Endocrine HTN Flashcards

1
Q

Pressor vs volume overload type HTN

A
  • Pressor: result of circulating vasoconstriction agents, such as elevated RAS and catecholamines (seen in pheochromocytoma)
  • Volume overload: abnormality of Na and H2O regulation (seen in 1o hyperaldosteronism and low renin HTN)
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2
Q

Activation of RAS

A
  • Increased renal BP leads to increased stretch of arterioles and decreased renin release
  • MD cells notice a drop in Na delivery to TAL and increase renin release
  • ATII: causes vasoconstriction, release of aldosterone from zone glomerulosa of the adrenals
  • Aldo: promotes Na (and H2O) reabsorption and K secretion
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3
Q

Na state of pts w/ hyperaldosteronism

A
  • These pts are eunatremic for a number of reasons:
  • Increased intravascular volume due to water retention
  • ANP released due to stretch of the atria, which causes Na dumping
  • Pressure natriuresis causing Na dumping
  • Overall: normal serum Na
  • However, the pts are hypokalemic and alkalotic
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4
Q

1o vs 2o hyperaldosteronism

A
  • Both cause hypokalemia and alkalosis, HTN
  • In 1o hyperaldo the renin levels will be LOW to try and compensate
  • In 2o hyperaldo the renin levels will be HIGH b/c that is whats leading to the hyperaldo
  • Causes of 1o: aldo producing adenoma, primary adrenal hyperplasia (most common), adrenocortico CA
  • Causes of 2o: renal artery stenosis, renin-secreting tumor, CKD, malignant HTN
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5
Q

Pheochromocytoma

A
  • Rare tumors that cause pressor type HTN by releasing large amounts of catecholamies
  • Tumors usually develop in adrenal medulla, they produce NE and/or epi
  • Can be Dx w/ 24 hr urine and looking at metanephrine and nor-metanephrine levels (break down products), which must be >2-3x ULN
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6
Q

Sx of pheochromocytoma

A
  • HTN (may be severe) w/ paroxysms of severe HTN + pallor, headache, flushing, sweating, palpitations, hyperglycemia
  • These paroxysms last less than 15 min
  • Pheo tumors may be sporadic or associated w/ MEN II syndromes
  • Epidemiology: ages 30-50, usually solitary (if bilateral think familial/MEN)
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7
Q

Rx of pheochromocytoma

A
  • Surgical removal of the tumor after medical therapy

- First alpha blockade, then beta blockade, then surgery

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8
Q

When to consider excess aldo for a pt

A
  • Any individual w/ HTN + hypokalemia

- Any individual on the extremes of age w/ HTN

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9
Q

Differentiating primary adrenal hyperplasia vs aldo-producing adenoma

A
  • Look at 18-OHcorticosterone (18OHB, precursor to aldo) levels, if above 50 its an adenoma, if less than 50 its primary adrenal hyperplasia
  • Can also do posture test (blood test when supine and then standing after 30 min of supine)
  • If the 18OHB levels are stable then its adenoma, if the 18OHB levels rise its adrenal hyperplasia
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10
Q

MEN type II

A
  • Both are associated w/ RET oncogenesis, causes constitutively active tyrosine kinase
  • Both are associated w/ pheochromocytoma (and medullary thyroid CA), familial, and bilateral
  • MEN IIA (codon 634 of RET): pheochromocytoma, medullary thyroid CA, hyperparathyroidism
  • MEN IIB (codon 918 of RET): pheochromocytoma, medullary thyroid CA, neurofibromas
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