Contents
Unit 1: Chronicity with Related Concepts...................................................................................................................................................4
Unit 2: Introduction to the Care of the Paediatric Client.............................................................................................................................7
INTRODUCTION........................................................................................................................................................................................7
COMMUNITY............................................................................................................................................................................................8
Unit 3: Fluid & Electrolyte........................................................................................................................................................................10
FLUID.....................................................................................................................................................................................................10
ELECTROLYTES......................................................................................................................................................................................16
CASE STUDY FLUID & ELECTROLYTE................................................................................................................................................17
Unit 4: Principles of Hemodynamics.........................................................................................................................................................19
CLIENTS WITH HYPERTENSION..............................................................................................................................................................19
CASE STUDY HEMODYNAMICS...........................................................................................................................................................25
Unit 5: Pain Theory and Assessment.........................................................................................................................................................26
Unit 6: Care of the Client with Chronic Pain both Adult and Child.......................................................................................................29
Unit 7: Clients with Rheumatic Disorders.................................................................................................................................................37
ARTHRITIS..............................................................................................................................................................................................37
Unit 8: Paediatric Client with Upper Respiratory Disorders.....................................................................................................................42
Unit 9: Clients with Altered Endocrine Function......................................................................................................................................50
Unit 10: Head-to-Toe Sexuality and Illness............................................................................................................................................61
Unit 11: Clients with Altered Glucose Homeostasis (Diabetes Mellitus).................................................................................................63
Unit 12: Paediatric Client with Chronic Respiratory Disorders................................................................................................................70
ASTHMA.................................................................................................................................................................................................75
CYSTIC FIBROSIS....................................................................................................................................................................................79
Unit 13: Clients with Altered Nutrition and Absorption Liver and Pancreas.........................................................................................83
Unit 14: Adult Chronic Respiratory Disorders..........................................................................................................................................94
ACIDBASE BALANCE AND ARTERIAL BLOOD GASES (ABG)..............................................................................................................94
CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)....................................................................................................................100
TUBERCULOSIS.....................................................................................................................................................................................104
Unit 15: Care of the Client with Hematologic and Immune Disorders...................................................................................................106
IMMUNE SYSTEM.................................................................................................................................................................................117
Unit 16: Care of the Client with Dysrhythmias.......................................................................................................................................122
Unit 17: Clients with Coronary Artery Disease and Acute Coronary Syndrome....................................................................................130
CORONARY ARTERY DISEASE (CAD)..................................................................................................................................................130
ACUTE CORONARY SYNDROME (ACS)................................................................................................................................................132
Unit 18: Clients with Heart Failure.........................................................................................................................................................146
CORONARY ARTERY DISEASE (CAD)..................................................................................................................................................146
Unit 19: Clients with Cancer...................................................................................................................................................................156
SURGERY..............................................................................................................................................................................................167
experience upward, downward or stable periods for several weeks or months. The following is a synopsis of the phases of an
illness trajectory and the implications for nursing management.
o Corbin and Strauss 1991.
o Updated 2002 page 30 of your text.
Coping tasks change throughout course of illness.
Illness trajectory = course of illness.
Illness trajectory can be uncertain:
o Textbook trajectory (i.e., it progresses as expected)
o Patients perception of own trajectory
o Health care providers perception
o Actual trajectory of illness as it unfolds
Influences of the Trajectory:
o Individuals perception
o Familys perception
o Resources (recall the determinants of health, especially the social determinants of health)
o Past experiences
o Lifestyle, beliefs, values, culture
Its important to consider ones culture and lifestyle as these elements often do not change (e.g., a fatty diet in
certain cultures).
o Motivation (individual and family)
o Relationship with care provider
The trust established between the HCP and the patient is very important.
Health problems
o Unique to paediatrics
Bronchiolitis is more common in children.
o Frequency in paediatrics
o Signs and symptoms
Some children display different signs and symptoms than adults for similar problems.
o CPR/BLS
Pharmacokinetics (ADME)
Safe med administration
o All medications are delivered based on weight and surface area.
o Their physiology is also different than adults (e.g., blood proteins).
Family & caregiver dynamics
o Therapeutic relationship vs. Friendship
o Bonding vs. Conflict vs. Control
Families and children
o Variety and values
o Culturally different parenting? Parenting that is less than optimal? Parenting that is different? Parenting that may be
harmful??
Play!
o Child Life Specialists
Education
o Health
o Development
o Hospitalization
Child decision-making
o Consent vs. assent
Abuse and neglect
Advocacy
o but peds
You need glucose and O2 to make ATP. Bi-products of Glycolysis and the Citric Acid Cycle are CO2 and H2O.
10
Osmosis
Going back to our question earlier, how do we maintain fluid volume (and essentially blood pressure) when we lose fluid either
through insensible volume loss or failure to replenish?
o Hydrostatic pressure shifts fluid out of the capillaries. When this happens, albumin is left behind in the capillaries.
When the levels of albumin start to rise due to all this fluid loss, it will draw fluid back in the capillaries (i.e., oncotic
pressure).
More on this later..
Fluid Shifts
What happens when the fluid shifts from the plasma to interstitial?
o The cells will swell and there will be a decrease in plasma volume (which will lead to blood pressure and edema).
Interstitial fluid to plasma?
o The cells will shrivel and there will be an increase in plasma volume (which will lead to blood pressure).
If the fluid is in your blood, that fluid will be strained by the kidneys and excreted. If the fluid is in the interstitial space, it will
not be excreted and the patient will therefore gain weight.
The pressure in the lungs is quite low so it can take O2 in the body. Recall that blood pressure is 120/80, which is the pressure the
body has to overcome.
11
Second spacing
o Abnormal accumulation of interstitial fluid (e.g., edema).
Third spacing
o Fluid accumulation in part of body where it is not easily exchanged with ECF (e.g., ascites, edema with burns).
Burns often look shiny due to the edema.
It also secretes hormones that control the release of hormones from the anterior pituitary.
ADH, also called vasopressin, is a nonapeptide that is produced in the magnocellular system of the
hypothalamus, specifically within cells of the supraoptic and paraventricular nucleus. The hormone is synthesized
and packaged in neurosecretory granules with a protein, neurophysin. The granules flow along the axons of these
cells to the nerve endings in the posterior pituitary where they are stored. ADH is released from the nerve endings
by exocytosis in response to stimulation of the neurons.
Pituitary regulation
o Anterior Pituitary Hormones
FSH, LH, ACTH, TSH
(Tropic Hormones)
Prolactin
, GH
(Direct Hormones)
o Posterior Pituitary Hormones
As mentioned above, ADH/Vasopressin is synthesized in the hypothalamus and is transferred to the
posterior pituitary, where it is eventually released.
Adrenal cortical regulation
o Renin is synthesize in the kidneys and via the Renin-Angiotensin-Aldosterone system, causes an increase in water
retention.
Renal regulation
Cardiac regulation
Gastrointestinal regulation
Insensible water loss
Renin-Angiotensin-Aldosterone System (see Human Phys notes and p. 511 & 517 of Human Physiology)
Know
this!
Renin comes from the kidneys and goes to the liver where it converts to angiotensin-I. It then goes to the lungs to become
angiotensin-II. The kidneys secrete renin when the blood pressure is too low, which will stimulate water reabsorption.
The aldosterone draws Na+ back in the body, which is followed by water. This water comes firstly from the interstitial space, and
if there is not enough there it comes from the intracellular space (when there is no water in the tubules).
Aldosterone belongs to a class of hormones called mineralocorticoids, also produced by the adrenal glands. It helps maintain
blood pressure, water, and salt balance in the body by helping the kidney retain sodium and excrete potassium. When aldosterone
production falls too low, the kidneys are not able to regulate salt and water balance, causing blood volume and blood pressure to
drop.
12
CO
BP
Neural
respons
e
Renal
respons
e
Sympathetic
NS activated
Renin (kidneys)
+
Angiotensinogen
(liver)
Norepinephrin
e
-blockers, 1
blockers
ADH
Retains
water
Angiotensin
I + ACE
Vasoconstrictio
n
BP
Hormon
al
respons
e
Angiotensin II
Increases
blood volume
Vasoconstricti
on
Aldosterone
(adrenal
cortex)
BP
Retention of Na+
and water
Sympatholyti
cs
BP
blood
volume
BP
Renal response
o ACE is found in the blood vessel epithelium.
o ADH comes from the posterior pituitary (ACTH comes from the anterior pituitary).
o Aldosterone comes from the adrenal cortex.
o Angiotensin II antagonist/ACE inhibitor (ACEi) in BP
o Giving a diuretic will cause a decrease in volume, thus decreasing BP.
Receptors Responses
Adrenergic agonists
- Arterioles (vasoconstriction)
1 - Pupils (dilation)
- Heart rate
1 - Contractility
- Automaticity
- Conduction
- Bronchioles (dilation)
2 - Arterioles (vasoconstriction)
13
Blood
vessels
Iris
Gut
Liver
Urinary
bladder
Piloerector
muscle
Sweat
glands
Vasoconstriction
Pupil
dilation
(mydriasis
)
Decreased
peristalsis
Glycogen
breakdow
n
Decreased
voiding
Goosebum
ps
Sweating
Blurred
vision
Constipati
on
Increased
blood
sugar
Urinary
retention
Reduction
in
congestio
n
Increase in
systemic vascular
resistance (SVR)
Increase
in blood
pressure
Nasal
decongestion
Ocular
decongestion
Hypertension
2 agonists
Bronchioles
Skeletal
muscles
Pancreas
Liver
Skeletal
muscle,
coronary,
and cerebral
circulation
Triggers
bronchodilati
on
Triggers fine
muscle
tremor
Increase
insulin
secretion
Trigers
glycogen
breakdown
Trigers
vasodilation
Fall in serum
K+ levels
Rise is blood
glucose level
Increase in
tissue
perfusion
Uterine
smooth
muscle
Heart
Induces
relaxation
Trigers
increased
rate and
force of
contraction
1 agonists
Juxtaglomerular
apparatus
Heart
muscle
Gut
Adipose
tissue
Increases
blood lipid
levels
Stimulates
renin
release
Increases
heart rate (+
chronotropic)
Increases
force of
contraction
(+
inotropic)
Decreases
peristalsis
Increase in
angiotensin
II
production
Increases in
cardiac
output and
workload
Increases in
cardiac
output and
workload
Constipatio
n
Increase in
blood
pressure
Increase in
blood
pressure
Increase in
blood
pressure
14
Hypovolemia
Hypervolemia
Dehydration
Edema
Fluid Assessment
History
o Conditions that affect F&E
Kidney problems, obesity, diabetes, endocrine disorders, metabolic disorders.
o Medications
Diuretics (e.g., loop and thiazide diuretics).
Loop diuretics will excrete Na+ and K+. Normal range of K+ is 3.5-5 mmol/L. The body cannot
tolerate large changes in K+ levels. It is important to look for patterns (e.g., in the last few days) and
not merely at a single point during the day.
o Abnormal loss
Nausea, vomiting, diarrhoea.
o Diet
Water, salt, proteins.
Strict vegan and vegetarian diets must have protein from another source (e.g., legumes, nuts, etc.).
A high sodium diet will cause an increase in water retention.
o Intake
Follow Canadas Food Guide.
Urine Volume/Concentration
1mL/kg/hr (range 0.5-2 mL/kg/hr)
Decreased urinary output (shock, renal/cardiac disease)
Increased urinary output (diabetes mellitus and diabetes insipidus)
Specific gravity
o Proportional to the amount of water in the body. This value is typically more important for that reason.
Urine Osmolality
o This is strictly the urine concentration.
In/Out/Weight
Accuracy NB
o In = ice, soup, ice cream
o Out = urine, feces, emesis, sputum
Note paediatric, weigh diapers.
Compare cumulative balance.
Frequency of checks depends on fluid status.
o WEIGHT 1kg = 1L of fluid.
o WEIGHT is the best way to monitor fluid balance!
15
Changes in GI tract
o Less able to absorb available fluids.
Considerations in Children
Larger total body water.
Larger ECF (both interstitial and plasma)
Need more fluid intake and output relative to size.
Exchange more fluid across capillary membranes daily than adults.
Immature renal function (i.e., it may not conserve as much Na+).
Infant has greater body surface area.
Skin and GI considerations.
Cardiovascular considerations.
o They will have a lower BP.
NOTE:
o Infant is less able to handle large quantities of solute free water than an older child.
o Should use Pedialyte (contains electrolytes) rather than water.
o It is important to rehydrate SLOWLY with Pedialyte.
ELECTROLYTES
Electrolytes Review
Substances that dissociate in solution = ions
Cations = positive charged electrolytes
Anions = negatively charged electrolytes
Functions:
o Help regulate water & acid/base balance.
o Contribute to enzyme reactions.
o Essential to neuromuscular activity.
Sodium
Imbalances are typically associated with parallel changes in osmolality. That is because where ever sodium goes, water follows.
Plays a major role in:
o ECF volume and concentration.
o Generation and transmission of nerve impulses.
o Acid-base balance.
Potassium
Potassium major ICF cation.
90% of potassium intake is eliminated by the kidneys.
o If someone has kidneys problems, they are likely unable to eliminate K+. This will lead to issues with the heart as it
cannot tolerate changes in K+ levels.
Potassium is necessary for:
o Transmission and conduction of nerve impulses.
o Maintenance of normal cardiac rhythms (e.g., may affect pulse).
o Skeletal muscle contraction.
16
Calcium
Obtained from ingested foods.
More than 99% combined with phosphorus and concentrated in skeletal system.
Aids coagulation.
Bones are a readily available store of calcium.
Magnesium
50-60% contained in bone.
A coenzyme in metabolism of protein (protein synthesis) and carbohydrates.
Modifies nerve impulse transmission and skeletal muscle response. These patients may have twitching.
Magnesium
(Mg2+)
Hypermagnesemia
Loss of DTRs (i.e., deep tendon reflexes)
Depression of CNS
Depression of neuromuscular function
Deficit
Hypocalcemia
Tetany
Chvosteks, Trousseaus muscle
twitching
CNS changes
EKG changes
Hypomagnesemia
Hyperactive DTRs
CNS changes
EKG changes
Phosphate
Phosphorus is primary anion in ICF.
Promotes energy storage and CHO, protein, and fat metabolism.
Deposited with calcium for bone and tooth structure.
Kidneys are major route of phosphate excretion.
Acts as hydrogen buffer in acid/base function (more on this later).
Deficit
Hypophosphatemia
Parasthesias
Muscle weakness
Confusion, delirium
Question
Several conditions will cause multiple imbalances of electrolytes. Identify three electrolyte imbalances that are caused by the
following:
17
b.
c.
Hyperaldosteronism (e.g., if you had too much aldosterone, what would your electrolytes look like?)
Aldosterone is a hormone that is produced by the adrenal glands. It works primarily on kidney (renal) cells to
help maintain the balance of fluids and electrolytes in our bodies. It mainly works to control reabsorption of
sodium and chloride and secretion of potassium and hydrogen. If aldosterone production is not functioning
properly, there can be serious consequences to the heart, kidneys and electrolyte balance.
They would have hypernatremia, followed by hypokalemia.
Chronic Renal Failure
Hyperkalemia, hyperphosphatemia.
Loop and thiazide diuretics
H4 may have many kidney infections.
Protein Imbalances
Plasma proteins, particularly albumin, are significant determinants of plasma volume. Recall how older adults and children have
fewer albumins in their blood, making them more susceptible to drug toxicity from the free drug in the blood stream.
Having too much protein is rare.
Client Profile
Kathleen B., a 74 year old woman who lives alone, is admitted to the hospital because of weakness and confusion. She has a
history of chronic heart failure and chronic diuretic use.
Objective Data
Neurological: confusion, slow to respond to questioning, generalized weakness
Cardiovascular: BP 90/62, HR 112 and irregular, peripheral pulses weak; ECG indicates sinus tachycardia (normal wave but it is
fast)
Pulmonary: respirations 12 per minute and shallow
Additional findings: decreased skin turgor; dry mucous membranes
Electrolyte
Normal
K.B.
V
levels
s Levels
erdict
Na+
135-145
141
N
mmol/L
mmol/L
ormal
K+
3.5-5
2.5
L
mmol/L
mmol/L
ow
Cl
98-106
85
L
mmol/L
mmol/L
ow
HCO3
24-30
43
H
mmol/L
mmol/L
igh
Mg2+
0.75-0.95
mmol/L
Calcium (serum)
2.18-2.58
total
mmol/L
Calcium (serum)
1.05-1.30
18
Albumin (serum)
Cholesterol
2)
3)
4)
5)
6)
mmol/L
35-50 g/L
<5.2
mmol/L
Osmolality
280-300
mmol/kg
Iron
11-32
mol/L
Which physical assessment findings support your analysis? Which laboratory results support your analysis? What is the most
likely etiology of these imbalances?
Physical assessment
o See above.
Lab values
o See table.
Etiology
Explain the reasons for Kathleens ECG changes.
Increased HR.
Why has Kathleens advanced age placed her at risk of a fluid imbalance?
With age comes certain physiological changes (e.g., decrease in plasma protein levels, decreased water volume,
decreased kidney function, decreased thirst).
Discuss the role of aldosterone in the regulation of fluid and electrolyte balance. How will changes in aldosterone affect
Kathleens fluid and electrolyte imbalances?
It works primarily on kidney (renal) cells to help maintain the balance of fluids and electrolytes in our bodies. It mainly
works to control reabsorption of sodium and chloride and secretion of potassium and hydrogen.
While she is in the hospital what daily assessments should be included in her plan of care?
Measure her I&O.
The K+ is dangerously low so that must be dealt with. Shell likely be on a KCl treatment.
Stop giving her diuretics.
Take her vital signs q4h.
19
Hemodynamics
Depends upon:
o Adequate blood volume.
o Adequate amount oxygen in blood.
o Effective pump (i.e., heart).
o Effective vessels (particularly the arteries).
o Effective nervous system.
Principles of Hemodynamics
Fluid flows from high to low pressure.
Pressure is generated by ventricular contraction.
Pressure gradient forces blood through arteries and capillaries into veins (recall hydrostatic and oncotic pressure).
Pressure gradient in pulmonary circulation are lower than systemic circulation.
Hemodynamics
Cardiac oxygen consumption
o Myocardium high need for oxygen.
o Volume of O2 is determined by the amount and type of exercise.
o The heart takes ~60-70% of oxygen from arterial blood. The brain also requires a lot of O2.
Workload
o Increased O2 demand = increased flow of O2 blood
Cardiac Output
o CO = HR X SV
o Amount of blood pumped from the ventricles in 1 min.
o Why is cardiac output so vital?
It delivers oxygen, glucose, electrolytes, etc. to the body.
iClicker time
What is cardiac reserve?
a. Peripheral resistance encountered by the left ventricle
This is afterload.
b. The force opposing the movement of blood
Systemic vascular resistance.
c. Ability to increase cardiac output
We can increase it by 3-4 times.
d. The addition of the diastolic pressure to 1/3 of the pulse pressure
Mean arterial pressure (MAP)
It is the difference between the amount of blood in the ventricles and the amount they eject during systole.
20
Afterload
o The resistance that the ventricles have to pump against during systole.
Contractility
Contractility is enhanced by:
o Catecholamines
Epinephrine and norepinephrine.
o Sympathetic Nervsous System (SNS)
o Meds
Digoxin: it increases the contractility and the heart rate slows down because the contractility is more efficient
Contractility depressed by:
o Hypoxia
The heart needs O2 to run optimally.
o Acidosis
Any increase in K+ depresses contractility because of the ions inability to repolarize is slower.
o Meds
Digitalis drugs: decrease the heart rate
Calcium channel blockers (CCB): Ca2+ is required for adequate contractility
Ejection Fraction
The percentage of blood that is ejected from the heart with each beat.
o ~67% +/ 9% is normal
When is someone symptomatic?
o Symptomatic with activity: <40% ejection fraction
o Symptomatic at rest: <25% ejection fraction
o These people may be tired, dizzy, and pale.
Afterload
Ventricular wall tension during systolic ejection.
With an increase in peripheral vascular resistance, the heart will have to work harder in order to overcome that pressure. With
time the heart will get stronger and enlarge. This is a problem because it will then affect the pre-load (i.e., the amount of blood
that can enter the heart during diastole).
Resistance to ejection of blood from ventricles.
Heart Rate
Autorhythmic, SA node is controlled by the ANS.
For a short period of time, a normal heart can increase its rate by 3.
Sustained HR over 180 bpm will lead to:
o Workload,diastole, CO
Its important to look at patterns!
21
BP Regulation Mechanisms
The radius of the small arteries and arterioles is the principle factor
Parasympathetic (cholinergic) HR, BP,
determining vascular resistance. A small change in the radius will lead to
GI motility
Autonomic Nervous
big changes in the systemic vascular resistance (SVR).
System
The mechanisms that affect BP can affect the cardiac output, the
systemic vascular resistance, or both.
Short Term
o Involve SNS and vascular endothelium.
Sympatheti
Parasympathetic
c
SNS activity
HR and contractility
Widespread vasoconstriction of peripheral
arteries
Fight or
Rest and Digest
Flight
Promotes the release of renin
Net effect is to CO and SVR.
Changes in blood pressure are sense by baroreceptors.
NE activates receptors in the SA node, myocardium, and
Stressful
Quiet
situations
activities
vascular smooth muscle.
1, 2, and 1 cause vasoconstriction when stimulated.
2 causes vasodilation when stimulated.
The sympathetic vasomotor centre in the medulla
Expend
Conserve energy
interacts with the brain to control blood pressure.
energy
Baroreceptors are located in arteries and the arch of the
aorta. When stretched by an BP, they send inhibitory signals to the sympathetic vasomotor centre to BP by
the HR, the force of contraction, and vasodilating the peripheral arterioles. A in BP causes
baroreceptors to SNS activity. With prolonged hypertension, the baroreceptors sense the BP as normal
and will stop sending messages to the vasomotor centre.
Vascular endothelium
Nitric oxide (NO), a potent vasodilator, helps maintain low arterial tone and prevent platelet
aggregation.
Endothelin (ET) is an extremely potent vasoconstrictor.
o Active in seconds to hours.
o Do not return BP to normal.
o Lose efficiency within hours to days.
Long Term
o Involves renal and hormonal processes (e.g., renin-angiotensin-aldosterone system).
Renal system
The kidneys regulate BP by controlling Na+.
Prostaglandins are vasodilators secreted by the adrenal medulla.
Angiotensinogen (from liver) Renin (from kidney) Angiotensin-I ACE (in lungs) Angiotens
22
The hypothalamus synthesizes ADH and stores it in the posterior pituitary. When sodium levels rise, it
signals it to release the ADH in order to retain water and thus [Na+].
Active in days to weeks.
Hypertension - Definition
Hypertension is sustained elevation of BP.
o Systolic blood pressure 140 mm Hg.
o Diastolic blood pressure 90 mm Hg.
Canadian Hypertension Society stipulates normal BP is 120/80.
o www.hypertension.ca
Classification of Hypertension
Primary (Essential) Hypertension
o Elevated BP without an identified cause (relating to disease processes such as kidney failure or diabetes). Having a high
Na+ diet would still constitute primary hypertension.
o This accounts for the majority of cases.
Secondary Hypertension
o Elevated BP with a specific cause (relating to disease conditions).
Primary Hypertension
Several contributing factors:
o SNS activity
o Sodium intake
Processed foods, canned drinks, sauces, certain dairy products, etc.
The average adult should have roughly 1,500mg of sodium. This amount decreases with age.
o Excessive alcohol intake
Obesity
Ethnicity (e.g., Aboriginals and African Americans are
more likely of getting high blood pressure)
Age
Secondary Hypertension
Contributing factors:
o Coarctation of aorta
o Renal disease
o Endocrine disorders
o Neurologic disorders
These factors must be dealt with in order to get rid of the hypertension more permanently.
iClicker time
While performing blood pressure screening at a health fair, the nurse counsels which of the following visitors as having the
greatest risk for developing hypertension?
a. A 56-year-old man whose father died at age 62 from a stroke
b. A 30-year-old female advertising agent who is unmarried and lives alone
c. A 68-year-old man who uses herbal remedies to treat his enlarged prostate gland
d. A 43-year-old man who travels extensively for his job and exercises only on weekends
Epistaxis (nosebleeds)
Dyspnea
Palpitations, angina
Fatigue, reduced activity tolerance
Hypertension Complications
23
24
Testing for secondary hypertension is not usually done as most hypertension is primary.
o
o Collaborative Care Strategies for Adherence to Regimens
What can we do as nurses?
o Encourage patients to stick to their medication regimens, diet by giving them realistic targets. It is important that
medications are taken regularly!
o Empathy increases patient trust, motivation, and adherence to therapy.
Consider patients cultural beliefs and individual attitudes in formulating therapy.
o
Goal is to reduce overall cardiovascular risk factors and control BP by the least intrusive means possible.
Follow-up monitoring of the BP is very important.
o
Health History
o Medications
o BP consistently >140 mm Hg
o Functional health patterns
o Presence or absence of target organ damage and CVD
o
Lifestyle Modifications
o Dietary changes
o Limitation of alcohol intake
o Regular physical activity
o Avoidance of tobacco use
o Stress management
o
Nutritional Therapy
o Sodium restriction
o Diet rich in vegetables, fruit, and non-fat dairy products
o Calorie restriction if overweight
o
o
Drug Therapy
o Reduce systemic vascular resistance (SVR)
o Decrease volume of circulating blood
ACE inhibitors and angiotensin-receptor blockers (ARBs) are not given together!
o Diuretics
o Adrenergic inhibitors
o Direct vasodilators
o Angiotensin inhibitors
o Calcium channel blockers
o
Drug Therapy and Patient Teaching
o Identify, report, and minimize side effects
o Achieve and maintain the individually determined target BP
o Understand and implement the therapeutic plan
o Experience minimal or no side effects of therapy
o
o Ambulatory BP Monitoring (ABPM)
It is when patients will be given the tools required to measure their blood pressure at home as they may get the white coat
syndrome.
o
o Hypertension in Older Persons
More than two-thirds of people over 65 have hypertension.
This population has the lowest rates of BP control.
Treatment, including those with isolated systolic hypertension, should follow same principles outlined for general care of
hypertension.
o
25
Joan is a lively 78-year-old Aboriginal woman who comes to your clinic for a follow-up visit. She was diagnosed with
HTN 2 months ago and was started on HCTZ 25 mg 4x/day. She stopped taking the pills as they made her dizzy and she
had to keep getting up at night to void. Her mother died from a CVA at age 70. Father died from MI at 67. Brother alivehas CAD, DM, and HTN. Initial vitals were BP: 160/102, P: 78, RR: 16, T: 37.
o
1) What is going on with Joan?
Her BP is high.
2) What clinical manifestations is she exhibiting?
Hypertension.
3) What should you do immediately? For discharge? Follow-up?
o
o
26
o Pain
Pain is one of the major reasons people seek health care.
Nurses have a central role in pain assessment and management.
o
o Nursing Roles
Assessing pain and communicating this information to other health care providers.
Ensuring the initiation of adequate pain relief measures.
Evaluating the effectiveness of these interventions.
o
o Magnitude of the Pain Problem
o Do not memorize numbers for test.
11-12% of Canadians aged 12 and over report moderates to severe pain interfering with ADLs.
Although 90% of cancer pain can be controlled, 40-80% of patients with cancer report moderate to severe pain.
50% of the elderly living in the community experience pain.
70% of the elderly living in personal care homes experience pain.
o
o Pain in Children
Headache (H/A) prevalence by:
o Age 7: 37-51%
o Age 7-15: 57-82%
Chronic knee pain: 11.3% boys, 12.6% girls
Fibromyalgia age 9 12: 57 per 100,000
Jaw pain 0.2 12%
o
o Patient Related Barriers to Pain Control
Belief that pain cannot be relieved.
Not wanted to be a complainer.
Not wanting to distract doctors from treating the illness.
Fear of addiction.
Fear of tolerance.
Fear of side effects.
o
o Health Care Provider Related Barriers to Pain Control
Pain relief is not seen as a treatment goal.
Inadequate or non-existent pain assessment due to lack of knowledge/skills.
Under-treatment.
Fear of addiction, sedation, respiration, depression, and other opioid side-effects.
Perceptual differences between patient and provider.
o
o Definition of Pain
Whatever the person experiencing the pain says it is, existing wherever the person says it does (McCaffery 1968).
An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such
damage (International Association for the Study of Pain).
o Description of Pain
Subjective experience.
Patients experience and self-report is essential if possible.
Affected by culture, meaning of situation, individual factors.
o
o Pain & Cultural Influences
Culture influences expression and perception of pain.
Beliefs/attitudes affect how one interprets, perceives, and responds to injury/illness.
Pain may have a personal meaning influenced by culture.
27
o It is very likely that a nurse will not treat their pain adequately.
o
o Nociception vs. Suffering
Suffering can occur independently of tissue damage.
o
o Nociception
Nociception is the activation of the primary afferent nerves with peripheral terminals (free nerve endings) that respond differently
to noxious (tissue-damaging) stimuli.
Nociceptors function primarily to sense and transmit pain signals.
o
o Suffering
State of severe distress associated with events that threaten the intactness of the person.
Pain is not synonymous with suffering.
o E.g., you can treat some pain with opioids, but you cannot treat suffering with opioids.
Suffering can occur in the presence or absence of pain.
Pain can also occur with or without suffering.
o
o Total Pain
Pain is a MULTI-DIMENSIONAL experience.
Need to consider all factors, not just physical. Other kinds of pain are nociceptive, somatic, visceral, neuropathic, behavioural,
sensory, cognitive, psychological.
o
These dimensions are
important!
o Dimensions of Pain Sensory
The sensory component of pain is the recognition of the sensation as painful.
Sensory-pain elements include:
o Pattern (i.e., location)
o Area (i.e., radiation)
o Intensity (e.g., pain scale; what is it now; what is the best it ever gets; what is the worst it ever gets)
o Nature (what does it feel like: this is very subjective is it aching, dull, burning, sharp, etc.)
Electricity: burning, shooting, tingling, etc.
o This could be from neuropathic pain, which requires a different set of medications than those required to deal with
visceral or somatic pain.
o
o Dimensions of Pain Affective
The affective component of pain refers to the emotional responses to the pain experience.
o Anger, fear, depression, anxiety, etc.
Someone who is very nervous and anxious will not deal with the pain as well as someone who is not.
o
o Dimensions of Pain Behavioural
The behavioural component of pain refers to the observable actions used to express or control the pain.
o Facial expressions such as grimacing
o Posturing
o A person adjusts their daily physical and social activities in response to pain
o
o Dimensions of Pain Cognitive
The cognitive component of pain refers to beliefs, attitudes, memories, and meaning attributed to pain.
Cognitions influence the ways in which a person responds to the pain and must be incorporated into the comprehensive treatment
plan.
This is different from the affective perspective.
o E.g. of a person who had a hip tumour that was cured. Should they get hip pain there in the future, that pain will be a lot
more anxiety provoking than that same pain in a person who never had the experience of the hip tumour.
Meaning of the situation! This cognitive element cannot be treated with opioids.
o
o Dimensions of Pain Sociocultural
The sociocultural dimension of pain encompasses factors such as demographics, support systems, social roles, and culture.
Age, gender, and education have been found to influence pain beliefs and coping strategies.
28
o
o Classification of Pain
According to its underlying pathology:
o Nociceptive pain physical
o Neuropathic pain electrical
Another way to classify pain:
o Acute
o Chronic
o
o Nociceptive Pain
Caused by damage to somatic or visceral tissue.
o Pain from a surgical incision.
o Arthritis.
o Cardiac ischemia.
Usually responsive to non-opioids as well as opioids.
o
o Somatic Pain
Aching or throbbing pain that is well localized.
Arises from bone, joint, muscle, skin, or connective tissue.
o
o Visceral Pain
May result from stimuli such as tumor involvement or obstruction.
Arises from internal organs such as the intestine and bladder.
o
o Neuropathic Pain
It is caused by damage or compression to nerve cells, or changes in spinal cord processing.
Described as burning, shooting, stabbing, or other terms that are electric in nature.
It can be sudden, intense, short-lived, or lingering.
It is not well controlled by opioid analgesics alone.
Treatment often includes the use of adjuvant analgaesics, including tricyclic antidepressants, anti-convulsants. By adding these
drugs, you can often decrease the opioid dose.
It can be centrally (e.g., fibromyalgia) or peripherally (e.g., shingles) generated.
E.g., shingles
o There is ongoing pathology in the nerve root.
o
o Acute and Chronic Pain
o Differences based on:
Causes
Course (acute pain has a shorter course; chronic pain lasts longer)
Manifestation
Treatment
o
o Acute Pain
Protective mechanism.
Informs of malfunction in the body.
Usually due to tissue damage.
Prevents further damage by limiting movement in injured area.
Time-limited: resolves when damage heals.
Even if severe, often tolerable b/c it is temporary (think of the process of labour).
As a nurse try get the patients mind on other things (e.g., walking about and moving other limbs if at all possible).
o
Sudden onset.
<3 months or as long as it takes for normal healing to occur.
Mild-to-severe pain (recall that this is subjective).
Generally can identify a precipitating event or illness (e.g., surgery).
o
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o Sociocultural
o
o Pain Treatment
Exercise is a great way for people to deal with back pain.
All pain treatment is guide by the same underlying principles:
1. The patient must always be believed.
2. Every patient deserves adequate pain management.
3. Treatment must be based on the patients goals (these goals must be realistic).
4. Treatment plans should use a combination of drug and non-drug therapies.
5. A multidisciplinary approach is necessary to address all dimensions of pain (e.g., nurses, physicians, Chaplin, etc.).
6. All therapies must be evaluated to ensure they are meeting a patients goals.
If drugs have been administered, it is vital to return to see how they are coping.
7. Drug side effects must be prevented and/or managed.
8. Patient and family teaching should be a cornerstone to the treatment plan.s
o
o Unit 6: Care of the Client with Chronic Pain both Adult and Child
o Myths about Pain in the Elderly
Pain is a natural consequence of aging. FALSE
Pain perception/sensitivity decreases with age. FALSE
Potential side effects of narcotics make them too dangerous to use in the elderly. FALSE
o Administer low doses and take it from there. The half-life is longer but that is no reason not to give them any.
Pain is a symptom of depression. FALSE
o Depression is sometimes a symptom of pain.
Narcotics are totally inappropriate for all patients with chronic non-malignant pain. FALSE
o
o Myths about Pain in Children
Newborn /infants dont feel pain due to immature nervous system. FALSE
o The opposite is in fact the case (i.e., they feel more pain).
Infants dont remember pain. FALSE
Children cry out of fear not pain. FALSE
Children need to learn to tolerate a little pain. FALSE
Children can become addicted; therefore its best not to expose them to strong opioids. FALSE
o
o Pain in the Elderly
Chronic pain often results in:
o Depression
o Sleep disturbances
o mobility
o health care utilization
o Physical and social role dysfunctions
Pain assessment tools may need to be adapted for the older adults:
o Vertical scales are better than horizontal.
o Most elders prefer using words be sure you both understand what they mean.
o Body outline draw or point to pain.
o Faces if non-English speaking or illiterate.
o Colour scale darkest color most painful.
o
o Pain Assessment in Children
Pre-verbal children
o It is important to listen to the family. The parents know their child best, ask them questions.
Differentiating anxiety/fear/pain
Health care providers knowledge deficit in pain assessment of children
o Again, the parents are a great source of information.
Presence of other symptoms
Role of parents/family members
Frequent or chronic uncontrolled pain: learned helplessness
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o
o Nursing Role Regarding Pain Management
Nurses are responsible for:
o Identifying the problem of inadequate pain management.
o Initial and ongoing assessment, communicate to colleagues.
o Develop plan of care with measurable goals and effective interventions.
o Implementing and coordinating pain management plan.
o Evaluating patient response & revising plan as needed.
o
o Nurses as Advocates
Pain must be recognized.
Nurse needs courage to be present.
Nurse must be ready to engage.
Nurse must be more empathetic than judgmental!
Nurse must be willing to educate self beyond nursing school education.
o
o Drug Therapy
Nursing role
o Obtain analgesic history
Ask them which medications they have taken in the last 24 hours.
When people have a migraine, they often have decreased gut motility, which will affect the drugs onset.
Differentiate between side-effects and allergies! For instance, nausea and constipation are side-effects of
morphine, not allergies.
Codeine: it is a pro-drug that metabolizes to morphine.
It is possible to be allergic to codeine but be able to take morphine. It is not possible to be allergic to
morphine and be able to take codeine. Some Asians lack the enzyme that breaks codeine down to
morphine.
o Codeine morphine
o 1/3 of Ethiopians and 1% of Caucasians are rapid metabolizers of codeine. This means that when
given codeine, their bodies will turn it into large amounts of morphine.
Opioid abusers have an altered threshold as their nervous system is shot.
o Opioid-induced neurtoxicity.
o Opioid-induced hyperalgesia: these people will require less drug!
o The cytochrome P450 pathway is used by codeine to turn into morphine.
o
o Paxil (an SSRI: anti-depressant) is a serious inhibitor of the Cytochrome P450 pathway! Many SSRIs will
inhibit the P450 pathway but Paxil is the strongest of the SSRIs. With that being said, a patient taking Paxil
and codeine (e.g., T3), they will not have any benefits of codeine as it will not get turned into morphine due to
the Cytochrome P450 pathway inactivation.
o
o Calculating equianalgesic dose
o Scheduling analgesic doses
o Titrating opioids
o Selecting from the prescribed analgesic drugs
o Monitoring and managing medication side effects
o Evaluating effectiveness of pain medication!
o Analgesic History
All medications used in past 24 hours.
PRN or scheduled use?
Current medications onset, duration, maximal analgesia.
Side effects, drug allergies, or phobias (i.e., many people are afraid to become addicted).
o
o Adjuvant Analgesic Therapy
Antidepressants
o Recall that they are also good to relieve headaches.
Anti-seizure agents
2-Adrenergic agonists
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33
34
Any longer and you may develop seizures from normeperidine toxicity. Using Narcan will not reverse the pain as it will
only release the Demerol from the receptors, therefore increasing the number of available receptors for the
normeperidine.
o Equianalgesia
Lack of knowledge of this is a common reason for under or over medication of patients.
Analgesics have different per mg potencies: 10 mg Drug X not necessarily equal to 10 mg Drug Y.
Need to know drug equivalence to properly assess efficacy/side effects when changing to different analgesic.
o In general, 10mg of Dilaudid = 50-75 mg of Morphine (i.e., Dilaudid is 5-7.5x stronger than Morphine).
Incomplete cross-tolerance: decrease dose by 25-50% when switching to a different medication.
o
o Dose Scheduling
Around the clock (ATC) or as needed (PRN).
PREVENTION is the key.
o ATC meds for constant pain.
o Give PRN meds as soon as pain starts (i.e., intermittent pain).
o Less analgesic is needed if the preventative approach is used.
Need to tech patients the importance of prevention.
The breakthrough dose is roughly 10% of the daily dose (e.g., if their daily dose is 100mg of a drug, the breakthrough dose is
10mg).
o
o Opioid Titration
Need to give enough medication to have the desired effect with the least side effects (i.e., the right dose).
May need to change route, interval, dose, or drug to get that effect. In general:
o If still in pain likely under-medicated
o If very sedated may be over-medicated
o If in pain but sedated possible wrong drug for patient
Nurse says The patient states he is in pain but he sleeps all day...this is a possible instance of this.
o If relief is adequate but not lasting inadequate frequency or dose
o
o Drug Selection
Patients will often have a range of medication or more than one analgesic ordered.
o It is not necessary to have a large drug list on the Kardex (e.g., Dilaudid, Morphine, T3, and percoset).
Tylenol #3 i-ii tabs q4-6h prn
How to decide which one to use:
o WHO ladder
o Use drug appropriate for pain
o
o Route Selection
PO route usually preferable.
Avoid IM route as there is variable absorption, and can cause scar tissue.
Sub-lingual: some meds absorbed via this route.
Transdermal fentanyl.
Peak concentration 24-72 hours after application.
Concentration decreases by 50% in 17 hours after removal.
o
o
o What is NOT an Analgesic
Pherergan (promethazine)
Valium (diazepam)
Ativan (lorazepam)
o
o All will increase sedation without enhancing analgesia.
o
o Pharmacotherapy in the Elderly
Increased sensitivity to analgesics due to age-related changes that alter absorption, metabolism, distribution, and excretion of
drugs.
35
More likely to have relief from lower doses and side-effects from higher doses.
No one drug is preferable.
START LOW and GO SLOW!
o
o Pharmacotherapy in Children
Should be managed as aggressively as in adults.
Use basic pain management principles.
Can be more difficult to assess pain and side effects.
Codeine in kids turns into morphine afterr being metaolized in the liver. Serious adverse effects. Genetically determined how
fast of a drug metabolizer you are. Variability in how one handles the drug. 1 in 10 people wont enjoy any benfits from codeine.
30% failure rate in Ethiopians. Important to ask if they have taken it before and what happened.
o
o Nursing and Collaborative Management
Effective Communication
o Patients need to feel confident that their reporting of pain will be believed and will not be perceived as complaining.
o The nurse needs to communicate concern and assure the patient that he or she is committed to helping the patient.
o If pt goals are not realistic, need to discuss honestly and compassionately.
o
o Addiction APS, AAPM, ASAM, 2001
It is a primary (its own entity), chronic, neurobiologic disease, with genetic, psychosocial, and environmental factors influencing
its development and manifestations.
It is not continuously asking for medications.
It is a primary, chronic disease of the brain reward, motivation, meemory and related to circuitry,
Dysfunction in these circuits leads to charisteristic biological, psychological, social and spiritual manifestations.
This is reflected in an individual pathologically pursuing reward and/or relief by substance use and other behaviouds.
o
o Characterized by the 4 Cs
Addiction is characterized by behaviours that include one or more of the following:
o Impaired control over drug use
o Compulsive use
o Continued use despite harm
o Craving
o
o Addiction
Craving a drug at escalating doses despite physical, psychological, and social consequences.
Pre-occupation with obtaining & using a substance, the use of which results in decreased quality of life.
NOT defined by symptoms of withdrawal ALONE.
Withholding opioid analgesics from chemically dependent patients with pain has NEVER been shown to increase the likelihood
of recovery from addiction. McCaffery
o
o
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37
Common language
o Pain rating scale, standardized tools.
Regular communication
Being honest with the patient.
o
o Ongoing, Consistent Evaluation
Monitoring the 4 As:
1. Analgesia (is there pain relief)
The problem is that deception is an inherent problem of addiction.
2. ADL (psychosocial functioning)
3. Adverse effects
When they come to the clinic/hospital, are they excessively sedated?
4. Aberrant drug taking behaviour
o
o Pain & Quality of Life: A Challenge
Talk to someone with chronic pain about:
o What quality of life means to them.
o How pain affects quality of life (QOL) for them and their family.
o How would life be different if they had no pain?
o
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39
Limitation of motion
Caused by the Pannus
Signs of inflammation
o
o
o Extra-articular Manifestations of RA
o Fig. 66-5 Image of woman
Every single system is affected (we will cover 3 of them).
Carpal tunnel syndrome
o This is because the nodules formed will take up space.
o
o Clinical Manifestations Extra-articular Manifestations
Three most common:
1. Rheumatoid nodules
They get bigger due to extravasation and will eventually decrease in size. They are typically not removed
(unless they cause extreme pain or are likely to open up).
Rheumatoid factors: autoimmune disease (meaning that the body produces antibodies)
o If the rheumatoid factor is high, 25% of people will develop nodules, which grow everywhere
(including the heart, cervical spine, any organ, the throat, etc.). These nodules can open up, causing
extreme pain.
2. Sjgren syndrome
10-15% of people with RA will develop this syndrome.
It can happen as a disease itself but often comes as a complication of RA. They have burning, gritty eyes,
decreased tearing, and photosensitivity.
Some anti-inflammatory drugs will cause the same signs and symptoms seen in Sjgren syndrome.
3. Felty syndrome
This is the worst case scenario of rheumatoid nodules. They are everywhere in your major organs.
o
o Complications
Flexion contractures and hand deformities seen in the joints.
Nodular myositis (i.e., the nodules are growing in the muscles) and consequently muscle fibre degeneration.
o
o Deformities of RA
o A ulnar drift
o B Boutrier
o C Hallus valgus (different from a bunion as there is less bone)
o D Swann neck
o
o Complications
Cataract development and loss of vision.
Rheumatoid nodules can ulcerate, similar to pressure ulcers.
Hoarseness.
Bone destruction from nodules in the vertebral bodies.
Cardiopulmonary effects later in the disease.
Carpal tunnel syndrome.
o
o Diagnostic Studies
Accurate diagnosis essential because you want to start treatment as early as possible
Positive Rheumatoid Factor (RF), which are antibodies, in 80% of patients
Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
o An elevated ESR is a sign of inflammation somewhere in the body (recall that this is characteristic of RA systemic).
o CRP responds to inflammation.
o
o Nursing Management
Goals are that the patient with RA will:
o Have satisfactory pain relief (look at this first).
o Have minimal loss of functional ability of the affected joints.
o Participate in planning and carrying out the therapeutic regimen.
o Maintain a positive self-image.
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41
o Osteoarthritis
Non-inflammatory disorder of the synovial joints (different from RA).
Slowly progressive.
More than 90% of adults are affected by age 40.
It occurs from damage to the cartilage.
Before 50 years, men are more likely to get OA. After 50 years, women are more likely to get OA due to menopause (i.e., in
bone mass and oestrogen levels).
o
o Etiology and Pathophysiology
Bodys attempts at repair cannot keep up with destruction (i.e., homeostasis becomes inadequate).
There are continued changes in collagen structure (its supposed to be white, soft, etc.) fissuring (at the level of the
chondrocytes) and erosion (the cartilage is not as pliable and it becomes yellow).
Central cartilage becomes thinner.
Cartilage and bony growth (osteophytes) increase at the joint margins (this causes the pain).
o During assessment you would feel crepitus.
o
o Clinical Manifestations
No systemic manifestations (unlike RA). There may still be heat, swelling, and other such signs of inflammation, but it is
localized within the joint in question.
Joint pain.
Most commonly involved joints:
o Distal interphalangeal (DIP)
o Proximal interphalangeal (PIP)
o Carpometacarpal joint of the thumb
o Weight-bearing joints (hips, knees)
o Metatarsophalangeal (MTP)
o Cervical and lower lumbar vertebrae
Deformity
o OA can also have nodules, like RA, only these nodes are painful (unlike RA, where the nodules are painless). As in RA,
these nodes are not typically removed.
o Heberdens nodes
DIP joints
o Bouchards nodes
Red and painful
PIP joints
o
o Diagnostic Studies
Bone scan
CT
MRI
X-ray
o This is because there is a problem with the cartilage and the bone.
ESR
o Localized ESR.
CBC
o Interested in the WBC count (due to synovitis).
o
o Collaborative Care
No cure.
Pain and inflammation management.
o Cortisone joint injections.
Prevent disability.
Maintain and improve joint function.
Drug Therapy
o Based on the severity of symptoms.
Mild anangelsics can cause more damage
o
42
o
o iClicker Questions
o To preserve function and the ability to perform activities of daily living, the nurse teaches the client with OA to:
a. Plan less stressful ways to accomplish ADLs.
o
o Naproxene, indomethacin, and ibuprofen are in the same family of drugs.
o
o Gout
Metabolic disorder of purine (protein) metabolism.
It is very painful and typically hurts the big toe.
o
Primary Gout
o Hereditary error: the body cannot metabolize the purine.
Secondary Gout
o Acquired disorder: too much meat and alcohol.
There are high levels of uric acid (i.e., an overproduction or the body cannot excrete it).
Acute gout: 1 joint affected
Chronic gout: up to 4 joints affected
o
o Complications
Pain
Joint deformity
TOPHI
o Formation of uric acid. If you cant excrete uric acid, it comes together to form crystals which are deposited in the big
toe. It can also ulcerate which may lead to infection.
Kidney stones
o Which may lead to pylonephritis.
o
o Pharmacology
Anti-inflammatory agents
o Ibuprofen, aspirin, acetaminophen.
The TOPHI is not supposed to be in the joints so the body will try fight it off.
Uricosuric Drugs
o Allopurinol.
It blocks the production of uric acid.
o Probenecid.
Anti-gout that increases uric acid excretion.
Antibiotics increase the synthesis of uric acid so Probenecid is sometimes used before the antibiotics are given
to ensure their half-life is extended.
o
o Nutrition
Limit red meat (e.g., sardines, muscles, moose).
Limit alcohol.
o
o Nursing Care
Immobilize the joint in question (for no more than a week for any joint!).
Avoid pain.
ROM exercises after the joint has been immobilized for no more than a week.
Lots of fluids for kidney stones
o
o Systemic Lupus Erythematosus
Chronic multisystem inflammatory disease.
Associated with abnormalities of immune system (i.e., autoimmune issues).
o Involves the lymphocytes (e.g., B cells and T cells).
Affects skin, joints, serous membranes, and renal, hematologic, and neurologic systems.
Africans, Natives & Asians are 3x more likely to get it than Caucasians.
o It is typically seen in women of childbearing age.
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o Etiology
o Clinical manifestations
o Therapeutic/nursing management
o Paediatric Upper Airway Differences
Smaller airways.
o Small amounts of secretions can block off the airway.
Smaller nasopharynx.
Rapidly growing lymph tissue.
Smaller nares.
Small oral cavity/large tongue.
High larynx and glottis.
Immature thyroid/cricoid and tracheal cartilage.
o This makes it easier to collapse.
Narrowest part of airway at cricoid cartilage (funnel shaped). Older child is vocal cords.
Underdeveloped respiratory muscles.
o They often use their abdominal muscles when breathing.
Upper A/W compliant, may narrow during inspiration.
Longer epiglottis.
Shorter trachea.
A/W increases in size and length after birth.
Steeper right mainstem bronchus.
Obligate nose breathers (for the first 4 weeks of life).
o Secretions in the nose make it hard to breathe. These patients will have their noses suctioned.
Chest wall more pliable.
Diaphragm primary chief muscle of inspiration.
o
o Why is this important?
Edema increases airway resistance 15X that of adult.
Proper positioning can open an airway.
o E.g., back rolls will be used when the child is lying down as this will force their airways open.
A paediatric airway can be quickly lost.
o
o Effects of Edema
o
o
o Why is this Important?
The primary type of arrest in children is respiratory arrest, often associated with loss of an airway.
Early recognition and treatment is essential.
Nurses are often the first to assess the paediatric patient.
Airway is the A in ABCs of Basic Life Support.
o
o Paediatric Respiratory Assessment
Never force a child to lie down.
Assess in the position they have chosen.
o Children often like to be in their parents lap. If theyre comfortable in their position, let them stay as such. Trying to
move them may cause them to get agitated and cause their airways to become closed off.
Care should be take with throat cultures or visual inspection
Keep with parent do not remove them from their parent.
45
Quality of voice/cry
Able to speak in full sentence
Position of child
Weight loss or gain
Chest pain
Vomiting
o When they cough often and hard, the vomiting
reflex is triggered.
Poor appetite or feeding
Sleeping patterns
Tonsillitis
Etiology
Viral (causes most cases): Herpes simplex, Epstein-Barr, Cytomegalovirus, Adenovirus, and the Measles virus
Bacterial: Streptococcus pyogenes is the cause for most bacterial tonsillitis
Pathogenesis
Infection/inflammation of palatine tonsils.
Clinical Manifestations
Frequent throat infections
Breathing /swallowing difficulties
Fever/headache
Ear pain
Redness +/- white patches to anterior pillars
Enlargement of cervical lymph nodes
46
Persistent cough
Therapeutic Management
Diagnosis is based on clinical manifestations and visual inspection.
Antibiotics usually Penicillin.
Treatment: symptomatic (i.e., treatment of the symptoms).
Nursing Management
Symptomatic
Acetaminophen
Cool fluids/popsicle/soft foods
o Use cool to decrease inflammation.
Salt water gargle
o The Na+ helps draw fluid out of the tonsilar beds.
Rest
Teach to take all antibiotics
Surgical Intervention
Removal of the tonsils.
o >3 years of age
3 infection/year X 3 years
Chronic tonsillitis
Obstructive sleep apnea
Malformation
+/- adenoids (pharyngeal tonsils)
Discharge
Pain management (e.g., Tylenol)
Fluid intake (e.g., cold fluids or soft food)
Activity restrictions
Complications
Follow-up appointment
Children are at a higher risk for bleeding 7-10 days following surgery.
Nasopharyngitis
Etiology
The common cold.
Most common illness of infancy and childhood.
Viral causes: rhinovirus and coronavirus.
Bacterial: streptococcus.
Pathogenesis
Pathogens spread when infected person touches hand of uninfected person.
Incubation 1-3 days.
47
Nursing Management
Symptomatic
Saline drops to nares of infants/suctioning
Humidifiers
Antipyretics
Decongestants over 6 months of age
Antihistamines
Encourage adequate fluid intake
Rest
Pharyngitis
Etiology
80% Viral: cause is a large number of enteroviruses
Bacterial: Strep. throat (group A beta-hemolytic Streptococcus)
Diagnosed with a throat swab (it is important to swab the entire throat, i.e., both sides).
Pathogenesis
Infection of pharynx +/- tonsils
Usually 4-7 year olds rare <1 year
Onset abrupt
Clinical Manifestations
Sore throat
Difficulty swallowing
Fever >38.3C
Headache
Tonsillar exudate +/ Abdominal pain
Tender nodes
Therapeutic Management
Penicillin
Erythromycin (if allergic to penicillin)
If drooling or dehydrated need to be seen by MD emergently
Nursing Management
Symptomatic
Antibiotics bacterial (Pennicillin)
Acetaminophen
Cool fluids/popsicle
Salt water gargle
Rest
Teach to take all antibiotics
Otitis Media
Etiology
48
Unknown
Related to eustachian tube dysfunction (typically because its blocked)
May be related to upper respiratory infection
75-95% all children by 6 years of age will have had an ear infection.
Boys typically get it more than girls
Bacterial: streptococcus pneumoniae, Haemophilus influenzae, moraxella catarrhalis
Highest in winter months due to the increase in upper respiratory tract infections.
Pathogenesis
Infection
Mucous membranes of eustachian tubes edematous
Air flow blocked, causing fluid to accumulate
Fluid pulled into air space
Medium for pathogens
Tympanic membrane and fluid infected
Clinical Manifestations
Tympanic membrane: red/bulging/retracted
Ear pulling
Fever
Hearing loss
Irritability
Ear popping
Rupture of TM
Therapeutic Management
Diagnosis based on otoscopic exam.
Antibiotics: Amoxicillin, Clavulin, Cefuroxime
Antibiotic use is controversial because it may be due to a viral upper respiratory tract infection.
Surgical Intervention
Children with bil. middle ear effusion and hearing deficiency > 20 decibels for >3 months
Myringotomy with
Typanostomy tube (T-tubes)
o Recommend ear plugs if going swimming.
Nursing Management
Centers on care of child at home
Antibiotics should see improvement in 24 hrs.
Prevention
Analgesia
Chew gum
Lie on unaffected side
Warm cloth
Bronchiolitis
Etiology
Viral: RSV respiratory syncytial virus (most common), Adenovirus
Bacterial
Most frequently in toddlers and preschoolers
Most severe if <6 months
< 2 months often hospitalized
Winter months - early spring
75-90% of PICU admissions
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Pathogenesis
Viruses invade bronchiole cells (lower respiratory tract)
Virus bursts Cell debris in airway
Edema from inflammatory process
Airway produces excessive mucous
Above causes obstruction of airways and diffusion impairment
Repeated in both lungs
Blocked airway stops expulsion of air, which leads to the wheezing/crackles
Air trapped below prevents normal gas exchange O2 less CO2 more
Respiratory failure
The virus can live on hospital gowns for up to 2 hours, 20-30 minutes on skin, and 6-7 hours on surfaces.
Clinical Manifestations
Nasal stuffiness
Cough
Fever
As progresses:
Wheeze
Deeper cough
Increased WOB (e.g., trach tugging, nasal flaring,
indrawing, etc.)
o Their respiratory rate may be in the 70s, 80s, 90s.
Off feeds
Bad cold
Therapeutic Management
Immunization (Palivizumab) for high risk patients (it is a short risk immunization that is to be given monthly).
Isolation for all suspected cases.
See Bronchiloitis Order Sheet and Clinical Scoring tool.
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<24 months of age with hemodynamically significant heart disease as assessed by paediatric cardiology.
Infants born 33-35 weeks gestational age and are living in or will reside in remote Northern communities
Other children <24 months of age may be considered on individual basis (e.g.,Respirology, infectious diseases, cardiology,
genetics, or haematology/oncology).
Other infants born 33-35 weeks gestational age deemed to be at high risk for hospitalization for RSV:
o Born November 2010 to March 2011
o Male
o Small for gestational age (BW<10th percentile)
o Patient or sibling attends daycare
o >5 people living in the home
o 2 or more smokers in household
Vaccines do not necessarily mean that the child will not get any health issues. It does, however mean that the severity will be
decreased.
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Laryngotracheitis
Parainfluenza I or II, RSV, influenza
T <39C
Hoarseness
Barking-seal cough
Sore throat
Stridor
Progresses to laboured respirations
Most common
Laryngotracheobronchitis
parainfluenza I or II, RSV, influenza
T <39C
Hoarseness
Barking-seal cough
Sore throat
Stridor
Progresses to laboured respirations, increasing stridor, cyanosis
Most serious if untreated
Bacterial Tracheitis
Staphylococcus
Fever>39C
Barking-seal cough
Stridor
Purulent secretions
Guarded prognosis requires close observation
Therapeutic Management
L-epinephrine
Dexamethasone
Antibiotics as appropriate (bacterial)
Cool air (i.e., open a window in the house, go for a car ride with the windows down, get a cool air humidifier)
Nursing Management
Frequent airway assessment due to the inflammation
Humidified O2 as tolerated
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Epiglottitis
H-flu (incidence less since vaccine introduced)
Fever>39C
Preceded by URTI (upper respiratory tract infection)
Intense sore throat
Drooling
Stridor
Increase HR and RR
Prefers sitting upright
Medical Emergency
o This is because the inflamed epiglottis can cause an obstruction.
o Looking at a lateral neck X-ray, you will see the characteristic thumb print of the swollen epiglottis.
Management
o Intubation
o Sedation
o IV fluids
o Antibiotics
o Cast arms when intubated so they will not try rip them out
Videos
RSV Patients
RSV and pertussis.
Exam Information
Know the information that relates to the objections outlined in the syllabus.
Lecture Plan
Introduction and Review of Endocrine System
Care of the client with thyroid and parathyroid dysfunction
Care of the client with imbalances of hormones produced by the adrenal cortex
Care of the client with endocrine disorders characterized by excess and deficits in fluid volume
Feedback Mechanism
Hypothalamus:
Releasing hormone
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Anterior pituitary:
Stimulating hormones
Effect!
Thyroid
When palpating for the thyroid, stand behind them, have their head turned to the side and swallow. In a healthy individual you
should not feel the thyroid.
It regulates metabolism. It produces T4 (thyroxine), T3 (triiodothyronine), and calcitonin. The measure is three T4 and TSH
levels. T3 is very potent and is not present in as large of quantities. These levels are important because it is important to
determine if a patient has primary or secondary thyroidism.
Hypothyroidism
Etiology and Pathophysiology
Iodine deficiency.
o Iodine is required for the thyroid gland to synthesize T3 and T4. Salt has been iodized but the reason there is deficiency is
because people are changing their lifestyles in the following ways:
Vegetarians do not consume meat and therefore consume soy as their protein. Soy blocks the uptake of iodine.
Atrophy is the end result of Hashimotos thyroiditis and Graves disease.
o These are autoimmune diseases.
Other reasons:
o Iatrogenic
Hyperthyroidism was treated and hypothyroidism was the result.
o Surgery
T4 is required for metabolism therefore hypothyroidism can lead to weight gain. This lack of metabolism will also lead to
lethargy.
Clinical Manifestations
Cardiovascular System
o There will be a decrease in CO so the body will compensate with an HR. A continuous increase in HR can lead to
cardiac hypertrophy. If a patient has cardiac hypertrophy, we may hear S4 sounds, murmurs.
o Decreased cardiac contractility.
o LDL levels because your metabolism has decreased, causing your cholesterol to stay in the body.
o Red blood cells are created every 120 days. If the body does not have the energy, these patients are likely to be anaemic.
Respiratory System
o breathing capacity.
GI System
o Slowed GI motility, leading to constipation (and thus a distended abdomen because the impacted feces are causing fluid
retention.
o Weight gain because the food energy you are consuming is not being used to help expel waste so it is accumulating.
Integumentary System
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o The skin is going to be dry, thick, and cold (people with hypothyroidism always feel cold).
o The nails are brittle, the hair is going to be sparse because the body does not have the energy to make it.
Musculoskeletal System
o Slow reflexes, muscle aches and pain, fatigue, and slowed movement. Tired, can hardly move, slow, no energy,
extremely fatigued.
Nervous System
o The nervous system slows down (e.g., decreased neuron firing) leading to slowed speech and thought processes. If it
progresses without treatment, the patient may end up in a stupor or coma.
Reproductive System
o Infertility, amenorrhea, decreased libido.
Other:
o Increased risk of infection as the entire body has slowed, meaning that the neutrophils, considering they have even been
made, will take longer to get to the site of infection.
o These patients are highly sensitive to narcotics and sedatives. This is because the body is not excreting them and they are
staying in the body.
o High cholesterol not burning it constipated cant move/excrete it
o Anemic not making cells (red blood cells gone after 120 days)
Myxedema Coma
o If untreated, patients may end up in myxedema coma.
o Accumulation of hydrophilic mucopolysaccharides in the dermis and other tissues. These polysaccharides attract water
from the intravascular space and the blood pressure drops. Hypovolemic!
o It is an emergency because there is a decrease in blood flow to the brain.
If you see this in a patient, give the patient oxygen!
Diagnostic Studies
Laboratory tests that measure TSH and free T4.
o Values correlated with symptoms confirm diagnosis.
Free T4
TSH Primary
The gland is not responding.
Free T4
TSH Secondary
The gland is not the problem here.
Other Tests:
o Elevated cholesterol.
o Goiter (which occurs as a compensative mechanism).
You will notice that goiter is a sign of body hypo- and hyperthyroidism.
Hyperthyroidism
A sustained increase in synthesis and release of thyroid hormones by thyroid gland. Catabolism (breaking down) and building
again.
Common form is Graves disease.
Groiter with hypo or hyper compensation creates more tissue (same thing but different reasons).
You make antibodies that act autoimmune thyroid enlarges and you make more thyroxine.
Exophthamlmos big white protruding eyes that push them forward. All you see is white and they cant close them.
Free T4
TSH Secondary
The problem is outside of the gland.
Free T4
TSH Primary
The problem is the gland.
Other causes:
o Thyroiditis
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Nodular goitre
Exogenous iodine excess
Pituitary tumors
Thyroid cancer
Clinical Manifestations
Cardiovascular system
o CO which will lead to systolic hypertension. This will also lead to murmurs, arrhythmias (as the contractility is not
strong enough), an increase in -adrenergic receptors (causing an increase sensitivity in catecholamine), and distant heart
sounds.
o The symptoms will be similar to hypothyroidism but for different reasons.
Exophthalmos
o Eyeballs forced outward and protrude.
o Impaired drainage from orbit, increasing fat and edema in retroorbital tissues which stretches the ligaments, causing the
eyes to push outward.
o Corneal surfaces become dry and irritated. (eye drops to help)(lot of white hyperthyroidism)
GI system
o Diarrhoea.
K+ levels will be high.
o appetite (with no associated weight gain).
*Although the elderly with hyperthyroidism have anorexia.
o thirst (as there is a lot of energy being made).
o Weight loss.
o Hepatomegaly (large liver) and splenomegaly (large spleen).
RBCs get broken down in the liver. With an increase in RBCs comes an increase in liver function.
The spleen stores both red and white blood cells. With the increase in metabolic rate due to the increase in T 4,
the body is making a lot more RBCs and WBCs and storing them in the spleen.
Integumentary system
o The skin will be warm and moist. The nails will be brittle and the hair will be sparse as the excess energy is going to
other things than hair and nail growth.
Musculoskeletal system
o Fatigue from continuously moving and trying to burn energy
o Muscle weakness
Nervous system
o Everything is being processed quicker. Your thoughts, movements, etc. all occur quicker and dont stop.
o Fine tremors
o Insomnia, phychotic
o Lability of mood, delirium
Reproductive system
o Menstrual irregularities
o Amenorrhea
o Decreased libido (by the time you think of it, the feeling is gone)
o Impotence
Other Clinical Manifestations
o Intolerance to heat
o Increased sensitivity to stimulant drugs
o Elevated basal temperature
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Collaborative Care
Drug Therapy
o Antithyroid drugs PTU and Tapazole
o Iodine
By giving exogenous iodine, the negative feedback mechanism will tell the gland to stop creating endogenous
iodine. Treatment is radioactive for non-pregnant adults in a storm or crisis. Blocks synthesis of thyroxine. Ptu
will stop conversion between T3s and T4s (more numerous). Short term tx is to give some excess iodine.
o -adrenergic blockers (e.g., Propanolol)
You want to decrease the HR.
o Radioactive Iodine Therapy (RAI)
The amount required is based on trial and error. By giving too much you risk killing all the thyroid cells,
essentially giving the patient hypothyroidism. Burnt out thyroid iotrogenic now you have hypothyroidism
now.
Surgical Therapy
o Subtotal thyroidectomy involves removal of significant portion of thyroid.
These patients will have high levels of thyroxin in the blood for ~72 hours following surgery.
Nutritional Therapy
o High-calorie may be ordered for hunger and prevention of tissue breakdown.
o Protein allowance 1-2 g/kg ideal body weight.
o Avoid caffeine, highly seasoned foods, and high-fibre foods (this will worsen the patients diarrhoea)(sensative to these
foods/stimulants).
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Parathyroid Review
There are 4 pea-sized glands located around the thyroid gland. The secrete PTH (parathyroid hormone) which regulates Ca 2+ and
PO32-. When PTH is increase, it increases calcium levels by:
Control calcium and phosphorous (have an inverse relationship like sodium and potassium)
o Taking the calcium from the bones or gut (after activating vitamin D).
o Causes increased reabsorption from the kidneys. (may cause kidney stones)
o Synthesizes Vitamin D
Calcium stops the transport of Na+ during an action potential and assists in nerve impulses. Calcium is for muscle contraction.
Doesnt take part in the reaction but must be present. Issues with clotting.
Beta Blocker or Calcium Channel blocker difference?
PTH says calcium is low so PTH is secreted once calcium is normal so the PTH stops.
Hyperparathyroidism
Problems with calcium and phosphorus.
o levels of calcium in the body, therefore low phosphorus levels in the body (recall that they are inversely proportional).
Causes:
Most common benign tumour in one of the glands.
o Primary: Disorder of calcium, phosphate, and bone metabolism 80%
Problems with bone metabolism.
o Secondary: Vitamin D deficiencies, electrolyte deficiencies, chronic renal failure (CRF) hyperphosphatemia
o Tertiary: Hyperplasia and loss of negative feedback from circulating Calcium (compensatory response)
The problem with the feedback system is that it does not shut off.
Cardiovascular
Too much calcium = disrhythmias
Hypertensive too many particles and same amount of fluid (move fluid from second space into first space (IS
into first space)
Gastrointestinal
N and V, diarrhea to constipation, cells getting dyhydration (they shrink and potassium is coming out so K+
is rising in first space so you will get nausea and vomiting and then abdominal pain).
o More common in women 30-70 years. Peak 60-70 years.
Bones
o Osteoporosis as the calcium is being pulled out.
Kidney
o Kidney stones. Polyurea due to increased glomular filtration so you will pee more and your first space fluid goes down
and we pull from second space and cycles. (gotta start an IV once it goes through the kidneys they are going to excrete
it).
Neuromuscular
o Muscle weakness as the muscle is over-contracting. Abnormal gait, psychosis bc you are conducting too quickly.
GI
o Constipation, loss of appetite.
Severe
o Gastric ulcers, pancreatitis, cardiac changes (e.g., dysrhythmias) and renal failure.
Symptoms
Moans, groans, stones, and bones.
It is insiduous, meaning that it will develop over time.
Diagnosis
Excess serum Calcium.
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Treatment
Focus on symptom management.
Prevention of complications.
Close monitoring.
Pharmacologic:
o Calciumemtic agents Plicamycin (lowers the calcium levels within 48 hours)
o Biphosphonates (Fosamax)
Puts calcium back into the bones in order to prevent people from getting fractures.
It does not treat hyperparathyroidism as the PTH is still being secreted.
o Estrogen/progestin
Given to those with osteoporosis as it puts calcium back into the bones.
Surgical one or all glands (if you take them out we will have iotrogenic hypoparathyroidism)
Increase phosphate levels within the body in order to decrease calcium levels.
Hypoparathyroidism
Cause
Primarily iatrogenic (i.e., treatment of hyperparathyroidism).
Pseudohypoparathyroidism (genetic usually).
Acute symptoms: muscle cramps (due to low calcium levels)
o Sudden hypocalcaemia leads to tetany.
o Hyperkalcemia breathing from a paper bag breathe in CO2 will help short term.
Treatment
Normalize Ca2+ levels by administering calcium with Vitamin D. PTH expensive and IM so not convenient.
Mild treatment: breathe in a paper bag in order to CO2 levels, thus making the bodys internal conditions acidic. Recall that
acidosis prevents calcium from binding to albumin.
Administering a patient with synthetic PTH is not typically done because it is expensive and must be injected.
Question
If a client has hyperparathyroidism, the nurse should:
Encourage a daily intake of 4,000mL of fluid to flush out the calcium thus preventing kidney stone formation.
The nurse should NEVER encourage a patient to decrease their intake of calcium. The calcium is being taken from the bones
which may lead to osteoporosis.
Adrenal Disorders
There are two adrenal glands located on top of the kidneys.
There are two parts to the kidneys:
1. Adrenal medulla
epinephrine and norepinephrine
2. Adrenal cortex
Produces corticosteroids:
o Glucocorticoids
o Mineralcorticoids
o Androgens
(hypothalamus)
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Corticotropin/ACTH
Corticosteroids
(adrenal glands)
Corticosteroids
Main functions:
o Glucocorticoids
Main glucocorticoid: cortisol
Function: stress hormone that increases blood glucose levels by gluconeogenesis (i.e., formation of glucose
from a non-glucose source; supresses inflammation). Cons: suppresses immunce system, sickness.
o Mineralcorticoids
Main mineralcorticoid: aldosterone
Function: help regulate blood pressure by control sodium
High corticosteroid levels: hypertension and hyperglycaemia
Low corticosteroid levels: hypotension and hypoglycaemia
o Androgens
Increases weight gain and makes more prone to infection.
Cushing Syndrome
Etiology and Pathophysiology
Caused by an excess of corticosteroids, particularly glucocorticoids (clinically).
Mot often because they received corticosteroids (using it as a treatment hydrocortisone for a number of diseases)(they end up with
Cushings).
Symptoms: Moon face, buffalo hump, weight gain (from the excess glucose stored as fat).
Most common cause:
o Iatrogenic administration of exogenous corticosteroids (e.g., hydroclorozone).
Treatment:
o Stop taking exogenous corticosteroids slowly. The reason being that when taking exogenous corticosteroids, your body
will stop making them. A sudden decrease in exogenous corticosteroids will leave the body without any (which can be
life-threatening).
85% of endogenous is due to ACTH-secreting pituitary tumour.
Other causes include adrenal tumors and ectopic ACTH production by tumors outside hypothalamic-pituitary-adrenal axis.
Common Characteristics
Weight gain and stretch marks (i.e., purple striae).
Acne (due to the excess oil; androgens, females will have more testosterone, men get female characteristics).
Moon face (from the weight gain).
Buffalo hump (fat storage).
Slow wound healing (corticosteroids suppress the immune response).
Bruising / atrophy we are stealing protein and using it for glucose.
Thinning of hair.
Diagnostic Studies
24-hour urine for free cortisol. (throw away first urine and collect everything from 6-6)
o Urine (not blood), because it gives a 24-hour pattern of how a person secretes cortisol.
o The first urine sample of the day is to be discarded and the following samples should be collected until 0700 hrs the
following morning.
Low-dose dexamethasone suppression test (give a low dose of dexamethasone at night time and draw it in the morning)
o Dexamethasone (corticosteroid)
o Will do a high dexamethasone test if the urine is borderline
o ACTH normal = fine, keeps coming or is high (problem not with the gland but outside the gland) low = normal
CT and MRI are used for tumor localization
Plasma ACTH may be low, normal, or elevated depending on problem.
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corticosteroids (from an exogenous source), plasma ACTH would be low because it is not secreted in the body.
If the anterior pituitary is the problem, there would be an in ACTH because the negative feedback is not working
properly.
If the problem lies outside the gland (e.g., lung), the ATCH levels could be normal.
corticosteroids
ACTH
corticosteroids
ACTH
corticosteroids
Problem is occurring outside the glands (i.e., the lungs).
Normal ACTH
Have to give time via dose reduction or alternate days (20mg of prednisone). Drop doses each week or alternate days but cannot
be stopped abruptly.
Collaborative Care
If developed during use of corticosteroids:
o Gradual discontinuance.
o Reduction of dose.
o Conversion to alternate-day regimen.
Avoids potentially life-threatening adrenal insufficiency.
Goal is inhibition of adrenal function.
Drug therapy is indicated when surgery is contraindicated.
Mitotane (medical adrenalectomy) drug may be used, which will lower corticosteroid levels.
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Addisons Disease
Etiology and Pathophysiology
Adrenocortical insufficiency from a primary cause.
Main reason a person gets Addisons disease is from autoimmunity.
o The gland itself is not secreting corticosteroids.
Other causes:
o TB (rare cases)
o Infarction
o Fungal infections
o AIDS
o Metastatic cancer
o Iatrogenic Addisons
Clinical Manifestations
Insidious onset.
o Progressive weakness, fatigue, weight loss, anorexia are primary features. (Primary in the gland, secondary outside of the
gland)
o Skin hyperpigmentation (high levels of ACTH secreted instead of other corticosteroids in its place)
Areas exposed to sun.
Pressure joints.
Over joints.
In creases of the body.
The effects of aldosterone will cause the following: (all low)
o Hypotension
o Hyponatremia
o Hyperkalemia
Acidosis because the K+ holds on to H+ and is unable to enter the cell.
o N/V
Due to hyperkalemia.
o Diarrhoea
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Due to hyperkalemia.
Cramping from the N and V and diarrhoea.
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Primary
corticosteroids
ACTH
Secondary
corticosteroids
ACTH
ACTH increases with the hormones are down and are not secreted when hormones are up.
ACTH test without Addison the corticosteroid should go up if they dont go up there is a problem in the gland.
Diagnostic Studies
Subnormal levels of cortisol or levels fail to rise over basal levels with ACTH stimulation test.
o Indicate primary adrenal disease.
o Positive response to ACTH stimulation indicates functioning adrenal gland.
Abnormal lab findings:
o Hyperkalemia
o Hypochloremia
o Hyponatremia
o Hypoglycemia
o Anemia
o BUN
Indicates kidney failure because of low BP, low volume, glomerular filtration rate, blood flow to the
kidneys, and therefore signs of kidney failure. Hypotensive so kidneys dont diffuse.
Urine levels of cortisol are low
ECG
o Due to hyperkalemia, there is a risk for arrhythmias and an elevated T-wave. PQRS T=(repolarization) will take longer to
repolarize due to potassium
CT and MRI
o Check for tumours and cancer.
Collaborative Care
If the body is not producing the corticosteroids, they must have it administered.
o Hydrocortisone most commonly used as replacement therapy.
o Going to increase corticosteroids during a cycle fashion (three times per day) to match circadian rhythem.
Glucocorticoid dosage must be increased during times of stress to prevent Addisonian crisis.
Treatment directed at shock management.
o Isotonic fluid, put the head of the bed down.
(isotonic unless they have heart disease so NS 0.45%)
Nursing Implementation
Frequent assessment (particularly BP, Temp, RR, HR, chest-CHF(no crackles) checks).
Medication
o Glucocorticoids usually given in divided doses (typically 3x per day).
Increase glucocorticoids during times of stress.
o Mineralcorticoids usually given once in the morning.
o Reflects normal circadian rhythm
Teach signs and symptoms of corticosteroid deficiency and excess and to report findings.
Instruct to wear Medic Alert bracelet at all times. (need to learn how to give themselves a hydrocortisone IM injections)
Provide handouts on medications causing increased need for glucocorticoids.
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Hypothalamus
Senses serum osmolarity
Posterior Pituitary
Secretes ADH
Stimulates the reabsorption of H2O in the renal tubules
Kidney: reabsorbs fluid
serum osmolarity
Osmolarity more condesnsed particles. Increased serum osmolariy. Will act on posterior pituitary to produce increased ADH to
act on the kidney to bring back water. Norm is same particles with more fluid/water. Guess what? ADH stops. IfI bring back water
it means there is less water going out. Kidneys will do that and you will feel thirsty and it will shut off once we get enough water.
Dysfunction of ADH
Provides two extremes
o Diabetes Insipidus
o Syndrome of Inappropriate Antidiuretic Hormone Secretion-SIADH
o Normal Serum Osmolality 280-300mOsm/kg of water
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Presentation Symptoms
Abrupt polyuria
Polydipsia
Dehydration
Needs a catheter way too much fluid and output.
Neurological
o Na+ levels are up related to hypernatremia. The K+ levels will therefore be low.
o If Na+ levels >160mmol/L the patient is at risk for seizures and coma.
Lab values
o Different for Primary/Psychogenic
Water deprivation test
o Used to distinguish between Central DI, Nephrogenic DI, and Dispogenic DI. The patient are instructed not to
consuming any water or smoke beginning at midnight. They are then given exogenous ADH. In a normal clients and
patients with Dispogenic DI, urine osmolality and plasma osmolality are normal after ADH administration. In clients
with Central DI, urine osmolality increases after ADH administration. In clients with Nephrogenic DI, there is little or
no response to the ADH.
o Lose 3-5% of body weight and then give ADH = if you dont have DI you should reduce less urine and osmolarity and
urine should rise. Osmolarity in urine shouldbe higher and you put out less urine. (should be more concentrated).
Head
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Depression
o For humans, touch is an absolutely essential need.
o Touch releases the hormone oxytocin (which is also released after birth to help the mother bond with her child). When
depressed, some people become hypersexual as their bodies want the oxytocin release. Some anti-depressant drugs (i.e.,
SSRIs) have terrible side-effects on peoples sexual health.
Substance abuse
o Mind-altering substances have the ability to make people feel sexy.
People who are high on cocaine feel horny and they just cant get enough.
People on crystal meth also feel intense desires for sex.
Head injury/Brain tumour
o People who have impaired sexual function due to a head injury will often have a change in personality (e.g., some
patients may become more demanding and also more violent with their demands).
Multiple sclerosis
o It is a neurological disease. Neurological processes are required for adequate sexual functioning.
o Some people have had sexual numbing in their genital region and later been diagnosed with MS.
Torso
Respiratory diseases (e.g., asthma, COPD)
o These may affect ones sexual function.
Cardiovascular disease
o If an otherwise healthy man in his 40s or 50s experiences erectile dysfunction, he should not take Viagra or other such
drugs. This may be a sign of cardiovascular disease (as smaller blood vessels are affected first) and blood tests should be
taken.
o Climbing two flights of stairs comfortably is the test of whether an individual is physically able to have sex.
Diabetes
o It is a disease of blood vessels and may affect ones ability to attain an erection.
Pelvis
Hysterectomy
o Blood vessels are often ruined during a hysterectomy.
Radical prostatectomy
Bowel disease (malignant or benign)
o The rectum supports the vagina during sexual intercourse. When a bowel resection has occurred, there is often less
support for the vagina, making sex more uncomfortable.
Combat Injury
Burns
Amputation
PTSD
o This is very common in individuals who have served.
o Hypervigilance, over-reactive, anxiety.
Closed brain trauma
Cancer
Childhood
Adult
Reproductive organs
All cancers
Body image; libido; hormonal changes; anatomical changes; functional changes
o 80% of cancer survivors experience sexual dysfunction, most often relating to body image (e.g., breast cancer, loss of
hair in men, breast enlargement in men).
PLISSIT Model
Permission
o Give the patient permission to talk about this.
Limited Information
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BETTER Model
Bring up the topic.
Explain you are concerned with quality of life issues, including sexuality.
Tell patients you will find appropriate resources to address their concerns.
Timing may not seem appropriate now, but they can ask for information or help at any time.
Educate patients about the side effects of their cancer treatment.
Record your assessment and intervention in the patient chart.
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Outline
Physiology and pathophysiology
Etiology
Classification and clinical manifestation
Diagnosis
Management
Acute complications
Chronic complications
Diabetes Mellitus
Insulin and Carbohydrate Metabolism
Its about protein and fat metabolism as well (i.e., not only carbohydrates).
Insulin
o Insulin is a hormone (i.e., small protein). It must be given via injection because its a protein and will become denatured
if swallowed (by the acid in the stomach).
o It is produced in the pancreas, specifically in the beta cells of the Islets of Langerhan.
o It is continuously secreted by the body, but greater amounts are secreted when food is consumed.
o Carrier molecule
o If I put it in the cell blood levels will go down stores in the liver and skeletal muscles as glucogen (increases
glycogen stores) (facilitated diffusion).
What are the effects of insulin on carbohydrate metabolism?
o To increase the rate of glucose metabolism.
o To decrease blood glucose concentration.
o To increase glycogen stores.
How?
o Via facilitated diffusion. It will not move glucose against a concentration gradient. Insulin helps glucose move into the
cell. Doesnt require actions but a carrier.
o Brain doesnt need it, liver doesnt need it muscle needs insulin. Brain needs available source of glucose (no other
kind). Fructose, glucose, galactose, sucrose.
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Absence of Insulin
Results in:
o Hyperglycemia
The sugar will not enter the cells so it will accumulate in the blood.
o Lipolysis
If you cant get sugar into the cells, the body will respond by using fat for energy.
o Osmotic diuresis
The water from the ISF and cell will move into the plasma in order to balance out the extra glucose. This
increase in volume will increase the GFR, thus increasing urinary output.
This will lead to dehydration, which will lead to an increase in K+.
o Ketone bodies
This is a by-product of fat breakdown. It will also cause acidosis. This acidosis will interact with the fact that
there is an increase in K+.
Ketones in the urine imply ph is becoming more acidic 7.35-7.45. average is in the middle.
Diabetes Mellitus
Imbalance between insulin supply and demand.
It is characterized by hyperglycemia and is associated with abnormal carbohydrate, protein and fat metabolism.
Statistics
4.8% of Canadians have been diagnosed with diabetes. Many more have it but are not diagnosed.
Aboriginal people have a 3-5X higher incidence in developing Type II diabetes.
Children typically only ever had Type I diabetes, however this trend is changing due to obesity and lifestyle modifications.
o Refined foods (e.g., white flour, white bread) break down a lot faster than non-refined foods. This quick breakdown is
likely to lead to diabetes.
Risk Factors
Family history
o You cannot prove that diabetes has a gene, but family history is certainly a big factor (e.g., may be due to lifestyle).
Ethnicity
Obesity
o Especially central obesity (i.e., greater central obesity is linked with greater insulin resistance).
History of delivering infants weighing more than 9lbs.
Classification
Terms were created in 1997.
Type 1 diabetes (formerly known as insulin-dependent DM or juvenile)
Type 2 diabetes (formerly known as non-insulin dependent DM)
Gestational diabetes
Other types of glucose intolerance (e.g., Cushings syndrome, pancreatitis).
Etiology
Research suggests that it is an autoimmune disease.
The body is not producing any insulin.
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Polydipsia
o The increase in urine volume will cause the person to be thirsty.
Polyphagia
o The cells are not getting the glucose so they keep triggering the body to consume food energy.
o Will lose weight.
Type II Diabetes
Etiology
Most prevalent. Lifestyle.
Main characteristic is insulin resistance.
Available insulin is unable to bind with cell receptor sites (very little of the insulin can bind to the receptor sites). The more fat
present, the greater the resistance of the receptors to insulin.
Blood sugar should never go above 9 (regardless of whether a meal was consumed).
Blood tests for blood sugar are in the capillaries.
Inappropriate release from the liver, the liver makes more. Glucogon works on the liver to make glucose. Adipose tissue produce
signy with prevent use of insulin.
Clinical Manifestations
Non-specific
o Persistent infection (e.g., yeast infections in women).
o Still produce insulin but there is a resistance.
Risk factors family hx, ethnicity, obesity (II), hx of macro infant (II), hypertension autoimmune (II), polycystic ovary
syndrome (II), acanthosis nigricans (II).
Gerontologic Considerations
Elevation of blood glucose levels appear in the 5th decade.
Components of Management
Nutrition
Exercise
Monitoring
Pharmacologic therapy
Education
To teach diet principles to help in meal planning (see Appendix).
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Exercise
Lowers blood glucose.
Improves circulation and muscle tone.
Increases resting metabolic rate.
Alters blood lipids.
Increases levels of HDLs.
Decreases total cholesterol and triglyceride levels.
Type I individuals cannot benefit from exercise unless they take insulin beforehand. It is also important that these people have a
sugar source on hand in case their BS levels drop dramatically. It should also be noted that these patients can experience a
hypoglycaemic reaction up to 48 hours following the period of exercise.
Type II individuals will benefit from exercise because it helps decrease insulin resistance. These patients who are taking
medications such as glyburide can also have a hypoglycaemic effect up to 48 hours following the exercise period. They should
also have a snack nearby.
Monitoring
Self monitoring of blood glucose requires:
o Good visual acuity
o Fine motor coordination
o Cognitive ability
o Comfort with technology
o Willingness
o Costs (the machines are free but the strips are very expensive)
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Complications and breaking fats and becoming acidis and will go into diabetic acidosis (regular person means they are starving).
Complications of Insulin
1) Local allergic reaction
Due to lipolysis. That is why we have intrasite and other such rotations.
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Nursing Management
Education
o Focus should be on self care.
These patients will know more about their diabetes than you. It is important to listen to them.
o Develop a diabetic teaching plan.
o General approach:
Basic, initial, or survival skills (e.g., diet, exercise). Teach the patient, and if they are avoiders, teach the family
(recall FCC).
Continuing education.
Foot care
o Always wear shoes (even in the house), check your feet daily, maintain eye care (recall
retinopathy) as the triglycerides will be deposited in the eyes, etc.
Teaching Strategies
Assess readiness to learn (e.g., avoider or approach style).
Assess coping strategies.
Ask about major concerns or fears.
Understand misconceptions.
Hypoglycaemia
Abnormally low blood glucose levels (2.7-3.3mmol/L).
Causes:
o Too much insulin
o Exercising too much
o Not consuming enough food
o Defect in the counter-regulatory hormones (e.g., glucagon, epinephrine, etc.).
Clinical Manifestations:
Adrenergic Symptoms (ANS)
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Medical Management
Mild to Moderate
o Give 10-15mL of a fast acting simple carbohydrate (e.g., orange juice, coke, or other such products containing sugar).
o Retest the blood glucose in 15mins after treatment.
o If its greater than 4mmol/L, then give a protein and starch (e.g., peanut butter on whole wheat toast) or a meal.
o If that doesnt help it rise, administer another 10-15mL of a fast-acting carbohydrate.
If client unconscious
o Inject Glucagon 1mg subcutaneously or IM.
o After conscious, give simple sugar then protein starch snack.
Hypoglycemia is preventable always carry a simple sugar (Lifesavers were created for diabetics). Family and friends need to
know S&S and what to do.
3 Main Causes:
1. Decreased or missed dose of insulin
2. Illness or infection
Stress hormones (cortisol) will be released, thus increase blood glucose levels.
3. Undiagnosed and untreated diabetes
Clinical Manifestations
Hyperglycemia
Blurred vision, weakness, headache
Orthostatic hypotension
Anorexia, N&V, abdominal pain
Acetone breath
Hyperventilation
Mental changes vary individually
Assessment and Diagnostic Findings
Blood glucose levels vary >14-44.4mmol/L
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Prevention of DKA
Adherence to SICK DAY rules
o S = Sugar
o I = Insulin
o C = Carbohydrates
o K = Ketones
When people are under stress, their body will still be making glucose. For that reason, you should not tell a patient who is not
eating not to take their insulin (if anything, recommend a smaller dose).
Collaborative Care
Dehydration
o NS (no heart issues)
o NS (if patient has heart issues)
o If a patient has a blood glucose of 44 that has finally been lowered anywhere between 13-16, stop the NS and start
administering D5W. This is to prevent hyperglycaemic rebound of lowering the blood sugar too quickly.
Electrolyte Loss
o K+ may be given.
Acidosis
o Administer insulin.
This is based on how acidic this person is. Insulin helps put K+ back into the cells, therefore causing the H+ ions
to leave, thus creating a more basic environment. The insulin will also help the glucose to enter the cell,
decreasing lipolysis and azthus acidicosis.
o Arterial blood gases (ABGs) are done to determine ones acidity.
Clinical Manifestations
Hypotension
Profound dehydration
Tachycardia (the body is trying to move the little fluid in the body to the cells)
Variable neurologic signs
Assessment and Diagnostic Findings
Blood work including:
o Glucose, electrolytes, BUN CBC, serum osmolality and ABG
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Vascular
Macrovascular
o Damage to the large blood vessels providing circulation to the brain, heart and extremities.
Microvascular Complications
o Abnormal thickening of basement membrane in the capillaries by chronic hyperglycaemia. The constant sugars trying to
get through the vessels will damage the capillaries.
Retinopathy
Nephropathy
Even if the blood sugars have been well controlled, 50% of diabetics will get kidney damage.
Albumin in the urine (i.e., proteinuria) is a sign of kidney damage.
Neuropathic
40-50% of those with diabetes will develop detectable neuropathy within 10 yrs of onset.
Paresthesia
o Numbness, tingling, touch sensation not what it used to be.
Autonomic complications, sensory disturbances
o Polyneuropathies
The worst case is the inability to feel pain.
Infection
Defect in the mobilization of inflammatory cells and impairment of WBCs in phagocytosis.
o This makes the person more susceptible to infections.
Skin Complications.
o Acanthosis nigricans (dark ring around the neck caused from hyperinsulinism).
Note
Patients with Type I diabetes are typically very thin from lipolysis.
Assignment
Choose 1 case study.
Complete the focused assessment (typed).
Weve got to decide what the patient is being admitted with (otherwise its a fail).
80% is allocated for content.
o Do not waste time regurgitating the case study.
o Use as many references as needed, but tie up your own paper (i.e., do not have a paper full of quotes).
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Cystic fibrosis
Related pharmacology integrated
o Review notes from Pharmacology and texts; power point notes as a guide.
Immature systems
Smaller nares (OBSTRUCTION) (NOSE breathers)
Large tongue (POSITIONing important)
Underdeveloped sinuses (sometimes worriesome when children snore re sleep apnea)
Larger epiglottis prevents aspiration
Larynx and glottis sit igher and more anterior which makes them more likely to aspiration
Tracha shorter and funnel shapped
Narrowest part at cricoid cartilage until 8 yo resp arrest (contributes to cardiac failure)
Smaller narrow airways
Non compliant ribcage more cartilage than bone
Respiratoy distress
Bradypnea
Breathing rates slower than normal.
Often an omnious sign in an acutely ill child
Resp failure to arrest (CPCP or BIPAP - ventilation)
Poor prognosis
Grunting air being forced out of a partial closed epiglottis to increase negative pressue and help gas exchange (big
red flag for Resp distress)
Combined with retractions indiciitive of pneumonia or cardiac conditions
Grunting could also be from abdominal paid or fever
Stridor upper airway obstruction croup, foreign body, congenitial abnormalities, upper airway edema (allergy)
Wheezing lower airway obstruction,
Risk factors young age, daycare, recurrent URTIs abnormalitis, not breatfed, bottle propping, pacifier use
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Clinical manifestations: tympanic membrane, red bulging-retracting, ear pulling, fever, hearing loss, irritability,
ear popping, rupture of TM
Therapeutic management
Tx with antibiotics based on age, reoccurance and severity. Amoxil first line therapy
Nursing management
Supportive
Analgesia- no codeine
Heat
Antibitotics
Educate family good hand hygiene, flu vaccine/pneumonococcol, dont prop bottle, vit D
Nasopharyngitis etiology
Most common illness of infancy and childhoos
More commone in daycare and winter
Pathogenesis
Droplet or person to person contact
Incubation 1-3 days
Viral causes usually
Edema and increased mucuse production increased liklihood of obstruction or you could start viral and end up
with a secondary bacterial infection
Secondary bacterial infections
Self limiting 7-10 dyas
Symptoms
Lethargy
Irriatably
Fever,
Eating?
Sneezing
Nasal discharge
Headache
Dry irritated throat
Poor feeding/no appetite
Bulb suction
Humidifiers
Antipyretics
No cough and cold preparations unter 6 years of age
Fluids
rest
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viral
bacterial
abrupt onset
winter
clinical manifestations
sore throat
difficulty swallowing / voice
fever greater than 38.3
headache
bdominal pain
cervical adenopathy
soft palate petchiae
tonsillar exudate + or
theraputic management
antibiotics bacterial
analgesias
cool fluids
salt water gargle
rest
croup pathogenesis
inflammation and edma cause obstruction of the upper airway
narrowing of the subglottic are
edema of the larynx
increased mucus producation
peaks 3-5 days
clinical fidnings
anxiety / restlessness
inbility to sleep
hoarse voice or barky cough
inspiratory stridor
subcostal, substernal retractions
fever
steeple sign on x ray
manaement
humidification
oral steroids (dxamethasone)
inhaled epinephrine
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Pathogenesis
Bacterial iasuion and cause inflammation and swelling of the epuction
Ssore thoat
High fever
Mufflvoice
Drooling
Stridor
Pain
Anxieity / not vigorous
Tripod position / resp distress
Do not disturb
Upright position
NPO
Aanalgesia
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Droplet precautions
Observe for airway obstructions
High humidity oxygen
Suction
Encourage fluids
rest
anaphlaxis etiology
incidence unknonw (increasing)
epinepherine dispensed to aprox 1% of MB poulation
1/3 of childrens emerg visits
Seeing more reactions to milk proteins
Triggers
Food
Bees and hornets
Insect stings
Medications
Latex
Pathogenesis
Histamines aand secondary mediators released from mast cells and eosinophils following contact with allergen
Vasodilation
Anxiety, swelling, itchy, drooling, abnormal upper airway sounds, chest tightness, flushing, hives, abdominal cramps
Im epinepherine
Followed by dose of H1 antagonist such as ceterizine (reactine) or desloradetein (Aerius)
Child observed for 6 hours after for 2nd reaction
Use of epi pen teaching critical
teaching
Epi pen
Hold is fist
Remove blue cap
Place orange end against mid outer thigh
Press quickly and firmly to hear a click
Hold for ten seconds
Remove and carefully carry to emergency dept
Avoid triggers
Epi should always be with child
Follow up with allergist
Further education
83
ASTHMA
Paediatrics
Alveoli (by the age of 12 the alveoli are adult-like)
Peripheral bronchioles
Smooth muscle
Muscles of respiration (the diaphragm is the largest breathing muscle).
Additional symptoms
o The childrens respiratory rate is higher than that of adults.
o The ribs and cartilage are flexible.
o The chest walls are more pliable.
o The epiglottis is closer to the palate.
Airway Edema
Edema
o More dangerous in paediatric airway.
o 1 mm of circumferential edema can resistance to airflow by 16x.
Cross sectional area by 75%
o The paediatric airway can by quickly lost!
Most common cause of cardiac arrest in children = respiratory arrest.
Asthma
Incidence
o 15.6% from 4 to 11 yrs of age.
o 8.3% 12 yrs of age.
The incidence is decreasing due to asthma education.
Hospitalization and death
Risk factors:
o Allergies (i.e., dust mites)
Etiology
o Familial and environmental
The 3 contributors to asthma are:
Mucous
production
Mucosal
Bronchiol
inflammation
constriction
Pharmacologic Interventions
Two main groups are:
1. Controllers
2. Relievers
Pathophysiology
Early response to trigger:
o Bronchial constriction.
o Increase smooth muscle response and bronchospasm.
Pharmacological interventions?
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Later:
o * Mucosal inflammation
o Mucous production
Pharmacological interventions?
Continued hyper-reactivity
Early:
o Bronchiol constriction
Late:
o * Mucosal inflammation
o Mucous production
Continued hyper-reactivity
Triggers
What they are:
o Substance (allergen)
Trigger + IgE + mast cells
o Health conditions (non-allergic) that may cause an asthma attack:
Respiratory infections, fever.
Maintenance is the key to preventing asthma attacks.
o Other
What they are not
What is the role of nurses?
o Education!
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Characteristic
Daytime symptoms
Night time symptoms
Physical activity
Exacerbations
Absence from work or school due to
asthma
Need for fast-acting 2-agonist
FEV1 or PEF1
Frequency or
Value
<4 days/week
<1 night/week
Normal
Mind, infrequent
None
<4 doses/week
>90% personal
best
PEF diurnal variation2
<10-15%
1FEV1 = forced expiratory volume in 1s; PEF = peak expiratory flow.
2Diurnal variation is calculated as the highest PEF minus the lowest divided by the highest PEF multiplied by 100 for morning
and night (determined over a 2 week period).
Asthma Severity
See also box 46-13 in text
Care and treatment follows a stepwise progression based on age. Education must take place at every stage.
Educational Tools
Targeted resources:
o Asthma Action Plans
o Asthma diaries
Childrens Asthma Education Centre Wpg
o http://www.asthma-education.com/content/
Status Asthmaticus
It is a life-threatening emergency indicating that asthma is not being controlled.
Causes
o Seasonal factors (e.g., farmers burning fields, environmental pollution)
o Infections most common
o Self d/c drug therapy (typically seen in adolescents)
Symptoms
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Pharmacologic Education
Refer to Pharmacology notes and text.
Two main groups are.
o Controllers and Relievers
When to use it depends on the severity.
When to change your plan depends on the action care plan.
Controller Medicines
Inhaled steroids are the most common controller medications.
o or prevent swelling and extra mucous inside the airways
o Work slowly
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Controller Medicines
Leukotriene Receptor Antagonists (LRA)
o E.g., montelukast (Singular).
o Increasingly popular for complex asthma, with persistent allergies.
Reliever Medicines
Action: reduces bronchoconstriction
Use: if the patient has to use it more than q4h, they should see a doctor
Side effects: HR, supraventricular tachycardia, the children will vibrate.
Salbutamol (Ventolin), Airomir, terbutaline (Bricanyl)
Inhalers
There are many type and varied techniques.
Cleaning
Ability to use (child development)
Valved spacer recommended
CYSTIC FIBROSIS
Diskus
65 Roses
Cystic fibrosis affects the bodys endocrine glands. The respiratory and GI systems
are affected.
88
Exocrine Glands
Exocrine glands
o Exocrine glands and CF
o Sodium and chloride transport
Respiratory tract is affected (i.e., mucous becomes quite thick)
Pancreas
Sweat glands (there is a high content of salt on their skin)
Dehydration is a big problem in these children.
o See also text for detail.
Diagnosis
If symptomatic:
o Respiratory symptoms
o GI/nutrition:
4 Fs
Frothy, fat, foul, floaty stools
Meconium ileus
Failure to thrive (no matter how much they, they will not gain weight
There will be respiratory symptoms (e.g., wheezing)
o Median age at dx = ~ 6 months of age
How:
o Newborn screening and further evaluation.
o Sweat chloride via a pilocarpine test chemical.
o DNA testing for gene mutation.
Prognosis
Median life expectancy tends to be 37 years.
# Canadians with CF
# Manitobans with CF
Screening for CF
Genetic screening for most common mutation(s) all or high risk groups?
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Prenatal
At birth:
o IRT: a leak of tryptic-like substances into the blood detected by the IRT blood test.
Canada Ont/Alberta/Sask
A first step only confirm with retest and/or DNA +/- sweat chloride
o The pancreas secretes trypsinogen which is converted into trypsin.
Goals of Treatment
1) Prevent or minimize pulmonary complications
2) Optimize growth and nutrition
3) Assist family/child in coping
Infection/Inflammation/Destruction
Airway
destruction
Airway infection
(colonization)
Airway
inflammati
on (WBC)
Mucous is very thick and destroys the cilia.
Infection is caused by the thick mucous sitting in the respiratory tract.
Inflammatory response (early and chronic).
Progressive destruction.
Numerous respiratory symptoms.
Respiratory issues is the major cause of death.
Expiration
Inspiration
A+B = healthy
C+D = CF
Transplant
Theres a lot of risk associated with transplantation. There is only a 50% chance of living after a transplant has taken place.
Physiotherapy
Respiratory:
o Multiple methods:
Positioning, pummelling, and blowing devices.
External manoeuvres such as huffing.
o Oscillatory vest (the vest vibrates and is extremely expensive) in conjunction with other techniques.
Other physiotherapy:
o Upper body strength.
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Respiratory Infections
Organisms:
o Staphylococcus aureus seen early
o Pseudomonas aeruginosa
*colonization = mortality
o Burkholderia cepacia (this is associated with a rapid respiratory deterioration)
Treatment
o Antibiotics (although the prolonged use may lead to antibiotic resistance).
Nutrition
CF interferes with the passage of pancreatic enzymes.
Poor fat absorption
o Stools tend to be bulky and oily (see 4 Fs above).
o Other GI symptoms.
Therapy
o Goal
o Up to 30% more calories and protein
o Pancreatic enzymes (e.g., pancrease)
o Vitamins A, D, E and K
Routes
o Breastfeeding is encouraged by supplemental calorie sources may be needed.
o Enteral access devices may also be required.
Additional Medications
rhDNAse/Pulmazone (costs roughly $16,000/year)
o Promotes mucous thinning. It only benefits 30% of patients.
Inhaled NS (this may irritate some children).
High dose Ibuprofen.
Additional Issues
Transition to adult health care (this is needed since the average age is increasing).
(Fertility)
o The sperm and eggs are affected (recall that it is an exocrine gland disorder).
Expansion of adult clinics.
Cystic Fibrosis Related Diabetes (CFRD)
o This is due to the pancreas being affected (i.e., insulin release).
Resources
o Financial
o Family
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Review of Liver
There are 2 main lobes.
What else?
o There are 4 quadrants of the liver.
o It is located in the right upper quadrant.
You should not be able to feel it during an assessment (i.e., other than the lower edge).
o It will have a dull sound when percussed.
o A normal liver weighs 1.5kg in a male.
Hepatic circulation
o Hepatic Artery
Brings oxygenated blood to the liver.
o Portal Vein
Takes all the nutrients from the gut to the liver for phagocytosis to occur.
Portal hypertenstion the blood backs up to the spleen cause it cant go forward.
o Hepatic Vein
Bring deoxygenated blood (but it is in nutrients) to the inferior vena cava to be distributed to the body.
Functions:
1. Production of Bile
This is its only digestive function.
It makes 700-1,200mL per day. The bile is required for fat breakdown.
Comes together and emulsifies fat. Empties into the common bile duct.
No bile? Lot of fat gowing around fatty stool (not being emulsified) (frothy, floaty, foul, clay colored)
2. Carbohydrate Metabolism
The liver regulates blood glucose levels via gluconeogenesis.
If there is a problem with the liver, the patient may be lethargic.
Coverts monosaccarides to glucose.
3. Amino Acid Metabolism
There are 20 amino acids needed to make proteins.
It synthesizes non-essential amino acid (it makes 12 amino acids).
Non-essential amino acid synthesis
4. Deamination
Production of urea
Ammonia (NH4) is a toxic by-product of protein breakdown that will destroy brain cells.
The liver must convert the NH4 to urea so it can be excreted.
The deamination refers to the removal of NH4. Cant break it down? Pt will die.
5. Synthesis of Plasma Proteins
Over 50% of the plasma proteins are albumin. If the body cannot synthesize albumin there will be a decrease in
plasma volume as the oncotic pressure will not be great enough to draw fluid back in the plasma. This will lead
to edema and ascites (recall third space shifting). Keeps Water in the vessle. Its going to end up with third
space shifting. Hypervolemia.
Clotting factors (e.g., thrombin, prothrombin, fibrinogen) will also not be made. Dont make it? Bleeding.
Globulins are required to immune system functioning. They make antibodies. Make lipo-protiens to help
transfer fat. (stored in lymph). Liver doesnt work? All this is screwed (immune system)
6. Lipid Metabolism
The liver synthesizes lipoproteins (e.g., HDL, LDL, VLDL), which act as carrier molecules to get other
substances into the cells.
7. Formation of Bilirubin
Bilirubin is a pigment derived from the breakdown of haemoglobin (i.e., the breakdown of RBCs). Since it is
water insoluble, it is bound to albumin for its transport to the liver.
Red blood cell destruction (the heme is separated from the globulin).
Unconjugated Bilirubin + Albumin (this is not water soluble and can thus not be excreted)
Conjugated Bilirubin + Glucuronic Acid (this is water soluble and can be excreted by the kidneys)
If it is unable to conjugate, it will not be excreted and will lead to jaundice. It will also cause the feces to be
white.
8. Storage
It stores glucose in the form of glycogen.
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Hepatitis
Description
Inflammation of the liver.
Acute viral hepatitis
o Most common cause of why someone will get hepatitis.
o Other causes.
Drugs (e.g., acetaminophen), alcohol, chemicals (e.g., aerosols), genetic, autoimmune diseases.
If a person overdoses on Tylenol, you want to try prevent liver failure by giving Mucomyst IV.
Types of infectious viral hepatitis:
93
Etiology
Hepatitis C Virus (HCV)
o RNA virus
o Transmitted percutaneously (e.g., injections, IV drug users, and blood transfusions and haemodialysis prior to the
1990s).
o 80% of the people who have Hep C do not know they have it.
o These patients will also have co-infections (e.g., Hep B, HIV).
Hepatitis D Virus (HDV)
o Also called delta virus.
o Defective single-stranded RNA virus.
o It cannot survive on its own (i.e., it can only survive if Hep B is cured).
o Requires the helper function of HBV to replicate.
94
Pathophysiology
Liver
o Widespread inflammation of liver (the cardinal signs of inflammation are present).
o Pathophysiologic changes in the various types of viral hepatitis are similar.
During an acute infection:
o Liver cell damage results in hepatic cell necrosis.
o Proliferation and enlargement of Kupffer cells (these macrophages will enlarge to take up the extra debris).
o Basophils and eosinophils come too (very big). Inflammation and swelling. Swelling of periportal areas.
o Inflammation of the periportal areas may interrupt bile flow (recall that bile is made in the liver and stored in the
gallbladder). If the bile cannot make it to the gallbladder it will sit in the liver and cause damage.
o Cholestasis may occur.
Systemic effects
o Acute Phase table 46-2
o Basophils release histamine (itchy)
o Lasts from 1-4 months
o Icteric or anicteric
o (fill in more)
o Rash (bile salts will come out of the skin)
o Angioedema
o Arthritis (because the liver is not excreting everything it should be)
o Fever
o Malaise
Clinical Manifestations
30% of patients with HBV asymptomatic and 80% of patients with acute HCV will be asymptomatic.
It doesnt matter which type of hepatitis is present, the body will go through all 3 phases.
2) Icteric phase
o Lasts 2 to 4 weeks
o Characterized by jaundice
o Pruritus due to:
Bile salts
Inflammatory response
Increase in neutrophils, eosinophils, and basohpils, which produce histamines and cause pruritis. This
patient must therefore be given anti-histamines.
o The differential will give you the difference between WBCs.
3) Posticteric phase
o Begins as jaundice is disappearing
o Lasts weeks to months
o Malaise
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Easy fatigability!
This is because there are no stores of glycogen.
General considerations
o Not all patients with viral hepatitis have jaundice (i.e., termed anicteric hepatitis). For this reason it is important to treat
every patient as if they have Hepatitis.
See Appendix
Complications
Most patients with acute viral hepatitis recover completely with no complications.
Overall mortality rate <1%.
Fulminant hepatic failure.
o This is a syndrome. With continued damage in the liver will come liver failure.
Chronic hepatitis.
o This is like the carrier state.
Cirrhosis.
Hepatocellular carcinoma
Collaborative Care
No specific treatment or therapy for acute viral hepatitis.
No specific drug therapy antiemetics, diphenhydramine (benadryl).
Most patients can be managed at home.
Drug Therapy
No specific drug therapies.
Supportive therapy:
o Antiemetics (e.g., gravol, Maxeran)
o Diphenhydramine (e.g., Benadryl)
o Chloral hydrate (its a sedative used to decrease the metabolic rate and thus give the liver some time to rest)
Nutritional Therapy
No special diet is require, but:
o High-carbohydrate and protein for repair
o Low-fat (do not force the liver to have to make a lot of bile)
o Adequate calories
o Vitamin supplements (give the fat soluble vitamins and the B complexes)
Drug Therapy
Chronic hepatitis B
o -interferon
These are biologic modifiers that decrease the viral load. These may cause flu-like symptoms.
Have to take these all the time. Dont take them? Virus comes back another way. Then what youre taking wont
work. (e.g MRSA).
Chronic hepatitis C
o -interferon
o ribavirin (Rebetol)
o different drugs for different non genotypes 2/3
Prevention
Hepatitis A
o Hepatitis A vaccine
o Immunoglobulin (Ig) (Passive immunity if I had the vaccine)
o When travelling, do not consuming the water or foods that have come in contact with water (e.g., salad, cool foods, ice).
Hepatitis B
o Immunization
Most effective method.
Hepatitis C
96
97
This is due to long-standing heart failure (especially the right side because the blood will not flow onward but
will back up into the inferior vena cava and then the liver).
Diagnostic Studies
Liver function tests
Liver biopsy
Liver scan
Liver ultrasound
Esophagogastroduodenoscopy
Prothrombin time
o Would expect an increase in prothrombin time. Can expect Coumadin and Heparin to be administered.
Testing of stool for occult blood
o This is when there may be blood in the stools but it will not been seen by the naked eye.
Jaundice
o This is because the bilirubin is unable to conjugate.
Skin
o
Spider angiomas (telangiectasia, spider nevi), palmar erythema (the old blood cells are not being broken down and are
thus stored in the hands), petechiae (due to bleeding).
Endocrine Disturbances
o This is because the hormones (e.g., aldosterone, cortisol, androgens) are not being metabolized. This increase in serum
hormones will cause problems (e.g., edema, male/female characteristics due to the increase in serum androgens). Low in
potassium. Hair distribution different.
Hematologic Disorders
o Due to the decrease in clotting factors and an inability to store vitamin K. These patients have an increased likelihood of
bleeding and anaemia. Prothrombin. Anemia. Low in thrombocytes (thombocytpenia). Spleenomegly. Lymphopenic.
Palmar erythema Circulating estrogen we arent circulating the corticosterioids (red hands) affect red blood cells.
Peripheral Neuropathy
o This is because we are no longer storing the B vitamins.
98
Splenomegaly
o Back pressure caused by portal hypertension chronic passive congestion as a result of increased pressure in the
splenic vein.
o The spleen stores RBCs and 30% of platelets, which are used for clotting. Platelets live for 10 days (as opposed to 120
days for RBCs). It also stores lymphocytes (T-cells and B-cells) which are responsible for an immune response.
These patients will therefore have increased infections and risk of bleeding.
Esophageal Varices (i.e., dilated veins).
o Increased blood flow through the portal system results in dilation and enlargement of the plexus veins of the esophagus
and produces varices. An increase in pressure (e.g., cough, roughage) can cause these varices to burst.
Caput Medusae
o Collateral circulation involves the superficial veins of the abdominal wall leading to the development of dilated veins
around the umbilicus. To try and reduce pressure in systemc circulation.
Peripheral Edema and Ascites
o Ascites:
Intraperitoneal accumulation of watery fluid containing small amounts of protein. The body cannot make
albumin, which is responsible for drawing fluid back into the vascular space. Hypoalbuminia and increased
aldosterone.
Hepatic Encephalopathy
o This is usually a terminal condition. Ammonia not going through due to portal pressure. Its backing up and getting
into circulation and gets through the blood brain barrier this will kill brain cells. Terminal Condition.
Asterixis encephalopathy you can see. (liver flap arms cant stay up/tremors)
Fetor Hepaticus
o Musty, sweetish odour detected on the patients breath (it typically smells like feces).
o From accumulation of digested by-products.
Portosystemic/Peritovenous Shunt
This is done to prevent multiple needles as the patient is at an increased risk of infection and bleeding.
Esophageal Varices
Sengstaken-Blakemore Tube
o There are balloons down the side that put pressure on the capillaries when inflated in order to stop bleeding.
o This is a short-term treatment.
o Perienteral nutrition.
Portosystemic Shunts- Fig: 45-10
o This is a more long-term treatment.
99
The splenic vein is shunted from the liver directly into the kidney. This puts the patient at a higher risk of septicaemia.
Drug Therapy
There is no specific drug therapy for cirrhosis.
Drugs are used to treat symptoms and complications of advanced liver disease.
Nutritional Therapy
Diet for patient without complications:
o High in calories (from carbohydrates)
o CHO
o Moderate to low fat
o Amount of protein varies with degree of liver damage
Acute Pancreatitis
Review exocrine functions of the pancreas!!
o Pancreatic enzymes necessary for digestion to occur are amylase, protease, and lipase. These enzymes are carried in a
NaHCO3- solution in order to neutralize the HCl of the stomach.
o The hormone secretin (in the duodenum) signals the pancreas to secrete NaHCO3.
Acute Pancreatitis
The biggest reason for pancreatitis is alcohol abuse. Other reasons may be trauma, infection, drugs, autoimmunity, and following
surgery to the GI tract. Birth control.
If secretin is not secreted soon enough, NaHCO3- from the pancreas will not neutralize the HCl from the stomach. This is
problematic because if the chyme is released too soon into the duodenum, it will damage the pancreatic duct (thus causing
inflammation).
100
Clinical Manifestations
Abdominal pain is the predominant symptom.
o Pain located in the left upper quadrant.
o Pain may be in the midepigastrium.
o Commonly radiates to the back.
Complications
Pseudocyst
o A cavity surrounding the outside of pancreas that is filled with necrotic products and liquid secretions.
o Abdominal pain.
o Palpable epigastric mass.
o Internal complications (pulmonary complications due to swollen cavity).
Pancreatic abscess
o A large fluid-containing cavity within the pancreas.
o Results from extensive necrosis in the pancreas.
o Large and seen as worse.
Pulmonary (this is because the diaphragm cannot drop if there is an inflamed organ directly below it)
o Pleural effusion
o Atelectasis
o Pneumonia
Cardiovascular
o Hypotension (there is a lot of inflammation which can lead to haemorrhage).
o (skin might give a blueish-greenish circulation).
Tetany (caused by hypocalcaemia)
o The reason for this hypocalcaemia is unknown.
Diagnostic Studies
Serum amylase
Lipase
Urinary amylase is low (this is because the serum amylase is also )
Other lab abnormalities
Why?
o Hyperglycaemia damage to islets of landerhands they may become diabetic (because the insulin is not being
produced), Hypocalcaemia (reason unknown)
o Hyperlipidemia (the excess glucose from the hyperglycaemia will turn into fat)
Collaborative Care
Objectives include:
o Relief of pain
o Prevention or alleviation of shock
o Reduction of pancreatic secretions
o Fluid and electrolyte balance
o Removal of the precipitating cause
Drug Therapy
Demerol (reduces the spasms), IV morphine (step 3 morphine pain) (step 2 moderate codeine pain)
Nitroglycerin or papaverine (give these vasodilators, even though the patient is hypotensive, because it relaxes smooth muscle)
(vasodilates) (severely hypotenzive do not give right? Right). Hypotensive or shock would not geet this (very constricted
hypertensive then yea).
Antispasmodics (spasms from pain) (Never give demerol for chronic pain). Too short lifed.
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Carbonic anhydrase inhibitor (carbonic anhydrase makes NaHCO3 , which would typically be useful but if it cannot leave the
pancreas there is no point). Its an enzyme this inhibits the production of NaHCO3.
Antacids you wont be eating so why produce acid in the stomach. Well give you antacids.
H2-receptor antagonists (decrease gastric acid) prevents the production of hydrochloric acid.
Collaborative Care
Nutritional Therapy
o NPO status initially to reduce pancreatic secretion (not for long or youll start breaking down muscle mass and stores)
o Small, frequent feedings
o High-carbohydrate, low-fat, high-protein diet because it is good for repair, low fat.
o Bland diet
o Supplemental fat-soluble vitamins
o Enteral feeding (J or G tubes)
o TPN risk of infection, clots, fat embolisms, etc.
o Supplemental commercial liquid preparations
o Total parenteral nutrition (TPN): it is pre-digested food inserted via a central line
o No caffeine or alcohol
Nursing Implementation
Acute Intervention (risk of shock, risk of pneumonia, etc.)
o Monitor vital signs depending on the patient (e.g., q15min, q30min, q1hr)
Listen to the chest when doing vital signs!
o IV fluids
o Assess respiratory function
o Monitor for signs of hypocalcaemia (e.g., Trousseau and Chvotseks sign)
Ambulatory Home Care
o Physical therapy (due to muscle atrophy from not metabolizing protein).
o Counselling regarding abstinence from alcohol, caffeine, and smoking.
Notes
A person with acute pancreatitis can recover (i.e., the swelling will decrease and the pancreas will repair itself). Recall that the
main reason for acute pancreatitis is alcoholism.
Chronic Pancreatitis
Definition
Progressive destruction of the pancreas with fibrotic replacement of pancreatic tissue.
Strictures and calcifications may also occur in the pancreas.
Clinical Manifestations
102
Abdominal pain
o Located in the same areas as in acute pancreatitis.
o Heavy, gnawing feeling, burning, and cramp-like.
Malabsorption with weight loss
Constipation
Mild jaundice with dark urine
Steatorrhea (floaty, frothy, foul, fatty stools: recall the 4 Fs) (we dont have lipase to break up the stool looks like oil and
water).
Diabetes mellitus (it can be caused by pancreatitis, but not the other way around)
Diagnostic Studies
Increased serum amylase
Increased serum bilirubin
Increased alkaline phosphatase (indication of inflammation in either the liver or bone)
Mild leukocytosis (the number of WBCs will be increased)
Elevated sedimentation rate (ESR) indication of inflammation (how quickly red blood cells are going to fall out suggests
inflammation or infection somewhere). (heavier because of inflammation or infection so they will fall out of solution quicker).
Secretin (in the duodenum) stimulation test
Hyperglycaemia
Arteriography (want to see what is going on with the blood vessels)
X-ray
Endoscopic Retrograde Cholangio Pancretography (ERCP) (inside, with a dye, in the bile duct and pancreatic duct)
Collaborative Care
Prevention of attacks
Relief of pain
Control of pancreatic exocrine and endocrine insufficiency (pt will need to take enzymes since they arent making them and they
will likely be diabetic and will need insulin)
Surgery (not many successful transplants pancreatic cancer is typically short lived).
Nursing Management
Focus is on chronic care and health promotion.
o Dietary control
o Control of diabetes (because pancreas is destroyed).
o Patient and family teaching
103
Purpose
Arterial blood shows the make-up of blood before it is distributed to the tissues.
The radial artery is typically chosen. This is a very painful procedure.
By treating the underlying condition, the ABGs will typically resolve themselves.
pH
pH is measured on a scale from 1-14, with 1 being extremely acidic and 14 being extremely basic.
The pH is an indirect measure of H+ ion concentration.
Ratio of base (HCO3-) to acid (CO2).
o Bicarbonate is a weak base and carbon dioxide is a weak acid (i.e., the requirements for buffers).
Acids give up (donate) H+ ions, while bases pick up H+ ions.
The expected pH of the body is between 7.35-7.45 (i.e., slightly alkaline).
PaCo2 35-45 mmHg (resp component)
HCO3 22-26 mEq/L (metabolic component) (low is acidic; high alk)
Regulators of Acid/Base
Buffers (there are many buffers in the body used to maintain homeostasis).
o Lots of albumin in the body as buffers
Respiratory system (works to control the bodys acidic conditions via CO2 excretion or retention).
o This works faster than the renal system.
Renal system (works to control the bodys basic conditions via HCO3- by absorbing, retaining, or creating HCO3-).
o Metabolic system
o First buffers, then lungs, then kidneys
Buffers
Primary regulators of changes in acid-base balance.
Act immediately.
Present in blood and tissues.
Take up or release extra H+ ions (e.g., bicarbonate, proteins, globulins).
o Proteins are amphoteric (i.e., both acid and base properties) and are therefore very important regulators.
Respiratory System
Eliminates CO2.
Increased respirations leads to CO2 eliminated from body and CO2 in blood.
Decreased respirations leads to CO2 elimination from body and CO2 in blood.
Responds within minutes to hours to changes in acid/base.
Only 50%-75% effective as a buffer.
o In order to be completely balanced, you need both the respiratory and metabolic systems functioning.
Acid-Base Balance
CO2 + H2O
H2CO3
H+ + HCO3
Lungs
Respiratory
Fast
Kidneys
Metabolic
Slow
Renal System
Secretes hydrogen (H+) ions and reabsorbs bicarbonate (HCO3-) ions.
Reabsorption and secretion of electrolytes (e.g., Na+, Cl-, K+).
o In order to reabsorb sodium in the kidneys, there must first be the excretion of hydrogen.
o The bicarbonate plays an important role.
Responds within hours to days.
104
Exam Question!
iClicker Question
What of the following is true regarding SaO2 and PaO2?
a) SaO2 and PaO2 refer to the same thing.
False. SaO2 refers to oxygen saturation (i.e., the percentage of heme binding sites occupied by O 2), whereas PaO2 refers to
oxygen pressure (i.e., pressure exerted by O2 molecules not bound to haemoglobin).
b) SaO2 is the amount of Hgb saturated with oxygen.
c) PaO2 is the pressure of Hgb.
False. PaO2 is the pressure exerted by the O2 molecules not bound to haemoglobin.
d) PaO2 is measured with a pulse oximeter.
Interpretation of ABGs
Evaluate pH: this determines acidosis or alkalosis.
A pH value of 7.40 is in the middle of the normal range of 7.35-7.45.
o Value below 7.40 is moving towards acidosis.
o Value above 7.40 is moving towards alkalosis.
105
Respiratory
o pH, PaCO2
o pH, PaCO2
Metabolic
o pH, HCO3
o pH, HCO3
alkalosis
acidosis
alkalosis
acidosis
If both the respiratory and metabolic components match the pH, it may be a mixed disorder, which is rare, or there may have been
an issue with the ABG (i.e., the blood may have accidently been taken from a vein as opposed to an artery).
Interpretation of ABGs
If appropriate, treat the underlying cause and then treat acid-base imbalance. Often times, once the underlying cause has been
treated, the acid-base imbalance will correct itself.
ABG Interpretation
Example #1:
We are in acidosis (i.e., low pH).
CO2 47 (normal range is 35-45 it is high and acidotic)
HCO3- 24 (normal range is 22-26 it is normal)
Since the pH is outside the range and the HCO3- is normal, we are not compensated (therefore partially compensated or
absent).
Ac Nor Alka
idi
mal
line
c
p
H
O2
HC
O3
The acidosis appears to be respiratory in nature (due to the CO2 value). Since the HCO3- value is within normal ranges, we have
uncompensated respiratory acidosis.
106
Respiratory Acidosis
pH
low
PaCO2
high
What could cause this condition?
COPD, sedatives, overdose. pneumonia, anything that
causes hypoventilation, low resp rate, shallow breaths,
quiet death decreased resps
o
Respiratory Alkalosis
pH
high
PaCO2
low
What could cause this condition?
o Hyperventilation (due to anxiety, pain, sepsis).
Metabolic Acidosis
Metabolic Alkalosis
pH
low
pH
high
HCO3
low
HCO3
high
What could cause this condition?
What could cause this condition?
o Kidney failure, overconsumption of antacids.
Kidney failure, diabetes (i.e., DKA). Drugs, meds,
overdosing,
More Fun with Acid-Base
Mixed diagnoses:
o More than one problem:
Acute and compensated respiratory acidosis.
Respiratory and metabolic acidosis.
If you treat the underlying cause, the acid-base imbalance will sort itself out.
Hyperkalemia
o H+ drives K+ out of cells into serum (recall that alkalosis cause K+ to enter the cells).
o Treat acidosis, hyperkalemia resolves.
iClicker Question
A client with an acid-base imbalance has an altered potassium level. The nurse recognizes that the potassium level is altered
because of which following reason?
a. Potassium is returned to extracellular fluid when metabolic acidosis is corrected.
False, K+ is returned to the cell when acidosis is corrected. Alkalotic conditions cause K+ to enter the cell.
b. Hyperkalemia causes alkalosis that results in potassium being shifted into the cells.
c. Acidosis causes hydrogen ions in the blood to be exchanged for potassium from the cells.
d. In alkalosis, potassium is shifted into extracellular fluid to bind excessive bicarbonate.
False, K+ is shifted into the cells during alkalosis.
Interpretation of ABGs
Example #1
pH 7.36
PaCO2 67
PaO2 47
HCO3- 37
What is this? Fully compensated respiratory acidosis.
o Acidosis because the pH is lower on the normal scale.
o Respiratory in nature.
o Fully compensated (because both the CO2 and HCO3- are outside the normal ranges).
Ac
idi
c
Nor
mal
pH
Alka
line
107
HC
O3-
Example #2
pH 7.18
PaCO2 38
PaO2 70
HCO3- 15
What is this? Absent/uncompensated metabolic acidosis.
o Acidosis.
o Metabolic.
o Absent/uncompensated because the CO2 is
normal. It cannot be fully compensated because
the pH is not within normal ranges.
Ac
idi
c
p
H
Nor
mal
H
C
O3-
Alka
line
CO2
Example #3
pH 7.58
PaCO2 35
PaO2 75
HCO3- 50
What is this? Uncompensated metabolic alkalosis.
o Alkalosis.
o Metabolic due to the HCO3-.
o Uncompensated because CO2 is normal.
108
Ac
idi
c
Nor
mal
pH
CO2
Alka
line
HC
O3-
Example #4
pH 7.60
PaCO2 30
PaO2 60
HCO3- 22
What is this? Uncompensated respiratory alkalosis.
o Alkalosis.
o Respiratory.
o Uncompensated.
Ac
idi
c
Nor
mal
Alka
line
Example #5
pH 7.28
PaCO2 28
PaO2 70
HCO3- 18
What is this? Partially compensated metabolic acidosis.
o Acidosis.
o Metabolic.
o Partially compensated (i.e., the CO2 is trying to
correct the acidity).
pH
CO2
HC
O3-
109
Ac
idi
c
p
H
Nor
mal
H
C
O3Case Studies
Case Study #1: Jeri
Alka
line
CO2
110
pH low
Sats are: 85
Pao2 are: 50
CO2 high (due to retention)
HCO3- maybe a change
Respiratory acidosis.
2) What is your treatment?
DB&C.
Increase fluids.
Antibiotics therapy.
pH acidosis
CO2 high
HCO3- low
2) What is your treatment?
Insulin
Electrolyte replacement/fluids
r/a
111
Case Study #6
ABG results are: pH 7.20, PaCO2 58, PaO2 59, HCO3- 24
Case Study #7
ABG results are: pH 7.39, PaCO2 38, PaO2 44, HCO3- 24
Case Study #8
ABG results are: pH 7.50, PaCO2 28, PaO2 85, HCO3- 24
Case Study #9
ABG results are: pH 7.57, PaCO2 46, PaO2 87, HCO3- 38
Air gets trapped and we cant expel it. We have to make room somehow, so we press on the diaphragm and gets pushed down.
Intercostal cartilage as you get older become more calcified. Mostly d/t cigarette smoking (and being older). Smoking is bad.
Cigarette Smoking
80-90% of COPD deaths in North America are related to tobacco smoking.
~4,000 chemicals and gases inhaled with cigarettes.
Nicotine acts as a SNS stimulant.
o It causes vasoconstriction of the peripheral blood vessels which causes an increase in heart rate and workload. This will
lead to an increase in blood pressure.
Questions to ask patients with COPD:
o Do you experience SOB? When (i.e., how much exercise/how far/how long)?
o Do you have a cough? Is it productive? What does it look like? When does this occur (e.g., on exertion, in the morning,
during the night)?
o Do you get frequent colds/flues in the winter?
Inflammatory response goes on with cellular hyperplasia, ciliary activity cant move things through, build up of mucous. CO2
breathing in and less oxygen able to use for the rest of the body.
How much they smoke and for how long. Biggest questions to ask.
Have they tried to quit?
D/t hyperplasia crackles.
112
Infection
Major contributing factor to the aggravation and progression of COPD.
Recurring infections impair normal defence mechanisms.
o The excess mucous trapped in the bottom of the lungs is a lot harder to excrete, which may lead to pneumonia.
Bacteria like moist dark areas. COPD + cough (say green sputum) pt may automatically be put on antibiotics because we know
they wont be able to move the secretions d/t COPD. Sometimes prophalyaxily. If you dont they may die vs resistant strains
(Catch 22 there).
Heredity
-Antitrypsin (AAT) deficiency is the only known genetic abnormality that leads to COPD.
AAT deficiency accounts from <1% of COPD. These patients will have COPD at a young age.
It breaks down the elastin in the lungs.
PaO2 falls as a rate of 4 mmHg for each decade of life, beginning after age 20.
Thoracic cage changes from osteoporosis and calcification of costal cartilages.
Emphysema
There is a decrease in number of alveoli and the ones that are present enlarge, decreasing the surface area and ability to exchange
gas.
This destruction of alveoli is permanent.
2) Panlobular
The alveoli are all enlarged. boule are cauliflower like
The tripod position allows the chest to expand and help the person breathe.
Pathophysiology
There is a decrease in number of alveoli and the ones that are present enlarge, decreasing the surface area and ability to exchange
gas.
This destruction of alveoli is permanent.
What do bullae have to do with anything?
o They are cyst-like blobs in the alveoli that are fluid encapsulated.
How does the body compensate?
113
Clinical Manifestations
What would this person look like?
o Emaciated (the body is working hard and using a lot of calories just to breathe; these patients are also not hungry)
o Tripod position
o Using all the respiratory muscles (e.g., intercostals, diaphragm, sternocleidomastoid)
Will hear hyper resonate sounds d/t trapped air. (99 Tactile fremulis)
Use of tripod muscles, accessory muscles
Weight loss less calories, more fluids, difficulty eating so need nutrient dense calories.
Earliest symptoms:
o Frequent productive cough during winter (especially at the change between fall and winter).
o Frequent respiratory infections.
Bronchospasm can occur at end of paroxysms of coughing (i.e., the inability to stop coughing).
Cough usually exacerbated by respiratory irritants or cold air.
Chronic Bronchitis
Description
o Presence of chronic or productive cough for 3 or more months in each of 2 successive years in a patient whom other
causes of chronic cough have been excluded (e.g., asthma).
Tend to do it within the first year. Will start them on things like ventolin, etc.
Narrow airways, hypersecretions, Co2 levels go up/elevated (responsible for the urge to breath), hypoventilating d/t
hypercapnia.
Hr increases, not very oxygenating blood = pulmonary vasoconstriction
Resp acidosis confusion, forgetful,
More red blood cells are present, will increase in viscosity (like jelly) of deoxygenated blood.
Too much preload, end up with pulmonary (right sided) failure
Pathophysiology
Hypoxemia ( O2), hypercapnia ( CO2), and respiratory acidosis (due to CO2) usually develop late in disease.
o The alveoli are working fine; they just cant enough O2 because of the mucous present.
o The body will increase their production of RBCs in order to have more receptor sites for O2. These patients will have a
very high haemoglobin.
o Acidosis will eventually cause vasoconstriction, which is problematic because there is also an increase in RBCs that will
try squeeze through a constricted vessel, therefore increase the BP.
Inflammatory swelling + thick mucous = narrowing of airway lumen and diminished airflow.
Cough is often ineffective to remove secretions.
o This is because there are no cilia to move the mucous and the patient is unable to take a deep breath.
Chronic Bronchitis
114
Knowing all of this, what do you think this person would look like?
Haemoglobin may reach 200 g/L or more.
o This is because of the lack of O2. Many of these haemoglobin molecules will not get the O2 they need.
Normal hgb (120-130) 200 is high.
Pt will be cyanotic
iClicker Question
When reviewing the arterial blood gases of a client with COPD, the nurse identifies late-stage COPD based on which of the
following results?
1. pH 7.26, PaCO2 58 mm Hg, PaO2 60 mm Hg, HCO3 30 mmol/L
2. pH 7.30, PaCO2 45 mm Hg, PaO2 55 mm Hg, HCO3 18 mmol/L
False. The PaCO2 is high, but still within normal range. Wed expect it to be higher and also have a high HCO3-.
3. pH 7.40, PaCO2 40 mm Hg, PaO2 70 mm Hg, HCO3 25 mmol/L
False. The pH is within normal range. We would expect an acidic pH due to the retention of CO2.
4. pH 7.52, PaCO2 30 mm Hg, PaO2 80 mm Hg, HCO3 35 mmol/L
False. The pH is high and thus basic. We would expect an acidic pH due to the retention of CO2.
COPD
Complications
Cor Pulmonale (i.e., failure of the right side of the heart brought on by long-term high blood pressure in the pulmonary arteries
and right ventricle of the heart.)
Pulmonary Hypertension
Acidosis
Polycythemia (i.e., in RBCsdeveloped secondary to a resp problem)
o This blood is extremely viscous and may lead to pulmonary hypertension.
Distended neck veins (due to problems with the right side of the heart).
Hepatomegaly (due to portal hypertension) with upper quadrant tenderness.
Ascites (due to third space shifting).
Epigastric distress (due to the increase in pressure on the diaphragm).
S3 & S4 heart sounds.
hyperviscosity so extra heart sounds
Peripheral edema.
Weight gain.
Acute exacerbations of chronic bronchitis.
Peptic ulcer disease and GERD (due to ascites, and hypertension).
Pneumonia. and ? Part off Right sided failure are really important to tx before going into acute resp failure. ACP status important
re intubation.
Acute respiratory failure.
People with COPD have their breathing triggered by O2 levels (not CO2 levels as in normal, healthy individuals). If they have too
much O2, their breathing mechanism will not shut off altogether, as previously believed, but their breathing will be hindered.
Diagnostic studies
What would you want to do?
o Vital signs
o Dark patches (pneumonia)
o PFTs litres you can breath in and inspiratory and expiratory capacity
115
o pH decreased
o PaO2 decreased
o CO2 increased
o HCO3- increased (in time as a compensatory mechanism)(increasing trying to buffer acid and high CO2)
Typical findings include reduced FEV/FVC (forced expiratory volume/forced vital capacity) and increased residual volume and
total lung capacity.
Ratio of <70% suggests presence of obstructive lung disease.
Collaborative Care
Smoking cessation
Drug therapy
o Corticosteroids
o Bronchodilators (e.g., Ventolin) (some for large and some for small),
o Anticholinergic (e.g., Atrovent)
Check medication book.
inhaled epi
To prevent bronchospasms
O2 therapy
o O2 narcosis (too much O2). You want to keep this persons SaO2 around 92%.
Respiratory therapy
o Pursed-lip breathing (blowing out candle breathing)(this enables a person to expel more CO2).
o Diaphragmatic breathing.
o Chest physiotherapy (e.g., pummelling).
o Cough in the later afternoon in evening if asthmatic, other might be in the morning
Aerosol-nebulization therapy.
Nutritional therapy: high calories, high protein, avoid foods that may cause gas, small frequent meals
Nursing Management
Nursing Assessments
o Health history
o Physical assessment
What symptoms would you expect to find in an acute exacerbation of COPD?
Cough, sputum, SOB, may see a barrel chest, use of accessory muscles,
Crackles if there is bronchitis component, pale color, pulse elevated (depending on progression of disease), increased Co2 =
hypoventilating (urge suppressed),
Nursing Assessments
Acute exacerbation
What are you going to do about it?
o Activity (not to the point of tiring the patient).
o Pt may be leaning forward, keep HOB elevated,
Nursing Implementation
Ambulatory and Home Care
o What would you expect to do for patients in these environments?
Encourage patient to pace themselves.
Encourage adherence to medication therapy.
Use several pillows to stay propped up while sleeping.
Get rest.
116
TUBERCULOSIS
Mycobacterium tuberculosis
Kills more people worldwide than any other infectious disease.
19-34% of worlds population estimated to be infected.
8 million new cases each year with 3 million deaths.
Endemic of TB with HIV infection.
Multidose resistant strains of Mycobacterium tuberculosis.
It is reversible if treated early.
Vulnerable, overcrowding, new immigrant populations.
Airborne, droplet.
Tuberculosis
It is seen in developing countries, over-crowded housing, and with poor nutrition.
It is spread by airborne droplets (e.g., sneezing, coughing) that are inhaled after prolonged exposure.
It likes to grow down low in the lungs.
Healing of primary lesion occurs by resolution, fibrosis, and calcification. The granulation tissue surrounding the lesion may
become more fibrous and form a collagenous scar around the tubercle.
If the initial immune response is unsuccessful at controlling the organism, clinical disease results.
Clinical Manifestations
Early stages are usually free of symptoms!
Systemic symptoms:
o Fatigue
o Weight loss
o Malaise
o Low-grade fever (e.g., 38.1C)
o Anorexia
o Night sweats
Acute symptoms:
o High fever
o Pleuritic pain
o Chills
o Productive cough (especially blood)
o Generalized flu symptoms
o Bloody cough severely sick, people must take precautions when it comes to coughing,
o Initially flu-like symptoms, malaise, not hungry
o
o Complications
Military TB/Necrotic Ghon
o It has spread beyond the lungs and reached other organs.
Pleural effusion and empyema (puss in the lungs)
TB pneumonia
o
o These types of TB are hard to treat.
o
o Diagnostic Studies
Skin testing (Mantoux) does not necessarily mean you have it, but that youve been exposed to it
Chest X-ray (this may reveal a Ghon complex)
Sputum studies
Bacteriologic studies
Gastric washings
CSF
Cultures
Nucleic Acid Amplification
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Collaborative Care
Latent TB infection
o Individual is infected with bacilli but is not actually ill.
o Usually treated with INH for 6-9 months.
Not ill but bacilli (not sick and not contagious) lots of nurses or a family if one member has tb
Vaccine
o Bacille Calmette-Gurin (BCG)
Efficacy not clear.
Nursing Implementation
Screening programs in high risk groups.
Identify contact of patients with TB.
Teach:
o Tissues in paper bag then garbage (i.e., double bag Kleenex).
o Cover mouth when coughing/sneezing.
o Handwashing.
o Medicine regime and encourage compliance (it is necessary).
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Stem cell
Erythroblast
Normoblast
Basophilic
metamyelocy
te
Reticulocyt
e
Basophil
(histamine
)
Erythrocyt
es (RBC)
Myeloblast
Eosinophilic
metamyeloc
yte
Monoblast
Neutrophilic
metamyelocy
te
Band cell
Monocytes
Lymphoblas
t
Megakaryoblast
Lymphocytes
Megakaryocy
te
Found in bone
marrow
Found in blood
Leukocytes (WBCs)
Thrombocytes
(platelets)
Eosinophil
Neutrophil
You should not see erythroblasts in the blood! This is only seen in the bone marrow. The reticulocyte will be seen in the blood
and will mature into an erythrocyte.
What would be worse to live without, monoblasts or myeoblasts? The myeoblasts, because this the second line of defence (i.e.,
the inflammatory response).
If you reduce the formation of RBCs, you may not have a lot of platelets.
3rd line of defense is the immune system
RBC live for 120 days
o WBC between 4-10,000
o Myloblasts = granlocytes
o Need leukocytes for inflammation
o Monoblasts and lymphocytes 3rd line of defence (in the blood, spleen, lympth nodes)
o
Types and Functions of Leukocytes
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Type
Cell Function
Granulocytes (Myeoblasts)
Neutrophils
Phagocytosis, early phase of inflammation
Eosinophils
Phagocytosis, parasitic infections
Basophils
Inflammatory response, allergic response
Agranulocytes
Lymphocytes (T cells)
Cellular, humoral immune response
Thelper cells, Tkiller cells
Monocytes
Phagocytosis; cellular immune response
If the eosinophils levels are increased, you can assume a parasitic infection.
Anaemia
It is a broad category of disorders involving a deficiency of RBCs. It is not seen on its own (a lot of diseases come with anemia).
Anaemia is reflected in:
o Haemoglobin
This explains the O2 carrying capacity of the blood (recall that every haemoglobin molecule can carry 4 O2
molecules). Travels as carbolic acid (switches in the lungs to carbon dioxide).
Little volume = lots of cells hgb HIGH? Dehydrated?
Normal values:
Females: 120-160
Males: 140-180
o Hematocrit (Going to tell you if youre dilutional, or dehydrated)
The percentage of the pack cells (i.e., RBCs) to the total volume.
This is the value you want to look at to determine if someone is haemorrhaging.
Normal values:
Females: 38-47%
Males: 40-54%
o RBC count
Normal values:
Females: 4-4.5 million
Males: 4.5-6.5 million
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Classification by red cell morphology (recall that cytic means cell; chromic means haemoglobin)
o Cell size/HGB content
o Classification
o Decreased red blood cell production
o Increased red blood cell destruction
o Blood loss
There are many combinations possible:
Normocytic
Normochromic
Microcytic
Hypochromic
Macrocytic
Hyperchromic
o Tablee 33-1
o Types:
Normocytic Normochromic Anaemia
Normal cells and normal amount of haemoglobin.
This could be due to haemorrhage (i.e., acute blood loss), haemolysis, chronic renal disease,
pregnancy, aplastic anaemia, or other conditions that destroy RBCs.
Treatment: administer pack cells or blood.
Microcytic Normochromic Anaemia
Small cells with normal amount of haemoglobin.
Seen with tumours, infections, viral illnesses.
Macrocytic Normochromic Anaemia
Large cells and normal amount of haemoglobin.
This is also known as pernicious anaemia. There is a problem with B12. Recall that the gut has
intrinsic factors that will help the body absorb the vitamin B12. These patients will require monthly IM
injections. Orally if IF, injection if no IF
Cobalamin (Vitamin B12 deficiency), liver disease, folic acid deficiency.
Treatment: give patient B12.
Microcytic Hypochromic Anaemia
Small cells and low amount of haemoglobin.
Seen in iron and folic acid deficiency, thalasemia, lead poisoning, as well as slow bleeds (e.g.,
prolonged menstrual periods).
Treatment: give patient folic acid.
Classification by etiology/cause
o Dietary Deficient States
Deficiencies of B12, folic acid, and iron.
o Hereditary Disorders
Sickle cell anaemia, thalasemia.
o Bone Marrow Disease
The body could not be making enough, breaking too much down, or making too much.
Aclassic anaemia means that all blood types and cells are low.
o Bleeding States
Acute (e.g., haemorrhage)
Chronic (e.g., prolonged menstrual bleed)
o
o Key Features of Anaemia
Skin
o Pallor: due to reduced amount of haemoglobin and reduced blood flow to the skin.
o Jaundice: occurs due to the increased breakdown of RBCs which causes an accumulation of bilirubin.
o Pruritis: due to increased serum and skin bile salt concentrations.
o In addition to the skin, the sclera of the eyes should be evaluated for jaundice as it is a better representation of the
integumentary system.
CVS
o The CVS changes that are seen results from the hearts attempt to increase the distribution of O 2 via the blood to the
bodys cells.
o Cardiac output is maintained by increase the heart rate (as seen below) and stroke volume).
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Tachycardia (i.e., a compensatory mechanism) which may lead to palpitations, chest pain, and murmurs (because the
heart does not have the time to adequately fill before sending blood throughout the body). The decrease in blood
viscosity will also contribute to the murmurs and bruits.
A person with a murmur will have to take antibiotics before going to the dentist in order to prevent endocarditis.
In extreme cases, angina pectoris or an MI can occur if myocardial O2 needs are not met.
o
Lungs
o The pulmonary changes seen reflect the lungs attempt to increase the amount of O2 reaching the lungs.
o Dyspnea at rest, tachypnea, tire easily.
Neurologic
o Dizziness, syncope, headaches, and brain damage if the body does not get enough O2 (i.e., 3 minutes without O2 will lead
to brain death).
Other
o Chronic fatigue.
o
o Collaborative Management
History
o Recent blood loss or trauma; chronic liver, endocrine, or renal disease (including dialysis); medications; surgery or other
treatments.
Lab
o Haemoglobin (Hgb) and hematocrit (Hct) are both expected to be low.
RBC indices MCV, MCH, MCHC
MCV = mean cell volume (i.e., cell size)
MCH = mean cell haemoglobin (i.e., amount of haemoglobin)
MCHC = mean cell haemoglobin concentration (i.e., the saturation of haemoglobin)
TIBC and Serum Iron
TIBC = total iron-binding capacity (i.e., the amount of iron stored in places other than the serum)
Feritin in liver (called)
Reticulocyte count
You do not want a lot of reticulocytes. Too many reticulocytes will indicate that bone marrow is
sending out the RBCs too early.
o
o Treatment
This will depend on the cause (e.g., some types may require Vitamin B12, others folic acid, etc.).
o
o Polycythemia
This is an absolute increase in RBC mass.
Erythropoietin is a hormone produced by the kidneys in response to low levels of O2. It stimulates the production of erythrocytes.
Types:
o Primary (a.k.a., polycythemia Vera)
It is insidious disease due to a chromosomal mutation.
The RBCs, granulocytes, and platelets will be affected.
The erythropoietin will be either decreased or normal.
Splenomegaly and hepatomegaly are often manifested.
o Secondary
This is a normal physiologic response to hypoxia.
Long-distance athletes will often train in high altitudes so their bodies will have more red blood cells. These
red blood cells will last up to 120 days, meaning that when they get to a lower altitude, their muscles will have
more O2 available due to the increase in RBCs.
The erythropoietin will be increased.
o
o Clinical Manifestations & Complications Polycythemia Vera
Manifestations will be hypertension due to hypervolemia, and hyperviscosity.
o The body will move from second to first space shifting.
o The heart rate will be increased, there will be clotting problems (e.g., DVT)
o Blood vessels breaking as well as clotting.
o Headaches, dizziness, vertigo, tinnitus, and visual disturbances.
o
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1)
2)
3)
4)
Complications:
o Most serious stroke (due to a thrombus).
o Haemorrhage (due to the hypertension and the bursting of the over-distended vessels).
o Generalized pruritis (due to the increase in basophils).
Recall that the granulocyte production (i.e., basophils, neutrophils, and eosinophils) has increased.
o Uric acid is a by-product of cell breakdown (which is common as so many RBCs are being destroyed). A form of gout
may therefore be seen due to this increase in uric acid crystals. Hyperuricemia (increase of uric acid in the urine) may
also be exhibited.
o
o Diagnosis
CBC (it is expected that the RBC count is going to be increased)
Alkaline phosphatase (will increase as an indication of bone or liver disease)
Uric acid (will be increased; it is a by-product of protein breakdown)
Histamine (increased due to the increase in number of basophils)
Bone marrow (bone marrow aspiration would reveal increased number of erythroblasts)
Splenomegaly
o This is never found in secondary anaemia, only primary.
o The spleen is responsible for destroying old and defected blood cells, meaning that it is working harder to accommodate
all the extra RBCs and therefore increasing in size.
o Erythropoietin expecting it ti be high. Its released when you are hypoxic, primary its low or normal. Secondary its
high.
o
o Collaborative Management
Directed at reducing blood volume and viscosity and bone marrow activity.
Reduce hct to less than 45-48%
o
o Nursing Management
Phlebotomy
o Done until the hematocrit is near 50%.
Hydration if the person stands to become dehydrated
o I&O is extremely important.
Myelosuppressive Agents (e.g., Methotrexate)
o This is to suppress the bone marrow from producing a lot of RBCs.
Allopurinol (recall that this is anti-gout)
o Used to decreased your uric acid
Anti-platelet Agents (e.g., Plavix/ASA)
This person can become anaemic. Supplemental iron should not be given as the body will then start to make more RBCs.
o
o Thrombocytopenia
Thrombocytopenia is when platelet count is decreased.
o Normal 150,000L-440,000L.
o Thrombocytopenia <150,000L.
Normal Platelet function:
o Platelets form haemostatic plugs in a fibrin mesh in order to prevent bleeding/promote clotting.
o Normal lifespan of 10 days
Thrombocytopenia can be either inherited, as seen in Fanconi syndrome (pancytopenia) and hereditary thrombocytopenia, or
acquired, as seen in aplastic anaemia, chronic alcoholism, and other conditions.
o
o Causes
Failed Platelet production
Certain drugs (e.g., myelosuppressant), radiation, leukemia.
Increased Platelet destruction
Autoimmune disorders, alcohol, sepsis.
Loss of Platelets
Haemorrhage.
Intravascular Dilution
o
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o Implications
>50,000L potential haemorrhage from minor trauma (e.g., nose bleed).
10-50,000L spontaneous bleeding.
<10,000L often fatal, severe bleeding risk.
o
o Signs and Symptoms
Purpura, which is a combination of ecchymosis and haemorrhages.
Petechiae and blood blisters are usually seen.
o
o Sites to Monitor
Generally limited to skin and mucous membranes.
Arms, legs, upper chest and neck.
o
o Treatment
Withdraw or treat stimulus (e.g., drugs, therapy).
Precautions to avoid bleeding.
Corticosteroids (they suppress the immune response).
Administer platelets.
o Except during DIC = Disseminated Intravascular Coagulation, which occurs during abdominal surgery.
Attempts to clot, but it doesnt work, so it just results in a bigger hemmorahge.
Splenectomy.
o
o Immune Thrombocytopenia Purpura (previously known as Idiopathic Thrombocytopenia Purpura) ITP
It is an autoimmune disease causing platelet destruction (#1 reason why this disease happens)
Acute
o Occurs in patients with acute, post-viral infections (e.g., chicken pox).
Chronic
o Is typically linked with HIV and Lupus.
The platelets are coated with antibodies, which, when passed through the spleen are seen as foreign and destroyed by
macrophages. Platelets typically survive for 8-10 days; however, in patients with ITP, the lifespan of the platelets is between 1-3
days.
o
o Clinical Manifestations
Fever
Enlarged spleen
Bleeding mouth, nose
Risk factors such as HIV
o
o Diagnosis
History and lab
Includes all medications, including OTC and herbal medications
Bone marrow aspiration
o The megakaryocytes will be high because the thrombocytes are being destroyed from the autoimmune process. This will
cause the body to increase the megakaryocyte production.
Decreased platelet count
If bleeding decreased Hgb and Hct
Idiopathic Thrombocytopenia Purpura
o
o Treatment
Bleeding precautions (apply pressure)
Oral corticosteroids (e.g., prednisone) help suppress the immune function of the spleen. In addition, corticosteroids suppress
antibody formation. (suppress immune sytem)
IV Immunoglobulins (as the person has developed antibodies) (more at risk for infection)
Blood replacement therapy (never give with abdominal sx d/t dic risk, can give constuient blood)
Splenectomy
Avoid use of ASA anti-platelet inhibitor, dont t take otc St. Johns wort.
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o
o
o
o Note
An antidote for heparin is Vitamin K.
o
o Heperain Induced Thrombocytopenia and Thrombosis Syndrome/HITTS
Platelet destruction(possible immune response of body rejecting heparin so will need to give more and more heparin. If INR is
really high - Antidote is Protamine Zinc.
Vascular endothelial injury
Exchanging blood more serious
Believed to be an immune mediated response to heparin
Treatment d/c heparin, plasmaapheresis (exhchanging plasma more serious), individual reaction, INR raises significantly ,
protamine zinc to reveerse.
Thrombocytopenia
50,000 potential haemorrhage from minor trauma
10-50,000 spontaneous bleeding
<10,000 often fatal, severe bleeding risk.
o
o Neutropenia
It is a decrease in number of neutrophils (i.e., <1,000-1,500 L). Granulocytes in particular.
It may be a primary hematologic disorder but it is more often associated with other disorders:
o Ca chemotherapy
o SLE
Chemotherapy kills fast growing cells.
o Adverse drug reactions
o Mononucleosis its transient
o TB
o Reasons for becoming Neutropenic: Drug therapy, haematological disrders, leukemia, HIV, autoimmune disorders,
infections, severe sepsis, bone marrow infiltration, transfusion reactions, dialysis.
o
o Skin first line of defence, then immune system (neutrophils) very at risk for infections.
o
o Know aplastic anemia low everything.
o
o Clinical Manifestations
Depends on severity
o Diminished phagocyte response
There is diminished phagocytosis (i.e., inflammatory response), thus making the patient more susceptible to
infection. Might think UTI. Must get sample. If suspected of neutropenia dont wait. Dont want to mask a
fever either. Temp is 38 or 38.5 for fever. Treat or they will die. Cant wait for the results. Tx immediately. Dx:
differentials (wbc with differential including ANC (absolute neutrophil count), hgb, hct, reticulocyte count and
platelets, drug hx, bone marrow aspiration)
o Fever
The cardinal signs of inflammation are not greatly exaggerated. For example, the patients temperature may rise
from 36.8C to 37C.
o Infection
If the urine is cloudy and smells, send a sample down for C&S but start antibiotics immediately (i.e., broad
spectrum antibiotics) as the patient may be dead by the time the C&S comes back from the lab. Once the results
come back, use an antibiotic specific to the cause.
o Changes in mentation
The person may become septic (i.e., infection flowing through the blood). Since there is no acute inflammation
response, this person may not have a fever.
o
o Diagnosis
CBC with differential (i.e., to differentiate between the WBCs).
Bone marrow aspiration.
o
o Collaborative Care/Nursing Management
Determine cause / Remove offending agent (e.g., the chemotherapy).
Prophylactic, therapeutic antibiotics
Administer granulocyte stimulating drug (G-CSF and GM-CSF)
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Reverse isolation, screen visitors, only cooked food, more at risk for fungal infections
Granulocyte infusion (i.e., neutrophils, basophils, eosinophils).
Neupogen.
o It is a stimulant for the bone marrow to produce more neutrophils.
This patient will be on reverse isolation (wash your hands, wear a mask)!
o Protecting the patient from us
If the patient is given raw fruit, ensure they have been washed with soap and water.
Notify a doctor is you notice a possible elevated temperature.
o
o Leukemia
A group of malignant disorders affecting the blood and blood-forming tissues of:
o Bone marrow
o Lymph system
o Spleen
Occurs in all age groups.
Results in an accumulation of dysfunctional cells because of a loss of regulation in cell division.
Fatal if untreated.
o Progressive.
Patients who are leukemic, are also going to be anemic and have a lot of bleeding (making lots of WBC so not making as many
RBC and platelets)
o
o Etiology and Pathophysiology
No single causative agent.
It occurs most likely due to a combination of factors (i.e., genetic and environmental influences).
o
o Classification
Cell maturity and nature of onset
o Acute
The cells are not mature (i.e., they are pushed out of the bone marrow too early).
o Chronic
The cells are mature.
Type of white blood cell (WBC)
o Granulocytes (i.e, basophils, eosinophils, neutrophils)(responsible for inflammation our second line of defense VERY
BAD Dont want this one)
o Agranulocytes (i.e., lymphocytes, monocytes)
o Types:
Acute lymphocytic leukemia (ALL)
Acute myelogenous leukemia (AML)
Also called acute nonlymphoblastic leukemia (ANLL). This type has the worst prognosis because it deals with
myeloblasts (i.e., the granulocytes), which are involved in inflammation.
o Chronic myelogenous leukemia (CML)
o Chronic lymphocytic leukemia (CLL)
o There are also some unclassified types, the prognosis of which is really, really poor as the drugs do not work.
o
o Acute Myelogenous Leukemia (AML) also referred to as Acute Non-Lymphoblastic Leukemia (ANLL)
One fourth of all leukemias.
o 85% of the acute leukemias in adults.
Abrupt, dramatic onset.
o Serious infections (as there is no inflammation process), abnormal bleeding (if a whole lot of white cells are made, the
body cannot make many platelets).
Characterized by uncontrolled proliferation of myeloblasts, the precursors of granulocytes.
o Hyperplasia of bone marrow and spleen (as they are working overtime to make the WBCs).
Clinical manifestations:
o Fatigue and weakness, headache, mouth sores, anaemia, bleeding, fever, and infection.
o
o Chronic Myelogenous Leukemia (CML) also referred to as Chronic Granulocytic Leukemia (CGL)
o
o
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o Clinical Manifestations
Insidious onset.
Enlargement of cervical, axillary, or inguinal lymph nodes.
Nodes remain moveable, non-tender (recall that the tenderness only occurs during inflammation).
Painless nodes exert pressure on adjacent nerves, which may cause some discomfort.
o
May experience:
o Weight loss, fever, and night sweats occur and are known as the B symptoms. B symptoms are correlated with a worse
prognosis (i.e., Hodgkins + B symptoms).
o Fatigue, weakness, chills, tachycardia, palpitations followed by chest pain, dyspnea also occur.
o Alcohol induced pain at the located of the disease (for unknown reasons).
o Generalized pruritis (due to the granulocytes).
o Mediastinal node involvement.
Would expect to see cardiovascular problems, pulmonary problems.
Advanced cases:
o Hepatomegaly, splenomegaly.
o Anaemia (microcytic, hypochromic anaemia).
Since so many WBCs are being made, there is less focus towards making RBCs.
o Other physical signs vary depending on disease location.
If the cervical node is affected, it can lead to supra vena cava syndrome, hypertension, and coma.
If its below the diaphragm, it can be lead to spinal cord compression, hepatomegaly, splenomegaly, and bone
pain.
o
o Diagnostic Studies
Peripheral blood analysis.
Lymph node biopsy (in order to check for Reed Sternberg cells).
Bone marrow examination.
Radiologic evaluation.
o Chest X-rays, CT scans, MRIs, PET scan (displays heat spots).
o
o Nursing & Collaborative Management
Using diagnostic studies, a stage of disease is determined.
Stages:
o A (without symptoms) & B (with symptoms) classification
Roman numeral (I to IV).
This reflects the location and disease extent.
o IVB is the worst.
Management focuses on selecting a treatment plan.
Radiation therapy
o 95% of stage I or II (for both A and B) patients are cured within 4-6 weeks of radiation.
Combination therapy
o ABVD = standard regimen for chemotherapy
o BEACOPP = aggressive regimen
o 90% of stage I or II patients 10 yr survival 2-4 cycles.
o Presence of B symptoms 4-6 cycles
o MOPP
o There are different cells growing at different stages, so combination therapy is used to wipe out that variety of cells.
Radiation and Chemotherapy
o Stage IIIA
High-dose chemotherapy and bone marrow or peripheral stem cell transplantation
o Stage IIIB and stage IV (A and B)
Once cured, there is a risk of secondary malignancies. The most common include:
o Acute lymphoblastic leukemia
o Non-Hodgkins lymphoma
o Solid tumours (in the lung, breast, brain)
o
o Nursing Considerations
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When the symptoms return, chemotherapy will no longer work. Stem cell transplant then nothing.
IMMUNE SYSTEM
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b.
o
o Immunosuppression (e.g. transplant)
Consequences
o Infections
1. Persistent or recurrent infections
2. Opportunistic
This occurs when your normal microflora take over.
3. Severe infections by organisms that are normally mild
E.g., Staphyloccocus aureus found on your skin may cause a small localized infection in a healthy
person but cause a flesh eating disease in a person who is immunocompromised.
Incomplete Recovery: the bug is never truly gone.
Increased incidence: cancers and tumours are more likely to occur. These cancers are thought to be viral in origin.
o
o Patient Education is Key Treatment
Immunosuppression is often intentional.
o Education is key (e.g., wash your hands all the time, avoid large crowds).
Protection against and treatment of diseases and infections. (may be taking prophylaxis antibiotics)
Immunostimulant drugs may have to be given in order to spark the immune system (e.g., Neupogen).
Bone Marrow Transplant is required if the immunosuppression was not intentional.
o
o Human Immunodeficiency Virus (HIV) Infection
o Significance of Problem
Globally
o 33 million living with HIV (2009).
In Canada
o 1 million
o 65,000 (2008).
o 2,300-4,300 diagnosed each year in Canada.
o RNA virus discovered in 1983.
o Virus binds to specific CDA receptor sites and then enters the cell. (loves T-cells)
o It attaches and injects the virus and an enzyme (reverse transcriptase).
o Injected into the nucleus (where your DNA is), reverse transcriptase decides not to make your own DNA but well make
our own DNA (the virus) single stranded DNA. Every cell will reproduce a daughter cell that is infected. Every cell
divides. Each one infected. You will lose billions of cells.
o Every cell you produce now will have that virus.
o Reverse transcriptase assists to make a single viral DNA.
o Virus enters the cell nucleus.
o
There is no vaccine available (as seen in Hepatitis C) because the virus mutates so quickly.
The rates of TB are a good indication of HIV infections. If you cannot test for HIV (e.g., in some countries, such as the Soudan,
testing for HIV is prohibited), test for TB to possibly get an indication (the reason being that TB is an opportunistic infection).
HIV used to be called Slims disease, as there is so much muscle wasting.
As of 2011, the majority of transmission occurs via heterosexual couples (and not homosexual couples).
o
o Side-Effects of HIV
Diarrhoea, changes in mentation, muscle wasting.
o
o Pathophysiology of HIV (17.1)
RNA virus was discovered in 1983 and is called a retrovirus because it replicates in a backwards manner (going from RNA to
DNA).
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o 1iClicker Questions
o The component of the conduction system referred to as the pacemaker of the heart is the:
a) atrioventricular (AV) node.
b) sinoatrial (SA) node.
c) bundle of His.
d) bundle branches.
o
o The electrical stimulus of the cardiac cycle follows which sequence?
a) AV node SA node bundle of His
b) Bundle of His AV node SA node
c) SA node AV node bundle of His bundle branches
d) AV node SA node bundle of His bundle branches
o
o Review of Physiology Normal Heart Beat
The heart is made up of 2 types of cells:
1. Contractile cells
Make up 99% of cardiac muscle cells. These cells do not normally initiate their own action potentials.
2. Autorhythmic cells
Make up 1% of cardiac muscle cells. They do not contract but are specialized for initiating and conducting the
action potentials responsible for the contraction of the working cells.
They display pacemaker activity.
Cardiac autorhythmic cells (unlike any other type of cell) do not have a resting potential. The membrane
potential slowly depolarizes, or drifts, between action potentials. These cells initiate action potentials, which
then spread throughout the heart to trigger rhythmic beating without any nervous stimulation.
These cells are located in 4 different area of the heart:
1. The sinoatrial (SA) node
It is the normal pacemaker of the heart, located in the right atrium.
60-100 beats per minute (bpm).
o <60bpm = bradycardia.
o >100bpm = tachycardia.
2. The atrioventricular (AV) node
It is a small bundle of specialized cardiac cells located at the base of the right atrium near the
septum, just above the junction of the atria and ventricles.
Transmits pulses to ventricles.
Should the SA node suffer damage or trauma, the AV node will assume the role of pacemaker.
3. The bundle of His (atrioventricular bundle)
A tract of specialized cells that originate at the AV node and enters the interventricular
septum.
4. The Purkinje fibres
They are small terminal fibres that extend from the bundle of His and spread throughout the
ventricular myocardium.
Transmits pulses to the ventricles to make them contract.
o Normal Heart Beat
Effective electrical system.
Reacts to needs of body quickly.
Sometimes it breaks down, resulting in dysrhythmias (i.e., abnormal heart beats).
o
o Rhythm Identification and Treatment
Prompt assessment of abnormal cardiac rhythms, dysrhythmias, is crucial.
Conduction system.
Nervous control of the heart.
An ECG is the only accurate way to know exactly what is going on in the heart.
o Telemetry monitoring.
Heart palpitations (atrial flutter) may be transient.
o Review on Your Own
Electrophysiologic properties of the heart.
K+ out of the
cell
(repolarizatio
136
Action potential.
Na+ in the cell
o Every heart beat has its own action potential.
(depolarizatio
o Steps:
n)
0 = Depolarization
Sodium rushes into the ICF in large amounts; calcium
enters the ICF in smaller amounts.
1 = Early rapid repolarization
Sodium gates close and potassium gates open.
2 = Repolarization
Calcium moves into the ICF; potassium moves out of the
ICF (i.e., into the ECF).
3 = Repolarization
Polarized
Calcium channels close; potassium moves out of the ICF (i.e., into the ECF).
state
4 = Resting Membrane Potential/Polarized State
This is also a refractory period (i.e., a time during which depolarization cannot occur). The sodium
channels are blocked.
o There are two types of refractory periods:
1. Absolute refractory period
2. Relative refractory period
This is relative because of the T-wave.
o
o
Na+ in the cell
K+ out of the
(depolarizatio
cell
n)
(repolarizatio
Polarized
state
o
o
o
o
o Electrophysiologic Properties
Automaticity
o The ability to initiate an impulse spontaneously and continuously.
Excitability
o The hearts ability to receive the electrical impulses and contract.
Conductivity
o The hearts ability to transmit the impulse from one end of the heart to the other.
Contractility
o The hearts ability to respond to the electrical stimulus.
o
o *A problem with any of the four properties listed above will lead to dysrhythmias (i.e., abnormal heart rhythms).
o
o Refractory Periods
Many dysrhythmias are triggered at relative refractory periods.
o T wave most vulnerable.
Another action potential cannot take place during the absolute refractory period, but
o can, in some instances, take place during the relative refractory period.
T wave
o
o
o Dysrhythmias
They are abnormal heart rhythms.
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o Anti-Arrhythmic Drugs
Class I Drugs that depress the upstroke of action potential
o Block influx of Na+ into cells in phase 0.
o Sodium channel blockers or fast channel blockers.
o These drugs are based on the patients weight.
o Procainamide, Quinidine.
o Lidocaine, Mexiletine.
o Encainide.
Class II -adrenergic receptor blockers
o Blocks -receptors and therefore the SNS, depresses depolarization, slows SA node impulses, increases atrial and AV
nodal refractories.
o General myocardial depressants.
o This leads to a slower and stronger heart rate.
o Atenolol, Metaprolol, Propranolol.
Class III Drugs that prolong repolarization
o Blocks K+ movement in phase 3, therefore prolonging repolarization and refractory period.
o Ventricular tachycardia (TxVT), ventricular fibrillation (VF), atrial flutter/fibrillation (AF/F) resistant to other treatment.
Ventricular tachycardia is life-threatening. This is why too much potassium is bad.
Normal K+ levels are 3.5-5mmol/L.
o Amiodarone, Bretylium, Sotalol
These drugs are all ACLS (Advanced Care Life Support) drugs.
Class IV Calcium-channel blockers
o Blocks Ca2+ in phase 2, calcium channel blockers, slow channel blockers, prolongs conductivity and increases refractory
period and AV node.
o Paroxismal supraventicular (TxPSVT), atrial flutter (AF).
o Diltiazem, Verapamil.
o Increased use will increase risk of mobidity and mortality
o
o Anti-Arrhythmic Drugs that Dont Fit Into Classes
Potassium-channel opener
o Adenosine: decreases conduction at AV node (PSVT, WPWS).
WPWS: Wolf-Parkinsons white syndrome.
Atropine: anti-cholinergic blocks vagal effect on SA and AV node Increases heart rate.
Digoxin: strengthens myocardial contraction and slows conduction at AV.
Epinephrine: acts on alpha and beta adrenergic receptor sites of SNS, helps restore NSR (Normal Sinus Rhythm) post cardiac
arrest.
Magnesium Sulfate: decreases excitability and conduction.
CAUTION overdose = cardiac standstill.
o 2 nurse checks are done.
o
o Dysrhythmias
Dysrhythmias are triggered by internal and external forces.
o Internal: electrolyte imbalances, oxygen deprivation (due to a lack of haemoglobin and thus lack of oxygen), acidosis,
etc.
o External: trauma, drugs, haemorrhage, stress (i.e., prolonged stress that increases the bodys metabolic demands), etc.
Dysrhythmias are characterized by:
o Alteration in impulse formation.
Rate, rhythm, ectopics (beats that are coming somewhere else).
o Alteration in conductivity.
Failure or delay impulse transmission heart blocks.
Cardiac rhythms are classified according to:
o Site of impulse formation.
o Site/degree of conduction block.
o
o
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o Atrial Fibrillation
Total disorganization of atrial activity without effective atrial contraction.
The arrhythmia may be chronic or intermittent.
Manifestations:
o Hypo- or hypertension (this depends on the CO).
Significance:
o Can result in decreased CO (due to ineffective atrial contractions and rapid ventricular response).
o Risk for stroke (due to stasis).
o Risk for heart failure or hypertension.
Treatment:
o Same as for atrial flutter.
ECG characteristics:
o Multiple, short impulses.
o QRS complex is normal in shape but smaller (as the ventricles are not getting enough blood from the atria).
o
o First-Degree AV Block
It is a type of AV block in which every impulse is conducted to the ventricles, but the duration of AV conduction is prolonged.
Once the impulses move through the AV node, it is usually conducted normally through the ventricles.
Significance:
o May lead to other blocks.
No treatment.
ECG characteristics:
o Rate is normal.
o Rhythm is regular.
o P wave is normal.
o PR segment is prolonged.
o QRS typically normal.
o
o Second-Degree AV Block Type 1
Includes gradual lengthening of the PR interval, which occurs because of prolonged AV conduction time (known as Wenckebachs
phenomenon).
Most commonly occurs at AV node, but can occur in His-Purkinje system.
Significance:
o Second-degree heart block is usually due to an inferior MI or ischemia.
o It may be a warning.
Treatment:
o Atropine.
o Pacemaker.
ECG characteristics:
o Atrial rate is normal but ventricular rate may be slower as a result of dropped QRS complexes.
o Ventricular rhythm is irregular.
o
o Second-Degree AV Block Type 2
P wave is not conducted without progressive antecedent PR lengthening.
o It almost always occurs when bundle branch block is present.
It is a more serious type of block as a certain number of impulses from the sinus node are not conducted to the ventricles.
Type II AV block almost always occurs in the His-Purkinje system.
Significance:
o Often progresses to third-degree.
o May result in decreased CO due to BP and myocardial ischemia.
Treatment:
o Temporary drug measures to increase HR until pacemaker is available.
o Pacemaker.
ECG characteristics:
o Atrial rate is normal.
o Sinus rhythm is regular but ventricular rhythm may be irregular.
o Third-Degree AV Heart Block
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o Ventricular Fibrillation
Severe derangement of the heart rhythm characterized on ECG by irregular undulations of varying contour and amplitude.
No effective contraction or CO occurs.
Significance:
o Results in unconsciousness, absence of pulse, apnea, and seizures.
o If untreated, patient will die.
Treatment:
o CPR and ACLS (advanced cardiac life support) with the use of defibrillation.
o Drug therapy.
ECG characteristics:
o Hear rate is not measurable.
o Rhythm is irregular or chaotic.
o
o iClicker Question
o A client with a large myocardial infarction has been having premature ventricular contractions (PVCs) on his cardiac
monitor. Which pattern does the nurse recognize as being most characteristic of PVCs?
a) Irregular rhythm
b) Inverted T wave
o Characteristic of MIs.
c) Wide, distorted QRS complex
d) Increasingly long PR interval
o
o Sudden Cardiac Death
Death by an arrhythmia.
o
o Defibrillation
It is the most effective method of terminating ventricular fibrillation and ventricular tachycardia without a pulse.
It is most effective when the myocardial cells are not anoxic (i.e., having suffered damage due to hypoxia) or acidotic. For that
reason it is ideally performed within 15 to 20 seconds of onset of arrhythmia.
Defibrillation is accomplished by the passage of a direct current electrical shock through heart to depolarize cells. The intent is to
allow the SA node to resume the role of pacemaker.
The recommended energy for a first shock is 200J, with a second shock ranging between 200-300J as needed, and a third shock of
360J if defibrillation is unsuccessful. These shocks have been shown to cause myocardial damage, so it is important to start low
and work up as needed.
It is used in an emergency when the patient is unconscious.
o
o Cardioversion
It is not an emergency.
It is the therapy of choice for haemodynamically unstable ventricular or supraventricular tachyarrhythmias.
A synchronized circuit in the defibrillator is used to deliver a counter-shock that is programmed to occur during the with QRS
complex of the ECG.
Done on non-emergency basis.
During a cardioversion, the paitent is conscious, signs consent, start at 50J to 200J.
o
o Implantable Cardioverter-Defibrillator (ICD)
Treatment for life-threatening ventricular arrhythmias.
Education to the client receiving ICDs is extremely important.
o
o Pacemakers
They are pulse generators used to replace the SA node.
o Provide electrical stimulus to heart that cannot conduct own impulse to supply adequate CO.
o Used for transient and permanent conduction defects.
o They may have to be replaced over time.
o
o
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Unit 17: Clients with Coronary Artery Disease and Acute Coronary Syndrome
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Complicated lesion
o Thrombus forms or can act ike a flap which may occulude the area or break off and travel somewhere and create a
partial or full occlution
o
o Endotherlial lining altered as a result of chemical injuries
o
Hyperlipidemia (nonendenuding
o
Hypertension (denuding)
o
o Response to endothelial injury can inject a dye and with another screen view occlusions and dan instrument with a
balloon that we can go in and smooshes these deposits to the side (plaque)
o Hyperension not usually enough
o Hyperlipidemia combine hypertension and boom increased pressure on thrombus
o Lipids attracted to coronary arteries
o
o Collateral Circulation
Growth of collateral circulation (i.e., creating of new, smaller arteries when the main ones become occluded) is attributed to two
factors:
1. The inherited predisposition to develop new vessels.
2. The presence of chronic ischemia.
Relation to age:
o Collateral circulation is typically seen in older individuals, as this process occurs with time.
o People who have MIs at a younger age are more like to die than their older counterparts as their bodies have not had a
chance to develop collateral circulation.
o
o Risk Factors for Coronary Artery Disease
Risk factors can be divided:
o Unmodifiable risk factors
Gender, ethnicity, age.
o Modifiable risk factors
Diet (low fat, high fibre, low sodium), smoking (stop), exercise (30 minutes/day is optimal), diabetes, alcohol
intake (increased intake stimulates the release of renin, which will eventually increase BP), stress.
o
o iClicker Question
o Which two risk factors for coronary artery disease increase the workload of the heart and increase myocardial oxygen
demand?
a) Hypertension and cigarette smoking
b) Elevated serum lipids and diabetes mellitus
c) Physical inactivity and elevated homocysteine levels
d) Obesity and smokeless tobacco use
o
o Health Promotion
Identification of high-risk persons.
o This is done through a history.
o Some people may want to have their lipids checked every 5 years.
Management of high-risk persons
o Physical fitness
o Nutritional therapy
o
o iClicker Question
o The nurse determines that teaching about implementing dietary changes to decrease the risk of CAD has been effective
when the client states which of the following?
a) I should have some type of fish at least three times a week.
b) Most of my fat intake should be from olive oil or the oils in nuts.
c) If I reduce the fat in my diet to about 5% of my calories, I will be much healthier.
d) I should not eat any red meat such as beef, pork, or lamb.
o
o Health Promotion
Drug Therapy
o When do we start drug therapy?
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o
o True or False
1) The leading theory of atherogenesis proposes that aging is the basic underlying cause of atherosclerosis.
o False lipids and hypertension
2) Endothelial alteration may be caused by chemical irritants such as hyperlipidemia or by hypertension.
o True
3) During development of the raised fibrous plaque, arterial wall changes may be initiated by carbon monoxide produced by
smoking.
o True
4) Partial or total occlusion of the coronary artery occurs during the stage of raised fibrous plaque.
o False (due to the complicated lesions)
5) Collateral circulation in the coronary artery is more likely to be present in the young client with CAD.
o False
o
o Case Study
o You are working in the internal medicine clinic of a large teaching hospital. Today your first patient is 70yearold J.M.
who has been coming to the clinic for several years for management of CAD, hypertension and anemia. A cardiac
catheterization done a year ago showed 50% occlusion of the circumflex artery. He has had episodes of dizziness for the
past 6 months and orthostatic hypotension, shoulder discomfort, and decreased exercise tolerance for the past 2 months.
On his last clinic visit 3 weeks ago, a chest xray and 12lead ECG were done, showing cardiomegaly and a left bundle
branch block (LBBB).
o Results of chemistries drawn at the time were as follows: Na 136 mmol/L, K 5.2 mmol/L, BUN 5.7 mmol/L, creatinine
120 mcmol/L, glucose 5.1 mmol/L, Cl 95 mmol/L, CBC: WBC 4.4x109/L, Hgb 105 mmol/L, Hct 31.4% and platelets
229x109/L.
o This morning his daughter has brought him to the clinic because he has had increased fatigue, significant swelling of his
ankles, and SOB for the past 2 days. His VS are 142/83, 105, 18, and 36.6C.
o
o General Information
o His vascular flow will not be good, and he has anaemia, meaning that they will have decreased vascular flow to
everything. The LBBB will decrease the CO. Cardiomegaly (enlarged heart) will lead to a decrease in heart filling.
o
o K+ levels are a little high (may lead to arrhythmias).
o Haemoglobin is low (this is due to his anaemia).
o
1) Knowing this history and seeing his condition this morning, what further questions are you going to ask J.M. and his daughter?
Does he have pain?
o Where is it? Is it radiating? What kinds of pain is it?
These questions are to rule out an MI.
Is his SOB while at rest or on exertion?
o Position while sleeping (e.g., how many pillows does he use).
Has he had any pallor, diaphoresis, pain, shortness of breath (how long has he had it for)
o This would be due to the increased K+.
o
O
ACUTE CORONARY SYNDROME (ACS)
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st
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o When playing around with the arteries, it is possible for some clots to become loose.
Serum lipid levels
Cardiac markers
C-reactive protein (CRP)
Treadmill exercise testing
o
o iClicker Question
o The clients cardiac catheterization report reveals a 95% blockage of the LAD. The client is at greatest risk for an
infarction of the:
a. Lateral wall
b. Inferior wall
c. Anterior wall
d. Posterior wall
o
o Diagnostic studies Myocardial Infarction
Start with
o History of pain
Radiation, onset.
o Risk factors
o Health history
ECG
Serum cardiac markers
Other blood work?
o WBC count (sign of inflammation)
o Serum electrolytes (want to check K+ levels)
o C-Reactive Protein
o Creatinine, glucose
o
o Collaborative Care Angina
Treatment for stable angina:
o Nitrate therapy (vasodilation, decreasing pre-load)
o Stent placement
o Percutaneous coronary intervention (i.e., angiography)
o Atherectomy
o Laser angioplasty (i.e., reconstruction of the vessels)
o Myocardial revascularization
Drug Therapy
o Antiplatelet aggregation therapy
Aspirin (baby aspirin 81 mg): drug of choice
o -adrenergic blockers
Decreased heart workload.
o Calcium channel blockers
Decreased heart workload.
o Nitrates
Dilation of vessels
Percutaneous coronary intervention
o Surgical intervention alternative.
o Performed with local anaesthesia.
o Ambulatory 24 hours after the procedure.
Stent placement
o Used to treat abrupt or threatened abrupt closure and restenosis following PCI.
Atherectomy
o The plaque is shaved off using a type of rotational blade.
o Decreases the incidence of abrupt closure as compared with PCI.
Laser angioplasty
o Performed with a catheter containing fibres that carry laser energy.
o Used to precisely dissolve the blockage
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o
o
o
o
Hypertension.
Cardiomegaly.
Ejection fraction < 40%.
History of ventricular arrhythmias.
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1)
2)
3)
4)
5)
6)
7)
o iClicker Question
o What is the most significant factor in the positive outcome of a client with sudden cardiac death?
a. Absence of underlying heart disease
b. Rapid institution of emergency services and procedures
c. Performance of perfect technique in resuscitation procedures
d. Maintenance of 50% of normal cardiac output during resuscitation efforts
o
o Gerontologic Consideration Coronary Artery Disease
Collagen and fat deposition.
Myofibrillar degeneration.
Endocardial thickening.
Calcification of the heart valves.
Degeneration of the conduction system.
Resting heart rate.
Loss of elastic fibres.
Systolic BP and SVR.
Circulating norepinephrine.
o
o Women and Coronary Artery Disease
About 500,000 deaths occur in women per year.
Kills almost 10 times more women than breast cancer.
Manifest CAD 10 years later in life than men.
Most have symptoms present differently than men.
Diabetes mellitus found to be the single most powerful predictor of CAD in women.
o
o Case Study #1 Martin
o 57 year old Martin came to ER at 02:44, c/o chest pain. His worried wife accompanied him. He stated he was seldom ill
but for the past 3 weeks hed had tightness in his chest & left arm pain. On admission he was SOB, pale & ashen &
nauseated. VS: BP 95/60, P 112 irregular, R 36, T 39, wheezes in chest.
o
What are the pertinent facts of this case?
Chest pain, high respiratory rate, high temp, fast, irregular pulse, low BP, SOB, ashen, pale, and nauseated.
What nursing care issues/concerns should you address?
ECG, blood work, oxygen, when did this start, productive cough (i.e., pink, frothy sputum).
Need more detail about the pain (e.g., radiation, type of pain).
O2 sat?
What is your highest priority concern for this patient?
Deal with the patients chest pain.
Put patient on O2.
What should you be assessing for?
MI or angina:
o Perform an ECG.
o Ask pain questions: we know it radiates and hes had it for 3 weeks. How is the pain?
Angina and MI pain is differentiated based on when it occurs (i.e., at rest vs. on exertion).
What information is missing?
O2 saturations.
Medications taking.
Onset of pain.
What do you anticipate this patient will require for treatment?
Give patient nitro.
Oxygen therapy.
Take patients vital signs.
Give patient morphine.
ECG.
Blood work.
What assessments will the nurse need to anticipate/avoid complications to which the patient is susceptible?
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Other compensations:
Endothelin potent vasocontrictor, NO
Cytokines inflammation depression
Atrial natriuretic peptides (ANP) and B-type natururetic peptide (BNP)
Naturesis excretion of NA in the urine
Counterbalanances aldosterone effect
BNP for monitoring HF
Cardiac compensation
Cardiac decompensation
Plus
Cardiac remodeling
Heart failure (immediately like an acute MI but chronic compensation can change the heart permanently)
Right sided heart failure:
Pt will look or symptoms will be: peripheral edema, Liver, kidneys, bowel and edema in ankles and hands and bellies.
Elevated liver function enzymes. JVP increased, fatigue and exhausted, no appetie. Rapid increase of water weight gain.
Left sided Heart Failure:
supposed to go to the body and lungs
Rapid breathing, SOB with activity and then at rest, nocturnal dyspnea, orthopnea (lay down and immediately have a
problem this is not the same as nocturnal dyspnea)
Other manifestations: fine crackles, pink frothy sputum (little blood), decreased aire entry to baes
Depression, confusion, altered memory and concentration
Arrhythmias fluttering in chest (tachy or brady)
Chest pressure or pain; diaphoresis
Positive HJR; S3, S4 present
Pallor, cyanoisis
Low BP, HR over 100
Lightheaded, dizzy, syncope
Nocturia
Upright assessment; JVP (up somewhat; down the jVP will go up automatically)
Chest xray cardiomegaly
On leads to the other
Right left
Biventricular failure
Cardiomyopathy
(not often it will just be one sided failure usually a mixture because its a cicuit or system).
Systolic Heart Filure
Inability to move blood forward
Unable to overcome SVR/PVR
Poor contraction
High afterload
Mechanical abnormalities
EF % of blood in ventricle that I am movving forward can still be compensating but the EF may be decreasing and
failing
Systolic ability staartss to fail (but Im going down hill slowly)
Diastolic Heart Failure
HF with preserved systolic function is now used
Stiff ventricle
Common to diabetes pts
Impaired filling pressures
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Venous engorgement
Little stressor tips really quickly into bd heart failure but where going along with diastolic heart failure.
NYHA Funcational Classification
Class I no limitation with oridinary changes, no symptoms
Calass II slight limitation of physical activities
Class III marked limiation of physical activities (a and B)
Class IV UNABLE TO CARRY OUT ANY PHYSICAL ACTIVITY without discomfort. Symptoms at rest. (hospital
or end stage)(caardiac cripple)
Regression of stages (can be a 4 then 1 than 3, etc.)
ACC/AHA HF Stages
Stage A high risk, no structural changes, no symptoms (want to catch; at risk)
Stage B structural changes, no symptoms (at least an episode of symptoms)
Stage C structural changes, past or present symptoms
Stage D structural changes, refractory symptoms, specialized interventions (end stage; heart reached maximal damage;
heart transplant and unmanageable heart failure)
No regressions of stages.
Case Study
Manifestations? CNS, CVS, Resp, GI, GU, P/S (biventricular)
Longer term (later stage)
Pleural effusions
Air hunger (palliative conceern)
Hypotension (particularly orthostatic)
Ventricular thrombus
Arrythmias (the more stretched out the more prone it iss to arrhthmias) (pacemakers, implantable defibulators)
- Tachy/brady
- High risk of sudden death
Longer term later stage
Mental changes (especially in the elderly)
Hepatomegaly (splenomegaly)
Renal failure (ace inhibitors hard on the kidneys watch creatine)
Gross ascites, anasarca (drains can be inserted peritoneal dialysis) (massive accumulation in the abd compressed the
bowel difficulty digesting food)
Anorexia
Muscle wasting common in late stages of heart failure (lose body mass)(immunological changes most likely culprit)
Function tatisnd trajectory:
NYHA Functional Classifications
ACC/AHA HF Stages
How do you classify and Stage? Pts know which class they are.
Tests:
Labs (cardiac enzymes, BNP, lytes (Potassium, magnesium, calcium, sodium, Creatinine), LFTs, T3/T4
(hyperthyroidism), CBC - hgb)
Hemodynamics blood pressure, pulse
ECG
CXR (enlrged heart, pleural effusion), Cardiac CT
Before tx: determine underlying cause
What do the tests tell you?
ECHO, MUGA, MRI (EF, architecture)
Cardiac catheterization (PCI) angiogram
Exercise Stress Test (debutamine drug to do the test)
6 Min Walk Test (how far can you walk in 6 min)
Sleep studies (obstructive apneic episodes during the night affects oxygen sats monitor on, orthopnea)
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NCP
Outline your intitial assessment H2T
CNS, CVS, Resp, GI, GU, P/S
Heart booklet/guidelines
Desired tx outcomes
Maintenance of adequate tissue oxygenation
Hemodynamic stability
Optimized fluid volume status (daily wt) (JVP down)
Minimized cardiac remodeling (get rid of alcohol, etc.)
Optimized functional sstatus (NYHA Class) ie. Symptom control
Medication adherance max dose titration, renal tolerance
Pt understanding of symptom maintenance and management (self-care)
Lifestyle modification (diet, obesity, smoking, exercise)
Knowledgeable family / community supports
(High potassium means failing kidneys)
#1 underlying cause ischemia***
HTN
Fluid Overload
Arrhythmias, electrolytes.
Medication therapy
ace inhibitors and beta blockers titrate!
Intolerant to either - > ARB
Intolerant to ACE-I/ARB
->nitrate/hydralazine
- tailor diuretic furosemide, metolozone
Electrolytes/creatinine within 7-10 days
If clinically stablee good! If not ->
Persistant NYHA II-IIIa on:
ACE-I and Beta Blcoker (ARB)
Tailored Diuretic
Then
Add ARB
Spironolactone or e[plerenone (MRA)
(**ACE-I + MRA + ARB not recommended)
If clinically stable good! If not ->
Digoxin )not a great ionotrope), nitrated increased
Other things to consider:
Statins
Antiplatelet agents
ACUTE/unstable
IV vasodilators
IV inotrpe (norepi, .
Devices and Interventions:
Revascularization (PTCA, Stent, CABG)
IABP
Pacer (temp/permananet)
ICD (implantable cardiaversion defibulator)
CRT (Cardiac resyncronization therapy for HF with some heart block where ventricles are not coordinated)
VAD (Ventricular assist device pump implanted with an external generator)
Transplant
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PTCA (percutaneous transluminal coronary angioplasty) in coronary artery through femoral artery up the left side of the
heart (very risky and controlled),
CABG take a vessel from another thigh or calf (vein) flip it around to change valves and move it to bypass the vessle
in the heart (Coronary artery bypass graph)
Intraaortic balloon pump temp lifesaving solution through artery into heart holds fluid and then deflates to allow
easy forward flow of the blood. Must be incredibly syncronized with how the heart contracts and it cant slide out of its
location.
Pacer/Pacemaker internal, external, temp with pain medication it delivers a shock each time. It will pace their heart.
Burnng or pain in chest in external pace
Temp goes into heart through another vein and can work for few days to get an internal pacer inserted via sx through the
vessles
Use vessle to attach patch to heart. Mimics the SV node.
Implantable cardioverter defibrillator and cardiac resyncronization therapy
- pacemaker clinic can monitor th pacers.
Will test pacemaker by setting it off.
CRT chambers are no longer coordinated
Carry a card in their wallet or have a bracelet or necklace what they have implanted.
Ventricular Assist Device implanted under ribs and physically pumps with th heart external device that requires lots
of power. Must carry the pack. Good for bridging to transplant.
Heart transplant steroid junkies, severe alcoholics,
Diet reduce obesity, controlled DM
Low salt
Fluid restriction
Daily weights (morning, dry, 2kg in two days)
Cardiac diet
Lifestyle diet, foo, stress, exercise, ADLs
Education self care
Family Caregivers:
Invaluable resource.
Consolidate notes..
o
O
o Heart Failure
What is it?
o It is typically a grouping of symptoms, making it more of a syndrome than a disease in itself. It is characterized by
impaired cardiac pumping.
o It is viewed relating to anatomical location, that is, right and left sided heart failure, with the side pertaining to the
ventricles.
Left sided heart failure
Will affect the body systemically.
As the ventricles enlarge, they are less able to fill adequately, thus decreasing cardiac output.
Right sided heart failure
Will affect the lungs and pulmonary system.
Who is at greatest risk of developing heart failure?
o It is insidious and is therefore seen in the older populations.
o Individuals who have had a history of hypertension are also more susceptible to developing heart failure.
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Individuals who would have an increase in systemic vascular resistance for any particular reason, such as smokers, due
to the increase in blood viscosity, people with hyperlipidemia, and people with diabetes.
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1)
2)
3)
4)
o
o Pathology of Ventricular Failure Diastolic Failure
It is an impaired ability of the ventricles to fill during diastole.
Diastolic failure is characterized by high filling pressures and the end-result is pulmonary congestion due to a decrease in stroke
volume (i.e., the amount of blood expelled by the ventricles in one contraction) and impaired ventricular filling. There is
continuous venous engorgement in both the pulmonary and systemic vascular systems.
There is normal ejection fraction as the problem lies with heart filling (and not heart expulsion of blood to the body).
It is usually the result of left ventricular hypertrophy from chronic systemic hypertension.
o
o Pathology of Ventricular Failure Mixed Systolic and Diastolic Failure
Seen in diseased states such as dilated cardiomyopathy.
There is biventricular failure (neither ventricle can compensate).
Patient has extremely poor ejection fractions.
This will lead to a decrease in cardiac output, decrease in blood pressure, and decrease in renal perfusion.
o
o 4 Basic Factors Causing Heart Failure
Increase in volume of blood to be pumped (i.e., problems with preload).
Increase in resistance against which blood must be pumped (i.e., problems with afterload).
Decreased contractility (e.g., dysrhythmias, patients with a history of MIs).
Decrease in filling of cardiac chambers (the chamber volume has decreased due to myocardial hypertrophy).
o
o iClicker Question
o A client with a history of chronic heart failure is hospitalized with severe dyspnea and a dry, hacking cough. She has
pitting edema in both ankles, and her vital signs are BP 170/100, P 92, and R 28. The nurse recognizes that the clients
symptoms indicate which of the following?
1. The venous return to the heart is impaired, causing a decrease in cardiac output.
2. There is impaired emptying of both the right and left ventricles, with low forward blood flow.
3. The right side of the heart is failing to pump enough blood to the lungs to provide systemic oxygenation.
4. The myocardium is not receiving enough blood supply through the coronary arteries to meet its oxygen demand.
o
o Cardiac Reserve
It is the difference between the total amount of blood in the ventricles and the amount ejected during systole (i.e., stroke volume).
Not all the blood in the heart is expelled during ventricular contractions.
o During times of stress, the heart can increase its cardiac output with the help of this reserve.
o
o
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o Compensatory Mechanisms
o The overloaded heart resorts to certain compensatory mechanisms to try to maintain adequate cardiac output.
o
Ventricular dilation
o This is an enlargement of the chambers of the heart. It occurs when the pressure the heart chambers (typically the left
ventricle) is elevated over time. The muscle fibres of the heart stretch and increase their contractile force. This initially
increases the cardiac output and maintenance of arterial blood pressure and perfusion. This is an adaptive mechanism to
cope with increasing blood volume. With time this mechanism becomes inadequate as the elastic element of the muscle
fibres are overstretched and can no longer contract effectively, thus cardiac output.
Ventricular hypertrophy
o This is an increase in muscle mass and cardiac wall thickness in response to overwork and strain. This typically follows
persistent or chronic dilation. This will lead to an CO and maintenance of tissue perfusion but hypertrophic heart
muscle has poor contractility (i.e., the hearts ability to respond to an electrical stimulus).
Increased sympathetic nervous system stimulation
o SNS stimulation is often the first mechanism triggered in low CO states; however, it is the least effective compensatory
mechanism. Due to the inadequate stroke volume and CO, there is an increased release of epinephrine and
norepinephrine. This results in an increase in heart rate, myocardial contractility, and peripheral vasoconstriction, which
initially leads to an increase in HR and contractility, which increase the CO. Over time this becomes detrimental as it
increases the workload on the already weakened heart, which increases the hearts demand for O 2.
o The vasoconstriction increases the preload, which is problematic because the heart is already overloaded.
Neurohormonal responses
o A decrease in CO leads to a decrease in blood to the kidneys, which interpret this decreased flow as being a decreased
volume. The kidneys will release renin in response to a decrease in blood pressure. This will lead to vasoconstriction
and an increase in Na+ retention in the hopes of increase the blood pressure. Angiotensin-II will also secrete aldosterone,
which will cause Na+ retention and also increase the blood pressure.
o A decrease in blood flow to the brain causes the posterior pituitary to secrete ADH, which increases water retention and
thus the blood pressure.
o Natriuretic peptides are potent vasodilators.
Ventricular remodelling
o The neurohormonal response contributes to ventricular remodelling. This involves hypertrophy of the cardiac myocytes,
resulting in large, abnormal cells. This eventually leads to increased ventricular mass.
o
o *Cardiac compensation occurs when compensatory mechanisms succeed in maintaining adequate CO that is needed for
tissue perfusion. Cardiac decompensation occurs when these mechanisms can no longer maintain adequate CO.
o **Although these mechanisms are meant to be compensatory, their cumulative effects are harmful on the body because
the heart is unable to handle the compensatory effects.
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CHF can lead to severe hepatomegaly, especially with right ventricle failure. The liver lobules become
congested with venous blood and this hepatic congestion leads to impaired liver function.
Splenomegaly.
CHF can lead to splenomegaly, especially with right ventricle failure.
Jugular venous distension.
o The primary cause is left-sided failure (recall that one-sided heart failure will lead to biventricular failure). This is
because left-sided failure causes an increase in pulmonary congestion and increased pressure in the blood vessels of the
lungs (i.e., pulmonary hypertension). Eventually, chronic pulmonary hypertension results in right-sided hypertrophy and
failure.
o Cor pulmonale (i.e., right ventricular dilation and hypertrophy caused by pulmonary pathology (e.g., COPD)) may be a
cause of right sided-failure.
Forward & Backward failure.
o Based on the effect of circulation.
Forward failure: unable to propel the blood forward (i.e., during systole) due to decreased contractility. This
leads to an increase in sodium and water retention due to decreased renal perfusion and the release of renin.
Sodium and water are retained due to decreased renal perfusion.
Backward failure: unable to accommodate volume returning (i.e., preload) due to hypertrophy of the ventricles.
Sodium and water are retained due to decreased renal perfusion.
High output & Low output failure.
o High output failure: occurs when the cardiac output is normal or high but a condition exists that abnormally increases the
demand for oxygenated blood (e.g., hyperthyroidism, anaemia, pregnancy, arteriovenous fistulas, beriberi, and Pagets
disease).
o Low output failure: occurs when the cardiac output is low but the bodys demand of oxygen is normal (e.g., this may
occur due to ischemia coronary disease, hypertension, dilated cardiomyopathy, or valvular and pericardial disease).
Systolic & Diastolic failure.
o Systolic failure: the most common cause of CHF results from the hearts inability to pump blood (as the left ventricle
loses its ability to generate enough pressure to move blood past the aorta). It is a defect in the ability of the ventricles to
contract. The hallmark of systolic dysfunction is a decrease in the left ventricular ejection fraction. It is caused by
impaired contractile function (e.g., hypertension), cardiomyopathy, and mechanical abnormalities (e.g., valvular heart
disease).
o Diastolic failure: it is an impaired ability of the ventricles to fill during diastole. Decreased filling will lead to decreased
stroke volume (and thus decreased CO). It is usually due to left ventricular hypertrophy from chronic systemic
hypertension, aortic stenosis, or hypertrophic cardiomyopathy.
o This is similar to forward and backward failure (i.e., forward failure = systolic failure and backward failure = diastolic
failure).
o
o Clinical Manifestations
o Left-sided Heart Failure
o
o Right-sided Heart Failure
o Dyspnea (due to pulmonary
o
o Epigastric and RUQ
congestion)
abdominal pain
o Fatigue
o
o Increased abdominal girth
o Orthopnea, nocturia
o
o Anorexia
o Dry, hacking cough
o
o Bloating
o Pulmonary edema
o
o
o Acute Congestive Heart Failure Clinical Manifestations
Pulmonary edema.
o Agitation (due to decreased O2 to the brain).
o Pale or cyanotic.
o Cold, clammy skin.
o Severe dyspnea (the most common characteristic; due to severely impaired gas exchange).
o Tachypnea.
o Above is related to inadequate gas exchange as well as having fluid backing up into the lungs (more specifically, the
alveoli).
o Pulmonary Edema
o The pooling of blood in the lungs increases the hydrostatic pressure, pushing
the blood into the pulmonary interstitial space. This fluid will eventually
move into the alveoli. The most common cause of pulmonary edema is left
ventricular failure.
Every alveolus is surrounded by
lymphatics, which act as drains.
165
o
o
This increase in pulmonary pressure due to a decrease in left ventricular efficiency results in engorgement of the
pulmonary vascular system. In order to help maintain a constant volume of the pulmonary extravascular fluid, the
lymphatic system increases its flow. This early stages is associated with a mild increase in the respiratory rate and a
decrease in PaO2.
If the pulmonary venous pressure continues to increase, the increase in intravascular pressure causes more fluid to move
into the interstitial space than the lymphatics can drain. Interstitial edema occurs at this point and severe tachypnea is
present.
Clients with pulmonary edema will be pale, agitated, and possible cyanotic. The skin is clammy and cold and the client
has severe dyspnoea, exhibited by the obvious use of accessory muscles, and orthopnea (i.e., severe dyspnea that is
relieved when seated upright). There may be frothy, blood-tinged, sputum upon coughing.
o
o Chronic Congestive Heart Failure Clinical Manifestations
Fatigue (due to decreased cardiac output, impaired circulation, tissue oxygenation, and anaemia)
Dyspnea
o Paroxysmal nocturnal dyspnea (PND) occurs when the client is asleep. It is caused by the reabsorption of fluid from
dependent body areas when the client is recumbent. The client will awaken in a panic and have feelings of suffocation as
well as the need to sit upright.
o Orthopnea.
These individuals are often sleeping with multiple pillows as lying supine is uncomfortable due to the PND.
Tachycardia (this is the body trying to compensate)
o It is one of the first symptoms. It occurs as a result of an increase in SNS stimulation.
Edema (this is due to a non-functional cardiac system)
Nocturia
o A person with chronic CHF who has decrease CO will also have impaired renal perfusion and decreased urinary output
during the day. When the person lies down at night, fluid movement from the interstitial spaces back into the circulatory
system is enhanced, which causes increase renal blood flow and diuresis.
Behavioural changes
o Cerebral circulation may be impaired with chronic CHF secondary to a in CO. The patient may display restlessness,
confusion, and attention span. This may be secondary to poor gas exchange and worsening renal failure.
Chest pain (this is similar to an angina-type pain due to a decrease in coronary perfusion)
Weight changes
o There will initially be weight gain, secondary to fluid retention; with time, the individuals may become too ill to eat and
will therefore lose weight. Renal failure may also contribute to fluid retention. In many cases, the persons weight loss
is masked by the edematous condition.
Skin changes (due to a general lack of circulation)
o Dusky appearance.
Cough (due to fluid build-up in the lungs)
o At first this will be a dry, hacking cough that is unrelieved by positional changes or over-the-counter medications. In
time (as the alveoli become flooded), the cough will be productive (i.e., pink and frothy).
Pulse Alterans (i.e., an alteration between a strong and weak pulse)
Enlargement of heart
o This is often due to the heart overworking for so long. This will lead to S3 and S4 heart sounds.
Atrial fibrillation
o These are common.
o The atrium quivers, leaving heart to pool in the ventricles and increases the likelihood of clot formation.
CheyneStokes Respiration
o An abnormal pattern of breathing characterized by alternating periods of apnea and deep, rapid breathing. This type of
breathing is typically seen as a person nears death (death breath).
o
o Heart Failure Complications
Pleural effusion
o The increase in pressure in the pleural capillaries leads to pleural effusions. This will be lead to dyspnea and bloodtinged frothy sputum.
Arrhythmias
o When the hearts chambers become enlarged, an alteration in the normal electrical pathway occurs, giving rise to atrial
fibrillation. The person may feel palpitations.
Left ventricular thrombus
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167
Aldactone/Spironolactone helps prevent the release of aldosterone, which leads to a decrease in Na+
and water reabsorption).
o Improving cardiac function
Hemodynamic monitoring for the following 3 drugs.
Digitalis.
It increases contractility but also increases myocardial oxygen demand.
Apical pulse must be >60bpm to receive this drug as it is a negative chronotropic and positive
inotropic.
Hold if the patients blood pressure is too low.
There are newer inotropics (e.g., dobutamine).
Dobutamine (this is not typically used on the average ward; it is usually in acute care settings).
o This drug enhances contractions but does not increase myocardial oxygen consumption.
o Reducing anxiety
Stress will exacerbate CHF.
Morphine.
This is not used for pain. It helps take the edge off and is used instead of sedatives as they will
decrease the patients respiration rate.
IV
inotropic
drugs.
Open vessels,
Enhance
contractility.
clear lungs,
Vasodilators.
and improves
ACE inhibitors.
heart rate
Prevent vasoconstriction.
o
Treat the underlying cause.
Maximize cardiac output.
Alleviate symptoms.
Oxygen treatment (especially at night).
Rest.
Biventricular pacing (this is typically done in more emergency-type situations when the patient experiences an HR).
Cardiac transplantation (severe; it is reserved for younger individuals).
o
o Chronic Heart Failure Drug Therapy
ACE inhibitors
o Prevent vasoconstriction by inhibiting the action of the angiotensin converting enzyme.
o They are the first line therapy for patients with CHF as they are useful in both systolic and diastolic failure.
Inotropic drugs
o They enhance heart contractility.
Vasodilators (e.g., nitro)
o It is the first line given to patients with heart failure (it is not for chest pain).
Diuretics
o The diuretics help decrease the fluid volume.
o The dose will increase with time and a combination of different diuretics is often used.
o Loop diuretics (e.g., Lasix) are the strongest type of diuretics.
Patients with allergies to sulfa drugs are cautioned against loop diuretics.
o Thiazide diuretics decrease the reabsorption of Na+, thus promoting its excretion along with water.
Adrenergic blockers
o Directly block the sympathetic nervous systems negative effects on the failing heart, such as increased heart rate.
o -adrenergic blockers must be started slowly as dizziness and edema are prevalent.
o Slows things down, enhances contractility of the heart.
o
o Question
o Match the following drugs used in the treatment of acute and chronic congestive heart failure with their therapeutic
effects.
a. Spironolactone (aldactone)................11
e. IV nitroprusside (nipride)..................6
b. IV nitroglycerin.................................4
f. Enalapril (vasotec).............................7
c. Digoxin (lanoxin)..............................10
g. Dopamine (Inotropin)........................5
d. Furosemide (lasix).............................8
h. Milrinone (Primacor).........................1
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IV morphine......................................2
Carvedilol (Coreg).............................5
Nesirtide (natrecor)...........................3
1.
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Evaluation
Respiratory status (first and foremost)
Sleep
Fluid balance (strict I&O are not done, but daily weights are taken to ensure there is no fluid retention occurring)
Activity tolerance
Anxiety control (they may feel as though they are drowning and will therefore be quite anxious)
Knowledge: disease process
Questions
A client with leftsided heart failure has oxygen at 4 L/min per nasal cannula, furosemide (Lasix) 40 mg po daily, spironolactone
(Aldactone) 25 mg po daily, and enalapril (Vasotec) 5 mg po bid. Which of the following actions is most important for the nurse
to implement?
1. Auscultate lung sounds.
2. Measure intake and output.
3. Assess skin turgor.
4. Draw a blood sample for arterial blood gases.
A client with chronic heart failure who is taking digoxin (Lanoxin) 0.25 mg po daily with furosemide (Lasix) 60 mg po daily
develops nausea and vomiting. Based upon these findings, what is the most appropriate intervention for the home care nurse?
1. Instruct the client to increase intake of high-potassium foods.
2. Notify the physician.
3. Perform a dipstick urine test for protein.
4. Ask the client to weigh himself each morning and call the nurse in 3 days.
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Cancer
It is a group of more than 200 diseases characterized by uncontrolled and unregulated growth of cells.
Cancer is the second leading cause of death (second to heart disease).
Males: prostate cancer is the most common.
Females: breast cancer is the most common.
For both men and women, lung cancer is the deadliest type of cancer.
In Canada:
2 in 5 will be dx with cancer in their lifetime. 1 in 4 will die of cancer
At the beginning of 2009, 838,724 canadians alive who had been diagnosed with cancer in past 10 years.
A disease resulting from the interaction of multiple factors at the cellular, genetic, immunological and environmental levels.
An estimated 173,800 new cases of cancer (excluding about 75,500 non-melanoma skin cancers) and 76,200 deaths will occur in
Canada in 2010.
Approximately 83,900 Canadian women will be diagnosed with cancer and an estimated 36,200 women will die of cancer.
Approximately 90,000 Canadian men will be diagnosed with cancer and an estimated 40,000 men will die of cancer.
Lung, prostate, breast and colorectal cancer account for 50% of all new cancer cases every year.
Lung cancer accounts for over a quarter (27%) of all cancer deaths each year.
Breast cancer accounts for over a quarter (28%) of new cancer cases in women.
Prostate cancer accounts for over a quarter (27%) of new cancer cases in men.
Prevalence
At the beginning of the year 2005, there were approximately 723,000 cases of cancer that had been diagnosed in the previous 10
years.
Survival
Based on 2002-2004 estimates, 62% of people are expected to survive for 5 years after their cancer diagnosis compared to the
general population of the same age and sex. Survival rates differ according to the type of cancer.
In Manitoba in 2010
Lung cancer
Colorectal cancer
o 850 new diagnoses
o 820 new diagnoses
o 780 deaths
o 350 deaths
Breast cancer
Prostate cancer
o 800 new diagnoses
o 760 new diagnoses
o 200 deaths
o 180 deaths
Estimated 6,200 new cancer diagnoses.
Estimated 2,800 cancer deaths.
In Canada
40% of women, 45% of men will develop cancer during their lifetimes.
o Approximately 1 in 4 will die of cancer.
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Paediatric Cancer
Much less common
Average of 1,271 new cases diagnosed in Canada.
Average of 208 deaths per year in Canada.
Most common types:
o 25% - Leukemia (most common: ALL)
o 18% lymphoma
o ~17% - Brain (gliomas, medulloblastomas)
o Less common:
Neuroblastoma
Wilms (kidney)
Sarcomas (rhabdomyosarcoma, osteosarcoma)
Survival Rates
Current 5-year overall survival:
o Adults: 65%
Death rate from breast cancer has decreased 24% since 1980.
o Children: 77%
1930s <30%
Development of Cancer
The following is a theoretical model to explain cancers development. The cause and development of each type of cancer are
likely to be multifactorial.
Growth factors will interact with its receptors to stimulate the cell.
Problems with cancer occur in and on the cell.
There are thought to be 3 main stages in the development of cancer:
1) Initiation
o Mutation of genetic structure (which can occur for many reasons) has the potential to develop into a clone of neoplastic
cells.
o Many carcinogens that enter the body are excreted; however, there are those that alter the bodys cells. If those cells do
not repair themselves or die, they will replicate into daughter cells, each of which will contain the alteration.
o Caused by things such as smoking
2) Promotion
o A single alteration of the genetic structure of a cell is not sufficient to result in cancer; however, the odds of cancer
development are increased with the presence of promoting agents (carcinogens).
o Promotion is characterized by the reversible (this characteristic distinguishes it from the initiation phase) proliferation of
altered cells.
o Promoting factors include dietary fat, obesity, cigarette smoking, alcohol consumption, and prolonged stress. The
withdrawal of these factors can reduce the risk of cancer development. Some carcinogens (known as complete
carcinogens) have the ability to initiate and promote the development of cancer (e.g., tobacco).
o A latent period is said to the time between the initial genetic alteration and clinical evidence of cancer. This period can
range between 1 and 40 years.
o A 0.5cm tumour is the smallest tumour that can be detected via MRI. A 1cm tumour is said to contain 1 billion cancer
cells.
3) Progression
o Progression is characterized by growth rate of the tumour, an increase in its invasiveness, and metastasis (i.e., the
spread of cancer from its original site to a distant site).
o Some cancers have certain sites in which they like to metastasize whereas others will metastasize randomly (e.g.,
melanoma). Frequent sites of metastasis are the lungs, brain, liver, bone, and adrenals (mnemonic: bball).
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The metastatic process is a multistep process that begins with rapid growth of primary tumour. As the tumour increases
in size, it requires its own blood supply. This development of blood supply is critical for survival and is termed tumour
angiogenesis, which is promoted by tumour angiogenesis factors created by the cancer cells. Certain subsections of a
tumour are able to detach from the primary tumour and enter a different area of the body.
Biology of Cancer
Cancer is a group of many diseases of multiple causes that can arise in any cell of the body capable of evading regulatory controls
over proliferation and differentiation. Two major dysfunctions present in the process of cancer are defective cellular proliferation
(growth) and defective cellular differentiation.
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The distribution and activity of the microfilaments and microtubules may change. These alterations
change the ways in which the cell interacts with neighbouring cells and alter the appearance of the
cells. Changes in the cytoskeleton also affect cell adhesion and movement (motility).
Cell adhesion/motility
The reduction of cell:cell and cell:extracellular matrix adhesion allows large masses of cells to form.
As described in the section on cell division, cancer cells do not exhibit contact inhibition and are able
to continue to grow even when surrounded by other cells. The alterations in cell adhesion also impact
on the ability of the cells to move. Cancer cells must be able to move and migrate in order to spread,
and cell adhesion plays a major role in regulating cell movement.
Nuclear changes
The shape and organization of the nuclei of cancer cells may be markedly different from that of the
nuclei of normal cells of the same origin. This change in appearance may be useful in the diagnosis and
staging of tumours.
Enzyme production
Cancer cells often secrete enzymes that enable them to invade neighbouring tissues. These enzymes
digest away the barriers to migration and spread of the tumour cells.
Cancer cells that get past this have acquired the ability to avoid the cell death signals triggered by their abnormal behaviour.
Changes in Physical Properties of Cancer Cells
The changes in cell behavior that occur as cancer develops are, in part, dependent on changes in physical properties of the cells.
Some of the changes have been identified and may be used to identify cancer cells.
Tumor cells display a characteristic set of features that distinguish them from normal cells. These traits allow the individual cells
to form a tumor mass and eventually to metastasize to other parts of the body. We will briefly consider the changes that affect cell
functions and then discuss some of the capabilities that must be acquired by the tumors as a whole to enable them to grow and
spread.
A wide range of changes occur during the transformation of a normal cell to a cell capable of forming a cancerous growth. All
cancer cells acquire the ability to grow and divide in the absence of appropriate signals and/or in the presence of inhibitory
signals. There are also detectable changes in the physical properties of the cells. These changes include the following:
Cytoskeletal changes- The distribution and activity of the microfilaments and microtubules may change. These alterations
change the ways in which the cell interacts with neighboring cells and alter the appearance of the cells. Changes in the
cytoskeleton also affect cell adhesion and movement (motility).
Cell adhesion/motility- The reduction of cell:cell and cell:extracellular matrix adhesion allows large masses of cells to form. As
described in the section on cell division, cancer cells do not exhibit contact inhibition and are able to continue to grow even when
surrounded by other cells. The alterations in cell adhesion also impact on the ability of the cells to move. Cancer cells must be
able to move and migrate in order to spread, and cell adhesion plays a major role in regulating cell movement.
Nuclear changes- The shape and organization of the nuclei of cancer cells may be markedly different from that of the nuclei of
normal cells of the same origin. This change in appearance may be useful in the diagnosis and staging of tumors.
Enzyme production- Cancer cells often secrete enzymes that enable them to invade neighboring tissues. These enzymes digest
away the barriers to migration and spread of the tumor cells.
Cancer cells that get past this have acquired the ability to avoid the cell death signals triggered by their abnormal behavior.
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175
T cells are also important in the production of cytokines (e.g., interleukin-2 and -interferon), which
stimulate T-cells, natural killer cells, B cells, and macrophages.
o Natural killer (NK) cells are able to directly lyse tumour cells spontaneously without any prior
sensitization. Their killing ability is boosted by -interferon.
o Macrophages also secrete cytokines (i.e., interleukin-1) and tumour necrosis factors (TNF).
Escape mechanisms by which cancer cells evade immune system:
o The process by which cancer cells evade the bodys immune system is known as immunological escape. Theorized
mechanisms by which cancer cells can escape immunological surveillance include:
1. Suppression of factors that stimulate T cells to react to cancer cells.
2. Weak surface antigens allow cancer cells to sneak through surveillance.
3. Development of tolerance of immune system to some tumour antigens.
4. Suppression of immune response to products secreted by cancer cells.
5. Induction of suppressor T cells by the tumour.
6. Blocking antibodies that bind TAAs, thus preventing their recognition by T cells.
Oncofoetal Antigens
o They are a type of tumour antigen found on both the surface and inside of cancer cells, as well as foetal cells. These
antigens are an expression of the shift of cancerous cells to a more immature metabolic pathway, an expression usually
associated with embryonic or foetal periods of life. The reappearance of foetal antigens in malignant disease is not well
understood, but it is thought to be a result of the cell regaining its embryonic capability to differentiate into many
different cell types. Examples of oncofoetal antigens include carcinoembryonic antigen (CEA) and -fetoprotein. CEA
levels are currently used to determine the efficacy of cancer treatment.
Immune system response is to reject or destroy cells perceived as nonself
Immunologic surveillance
o Lymphocytes continually check cell surfaces, detect and destroy cells with abnormalities
o Involves cytotoxic T-cell natural killer cells, macrophages, and B lymphocytes
Some cancer cells have changes on their surface antigens
o Tumor-associated antigens (TAAs)
Escape mechanisms by which cancer cells evade immune system
o Suppression of factors that stimulate T-cells
o Weak surface antigens allow cancer cells to sneak through surveillance
o Development of tolerance of immune system
o Suppression of immune response to products secreted by cancer cells
o Induction of suppressor T-cells
o Blocking antibodies that bind TAAs
Cell Biology:
Immortality: unlimited number of cell divisions
Growth without GO signals
Growth factors, cell-to-cell adhesion molecules, extracellular matrix components
Ignoring STOP signals
Loss of contact inhibition: invade neighboring cells, keep dividing
Loss of restrictive point control: keep dividing without adequate nutrients
Loss of anchorage-dependent growth
Loss of cell cycle control
Avoidance of APOTOSIS (programmed cell death)
- apoptosis = auto destruct sequence (they dont self-destruct. They continue to grow.
- Angiogenesis can create their own blood supply. Secrete factors and androgen (vascular epidural growth factors)
Property
Cytological changes
Altered cytoskeleton
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Immortality
Reduced apoptosis
Types of Tumours
Benign neoplasms
o Well differentiated.
o Encapsulated.
o Expansive mode of growth.
o Characteristics similar to parent cell.
Malignant neoplasms
o Poorly differentiated.
o Infiltrative and expansive.
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Risk Factors
External stimuli (carcinogens)
o Diet colon cancer
Estimated that 1/3 all cancers and 90% of colon cancer are related to diet.
Tobacco small cell lung cancer (SCLC), oropharyngeal, bladder, cervical, gastric, lip, pancreatic, breast.
o As much as 50% of bladder cancer is related to smoking as a lot of carcinogens are excreted by the kidneys (meaning
that the carcinogens will sit in the bladder).
Bacteria H. pylori ulcers cancer risk.
UV radiation (e.g., from the sun) basal cell, squamous cell.
Chemicals
o Asbestos mesothelioma.
o Vinyl chloride liver.
o Arsenic sinuses, liver.
o Benzidine, aniline dyes bladder.
o Wool, leather, dust nasal sinuses.
Viruses
o Most common: HBV/liver cancer
o HTLV-1: T-cell lymphoma & T cell leukemia
o HTLV-2: Hairy cell leukemia
The prognosis is better with this type of cancer.
o Epstein Barr: Burkitts lymphoma
o HCV: liver cancer
o Human papilloma virus: cervical cancer
Immune System Abnormalities
o Immunosuppressive medications
Prednisone, cyclosporin, Immuran, etc.
Disorders affecting immune system
o Lupus, HIV/AIDS
Kaposis sarcoma is an AIDS-defining malignancy.
Age-related immune susceptibilities
o Children, Elderly
Inheritable Genetic Mutations
o BRCA-1: breast, ovarian, prostate
o BRCA-2: breast
o RB1: retinoblastoma (only in children up to the age of 2)
o
o
o
o
178
o
o
Phase
Psychosocial Impact
Pre-diagnosis
Diagnosis
Treatment
Recovery
Survivorship
OR
Progression or recurrence
Diagnosis
History and physical
o In many cases, the patients will have vague, non-specific symptoms which will lead them to see a health care provider.
Blood work
o A man with prostate cancer will test positive with a pregnancy test.
Tumour markers (e.g., oncofoetal antigens)
o As successful treatment progresses, the level of these markers will decrease.
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Classification of Cancer
Cancer can be classified according to:
1. Anatomical site classification
2. Histological analysis classification/degree of differentiation (i.e., grading).
3. Extent of disease classification (i.e., staging).
Classifying cancer in such ways is intended to provide standardized ways to communicate the status of cancer within the health
care team, assist in finding the best treatment plan, evaluate the plan, help determine prognosis, and compare like groups for
statistical purposes.
HER2/neu (also known as ErbB-2) stands for "Human Epidermal growth factor Receptor 2
HER2 is a cell membrane surface-bound receptor tyrosine kinase and is normally involved in the signal transduction pathways
leading to cell growth and differentiation. It is encoded within the genome by HER2/neu, a known proto-oncogene. HER2 is
thought to be an orphan receptor, with none of the EGF family of ligands able to activate it. However, ErbB receptors dimerise on
ligand binding, and HER2 is the preferential dimerisation partner of other members of the ErbB family.[1] The HER2 gene is a
proto-oncogene located at the long arm of human chromosome 17(17q21-q22).[2]
In clinical usage, HER2/neu is important as the target of the monoclonal antibody trastuzumab (marketed as Herceptin).
Trastuzumab is effective only in cancers where the HER2/neu receptor is overexpressed. One of the mechanisms of how
trastuzumab works after it binds to HER2 is by increasing p27, a protein that halts cell proliferation.[8]
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Classification systems are a means of categorizing the extent of disease into groupings that have clinical similarities rather than on
cell appearance. Its purpose is for treatment, research, and prognostication.
Clinical staging:
o Stage 0: cancer in situ (i.e., in a natural or original position)
o Stage 1: tumour limited to tissue of origin; localized tumour growth
o Stage 2: limited local spread
o Stage 3: extensive local and regional spread
o Stage 4: metastasis
If there is any metastasis, it is automatically stage 4.
This classification system has been used as a basis for staging cancer of the cervix and Hodgkins disease.
TNM Classification (one example of a classification system) there are MANY staging systems that are disease-specific.
This classification system is used to determine the extent of the disease process according to 3 parameters: tumour size (T),
degree of regional spread to the lymph nodes (N), and metastasis (M). After the extent of the disease is determined, the stage
classification is not changed. The original description of the extent of the tumour remains part of the original record.
o Tumour size
T0 No evidence of primary tumour
Tis Carcinoma in situ
T1-4 Ascending degrees of increase in tumour size and involvement
o Spread to lymph nodes
N0 No evidence of disease in the lymph nodes
N1-4 Ascending degrees of nodal involvement
Nx Regional lymph nodes unable to be assessed clinically
o Metastasis
M0 no evidence of distant metastases
M1-4 Ascending degrees of metastatic involvement of the host, including distant nodes
In general, the bigger the tumour, the greater the number of nodes, or the more metastasis, the worse the prognosis. Also, the
more primitive the cancer (i.e., the more the cell looks unlike healthy cells), the worse the prognosis.
Childhood Cancer
Children tend to develop different cancers than adults.
Usually embryonic in origin or due to oncogenes.
Major difference: immune system function.
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Developmental Considerations
Impact of cancer and treatment is variable depending on age/stage of life and associated developmental tasks/roles.
Children
o Potential impact on normal growth and development, future health, schooling.
Young adult
o Potential impact on career choices, education, relapses, $$.
Middle adult
o Potential impact on family functioning, finances.
Older adult
o Potential impact on ability to live independently, finances, retirement plans.
Cancer Treatment
Curative therapy: eradication of disease using modalities appropriate to the type of cancer.
Control: disease is present but treatment is controlling growth.
Palliation: relief or control of symptoms and maintenance of quality of life.
In reality, treatment does not always fit into neat/discrete categories (e.g., BMT for multiple myeloma is life prolonging, not
curative; disease temporarily eradicated but relapse is certain, or may have partial remission with eventual progression.
SURGERY
Surgical Therapy
Surgical therapy can be used for curative intent, for disease control, or for palliative reasons.
o Several principles are applicable when surgery is used to cure the disease process of cancer:
1. Cancer that arises from a tissue with a slow rate of cellular proliferation or replication is the most amenable to
surgical treatment.
2. A margin of normal tissue must surround the excised tumour.
3. Remove only as much as necessary and use adjuvant therapy. Less radical surgery is the current trend among
health care providers.
4. Preventative measures used to reduce surgical seeding of cancer cells.
5. Usual sites of regional spread may be removed.
Debulking is a procedure that may also be used when the tumour is attached to vital organs and cannot be completely removed. In
this case, as much tumour as possible is removed and the patient is then put on radiation and/or chemotherapy. This greatly
increases the effectiveness of the radiation/chemotherapy (as compared to no debulking).
RADIATION THERAPY
Radiation Therapy
It is the use of high energy particles or waves to treat disease.
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CHEMOTHERAPY
Chemotherapy
The use of cytotoxic medications to kill cancer cells
First drug: nitrogen mustard, 1940s
1960s/70s: platinum-based tx & combo chemtox
Goal: reduce and/or eliminate visible and invisible (micrometastases) disease
Cancer cells can develop resistance to chemotx
It is most often a SYSTEMIC therapy; therefore systemic side effects are expected. Chemotherapy works at the cellular level.
Drugs have expected side effects (e.g., nausea) that are to be managed aggressively. There are two types of chemotherapeutic
drugs: cell cycle-non-specific drugs and cell cycle phase-specific drugs. These two types of drugs are often administered in
combination with one another.
Drugs also have less common, unexpected toxicities (e.g., cardiotoxicity) assess carefully to allow for early identification.
Goal is to reduce and/or eliminate visible and invisible (micrometastases) cancer cells.
o Several factors determine response of cancer cells (e.g., mitotic rate of the tissue from which the tumour arises).
o Cancer cells can escape death by staying in the G0 phase (i.e., rest/non-active period).
o Main problem is the presence of drug-resistant resting and non-cycling cells.
Chemotherapy can be used in a number of ways:
o Primary therapy
o Adjuvant therapy
Women with breast cancer will often receive chemotherapy as an adjuvant.
o Neoadjuvant therapy (i.e., before other therapies)
This may be seen in order to shrink large masses before they can be removed.
o Combination therapy
Numerous regimens (recipes).
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Central vascular access devices permit frequent, continuous, or intermittent administration or for vesicants.
o Can be used to administer additional fluids, supplemental medications, nutrition, and blood products.
Major types:
o Central line (subclavian)
o PICC
o Implanted infusion ports
Chemotherapy Effects
Chemotherapeutic agents are cytotoxic to both normal and cancer cells.
The effects of chemotherapeutic drugs can either be acute, delayed, or chronic.
Bodys response to products of cellular destruction in circulation may cause fatigue, anorexia and taste alterations
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Acute reactions:
o Vomiting prevent with anti-emetics.
Nausea and vomiting is important to treat with the first treatment. This is due to anticipatory nausea and
vomiting. Lorazepam is used to treat this.
o Allergic reactions may pre-medicate to prevent.
o Arrhythmias
Delayed effects:
o Mucositis
o Alopecia (i.e., loss of hair)
o Bone marrow suppression
Bleeding due to decreased platelets.
o Fatigue
Due to decreased Hgb (which will lead to fatigue) and other factors.
o Skin changes (this is because skin is a rapidly dividing tissue)
o Nausea and vomiting
o Diarrhoea
o Decreased white blood cells infection.
Chronic toxicities
o Unique to each medication
o Assess carefully to allow for early identification
o Damage to
o Heart: e.g. anthracyclines follow with serial MUGA, assess s/sx CHF, D/C meds if LV dysfunction. These meds have
maximum lifetime doses even in absence of cardiac dysfunction.
o Kidney: e.g. cisplatin, carboplatin monitor serum Urea/Cr & creatinine clearance (24 hour urine), monitor I/O
o Liver: e.g. - monitor LFTs, jaundice, edema
o Lungs: e.g. bleomycin follow with serial PFTs, assess resp fctn
o Bone marrow: most drugs can cause chronic bone marrow failure if used over a prolonged period of time follow with
CBC and bone marrow bx if signs of bone marrow failure
o Reproductive: sterility depends on drugs & dose, assisted fertility
o Damage to:
Heart (the ejection fraction will be effected)
(bone marrow failure may occur from repeated doses of chemotherapy)
Late Effects
o Risk for leukemias and other secondary malignancies
Radiation and chemotx can induce DNA damage that can lead to new malignancies other than original dx
o Secondary malignancies other than leukemia have been reported
Includes breast (esp women who had chest radiation without shielding prior to 1980s), uterine, thyroid, lung
o Secondary malignancies are usually tx-resistant
Acute reactions: immediate with infusion
Delayed effects: days to weeks after treatment
Chronic toxicity: known but not typically expected to occur with each patient; usually weeks/months/years after treatment
Late effects: years after treatment
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Patient education is essential to decrease anxiety and ensure adherence to treatment plant.
o Treatment protocol
o Supportive care
o Expected side effects, toxicities, monitoring parameters
o Self-care
o Activity restrictions
Psychosocial care.
BIOLOGIC THERAPY
Biological therapy consists of agents that modify the relationship between the host and tumour by altering the biological response
of the host to the tumour cells.
Biological agents may affect the host-tumour relationship in 3 ways:
1. They have direct anti-tumour effects.
2. They restore, augment, or modulate the host immune system mechanism.
3. They have other biological effects, such as interfering with the cancer cells ability to metastasize or differentiate.
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Chimeric (mouse/human) monoclonal antibody that targets CD20 cell surface receptor.
CD20 is present on B-cells
90% of NHL have CD20
o Bevacizumab
Biological/Targeted Therapies
Monoclonal Antibodies:
Trastuzumab/Herceptin: HER-2+ breast ca, gastroesophageal junction adenoca
Cetuximab/Erbitux: squamous H & N, colorectal
Bevacizumab/Avastin: glioblastoma, NSCLS, met. colorectal & renal
Rituximab/Rituxan:
Tyrosine Kinase inhibitors:
Imatinib/Gleevec : CML, myelodysplatic/myeloproliferative, gastrointestinal stromal tumor
Dasatinib: CML, Philadelphia + ALL
Nilotinib: CML
Erlotinib/Tarceva: NSCLC, pancreatic
EGFR inhibitor:
Gefitinib/Iressa: NSCLC
mTOR inhibitors (mammalian target of rapamycin) a kinase enzyme:
Temsirolimus/Torisel: advanced renal cell
Everolimus/Afinitor:advanced renal
Retinoid (carboxylic acid form of Vitamin A) differentiating agent:
Tretinoin/Vesanoid: acute promyelocytic leukemia (can be very lethal from bleeding)
Proteasome inhibitor (promotes apoptosis):
Bortezomib/Velcade: multiple myeloma, mantle cell lymphoma
Angiogenesis inhibitors:
Thalidomide, lenalidomide/Revlimid: multiple myeloma
o
o Hematopoietic Therapy
Granulocyte Colony-stimulating Factors (G-CSF)
o Colony-stimulating factors (CSF) are a family of glycoproteins produced by various cells.
o These glycoproteins stimulate the production, maturation, regulation, and activation of cells in hematologic system.
o Hasten recovery from bone marrow depression or stimulate stem cell mobilization for transplantation.
o It is a supportive care measure rather than a treatment for cancer.
o Very important part of many cancer treatment protocols.
Erythropoietin is used more commonly in renal failure.
Platelet stimulating factors none on market in Canada.
Transfusions of RBC and platelets are more commonly used than growth factors in cancer treatment.
o
o Stem Cell (Blood) & Bone Marrow Transplantation (aka Hematopoietic Stem Cell Transplantation)
Myeloablative: use lethal doses of chemo/radiation.
o Administer large doses of chemo +/- radiation.
Eradicate diseased bone marrow (myeloablative).
Dose-escalation to treat disease outside bone marrow.
Stem cell rescue.
Engrafts and repopulates marrow with healthy donated cells or previously collected autologous cells.
Today we are also doing:
o Reduced intensity transplants.
o Non-myeloablative transplants.
o Both transplants depend on the graft-versus disease effect for success and use lower doses of chemo/radiation.
o Allows for older patients to receive treatment.
Other types of BMT:
o Reduced intensity
o Non-myeloablative
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Both depend on the graft-versus-disease effect for success & use lower doses of chemo/radiation
Allows for older patients (up to 65) & those with certain co-morbid conditions to be transplanted
o
Allows use of very high doses of chemotherapy +/- radiation therapy.
Highest tolerable doses of chemotherapy.
Goal is to administer large doses of systemic therapy.
Eradicate diseased bone marrow (i.e., myeloablative).
Dose-escalation of disease outside bone marrow.
Bone marrow rescue is required after myeloablative therapy.
Engrafts and repopulates marrow with healthy donated cells or previously collected autologous cells.
Whether the disease is malignant or non-malignant, the goal of BMT is cure.
o BMT Complications
Graft-versus-host disease
o T-lymphocytes from donated marrow recognize recipient as foreign and attack organs such as skin, live and intestines
o Beneficial graft-versus-disease effect
T-lymphocytes also attack residual malignant cells
Essential component/benefit of BMT
Can induce this to treat early relapse
Reduce immunosuppression or give DLI
o
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o
o Complications of Cancer and Treatment
Infection (the client may have neutropenia and may therefore not display the cardinal signs of inflammation)
Fatigue
Bleeding
Mucositis
Cachexia/Anorexia
o Malnutrition (once a weight loss of 10lbs has occurred it is difficult to maintain nutritional status).
o Altered taste sensations.
o
o Oncologic Emergencies (cancer equivalent of chest pain or GI bleed)
Emergency
Sx
Tx
FNE/Septic Shock
Bld cultures
Urgent Abx
Assess focus: CXR, MSU
Hypercalcemia of
Malignancy
calcium
Pamidronate
Hydrate
TLS
K, uric acid
Prevent
Rasburicase
Hydrate/alkalinize
SIADH
Fluid restriction
Treat cancer
DIC
Tx underlying malignancy
Transfuse & anti-coagulate
Febrile (i.e., >38.5C at one measurement or >38C measured twice within an hour) neutropenia/Septic Shock
o They need antibiotics within 1 hour.
Obstructive emergencies:
o Spinal cord compression (SCC)
This occurs when there is the presence of a malignant tumour in the epidural space of the spinal cord.
o Superior Vena Cava Syndrome (SVC Syndrome)
This occurs when the superior vena cava is obstructed by the tumour.
o Metabolic emergencies:
o
o
o
o
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Emergency
Sx
Tx
SCC
Urgent radiation
Steroids
SVC syndrome
Cardiac tamponade
Carotid artery
rupture
Exsanguination
Infiltrative emergencies:
o Cardiac Tamponade
Tumour is pressing on the heart.
o Carotid Artery Rupture
Cancer in the head and neck area can cause it to chew through the carotid artery. There is no management
possible.
Spinal Cord Compression
o
o Nutritional Problems:
o
o Symptoms:
N/V
Diarrhea
Anorexia/cachexia
Mucositis/dysphagia
Xerostomia
Taste changes
Fever/infection
Medication side effects
Disease effects
Fatigue
Edema/fluid retention
o Consequences:
Malnutrition d/t intake
Lytes, albumin, protein abnormal
Dehydration
Weight loss
Weight gain
Decreased wound healing
Fatigue
Weakness/difficulty ambulating
o
o Radiation Induced Xerostomia
o Nutritional Interventions
Manage symptoms optimally (n/v, pain)
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Stage
Potential Impact
Child/Teen
o G & D, future health, schooling, fertility, family $$ if parent needed to care for child at
home/hospital
Young Adult
Middle Adult
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Older Adult
Assessment:
Physical, psychological, developmental, family
How would you do an oral assessment on a 3 year-old with mucositis??
Interventions:
Nutrition/hydration: how to encourage if decreased appetite, nausea
Med administration: oral meds?
Infection prevention: crawling? Oral phase?
Pain/sx management: appropriate drugs/doses
School-age children: maintaining normalcy, keep up with class
Family care:
Parental psychosocial support
Information/resources
o
o
Recovery
Survivorship
OR
Progression or recurrence
o
o
o
o
o
o
o
o
Psychosocial Impact
Often caught off guard, sometimes suspected it
Overwhelmed, information overload
Dealing with side-effects, life revolves around
treatment
Re-entering normal world
Living beyond cancer
Approaching and dealing with death
o
o Cancer Survivorship
Preferred term over cure
o Cure is a prophetic statement that cancer will never come back. Almost impossible to determine prospectively.
Refers to a dynamic process of living with, through, and beyond cancer.
o
o Treatment Goals:
Curative: eradication of disease using modalities appropriate to the type of cancer
Control: disease is present but treatment is controlling growth
Palliation: relief or control of symptoms and maintenance of quality of life
In reality, treatment does not always fit into neat/discrete categories e.g. BMT for multiple myeloma is life prolonging, not
curative; disease is temporarily eradicated but relapse is certain, or may have partial remission with eventual progression
Cancer survivorship care needs to take this into account
o
o Seasons of Survival
Acute
Extended survival
Permanent Survival
o Long-term disease free survival.
o
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o Survival Rates
838,724 people alive in 2009 who had cancer dx in previous 10 years.
Current 5-year overall survival
Adults: 63%
Range: Thyroid 98%, Pancreatic 8%
Death rate from breast cancer ing since 1980s, ~2.4% /year. 42% since 1986.
Children: 82%
1930s <30%
o
o Impact of Survival
Physiologic
o Disease recurrence: variable depending on diagnosis.
o Second malignancies low but real risk
o Long term effects:
Chronic S/E persisting beyond treatment:
Cognitive dysfunction, lymphedema, scars, ostomies, fatigue, N/V
o Late effects:
Occur months to years post treatment:
Cardiac changes, pulmonary fibrosis, cataracts, thyroid dysfunction, arthritis
Psychologic
o Fear of recurrence.
o Sense of vulnerability.
o Anxiety at cancer anniversaries.
o Body/self image changes.
o Sexuality issues.
Social
o Stigma.
o Perception of health by others (work, family).
o Employment issues, financial issues.
o Altered family roles/relationships.
o Loss of friends.
o Impact of Survival.
Spiritual
o Changes in priorities, values, lifestyle.
o Re-evaluation of goals, career.
o Search for meaning, enhanced meaning in life.
o Deepened sense of spirituality.
o Concerns about QOL, altered QOL.
o Increase self-acceptance.
o Increased passion or zest for life.
o Feel need to give back.
o Survivors guilt.
o
o Community resources (see slides 121-128)
o
o
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o Outline
Definition
First aid
Etiology
Nursing care
Classifications and symptoms
Psychosocial issues
Diagnosis
Seizures
What is a seizure?
o Sudden disturbances of brain function that can cause:
Changes in involuntary muscle activity.
Behavioural and sensoral manifestations.
Alterations in consciousness/awareness
Goals of Treatment
The ultimate goal is to stop the seizures from occurring, but realistically speaking, this may not be possible due to different
etiologies. Maximum control of seizures is desired.
Maintain quality of life.
o Many seizure drugs have side-effects that may interfere with ones quality of life (e.g., sedation).
Etiology
Acquired (secondary); idiopathic/cryptogenic (i.e., the cause is unknown).
First month of life:
o Brain injury (e.g., asphyxia, birth trauma, intercranial haemorrhage)
Premature children are susceptible to intercranial haemorrhage.
o FAS
o Inborn errors of metabolism
o CNS infection (e.g., meningitis, encephalitis)
o Drug withdrawal (maternal)
Young Children
o Symptoms vary (e.g., sucking, yawning, lip smacking, staring, abnormal cry).
o Brodies seizures: http://www.youtube.com/watch?v=6Fje2AltD1A
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1) Partial
a. Simple Partial
b. Complex Partial
2) Generalized (6 types)
3) Unclassified
4) Status epilepticus
Partial Seizures
Initiated in a localized area within brain.
1) Simple partial:
o No loss of consciousness. They are also likely to remember what happened.
o Symptoms vary: emotions (e.g., bliss), sensory response (e.g., visual disturbances), and motor response.
2) Complex partial:
o Most common type.
o Some alteration of LOC/awareness.
o Onset: blank stare, appears dazed or confused.
o Automatic, unorganized (they may be able to speak, but their sentences wont make sense), non-purposeful repetitive
movements, and lip-smacking.
o May have a post-dictal phase.
o May evolve into generalized.
Nursing care
o Remain calm and by their side.
o Turn the lights down/off.
o Ensure the surroundings are safe.
o Time the seizure.
Generalized Seizures
Convulsive or non-convulsive
Absence
Generalized
Status
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o No loss of consciousness.
o Quick recovery; excellent response to treatment.
Benign Myoclonic jerks
o Drowsy falling asleep.
o May occur from changes in visual perceptions (e.g., flickering lights, TV).
Absence seizures (formerly known as petit mal)
o Brief (2-10 seconds) lapse of consciousness making them hard to spot (an EEG is required for diagnosis).
o How to distinguish: age, frequency, and family history.
o Respond well to treatment.
o Some patients outgrow this type of seizure whereas others move onto the tonic/clonic seizures.
o http://www.youtube.com/watch?v=z9V2sNmIoJk
o http://www.youtube.com/watch?v=kawYuUeXg4U
o http://www.youtube.com/watch?v=DruJDZVO7Ko
o http://www.youtube.com/watch?v=H3iLQi6wt94
Tonic/clonic (formerly known as grand mal)
o Grand mal.
o Bilateral; lose consciousness.
o Tonic phase: muscle contraction/rigidity.
o Clonic phase: contraction and relaxation, intense jerking.
o When they regain consciousness they will be groggy and have a headache.
o Recovery time is different for everyone (may range from a few minutes to the entire day).
o http://www.youtube.com/watch?v=FSkwXUi6ie0
Post-dictal state
o http://www.youtube.com/watch?v=Tk6HyxSI4Ag
o Recovery
o Duration
Triggers
Role of triggers
Common triggers:
o Fatigue
o Fever/infection
o Stress
o Sleep deprivation
o Flashing lights
o
o
o
o
Photosensitivity
Prolonged use of video games/computer
Non-compliance with anti-epileptic drugs
(AEDs)
Hormonal changes (often associated with growth
spurts)
Action to take:
o Vigilance
o Emphasize normal family life
Jett Travolta
Died while taking a shower as a he hit his head during a shower.
Status-Epilepticus
Definition:
o Continuous generalized tonic-clonic activity with loss of consciousness for longer than 30 minutes, or two or more
discrete seizures without a return to baseline mental status.
or
o Continuous or intermittent seizures lasting longer than 5 minutes without full recovery of consciousness between
seizures.
During this time the patient will have an increased HR and BP as well as a decrease in SaO 2. This decrease in SaO2 can be very
dangerous if the patient is seizing for >5 minutes.
It most commonly occurs in children <2 years of age.
Nursing care:
o Check blood sugars.
They will often be hypoglycaemic as the body uses a lot of sugar during a seizure.
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o
o
Treat ABCs.
They may need help with ventilation.
They will have to be placed side-lying if they start vomiting.
Apply oxygen mask (even if their SaO2 appears normal) and monitor SaO2.
Monitor BP.
Common Etiologies
Acute (17-52%):
o Acute CNS infection
o Metabolic derangement
Hyperglycaemia, hypocalcaemia.
o Antiepileptic drug noncompliance, withdrawal or insufficient pharmacological treatment
o Antiepileptic drug overdose
o Non-antiepileptic drug overdose
o Prolonged febrile convulsion
o Trauma
Remote (16-39%)
o Cerebral migrational disorders
The brain lacks the grooves that develop with normal growth. This will alter the patients electrical conduction.
o Cerebral dysgenesis
o Perinatal hypoxic-ischemic encephalopathy
o Progressive neurodegenrative disorders
Idiopathic/cryptogenic (5-19%)
Objectives for Acute Management
Maintenance of adequate ABCs.
Termination of seizure and prevention of recurrence.
Diagnosis and initial therapy of life-threatening causes of status.
Arrangement of appropriate referral for ongoing care or transport to secondary centre.
Management of refractory status (i.e., period in time where the body does not respond to treatment).
Cell damage occurs after 30 minutes and is secondary to a decreased blood flow to the brain.
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Medications
Constant adjustments and on-going monitoring.
o Therapeutic index
o Long half-life
o Increase the drugs dose in small increments
o Serum levels
o When to discontinue
o Risk/benefit ratio
Drug interactions +++
Common side effects:
o Drowsiness, fatigue, nausea, clumsiness.
o Dilantin gingival hyperplasia.
o Teratogenic effects to be considered if contemplating pregnancy.
o Liver metabolizing enzymes.
Ketogenic Diet
This is used as a last effort to control seizures. The goal is to put the body in starvation mode.
Febrile Seizure
Does not = epilepsy.
Refer to text.
Characteristics:
o Generalized any kind.
o Associated with fever usually due to viral infection.
o Brief.
o Occur only once in 24 hours.
o 6 months to 5 years of age.
Diagnosis: by history and assessment.
Risk for recurrence,
Treatment:
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Review
Acute and chronic renal failure:
o Acute renal failure can lead to chronic renal failure. If treated early
enough, acute renal failure can be reversible.
Notes:
o Blood flow determines how the kidney will react (e.g., release of renin).
o Renal filtrate is very much like blood plasma.
Nephrons
o It is the basic structural unit of the kidney.
o It contains the Loop of Henle, the glomerulus, the Bowmans capsule, etc.
Formation of urine
Loop of Henle
o It is responsible for the reabsorption of Na+, Cl-, and water, which follows
sodium.
Primary function(s) of the kidney
o Filter blood.
o Regulates acid-base balance by controlling HCO3-.
o Reabsorption of sodium.
o It is one of the primary regulators of homeostasis in the body.
o 3-5L of blood is ejected from the heart in one minute.
~25% of this is seen by the kidneys.
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iClicker Questions
The client is admitted to a nursing unit from a long term care facility with a hematocrit of 0.56 (56%) and a serum sodium level of
152 mEq/L. Which condition would be a cause for these findings?
a) over-hydration
The sodium value is high.
b) anaemia
The hematocrit is a normal-high value (normal values are between 37-47% for women and a little higher for men).
c) dehydration
d) renal failure
The hematocrit is normal-high.
True or False
1) Glomerular filtration rate (GFR) is primarily dependent on adequate blood flow and adequate hydrostatic pressure.
True
2) The primary function of the kidney is to excrete nitrogenous waste products.
It does do that, but it is not the primary function. The primary function is to regulate volume, fluid and electrolyte
composition, etc.
3) Atrial natriuretic factor (ANF) is secreted by the right atrium when atrial blood pressure is low, and it blocks the action of
aldosterone.
False. ANF is secreted by the right atrium when atrial blood pressure is high. It then blocks the action of aldosterone.
4) Increased permeability in the glomerulus causes loss of proteins into the urine.
True
A client with an obstruction of the renal artery causing renal ischemia exhibits hypertension. One factor that may contribute to the
hypertension is:
a) Increased renin release
b) Increased ADH secretion
c) Decreased aldosterone secretion
Renin is secreted before aldosterone and both are responsible for an increase in blood pressure.
d) Increase synthesis and release of protaglandins
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A clinical situation in which the increased release of erythropoietin would be expected is:
a) Hypoxemia
b) Hypertension
c) Hyperkalemia
d) Fluid overload
Causes of ARF
They are divided according to similar pathogenesis into:
o Pre-renal (55-60% of all cases)
Due to factors external to the kidneys that reduce blood flow and lead to decreased glomerular perfusion and
filtration.
Hypovolemia (the most common cause), trauma, obstruction, and anything that decreases cardiac
output (e.g., MI, cardiac disease, etc.).
Pre-renal ARF can lead to intra-renal disease if the renal ischemia is prolonged.
o Renal/Intra-renal (30-40% of all cases)
Due to conditions that cause direct damage to the renal tissue (parenchyma), resulting in impaired nephron
function.
Glomerular nephritis, rhabdomyolysis, trauma, nephrotoxic drugs, and anything that affects the inside
of the kidneys. Strep throat and urinary tract infections can cause glomerular nephritis.
Acute tubular necrosis (ATN) is a type of intra-renal ARF caused by ischemia, `xins, or pigments.
o Post-renal (<5% of all cases)
Involve mechanical obstruction of urinary outflow. As the flow or urine is obstructed, it refluxes into the renal
pelvis, thus impairing kidney function.
Benign prostatic hyperplasia, kidney stones, prostate cancer, trauma, pylonephritis.
It is important to determine the cause of renal failure.
Treatment
Treatment must be prompt and appropriate. There is a 50% mortality rate.
iClicker Question
The nurse is admitting a client diagnosed with ARF. Which question would be most important for the nurse to ask during the
admission interview?
a) Have you recently traveled outside of Canada?
ARF is not caught.
b) Did you recently begin a vigorous exercise program?
The amount of exercise would have to be extremely vigorous (e.g., a triathalon).
c) Is there a chance you have been exposed to a virus?
A virus is generally not the cause.
d) What over-the-counter medications do you take regularly?
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1) Onset/Initiating Phase
Precipitous event (e.g., taking nephrotoxic drugs, a hypovolemic event such as a trauma).
2) Oliguric Phase (i.e., decrease in urine output: <400mL per day)
Recall that 30mL/hour is the absolute minimum urine output.
This is the most common initial manifestation of ARF. It is caused by a decrease in GFR.
~50% of people will not display this oliguric phase.
It is usually seen within 1-7days following the onset. It can last 1-2 weeks; can be up to 8 weeks or more.
BUN and creatinine.
Pre-renal oliguric phase:
o Increased specific gravity (i.e., >1.015).
o Na+ retention (and thus low Na+ concentration in the urine).
Intra-renal oliguric phase:
o Normal specific gravity (i.e., 1.010).
o High Na+ concentration in urine.
Fluid retention, edema, and weight gain.
Fluid and electrolyte imbalances.
Metabolic acidosis occurs as the kidneys are unable to produce ammonia that is used to bind the excess H +. This, couple
with the fact that the HCO3- in the kidneys is now being used to buffer the H+ (rather than ammonia) causes an acidotic
state.
Na+ spill as the damaged tubules are no longer able to retain Na+.
3) Diuresis
Over 2,000mL/day.
Marks return of glomerular filtration due to osmotic diuresis. The bodys ability to excrete waste products has returned
but the kidneys have not regained the ability to concentration urine.
BUN and creatinine begin to stabilize.
Risk of hypovolemia**.
o This can be determined by the patients blood pressure, their mucous membranes (check moisture), etc.
4) Recovery
Takes 3-12 months.
Begins when BUN is stable.
Case Studies
Karl is a healthy 42 year old bachelor who enjoys hunting by himself. While...
He has decreased urine output, possibly relating to decreased renal perfusion. He is at risk for acute renal failure.
What nursing measure would be beneficial for Karl?
o Fluids: strict I&O, daily weights, IV running to help replace the lost fluid
o Nutrition: low protein (as the BUN and creatinine [breakdown of creatine phosphate in the muscle][closest youre going
to measure the GFR] are high), low K+, increased carbohydrates for energy.
o Medications: medications to remove K+ (e.g., Kayexalate), ACEi (help slow the progression of acute renal failure),
diuretics.
o Dialysis: this may be started if the diuretics dont work (this is indicated when the GFR is decreased).
Clinical assessments:
o Vital signs, I&O.
Signs and symptoms of an elevated urea level:
o LOC, gout, pruritis.
Metabolic acidosis was developed as the H+ ions were not excreted and the HCO3- was not reabsorbed.
o This may lead to Kussmauls respirations (i.e., fast and deep respiratory rate).
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Etiology
There is a high incidence of diabetes in Manitoba (30% of the patients with renal failure are diabetics)*
Hypertension*
Glomerulonephritis
Renal vascular disease
Pyelonephritis
Polycystic disease
There are usually no symptoms until the GFR is 20% of normal (i.e., 80% of the kidneys can be damaged before an individual
recognizes symptoms). This is because the remaining nephrons hypertrophy to compensate.
Clinical Course
1) Decreased renal reserve (stage 1)
Renal function 40-70% of normal.
Asymptomatic.
BUN and Cr are normal/high normal.
2) Renal insufficiency (stage 2)
GFR 60-89 mL/min. (Never going to ask about values)
Residual renal function 40% of normal.
Slight increase in BUN and Cr.
Polyuria with decreased ability to concentrate urine.
Anaemia (this is due to impaired erythropoietin production by the kidneys).
Symptoms worsen with stress (e.g., infection, emotional stress, etc.).
3) Chronic Renal Failure (stage 3-4)
GFR 15-59 mL/min.
15-20% normal function.
Azotemia (i.e., high BUN and Cr).
Metabolic acidosis due to a in ammonia excretion (this also leads to K + levels as acidosis prevents it from entering
the cells).
Fluid retention due to Na+ retention from a lack of its excretion.
Increased Na+, K+, and PO4- due to a lack of their excretion by the kidneys. PO4- also increases due to PTH release.
209
2+
210
Retained Substances
Urea
Hormones
Creatinine
Electrolytes (e.g., Na+, K+, PO4-)
Phenols
Water
iClicker Question
A client with an elevated BUN:
a) Has decreased urea in the urine.
b) May have non-renal tissue destruction.
c) Definitely has impaired renal function.
d) Will always have a rise in serum creatinine.
a. Note* BUN and Creatine will always be read together, BUN only reads the kidneys
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Electrolyte imbalance
Hypoxia
Respiratory
o Uremic lung aka pneumonitis (depressed cough reflex).
o Related to immune response.
o Leads to secondary infections.
o Pneumonia.
o Death.
o Pulmonary edema.
o SOB and Kussmauls breathing in order to excrete CO2.
Gastrointestinal
o Every part of the GI system is affected due to the mucosal inflammation due to the increase in urea.
o Nausea, vomiting, anorexia, hiccoughs.
o Bleeding and ulceration are prevalent due to irritation of the GI tract by waste products coupled with platelets.
o Uremic fetor (urinous odour of the breath).
o Stomatitis.
o Tongue yellow/brown.
o Altered sense of taste.
o Constipation/diarrhoea (due to K+).
o Altered CHO metabolism triglycerides.
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Serum
BUN and creatinine
Anaemia (Erythropoietin Epogen)
Hgb/Hct (decreased haemoglobin)
Coagulation defects
protein albumin
Hyperkalemia
Hypo/hypernatremia (edema, HF, HTN)
Magnesium imbalance
Calcium/phosphate imbalances (Ca++based phosphate binders)
Urine test
ABGs
o Bicarbonate IV, oral Shols solution (which is another form of bicarbonate)
o Monitor dysrhythmias, LOC
Management of hyperkalemia
o Diet (Leafy greens, bananas, etc.)
o Avoid catabolic states
o Transfuse during dialysis
o Kayexalate (cation-exchange resin)
o Glucose and insulin (shifts the K+ into the cell out of the vascular blood, where is cannot harm our hearts)
o K+ wasting diuretics
o Teach
o
o Other Major Concerns
1) Potential for infection.
o This is due to a change in leukocyte function.
o Altered immune response.
o Diminished inflammatory response.
2) Potential for injury related to diminished drug excretion.
o Drug toxicity digoxin antibiotics pain medications.
3) Psych-social aspects.
o Personal behavioural changes, emotional liability, withdraw, and depression.
o
o Diagnosis of Renal Failure
History
Physical
o Pre-renal (volume depletion)
o Renal (ischemia nephrotoxin)
o Post renal (obstruction)
Lab Work
o
o Diagnostic Tests
KUB
CT scan
IVP
Renal scan
Renal arteriogram
Blood work
U/S
Urinalysis
Management of ARF
ID, eliminate and treat
ACE Inhibitors
Monitor blood work (lytes)
Phosphate binders
Treat hyperkalemia
Monitor ABGs
o IV glucose and insulin
Diet restriction protein & phosphate/oliguric phase
o Calcium gluconate
Calorie requirements met by CHO
o Kayexalate
Dialysis
Diuretics
Diuresis phase: diet low in protein and CHO
Albumin
Management of CRF
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DIALYSIS
Indications for Dialysis
Fluid overload.
Hyperkalemia.
Severe metabolic acidosis (determine by ABGs).
Uremic pericarditis.
Uremic encephalopathy (i.e., mental changes).
When the GFR <15mL/min.
Dialysis
It is the movement of fluid and molecules across a semi-permeable membrane from one compartment to another.
Purpose
Remove end-products of metabolism (i.e., metabolic wastes).
Remove excess fluid.
Restore electrolyte and acid balance.
Principles
Diffusion
Osmosis
Filtration (i.e., microfiltration)
Dialysis
Started when patients uremia can no longer be adequately managed conservatively.
Initiated when GFR <15 mL/min.
Peritoneal access is obtained by inserting a catheter through the anterior abdominal wall.
Complications of PD
Infection******
Bleeding
Abdominal/back pain
Protein loss
Outflow problems due to obstruction
Pulmonary complications
Hernias
3 Phases of Dialysis
Inflow (10 min)
Dwell (4-6 hrs)
Drain (15 min)
Effectiveness
Independence.
Ease of traveling.
Fewer dietary restrictions.
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Haemodialysis Complications
Hypotension (#1 complication)
Muscle cramps
Loss of blood
Hepatitis
Sepsis
Disequilibrium syndrome
Effectiveness
It cannot fully replace the metabolic and hormonal functions of the kidneys.
It can ease many of the symptoms.
It can prevent certain complications.
Kidney Transplantation
Selection
o This is based on a variety of medical and psychosocial factors. Clients with cardiovascular disease and diabetes mellitus
are considered to be high risk. As are those who have displayed non-compliance with medication regimens, those who
are alcoholics, and those with drug addictions. The presence of hepatitis B or C is not a contraindication to
transplantation.
Histocompatability studies
Donor sources
o Polycystic kidney disease is hereditary, making other family members poor potential donors.
Treatment pre-, intra-, and post-op
o Pre-operation preparations include removing any dialysate from the
patient.
Complications
Acute Glomerulonephritis
Immunological processes involving the urinary tract predominantly affect the renal
glomerulus. The disease process results in glomerulonephritis, which affects both
kidneys equally.
There are 2 types of antibody-induced injury that can initiate glomerular damage.
1. The antibodies have specificity for antigens within the glomerular
basement membrane. Immunoglobulins and complement are deposited
along the basement membrane. Production of auto-antibodies (i.e.,
antibodies to ones own tissues) may be stimulated by a structural alteration in the glomerular basement membrane or by
a reaction of the basement membrane with an exogenous agent (e.g., hydrocarbon, virus).
2. The antibodies react with circulating non-glomerular antigens and are randomly deposited as immune complexes along
the glomerular basement membrane.
It is usually due to -haemolytic streptococci group A, which are nephrotoxic.
In both cases, the inflammation comes from the activation of complement.
Glomeruli become obstructed due to the inflammation which leads to a decrease in GFR.
Increase water and Na+.
Symptoms patients MAY have:
o Microscopic hematuria (if it is not microscopic, that is it can be seen by the naked eye, it may be bladder cancer)
o Hypertension & edema
o Excretion of formed elements (e.g., RBCs, WBCs, and casts)
o Oliguria (decrease in urine output)
o Transient anaemia
o Proteinuria
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Nephrotic Syndrome
Nephrotic syndrome describes a clinical course that can be associated with a number of disease conditions. In adults, about one
third of clients with nephrotic syndrome will have a systemic disease such as diabetes or systemic lupus erythematosus (SLE).
The rest will be categorized as having idiopathic (i.e., arising spontaneously or having unknown origin) nephrotic syndrome.
The increased glomerular membrane permeability causes:
o Abnormal loss of protein (proteinuria)
o Hypoalbuminemia
Ascites and anasarca (i.e., generalized edema with accumulation of serum in the connective tissue) will develop
from severe hypoalbuminemia.
o Hyperlipidemia
This results from the decreased serum proteins which stimulates hepatic lipoprotein synthesis.
o Both lead to edema (due to decreased serum protein) and hypercoagulable state
Hypercoagulability and thromboembolism is potentially the most serious complication of nephritic syndrome.
Uremic Syndrome
Collective systemic responses to renal failure.
It is caused by retention of metabolic by-products.
iClicker Questions
Restriction of dietary protein may be indicated in management of acute post-streptococcal glomerulonephritis when the client has:
a. Hematuria
b. Proteinuria
c. Hypertension
d. Elevated BUN
Which following assessment would evaluate the effectiveness of treatment for the client with nephrotic syndrome?
a. Blood pressure q4h
b. Abdominal girth daily
c. Urine of each voiding for protein
d. Daily dietary protein intake
The edema associated with nephrotic syndrome occurs as a result of:
a. Hypercoagulability
b. Hyperalbuminemia
c. Decreased plasma oncotic pressure
d. Decreased glomerular filtration rate
216
Review
Levels of unconsciousness
o Check Appendix Y.
o The first sign that a patient has an increase in intracranial pressure is a change in level of consciousness. Another sign is
when the pupils are not the same size.
o The worst case scenario is when a patients pupils are fixed (this occurs from a lack of O2).
o Pinpoint pupils occur from pressure on the pons medulla.
Review assessment of cranial nerves
I.
Olfactory nerve
VII.
Facial nerve
II.
Optic nerve
VIII.
Vestibulocochlear/Auditory nerve
III.
Occulomotor nerve
IX.
Glossopharyngeal nerve
IV.
Trochlear nerve
X.
Vagus nerve
V.
Trigeminal nerve
XI.
Accessory/Spinal accessory nerve
VI.
Abducens nerve
XII.
Hypoglossal nerve
Review musculoskeletal positions
o Decorticate
o Decerebrate (more serious)
217
Clinical Manifestations
Change in level of consciousness (this is the first thing that will occur).
Changes in vital signs (known as the Cushings triad).
o Increasing systolic blood pressure and decreasing diastolic blood pressure (i.e., widening pulse pressure).
o Bradycardia with a full and bounding pulse.
o Irregular respirations.
Ocular signs (i.e., cranial nerve III)
o The ocular signs are third, making it important not to wait for the pupils to change.
o Signs:
Having one dilated pupil. If the occulomotor nerve (i.e., cranial nerve III) is compressed, the pupil ipsilateral
(i.e., on the same side) to the mass of lesion will be dilated.
Pinpoint pupils indicate pressure on the pons medulla.
Papilledema, a choked optic disc seen on retinal exam, is also noted and is a non-specific sign associated with
long-standing increased ICP.
Decrease in motor function
o A contralateral (i.e., opposite side as the mass or lesion) hemiparesis or hemiplegia may be seen depending on the source
of the increased ICP.
o Decorticate Posturing
Arms come to the middle.
Theres an interruption in the voluntary motor tracts.
o Decerebrate Posturing
Palms are outward on the sides.
The nerve fibres are damaged.
Once the decerebrate posturing has occurred there is really no going back.
Headache
o Continuous headache that is worse in the morning and when the patient is lying.
Vomiting
o There is no nausea preceding the vomiting and it is projectile.
Complications
There are 2 major complications of uncontrolled ICP:
1. Inadequate cerebral perfusion
2. Cerebral herniation
With an increase in pressure, the brain will push downward (as the skull prevents it from moving anywhere else) and put pressure
on the medulla.
o This will lead to altered temperature (i.e., the patient will become extremely hot), pulse, and respiratory control.
Diagnostic Studies
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Collaborative Care
Drug therapy
o Mannitol, glycerol, and urea are all used as osmotic diuretics.
Mannitol is a sugar solution and strong diuretic that is kept in an incubator to prevent crystallization. This will
be given with loop diuretics. The mannitol will draw fluid out of the brain and the loop diuretics will help
excrete those excess fluids.
o Loop diuretics
o Corticosteroids
Decrease inflammation.
o Barbiturates
You want to slow the hypermetabolic state which will decrease the need for O2.
o Antiseizure drugs
The increase in pressure can lead to seizures.
Seizures can also occur if Na+ is below 125mmol/L or greater than 160mmol/L.
o Antipyretics
Nursing Management
Nursing Assessment
Subjective data from client or family members.
Glasgow Coma Scale.
o Vitals signs are completed q4h.
o Neurological tests are done q4h.
Vasomotor response.
Eye opening.
Muscle coordination.
o It is scaled up to 15 for adults.
When the patient scores 8, they have an increase in ICP.
The scale is a little different for children because of different developmental levels.
Neurological assessment.
o You typically only check the cranial nerves that are relevant to the patient.
Nursing Implementation
Goals for a patient with increased ICP:
o Normalize the ICP.
o Maintain a patent airway.
Positioning (e.g., side-lying, chin-tuck with the chin being midline).
Adequate oxygenation.
The amount of O2 administered will be based on the ABGs.
Oral airway if the patient is unconscious.
Mouth care is very important due to the increased secretions.
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Safety
o Side rails up.
o Patient side-lying.
o Ensure the environment is safe in case a seizure occurs.
o Changing positions.
o Have the patient blink to ensure the eyes dont dry out.
o Perform mouth care.
o Ensure there is a gag reflex.
o If a patient is tube feeding you want to check for residuals.
o If the blankets are too tight it may cause foot drop. This can be prevented if the patient is wearing shoes while in bed.
o The patient must be fed calories (e.g., TPN) to ensure they are not breaking down their protein.
GI & GU
o Catheters.
o Once the catheter is removed, put the patient on a schedule to retrain them.
Musculoskeletal
o Range of motion exercises as osteoporosis can occur from bed rest.
Skin
o Skin breakdown can be prevented by repositioning the client frequently.
o Skin assessments should be done frequently.
o Integumentary care and nutrition go hand-in-hand.
Psychosocial
o The patient in a coma is still able to hear what you are saying.
o Support the family.
Rehabilitation
Review
Anatomy of cerebral circulation and cerebral blood flow.
Review neurological assessments.
o Pupils unequal = increased ICP.
o Pinpoint = pressures on the pons medulla.
Terminology Review
Aphasia/Global aphasia
o Inability to express oneself (i.e., speak) as well as a loss of comprehension.
Brocas aphasia
o Inability to express oneself (i.e., speak). Anything that comes out of the mouth will be gibberish. They are able to
understand.
Wernickes aphasia
o Inability to comprehend the sounds or meaning of speech. They can express themselves but what they are saying will
not make any sense.
o This is often seen in patients with encephalopathy (liver failure).
Dysphasia (to be distinguished from dysphagia)
o Inability to arrange the words in proper order.
Apraxia
o Inability to carry out a motor activity in response to a command.
Dyspraxia
o Impairment of the ability to perform coordinated movements.
Anomia
o Difficulty in selecting the appropriate word.
Agnosia
o Unable to recognize objects by feeling them (while their eyes are closed). Their sensory stimuli are not good.
Unilateral neglect
o Typically affects the left side, which is a right-sided stroke (this greatly impacts safety). They cannot move their affected
sided. It is as though it does not belong to them.
A person with a left-sided stroke will lose the ability to speak.
o It is often accompanied by hemanopsia (i.e., the loss of peripheral vision; they only have central vision).
220
STROKE
Terminology
Brain attack
o Term increasingly being used to describe a stroke and communicate the urgency of recognizing stroke symptoms and
treating their onset as a medical emergency.
Stroke
It is the third most common cause of death in the Canada.
If people survive a stroke, it is the leading cause of serious, long-term disability.
Approximately 25% of individuals who have an initial stroke die within 1 year, even if treated with drugs such as t-Pa and
streptokinase.
In Canada, someone has a stroke every 10 minutes.
A stroke occurs when there is ischemia (i.e., inadequate blood flow to the brain) to a part of the brain or haemorrhage into the
brain that results in the death of brain cells.
o Transient ischemic attacks (TIA) are when there is ischemia to the brain for an extended period of time. When TIA lasts
for 24-48 hours, a stroke occurs.
Risk Factors
Non-modifiable:
o Age
2/3 of all strokes occur in people >65 years of age.
The incidence of a stroke doubles every decade after 55 years of age.
o Gender
The rate is equal among men and women until 75 years of age, after which there is a greater number of women
getting strokes (this is due to the fact that women are more likely to live longer than men).
Women are more likely to die from a stroke than a man.
o Race
Asians, Aboriginals, African Americans all have a greater likelihood than Caucasians due to their increased
incidences of diabetes.
o Genetic factors (i.e., heredity)
Modifiable:
o Hypertension*
o Hypercoagulability
Single most important risk factor.
o Hyperlipidemia
o Obesity
o Asymptomatic carotid stenosis
o Oral contraceptive use
o Diabetes mellitus
o Physical inactivity
o Heart disease, atrial fibrillation
o Sickle cell disease
o Heavy alcohol consumption
o Smoking
o Table 59-1
o
o Cerebral Arteries
There are 2 main arteries that feed the brain:
o Internal carotid arteries (anterior circulation)
o Vertebral arteries (posterior circulation)
The major branches of the internal carotid arteries are the middle cerebral and anterior cerebral arteries. The middle cerebral
artery is where most strokes occur. This is because there is a lot of branching in that area, making it a prime location for clot
deposition.
A lot of vision problems occur with strokes because the optic chiasm is located directly below the middle cerebral arteries.
o Etiology and Pathophysiology
221
o
o
Cerebrovascular
Accident (CVA)
24-48 hours
Neurological deficits
Completed Stroke
(following 72
hours of ischemia)
Stroke in evolution
o
o Transient Ischemic Attack (TIA)
It is a temporary focal loss of neurological function caused by ischemia of one of the vascular territories of the brain, lasting less
than 24 hours and often lasting less than 15 minutes. They may be due to microemboli that temporarily block the blood flow.
Most TIAs resolve within 3 hours.
o
o Types of Stroke
Strokes are classified based on the underlying pathophysiologic findings:
1. Ischemic stroke
o Ischemic strokes account for 85% of all strokes and result from inadequate blood flow to the brain from a partial or
complete occlusion of an artery.
a. Thrombotic stroke
These kinds of strokes account for 61% and they are usually preceded by TIAs. They occur due to
narrowing of the blood vessels by plaque. This narrowing increases the risk of a blood clot to occur.
b. Embolic stroke
Occurs when an embolus (i.e., blood clot) that is circulating in the blood gets caught in a cerebral
artery that is too small for it to pass through.
It is the second most common cause of strokes.
The client with an embolic stroke will have a sudden onset of symptoms (i.e., there are no warning
signs as in thrombotic strokes). With that in mind, these strokes are also more dangerous as collateral
circulation has not had a chance to develop. Recurrence of an embolic stroke is common unless the
underlying cause is aggressively treated.
2. Hemorrhagic stroke
o Hemorrhagic strokes account for 15% of all strokes. Results from bleeding into the brain tissue itself (i.e.,
intracerebral) or into the subarachnoid space or ventricles (i.e., subarachnoid).
a. Intracerebral haemorrhage
Results from bleeding the in brain tissue as result of a ruptured vessel. These ruptures may occur due
to trauma, or more commonly, hypertension.
Haemorrhage typically occurs during periods of activity as the heart rate and blood pressure rises.
o
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Subarachnoid haemorrhage
This occurs when there is intracranial bleeding into cerebrospinal fluid-filled space between the
arachnoid and pia mater membranes on the surface of the brain (or ventricles)
It is commonly caused by rupture of a cerebral aneurysm.
o Clinical Manifestations
Most obvious effects of stroke include impairment of:
o Mobility
o Respiratory function
o Swallowing and speech
o Gag reflex
o Self-care abilities
o
o Motor Function
In a person with a right-sided stroke, their left side will be affected due to the neural pathways crossing over in the brain. This is
the contralateral side (i.e., opposite side as the stroke).
Characteristic motor deficits:
o Loss of skilled voluntary movement (i.e., akinesia).
o Impairment of integration of movements.
o Alterations in muscle tone.
o Alterations in reflexes (the initial hyporeflexia gradually progresses to hyperreflexia).
o
o Communication
This will occur in patients with a left-sided stroke.
Patient may experience:
o Aphasia (i.e., total loss of comprehension and use of language).
o Dysphasia (i.e., difficulty with comprehension and use of language).
o Dysarthria (i.e., a disturbance in the muscular control of speech).
o Expressive, receptive
o It can be classified as non-fluent or fluent.
o Impairments may involve pronunciation, articulation, and phonation.
o
o Affect
Affect is a persons facial expression. Patients who suffer a stroke may have difficulty controlling their emotions.
o
o Intellectual Function
Both memory and judgment may be impaired as a result of stroke.
o People with right-sided strokes will have really poor judgement.
Manifestations of Right-Brain and Left-Brain Stroke
Exam Question!
o
Right-brain damage
o
Left-brain damage
o
Paralyzed left side: hemiplegia (i.e., total or
o
Paralyzed right side: (hemiplegia)
partial paralysis of one side)
o
Often have proprioceptive damage (i.e., loss of o
Impaired speech; language aphasias
spatial awareness)
o
Spatial-perceptual deficits
o
Impaired right/left discrimination
o
Tends to deny or minimize problems
o
Slow performance; cautious
o
Rapid performance; short attention span
o
Aware of deficits: depression, anxiety
o
Impulsive; safety problems
o
Impaired comprehension related to language and math
o
Impaired judgment
o
o
Impaired time concepts
o
o Spatial-Perceptual Alterations
Stroke on the right side of the brain is more likely to cause problems in spatial-perceptual orientation.
There are 4 categories:
1. Incorrect perception of self and illness
2. Erroneous perception of self in space
This may be worsened by homonymous hemanopsia (i.e., blindness that occurs in the same half of the visual
field of both eyes).
3. Inability to recognize an object by sight, touch, or hearing (i.e., agnosia)
223
o Elimination
Most problems with urinary and bowel elimination occur initially and are temporary if care was quickly initiated.
o
o Diagnostic Studies
When symptoms of a stroke occur, diagnostic studies are done to:
o Confirm that it is a stroke.
o Identify the likely cause of the stroke (i.e., you do not want to give anticoagulants to a patient with a haemorrhagic
stroke).
CT is the primary diagnostic test used after a stroke.
o
Cerebral blood flow measures.
o Cerebral angiography
o Transcranial doppler
o Carotid angiography
o
Cardiac assessment:
o Electrocardiogram (want to check for dysrhythmias)
o Chest X-ray (want to check for emboli, pulmonary edema)
o Cardiac enzymes (want to see if the patient has had an MI)
o Echocardiography
o Holter monitor (does a continuous reading of the heart, whereas an ECG measures the heart at a point in time)
o
Additional studies:
o Complete blood count
o Platelets, PT (prothrombin time), APTT (activated partial thromboplastin time)
APTT is similar to INR.
o Electrolytes, blood glucose
o Renal and hepatic studies
A decreased GFR may lead to an increase risk of kidney failure. This is particularly likely in patients with
haemorrhagic stroke.
o Lipid profile
Recall that lipids are modifiable risk factors.
o
o Collaborative Care
Prevention
Priority for decreasing morbidity and mortality from stroke.
Surgical interventions for the patient with TIAs from carotid disease include:
o Carotid endarterectomy (rotor rooter)
o Transluminal angioplasty (i.e., reconstruction of a vein)
o Stenting (i.e., widen the vessel)
o Extracranial-intracranial bypass
The affected vessel is brought down, the poor piece excised, the two ends brought together, and the vessel is put
back in place.
o
o Acute Care
Goals for collaborative care during the acute phase are:
1. Preserving life.
The #1 priority is to check the airway!
2. Preventing further brain damage.
3. Reducing disability.
o
Etiology must be determined before treatment can occur.
o This is determined with the use of a CT scan.
Assessment findings:
o Altered level of consciousness
o Weakness, numbness, or paralysis
224
o
o
o
o
o
o
o
Hypertension
Recall the widening pulse pressure
associated with Cushings triad.
Facial drooping on affected side
Difficulty swallowing
Seizures
Bladder or bowel incontinence
Nausea and vomiting
Vertigo
Interventions Initial
o Ensure patient airway.
o Obtain CT scan immediately.
o Remove dentures.
o Perform baseline laboratory tests.
o Perform pulse oximetry.
o Position head midline with the chin down in
o Maintain adequate oxygenation.
order to prevent an increase in ICP.
o Elevate head of bed 30 if no symptoms of shock
o IV access with normal saline.
or injury are present.
o Maintain BP according to guidelines.
o Institute seizure precautions.
By decreasing the BP too quickly, you
o Anticipate thrombolytic therapy for ischemic
decreasing perfusion to the brain.
stroke.
o Remove clothing.
Recombinant tissue plasminogen activator (tPA) [tPA = clot buster] is used to:
o Reestablish blood flow through a blocked artery to prevent cell death in patients with acute onset of ischemic stroke
symptoms.
Thrombolytic therapy must be given within 3 hours of the onset of symptoms in order to decrease disability.
Surgical interventions for stroke include immediate evacuation of:
o Aneurysm-induced hematomas.
o Cerebellar hematomas (if >3 cm).
Drug Therapy
Mannitol (osmotic diuretic)
Anti-seizure
Loop Diuretics
Continuous anticoagulants (heparin, Coumadin)
Corticosteroids (dexamethasone)
Platelet Inhibitors (ASA, Ticlid, Plavix, Persantine)
Barbiturates
Calcium channel blockers
225
Nutrition
Hypermetabolic and hypercatabolic state.
o Increase need for glucose (glucose is the only sugar the brain can use).
o Keep patient normovolemic with NS or NS.
Rehabilitation Care
After the stroke has stabilized for 12-24 hours, collaborative care shifts from preserving life to lessening disability and attaining
optimal functioning.
Patient may be transferred to a rehabilitation unit.
Goals are that the patient will:
o Maintain adequate nutrition.
o Avoid complications of stroke:
Pressure ulcers.
Foot drop.
Muscle atrophy.
Osteoporosis.
Injuries from falls.
Catheters may cause urosepsis.
o Maintain effective personal and family coping.
Anatomy Review
Functional unit of the nervous system is the neuron.
o This class will deal with the neurons taking the message from the brain to the muscle cells.
Neuron composition:
o Dendrites
o Axons
Myelinated
Myelinated axons increase the speed of conduction. This is further increased if Nodes of Ranvier are
present.
Unmyelinated
o Terminal end
MS: Diagnosis
It is primarily based on the clinical signs and symptoms.
o Since many of the signs and symptoms are vague, there must be 2 or more seemingly unrelated problems (e.g., eye
twitching and numbness in the right foot).
Once 2 or more signs and symptoms have occurred, an MRI will be done, which will show the damage along the axons.
The CSF may be monitored. If the patient has MS there will be an in Oligoclonal immunoglobulin G.
Medical/Nursing Management
Goals:
1. To treat/halt the disease process.
Drugs!!
o See Table 60-15
Immunomodulators
Avonex
Betaseron
Rebif
Copaxone
o New: Antegren
o New: Novantrone (this drug is used for patients with a progressive kind of MS)
Alemtuzamab
These two drugs were initially designed for patients with cancer.
2. To promote symptomatic relief
Regarding exacerbations:
o Immunosuppressives (e.g., Imuran, Cytoxan).
o Steroids (e.g., prednisone).
This will deal with the inflammatory element of the illness.
Regarding signs and symptoms:
o Related to cranial nerve dysfunction.
Diplopia/visual disturbances
Safety becomes a big issue in these patients.
Dysarthria
Rest is important for these patients.
Dysphagia
The diet will be important (i.e., what types of food can be handled).
Ataxia
Tremors
Related to Bladder
There are usually two problems associated with the bladder.
o Spastic bladder
The patient will always have the urge.
Medications (antispasmotics).
o Hypotonic
The patient will have retention.
Treatment (straight catheter).
Related to Bowel
Constipation!!
o Treatment:
Increase activity.
Increase fibre in diet.
Cognitive
o Difficulty with word-finding.
Emotional
o This has both physical and psychological implications.
Related to Depression
MS Patient Teaching
Self-awareness!!
o Be aware of triggers (this is often seen in patients in patients with exacerbations and remissions).
Build resistance/maintain balance!
o Rest!
o Exercise (physiotherapy).
Avoid temperature extremes.
Avoid infection exposure.
Diet!
o Fibre and fluids.
o protein intake as the basal metabolic rate is very high.
Multidisciplinary team consult?
New/Alternative Therapies
Diets
Vitamins
Apitherapy
o Deliberate bee stings is a therapy (it is done following ice to numb the arm). This has to do with initiating an
inflammatory response.
Hyperbaric O2 therapy
o The idea is that the copious amounts of O2 will have a healing effect on the axons.
Vitamin D/sunshine!
Cannabis
Research: BMTs/stem cells; repair/grow myelin?
LATEST: CCSVI (Chronic Cerebrospinal Venous Insufficiency) a jugular venous obstruction?
Neuromuscular Transmission
I.
UMNs
II.
LMNs
III.
M/N Junction
a. This is where the axon meets the muscle cell.
GUILLIAN BARR
It is a post-infectious polyneuritis.
It occurs because the immune system is stimulated that results in the post-infectious polyneuritis.
It is similar to MS in that it affects the axon, but in this case the axons can regenerate.
CTQ: Key health history data?
o It is important to determine if infections occurred 2-3 weeks prior. It is typically triggered by a virus.
CTQ: Hallmark signs and symptoms.
o It is weakness and paralysis that starts at the feet and moves up bilaterally. It then recedes the way it came.
It starts at the toes and moves up to the nose.
o This is problematic because the diaphragm is involved, therefore cutting out their respiratory system.
Management: *CTQ: watch for the respiratory rate and effort (e.g., O2 sat).
o Supportive++
o IV immunoglobulin/plasmapheresis
o Recovery??
It generally recovers the way it came.
MYASTHENIA GRAVIS
CTQ: This will lead to fatigue with repeated use of a particular muscle.
CTQ: Hallmark signs and symptoms?
o It starts proximally and moves distally.
o Fatigue++
Is it with repetition? Does it resolve with rest?
o Ptosis
Eye drooping (early sign; can be bilateral or unilateral)
o Dysarthria
o Dysphagia
o Exacerbations and remissions
CTQ: Function best in the morning
Diagnosis:
o Gaze up!
In a patient with myasthenia gravis, the eyes will droop.
o Tensilon Test
It is a short-acting cholinergic/acetylcholine-like drug.
CTQ: Should always have atropine on hand when performing the tensilon test.
o ACh antibody titres
o Acetylcholine is the major neurotransmitter for the parasympathetic nervous system.
Treatment:
o Anti-Che meds
o Thymectomy
This is usually only done when the medications do not work. The success rate is very good.
o The medications must be given on time! Their food should be given shortly after their medications have been given.
Patient teaching
o Crises: Myasthenic vs. Cholinergic
o See Table 57-21
PARKINSONS DISEASE
Management
Goals: Balance dopamine and acetylcholine with the least amount of drugs.
Drugs!!