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36 Cards in this Set
- Front
- Back
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Categories of hypertension by blood pressure |
Optimal High normal Grades 1-3 Isolated systolic hypertension (SBP > 140, DBP < 90) |
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Definition of hypertension in children |
Reading greater than 95th percentile on 3 occasions |
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Diagnosis of hypertension |
In-office: Two readings, five minutes apart, sitting in chair. Arm at level of heart. Deflate cuff at 2 mmHg/sec. Confirm in both arms. In children, check legs to exclude coarctation of aorta. Confirm with ambulatory and home blood pressure monitoring. |
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Malignant hypertension |
Severe increase in blood pressure, epspecially diastolic blood pressure. Manifests as: - Retinal hemorrhages, papilledema with visual loss - Renal failure - Left ventricular failure and angina |
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Patterns of Age-Related Changes in BP |
Systolic blood pressure increases with age, even in normotensive. Diastolic blood pressure increases until age 50, then decline as vessels become stiff and lose elasticity. Overall, pulse pressure increases with age. |
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Patterns of change in BP throughout day |
When wake up, blood pressure rises 10-20 mmHg. Nocturnal dip - declines at night. Hypertensive people lose nocturnal dip. Remain at same blood pressure all day long. |
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Predictors of mortality from hypertension |
Elevated systolic Elevated diastolic Loss of nocturnal dip Wide pulse pressure - best predictor of CV mortality from HTN |
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Mean arterial pressure calculation |
MAP = 1/3 SBP + 2/3 DBP. Normally, 86. |
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Hemodynamic progression of HTN (contributions) |
Early years - Greater contribution of cardiac output. "Hyperkinetic phase". Later years - Vessels tiffen so greater contribution of peripheral resistance. Recall BP = CO x TPR |
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Causes of hypertension |
Primary - 90%. Unknown cause Secondary - 10%. Includes chronic kidney disease (5%), renovascular disease (4%), adrenal disease, pheocyromocytoma, genetic disease, obstructive sleep apnea, and coarctation of aorta. |
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Pathophysiology of primary hypertension. |
Largely unknown. Interplay between: - Inappropriately high sympathetic outflow, leading to: - Abnormal venoconstriction and high venous return - Inappropriately high renin release - Inappropriately high cardiac output (hyperkinetic phaes) - Abnormal renal salt/water handling |
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Hypertension and renal disease |
Parenchymal renal disease Kidney damage causes reduction in number and function of nephrons. Remaining nephrons work harder, increasing glomerular HTN. Causes further glomerular damage and death. Glomerular damage continually exacerbates hypertension d/t reduction in ability to secrete sodium and water. Vicious cycle. |
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Hypertension and renovascular disease |
Triggered by: - Constriction in renal artery perceived as decreased renal perfusion - Decreased distal delivery of sodium - Increased sympathetic activity - Increased prostaglandins Causes J cells in kidney to secrete renin. Renin cleaves angiotensinogen to angiotensin 1, converted by ACE into angiotensin II. Angiotensin II causes vasoconstriction and sodium retention from aldosterone. Both contribute to hypertension. |
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Surgical and medical management of renovascular disease |
Surgical - angioplasty balloon or stent to improve flow to renal artery. Medical - antihypertensives, antilipidemics, antiplatelet agents. Studies show no difference between medical vs surgical amnagement so medical management usually used. |
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Screening for renal artery stenosis |
Magnetic resonance angiogram - most sensitive, noninvasive. Captopril nuclear scans or Dopplers can also be used to assess blood flow. |
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Primary hyperaldosteronism |
Cause of 2% secondary hypertension. Two primary causes: Hypertrophy of adrenal gland Benign adenoma Result in high aldosterone independent of renin feedback, which acts on kidney to increase Na+ reabsorption and increase K+ excretion. Causes hypokalemia and hypernatremia (hypertension). |
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Primary hyperaldosteronism diagnosis |
Look for hypokalemia |
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Management of adrenal hypertension (primary hyperaldosteronism) |
Adrenal hypertrophy - Aldosterone inhibitors spironolactone or aplerenone (fewer side effects, more costly) Benign adneoma - Monitor and medical management. Surgical excision if high cost of meds or complications. |
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Monogenetic hypertensions with GOF sodium retentoin |
- Liddle's Syndrome - increased ENaC activity - Gordon's Syndrome - increased NaCl transporter |
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Hypertension due to apparent mineralocorticoid escess |
Renal mineralocorticoid receptor is activated by both aldosterone and cortisol, but cortisol is broken down rapidly by 11b-HSD into cortisone. If cortisol degradation is inhibited, it causes hypertension due to apparent mineralocorticoid excess. - 11b HSD deficiency - Glyccorrhetinic acid from black licorice or chewing tobacco (blocks 11b HSD) |
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Glucocorticoid remediable hypertension |
AD form of low renin hypertension. Crossover results in aldosterone production under control of 11 hydroxylase (usually converts ACTH to cortisol) rather than aldosterone synthase. Anytime stressed, extra aldosterone made. Treat with glucocorticoids to block formation of aldosterone from ACTH. Aldosterone secretion is controlled by ACTH |
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Differential for low and high aldosterone and renin |
High aldosterone, high renin: Renovascular hypertension, hypovolemia, or renin secreting tumor High aldosterone, low renin: Adrenal adenoma or hyperplasia (aldosterone producing), or familial remediable hypertension Low aldosterone, low renin: Apparent mineralocorticoid excess syndrome, Cushing's syndrome, Liddle's syndrome |
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Pheochromocytoma |
Neuroendocrine tumor of adrenal medulla, originating in chromaffin cells Causes hypertension (99%) ,headache, flushing/sweating, and palpitations. Fluctuating hypertension because regulatory mechanisms restore blood pressure between surges of E and NE from tumor. |
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Diagnosis of pheochromocytoma |
Look for elevated plasma metanephrines and urinary VMA, MHPG. |
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Medical management of pheochromocytoma |
Give alpha blockers, then beta blockers (prevent unopposed alpha vasoconstriction = stroke, heart attack) |
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Obstructive sleep apnea and hypertension |
Normally, neural pathways maintain patency of airway during sleep. Occurs when pathways fail, often due to excess tissue in pathway. Causes intermittent asphyxia, sleep fragmentation, excess CV death. Excessive daytime hypersomnolence. 50% have hypertension. Treatment - weight reduction, CPAP |
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When to look for secondary vs primary hypertension? |
- Age <30 or >50 (primary HTN usually presents in 40s) - Sudden deterioration in previously stable hypertension - Severe onset - Presence of target organ damage at diagnose (LV hypertrpohy, retinal, renal findings) - Special clinical features - hypokalemia (primary hyperaldosteronism), abdominal bruit (renovascular disease), headache/tachycardia/sweating (pheo), or heavy smoker - Poor response or rise in creatinine with routine antihypertensive therapy - Sudden drop in blood pressure if interfere with angiotensin II (renal artery stenosis - angiotensin II needed to maintain renal blood flow by constricting efferent arteriole) |
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Organ damage from hypertension |
Brain: - Hemorrhagic stroke - Ischemic stroke with multiple lacunar infarcts - cavities caused by WBC activity following embolus - Dementia Peripheral vascular disease - reduced ability for endothelial cells to relax smooth muscle, greater risk of arterial wall hypertrophy due to high pressure LV hypertrophy - Can lead to CHF and arrhythmias. Retinopathy Renal failure |
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Eye complications from hypertensoin |
Flame hemorrhages Cotton wool spoots - ischemic infarcts Hard exudates - cholesterol plaques In malignant HTN only - papilledema |
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Increase in CV Mortality with BP increment in hypertension |
CV mortality risk doubles with each increment of 20/10 in blood pressure. |
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Blood pressure goals |
All patients should be < 140/90 Patient > 60 yo should be < 150/90 |
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Reduction in CV event risk with reduction in blood pressure |
2 mmHg decrease in SBP results in a 7% decrease in heart disease mortality and 10% decrease in stroke mortality. |
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Life style modification for hypertension |
Weight loss - 10 kg loss reduces BP by 20 mmHg Dietary sodium restriction - <2g intake /day reduces BP by 8 mmHg Physical activity Moderation of alcohol and smoking In reality, patients rarely respond merely to lifestyle modification. |
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Rule of TENS for hypertension |
Each drug only reduces blood pressure by 10 mmHg Most patients require multiple medications |
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First line therapy for uncomplicated HTN |
ACE inhibitors Angiotensin receptor blockers Beta blockers Ca2+ channel blockers Diuretics Caucausians respond better to ACE inhibitors and beta blockers; African-Americans to Ca2+ channel blockers, diuretics. But all people respond to all agents. Initial therapy depends on other comorbidities |
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First line therapy for HTN with proteinurea |
Start on ACE inhibitor or Angiotensin receptor blocker (ARB) |
