Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Cards HTN Dx
Cardiology
| Question | Answer |
|---|---|
| Goals of Diagnosing HTN | Detect & stage HTN severity; detect TOD; assessing overall CV risk; detect secondary causes of HTN |
| HTN stats | 1 in 3 in US = HTN; 66 mil in US 20 yo & older; 95% are essential HTN; 2005 in US, direct & indirect cost of HTN = $59.7 Billion |
| HTN pt awareness stats | 63% aware of the dx; only 45% receiving tx; 34% under ctrl using a threshold criterion of 140/90 |
| Factors of essential HTN: | Genetic defect, inc dietary Na intake, intrinsic renal differences, stress, obesity, drug or substance abuse |
| Primary HTN: other factors: | Variable plasma renin activity; variable symp n.s. response & catecholamines; insulin resistance & DM; inadequate dietary K+ & Ca+ ; resistant vessels |
| Renal artery stenosis in HTN: MOA | Excessive renin release in response to decrease in renal blood flow & perfusion pressure |
| Renal vascular HTN: 2 pathologic processes (resulting in stenosis) | 85% atherosclerosis of proximal renal arteries (pts usu also have CAD); 15% fibromuscular dysplasia (esp in F 15–50 yrs; genetic predisposition) |
| Fibromuscular dysplasia (FMD) is characterized by: | fibrous thickening of the intima, media, or adventitia of the renal artery |
| Congenital abnormality which results in narrowing of the aorta, usually in the ascending region, which increase PVR due to the stenosis | Coarctation of the Aorta |
| Coarctation of the Aorta: incidence | Rare (1:10,000) & usually accompanies other abnormalities such as bicuspid aortic valve or Turner Syndrome |
| Hyperaldosteronism: most common etiologies: | unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia |
| If Pheochromocytoma undiagnosed: | Outpouring of catecholamines during unrelated surgical/ radiologic procedure can lead to severe, abrupt hypertensive crisis & mortality rate over 80% |
| Obstructive sleep apnea & HTN | HTN = response to chronic, intermittent hypoxia during nocturnal apneic episodes |
| HTN & chronic kidney dz: epidemiology | HTN is second most common cause of chronic kidney disease (> 25% of cases) |
| Most easily recognized treatable risk factor for stroke, MI, CHF, peripheral vascular dz, aortic dissection, atrial fibrillation & end-stage kidney disease | HTN |
| HTN in younger pts (< 50 yrs): Hemodynamic fault = | vasoconstriction at the level of the resistance arterioles |
| Isolated systolic HTN: associated risks | BP of 160/60 (pulse pressure of 100 mmHg) carries 2x the risk of fatal coronary heart dz as 140/110 (pulse pressure of 30 mmHg) (PP = SBP – DBP) |
| Diastolic BP age pattern | Peaks in the early 50’s, then declines for men and women (Systolic BP continues to rise for both throughout life) |
| Resistant Hypertension | Defined as persistence of BP > 140/90 despite tx with full doses of 3 or more different classes of meds in rational combination (& including a diuretic); important to know pt is compliant |
| 4 Categories of Resistant HTN | Pseudoresistance; Inadequate medical regimen; Nonadherence or ingestion of pressor substances; secondary HTN |
| Pseudoresistance: | Usually caused by white coat effect superimposed on chronic HTN that is well controlled with meds outside the office |
| Resistant HTN: Inadequate medical regimen | Absence of appropriate diuretic; Renal fn impairment which affects drug clearance; monotherapy or inadequate dosing of meds |
| Resistant HTN: Nonadherence or ingestion of pressor substances | a. Medication nonadherence; b. Lifestyle modification noncompliance; obesity, high salt diet, excessive alcohol intake; c. Habitual use of tobacco, cocaine, meth, phenylephrine or NSAIDS (cause renal Na+ retention) |
| Resistant HTN: Secondary HTN: | If you’ve exhausted the first 3 categories, time to look for secondary cause of HTN |
| Most commonly overlooked secondary causes of Resistant HTN: | Chronic kidney dz & primary aldosteronism |
| Hypertensive Urgency | Severe elevation of BP; No evidence of progressive TOD; benefit from BP lowering in a few hrs; absence of raised intracranial pressure |
| Hypertensive Emergency | Acute, severe elevation in BP; evidence of rapidly progressive TOD (eg, MI, pulmonary edema or renal failure); requires immediate, gradual reduction of BP (NOT to the normal range); always look for secondary causes |
| Malignant Hypertension: | Type of Hypertensive Emergency; usually accompanied by other end organ damage |
| Malignant Hypertension is most common in: | Young adults, prior renal dz, AA males, PG, or collagen vascular dz |
| Dz w/ Compelling Indications for tight HTN ctrl | CHF; High Coronary Dz Risk; Chronic Kidney Dz; DM; Post-MI; Recurrent Stroke Prevention |
| Fn of Angiotensin II | Stimulates release of Na+-retaining hormone aldosterone (adrenal corticol cells); amplifies vasoconstriction (systemic and renal) |
| BP = | CO X PVR |
| Essential HTN = | established primary HTN |
| Hallmark of essential HTN = | elevated peripheral vascular resistance |
| Variations in BP determined by: | variations in ECF volume, heart contractility, & vascular tone |
| Def of HTN = repeated readings of: | SBP over 140 &/or DBP over 90 |
| Evidence supports tx of high risk pts at lower threshold of: | of 130/80 mmHg. |
| HTN: High risk groups include: | DM, chronic kidney dz, CV or Cerebrovascular dz, or LVH on EKG |
| Factors of essential HTN affect: | ECF volume, heart contractility, or vascular tone |
| HTN contributes to what % of M/F AA deaths? | 30% M & 20% F |
| Most common secondary cause of HTN | Chronic renal dz (proteinuria, high creat) |
| ?% of pts w/ chronic renal dz have HTN | 85% |
| Chronic renal dz & HTN: MOA | expanded plasma volume & peripheral vasoconstriction |
| Renal artery stenosis prevalence in HTN pts | less than 2% |
| HTN pts w/ renal artery stenosis: proportions | 75% unilateral stenosis; 25% bilateral |
| Renal artery stenosis causes what % of medically refractory HTN? | 30% |
| Catecholamine-producing large tumors of adrenals | Pheochromocytoma |
| HTN & CPAP use for OSA | CPAP improves risk of developing HTN & CV dz |
| HTN prevalence in DM pts | 75% of diabetics have HTN |
| Aldosterone-like effect precipitates persistent HTN in: | Cushing Syndrome |
| Leading cause of death worldwide | arterial HTN |
| Using standard size cuff on obese pt: | Gives falsely elevated result |
| Ambulatory BP monitor can detect: | Lack of nocturnal dip (assoc w/higher CVD risk) |
| BP & substances | Avoid tobacco/caffeine 30 min prior; document if pt took meds |
| Ambulatory BP monitor & TOD | Better TOD predictor than office measurements |
| What symptom must be present for a dx of Malignant Hypertension? | Papilledema |
| Most patients who develop HTN after 50 yrs have: | Isolated Systolic HTN |
| Defn Isolated Systolic HTN | systolic BP over 140 mmHg with diastolic BP <90 mmHg |
| Isolated Systolic HTN: hemodynamic fault = | decreased distensibility of the large conduit arteries |
| Majority of uncontrolled HTN occurs among: | older pts with isolated systolic HTN. |
| JNC8: SBP opinion | In pts over 50, SBP over 140 is a more important CVD risk than DBP |
| Most common cause of Hypertensive Emergency | Acute CHF with pulm edema (37%) |
| HTN eval labs | UA; serum Cr, glu, K+, Na+ ; Lipids (TC, trigs, HDL, LDL); 12-Lead EKG (LVH) |
| HTN TOD | Neuro; Ophthalmologic; CV; Renal; Vascular |
| Excessive Na+-K+ exchange which results in hypokalemia; associated with HTN | Hyperaldosteronism |
| Hydralazine MOA: | Direct vasodilation of arterioles (with little effect on veins) with decreased systemic resistance |
| Ca Channel Blockers = | Nifedipine, verapamil, diltiazem, amlodipine, felodipine |
| Amlodipine MOA: | CCB without negative inotropic effects but with vascular smooth muscle relaxing activity |
| Dash diet = | low in Na, fat; high in K+, fiber, calcium; lowers SBP 8-14 |
| HTN BP goals (for nl, CAD, DM) | Nl: <140/90; DM or CKD: <130/80 |
| HTN med choices: w/o CE | stage 1 thiazide, ACE/ARB, BB, CCB; stage 2: 2 drug combo (usu HCTZ + ACE etc) |
| HTN med choices: w/ CE | thiazide: HF, CVD risk, DM; ARB: HF/DM; BB: any but CKD/stroke prevention; CCB: CVD risk/DM |
| Hypertensive emergency etiology | fibrinoid necrosis of small arteries causes end organ damage (heart, brain, kidneys, eyes) |
| Hypertensive emergency definitions | crisis >180/110; urgency DBP >130; emergency is EOD; malignant is papilledema |
| Grossly elevated blood pressure esp. w/ signs of TOD | Malignant HTN, hypertensive crisis: tx sodium nitroprusside to rapidly lower BP |
| HTN with idiopathic hypokalemia may be 2/2 = | hyperaldosteronism (check renin/ aldosterone level); usu 2/2 adenoma |
| HTN & PG | OCP can increase BP (HRT does not); PG tx with methyldopa, BB, vasodilators (hydralazine) |
| HTN urgency vs emergency | emergency: TOD, admit, IV tx; urgency no/stable TOD, observe 3-6 hr, PO tx (captopril, clonidine, or labetalol) |
| Factors of essential HTN: | Genetic defect, inc dietary Na intake, intrinsic renal differences, stress, obesity, drug or substance abuse |
| Renal artery stenosis in HTN: MOA | Excessive renin release in response to decrease in renal blood flow & perfusion pressure |
| Renal vascular HTN: 2 pathologic processes (resulting in stenosis) | 85% atherosclerosis of proximal renal arteries (pts usu also have CAD); 15% fibromuscular dysplasia (esp in F 15–50 yrs; genetic predisposition) |
| HTN & chronic kidney dz: epidemiology | HTN is second most common cause of chronic kidney disease (> 25% of cases) |
| Isolated systolic HTN: associated risks | BP of 160/60 (pulse pressure of 100 mmHg) = 2x risk of fatal CHD as 140/110 (pulse pressure of 30 mmHg) (PP = SBP – DBP) |
| Diastolic BP age pattern | Peaks in early 50s, then declines for men and women (SBP continues to rise for both thru life) |
| Resistant Hypertension = | persistence of BP >140/90 despite tx w/full doses of 3 or more diff classes of meds in rational combo (& including a diuretic); important to know pt is compliant |
| Most commonly overlooked secondary causes of Resistant HTN: | Chronic kidney dz & primary aldosteronism |
| Hypertensive Urgency = | Severe elevation of BP; No evidence of progressive TOD; benefit from BP lowering in a few hrs; absence of raised intracranial pressure |
| Hypertensive Emergency = | Acute, severe elevation in BP; sxs of rapidly progressive TOD (eg, MI, pulmo edema, ARF); req immed, gradual reduction of BP (NOT to normal range); look for secondary causes |
| HTN: High risk groups include: | DM, chronic kidney dz, CV or Cerebrovascular dz, or LVH on EKG |
| Factors of essential HTN affect: | ECF volume, heart contractility, or vascular tone |
| Ambulatory BP monitor can detect: | Lack of nocturnal dip (assoc w/higher CVD risk) |
| Most patients who develop HTN after 50 yrs have: | Isolated Systolic HTN: systolic BP >140 with diastolic <90 |
| Most common cause of Hypertensive Emergency | Acute CHF with pulm edema (37%) |
| Hyperaldosteronism: most common etiologies: | unilateral aldosterone-producing adenoma or bilateral adrenal hyperplasia |
| If Pheochromocytoma undiagnosed: | Outpouring of catecholamines during unrelated surg/ radiologic procedure can lead to severe, abrupt hypertensive crisis & mortality rate over 80% |
| Malignant Hypertension is most common in: | Young adults, prior renal dz, AA males, PG, or collagen vascular dz |
| Normal angiotensin function | Renin promotes angiotensin I production -> ACE converts to angiotensin II -> vasoconstriction, aldosterone secretion (-> Na reabsorption & K secretion) -> higher BP |
| Normal adrenergic function | Adrenergic stimulation -> stimulate beta 1 receptors (inc HR) -> increase BP; also stimulate alpha 1 receptors -> vasoconstriction |
| HTN funduscopic exam: | may see AV nicking, narrowed arteries, copper / silver wiring of arterioles, hemorrhages, exudates, papilledema |
| Cardiogenic shock = | SBP <90 (or 30 mmHg below baseline >30 min); sxs poor tissue perfusion, persistence of shock after correction of non-myocardial factors |
| Cardiogenic shock: non-myocardial factors include: | 6 H's (hypovolemia, hypoxia, acidosis, etc), arrhythmias, MI & comps (valve dz, LV aneurysm, CM), myocarditis, LVOT obstruction (eg, AS) |
| When to suspect RAS: | Onset <20 yo or >50 yo; HTN resistant to >2 meds; renal arter / epigastric bruit; atherosclerosis (aorta or peripheral arteries); abruptly worse renal fn after starting ACEI |
| RAS dx studies | Renal arteriogram is definitive. If low suspicion: noninvasive angiography (MRI or CT). US |
| RAS mgmt | BP meds: ACEI, ARB, diuretics. Surgery (perc transluminal angioplasty +/- stents). Nephrectomy in severe dz & risk of kidney loss 2/2 ischemia |
| JNC 8 BP goals | >60 yo: <150/90. 30-59 yo: <140/90 |
Created by:
Abarnard
Popular Medical sets