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Stephanie Talbot

Diabetic Ketoacidosis- caused by lack of insulin in body causing severe hyperglycemia


Acute Complications: s/s: 1. Dehydration 2. Kussmals bx 3. Acetone breath 4. Glucose, ketones, protein in urine 5. Tachycardia ,hypotension 6. Weight loss and anorexia 7. Glucose>300mg/dL, pH<7.35, bicarb <15meq/L, BUN>20mg, creatinine >1.5 8. Hyperkalemia 9. Abdominal pain 10. N& V

Hyperglycemia increases serum osmolalitypolyuria

Treatment: 1. Maintain patent airway 2. O2 therapy 3. IV bolus insulin, then cont infusion 4. Fluid resuscitation 0.9% NaCl infusion 1L/hr until BP stable and blood glucose approaches 250 mg/dL 5% dextrose added to prevent hypogylcemia 5. Regular insulin via bolus then drip 0.1U/Kg/hr 6. Monitor K+- cause initially high but as add insulin, pushes K+ into cells resulting in vascular depletion K+

Hyperosmolar Hyperglycemic Syndromecharacterized by hyperglycemia, osmolar diuresis, and dehydration Acute Complications: S/S: 1. Dehydration 2. Tachycardia, hypotension 3. Hemiparesis 4. Somulance, decreased LOC 5. Hypernatremia & hypokalemia 6. Blood glucose>600mg/dL 7. Osmolality >330mOsm 8. Lactic acidosis, Azetemia (kidney), Lack ketones 9. Aplasia 10. E-lytes- hypernatremia, hypokalemia, hypochloremia, increased BUN, creatinine HCT & HgB

Treatment: -treat cause- infection,


stress, surgery, TPN, tube feeds or conditions like MI, sepsis, pancreatitis, stroke, drugs, like diuretics, glucocorticoids, Ca2+ channel blockers, propanolol

Maintain patent airway O2 therapy IV access Immediate Fluid resucitation 0.9%/.45% NaCl infusion 1L/hr until BP stable 5. Regular insulin via bolus, then by infusion 0.1U/Kg/hr. When glucose 250mg/dL dextrose added 6. Monitor VS, I/O, heart and elytes
1. 2. 3. 4.

EO 1.1: Define The Following Terms

Bradycardia:

Originates SA node Rate <60bpm

s/s:

Pale skin Cyanosis Dizziness or synchope Confusion Weakness SOB

Cause: hypothermia, sleeping, athlete, parasympathomimetic drugs, carotid artery massage, valsalva manoeuvre, increased intracranial pressures, alcohol intoxication. Treatment: Atropine Pacemaker

Ventricular Tachycardia:
3 or more PVCs Life threatening because of decreased

CO Deteriorates to V-fib cardiac arrest

Cause: fever, exercise, stress, heart dx stimulants Treatment: Administer prescribed meds: lidocaine, amiodarone, procainamide Cardioverson Defib if deteriorates to v-fib

Atrial Fibrillation

Ectopic foci cause atrium to have a rapid beat Rate 300-600bpm Ventricular rate 50180bpm No p wave- replaced by fibrillation waves Leads to stroke due to emboli

goal slow down ventricular rate

Cause: 1. Hypoxia 2. Mitral stenosis 3. Pericarditis 4. Hypertensive heart dx 5. HF 6. Cardiomyopathy 7. throxotoxicosis TX: Treat the cause Cardiac glycoside: Digoxin B- blocker: propanolol Ca2+ channel blocker: Verapamil Cardioversion: amiodarone, procainamide Coumadin (Warfarin) if cardioversion doesnt work

EO 1.1: Define The Following Terms

Ventricular Fibrillation:
3+ PVCs

Ventricles vibrating in a

chaotic manner. No effective contraction or C.O

Cause: 1. Acute MI 2. Hyperkalemia 3. Hypoxia 4. CAD: MI, cardiomyopathy 5. Acidosis 6. Drug toxicity TX: CPR, ACLS, countershock (defibrillator)

Premature Ventricular Contraction


Ventricle contracts before the atria due

to increased ventricular irritability P waves are lost in QRS complex Wide, bizzar QRS complex Can lead to ventricular tachycardia Not strong enough to generate a pulse

Cause: 1. E-lyte imbalance 2. Hypokalemia 3. Digoxin toxicity 4. hypoxia 5. Stimulants 6. exercise TX: treat the cause 1. Na+ channel blockers: lidocaine, procainamide, amiodarone 2. B-blockers

CAD-Disease of the blood vessels


s/s:

Chest pain 2. SOB, Dypnea, weakness 3. Diaphoresis, increased temp 4. Palpitations & dysrhythmias 5. Tachycardia & tachypnea 6. EKG: elevated/depressed ST segment, inverted T wave, new Q wave 7. Increased heart enzymes 8. Hyperlipidemia 9. Increased homocystene levels 10. Increased c-reactive protein levels 11. Decreased/absent pulses 12. S3/s4 heart sounds 13. Denial symptoms, anxiety, fear
1.

Cause: ATHLEROSCLEROSIS TX: 1. Manage risk factors 2. Acute manifestations:

EKG, O2, IV, nitroglycerin, morphine, aspirin, heparin, bblockers, ace inhibitor

3. ECG 4. PCI CABG 5. Rest 6. Monitor v.s and level fatigue 7. If dysrhythmias occur-assess BP,

pulses, LOC, chest pain 8. Assess heart failure

Chronic stable angina- chest pain that occurs intermittently over a long period of time

Cause: ischemia due to narrowed arteries

s/s: Choking, burning heavy sensation Substernal, radiates arm, jaw, shoulders Last 5-15min Provoked by exertion ECG=ST depression=ischemia

TX: sublingual nitroglycerin, aspirin, antiplatelet therapy, ACE inhibitor, b-blocker, smoking cessation, diet, control diabetes, exercise.

Acute coronary syndrome (ACS)encompasses UA, NSTEMI, STEMIs/s:


1. 2.

Unstable angina- occurs at rest, sleep, or worseningEMERGENCY Myocardial infarction-result of sustained ischemia necrosis due to halted perfusion
1. 2.

3. 4. 5. 6.

7.
8.

Pain not relieved by rest, position change or nitro SOB, weakness, pulmonary edema, dizziness, dysrhythmias Increased glucose, BP, HR Ashen, clammy skin Abn heart sounds Nausea & vomiting Fever Bibasilar crackles, sings rsided heart failure

Cause: rupture of athlerosclerotic plaque TX: ACS: 12 lead EKG, O2, IV access, Nitro, morphine, aspirin, heparin, beta blocker, ace inhib.

STEMI and NSTEMI


NSTEMI:

Drug therapy: nitro, low molecular weight heparin, antiplatelet (plavix), glycoprotein IIb/IIIa; 2. Coronary revascularization: PCI
1.

STEMI: immediate reperfusion therapy 1. PCI 2. Fibrinolytic therapy w/ streptokinase, alTplase 3. Emergent CABG

Defn: Diabetes Mellitus: abnormal insulin production, impaired insulin utilization, or both (type I/II).
Diagnostic tests: 1. Fasting glucose 126mg/dL 2. Random/casual plasma glucose level 200mg/dL 3. OGTT 200mg/dL w/ 75mg glucose load 4. A1C (glycosylated hemoglobin ), lipid profile, BUN, creatinine, elytes, TSH, 5. Urinalysis for ketones & glucose NSG: 1. Drug therapy: Insulin, Oral agents 2. Nutrition therapy 3. Exercise 4. Teach self- monitoring 5. transplant

S/S: Type 1:Chronic hyperglycemia, Polydipsia, Polyuria, Polyphagia, Weight loss, Weakness, Fatigue Type 2: fatigue, recurrent infections, prolonged wound healing, & visual changes

Definition: Head & Neck Cancer-squamous cell carcinoma arising from the mucus membranes: affects larynx, throat, trachea, tongue, salivary & parotid glands. Diagnostics: 1. CBC, PT, PTT, INR, urinalysis, renal & liver fxn tests, protein & albumin levels 2. X-ray of skull, neck, chest & sinuses 3. CT-head & neck, MRI, PET 4. Bone, brain & liver scan 5. Direct/indirect laryngoscopy 6. Panendoscopy 7. Biopsy NSG: radiation therapy, chemotherapy, targeted therapy, surgery, pre/postop care, teach about surgery, self-care airway, methods communication, sxn, pain control, critical care environment

Signs/symptoms: 1. Persistent sore throat or otalgia 2. Change voice quality, hoarseness, feeling of lump in throat 3. Oral leukoplakia or erythroplakia 4. Pain, dysphagia, decreased mobility tongue, cranial neuropathies, & airway obstruction 5. Weight loss 6. Lumps on head & neck 7. Laryngeal abnormalities

Defn: an inflammatory process characterized by an excess of fluid in the lungs


Diagnostics: 1. Presence s/s 2. +ive C&S 3. Chest x-ray 4. Gram +ive sputum &blood stain 5. ABG & pulse-ox: decreased PaO2/SaO2 6. CBC w/ WBC- leukocytosis w/ band neutrophils NSG: 1. Admin antiinfectives 2. Supportive therapy: O2, analgesics, 3L fluid, bronchodilators & corticosteroids, 3. Monitor for hypoxemia, resp. Failure, atelectasis, pleural effusion, & pleurisy.

Signs/symptoms: 1. Sudden onset fever, chills, productive cough 2. Dyspnea, cyanosis, Pleuratic chest pain 3. Foul smelling sputum 4. Tachycardia, hypotension, fatigue 5. Anxiety & confussion, Change LOC & dehydration in elderly 6. Dullness to percussion, Bronchial BS, Wheezes & crackles 7. Flushed cheeks, resp. Grunting, nasal flaring 8. Decreased SaO2 & PaO2

Defn: destruction & cavity formation of lung tissue caused by mycobacterium tuberculosis.
Diagnostics: 1. Presence s/s 2. +ive acid-fast bacillus test, PPD or quantiferron TB gold test 3. +ive C&S 4. Chest x-ray NSG: 1. Combination therapy 2. Care hospitalized pt: use airborne precautions, teach about drugs, resistant strains TB, infection control, health & general care issues.

Signs/symptoms: 1. Persistent cough 2. Night sweats 3. Weight loss & anorexia 4. Dyspnea, hemoptysis, malaise & fatigue 5. Fever & chills 6. Dullness w;/ percussion 7. Bronchial BS 8. Crackles & wheezes 9. Enlarged lymph nodes

Lung caner
Diagnostics: 1.Chest x-ray, CT scan, MRI, PET 3.Thoracoscopy & thoracentesis 4.Sputum culture 5.Fiberoptic bronchoscopy & biopsy NSG & Collaborative: 1.Chemotherapy,Radiation therapy, Targeted therapy, Photodynamic therapy 3.Surgery 4.Pre & post-op care 5.Teach about procedure 6.Apply closed chest drainage 7.Drug therapy 8.Thoracentesis & pleurodesis 9.Pain management 10.Refer to hospice (terminal) 11.Refer family to American cancer society

Signs/Symptoms: Persistent Pneumonitis Persistent cough Anorexia Weight loss Nausea & vomiting Fatigue Hoarseness Unilateral diaphram paralysis Chest pain

Defn: reversible & intermittent airway obstruction due to chronic inflammation


Diagnostics: 1.Increased IgE, increased eosinophil count, Cushmans spirals in sputum 2.Decreased pulmonary fxn test results: FVC, FEV, PEF 3.Increased AP chest diameter on chest x-ray 4.Decreased/absent BS, ABG: respiratory acidosis NSG & Collaborative: 1.Education:s/s, asthma diary 2.drug therapy 3.regular exercise- strengthen muscles 4.supplemental O2 5.heliox therapy (O2 & helium)

Signs/Symptoms: Increased RR Change LOC Respiratory acidosis Cyanotic mucous membranes Decreased BS Increased AP chest diameter Increased intercostals space Increased expiratory phase Use of accessory muscles Pursed lipped bx Tachycardia Wheezes Inability to complete sentence

Defn: irreversible chronic lung dx: Emphysema & chronic bronchitis


Diagnostics: Chest x-ray NSG & Collaborative: 1.maintain patent airway 2.check respiratory status q2 3.teach coughing & deep bx 4.administration O2 as prescribed 5.administer drug therapy as prescribed 6.pulmonary rehab to improve fxn 7 endurance 7.teach need exercise to prevent muscle de-conditioning 8.lung transplant for those w/ endstage COPD 9.lung reduction surgery 10.pre & post op care

Signs/Symptoms: Rapid, shallow, paradoxical respirations Chest retraction Dyspnea Wheezes Hyperressonant on percussion Tachycardia Peripheral edema Decreased cap. Refill Clubbing of fingers Cyanosis of mucous membranes & nail beds Polycythemia Weight loss anorexia

Labs
Whole Blood:Plasma-55% blood volume, Blood cells-45% blood volume
Erythrocytes-4-5million/uL, lives 120dys 2. Thrombocytes-150,000-400,000uL, lives 5-9dys 3. WBC=4000-10000/mm Granulocyte
1.

Neutrophils-50-70%-acute inflammatory response Eosinophil-1-2%-antigen-antibody Basophil-0-2%-allergic rx Lymphocyte- B & T cell20-40% Monocyte-4-8%, Macrophage

Agranulocyte

ESR measures sedimentation rate RBCs in 1hr. Increase=acute/chronic inflammatory rx, malignacy, MI, & endstage renal dx 2. D-Dimer- measures fragment of fibrin that is formed as result fibrin degrdation & clot lysis N<250mcg/L
1.

Labs
Whole Blood:

1. Hgb- w=12-16g/dL, M=13.5-18g/dL 2. HCT- W=38-47%, M=40-54% 3. Red cell indices:


MCV=82-98, low=microcytosis, high=macrocytosis MCH =27-33%, same as MCV MCHC=32-36% low=hypochromia,

high=spherocytosis 4. Pt=12-15 sec, aPTT=30-45sec, INR <1

Labs
3. Iron Studies:

4.

Serum iron- measures tot. Amt. Protein bound Fe circulating N=50-150mcg/dL Total iron-binding capacity (TIBC)- all proteins that act to bind/transport between tissues & bone marrow N=250-410mcg/dL Serum ferritin- iron storage protein N=10-300mcg/L Transferrin saturation-binds to iron. Increases in those w/ deficiency anemia N=215380mg/dL Best indicator of availability of iron

5. 6. 7.

Sickle cell test- exposes cells to deoxygenating agent Blood typing & Rh factor Bone Marrow & lymph node biopsy Schillings test (urine) N=10-40%

Summary
The hematological system consists of : 1. Blood-transports O2/CO2, wastes, & nutrients to and from the cells, maintain e-lyte & acid-base balance as well as protection from foreign invaders 2. Lymphatic system- carries fluid from interstitial spaces to the blood via subclavian veins as well as filters pathogens & foreign particles 3. Liver-filters, production procoagulants & hepcidin (regulates Fe3+ balance) 4. Spleen-storage of lymphocytes, monocytes, immunoglobins, RBCs & platelets. Also produces RBCs in the fetus & removes old & defective RBCs & recycles iron.

Summary
There are two types of bone marrow:
1. 2.

Red- active site blood production Yellow- fat storage

Red marrow is found in the flat & long bones of the body ex. Pelvic bones, flat bones of skull, ends long bones, scapula, sacrum, sternum, ribs & vertebrae. RBCs, WBCs & platelets arise from hematopoietic stem cell (erythropoietin causes differentiation).

Phases of Hemostasis
Vascular response
Platelet plug

Plasma clotting factors

Lysis of clot

Phases Hemostasis
1.
2.

3.

4.

Vascular response- upon injury immediate vasoconstriction occurs (20-30min), allowing platelets & clotting factors to be activated (activated injury & release factors like tissue factor). Platelet plug when activated, platelets release platelet factor 3, serotonin & adenosine diphosphate to enhance coagulation, adhesion (stickiness) & aggregation (clumping). Plasma clotting factors plasma clotting factors are stimulated via the intrinsic pathway by exposure to collagen due to endothial cell injury or via the extrinsic pathway due to exposure to tissue factor/tissue thromboplastin release from the tissues. These all lead to thrombin converting fibrinogen to fibrin. Lysis of the clot- the anticoagulation and fibrinolysis of the clot to limit its size or eliminate it. In anticoagulation , antithrombins like endogenous heparin & protein C& S are released. In fibrinolysis the clot is attacked when plasminogen is converted to plasmin (plasmin attacks and breaks fibrin into small pcs).

Hematological Points of interest


The clotting process is

partially regulated by throbopoeitin Hypoxia stimulates release of erythropoeitin from the kidneys To evaluate rate & adequacey of erythrocyte production, do a reticulocyte count Iron is stored as either ferritin or hemosiderin in the bone marrow, spleen, liver & macrophages

The degree to which

transferrin saturated with Fe3+ indicates Fe3+ supply for developing RBCs Plasmin attacks either fibrin or fibrinogen by splitting the molecules into smaller elements- fibrin split products (FSP) or fibrin degradation products (FDP). Increased FSP leads to impaired platelet aggregation, reduced prothrombin & inability to stabilize fibrin

Hematological Points of interest


The most essential enzyme Pts cannot use diet to correct

for clotting is thrombin, which converts fibrinogen to fibrin Hgb levels are used to determine the severity of anemia Iron should be given deep IM in upper quadrant of buttocks, w/ 2-3inch, 1920gauge needle using Z-track method. DO not massage site.

cobalamin related anemia because they lack intrinsic factor Puritis occurs due to increased serum & skin bile salts Iv dextran should not be mixed, give undiluted rate 1mL/min, then flush with NS Hepsidin is produced by the liver and is stimulated by iron overload or inflammation

Hematological Points of interest


Superficial lymph nodes If a patient is

can be evaluated by light palpation...deep cant be felt in adult Normal nodes are mobile, firm, and nontender to be considered a normal finding.

thrombocytopenic, pressure may be required for 5-10min or longer Cover the needle aspiration site with sterile pressure dressing

Hematological Points of interest


Coagulation factor: I. Fibrinogen II. Prothrombin III. Throboplastin IV. Calcium Blood types: A, B, AB, O Named for the antigen attached to the cell membrane. Has the opposite antibody ex. Type A has antibody B, type AB has neither, type O has both

Hematological Points of interest


Classification & etiology anemias: 1. Normocytic, normochromic- acute blood loss, hemolysis, chronic kidney dx, aplastic anemia, sickle cell anemia, pregnancy 2. Macrocytic, normochromic- cobalamin & folic acid deficiency, liver dx, postsplenectomy 3. Microlytic, hypochromic (sm & pale colour)-irondeficient anemia

Altered Hematological fxn


Aplastic anemia
Characterized by pancytopenia

Hodgkins Dx
Malignant condition

(decreased production ALL blood cells) Tx: 1. Erythropoeitin 2. Blood transfusion Polycythemia: increased production RBC Tx: phlebotomy, hydration, myelosuppressive agent ex. hydroxyurea

characterized by the proliferation of giant & abnormal multinuclear cells called REED-STERNBERG cells in lymph nodes resulting in enlarged lymph nodes, spleen, & lymph tissue Tx: 1. chemotherapy

Pernicious Anemia- Vit


B12 deficiency resulting in production of large, immature, dysfxnl RBSs (Megoblastic)
Cause: 1. Cobalamin deficiency 2. Absence intrinsic factor 3. Decreased HCL secretion S/S:
1. 2. 3. 4. 5. 6.

1. Teach pts that they are not able ingest cobalamin from diet

7.
8.

s/s hypoxia Sore tongue, red, swollen , smooth, beefy, glossitis Anorexia, weight loss N&V, abdominal pain Weakness & fatigue Parasthesia of feet & hands Balance & gait disturbance Impaired thought process

2. Drug therapy: Parentral cycanobalamin or hydrocolobalamin Itnranasal (Nascobal) 100mg cobalamin IM qd 2wks, then weekly until HCT normal, then monthly for life 3. Encourage rest when needed

Iron Deficiency Anemiabelow normal total body iron & inadequate Hgb production
Cause: 1. Inadequate dietary intake 2. Malabsorption Fe3+ due to gastronomy, severe diarrhea, removal/bipass duodenum 3. Blood loss- PUD, gastritis, esophagitis, hemorrhoids, neoplasia 4. hemolysis S/S: 1. Pallor, fatigue, bone pain 2. Headache, restlessness, dizziness, slowing thought process, irritability, depression, vertigo 3. Tafchycardi, palpitations, angina, HF 4. Cold intolerance 5. Tachypnea, orthopnea, dyspnea 6. Anorexia, hepato/splenomegaly, dysphagia

1. Teach pts increase Fe3+ rich foods 2. Oral or parentral Fe3 3.

4.
5.

6.

suppliments For acute blood losstransfusion packed RBCs Teach Fe3+ colours stool black Monitor Hgb & RBC Teach cont take suppliment 2-3mths after HgB normal

Sickle cell anemia- an inherited disorder characterized by abnormal Hgb called Hgb-S. Cause: deprivation O2cell flattens and elongates
1.

2. 3.

4.

5.

6.

Instruct pt measures to prevent crisis ex. Avoid infections, dehydration, strenuous physical activity, emotional stress, tight clothing, & high altitudes Administer folic acid if indicated Provide support & family teaching- rev. Genetic implications & coping skills Manage priapism-instruct empty bladder @ onset attach, exercise & take warm bath. If persist >4hrs notify provider Inform experimental meds being evaluated-hydroxyurea, cetiedil citrate, pentoxifylline, & food additive vanilla Administer meds, OTC, opiods, increase oral/IV intake fluids, monito I/O, use small gauge needles, administer blood transufsion, encourage rest

S/S: 1. Jaundice 2. Enlarged skull & facial bones 3. Increased suscep. To infection esp. Osteomyelitis & pneumonia 4. Spleno/ hepato/cardiomegaly, gallstones 5. Tachycardia, flow murmurs 6. Thrombosis/hemorrhage causing paralysis, sensory deficits, death, retinal detachment, blindness, retinopathy 7. Acute chest syndrome, pulmonary HTN, pneumonia 8. Renal failure, hematuria 9. Hand-foot syndrome, osteonecrosis 10. Priapism 11. Stasis ulcers of hands, ankles, feet.

Sickle Cell Crisis


Occurs when experiencing deprivation of O2, result=

sickeling of cells increases viscosity blood stasis w/ enlargement & engorgement of organs, infarction w/ischemia & destruction RBCs

Summary: Urinary System


The urinary system consists of the 2 kidneys & ureters, and an urethra. The kidneys function to excrete waste, maintain the volume and composition of extracellular fluid, maintain acid-base balance and blood pressure, secrete erythropoietin & activate vitamin D. The kidney is surrounded by a membranous sac called the capsule. The tissue of the kidney is termed the parynchema and is divided into the cortex (outer layer) & medulla (inner layer). The medulla contains pyramids, whose apices are called papillae.

Summary: Urinary System


The hilus is the entry & exit point of all the renal veins, arteries and nerves. The renal papillae are connected to the minor & major calyces which drain into the renal pelvis (holds 3-5mL urine) ureters bladder outside of body.

Urinary System
A. Kidney- removal of waste, acid-base balance, control

BP, produce erythropoietin, activate vit. D


1.

Nephron- fxnl unit kidney


Glomerulus-blood is filtered, GFR=125ml/min Bowmans capsule Proximal convouted tube-reasorption80% H2O & e-lytess, all glucose & a.a, HCO3; secretes H+ & creatinine Loop of henle-reasorption Na, Cl & H2O Distal convuluting tube-secretion K+, H=, ammonia

Summary: Urinary System


, reabsorption H2O, bicarb, regulate Ca2+ & PO4Collecting duct- reabsorption water (ADH required)

2. 3.

4.
5. 6.

Renal artery & veins- 1200mL/min perfuse the kidneys Ureters- carry urine from kidneys to bladder Bladder- fxns store urine & help eliminate waste Urethra- conduit urine removal to outside body Urethralvesical unit0 bladder, urethra & pelvic floor

Urinary System & Aging


Decrease amt renal tissueless palpable 2. Decrease # nephrons, vessels, thickened basement membrane of bowmans capsuledecreased creatinine clearance, increased BUN, increased serum creatinine 3. Decreased fxn loop henle & tubles-alteration drug excretion, decreased ability concentrate urine 4. Decreased elasticity & muscle tone-palpable badder after urination
1.

Urinary System & Aging


5. Weakening of urinary sphincter- stress incontinence
6. Decreased capacity & sensor y receptors- frequency,

urgency, nocturia, overflow incontinence 7. Increased prevalence unstable bladder contractionsoveractive bladder 8. Prostetic enlargement- hesitancy, frequency, urgency, nocturia, retention

Urinary System
Azotemia- an

accumulation of nitrous waste products Glomerular filtration rateN-39-90mu/min, calculation of the rate of glomerular filtration Iterstitial cystitis- chronic & painful inflammation of bladder Uremic frost- deposits of urea crystals on the skin of one who has severely impaired kidneys

Nephrotic syndrom- the

massive loss fo protein in the urine due to increased glomerular permeability leading to decrease in oncotic pressure & edema Renal colic- intenser intermittent pain resulting from renal calculi in the kidney or uriter. Begins kideny radiates to abdomen, genitals & legs

Urinary System: Labs


1.

Creatine clearance- approximates GFR N=85135mL/min; evaluates glomerular filtration rate, levels increased as renal fxn diminishes
NSG: Collect 24hr urine specimen Discard 1st and collect rest 24hrs

2. Urine culture & sensitivity-clean catch/midstream,

confirms UTI & organism


<10,000 organisms=no infection; >100,000=infection NSG: sterile container, touch outside, clean genitals, start urinating, then in container

Urinary System
3. BUN- I.Ds renal problems. Concentration urea in

blood regulated by rate @ which kidney excretes urea N=10-30mg/dL


NSG: explain procedure, watch post puncture bleeding

4. Creatinine- more reliable for renal fxn N=0.5-

1.5mg/dL 5. Intavenous pyelogram (IVP)- xray of urinary tract after injection contrast material
NSG: assess labs, report BUN>40mg/dLcathartic enema before, NPO 8hrs, assess iodine allergy, metalic taste, after procedure force fluids to flush material

Urinary System
6.

Renal angiogram- to visualize renal vesselsdx arterial stenosis


NSG: cathartic enema before, check iodine allergy, notify warm & flush w/ contrast, after procedure place pressure dressing over femoral artery injection site, observe bleeding, maintain bed rest w/ affected leg straight, check peripheral pulses q30-60min, observe complications

7.

8.

Cystogram- visualize bladder & eval. Vesicoureteral reflux Renal scan- eval anatomical structures, perfusion, fxn kidney
NSG: inform pt no pain/discomfort should be felt

Urinary System
9.

Renal biopsy- det type renal dx or follow progress

NSG: type & cross-match, informed consent, pt hx coag, status, meds, CBC etc, after apply pressure dressing & keep on affected side 30-60min, bed rest 24hrs, VS q5-10min 1st hr, assess flank pain, hypotension, decreased HCTm increased temp, chills, urinary frequency, dysuria, & serial urine specimens, check blood urine, avoid lifting heavy objects 57dys 10. Glomerular filtration rate=amt. Blood filtered by

glomerulus N=125mL/min 11. Urinalysis- provides info kidney fxn note colour, opacity, odour, sp.gr, osmolality, pH, as well as presence glucose, ketones, proteins, RBCs

UTI- infection of the bladder, e. Coli most common organism


Upper UTI involves renal parynchema, pelvis & ureter s/s: fever, chills, flank pain, malaise Lower UTI 1. Weak urinary stream 2. hesitancy 3. Intermitancy- interuption while voiding 4. renetion or incomplete emptying 5. Dysuria 6. Pain on urination 7. Urinary frequency- increased 8. Urgency- increased 9. Incontinence 10. Nocturia 11. Nocturnal enuresis-loss urine during sleep

Labs: 1. Urinalysis- i.d presence nitrate (indicates bacteremia), WBC, & leukocyte esterase (indicates presence WBC) 2. Culture & sensitivity- clean catch, refrigerate on collection & culture w/in 24hrs 3. Intravenous pyelogram or CT when urinary obstruction suspected
INT:
1.

2.
3. 4. 5.

6.

Antimicrobial therapy- trimethoprim sulfamethoxazole (TMP-SMX), Fluroquinolones, OTC agents Provide pain relief- heat to perenium, encourage hot bath Promote measures to prevent infection Promote measures to maintain fluid & elyte balance Provide client & family teaching- empty bladder regularly & completely, evacuating the bowel regularly, wiping from front to back, drink adequate fluids daily Promote client & family coping

s/s: Polynephritis- inflammation of 1. mild fatigue, Sudden onset chills, the renal parychema & fever, vomiting, malaise, flank pain collecting system & costovertebral tenderness on Cause: affected side Infection of lower urinary tract by 2. Dysuria, Urinary urgency, Urinary way of ascending urethral rout e.coli frequency vesicoureteral reflux (backward
movement from lower to upper urinary tract), dysfxn lower urinary tract fxn- ex. Obstruction from benighn prostetic hyperplasia or urinary stone Long-term catherization Acute pyelonephritis leads chronic pyelonephritis which can progress to end-stage renal dx when both kidneys involved LABS: uranalysis, culture &sensitivity, gram stain, CBC, IVP, & CT

INT:
1. 2.

3.
4.

Administer oral/parentral antibiotics Teach need cont meds as prescribed &need for follow-up urine culture, encourage drink 3L fluid daily, rest to increase pt comfort, prophylaxis w/low dose antibiotics for those recurrent infections Maintain sufficient perfusion to kidneys to protect from injury Surgery: pyelolithotomy, nephrectomy, uretral diversion or reimplantation

Nephrolithiasis (renal calculi) calculi in the kidney


Cause: 1. Slow urine flow saturation with Ca2+ which crystalizes & becomes stone 2. Damage lining of urinary tract from crystal 3. Decreased inhibitor substance in urine to prevent crystallization 4. High urine acidity or alkalinity & drugs s/s:
1. 2. 3. 4. 5. 6. 7.

Renal colic (severe pain) N&V Heamturia, oliguria, anuria Flank pain Uretral spasm or colic Increased turbididty & odour urine Bladder distension, diaphoresis, pale ashen skin

INT: 1. Drug therapy: opiods, NSAIDS ex. Ketorolac, spasmolytic agents ex. Oxybutylnin chloride 2. Asses response drug therapy 3. Encourage ambulation & upright position to drain renal calyx & pass renal calculi 4. Assis pt comfortable position & use relaxation techniques 5. Lithotripsy or extracorporeal shock wave lithotripsy 6. Surgery: Stone removal via nephrolithotomy: post op- assess urine q 1-2hrs for 24hrs, strain pts urine, monitor for infection: obtain C&S, administer antibiotics, ensure nurtition& fluids 7. Administer drug therapy & assess adverse rx: broad spectrum antibiotics ex. Aminoglycosised & cephalosporines, acetohydroxamic acid (Lithostat) & hydroxyurea (hydrea) for those w/ struvite stones, thiazide diuretics tx hypercalciuria, allopuinol(Zyloprim)-tx hyperoxaluria or gout, alpha-mercaptopropionyl glycine (AMPG) & captopril (capotea) tx cystinure.

Bladder cancer- malignant tumours of the urotheluim in the kidney, renal pelvis, ureters, urinary bladder, & urethra (arise form transitional cells) Cause: Tobacco use, exposure chemicals, Schistosoma haematobium infection, excessive use drugs containing phenacetin, long-term use cyclophosphamide (lytoxan, procytox) s/s: 1. Gross, painless hematurea (RBC, WBC) 2. Bladder irritability w. Dysuria, frequency & urgency 3. Oliguria 4. Sp.gr=1.010, osmolality 300,Osm/KG 5. Fluid retention- distended neck veins, bounding pulse, edema, HTN, metabolic acidosis, altered K+, Na+, anemia, Ca2+ deficiency, neurologic changes 6. +ive cytoscopy & biopsy

INT: Non-surgical: 1. Prophylactic immunotherapy w/ intravesical instillation of bacille calmette guerin (BCG) to prevent recurrance of superficial bladder cancers 2. Multiagent chemotherapy 3. Radiation therapy Surgical: 1. Transurethral resection of bladder tumor or partial cystectomy 2. Complete cystectomy w/ ureter diversion into an ileal conduite (internal pouch), continent pouch, bladder reconstructed- neopbladder (constructed from bowel) & ureterosigmoidostomy- ureters placed in constructed segment sigmoid colon. *ureterostomy- ureters placed on skin surface as one /two stomas that drain urine into an external pouching system 3. Pre-op care 4. Post-op care: check UOP, assess wound & drainage, irrigation & intermittent catheterization of neobladder, teach pt cues to void that have neobladder,

Acute renal failureCause: 1. Pre-renal azotremia 2. Post renal obstruction 3. Intrarenal acute failure s/s: 1. Altered UOP (oliguria, anuria, polyuria) 2. HTN/hypotension 3. Tachypnea 4. s/ sfluid overload or dehydration 5. Uranalysis: pre-renal azotemia >900mOsm/Kg, post-renal =N, intra-renal failure <250mOsm/Kg 6. Urine sodium: pre-renal azotemia <20meq/L, postb=obstruction=N, intra-renal failure>27meq/L 7. Blood analysis: Increased BUN, serum creatinine K+, decreased pH, bicarb, Hb, HCT

INT: goal eliminate cause, tx s/s 1. Administer prescribed meds 2. Manage underlying problem 3. Monitor K+, restrict dietary K+, monitor heart, prepare administer insulin & glucose (drives K+ back into cell) 4. Assess fluid balance, restrict intake to 24hr output plus 500mL 5. Monitor for acidosis, administer alkalinizing agents, monitor ABG, prepare institute vent measures 6. Prevent infection: assess infection, do not leave catheter in place, admin. Prophylactic antibiotics, monitor: hyperphosphatemia, serum phosphate levels , admin phosphate binding agent 7. Instruct client restrict Na+ intake, drink fluids & follow low phosphate diet 8. Monitor hypercalcemia, admin Ca2+ suppliments, 9. Prevent GI bleed by administering histamine receptor antagonist & proton pump inhibitor 10. Promote comfort & bed rest 11. Provide high cal, low protein diet 12. If indicated prepare for dialysis to correct hyperkalemia, fluid overload, acidosis, or severe, uremia

INT: 1. Administer meds Chronic renal failure2. Maintain strict fluid control, I/O, daily result of irreversible loss of weights, encourage high calorie, low protein diet w/ low sodium, potassium, fxnal renal tissue activity & rest s/s: 1. decreased renal reserve, 3. Peritoneal dialysis if indicated- monitor renal insufficiency-polyuria, s/s peritonitis nocturia, s/s mild anemia 2. Endstage: edema, HF, e-lyte 4. Prepare hemodyalysis if indicatedimbalance, HTN, provide shunt care, assess complications tamponade, pericarditis, effusion, arrythmias, (bleeding, hypovolemia, hypotension, anorexia, N&V, stomatitis, dialysis, disequillibrium sydromeuremic halitosis, gastritis & bleeding, diarrhea, headache, confusion, seizures. constipation, pallor, 5. Prepare client transport- provide post-op jaundice, dryness, confusion, uremic frost, drowsiness, care, monitor s/s complications ex. Graft confusion, coma tremors, rejection, increased WBC, e-lyte twitching disturbance, abn renogram & infection stemming from immunosupressive LabsDx: anemia, increased BUN & therapy creatinine, P3+, decreased 6. Provide referral Ca2+, serum protein, pH

Prosthetic hypertrophy- enlarged prostate resulting in increased # epithilial cells & stromal tissue, causes bladder outlet obstruction, aging & endocrine changes
s/s:
1.

INT: 1. Watchful observation w. Yrly exam 2. Drug therapy:


a) b)

Urinary retention, difficulty voiding, dribbling @ end urination, urinary frequency, urgency, dysuria, bladder pain, nocturia, incontinence

Those decrease dihydrotestosterone (DHT) levels: finasteride (Proscar), utasteride (Avodart) Alpha-blocking agent that decrease urethral pressure & improve flow: Tamsulosin (Flomex), Alfuzosin (Uroxatral), Doxazosin (cardura), Terazosin (Hytrin)

3. 4. 5.

Labs/Dx: Physical exam- digital rectal exam (DRE) for prostate size, symmetry & consistency Urinalysis w/ C&S Post-void residual urine volume to assess degree of urine flow obstruction Prosthetic specific antigen (PSA) to rule our cancer RBC & WBC in urine

6. 7.

Release prostetic fluide w/ frequent sex Teach avoid bladder distension: avoid drinking large amts fluid, alcohol, diuretics & caffine, void as soon as possible, avoid drugs causing retention Minimally invasice-techniques: transurethral neddle abilation to shrink prostate (TUNA), transurethral microwave therapy (TUMT) to destroy excess tissue, interstitial laza coagulation, placement prostetic stent into urethra Surgery: transurethral transection of prostate (TURP) cuts prostate into pcs & removes via urethra Holmium laser enucleation of prostate (HoLEP) & transurethral ultrasound guided laser incision of the prostate (TULIP)

Prostate hypertrophy INT cont,


Provide pre-op care: assess anxiety, inform will have indwelling catheter for 24hrs, instruct will make him feel he has to void, inform there will be blood in urine after surgery 9. Post-op care: monitor UOP 2hrs, vs q4hrs, maintain traction on 3 way urinary catheter, monitor Hgb & HCT, remind pt not to try to void around the catheter 10. Administer antispasmotics
8. 11. Perform CBI w/saline 12. keep catheter free of

13. 14. 15.


16.

obstruction monitor UOP Instruct increase fluids Observe complications TURD Teach pt that sexual fxn should not be affected after TURP but that retrograde ejaculation is possible

Prostetic cancer- most adenocarcinomas,


s/s:
1.

2.

Dysuria hesitancy, dribbling, frequency, urgency, hematuriasm nocturia, retention Pain lumbosacral area radiating down hips or leg

Lab & DX: 1. Digital rectal exam (DRE) 2. Increase levels comlexed prostatespecific antigen (cPSA>3.4ng/mL 3. Icnrease serum acid phosphtase 4. Transrectal ultrasound (TRUS) of prostate 5. Prostate tissue biopsy 6. Lymph node biopsy 7. CT & MRI

INT: 1. Watchful waitin w/ PSA & DREs to monitor progress 2. Surgery for those w/ stage AB: radical prostectomy- TURP to promote urination, bilateral orchiectomy(removal testicles) to slow spread cancer by removing source testosterone, laparoscopic radical prostatectomy (LRP) for those w/ PSA<10ng/mL, tranditional open radical prostatectomy

Prostate cancer interventions cont:


3.

Pre-op care: teach about location incision, indwelling catheter, placement drains, & poss temporary erectile dysfxn, encourage express fears, reinforce surgeons explanation

4.

Post-op care:-encourage use PCA as needed, assist getting out of bed & in chair night surgery & ambulate next day, use compression stockings till ambulate, monitor DVT & PE, I/O, clean urinary meatus, avoid rectal procedures or tx, teach how use leg bag, teach not strain during bowel movement, external & internal radiation therapy, hormone therapy, chemotherapy, cryotherapy

Left sided HF leads to r. Sided HF


Cause: 1. Athlerosclerosis 2. MI 3. HTN 4. Cardiomyopathy 5. Dysrthmias 6. Valve disorders LABS: 1. CXR-pulmonary congestion L. Ventricular hypertrophy 2. Echo- cardiomegaly, decreased fxn 3. ABG: hypoxia, hypercapnea, resp. Acidosis 4. EKG: L. Ventricular hypertrophy 5. BNP >500mg/mL HF probable

s/s: 1. HTN 2. Paroxysmal nocturnal dyspnea, dyspnea on exertion, orthopnea 3. Wheezing & crackles 4. hypoxia, resp. Acidosis 5. Cough w/ pink frothy sputum, pulmonary edema 6. S3/4 heart sounds 7. Palpitations 8. Dysrhythmias

right sided HF leads to core pulmonale


Cause: 1. Athlerosclerosis 2. L. Sided HF 3. Lung dx- core pulmonale, r. Ventriculare dilation & hypertrophy due to pulmonary dx ABS: 1. CXR-congestion, cardiomegaly 2. Echo- cardiomegaly, decreased fxn 3. EKG: L. & R Ventricular hypertrophy

s/s: Weakness, fatigue, synchope Hepatomegaly, splenomegaly Ascites depedent pitting edema Jugular vein distention Hepatojugular reflex Oligura Dysrhythmias Elevate central venous/right atrial pressure 10. Nausia, vomiting, anorexia, abdominal distension 11. Weight gain
1. 2. 3. 4. 5. 6. 7. 8. 9.

R.L sided HF interventions


1. 2. 3. 4. 5. 6. 7. 8.

9.

Diet therapy O2, bed rest, semifowlers Assessemntscardiovascular, VS Foley catheter Morphine Diuretics: Lasix Cardiac glycosieds: Digoxin Cardiac stimulants: dopamine (Intropin), dobutamine (Dobutrex) Nitrates vasodilators

10. 11. 12. 13. 14. 15. 16. 17. 18. 19.

Fluid restriction Diet theapy teaching Daily weights Medication administration, teaching Measure abdominal girths Assess peripheral edema Cardiovasculare assessments CVP readings Rest periods Monitor e-lytes, I/O Skin care

R.L sided HF interventions


Discharge planning: 1. Stop smoking 2. Maintain ideal body weight 3. Activity restrictions/care 4. rehab

Digitalis preparations- not used new MI


Action: increase force contraction, slows HR, kkpromotes diuresis, decreases heart size Tx: CHF, atrial fibrilation or other tachyarhythmias NSG: monitor client response, check apical pulse: do not give <60bpm, monitor e-lytes, toxicity: 2.0ng/ml, N=0.52.0ng/mL s/s toxicity: 1. Anorexia, nausea, vomiting, diarrhea 2. Headache, lethargy, restlessness, irritability, convulsions, hallucinations 3. Coloured vision- yellow, blue hallo 4. Dysrhythmias, tachycardia, bradycardia , heart block, cardiac failure

Pulmonary edema- as result decompensated L. Sided failure


Cause: atherosclerosis, MI, fluid overload s/s:
1. 2. 3. 4. 5. 6. 7. 8.

Dyspnea Crackles Pink frothy sputum Tachycardia Anxiety, aggitation Diaphoresis Cold, clamy skin Chest pain

TX: 1. Diuretics 2. Vasodilators 3. Cardiac stimulantsdopamine, dobutamine 4. Nitrates 5. May be intubated 6. Bed rest 7. Cronchodilators: aminophylline 8. Nsg care

Pacemakers- inserted r. Atrium, r. Ventricle to provide electrical stimulation

Types: external temporary- surgery, emerg situations, control dysrhythmias, perminant- conduction system problems INT: 1. Cardiac monitor 2. Monitor s/s infection 3. Education:

Take pulse Send rhythm strip Avoid contact sports Wear medic alert braclet Carry info on pacemaker Safety measures s/s malfxn

INT:

MI- necrosis of myocardial tissue, sustained ischemia


Cause: atherosclerosis, coronary artery spasm, thrombosis Labs/DX: 1. Hx, physical 2. Cardiac enzymes: CPK, CPK-MB, troponin, myoglobin 3. EKG: q waves, ST elevation, Twave inversion, dysrhythmias 4. Increased WBC Complications: 1. dysrhythmias: PVCs, v-tach, v-fib 2. CHF 3. Cardiogenic shock: changes mentation, Vs, decreased UOP, cool, moist skin

Drug therapy: Lidocaine, pronestyl Potassium suppAntogoags- aspirin, heparin Nitrates- IV notroglycerin B-blockers-lopressor Morphine Pharmacologic INT Angina & MI: 1. Nitrates: NTG, NTG ointment, transder, nitrodur, isordil 2. B-blocker: inderol, corgard 3. Ca2+ channel blockers: procardia, calan, cardizem 4. Antianxiety: ativan, xanax 5. Anagesics: morphine 6. Antihyperlipidemics: lipitor, mevacor, zocar report jaundice, dark urine, RUQ tenderness, fatigue 7. Surgery: Laser angioplasty, PTCA
1. 2. 3. 4. 5. 6.

INT Angina & MI cont


Teaching: 1. Weight reduction 2. Diet therapy 3. Avoid activities result angina 4. Stress reduction 5. Stop smoking 6. Take meds as prescribed , report S.E, and follow up 7. How to take NTG 8. Exercise, space activities 9. Teach about drugs and cardiac catheterization

Cardiac drugs
Vasodilators: 1. Decrease preload, afterload, workload of heart 2. Vasodilate coronary arteries and indirectly peripheral vasodilation S.E: headache, hypotension Ca2+ channel blockers: 1. Vasodilation coronary & systemic 2. Slows HR 3. Decrease heart demand O2, afterload, BP S.E: hypotension, bradycardia

Cardiac drugs
B-Blockers: 1. Decrease contractility, HR, BP, heart demad O2 S.E: bradycardia, hypotension, wheezing, depression, sexual dysfxn Ca2+ channel blockers: 1. Vasodilation coronary & systemic 2. Slows HR 3. Decrease heart demand O2, afterload, BP S.E: hypotension, bradycardia

Angina-acute pain chest, imbalance between O2 supply & demand


s/s:
1. 2. 3. 4.

Vague sensation, feeling strange Choking, squeezing, suffocating sensation Pain down arms, neck, back Pain relieved by rest or cessation of activity, NTG admin

INT: 1. Bed rest 2. IV therapy: Heparin lock 3. O2 therapy 4. Monitor:


VS 2. I/O 3. EKG 4. Cardiac enzymes
1.

5. Diet therapy 6. Cardiovascular assessment 7. Obtain EKG during acute attack

PAD- result systemic atherosclerosis, partial/total occlusion


deprives lower extremities O2

Inflow obstructions involve distal end aorta, common internal and external iliac arteries Outflow obstructions involve femoral, popliteal & tibial arteries

Clinical course: 1. Asymptomatic 2. Claudication 3. Rest pain 4. Necrosis/gangrene

PAD- result systemic atherosclerosis, partial/total occlusion


deprives lower extremities O2 s/s: 1. Intermittent clausdication 2. Paresthesia 3. Pallor on elevation 4. Dependant rubor 5. Dry shiny skin 6. Loss hair on legs 7. Thickened toenails 8. Pulselessness 9. Poikiliothermia Complications: delayed wound healing, infection, necrosis, ischemic ulcers (ankle, gangrene)

PAD- result systemic atherosclerosis, partial/total occlusion


deprives lower extremities O2
INT: 1. RF modification: stop smoking, aggressive treatment hyperlipidemia, HTN, diabetes 2. Drug therapy: antiplatelets-plavix, aspirin, pentoxifyllin (Trental) & cilostazol (Pletal)-for intermittent claudication 3. Exercise therapy 4. Nurtrition therapy 5. Complimentary & alternative therapy 6. Maintain tissue integrity: foot care, inspect daily, avoid injury, good fitting shoes, trim nails carefully 7. Increase tissu perfusion: warmth, no constrictive clothing, no crossed legs Surgery: 1. Percutaneous transluminal angioplasty w/without stent placement 2. Lazer assisted angioplasty 3. Athrectomy (rotoblator) 4. Peripheral arterial bypass 5. Endatarectomy 6. Patch graft angioplasty 7. amputation

Acute arterial ischemic disorders- sudden and abrupt, caused by embolism,


thrombosis, trauma

s/s:
1. 6 Ps: pain, pallor, poulselessness, paresthesia,

poikiliothermia, paralysis Tx: anticoags, throbectomy, TPA, steptakinas, monitor for hemorrhage

Superficial thrombosis- due to trauma, irritation


s/s:
1.

Pain, reddness, warmth

Tx: 1. Rest, moist heat, elevation, mild anagesic

DVT-stasis of blood, damage endothelium, hypercoagability of blood


s/s: 1. 2. 3. 4. 5. 6. 7. Asymptomatic Unilateral leg edema Warm skin, elevated temp Calf tendernes, diff size +ive homans sign Peripheral pulses present Complications: pulmonary embolism, chronic venous insuffficiency, phlegmasia cerulea dolens- cold, blue leg sydrome TX: 1.
2. 3.

4. 5. 6.

Bedrest, elevate extremity (until thrombus stable) War, moist heat anticoag therapy: heparin, monitor PTT (have protamine sulfate availe), LMWH (enoxapprin lovenox admin SQ), coumadinonset 4872hrs, keep VitK on handNSG: bleeding precautions, SQ technique (no IM), give same time each day, S.E, teach importance blood draws, avoide Vit. K rich foods, med alert bracelt) Elastic stockings analgesics thrombectomy

Raynauds Phenomenon- arterial spasm feet & hands, assoc. Lupus & rheumatoid arthrisits
s/s:
1. 2.

3.

Pallor, cyanosis, hyperthermia (white, blue, red) Coldness & numbing, throbbing, aching pain, tingling swelling Pulse never lost Warm clothing Stop smoking Vasodilators, ca2+ channel blockers, sm. Relaxants Decrease stress Protect form cold

Tx: 1. 2. 3. 4. 5.