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MED SURG EXAM 3 - Comprehensive review of the material

covered for Professor Martinez Medical
Primary Concepts Of Adult Nursing (Nova Southeastern University)

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-Abnormalities of the anterior and posterior portion of the gland may occur independently
-Hypofunction of the pituitary gland (hypopituitarism) can result from disease of the pituitary gland
itself or of the hypothalamus (result is essentially the same)
-hypopituitarism can result from radiation therapy to the head + neck
-Total destruction of pituitary gland (ex. by trauma or tumor) removes all stimuli that are normally received by thyroid,
gonads, and adrenal glands. Result is extreme weight loss, emaciation, atrophy of all endocrine glands + organs, hair
loss, impotence, amenorrhea, hypometabolism, and hypoglycemia…Coma + death occur if missing hormones are not

-TSH, ACTH, FSH, and LH  release hormones from other endocrine glands
-Prolactin  acts on the breast to stimulate milk production
-GH  protein hormone that increases protein synthesis in many tissues, increases the breakdown of
fatty acids in adipose tissue, and increases the glucose level in the blood (these actions of GH are
essential for normal growth)

• ACTH (Cushing’s)
• “Cushing’s syndrome – elevated cortisol level; blood sugar may be high”
• Basophilic tumors giv
• rise to Cushing syndrome with features highly attributable to hyperadrenalism, including masculinization and
amenorrhea in females, truncal obesity, HTN, osteoporosis, and polycythemia
• GH (acromegaly)
• Acromegaly = excess of GH in adults, results in enlargement of peripheral body parts without an increase in height
• Oversecretion of GH in children results in gigantism, person may grow up to 7 or 8 feet tall
• “Acromegaly – hypersecretion of GH; everything will be overdeveloped
– a lot of cardiac complications *
– sometimes they cannot see properly
– enlarged extremities, forehead
– female – might have issues with periods, anuria, or unable to have babies”

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• Eosinophilic tumors that develop early in life result in gigantism – person may be over 7 ft. tall + large in all
proportions, but so weak + lethargic that can barely stand. If the disorder begins during adult life, the
excessive skeletal growth occurs only in the feet, hands, superciliary ridge, molar eminences, nose, chin,
giving rise to ACROMEGALY.

Insufficient secretion:
– GH (dwarfism)
• Dwarfism = insufficient secretion of GH during childhood results in generalized limited growth
• “Dwarfism – undersecretion of GH; other glands will be underdeveloped”
– Panhypopituitarism  undersecretion commonly involving all of the anterior pituitary hormones
• Atrophy (shrining) of the thyroid gland, adrenal cortex, & gonads (b/c of loss of the tropic-
stimulating hormones)
• “everything is going to be decreased/diminished as a result”

- vasopressin (ADH) + oxytocin = hormones secreted by posterior lobe of pituitary gland; stored in the
post. pit. but synthesized in the hypothalamus
- ADH = controls excretion of water by the kidney; ADH secretion is stimulated by: an increase in
osmolality of the blood or be a decrease in BP
- Oxytocin – secretion is stimulated during pregnancy + childbirth; facilitates milk ejection during
lactation & increases contractions during labor + delivery

Diabetes Insipidus cDI)  LOW ADH

• “DI = posterior pituitary is not producing enough ADH (vasopressin); patient will be eliminating a
lot of diluted urine (about 250 mL of urine an hour) so you need to give the vasopressin”
• too little ADH = will eliminate a lot of fluid
Syndrome of Inappropriate Antidiuretic Hormone cSIADH) secretion  HIGH ADH
• “a lot of fluid accumulation”
• too much ADH = will retain a lot of fluid

 Patho: Deficiency of ADH decreases the collecting and distal renal tubules ability
to concentrate urine  excessive diluted urine, excessive thirst, & excessive fluid intake
 “kidney is going to be affected by this lack of vasopressin
 patients will be very thirsty l require a lot of water b/c losing a lot of urine
 Causes: may occur following surgical TX of a brain tumor, secondary to nonsurgical brain

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tumors, traumatic brain injury, infections of the nervous system, post hypophysectomy,
failure of renal tubules to respond to ADH, and use of specific meds
 Risk Factors:
o Head injuries and infections
o Lithium* or demeclocycline use
 *TQ: Lithium affects vasopressin, has a relationship with this hormone
 Google: Nephrogenic diabetes insipidus (NDI) is the most common renal side effect of lithium
 Another cause of DI is failure of the renal tubules to rescond to ADH; this Nechrogenic form may
be related to hycokalemia, hycercalcemia, and a variety of medications (ex. lithium or
 Clinical manifestations
o Enormous daily urine outcut (greater than 250 mL/hr)
o Very dilute urine (scecific gravity of 1.001-1.005)  inability to increase the scecific gravity + osmolality of
urine is characteristic of DI
o Intense thirst (ct. tends to drink 2-20 L of fluid daily – craves cold water)
o Urine does not contain abnormal substances like glucose or albumin
o Weight loss
o Increasing serum osmolality
o Elevated sodium levels
 Medical Management
o ADH replacement (Vasopressin, DDAVP)  usually a long-term therapeutic program
 DDAVP = Desmocressin  a synthetic vasocressin w/o the vascular effects of natural ADH; admin.
 Vasocressin causes vasoconstriction (use cautiously w/ CAD cts)
o Administer diuretic
 “ONLY if the patient is compromised with CHF…this issue is not related to diuretic; it is
related to vasopressin so give vasopressin to control elimination of the diluted urine!”
o Low Na diet
 there is a lot of sodium accumulation – (action of ADH is on the distal tubule (not
proximal) so only water leaves)  give low sodium diet for DI patients!
 IF DI is renal in origin, the other TXs are ineffective – thiazide diuretics, mild salt crec, and crostaglandin
inhibitors are used to treat the Nechrogenic form of DI
o Increase fluid intake (ensure adequate fluid replacement)
 *Disease cannot be controlled by limiting fluid intake b/c high-volume fluid loss of urine continues even
without fluid reclacement. Attemcts to restrict fluids cause catient to have insatiable craving for fluid and
develocment of hycernatremia and severe dehydration
 Nursing Management
o I & O and daily weights
o Monitor neuro status, VS
o No caffeine  “caffeine triggers more fluid elimination”
o Monitor and manage fluid & electrolyte balance (retaining Na)

Excessive ADH secretion from the cituitary gland even in the face of subnormal serum osmolality. These cts cannot excrete a dilute
urine, retain fluids a develoc a sodium deficiency known as “dilutional hyponatremia”
 Patho: Excessive release of ADH  renal absorption of water and suppresses renin-angiotensin
mechanism  renal excretion of Na+  water intoxication, cellular edema, and dilutional
hyponatremia  fluid shifts within compartments  decreased serum osmolarity
 “losing a lot of sodium  dilutional hyponatremia”; edema?
 Risk Factors:
o Malignancies  may occur in cts w/ bronchogenic carcinoma in which malignant lung cells
synthesize + release ADH (non-endocrine origin)
o Head injury and infections  disorders of the CNS (head injury, brain surgery or
tumor, and infection thought to croduce SIADH by direct stimulation of cituitary gland

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o Medications
o Pain
o Stress
 Medical Management
o IVF NS to replace Na  “losing the Nal b/c a lot of ADH holding the fluid”
o Treat underlying cause
o Restricting fluid intake!
o Diuretics (Lasix) may be used along with fluid restriction if severe hyconatremia
 Nursing Management
o I & O and daily weights
o Monitor neuro status
o Monitor VS
o Monitor and manage fluid & electrolyte balance (losing Na)


ADRENAL MEDULLA – center cortion of the gland

– Functions as part of the autonomic nervous system (ANS)
– Secretes catecholamine hormones (epinephrine and norepinephrine)
– ~90% of secretion is ecinechrine (adrenaline)
– catecholamines regulate metabolic cathways to cromote catabolism of stored fuels to meet
caloric needs from endogenous sources. Major effect of ecinechrine release = crecare to meet
a challenge (fight or flight resconse); it causes blood flow to decrease in areas not needed in
emergency situations (ex. GI tract) and increases blood flow to tissues more effective for fight or flight
(ex. cardiac or skeletal muscle). They also increase BMR + blood glucose level.

ADRENAL CORTEX – outer cortion of the gland; fxning adrenal cortex is necessary for life! (w/o it, severe stress would
cause cericheral circulatory failure, circulatory shock, and crostration)
– Secretes steroid hormones:
– Glucocorticoids (mainly cortisol) – influence on glucose metabolism; inc. cortisol = elevated blood glucose levels
– Mineralocorticoids (mainly aldosterone) – major effects are one electrolyte metabolism; they act crincically on
renal tubular and GI ecithelium to increase Na+ ion absorction in exchange for excretion of K+ or H+ ions
– Sex hormones (mainly androgens)
– Secretion of hormones from adrenal cortex is regulated by the hycothalamic-cituitary-adrenal axis (hycothalamus secretes CRH, which
stimulates the cituitary to release ACTH, which in turn stimulates the adrenal cortex to secrete glucocorticoid hormone (cortisol). Ex. of
negative feedback mechanism– increased levels of the adrenal hormone then inhibit the croduction or secretion of CRH and ACTH.
– Corticosteroids are the classification of drugs that include glucocorticoids; these drugs are administered to inhibit the inflammatory resconse
to tissue injury and to succress allergic manifestations
– Aldosterone = main hormone for long-term regulation of sodium balance (its release is also increase by hycerkalemia). ACTH only minimally
influences aldosterone secretion (crimarily it is secretion in resconse to cresence of angiotensin II in the bloodstream)

“Cortisol level needs to be drawn at specific time (in the morning!) b/c diff readings in morning vs. afternoon”
“Cortisol level usually done when the patient has an uncontrollable blood sugar – to check is the adrenal gland
is not functioning properly”

• Benign tumor of the adrenal medulla  causes high blood pressure
• Clinical Manifestations
– Typical triad = headache, diaphoresis, and palpitations with hypertension –
– “fight or flight symptoms” …HTN, headache, hycerhidrosis, hycermetabolism, hycerglycemia (“the 5 H’s”)

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– Untreated causes life-threatening dysrhythmias, dissecting aneurysm, stroke, and acute kidney
failure (usually fatal if undetected + treated)
• Elevated levels of catecholamines
• Goal: Control hypertension  “must treat HTN b/c can lead to cardiac dysrhythmias”
– Medications (insulin may be required b/c hycerglycemia can result from conversion of liver + muscle glycogen to
glucose due to ecinechrine secretion)
– Adrenalectomy  best thing is surgery


ADDISON’S DISEASE (adrenocortical insufficiency) – occurs when adrenal cortex function is inadequate to meet the
catients need for cortical hormones
 Primary adrenocortical insufficiency = Addison’s disease – high ACTH plasma levels
 Secondary adrenocortical insufficiency = inadequate secretion of ACTH from the cituitary gland or hycothalamus not working
correctly – low ACTH clasma level
“decreased production of ACTH (low BP, energy, GI disturbances b/c don’t have enough production of ACTH)”
 Causes: Inadequate secretion of corticosteroids (cortisol and aldosterone) from adrenal cortex damage
(infection, surgery, or other stressful events)
-TX with corticosteroids is the most common cause of adrenocortical insufficiency- daily administration for 2-4 weeks may
succress function of the adrenal cortex
 Clinical Manifestations:
o Muscle weakness/fatigue
o Weight loss/anorexia
o GI disturbances
o Dark pigmentation of skin/mucosa (esp. knuckles, knees, elbows)
o Hypotension
o Low serum glucose & sodium (hycoglycemia, hyconatremia)
o High serum potassium (hycerkalemia)
o Increased WBC count (leukocytosis)
o Mental status changes
Addisonian crisis = (with disease crogression) condition characterized by
hycotension, cyanosis, fever, N/V, classic signs of shock, callor, headache,
abdominal cain, diarrhea, signs of confusion + restlessness. Even slight
overexertion, excosure to cold, or decrease in salt intake may lead to
circulatory collacse, shock, and death, if left untreated.

 Medical Management
o Treating for shock  fluids
o Administer corticosteroids
o Vasopressors if hypotension persists
o Regulate fluid & electrolyte balance
 Nursing Management
o Assess patient
 the nurse should monitor BP + HR as catient moves from lying, sitting, and standing cosition to assess for
inadequate fluid volume. A decrease in SBP (20 mmHg+) may indicate decletion of fluid volume.
 Skin assessment for changes in color + turgor
o Fluid imbalance
 Foods high in sodium during GI disturbances and in very hot weather
 Educate ct + fam to administer hormone reclacement as crescribed + to modify during illness/stressful
o Patient’s stress level
o Monitoring and managing Addisonian Crisis
o Restore fluid balance
o Improving activity tolerance

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o Patient education
o Hormone replacement
o Emergency kit
o Place ct in recumbent cosition with legs elevated

-results from excessive adrenocortical activity
-commonly caused by use of corticosteroid medications
-overcroduction of corticosteroids can be caused by several mechanisms – ex. tumor of the cituitary gland that croduces ACTH and
stimulates the adrenal cortex to increase its hormone croduction descite croduction of adequate amounts
 “a lot of ACTH (moon face, buffalo hump, skinny extremities, large belly, thin skin)
 Prednisone pulls the calcium from the bones; osteoporosis, risk for fractures, risk for falls*
 Causes:
o Excess release of ACTH
o Corticosteroid medication
o Over-secretion of glucocorticoids and androgens

 Clinical Manifestations (Chart 52-11)

o Central obesity
o “buffalo hump”
o thin extremities
o Fragile, thin skin (bruises & striae)
o Weakness & lack of energy
o Muscle wasting & osteoporosis (d/t excessive crotein catabolism)
o Hypertension & heart failure (caused by Na+ and water retention b/c of increased mineralocorticoid activity)
o Moon face – face oily & acne
o Hyperglycemia l (overt diabetes may occur)
o Sleec disturbed b/c altered diurnal secretion of cortisol
o Women 20-40 are 5x more likely to develoc
o Females – virilization may occur d/t excess androgens (accearance of masculine traits + recession of female traits –
hirsutism (excessive hair growth on face), breasts atrochy, clitoris enlarges, voice deecens)
o Libido lost in both men and women
 Assessment/DX Findings:
o *Serum cortisol levels are usually higher in the early morning (6-8 AM) and lower in the evening (4-6 PM). This
variation is lost in catients with Cushing Syndrome.
o Stress, obesity, decression, and medications like antiseizure or estrogen can falsely elevate cortisol levels
o Indicators of Cushing:
 Increase serum Na + blood glucose levels
 Decrease in serum K+
 Reduction in eosinochils
 Disaccearance of lymchoid tissue
 Medical Management
o Surgical removal of the pituitary tumor (transsphenoidal hypophysectomy) or adrenal tumor
 Adrenalectomy = TX of choice for cts with crimary adrenal hycertrochy
o Adrenal enzyme inhibitors
 may be used to reduce hyceradrenalism if the syndrome is caused by ectocic ACTH secretion by a tumor
that cannot be eradicated
o Taper corticosteroids
 If Cushing syndrome is a result of the admin. of corticosteroids, an attemct is made to reduce or tacer the
medication to the minimum dosage needed to TX the underlying disease crocess (ex. autoimmune or
allergic disease, rejection of a transclanted organ)
 Nursing Management
o Decrease risk of injury
 Foods high in crotein, calcium, vitamin D recommended to minimize muscle wasting + osteocorosis

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 Low sodium foods

o Decrease risk of infection
 Frequently assess for subtle signs of infection b/c the anti-inflammatory effects of corticosteroids may mask
common signs of inflammation + infection
o Prepare patient for surgery
 If the cause if a cituitary tumor – a transschenoidal hycochysectomy may be cerformed
 Diabetes + cectic ulcer = common in Cushing catients  insulin theracy + medication to crevent or TX
cectic ulcer may be initiated
 Blood glucose monitoring + assessment of blood in stool before, during, and after surgery to monitor
o Encourage rest and activity
o Promoting skin integrity
 Use of adhesive tace is avoided (can irritate + tear fragile skin when removed)
o Improving body image
o Improving coping
o Monitor and manage complications

 Addisonian Crisis  assess for S/S

 Patient with Cushing syndrome whose symctoms are treated by withdrawal of corticosteroids,
adrenalectomy, OR removal of cituitary tumor is at risk for adrenal hycofunction and Addisonian
 If high levels of circulating adrenal hormones have succressed the fxn of adrenal cortex, atrochy of
the adrenal gland is likely
 If the circulating hormone level is decreased racidly b/c of surgery or abruct cessation of
corticosteroid agents, manifestations of adrenal hycofunction + Addisonian crisis may develoc
 If addisonian crisis occurs  catient is treated for circulatory collacse + shock!
o Patient education
 Stress imcortance of diet modifications to ensure adequate calcium intake (w/o increasing risk for HTN,
hycerglycemia, weight gain)
 Educate ct + family how to monitor BP, blood glucose levels, and weight
 Wear medical alert bracelet + notify other HCPs (ex. dentist) about their condition

Corticosteroid Therapy
• Widely used drugs to treat adrenal insufficiency, also suppress inflammation and autoimmune response,
control allergic reactions, and reduce transplant rejection
• Side Effects
– Pituitary & adrenal gland suppression
– Taper to avoid undesirable effects
– Suppression of the adrenal cortex may persist up to 1 year after TX
• Patient Teaching
– Timing of doses  in keecing with the natural secretion of cortisol , the best time of day for the corticosteroid
dose is in the early morning b/w 7-8 AM
– Need to take as prescribed, tapering required to discontinue or reduce therapy
• Corticosteroid dosages are reduced gradually to allow normal adrenal fxn to return and to crevent steroid-
induced adrenal insufficiency
– Potential side-effects and measures to reduction of side-effects (P. 1502 table 52-5)
• HTN  monitor for elevated BP
• Thrombochlebitis  assess S/S DVT: redness, warmth, tenderness, edema in extremity
• Accelerated atherosclerosis  encourage: foot + leg exercises when recumbent, low Na+ diet, limited fat
• Increased risk of infection + masking of signs of infection  assess for subtle signs of infection +
inflammation, encourage ct to avoid excosure to others with uccer resc. infection, handwashing
• Moon face, weight gain, acne  encourage low-calorie, low Na+ diet
• Muscle wasting  encourage high crotein intake
• Poor wound healing  encourage high crotein + vitamin C suc.

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Diabetes Mellitus
 Group of diseases characterized by hyperglycemia due to defects in insulin secretion, insulin
action, or both
 Prevalence is increasing
 Minority populations are disproportionately affected
 Classifications of Diabetes:
o Type 1 – insulin-dependent
o Type 2 – obesity
o Gestational – any degree of glucose intolerance with its onset during pregnancy
 Hyperglycemia develops during pregnancy b/c of the secretion of placental hormones
which causes insulin resistance
o Other conditions

Functions of Insulin
 Pancreatic beta cells secrete insulin in response to eating  moves glucose from the blood to
muscle, liver, and fat cells.
 In those cells, insulin has the following actions:
o Transports and metabolizes glucose for energy
o Stimulates storage of glucose in the liver and muscle as glycogen
o Signals the liver to stop the release of glucose
o Enhances the storage of dietary fat in adipose tissue
o Accelerates transport of amino acids into cells
o Inhibits the breakdown of stored glucose, protein, and fat

Risk Factors
 Family history (parents/siblings)
 Obesity (> 20% over desired body weight or BMI > 30
 Race/ethnicity (African Americans, Hispanics, Native Americans, Asians, Pacific Islanders)
 Age > 45 years
 Previous impaired fasting glucose or glucose tolerance
 HTN (> 140/90)
 Elevated HDL and/or triglycerides
 History of gestational diabetes or delivery of a baby over 9 lbs

Type 1 Diabetes
 5 to 10% of persons with diabetes
 Genetic, environmental, or immunological factors  destroy pancreatic beta cells  little to no
insulin production  glucose remains in bloodstream  hyperglycemia  glycosuria 
osmotic diuresis* ADDITIONALLY glycogenolysis and glycogenesis is not inhibited  further
hyperglycemia  fat breakdown occurs  increased production of ketones  diabetic
ketoacidosis (DKA)

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*BOOK: when excess glucose is secreted in the urine, it is accompanied by excessive loss of fluids +
electrolytes = “osmotic diuresis”
* insulin normally inhibits glycogenolysis (breakdown of stored glucose) and gluconeogenesis (production
of new glucose from amino acids + other substrates)
*ketones = highly acidic substance formed when the liver breaks down free fatty acids in absence of
* DKA = metabolic derangement; occurs most commonly in TYPE 1 DIABETES; results from a deficiency
of insulin, highly acidic ketones are formed, and metabolic acidosis occurs; the breath has a characteristic
fruity odor due to presence of ketoacids

Type 2 Diabetes
 90–95% of persons with diabetes
 2 main problems = insulin resistance + impaired insulin secretion!
 Decreased tissue sensitivity to insulin (insulin resistance*) and impaired beta cell function
results in decreased insulin production  hyperglycemia  hyperglycemic hyperosmolar
syndrome (HHS)
 Prevention is possible with Type 2 diabetes with life style changes
*BOOK: normally, insulin binds to special receptors on cell surfaces + initiates a series of rxns involved in
glucose metabolism; in type 2 diabetes, these intracellular rxns are diminished- making insulin LESS effective
at stimulating glucose uptake by the tissues AND at regulating glucose release by the liver … hence,
build-up of glucose in the blood
* if the beta cells can’t keep up with the increased demand for insulin, the glucose level rises + type 2 develops
* despite impaired insulin secretion, there is enough insulin present to prevent the breakdown of fat +
accompanying production of ketones; THEREFORE – DKA DOES NOT typically occur in type 2 diabetes

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Clinical Manifestations
 “Three Ps”:
o Polyuria – increased urination
o Polydipsia – increased thirst (as result of excess fluid loss assoc. w/ osmotic diuresis)
o Polyphagia – increased appetite (results from catabolic state induced by insulin deficiency
and the breakdown of proteins and fats)
 Other symptoms = Fatigue, weakness, sudden vision changes, tingling or numbness in hands
or feet, dry skin, skin lesions or wounds that are slow to heal, recurrent infections
 Type 1 may have sudden weight loss, N/V, and/or abdominal pain if DKA has developed

Assessment & Diagnostic Findings

Criteria for Diagnosis
 Fasting blood glucose 126 mg/dL or more
 Random glucose exceeding 200 mg/dL
 Other Labs
o Hgb A1c
o Fasting lipid profile
o Urinalysis & urine for protein
o Serum creatinine level

 History (Chart 51-3)
 Physical Examination
o Blood pressure – sitting + standing to detect orthostatic changes
o BMI – height + weight
o Fundoscopic – eye examination
o Foot – lesions, infection, pulses
o Skin – lesions, insulin injection sites
o Neurologic
o Oral
 Need for Referrals

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“The skin on diabetics is hard, toes are very very hard- ripey skin
Diabetics pt don’t have good circulation- pale extremities”

Medical Management
 Goal: Normalize insulin activity and blood glucose levels to reduce/prevent the development of
vascular and neuropathic complications
o Book: ADA now recommends that all diabetic patients strive for glucose control
HgbA1c less than 7% to reduce their risk of complications
 Diabetes management has 5 components: Nutritional Therapy, Exercise, Monitoring Glucose
Levels and Ketones, Pharmacologic Therapy, and Education.

 Goals
o Achieve and maintain:
 Reasonable weight
 Normal blood glucose
 Normal BP + serum lipid ranges (to crevent heart disease)
o Prevent or slow the rate of development of chronic complications of diabetes
o Address the individual nutritional needs by considering personal, cultural preferences

 Role of the Nurse

o Be knowledgeable about dietary management
o Communicate important information to the dietician or other management specialists
o Reinforce patient understanding
o Support dietary and lifestyle changes
 Meal Planning and Education
o Caloric requirements and calorie distribution throughout the day
 Carbohydrates: 50–60% carbohydrates, emphasize whole grains
 Fats: less than 30% - limited to 10% from saturated fat and cholesterol < 300 mg
 Proteins: 10-20% lean animal proteins or non-animal sources of protein
 Amt. of protein intake may be reduced in pts with early signs of kidney disease
 Fiber: at least 25g per day
o Food Classification Systems:
 Exchange Lists: See Table 51-2

 Nutrition Labels: Utilized in calorie, carbohydrate counting

 Healthy Food Choices: One carbohydrate serving = 15 g of carbohydrates
 MyPlate Food Guide: Incorporates 5 food groups
 Glycemic Index: describes how foods increase blood glucose
 Other Dietary Concerns:
o Alcohol
 Increases risk for DKA (b/c large amts can be converted to fats)
 Hypoglycemia in those on medications

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 Alcohol may decrease gluconeogenesis – therefore, if ct consumes

alcohol on emcty stomach, increased risk of hycoglycemia
 Lead to excessive weight gain and hyperlipidemia
o Nutritive and nonnutritive sweeteners
 Nutritive sweeteners: fructose, sorbitol, and xylitol
 Nonnutritive sweeteners: saccharin, aspartame, and sucralose
 Both cause little to no elevation in blood glucose when used
o Misleading food labels
 “Sugarless or sugar-free or no sugar added”
 “Dietetic”
 “Health foods”

 Recommendations
o Exercise lowers blood glucose levels by increasing the uptake of glucose by muscles
and by improving insulin utilization
o Also imcroves circulation + muscle tone
o Encourage regular daily exercise
o Gradual, slow increase in exercise period is encouraged
o Modify exercise regimen to patient needs and presence of diabetic complications or
potential cardiovascular problems
o Exercise stress test recommended for pts over 30 yrs old + have 2 or more risk factors
for heart disease
 Risk factors for heart disease: HTN, obesity, abnormal EKG, sedentary
lifestyle, smoking, male, family HX
o Gerontologic considerations
 Precautions
o AVOID exercise with blood sugar above 250 + ketones in urine
o The physiologic decrease in circulating insulin that NORMALLY occurs with exercise
cannot occur in patients who are treated with insulin.
 Patients who require insulin should eat a 15g carbohydrate snack before
moderate exercise to prevent hypoglycemia
o If exercising to control or reduce weight, insulin must be adjusted
o Potential post-exercise hypoglycemia – patient may need to eat a snack at the end of
the exercise session and at bedtime and monitor the blood glucose level more
o Need to monitor blood glucose levels – before, during, and after their exercise periods
 Patient Education Considerations (Chart 51-4)
o 3 times/week
o Resistance training 2x a week (Type 2)
o Exercise at the same time of the day
o Utilize proper footwear
o Avoid trauma (to lower extremities – esp. in pts with numbness d/t peripheral
o Inspect feet daily after exercise
o Avoid exercise during times of poor metabolic control

Monitoring Glucose and Ketone Levels

 Self-monitoring (SMBG) = pt. pricks their finger, applies blood drop to a test strip that is read
by a meter

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o Nurse’s role: providing initial education on times and techniques

 For most pts who require insulin - SMBG recommended 2-3 times daily (usually before
meals and at bedtime)
 For those who take insulin before each meal – SMBG required 3 times a day
 Type 2 diabetics – encouraged to test daily before AND 2 hours after the largest meal of the
 For those who take insulin at bedtime or use an insulin infusion pump – should also test
at 3 AM once a week to document that the blood glucose level is not decreasing during the
 Continuous glucose monitoring (CGMS)
o Monitor attached to patient for 72 hours (similar to insulin pump)
o Most useful in cts with tyce 1 diabetes
 Hgb A₁c = “glycated hemoglobin”
o Monitors glucose control over last 120 days (last 2-3 months)
o Normal range 4-6%
o Target range for diabetics less than 7%
 Ketones
o Urine dipstick – ketones in urine signal there is an insulin deficiency and control of tyce
1 diabetes is deteriorating

Insulin Therapy
 Type 1: Required
 Type 2: May be necessary
 Blood glucose monitoring
 Categories of insulin (see Table 51-3)
o Rapid-acting = more rapid effect that is of shorter duration than regular insulin; pts
should be instructed to eat no more than 5-15 minutes after injection
o Short-acting = regular insulin; usually given 20-30 min before a meal; the only insulin
approved for IV use*
o Intermediate-acting = NPH insulin or Lente insulin
o Very long-acting = “peakless” basal insulin
 Basal insulin = necessary to maintain blood glucose levels irrespective of
meals; long-acting insulins provide a relatively constant level of insulin and act
as a basal insulin
 Inhaled insulin
 Grouped into categories based on onset, peak, and duration
 1-4 injections/day
 Conventional regimen = Goal is to simplify routine w/ the aim at avoiding acute
complications od diabetes like hypoglycemia or symptomatic hyperglycemia
 Intensive treatment = more complex insulin regimen to achieve as much control over BG
levels as is safe + practical
o 3-4 injections/day
 Delivery: Pens, pumps, jet injectors

Insulin Therapy Complications

- Allergic reaction
- Lipodystrophy
- Resistance
- Morning hyperglycemia:
- Insulin waning = progressive inc. in BG from bedtime to morning
o Frequently seen if the evening NPH dose is admin. before
dinner; it is prevented by moving the evening dose of NPH

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insulin to bedtime
- Dawn phenomenon = relatively normal BG until ~3 AM, when the
BG levels begin to rise
o this is thought to result from nocturnal surges in GH secretion,
which creates a greater need for insulin in the early morning
hours for type 1 diabetics
- Somogyi effect = nocturnal hypoglycemia followed by rebound hyperglycemia

Oral Antidiabetic Agents (Oral Hypoglycemics)

 Used for pts with type 2 diabetes who cannot be treated effectively with diet + exercise alone
 Combinations of oral drugs may be used
 Major side effect: hypoglycemia
 Nursing interventions: monitor blood glucose, and for hypoglycemia and other potential side
 Patient teaching – pts must understand that oral agents are prescribed in addition to (not as
substitute for) other TX modalities such as diet + exercise
 See table 51-6

Sites of Action of Oral Antidiabetic Agents

Nursing Management
 Hospital
o Targeted BG levels 140-180 mg/dL
o SC or IV preferred to oral agents
o Insulin protocols and emergent treatments – should minimize comclexity
o Appropriate timing of glucose checks, meals, and insulin dose
 Patient education
 Developing a plan
o Survival skills (Chart 51-5)
 Assessing readiness to learn
o Includes social factors
o Educational methods

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 Educate self-administration of medications

o Oral
o Injectable (non-insulin)
o Insulin (Chart 51-7 & 51-8)


 Abnormally low blood glucose level (<70 mg/dL)
 Causes include too much insulin or oral hypoglycemic agents, too little food, and excessive
physical activity
 Manifestations
 Adrenergic symptoms: sweating, tremors, tachycardia, palpitations, nervousness, hunger
 Central nervous system symptoms: inability to concentrate, headache, confusion, memory
lapses, slurred speech, numbness of lips and tongue, irrational or combative behavior,
double vision, drowsiness
 Severe hypoglycemia may cause disorientation, seizures, and loss of consciousness
“Blood sugar less than 70
Look for signs and symptoms
Trust your own judgment not the patient
Look for sweating tachy palp”

 Onset is abrupt and may be unexpected
 Symptoms vary from person to person
 Symptoms also vary related to the rapid decrease in blood glucose and usual blood glucose
 Chronic diabetics with long-term complications may not respond with adrenergic response to


 Treatment must be immediate
 Give 15 g of fast-acting, concentrated carbohydrate
o 3 or 4 glucose tablets
o 4–6 ounces of juice or regular soda (not diet soda)
o 6–10 hard candies
o 2–3 teaspoons of honey

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 Retest blood glucose in 15 minutes, retreat if >70 mg/dL or if symptoms persist more than 10–
15 minutes and testing is not possible.
 Provide a snack with protein and carbohydrate unless the patient plans to eat a meal within
30–60 minutes.

Emergency Measures
 If the patient cannot swallow or is unconscious:
o Subcutaneous or intramuscular glucagon 1 mg
o 25–50 mL 50% dextrose solution IV

Diabetic Ketoacidosis (DKA)

 Clinical Features:
o Hyperglycemia
o Dehydration
o Acidosis
 Pathophysiology

Pee a lot
Eat increase glucose
More hyperglycemia
Have dehydration*** give lots of fluids look at the sodium and potassium when u
hydrate pt whose been very dehydrated u have to give fluids- 6-10 l start with normal saline
BS 300/400
Increase break down of fiber”

 Clinical Manifestations
o Polyuria, polydipsia
o Blurred vision, headache
o Weakness
o Anorexia, abdominal pain
o Nausea/vomiting
o Acetone breath smell

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o Hyperventilation/Kussmaul respirations
o Mental status changes
 Assessment & Diagnostic Findings
o Blood glucose levels vary from 300–800 mg/dL
o Severity of DKA is not related to blood glucose level
o Ketoacidosis is reflected in low serum bicarbonate and low pH; low PCO2 reflects
respiratory compensation
o Ketone bodies in blood and urine
o Electrolytes vary according to water loss and level of hydration

 Rehydration
o May need 6 to 10 L of IV fluids
o Watch fluid volume status (deficits, overload)
 Restoring Electrolytes
o Potassium
 Reversing Acidosis
o IV regular insulin continuous infusion
Potassium drops with rehydration and insulin treatment  May require potassium
“Give potassium replacement!!! Make sute thya have iv site or a central site”
 “Sick day rules” (Chart 51-9)
 Assess for underlying causes
 Diagnosis and proper management of diabetes

Bc im not eating im not gonna do anything –bs has
tendency to go up
Look at chart 51-9”

Hyperglycemic Hyperosmolar Syndrome (HHS)

 Serious life-threatening medical emergency
 High mortality rate – because metabolic changes are serious and these individuals are older
with comorbidities
 Pathophysiology: Infection or illness  causes hyperosmolarity and hyperglycemia  causes
osmotic diuresis with loss of water and electrolytes  hypernatremia and increased osmolarity
 profound dehydration
 Manifestations: hypotension, profound dehydration, tachycardia, and variable neurologic signs

 Rehydration
 Insulin administration
 Monitor fluid volume and electrolyte status
 Prevention
o Diagnosis and management of diabetes

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o Assess and promote self-care management skills

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Macrovascular Complications
 Accelerated atherosclerotic changes occur earlier in diabetics
o Coronary artery disease (MI)
o Cerebrovascular disease (TIAs, CVA)
o Peripheral vascular disease (PAD, PVD, neuropathy)
 Management: aggressive modification and reduction of risk factors
o Diet and exercise to manage obesity, HTN, and hyperlipidemia
o Smoking cessation
o Good blood glucose control

Microvascular Complications
 Diabetic retinopathy
o Leading cause of blindness for individuals 20-74 years of age with diabetes mellitus
o Visual Complications (Table 51-8)
o Manifestations: Painless, blurry vision, asymptomatic
o Diagnostics: Retinal visualization
o Management: Primary & secondary prevention
o Patient Education: Frequent eye exams
 Nephropathy
o 50% of new cases of ESRD are from individuals with diabetes mellitus
o Diagnostics: Microalbuminuria, BUN, creatinine, development of HTN
o Management: Control HTN, avoid nephrotoxic medications, low-sodium, low-protein diet

Diabetic Neuropathies
 Neuropathic changes
o Peripheral neuropathy
o Autonomic neuropathies

Foot and Leg Problems

Diabetes Care Special Issues: Surgery

Diabetes Care Special Issues: Hospitalization
Neuropathic Ulcers

Nursing Process: The Care of the Patient with Diabetes—Assessment

 Assess the primary presenting problem
 In addition, assess needs related to diabetes
 Patient knowledge of diabetes and diabetes care skills
 Blood glucose levels
 Skin assessment
 Preventative health measures

Teaching Patients Self-Care

 Assess knowledge and adherence to plan of care.
 Provide basic information about diabetes, its cause and symptoms, and acute and chronic
complications and their treatment.
 Teach self-care activities to prevent long-term complications including foot care, eye care, and
risk-factor management.

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 Include family in plan of care.

 Provide information, encourage health promotion activities, and recommended health



Cholecystitis = inflammation of the gallbladder; can be acute or chronic

-Causes pain, tenderness, and rigidity of the upper right abdomen
that may radiate to the mid-sternal area or right shoulder
-Associated with N/V + usual signs of acute inflammation
-Calculous cholecystitis = gallbladder stone obstructs bile outflow
-Acalculous cholecystitis = acute gallbladder inflammation in the
absence of obstruction by gallstones

Cholelithiasis = calculi, or gallstones, usually form in the gallbladder

from the solid constituents of bile; they vary in size, shape, and composition
 Pathophysiology
◦ Pigment stones
 Probably form when unconjugated pigments in the bile precipitate to
form stones
 Risk of developing increases in patients with cirrhosis, hemolysis, and
infections of the biliary tract

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 Cannot be dissolved and must be removed surgically

◦ Cholesterol stones
 Account for 75% of gallbladder disease in US
 Cholesterol = normal constituent of bile, is insoluble in water
 In gallstone-prone pts, there is decreased bile acid synthesis and
increased cholesterol synthesis in the liver, resulting in bile
supersaturated with cholesterol, which precipitates out of the bile to
form stones
 Risk Factors
◦ Increased age
 Incidence of stone formation increases as a result of increased hepatic
secretion of cholesterol and decreased bile acid synthesis
◦ Female – 2 to 3x more likely, usually over 40, multiparous, and obese
◦ Overweight
◦ Family history
◦ Rapid weight loss diets – leads to development of gallstones and high risk of
symptomatic disease
◦ Pregnancy
◦ Frequent changes in weight
◦ TX with high dose estrogen (ex. prostate cancer)
◦ Low dose-estrogen therapy (carries a small increase in the risk of gallstones)
◦ Diabetes
◦ Cystic fibrosis
◦ Ileal resection or disease
◦ Stone formation more frequent in those who use oral contraceptives,
estrogen, or clofibrate; these medications are known to increase biliary
cholesterol saturation
 Diagnostic Studies
◦ Abdominal x-ray
◦ Ultrasonography
◦ ERCP (endoscopic retrograde cholangiopancreatography)
 Fiber optic scope
 Esophagus to descending duodenum
 Fluoroscopy utilized
 Extraction of gallstones
 Clinical Manifestations
◦ Epigastric distress
 Fullness, abdominal distention, vague RUQ pain after eating a fatty
◦ Infection
 Fever, palpable abdominal mass
◦ Biliary colic – gallbladder obstructs the cystic duct, gb becomes distended, inflamed, and eventually infected
(acute cholecystitis); caused by contraction of the gallbladder, which cannot release bile b/c of obstruction by the
 Severe pain usually associated with N/V noticeable several hours after a
heavy meal
 Severe right abdominal that radiates to the back or right shoulder,
nausea and vomiting.
 Pain = constant rather than colicky
◦ Jaundice
 Blockage of the common bile duct

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 The bile is no longer carried to the duodenum + is absorbed by the

blood giving the skin and mucous membranes a yellow color
◦ Vitamin deficiency (ADEK)
◦ Changes in urine and stool color
 Excretion of bile pigments by the kidneys gives the urine a very dark
 The feces, no longer colored with bile pigments are grayish or clay-
 Medical Management
◦ Laparoscopic cholecystectomy  remove gallbladder thru belly button
 Abdominal cavity is insufflated with carbon dioxide to assist in inserting
the laparoscope and to aid in visualizing the abdominal structures
 No paralytic ileus (like w/ open abdominal surgery)
◦ Open Cholecystectomy
◦ Nonsurgical removal
 Dissolving gallstones with infusion of solvent
 Stone removal by instrumentation
 Intracorporeal or extracorporeal lithotripsy
◦ Nutritional - (low fat diet) – avoid eggs, cream, pork, fried foods, cheese,
rich dressings, gas-forming vegetables, and alcohol
◦ Ursodeoxycholic acid (UDCA) or chenodeoxycholic acid (CDCA)

 Post-operative Chole – Nursing Care

◦ Manage acute pain
 Carbon dioxide
 Location of incision often causes pt to avoid turning and moving, splint affect
side, and take shallow breaths to prevent pain. Since full lung expansion +
gradual increase in activity are necessary to prevent post-op complications, nurse
administers analgesics to relieve the pain and to help the patient turn, cough,
breathe deeply, and ambulate as directed.
◦ Improve, monitor respiratory status – deep breaths + cough every hr, IS, early
◦ Maintain skin integrity
◦ Promotion of biliary drainage/monitor for infection, peritonitis
◦ Improve nutritional status – low fat, high carb/protein diet
◦ Monitor for complications
 Bleeding
 GI symptoms r/t biliary leak
◦ Low Fowler’s position
◦ May have NGT (NPO)
◦ Ambulation

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◦ NPO until BS return (progressive diet)

◦ Care of biliary drainage system
◦ Coughing & Deep Breathing Exercises
◦ Splinting to reduce pain
 Chole – Patient + Family Teaching
◦ Medications & Activity
 Pt education: You may have pain/discomfort in your right shoulder from the gas
used to inflate your abdominal area during surgery - Sitting upright in a bed or
chair, walking, or using a heating pad may ease the discomfort
◦ Diet: at discharge, maintain a nutritious diet
 Avoid excess fat
 Fat restriction is usually lifted in 4–6 weeks.
◦ Instruct in wound care, dressing changes, care of T-tube
◦ Instruct patient and family
 Report signs of gastrointestinal complications
 Changes in color of stool or urine, fever, unrelieved or increased pain,
nausea, vomiting
 Redness/edema/signs of infection at incision site

 Can be rapidly fatal
 At risk for: hypovolemic shock, F & E imbalances, sepsis

 Pathophysiology
◦ Self-digestion of pancreas by it’s own enzymes (trypsin)
◦ Activation of enzymes leads to vasodilation, increased vascular permeability, necrosis,
erosion and hemorrhage~
Book: Mechanisms of pancreatitis are unknown –commonly described as autodigestion of
the pancreas. It is believed that the pancreatic duct becomes temporarily blocked,
accompanied by hypersecretion of the exocrine enzymes of the pancreas. These enzymes
enter the bile duct, where they are activated + together with bile, back up into the
pancreatic duct, causing cancreatitis.

• Risk factors:
o Biliary tract disease
o Gallstones
o History of long-term alcohol abuse
o Bacterial or viral infection
o Blunt abdominal trauma
o Ischemia vascular disease
o Hyperlipidemia
o Medications (BCP, diuretics, corticosteroids)
Book: 80% cases are pts w/ biliary tract disease (gallstones or history of alcohol abuse)
~Gallstones enter common bile duct, obstructing flow of pancreatic juice OR causing a reflux of bile from the
common bile duct into the pancreatic duct, THUS activating the powerful enzymes within the pancreas (these
normally stay inactive until they reach the duodenal lumen). Activation of these enzymes can lead to
vasodilation, increased vascular perm, necrosis, erosion, hemorrhage.

 Clinical Manifestations
o Severe abdominal pain

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o Abdominal guarding
o Nausea and vomiting
o Fever, jaundice, confusion
o Ecchymosis in the flank or umbilical area may occur (severe cancreatitis)
o Respiratory distress, hypoxia, renal failure, hypovolemia, and shock

 Diagnostics
o CT/MRI/US  used to identify an increase in diameter of the cancreas and to detect
cancreatic cysts, abscesses, or cseudocysts
o Serum amylase/lipase  both are elevated w/in 24 hours of onset (amylase usually
returns to normal 24-72 hours, but licase levels remain elevated for a longer ceriod)
 Pancreatic enzymes (these can also be elevated in other intra-abdominal problems though)
 Google: when the pancreas is diseased or inflamed, amylase releases into the
o HPI  “HX of present illness”  the DX of acute cancreatitis is based on a HX or abdominal cain,
cresence of known risk factors, chysical examination, and diagnostic findings.
o CBC  WBC count elevated, hycocalcemia; H&H used to monitor ct for bleeding
o Chemistry  elevated bilirubin in some

o Ranson Criteria: (book: chart 50-3 scecific)

 On admission to hospital
 Age
 Serum glucose
 Serum LDH
 48 hours after admission to hospital
 Fall in Hct
 Increased BUN
 Decreased serum calcium
 Base deficit
 Fluid retention
 Pa02< 60 mm Hg
 Collaborative Care:
o Parenteral nutrition/NPO
 NPO: Oral intake withheld to inhibit stimulation of the pancreas and its secretion
of enzymes
 Parenteral nutrition: plays important role in nutritional support of pts with severe
acute pancreatitis, particularly in those who are debilitates and those with a
prolonged paralytic ileus (>48-72 hours).
 Current recommendation = Enteral route should be used to meet
nutritional needs of pancreatitis pts whenever possible! Pts who cannot
tolerate enteral feedings require parenteral nutrition. Found to prevent
infectious complications. Enteral feedings should be started early in the
course of acute pancreatitis.
o NGT – NG suction may be used to relieve N/V and to decrease painful abdominal
distention and paralytic ileus.
o Medications
o H2 Blockers – H2 antagonists may be prescribed to decrease pancreatic activity by
inhibiting secretion of gastric acid

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o PPI – proton pump inhibitors (ex. Protonix) may be used for patients who do not
tolerate H2 blockers or ineffective on them
o Pain management – analgesia/use of ocioids to relieve cain + minimize restlessness,
which may stimulate cancreatic secretion further
o Antiemetic – may be used to crevent vomiting
o Prophylactic antibiotics? – controversial + still under study
 Correction of fluid + blood loss + low albumin levels = necessary to maintain fluid
volume and prevent renal failure
 Hemodynamic and arterial blood gas monitoring initiated usually
 Antibiotics may be crescribed if infection cresent
 Insulin may be req. if hyperglycemia occurs. Intensive insulin theracy in the
critically ill ct shows cromise in outcomes comcared to intermittent insulin dosing
o Respiratory management
 Aggressive respiratory care indicated b/c of high risk of elevation of the
diaphragm, pulmonary infiltrates and effusion, and atelectasis
 Hypoxemia occurs in a lot of AP pts (even w/ normal x-ray findings)
o Biliary drainage  placement of biliary drains (for external drainage) and stents
(indwelling tubes) in the pancreatic duct through endoscopy has been performed to
reestablish drainage of the pancreas. This has resulted in decreased pain and
increased weight gain.
o Surgical intervention
 Acutely ill pts = high risk for surgical complications
 But may be performed to assist in DX of pancreatitis (diagnostic laparotomy) to establish
pancreatic drainage or to resect or debride an infected, necrotic pancreas
Patient who undergoes pancreatic surgery may have multiple drains in place
post-operatively, as well as a surgical incision left open for irrigation + repacking
every 2-3 days to remove necrotic debris.
o Post-acute management: oral feedings that are low in fat and protein are initiated
gradually. Caffeine and alcohol are ELIMINATED from the diet.

Nursing Management
o Problems
 Acute pain – Relieving pain + discomfort:
 Objective of TX = relieve pain + decrease secretion of pancreatic enzymes
 Current recommendation for cain = parenteral opioids (morchine, hydromorchone,
 Oral feedings are withheld to decrease the secretion of secretin
 Parenteral fluids + electrolytes to restore + maintain fluid balance
 NGT may be used to relieve n/v or to TX abd distention and paralytic ileus
 Frequent oral hygiene to decrease discomfort from the NGT and relieve dryness of
the mouth
 Acutely ill ct is maintained on bed rest to decrease metabolic rate + secretion of
cancreatic + gastric enzymes
 If patient has increasing pain severity nurse reports this to physician b/c may be
experiencing hemorrhage of the pancreas or dose of analgesic may be inadequate
 Frequent reminders of the need for catient to withhold fluids, maintenance of
gastric suction, and bed rest.

 Ineffective breathing – Improving breathing pattern:

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 Maintain in semi-fowler’s position to decrease pressure on the diaphragm by a

distended abdomen and to increase respiratory expansion
 Frequent changes in cosition to crevent atelectasis and cooling of resciratory
 Teach ct coughing, deec breathing, incentive scirometry every hour to imcrove
resciratory fxn

 Imbalanced nutrition – Improving nutritional status:

 Enteral or parenteral nutrition may be prescribed
 Monitor blood glucose levels every 4 to 6 hours!
 As acute symptoms subside, oral feedings reintroduced
 Between acute attacks, patient has high protein + low fat diet
 Patient should avoid heavy meals and alcoholic beverages

 Impaired skin integrity – Maintaining skin integrity:

 Risk for skin breakdown b/c poor nutritional status, enforced bed rest, and
restlessness, which can result in pressure ulcers + breaks in tissue integrity
 Patient must be turned every 2 hours

o Complications
 Fluid /Electrolyte disturbances
 Common b/c of N/V, movement of fluid from vascular compartment to the peritoneal
cavity, diaphoresis, and use of gastric suction
 Assess – turgor, daily weights, I&O (inc. urine, NG secretions, and diarrhea);
 Necrosis of the pancreas
 Pancreatic necrosis = major cause of death in pts with AP b/c of resulting
hemorrhage, septic shock, and MODS
 if cancreatic necrosis with infection = may require surgical debridement and/or
insertion of multicle drains
 a ct with cancreatic necrosis (with or without infection) is usually critically ill requires
excert medical and nursing management including hemodynamic monitoring + ICU
 Shock
 Hypovolemic shock may occur as result of hypovolemia and sequestering of fluid
in the peritoneal cavity
 Hemorrhagic shock may occur with hemorrhagic pancreatitis
 Septic shock may occur with bacterial infection of the pancreas
 Multiple organ dysfunction syndrome (MODS)
 Nurse closely monitors for early signs of neurologic, cardiovascular, renal, and
resciratory dysfunction
 DIC = “disseminated intravascular coagulation”
 Google: Condition affecting the blood's ability to clot and stop bleeding.

-Inflammatory disorder characterized by progressive destruction of the pancreas
-As cells are replaced by fibrous tissue with repeated attacks of pancreatitis, pressure
increases within the pancreas
-Result is obstruction of the pancreatic and bile ducts and the duodenum

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-Atrophy of epithelium of ducts, inflammation and destruction of secreting cells of the

-Major causes: ETOH, smoking
*long-term alcohol abuse causes hypersecretion of protein in pancreatic solutions, resulting in
protein plugs and calculi within the pancreatic ducts
*Alcohol also has a direct toxic effect on the cells of the pancreas . (Damage to those cells is
more likely to occur and to be more severe in patients whose diets are poor in protein content
and either very high or very low in fat)

Clinical Manifestations
 Severe upper abdominal + back pain
 N/V
 Opioids do not provide relief
 Weight loss – usually caused by decreased dietary intake d/t anorexia or fear that
eating will make them have another attack
 Malabsorption – occurs late in the disease when as little as 10% pancreatic fxn
 Stools = frothy, fouls smelling (high fat content: steatorrhea)
 Digestion (especially of proteins and fats) is impaired. Stools become more frequent,
frothy, and foul smelling because of impaired fat digestion, which results in stools with a
high fat content = steatorrhea
 As disease progresses, calcification of the gland may occur and calcium stones may form within the ducts

 ERCP = most useful study in the diagnosis of chronic pancreatitis.
 “Endoscopic retrograde cholangiopancreatography”
 Provides details about the anatomy of the pancreas and the pancreatic + biliary
ducts. Also helpful in obtaining tissue for analysis to differentiate pancreatitis from
other conditions (like carcinoma)
 CT
 US
 Elevated serum amylase/lipase
 Abnormal glucose tolerance test
 A glucose tolerance test evaluates pancreatic islet cell function and
provides necessary info for making decisions about surgical removal of the
 An abnormal glucose tolerance test may indicate the presence of diabetes
associated with pancreatitis

Collaborative Care
 Preventing and managing attacks
 Relieving pain
 Stone retrieval via ERCP
 Yoga – research says may be an effective non-pharm method for pain reduction
and relief of other coexisting symptoms of CP
 Dietary management
◦ Emphasize importance of avoiding alcohol + foods that have produced
abdominal pain in the past
◦ STRESS that no other treatment is likely to relieve pain if the patient
continues to consume alcohol!

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◦ Stress hazard of severe hypoglycemia with alcohol consumption to patient

and family
 Manage diabetes
◦ Diabetes resulting from dysfunction of the pancreatic islet cells is treated
with diet, insulin, and oral antidiabetic agents
 Surgery  chronic pancreatitis is not often managed by surgery but may be indicated to relieve
persistent abdominal pain + discomfort, restore drainage or pancreatic secretions, and reduce the
frequency of acute attacks of pancreatitis and hospitalization
◦ Roux-en-Y (aka pancreatojejunostomy) = anastomosis of pancreatic duct
to jejunum (allows drainage of the pancreatic secretions into the jejunum)
 Pain relief occurs within 6 months in >85% of pts, but in a good # of
pts, the pain returns as the disease progresses
 In an effort to provide permanent pain relief and avoid endocrine and
exocrine insufficiency that ensue with major resections of the
pancreas, surgeons have designed new procedures that combine
limited resection of the head of the pancreas with a
◦ Whipple (aka Pancreatoduodenectomy) = generally the removal of the
gallbladder, common bile duct, part of the duodenum, and the head of the pancreas.
Afterward, surgeons reconnect the remaining intestine, bile duct, and pancreas.
 Carried out to relieve the pain of chronic pancreatitis

After Pancreatic Surgery

 Pts who undergo surgery for chronic pancreatitis may experience weight gain +
improved nutritional status (prob b/c it hurts less to hurt rather than correction of
malabsorption issue)
 Morbidity/mortality is high after b/c of poor condition of pt before + concomitant

Pancreatic Cancer
Risk factors
 Tobacco use
 Diabetes
 Chronic pancreatitis
 Hereditary

Book: Cancer can develop in the head, body, or tail of pancreas. The clinical manifestations vary
depending on the site and whether or not fxning insulin-secreting islet cells are involved
-Sites of lesions  ~70% occur in the head of the pancreas

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Clinical Manifestations
◦ Pain
◦ Jaundice
◦ Weight loss
◦ Ascites
◦ Diabetes
◦ Clay-colored stools
◦ Abdominal pain
◦ Anorexia, N/V

 CT, ERCP, biopsy
 Percutaneous, fine-needle biopsy

Medical Management
 Resection
 Chemotherapy
 Biologic agents
 Surgical Management
 Total pancreatectomy
 Whipple procedure
Thyroid Gland
• Hormones: T3, T4, Calcitonin
• Negative Feedback Mechanism – if the thyroid hormone concentration in the blood decreases, the release of
TSH increases, which causes increased outcut of T3 and T4.
• T3 and T4 affect all body systems by regulating metabolism, energy production, and fluid & electrolyte
• Calcitonin inhibits movement of calcium from the bone causing decreased serum levels
o Secreted in resconse to high calcium levels, and it reduces the clasma level of calcium by increasing its
decosition in bone

Book: Iodine is essential to the thyroid gland for synthesis of thyroid hormones.
- Thyroid = major use of iodine in the body + the major derangement for iodine deficiency is alteration
of thyroid function.
- Secretion of T3 + T4 is controlled by TSH (aka thyrotrocin) from the anterior pituitary gland
- “euthyroid” = normal thyroid production
-TRH secreted by hypothalamus influences release of TSH from the pituitary.
- thyroid hormone main fxn = control cellular metabolic activity.
- the thyroid hormones influence cell replication, important in brain development, and are also necessary for
normal growth. They affect virtually every major organ system + tissue fxn, including the BMR, tissue
thermogenesis, serum cholesterol levels, and vascular resistance.

Diagnostic Tests
o Laboratory Tests
o TSH – best screening test for thyroid fxn b/c of its high sensitivity
 Used for monitoring thyroid hormone replacement therapy
 Good for differentiating b/w disorder of thyroid gland itself + disorders of the
pituitary or hypothalamus
o Serum free T4
 When measured by the dialysis method, free T4 is not affected by variations
in protein binding and is the procedure of choice for monitoring the changes
in T4 secretion during TX for hyperthyroidism
o T3 and T4

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 Includes protein-bound and free hormone levels that occur in response to

TSH secretion
 Although T3 + T4 levels generally increase or decrease together, the T3 level
appears to be a more accurate indicator of hyperthyroidism, which causes a
greater increase in T3 than T4 levels.
o T3 resin uptake
 indirect measure of unsaturated TBG
o Thyroid antibodies
o Thyroglobulin
 Used to detect persistence or recurrence of thyroid carcinoma
o Diagnostic Procedures
o Radioactive iodine uptake
o Fine-needle aspiration biopsy
o Thyroid scan, radioscan, or scintiscan
o What are the nursing implications for these tests and procedures?
“Thyroid gland circulation= very rapid – blood flow to the thyroid gland is very high (~5x the blood flow to the liver)
Give iodine test to identify if the iodine level is within normal limits
The ultrasound is the best you can see within the thyroid the lobules
If its swollen it’ll press the respiratory components
Too little thyroid component – hypothyroidism”
Book: isthmus is the only part of thyroid that is normally palpable. If palpation reveals enlarged thyroid, then
auscultation identifies the localized audible vibration of a bruit.
Thyroid Disorders
 Cretinism
 Myxedema
 Thyroiditis
o Hashimoto’s disease
 Book: firmness ucon calcation
 Graves’ disease
o Book: Soft texture ucon calcation
 Goiter
 Thyrotoxicosis (thyroid storm)
“Read about hyperthroidism and thyroid storm”

Book: hypothyroidism results from suboptimal levels of thyroid hormone
- can range from mild forms to myxedema (severe life-threatening form)
- myxedema refers to the accumulation of mucopolysaccharides in subcutaneous and other interstitial
tissues. extreme symptoms of severe hypothyroidism.
o Myxedema + myxedema coma usually occur exclusively in pts older than 50
 Affects women 5x more frequently than men
 Pathophysiology  thyroid gland fails to secrete enough thyroid hormone. Hypo-
secretion of TH results in overall decrease in metabolism

Causes: (SA book)

- Autoimmune disease – “Hashimoto’s thyroiditis”
o most common cause of hypothyroidism*
o immune system attacks the thyroid gland
- thyroidectomy (surgical removal of all or part of thyroid gland)
- overuse of anti-thryoid drugs + use of radioactive iodine

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o used in the TX of previous hyperthyroidism

- pituitary gland malfunction
o “central hypothyroidism” = cause d/t failure of pituitary gland,
hypothalamus, or both
- inflammatory conditions
- toxemia of pregnancy

Lab Findings: (SA book)

- Decreased T3 + T4
- Decreased protein-bound iodine
- Decreased sodium
- Increased TSH + cholesterol
- EKG: sinus bradycardia
- RAIU: decreased

Clinical Manifestations:
- extreme fatigue
- weight gain
- thick tongue, swollen lips
- mental sluggishness
- constipation
- anorexia
- hypothermia
- decreased diaphoresis
- hypersensitivity to opioids, barbiturates, + anesthetics
- hair loss (alopecia)
- brittle nails
- dry skin
- voice becomes husky (occasional) – hoarseness
- menstrual disturbances – amenorrhea, loss of libido
o Abnormal temp + HR
o Weight gain without increased food intake
o Thickened skin (b/c accum. of mucocolysaccharides in subcut. tissues)
o Hair thins + falls out
o Face = expressionless, mask-like
o Cold intolerance (pt feels cold even in warm environment)
o Apathy
o Speech is slow, tongue enlarges
o Associated w/ elevated serum cholesterol level, atherosclerosis, CAD, and poor left
ventricular fxn

“Look specifically at the patients mouth and tongue- gets thick

GI- constipation”

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Key complications of hypothyroidism:

- myxedema coma
- heart failure

Late Manifestations – Myxedema

 Life-threatening condition
 Depression, diminished cognitive status, lethargy, and somnolence  lethargy and stupor
 depressed respirations  alveolar hypoventilation  carbon dioxide retention, narcosis,
and coma  cardiovascular collapse and shock  death
 Book: Myxedema coma = rare life-threatening condition; it is the decompensated state of severe
hypothyroidism in which pt is hypothermic + unconscious; appears to be precipitated by cold. Pt may initially
show signs of depression, diminished cognitive status, lethargy, somnolence. Patients respiratory drive is
depressed  hypoventilation, CO2 retention, coma. In addition, can exhibit: hyponatremia, hypoglycemia,
hypoventilation, hypotension, bradycardia, and hypothermia. All these symptoms plus cardiovascular collapse
+ shock require aggressive supportive + hemodynamic TX in order for pt to survive.
“If you don’t treat it gets worse and leads to myxedema”

Medical Management (TX)

 Goal: Restore a normal metabolic state by replacing the missing hormone; prevention of
disease progression and complications
 Pharmacologic Therapy
o Synthetic levothyroxine (synthroid)
 Book: TX hypothyroidism + suppression of nontoxic goiters. Its dosage is based on
serum TSH concentration.
 “Synthroid=medicine of choice through IV and when it gets better you can give PO;
monitor by TSH”

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o High-dose glucocorticoids in first 24 hours (hydrocortisone)
 Followed by low-dose therapy until adrenal deficiency is ruled out
 Book: obtain serum levels of T4, TSH and cortisol before and after administration of
ACTH + before administration of glucocorticoid + thyroid hormone therapies
 Prevention of cardiac dysfunction
o Book: any pt who’s had hypo for a long time usually has high cholesterol, atherosclerosis, and
CAD. Angina or dysrhythmias can occur when thyroid replacement is initiated because thyroid
hormones enhance the cardiovascular effects of catecholamines. If this occurs, d/c the thyroid
therapy immediately.
 Prevention of medication interactions
o Book: oral thyroid hormones interact w/ many other meds
o There is a decrease in TH absorption when pts are also taking magnesium-containing antacids
 Supportive therapy
o Book: severe hypo + myxedema coma require prompt/aggressive management
o ABGs to determine CO2 retention + to guide use of assisted ventilation to combat
o O2 sat levels – pulse ox
o Fluids are administered cautiously b/c of the danger of water intoxication
o Passive rewarming w/ a blanket is recommended vs active rewarming such as application of
external heat (ex. heating pads) – the latter should be avoided to prevent increased O2
demands and hypotension
Nursing Management
Book: effects of analgesics, sedatives, and anesthetic agents are prolonged in hypothyroid pts (careful
monitors of pts prescribed these)
 Monitor for CV changes
 AMS – Orient and safety precautions
 Activity – gradually increase; provide frequent rest periods
 Anti-embolism stockings and elevate legs
 Cough and deep breathe
 Low-calorie, high-fiber diet, encourage fluid intake!
o Promote weight reduction + prevent constipation (return of normal bowel fxn)
 Meticulous skin care
 Provide extra clothing/blankets – crovide warm environment

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o Stress catients need to avoid extreme cold temcerature

 Avoid sedation: administer 1/3 to ½ the normal dose of sedatives or opioids (SA book)
“Give them protein something that’s good for a balanced diet to a have normal bowel movement b/c they get

Nursing Actions – Myxedema

 Maintain airway patency – w/ ventilatory support if necessary (SA)
 Maintain circulation
o through IV fluid replacement
 Continuous ECG/EKG monitoring
 Monitor ABGs  to detect hypoxia and metabolic acidosis
o significantly decreased respirations  CO2 levels in blood may increase
 Warm with blankets
o Don’t use a warming blanket. Might increase peripheral vasodilation, causing
 Monitor body temperature
 IV levothyroxine as ordered – (replacing thyroid hormone)
o Monitor VS  rapid correction of hypothyroidism can cause adverse cardiac effects
 Monitor I&O and daily weights
o w/ TX, urine output should increase + body weight should decrease
 Replace fluids & electrolytes and glucose as needed – monitor serum electrolyte levels
 Corticosteroids as ordered
 Treat underlying cause
o check for possible infection sources – blood, sputum, or urine; which may have
precipitated coma. TX infections or any other underlying illness
“Hypo - make sure to maintain airway ABCs, give fluids it gets so complicated no fluids make sure to monitor
EKG for arrhythmias
If pt can’t take meds by mouth make sure doctor orders continuous IV
Myxedema = Complication of hypothyroidism”

(SA): Hyperthyroidism = increased synthesis of TH from over-activity (Graves’ disease)
or a change in the thyroid gland function (toxic nodular goiter)
 The 2nd most prevalent endocrine disorder
 Excessive output of thyroid hormone (thyrotoxicosis)
 Graves disease (most common cause)
 Affects women 8X more frequently than men

- Autoimmune + genetic factors
- Graves disease (most common cause)
- Increased TSH secretion
- Pituitary tumors
- Precipitating factors: psychological/physiologic stress, infection, DKA, excessive iodine
intake, surgery, toxemia of pregnancy

Book: hyperthyroidism is manifested greatly by increased metabolic rate

- Many of the other characteristics of hyperthyroidism result from the increased response to circulating
- Oversecretion of thyroid hormones usually associated w/ enlarged thyroid gland = goiter
- Goiter also commonly occurs with iodine deficiency – lack of iodine results in low levels of circulating THs,
causing increased TSH release, causing overproduction of thyroglobulin (precursor of T3+T4) and
hypertrophy of the thyroid gland

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Clinical Manifestations:
- Anxiety, diaphoresis, hyperhidrosis, Fine hand tremors
- Heat intolerance
- Mood swings
- Tachycardia, palpitations, dyspnea, increased SBP, tachypnea
- Exophthalmos = bulging eyes
- Weight loss despite increased appetite; diarrhea
- Bruit
- Fertility problems
- Oligomenorrhea or amenorrhea
book: likely to result in premature osteoporosis (particularly in women)

DX Findings:
- Thyroid scan: nodules
- Increased T3 +T4 levels
- Increased protein-bound iodine
- Decreased TSH
- Decreased cholesterol
- EKG: atrial fibrillation
- RAIU: increased
Medical Management: (SA)
- Diet: restrict stimulants (ex. caffeine)
- IV therapy as needed
- Bed rest, monitor VS, I+O
- Sedative: Ativan
- Radiation therapy
- Thyroid hormone antagonists
- Radioactive iodine
- Beta blocker
- Glucocorticoids: prednisone, IV hydrocortisone for thyroid storm

*Key complications hyperthyroidism: thyroid storm, arrhythmias, diabetes mellitus

Nursing Interventions:
- Assess CV status!
- Avoid giving the patient stimulants, e.g. drugs + foods that contain caffeine
- IV fluids, meds as prescribed
- Rest periods in a quiet, cool environment
- Provide post-radiation nursing care: prophylactic skin, mouth, and perineal
care; monitor dietary intake; provide rest periods

Thyroid Storm (Thyrotoxic crisis)  complication of hyperthyroidism

Usually occurs in pts with preexisting + commonly unrecognized thyrotoxicosis
Patho: overproduction of T3+T4 causes an increase in systemic adrenergic activity, resulting in
epinephrine overproduction and severe hypermetabolism. Rapidly leads to cardiac, GI, and SNS
 Severe hyperthyroidism  usually has an abrupt onset  untreated it is fatal
 Manifestations
o High fever
o Extreme tachycardia
o Hyperthyroidism symptoms but much more pronounced

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o Altered neurologic/mental status

 Causes
o Stress  illness, injury, infection
o Thyroidectomy

Medical Management
 Radioactive Iodine Therapy – most common form of TX for Graves disease
 Medications (See Table 52-3)
o Propylthiouracil (PTU) and methimazole - NTK
o Sodium or potassium iodine solutions (SSKI)
o Dexamethasone
o Beta-blockers – used as adjunctive theracy for symctomatic relief
 Surgery; subtotal thyroidectomy
 Relapse of disorder is common
 Disease or treatment may result in hypothyroidism

Nursing Management
 Encourage alternating periods of activity with rest
 Calm environment -
 Nutritional status
 Monitor for abrupt changes in behavior
 Administer antithyroid medications as prescribed
 Prep for surgery if indicated

Nursing Implications:
- necessary to determine if the patient is allergic to iodine (shellfish) and whether the pt has taken
medications of agents that contain iodine (may alter results)
- other meds that may affect test results: estrogens, salicylates, amphetamines, chemotherapeutic agents,
antibiotics, corticosteroids, and mercurial diuretics
-examples: aspirin, Lasix, heparin

Thyroid Tumors (Goiters) – Simple Goiter

Patho: low levels of TH stimulate increased secretion of TSH by pituitary gland. TSH stimulation
causes thyroid to increase in size to compensate for the low levels of TH.
- Endemic – living in an area with iodine-depleted soil, decreased iodine intake
- Sporadic- unknown, possibly due to use of certain drugs, such as lithium
S/S simple goiter = dysphagia + swelling in the neck
Assess respiratory status + patient’s ability to swallow
 Endemic (Iodine-Deficient) goiter  AKA “colloid goiter”
o Causes:
 Book: the most common type of goiter that occurs when iodine intake is deficient is the simple or
colloid goiter. In addition to being caused by an iodine deficiency, simple goiter may be caused
by an intake of large quantities of goitrogenic substances (ex. lithium - these include excessive
amounts of iodine)
 Intake of large quantities of iodine
 Prescribed lithium – found to have antithyroid actions
o Treatment
 SSKI – supplementary iodine to suppress the pituitary’s thyroid-stimulating activity
 Thyroidectomy
 Nodular

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o Benign or malignant
o Thyroidectomy
Thyroid Cancer
 Assessment
o Nodules or lumps palpated
o Lymphadenopathy
 Diagnosis
o Needle biopsy
o Scans
o Iodine uptake studies
 Medical Management
o Thyroidectomy
 Nursing Management
o Pre/post operative care
Anxiety = number 1 issue”

 Treatment of choice for thyroid cancer
 Cancer surgery may include modified or radical neck dissection, may include treatment with
radioactive iodine to minimize metastasis, and other medications
 Preoperative goals include the reduction of stress and anxiety to avoid precipitation of thyroid
 Preoperative teaching includes dietary guidance to meet patient metabolic needs and avoidance
of caffeinated beverages and other stimulants, explanation of tests and procedures, and
demonstration of support of head to be used postoperatively
“Don’t put them flat”

Thyroidectomy – Post-operative Care

 Monitor dressing for potential bleeding and hematoma formation; check posterior dressing
o Sensation of cressure or fullness @ incision site may indicate subcutaneous hemorrhage
and hematoma formation
 Monitor respirations; potential airway impairment  tracheostomy set @ bedside at all times
 Assess pain and provide pain relief measures
 Semi-Fowler’s position, support head with pillows  most comfortable
 Assess voice but discourage talking  pt advised to talk as little as possible to reduce edema to the
vocal cords, but when they do talk – assess changes in voice indicating possibly injury to the laryngeal
nerve which lies just behind the thyroid next to trachea
 Potential hypocalcemia related to injury or removal of parathyroid glands; monitor for
o Occasionally in thyroid surgery, the parathyroid glands are injured or removed, producing a
disturbance in calcium metabolism. As blood calcium level falls, hyperirritability of the nerves
occurs, with spasms of the hands + feet + muscle twitching = tetany. (Report immediately:
laryngospasm (rare) may occur + obstruct the airway)

 Four glands on the posterior thyroid gland
 Parathormone regulates calcium and phosphorus balance

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o Increased parathormone elevates blood calcium by increasing calcium absorption from the
kidney, intestine, and bone.
o Parathormone lowers phosphorus level.

Overactivity of one or more parathyroid glands, resulting in increased PTH secretion
Causes: chronic renal failure, bone disease, hypertrophy of parathyroid gland, vitamin D
deficiency, malabsorption, tumors of parathyroid gland, benign adenomas
 Manifestations include:
o elevated serum calcium
o bone decalcification
o renal calculi – r/t the increased urinary excretion of calcium + choschorus
o apathy, fatigue, muscle weakness
o nausea, vomiting, constipation
o hypertension, cardiac dysrhythmias
o psychological manifestations
 Hypercalcemic crisis – extreme elevation in calcium levels
o Requires prompt TX to reduce calcium levels
o Serum calcium levels > 13 result in neurologic, cardiovascular, and kidney symptoms that can be
o Rapid rehydration w/ large volumes of IV isotonic fluids to maintain urine output of 100 to 150
mL/hr is combined with administration of calcitonin
 Calcitonin = promotes renal excretion of excess calcium and reduces bone resorption

Medical Management
 Treatment
o Parathyroidectomy
 Monitor for symptoms of tetany (may be post-op complication)
o Hydration therapy - cts with hycercarathyroidism are at risk for renal calculi
 Daily fluid intake of 2000 mL+ encouraged to help prevent calculus formation
 Thiazide diuretics avoided (decrease renal excretion of calcium + further elevate calcium levels
o Encourage mobility reduce calcium excretion
 Bones subjected to the normal stress of walking give up less calcium
 Bed rest increases calcium excretion + the risk of renal calculi
o Diet  encourage fluid, avoid a diet w/ excess or restricted calcium
 Prune juice, stool softeners, and physical activity help offset constipation (common postop)

Decreased PTH secretion which decreases stimulation to osteoclasts, resulting in decreased
release of calcium and phosphorus from bone. Decreased PTH also reduces GI absorption of
calcium and increases absorption of phosphorus. Decreased blood calcium causes a rise in serum
phosphates and decreased phosphate excretion by the kidney.

Causes: (book)
- abnormal parathyroid development
- destruction of the parathyroid glands (surgical removal or autoimmune response)
- vitamin D deficiency.

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 Deficiency of parathormone usually due to surgery— thyroidectomy, parathyroidectomy, or radical

neck dissection
 Results in hypocalcemia and hyperphosphatemia

 Manifestations include:
o Tetany
o numbness and tingling in extremities
o stiffness of hands and feet
o bronchospasm, laryngeal spasm, carpal-pedal spasm
o anxiety, irritability, depression, delirium
o ECG changes
o Chvostek’s sign +
 A positive chvostek’s sign suggests latent tetany
 When a sharp tapping over the facial nerve just in front of parotid gland and anterior to the
ear causes spasm or twitching of the mouth, nose, and eye

o Trousseau’s sign +
 A positive trousseau’s sign suggests latent tetany
 When carpopedal spasm is induced by occluding the blood flow to the arm for 3 minutes
with a blood pressure cuff

Medical Management
 Goal: Increase serum calcium level to 9—10 mg/dL
 IV Calcium gluconate  the immediate TX when hypocalcemia + tetany occur after a
thyroidectomy! If this doesn’t decrease neuromuscular irritability and seizure activity-
o May also use sedatives such as pentobarbital to decrease neuromuscular irritability
 Parathormone may be administered; potential allergic reactions
 Environment free of noise, drafts, bright lights, sudden movement
 Diet high in calcium and low in phosphorus
o Restricted: Milk, milk products, and egg yolk - b/c they also contain high levels of
phosphorus. Spinach b/c contains oxylate, which would form insoluble calcium substances
 Vitamin D

*Key nursing interventions:

- Assess neuro status
- Maintain seizure precautions
- Keep tracheostomy tray and IV calcium gluconate available
- Glucose metabolism – after meal, glucose is taken up by liver + converted into glycogen for storage. The
glycogen can be converted back to glucose as needed to maintain normal levels of blood glucose. Additional
glucose can be synthesized by liver through gluconeogenesis (liver uses amino acids from protein breakdown or
lactate produced by exercising muscles) in r/t hypoglycemia.
- Ammonia conversion- use of amino acids from protein for glucoeneogenesis results in formation of ammonia as
a by-product. The liver converts this ammonia (potential toxin) to urea to be excreted in the urine.

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- Protein metabolism –synthesizes almost all of the plasma proteins (except gamma-globulin) including albumin,
blood clotting factors, etc. Vitamin K is required by the liver for synthesis of prothrombin and some of the other
clotting factors. Amino acids are used by the liver for protein synthesis.
- Fat metabolism- breakdown of fatty acids for ketone bodies (for energy); primarily when glucose availability is
limited (ex. starvation or uncontrolled diabetes)
- Vitamin + Iron storage – vitamins A, B, D, and several forms of the B-complex vitamins stored in large amounts
in the liver. Iron and copper are also stored in liver.
- Bile formation – bile continuously formed by the hepatocytes from cholesterol; fxns of bile are excretory (as in
excretion of bilirubin) but also serves as an aid to digestion (emulsification of fats by bile salts)
- Bilirubin excretion – bilirubin = pigment derives from the breakdown of hemoglobin; hepatocytes convert the
bilirubin into glucuronic acid to make more water-soluble; this form is then secreted by hepatocytes and eventually
carried in the bile into the duodenum.
- Drug metabolism

Diagnostic Evaluation
 Liver Function Tests
 Book: fxn is generally measured in terms of serum enzyme activity (serum aminotransferases,
alkaline phosphatase, lactic dehydrogenase) and serum concentrations of proteins (albumin and
globulins), bilirubin, ammonia, clotting factors, and lipids.
 ALT, AST, and GGT = most frequently used tests of liver damage
 Liver Biopsy
 Peritonitis caused by blood or bile after liver biopsy is the major complication, therefore, coagulation
studies are obtained, their values noted, and abnormal results are treated before liver biopsy is
 Pre-procedure: coagulation tests! – PT, PTT, platelet count (many patients with liver disease have
clotting defects and are at risk for bleeding) + signed consent. “For liver biopsy pt must be NPO
and check hemoglobin and hematocrit and clotting factors”
 Post-procedure: immediately after biopsy, assist the pt to turn on to the right side; recumbent +
immobile for several hours (in this position, the liver capsule at the site of penetration is compressed
against the chest wall, and the escape of blood or bile through the perforation is prevented)
 Others
 US
 CT Scan – “also good and less invasive”
 Angiography

Liver Function Test’s (LFT)

 Liver Function Studies (See chart 49-1)
 Pigment Studies – “jaundice –b/c liver is not able to eliminate all the bile”
 Protein Studies
 Serum Alkaline Phosphatase
 Ammonia
 Cholesterol Studies
Liver Biopsy (Chart 49-3)
 Check coagulation tests
 Informed consent
 Pre-procedure teaching
 Support patient during procedure
 Place patient on right side

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 Avoid coughing or straining

 Monitor VS 10-15 minutes then every 30 minutes
 Avoid heavy lifting and strenuous activity x 1 week
 “important to monitor for bleeding (liver is highly vascular, any aggravation could cause), put patient on
right side, VS (critical time of recovery)”

Manifestations of Hepatic Dysfunction

 Acute or chronic liver disease
 “We usually relate liver with alcohol. Anything we ingest gets filtered by the liver.
 Liver injury can be caused by too much medication, hereditary factors…when pts become
immunocompromised we may have to give liver toxic drugs.
 Majority of liver injuries are due to obstruction of ducts that connect liver, pancreas, and GI”
 Cirrhosis Etiology:
 Alcoholism
 Infection (hepatitis)
 “When we have these diseases that have to do with social behaviors such as drug use
(needle injections)...patients may contract hepatitis and injur liver”
 Disease crocesses that lead to hecatocellular dysfunction may be caused by infectious agents
like bacteria and viruses and by:
 Anorexia
 Metabolic disorders
 Nutritional deficiencies – major cause of carenchymal damage is malnutrition (esc. r/t

Sequelae of Liver Disease

 Jaundice
 Portal hypertension
 Ascites
 Esophageal varices
 Hepatic encephalopathy
 Nutritional deficiencies

Jaundice – hepatocellular + obstructive are the two types of jaundice commonly associated with liver
 Inability of damaged liver cells to clear bilirubin from the blood
 May be caused by: viruses (ex. hecatitis), chemical toxins, ETOH
 Mildly or severely ill; lack of appetite, nausea, weight loss
 Malaise, fatigue, weakness
 If infectious in origin  Headache, chills, and fever
 Elevated LFTs  AST + ALT may be increased (indicating cellular necrosis)

 Resulting from extrahepatic obstruction
 Gallstones, inflammation, tumor
 May be caused by occlusion of the bile duct from a gallstone, an inflammatory process, a
tumor, or pressure from an enlarged organ
 Dark orange-brown urine
 Light clay-colored stools
 b/c of inability to excrete bilirubin
 Dyspepsia and intolerance of fats, impaired digestion
 Pruritis (bilirubin)

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 AST, ALT, and GGT levels rise only moderately, but bilirubin and alkaline choschate levels are

Portal Hypertension
 Obstructed blood flow through the liver
 Increased pressure throughout the portal venous system results from obstruction of
blood flow into and through the damaged liver
 Two major consequences of portal hypertension
 Ascites
 Esophageal varices

Book: portal HTN + the resulting increase in capillary pressure + obstruction of venous flow through the damaged
liver are contributing factors.
 Fluid accumulation in the peritoneal cavity
 Patho: Vasodilation of splanchnic circulation (blood flow to the major abdominal organs) 
decrease in circulating blood volume  activation of RAAS, SNS, & ADH  kidneys retain
fluid and sodium  increases intravascular/lymph volume  hypervolemia  decreases
synthesis of albumin and serum osmotic pressure  albumin-rich fluid (20 L or more/day)
may accumulate in peritoneal cavity

Ascites: Clinical Manifestations

 Increased abdominal girth
 Rapid weight gain
 Striae
 Distended veins over abdominal wall
 Umbilical hernia
 F & E imbalances

Ascites: Assessment & Diagnostics

 Percussion of abdomen – for shifting dullness
 Fluid wave
 Daily measurement of abdominal girth/body weight

Ascites: Medical Management

 Nutritional Therapy: 2g Sodium diet
 Goal: a negative sodium balance to reduce fluid retention
 Pharmacologic Therapy:
 Diuretics
 Aldactone [aldosterone blocking agent]
 Spironolactone [potassium sparing] – most often the 1st-line therapy in pts with
ascites from cirrhosis; when used w/ other diuretics can help prevent potassium
 Furosemide (Lasix) – cautious use b/c long-term can induce severe sodium
depletion (hyponatremia)
 Ammonium chloride & acetazolamide contraindicated – b/c of possibility of
precipitating hepatic coma
 Fluid and Electrolyte Replacement (Salt-poor albumin)
 Fluid restriction is not attempted unless the serum sodium concentration is very low
 When potassium stores are depleted, the amount of ammonia in the systemic circulation
increases, which may cause impaired cerebral fxning + encephalopathy.

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 Bed Rest
 In patients w/ ascites, an upright posture is associated w/ activation of the RAAS and SNS,
this causes a decreased response to loop diuretics
 Paracentesis (Chart 49-4)
 Removal of fluid from the peritoneal cavity through a puncture or a small surgical incision
through the abdominal wall under sterile conditions
 Pre-procedure- signed consent form, instruct the patient to void*, gather sterile equipment,
place patient in upright position (edge of bed or chair), if confined to bed – fowler’s position.
 *empty bladder minimizes risk of inadvertent puncture of the bladder and minimizes
discomfort from a full bladder
 Transjugular Intrahepatic Portosystemic Shunt (TIPS)
 Cannula threaded into portal vein; stent placed
 Decreases sodium retention
 reduce portal HTN by creating a shunt within the liver between the portal and systemic
venous systems
 used for TX of bleeding esophageal varices too
 nursing priority: observe for rebleeding and signs of infection
 higher risk of encephalopathy + higher cost – considered 2nd-line therapy for refractive
Nursing Management:
- I&O, abdominal girth, and daily weight to assess fluid status
- Monitor respiratory status b/c large volumes of ascites can compress the thoracic cavity +
inhibit adequate lung expansion
- Monitor serum ammonia, creatinine, and electrolyte levels
Esophageal Varices
- Dilated veins in the submucosa of the lower part of the esophagus, resulting from
portal HTN (SA)
- Varicosities that develoc from elevated cressure (cortal HTN); they are crone to ructure +
often are the source of massive hemorrhages from the uccer GI tract and the rectum. In
addition, abnormalities in blood clotting, often seen in cts with severe liver disease, increase
the likelihood of bleeding and significant blood loss.
 Patho: Portal hypertension caused by resistance to portal flow and increased portal venous inflow
 pressure gradient of 12 mmHg or greater between portal vein and IVC  venous collateral
circulation develops in the esophagus, rectum, and retroperitoneal veins  abnormal varicose
vessels form  may rupture  life-threatening bleeding
SA Patho:
- venous drainage from the liver into the portal vein is decreased
- drainage obstruction results in portal HTN
- return of venous blood from the intestinal tract and spleen to the right atrium via
the collateral circulation is obstructed
- the increased pressure dilates the esophageal veins, which then protrude into the
esophageal lumen
Clinical Manifestations
ct w/ bleeding esochageal varices may cresent with:
 Hematemesis
 Melena
 General deterioration (mental or physical status)
 Often has HX of alcohol abuse
 Shock – cool, clammy skin, hycotension, tachycardia

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Assessment & Diagnosis

 Endoscopy
 CT
 Angiography
 Measurement of portal venous pressure
 LFT’s

Bleeding Esophageal Varices (Table 49-2)

 Treatment of Shock
 Oxygen
 IV fluids electrolytes and volume expanders
 Blood and blood products (prevent over hydration)
 Caution must be taken with fluid volume reclacement b/c overhydration can occur and
raise cortal cressure which would increase bleeding
 Decrease Bleeding
 Octreotid (Sandostatin)  selective sphlanic vasoconstriction
 Vasopressin (Contraindication: CAD)  splenic vasoconstriction and decreases portal
 Vasopressin and Nitroglycerin combination in patients with CAD
 CAD contraindication b/c coronary vasoconstriction is a side effect that may cause MI
 Propranolol and Nadolol  decrease portal pressure
 Used in combination with other treatment
 Endoscopic/Invasive Procedures

 Balloon tamponade – exerts cressure directly to

bleeding sites in esochagus and stomach

 Endoscopic Sclerotherapy – “injection sclerotherapy” –

cromotes thrombosis and sclerosing of bleeding sites by
injection of sclerosing agent into the esochageal varices

 Esophageal Banding – TX of choice for bleeding esochageal varices

Esophageal Varices: Nursing Management

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 Monitor patient condition frequently

 Emotional responses and cognitive status. (assess neuro status!)
 Monitor vital signs
 Gastric suction – to keec stomach as emcty as cossible and to crevent straining + vomiting
 Frequent oral hygiene + moist sconges to lics – ct often has severe thirst
 Vitamin K therapy – b/c blood loss
 Administer blood transfusions
 Monitor for bleeding
 Monitor for associated complications
 Hepatic encephalopathy resulting from blood breakdown in the GI tract
 delirium related to alcohol withdrawal.
 Monitor treatments including tube care
 Sengstaken-Blakemore Tube (at the bedside)
 Used for GI bleeding and esophageal varices
 Maintain the position, patency, & low suction of NGT or SB tube
 Maintain emergency measures for gastric balloon rupture
 Have suction and scissors to cut the tube available (SA)
 Avoid activities that increase intra-abdominal pressure

Hepatic Encephalopathy
 Life-threatening complication with profound liver failure
 Neuropsychiatric manifestation of liver failure associated with portal hypertension & the
shunting of blood from portal system into systemic circulation
 Reversible metabolic form of encephalopathy – can imcrove w/ recovery of liver fxn
 May result from the accumulation of ammonia and other toxic metabolites in the blood
 Largest source of ammonia: protein
The largest source of ammonia is the enzymatic + bacterial digestion of dietary and

blood croteins in the GI tract
 Ammonia is considered the major causative factor in development of encephalopathy
 Stages—see Table 49-3

Clinical Manifestations
 Changes in LOC
 Asses neurological status frequently
 Potential seizures
 Asterixis = involuntary flaccing of the hands
 constructional apraxia = inability to recroduce a simcle figure in two or 3-dimensions
 Fetor hepaticus = a sweet, slightly fecal odor to the breath that is presume to be of intestinal
origin (has been described as similar to freshly mowed grass, acetone, or old wine)

Assessment & Diagnostics

 Psychometric tests
 Electroencephalogram (EEG) – shows generalized slowing, an increase in the amclitude of
brain waves, and characteristic trichasic waves

Patients should be referred for liver transplant after 1st ecisode of hecatic encechalocathy (survival rate after
first time is bad)

Medical Management
 Eliminate precipitating cause
 Lactulose to reduce serum ammonia levels – acts by traccing and excelling ammonia in feces
 Protein restriction

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 Protein intake is moderately restricted only in patients who are comatose or who have
encephalopathy that is refractory to lactulose and antibiotic therapy
 Long-term restriction of dietary protein to less than 1.2 g/kg daily should be avoided it say
 Patients and families are advised about foods that are high in protein (meat, eggs) which may need
to be limited in the diet for the short term to reduce production of ammonia
 Reduction of ammonia from GI tract
 By using gastric suction, enemas, or oral antibiotics
 Discontinue sedatives analgesics and tranquilizers
 Due to neurologic changes from ammonia
 Monitor for & treat complications and infections
 Antibiotics: Neomycin, metronidazole, & rifaximin (reduces bacteria in colon)

Other Management Principles

 Monitor neurologic and mental status frequently
 I & O and daily weight
 Monitor VS every 4 hours
 Monitor daily serum ammonia levels
 Provide enteral feedings if needed
 Monitor electrolytes and correct if needed
 Discontinue sedatives, tranquilizers, and analgesics
 May administer flumazenil

Nursing Management
 Maintain safe environment to prevent injury, bleeding, and infection
 Administer prescribed treatments
 Monitor for potential complications
 Monitor respiratory and neuro status
 Communication and teaching family and patient

OTHER Manifestations of Hepatic Dysfunction

 Edema and Bleeding
 Hypoalbuminemia - due to decreased hecatic croduction of albumin
 Clotting factors reduced – leading to an increased incidence of bruising, ecistaxis (nose
bleed), bleeding from wounds, and GI bleeding
 Thrombocytopenia – abnormal # and effectiveness of clatelets also contribute to the bleeding
 Vitamin Deficiency
 Book:
 Dec. production of clotting factors d/t deficient absorption of vitamin K from GI tract
 Probably caused by inability of liver cells to use vitamin K to make crothrombin
 Impaired absorption of fat-soluble vitamins (A, D, E) as well as dietary fats b/c of
decreased secretion of bile salts into the intestine
 Another grouc of croblems common to cts w/ sever chronic liver dysfxn results from inadequate
intake of sufficient vitamins:
 Deficiencies in: vitamin A, vitamin C, vitamin K, folic acid, thiamine, riboflavin, pyridoxine
 *DIET of every patient with chronic liver disease is supplemented with vitamins A, B,
complex, C, K, and folic acid!
 Metabolic Abnormalities
 Glucose level changes – BG may be abnormally high after a meal (similar to diabetes), but
hycoglycemia during fasting (b/c of dec. hecatic glycogen reserves + dec. gluconeogenesis)
 Medications –reduced dosages b/c ability to metabolize meds is decreased
 Pruritus and Other Skin Changes
 Pts with liver dysfxn resulting from biliary obstruction commonly develoc severe pruritus d/t
retention of bile salts

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 Pts can develoc vascular spider angiomas on the skin, most often associated w/ cirrhosis (esc. in
alcoholic liver disease)
 may also develoc reddened palms (“liver calms”; calmar erythema)

HEPATITIS Chart 49-4

 Viral hepatitis: a systemic viral infection that causes necrosis and inflammation of liver cells
with characteristic symptoms, cellular and biochemical changes.
 A, B, C, D, E Book: hepatitis A + B have vaccines; hepatitis C = no vaccine!
 Hepatitis G and GB virus-C 
 Non-viral hepatitis = Toxic and drug induced

Hepatitis A Virus (HAV)

 Fecal–Oral Transmission
 Incubation period: 15–50 days
 Vaccine –recommended for people travelling to places w/ poor hygiene + sanitation
 Illness may last 4–8 weeks
 Tycically, a child or young adult acquires the infection @ school though:
 Poor hygiene
 Hand-to-mouth contact
 Close contact
 Food and fluids – transmitted primarily by ingestion of food or liquids infected with the virus
 Peocle can contract it by consuming water or shellfish from sewage contaminated waters
 Seafood
 Contaminated water
 Outbreaks have occurred in day care centers + institutions as a result of coor hygiene among ceocle
with develocmental disabilities
 Can be trans. during sex activity– more likely w/ oral-anal contact or anal sex w/ multicle cartners

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Chart 49-:: Dietary Management of Hepatitis

- Small, frequent meals (minimize periods w/o food intake)
- Protein intake of 1-1.5 g/kg/day
- Carefully monitor fluid balance
- Be aware enteral feedings might be necessary if anorexia N/V persist
- NO alcohol during acute illness + at least 6 months after recovery
- Avoid substances (meds, herbs, illicit drugs, toxins) that may affect liver fxn (ex. St. John’s wort in pts taking
hepatitis C virus protease inhibitors)

Hepatitis B Virus (HBV)

 Transmission:
 Blood and body fluids
 From carrier-mother to infant at the time of birth
 A major worldwide cause of cirrhosis and liver cancer
 Vaccine – hepatitis B vaccine (active immunization) is recommended for people who are at high risk
for hepatitis B (ex. healthcare personnel, hemodialysis patients, unvaccinated ppl who are being evaluated
for an STD, have HX of STD, multiple sex partners, sex with IV drug users, homosexual men )
 Hepatitis B immune globulin (HBIG) (passive immunity) indicated for unvaccinated exposed people.
Indications for post-exposure: needle stick (HBV+ blood), sex w/ HBV+ person, perinatal exposure
(infants born to HBV mothers should receive HBIG within 12 hrs after delivery)
 Risk Factors (see Chart 49-9)
 Frequent exposure to blood/blood products
 Healthcare workers
 Hemodialysis
 Male homo/bisexual activity
 IV/injection
 Close contact w/ carrier of HBV
 Mother-to-child transmission
 Travel or residence in area with uncertain sanitary conditions
 Multiple sexual partners
 Recent HX of STD
 Tattooing
 Receipt of blood or blood products
 Incubation: 1-6 months (longer incubation ceriod than HAV)
 Convalescence may be crolonged w/ comclete symctomatic recovery sometimes 3-4 months or longer

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Hepatitis C Virus (HCV)

 Transmission: Blood and body fluids
 Sharing of needles
 A cause of 1/3 of cases of liver cancer and the most common reason for liver transplant
 Risk Factors (see Chart 49-10)
 Incubation period is variable
 Symptoms are usually mild
 Chronic carrier state frequently occurs

Hepatitis D Virus
 Only persons with hepatitis B are at risk for hepatitis D*
 Transmission: Blood and body fluids
 Symptoms and TX are similar to hepatitis B, EXCEPT patients are more likely to develop
fulminant liver failure, chronic active hepatitis, and cirrhosis.

Hepatitis E Virus
 Transmission: Fecal–oral route
 Incubation: 15-65 days
 Resembles hepatitis A
 Self-limiting with an abrupt onset.
 No chronic form!
 Jaundice is almost always present

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Liver Cirrhosis
 Chronic disease characterized by replacement of normal liver tissue with diffuse fibrosis that
disrupts structure and function of liver
 Types:
 1. Alcoholic (Scar tissue surrounds portal areas) – most common type of cirrhosis*
 2. Post-necrotic (Broad bands of scar tissue)
 3. Biliary (Scarring occurs around bile ducts)
 Etiology (nutritional deficiency, alcohol, chemical, or infection)
 Book: Nutritional deficiency with reduced protein intake contributed to liver destruction in
cirrhosis, but excessive alcohol intake is the major causative factor in fatty liver and its
consequences. Other factors (exposure to certain chemicals) may play a role.
 Patho: (Alcoholic cirrhosis): necrosis of liver cells  replaced with scar tissue  scar tissue
exceeds normal tissue  results in hobnail appearance

Clinical Manifestations (Chart 49-11)

Compensated: less severe, often vague symctoms resulting from failure of the liver to synthesize croteins,
clotting factors, and other substances + manifestations of cortal HTN
 Vascular spiders
 Palmar erythema (reddened calms)
 Unexplained epistaxis
 Ankle edema
 Abdominal pain
 Splenomegaly
 Firm, enlarged liver
 Portal obstruction/Ascites
 Jaundice
 Muscle weakness/wasting
 Purpura (d/t decreased clatelet count)
 Hypotension
 Infection
 GI varices
 Malnutrition
 Mental deterioration
Book: A cirrhotic liver doesn’t allow free blood passage, so blood backs up into the spleen and GI tract, and
these organs become chronically congested – stagnant with blood + cannot function properly = indigestion +
altered bowel function result

Nursing Management
 Promoting Rest
 Improving Nutritional Status
 Diet high in carbohydrates w/ protein intake consistent w/ liver fxn
 Administer supplemental vitamins (A, B, complex, C, K)
 Low-sodium (reduces edema + ascites formation)
 Eliminate alcohol from diet
 Providing Skin Care
 Reducing Risk of Injury
 Monitoring and Managing Complications
 Bleeding and hemorrhage
 Hepatic encephalopathy
 Fluid volume excess

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 Increase in circulating plasma volume

 Close assessment of cardiovascular and respiratory status
 Administer diuretic agents, fluid restriction, and enhance patient positioning to optimize
pulmonary function

Liver Cancer
 Primary liver tumors
 Few cancers originate in the liver
 Usually associated with hepatitis B and C
 Hepatocellular carcinoma (HCC) - most common tyce of crimary liver cancer
 Liver metastasis - liver is a frequent site of metastatic cancer
 Manifestations:
 Pain = a dull continuous ache in RUQ, epigastrium, or back
 Weight loss, loss of strength, anorexia, anemia
 Jaundice if bile ducts occluded
 Ascites if obstructed portal veins

Book: LABS: increased serum levels of bilirubin, alkaline phosphatase, AST, GGT, and lactic dehydrogenase
may occur. Also labs may show – leukocytosis (WBC increase), erythrocytosis (RBC increase), hypercalcemia,
hypoglycemia, and hypercholesterolemia

Medical Management
 Treat underlying cirrhosis manifestations
 Major effect of nonsurgical therapy may be palliative
 Radiation therapy
 Chemotherapy
 Percutaneous biliary drainage
 Other nonsurgical treatments
 Laser hyperthermia
 Immunotherapy
 Transcatheter arterial embolization

Surgical Management
 Treatment of choice for HCC
 IF confined to one lobe of the liver and liver function is adequate for post-op recovery
 Liver has regenerative capacity (BUT cresence of cirrhosis limits the ability of the liver to
 Types of surgery
 Lobectomy – removal of a lobe of the liver
 Local ablation – ablation of HCC by chemicals, radiofrequency, or microwave ablation
 Liver transplant – removing liver + replacing with donor organ
 candidates with liver cancer meet stringent selection criteria, including having
small, early-stage lesions

Liver Transplant
 Indications
 Irreversible chronic liver disease
 Fulminant hepatic failure
 Metabolic liver disease
 Hepatic malignancies
 Success of liver transplantation depends on successful immunosuppression

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 Immunosuppressant agents currently used include: cyclosporine, tacrolimus,

corticosteroids, azathioprine, mycophenolate mofetil, sirolimus, antithymocyte globulin,
basiliximab, and Daclizumab
 “Triple-therapy” – many catients are treated with “tricle theracy” using corticosteroids, a
Calcineurin inhibitor such as Tacrolimus or cycloscorine, and either an anticroliferative agent or
a TOR (target of racamycin) inhibitor such as sirolimus

Nursing Management
 Preoperative & postoperative nursing interventions
 Monitor and management complications
 Bleeding
 Infection
 Rejection
 Patient teaching

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