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chpt 33 HTN
HTN, rheumatic fever, valves, endo/peri/myocarditis
| Question | Answer |
|---|---|
| primary HTN contributing factors | stress, increased SNS, sedentary, genetic, smoking, altered renin, vasoconstictors, > ideal wt, mechanism, insulin resistance, endothelial cell dysfx, DM, increased Na intake, excessive alcohol, > ideal wt., sedentary, obesity, ethnicity, gender |
| primary HTN is... | idiopathic- no specific cause |
| secondary HTN | has specific cause- goal is to eliminate underlying issue |
| Angiotensin II causes | vasoconstriction, vascular hypertrophy, induces aldosterone secretion |
| high insulin concentration causes... | impairs NO mediated vasodilation, increases SNS activity, pressor effects include vascular hypertrophy and increased Na absorption |
| endothelin | prolonged vasocostriction |
| normalSBP/DBP | <120 <80 |
| prehypertention range | 120-139 80-89 |
| stage 1 HTN range | 10-159 90-00 |
| stage 3 HTN | >160 >100 |
| factors influencing BP | SVR, SNS, baroreceptors, renal system, endocrine(epinephrine & aldosterone), endothelin (ET1, ET2, ET3) |
| NITIC OXIDE | endothelium derived relaxing factor, helps maintain low tone, inhibits growth of smooth ms layer, inhibits platelet aggregation |
| pathophysiology of Primary HTN | environmental, demographic, and genetic combo |
| demographics for primary HTN | African american, obesity, increasing age, DM, renal dz |
| HTN is called | "silent killer" |
| S/S of HTN | secondary to TOD--> fatigue, dizziness, angina, dyspnea, palpitation |
| TOD involves which organs | heart, kidneys, eyes, brain, vascular(aneurysm, intermittent cladication) |
| "response to injury"hypothesis | HTN disrupts the coronary artery, exposing layer to WBC and Pltsgrowth factors induce smooth ms proliferation= stiffened arterial wall and narrowing |
| complications of HTN | LVH, HF, cerebrovascular dz (atherosclerosis-stroke) |
| DX studies for HTN | take BP on both arms and use highest reading |
| when is HTN @ highest & lowest | highest in the morning, lowest at night |
| office BP measurement | use auscultatory method- client has feet on floor, seated 5 min in a chair, arm supported @ heart level, appropriate size cuff, 2 readings obtained |
| "white-coat"phenomenon | anxiety is increased d/t clinical environment- may need ambulatory BP monitoring for 2 hours |
| Dx for HTN | UA, creatinine, lytes, glucose, BUN, serum lipid, ECG, echocardiograph |
| lifestyle modification for HTN | wt redux (22lbs) decreases SBP by 5-20mmHg, DASH diet, Na 2.4g/day, alcohol moderation, no tobacco, stress management, 30 min physical activity |
| primary actions of drugs to tx HTN | decrease preload and afterload |
| drug classifications for HTN | diuretics, adrenergic inhibitors, direct vasodilators, angiotensin inhibitors, CCBs |
| pt teaching for HTN | identify, report, and minimize s/s: sexual dysf, dry mouth, hypotension, frequent urination |
| Isolated systolic HTN | most common form in individuals >50 |
| the elderly have... | impaired baroreceptors & hypotension |
| African Americans | more at risk |
| Hispanic americans | seek tx less |
| Hypertensive crisis | severe abrupt increase in DBP (>140 mmHg)- rate of increase is most important. |
| Hypertensive crisis occurs to who | people who fail to comply w/meds or undermedicated |
| Hypertensive emergency | elevated in hours to days, evidence of acute TOD (CNS)and BP >180/120 |
| Hypertensive crisis causes... | acute renal failure, MI, HF, PE |
| hopitalization of hypertensive crisis | IV drug tx titrated to mean arterial pressure (HTN)- decrease by no more than 25%, monitor cardiac & renal fx, neuro checks, determine cause, educate to prevent |
| hypertensive emergency s/s | HA, confusion, N/V, blurred vision. coma |
| hypertensive urgency | developes in days-weeks; no TOD |
| clonidine/catapress | centrally acting alpha agonist, vasodilation, decrease SVR & BP; transdermal patch available- S/S:erectyle dysfx, depression, rebound HTN, chew gum for dry mouth, tremors, sedation-- do not stop abruptly |
| hydrochlorothiazede | diuretic, acts on distal convoluted tubule, inhibits NaCl absorption, lowers BP in 2-4 weeks. S/S: n/v/d, lyte imbalance, cardiac toxicity w/digoxin, pt should supplement w/K+ rich foods, monitor orthostatic hypotension |
| vasotec/enalapril | ACEI- inhibits A1-A2, S/S:loss of taste, rash, cough, hyperkalemia. ASA/NSAIDS decrease effectiveness, diuretics increase effect- do not use w/K+ sparing |
Created by:
arsho453
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