Hypertension

  1. What blood pressure measurements place pts at increased risk for CV disease?
    Blood pressure measurements higher than 120/80 mm Hg place patients at increased risk for cardiovascular disease.
  2. How is hypertension classified in adults?
    In adults, classification of hypertension is based on an average of two or more blood pressure readings obtained more than 1 minute apart at two or more visits.
  3. If single-agent antihypertensive therapy is ineffective, when do you add a second agent?
    If single-agent antihypertensive therapy is ineffective after 1 to 3 months of treatment, switching to or adding a drug with a complementary mechanism of action is indicated.
  4. What is a normal blood pressure according to JNC-VII?
    less than 120/80
  5. When do you start with an initial treatment with two antihypertensive agents?
    Initial treatment with two antihypertensive agents may particularly be warranted for patients whose blood pressure is more than 20 mm Hg above the blood pressure goal, and those with stage 2 or higher hypertension often require treatment with more than one agent
  6. What is diagnostic of primary aldosteronism?
    An elevated plasma aldosterone-plasma renin ratio accompanied by unsuppressed aldosterone excretion after correction of hypokalemia and adherence to a high-sodium diet for 3 days is diagnostic of primary aldosteronism.
  7. In pts with primary aldosteronism who cannot by treated surgically, what is the treatment?
    In patients with primary aldosteronism who cannot be treated surgically, aldosterone inhibition with spironolactone or eplerenone may be used.
  8. What is the most accurate method of diagnosing renovascular hypertension caused by fibromuscular disease?
    Catheter-based angiography is the most accurate method of diagnosing renovascular hypertension caused by fibromuscular disease.
  9. How do you diagnose pheochromocytoma?
    Diagnosis of pheochromocytoma requires confirmation of excess catecholamine production supported by positive findings on MRI or CT scanning.
  10. What is the treatment of choice for pheochromocytoma?
    Surgical resection is the treatment of choice for pheochromocytoma and can resolve associated hypertension.
  11. Define "white coat hypertension."
    White coat hypertension is characterized by at least three separate office blood pressure measurements above 140/90 mm Hg with at least two sets of measurements below 140/90 mm Hg obtained in non-office settings, accompanied by the absence of target organ damage.
  12. What is the gold standard for diagnosing white coat hypertension?
    Ambulatory blood pressure measurements
  13. Define resistant hypertension
    Resistant hypertension is defined as blood pressure that remains above goal despite treatment with the optimal dosages of three antihypertensive agents of different classes, including a diuretic.
  14. What is the most useful outcome predictor of CV morbidity and mortality in pts older than 50 years of age?
    An elevated systolic blood pressure is the most useful outcome predictor of cardiovascular morbidity and mortality in patients older than 50 years of age.
  15. What blood pressure patter is associated with increased CV risk, particularly stroke?
    Failure of the blood pressure to decrease by at least 10% during sleep, known as nondipping, as well as an excessive morning surge in blood pressure have been associated with increased cardiovascular risk, particularly for stroke.
  16. What is ambulatory blood pressure monitoring?
    Ambulatory blood pressure monitoring provides multiple blood pressure readings over a prolonged period of time. This method evaluates mean 24-hour blood pressure; mean daytime blood pressure; mean nighttime blood pressure; the average difference between waking and sleeping blood pressure to evaluate for nocturnal dipping (which may be defined as a decrease in mean arterial blood pressure of >10% during sleep); and blood pressure variability.
  17. What is the normal BP?
    <120 / <80
  18. What is the systolic and diastolic range for prehypertension?
    120-139 systolic or 80-89 diastolic
  19. What is the range for Stage 1 hypertension?
    140-159 / 90-99
  20. What is the range for Stage 2 hypertension?
    160 / 100
  21. What is the JNC-7 recommendation for Stage 1 hypertension?
    JNC 7 guidelines recommend lifestyle modifications and drug treatment for all patients with stage 1 or greater hypertension, regardless of absolute risk.
  22. What are the lifestyle modifications recommended for all pts with hypertension?
    • Reduce weight
    • Follow DASH diet
    • Participate in aerobic physical activity for 30 to 34 minutes most days
    • Reduce sodium intake to <100 mmol/24 h
    • Limit daily alcohol consumption to two drinks for men and one drink for women
    • Smoking cessation
  23. Pathogenesis of Liddle syndrome?
    Autosomal dominant; gain of function of epithelial sodium channel
  24. What are the clinical features of Liddle Syndrome?
    Elevated blood pressure, hypokalemic metabolic alkalosis, low renin and aldosterone levels, excess sodium retention
  25. What is the treatment for Liddle syndrome?
    Amiloride, thiazide diuretics, spironolactone
  26. What are the Monogenic forms of hypertension?
    • Liddle syndrome
    • Glucocorticoid-remediable aldosteronism
    • Apparent mineralocorticoid excess
    • Type 2 pseudohypoaldosteronism (Gordon syndrome)
    • Mineralocorticoid receptor activation
    • Mutations in peroxisome-activated receptor-γ
    • Hypertension and brachydactyly
  27. What is the pathogenesis of Glucocorticoid-remediable aldosteronism?
    Autosomal dominant; regulation of aldosterone secretion by ACTH
  28. What are the clinical features of Glucocorticoid-remediable aldosteronism?
    Elevated blood pressure, hypokalemic metabolic alkalosis, low renin levels, moderately high aldosterone levels
  29. What is the treatment for Glucocorticoid-remediable aldosteronism?
    Aldosterone blockade, corticosteroids
  30. What is the pathogenesis of Apparent mineralocorticoid excess?
    Autosomal recessive; activation of mineralocorticoid receptor by cortisol
  31. What are the clinical features of Apparent mineralocorticoid excess?
    Elevated blood pressure, younger age at presentation, hypokalemic metabolic alkalosis, low renin and aldosterone levels
  32. What is the treatment for Apparent mineralocorticoid excess?
    Thiazide diuretics, aldosterone blockade
  33. What is the pathogenesis of Type 2 pseudohypoaldosteronism (Gordon syndrome)?
    Autosomal dominant; mutations in WNK kinases 1 and 4
  34. What is the clinical presentation of Type 2 pseudohypoaldosteronism (Gordon syndrome)?
    Elevated blood pressure, hyperkalemia, hyperchloremic metabolic acidosis, low renin and aldosterone levels
  35. What is the treatment of Type 2 pseudohypoaldosteronism (Gordon syndrome)?
    Thiazide diuretics
  36. What is the pathogenesis of Mineralocorticoid receptor activation?
    Mutation in mineralocorticoid receptor
  37. What is the clinical manifestation of Mineralocorticoid receptor activation?
    Elevated blood pressure, younger age, low renin and aldosterone levels, mineralocorticoid receptor activation by steroids such as progesterone, exacerbation in pregnancy
  38. What is the treatment of Mineralocorticoid receptor activation?
    Thiazide diuretics
  39. What are compelling indications for thiazide diuretics?
    Heart failure, advanced age, volume-dependent hypertension, low-renin hypertension, systolic hypertension
  40. What are compelling indications for use of aldosterone antagonists?
    Primary aldosteronism, resistant hypertension, sleep apnea
  41. What are compelling indications for use of ACE-I?
    Heart failure, left ventricular dysfunction, proteinuria, diabetic nephropathy, chronic kidney disease, post–myocardial infarction
  42. What are compelling use of ARBs?
    Same as ACE inhibitors; useful when ACE inhibitors are not tolerated
  43. What are compelling indications for use of CCB?
    Systolic hypertension, cyclosporine-induced hypertension, angina, coronary heart disease
  44. What are compelling indications for use of beta-blockers?
    Angina, heart failure, post–myocardial infarction, migraine, tachyarrhythmias
  45. What are compelling indications for use of alpha-blockers?
    Prostatic hyperplasia
  46. What are some uncommon side-effects of ACE-I?
    rash, loss of taste, leukopenia (captopril)
  47. What are some side-effects of CCB?
    Headache, flushing, gingival hyperplasia, edema, constipation
  48. What are the side-effects of aldosterone antagonists?
    Hyperkalemia, increased creatinine level, painful gynecomastia, menstrual irregularities, gastrointestinal distress
  49. What is the target BP of those with minimal proteinuria (< 1 g/24h), and those with significant proteinuria (> 1 g/24h)?
    Target blood pressure measurements of less than 130/80 mm Hg are recommended for those with minimal proteinuria (defined as a 24-hour urine protein level below 1 g/24 h) and less than 125/75 mm Hg for those with significant proteinuria (defined as a 24-hour urine protein level above 1 g/24 h).
  50. Explain how Primary Aldosteronism is diagnosed.
    • The plasma aldosterone-plasma renin ratio (ARR) is a screening test for primary aldosteronism that is useful even in patients who are taking antihypertensive agents except for aldosterone blockers
    • ARR is helpful only if the serum aldosterone level is above 15 ng/dL (414 pmol/L)
    • ARR above 25 is generally considered abnormal.
    • An elevated ARR alone is not diagnostic of primary aldosteronism unless nonsuppressible or autonomous aldosterone excess is demonstrated by the presence of a urine aldosterone excretion of 12 µg/24 h (33.2 nmol/d) or higher obtained after correction of hypokalemia and adherence to a high-sodium diet for 3 days.
    • In some patients, administering an intravenous saline infusion also may demonstrate nonsuppressible serum aldosterone levels.
    • Once nonsuppressible or autonomous aldosterone production is demonstrated, adrenal imaging is indicated to reveal the adrenal anatomy and identify patients with unilateral disease such as an aldosterone-producing adenoma (Conn syndrome) or primary unilateral adrenal hyperplasia. High-resolution CT with thin cuts of the upper abdomen is the preferred imaging technique.
    • After biochemical confirmation of hyperaldosteronism, localization procedures differentiate aldosterone-producing adenomas or unilateral hyperplasia from bilateral hyperplasia. Adrenal vein sampling is considered the gold standard for demonstrating lateralization of aldosterone secretion and is recommended for patients who are candidates for adrenalectomy.
  51. Describe the management of Primary Aldosteronism.
    • Unilateral aldosterone-producing adenoma; unilateral adrenal hyperplasia; and, rarely, aldosterone-producing carcinoma can be resolved with surgery. Laparoscopic adrenalectomy without previous adrenal vein sampling may be warranted in patients less than 40 years of age if nonsuppressible hyperaldosteronism is documented and if CT scanning demonstrates unilateral adrenal abnormalities and a normal contralateral gland.
    • Bilateral adrenal adenomas or hyperplasia cannot be resolved with surgery. Glucocorticoid-remediable aldosteronism, a rare form of nonprimary aldosteronism that can cause hypertension, also is not able to be cured surgically.
    • If surgery is not indicated, aldosterone inhibition with spironolactone or eplerenone may be used to treat primary aldosteronism.
  52. What is the best known predictors of progression to ESRD in pts with ischemic nephropathy (renovascular kidney disease)?
    The best known predictors of progression to end-stage kidney disease are the glomerular filtration rate at presentation and the degree of fibrosis detected on kidney biopsy.
  53. Fractionated catecholamines and metanephrines can be measured in the serum or via a 24-hour urine collection.
    • MRI or CT scanning can localize the tumor in patients with a pheochromocytoma.
    • Metaiodobenzylguanidine adrenal scanning is highly specific for pheochromocytomas, is helpful in diagnosing extra-adrenal tumors, and can be used to confirm positive findings on CT and MRI scanning. Metaiodobenzylguanidine scanning also may be used when a patient’s clinical presentation raises strong suspicion for pheochromocytoma and biochemical testing demonstrates excess catecholamine production but results on CT or MRI are negative.
  54. Describe the management of Pheochromocytoma
    • Surgical resection is the treatment of choice for pheochromocytoma and can resolve associated hypertension.
    • Beginning 10 to 14 days before surgery, α- and β-blockers are indicated to control blood pressure and pulse rate during the preoperative period and to prevent massive outpouring of catecholamines during surgical manipulation.
    • The long-acting α-blocker phenoxybenzamine should be started first. The dosage of this agent should be titrated upward to achieve blood pressure control and until adverse effects such as nasal congestion, postural hypotension, fatigue, and diarrhea develop.
    • Metyrosine inhibits catecholamine synthesis and reduces tumor stores of catecholamines. This agent should be used when both α- and β-blockers are insufficient to control symptoms or are not tolerated, or when significant intraoperative manipulation of the tumor is anticipated.
Author
Mat
ID
106937
Card Set
Hypertension
Description
bp
Updated