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6 Cards in this Set

  • Front
  • Back
What are the two endocrine mechanisms for maintaining BP? Subtypes of these mechanisms?
Catecholamines
- nerve endings
- adrenal medullary secretion

Renin-angiotensin-aldo
- direct ang II effect
- indirect aldo effect on plasma volume
Is primary mineralocorticoid excess (adrenal adenoma secreting aldosterone) a relatively (common/uncommon) cause of HTN?
- characteristics (volume, Na, K)?
- must be distinguished from what non-pathological etiology?
- renin and ang II lvls?
relatively uncommon
- Na retention, V expansion, K excretion.
- pts w/ essential HTN taking diuretics
- low
Identify the dz at the top of the DDx for the following:
- ^Plasma Renin (PRA), ^ Plasma Aldo (PAC), PAC/PRA~10
- \PRA, ^PAC; PAC/PRA >2 w/ PAC > 15
- \PRA, \PAC
- 2ndary hyperaldosteronism (diuretic use, renovascular HTN, renin-secreting tumor, coarctation of aorta, malignant HTN)
- primary aldosteronism
- Congenital adrenal hyperplasia, DOC-producing tumor, Cushing's, 11B-HSD def, exogenous mineralocorticoid, Liddle's syndrome.
Explain the pathologenesis of secondary hyperaldosteronism in the context of renal artery stenosis.
decrease in blood flow --> ^renin --> ^ ang II --> ^ aldo --> ^ Na retention, \K rtn, increase plasma V
What are the 4 classes of drugs that are available to block various components of the RAAS system?
Renin inhibitors, ACE inhibitors, ARB's, Aldosterone receptor antagonists.
Should you use stimulation tests in pts with suspected pheochromocytoma?

What is the preferred tx?
- is there a sx focused medical therapy that works?
No, it's dangerous.

Surgerical removal.
- yes, a and b blocker combo tx is often useful to control HTN and cardiac arrythmias.