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Endo > Endocrine HTN (DJ) > Flashcards

Endocrine HTN (DJ) Flashcards

1
Q

HTN increases the risk of:

A

stroke, heart failure, MI, renal failure

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2
Q

Why do we treat essential HTN?

A

lowering BP = lower risk of diseases associated with HTN

CVA, CHF, MI, RF

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3
Q

How is pre-HTN defined?

A 
SBP = 120-139
DBP = 80-89

*note: these people progress to HTN at a rate of 10%/yr

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4
Q

CV risk is greater in patients with high levels of:

A

renin

compared to patients with low-renin HTN

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5
Q

BP response to diuretics and CCB’s is better in patients with what type of HTN?

A

low-renin

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6
Q

BP response to ACEI’s is better in patients with what type of HTN?

A

high-renin

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7
Q

T/F: Successful trx of essential HTN can be curative

A

F, trx of the underlying cause of secondary HTN*

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8
Q

What 3 endocrine diseases cause HTN in the majority of patients?

A

primary hypoaldosteronism
pheochromocytoma
Cushing’s

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9
Q

What are the 2 components of the sympathochromaffin system?

A
  1. sympathetic NS (NE)

2. chromaffin tissues, e.g. adrenal medulla (epi)

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10
Q

What is the major end product of catecholamine metabolism? What enzyme produces this?

A 
vanillymandelic acid (VMA)
MAO
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11
Q

Because there is a steep concentration gradient for ___, typical plasma levels must be substantially increased to affect BP.

A

NE

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12
Q

What are pheochromocytoma?

A

catecholamine-producing tumors comprised of chromaffin cells, which produce labile HTN and paroxysmal symptoms

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13
Q

Why is it important to detect pheochromocytoma?

A

1) usually curable
2) untreated patients are at risk for a lethal HTN paroxysm
3) 5-10% of them are malignant
4) may be a clue to a familial autosomal dominant syndrome

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14
Q

What malignancies are associated with pheochromocytoma?

A

multiple endocrine neoplasia:

  • -type 2A (hyperparathy + medullary carcinoma of the thyroid)
  • -type 2B (multiple mucosal neuromas + medullary carcinoma of the thyroid)
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15
Q

What are 2 conditions that may occur with familial pheochromocytoma?

A
  1. von Hippel-Lindau (abn tumor suppression)

2. neurofibromatosis (uncommon)

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16
Q

What clinical symptoms are associated with pheochromocytoma?

A
  1. paroxysmal symptoms (HA, diaphoresis, palpitations)
  2. labile HTN
  3. family hx
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17
Q

What stimuli may elicit pheochromocytoma symptoms?

A 
positional changes
stress
abd pressure
meds
direct pressure applied to tumor
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18
Q

What metabolic features are associated with pheochromocytoma?

A

increased metabolism
profuse sweating
hyperglycemia
wt loss

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19
Q

What causes glucosuria associated with pheochromocytoma?

A

catecholamines stimulate hepatic glucose production and inhibition of insulin secretion/action

20
Q

What hematologic and hemodynamic features are associated with pheochromocytoma?

A

catecholamine-induced vasoconstriction and plasma volume reduction cause:

  1. orthostatic hypotension
  2. elevated hct (volume contraction)
21
Q

What labs are performed to diagnose pheochromocytoma?

What drug should you use to treat HTN for these labs?

A
  1. 24h urine catecholamine (preferred)
  2. total metanepherines
  3. plasma catecholamine (but short t1/2)

clonidine–avoid false positives

22
Q

Where are most pheochromocytoma located?

A 
abdomen (99%)
adrenal medulla (90%)
23
Q

Where are familial pheochromocytoma located?

A

bilateral adrenals

24
Q

Treatment of pheochromocytoma?

A

surgery with pre-op trx with alpha-antagonists (to prevent BP increases during surgery)

25
Q

How do mineralocorticoids affect the kidneys?

A

stimulate distal tubules to reabsorb Na+ and excrete more K+ and H+

  • increase open Na and K channels
  • increase synth of Na/K/ATPase
26
Q

How do mineralocorticoids affect BP?

A

increased Na = expanded ECF volume + increased BP

27
Q

How do mineralocorticoids affect blood levels of Na, K and H?

A

increased Na
decreases K
decreased H (increased pH)

*evidence that effects on the brain may contribute to HTN

28
Q

What hormones activate the mineralocorticoid R?

A

aldosterone (*primary)
cortisol

(note: cortisol in converted to cortisone in renal tubule)

29
Q

How does inactivation of 11-beta hydroxysteroid dehydrogenase result in apparent mineralocorticoid excess?

A

enzyme inactivation (via hereditary defect or drug inhibition) prevents conversion of cortisol»cortisone; mineralocorticoid R is then activated by “normal” levels of cortisol

30
Q

What does mineralocorticoid excess cause?

A

HTN

hypokalemic acidosis

31
Q

What does mineralocorticoid excess NOT cause (unexpectedly)?

A

hypernatremia (regulated by thirst/ADH)

edema (regulated by ANP)

32
Q

What is primary hyperaldosteronism?

A

increased aldosterone secretion

**renin and AT are suppressed by negative feedback

33
Q

What is secondary hyperaldosteronism?

A

increased renin secretion due to deficient salt intake, decreased ECF volume or decreased kidney perfusion

34
Q

How is primary hyperaldosteronism diagnosed?

A

ratio of plasma aldosterone to plasma renin activity

aldosterone&raquo_space;> renin, ratio larger than nml

35
Q

What is the etiology of primary hyperaldosteronism?

A

aldosterone-secreting adrenal adenoma (66%)

bil adrenal hyperplasia (33%)

36
Q

What are the clinical findings in primary hyperaldosteronism?

A

HTN (due to increased Na)

hypokalemia

37
Q

How is primary hyperaldosteronism confirmed?

A

give IV saline; ECF expansion would suppress secretion in nml patient

38
Q

Clinically, when would you suspect primary hyperaldosteronism?

A

when a patient has HTN and spontaneously low K

39
Q

How is primary hyperaldosteronism often treated? Secondary?

A
  1. resection (if adenoma), which cures hypokalemia and usually HTN
  2. aldosterone agonist + anti-HTN drugs
40
Q

Why is dexamethasone used in diagnostic tests?

A

produces negative feedback in diagnostic tests but does not interfere with measurement of cortisol

41
Q

What symptoms is present in 80% of patients with Cushing’s?

A

HTN

42
Q

How are mineralocorticoids thought to play a role in Cushing’s?

A

high cortisol binds and cross-activates mineralocorticoid receptors, resulting in hypokalemia and HTN (Na and fluid retention suppress renin)

43
Q

How is angiotensin thought to play a role in Cushing’s?

A

GC stimulate hepatic synth of angiotensinogen, which is converted to ATII

44
Q

How is vascular reactivity thought to play a role in Cushing’s?

A

cortisol causes enhanced vascular reactivity to pressors, which results in vasoconstriction and increased peripheral resistance (and increased BP)

45
Q

What is the relationship between (non-HF) CV risk and natriuretic peptides?

A

less significant increases in plasma BNP and other natriuretic peptides may indicate an increased risk for CV disease (other than HF)

Endo (28 decks)

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