HTN2 Flashcards
what are the 4 main physiological categories of drugs that regulate BP
- diuretics
- RAA agents
- sympathoplegic agents
- vasodilators
what are the 4 classes of diuretics
- thiazides
- loop diuretics
- K-Sparing
- Aldosterone Agonists
the first 6-8 weeks of thiazide tx what happens to CO and TVR
- decrease in CO
2. initial increase in SVR
when are aldosterone agonists used for HTN
for pt’s with heart failure or post MI
What pt’s do not have much of a response to thiazides for HTN
CrCl< 30 ml/min
what diuretic shows a response that increases with an increase in dosing?
loop diuretics
what type of patients is HTN tx with loop diuretics appropriate for
pt’s with heart failure and cirrhosis (sodium retention)
when are K sparing diuretics used for HTN
to avoid K depletion and
in combo to enhance natriuretic effect
what are 3 classes of drugs that treat RAA system for HTN
- direct renin inhibitors
- ACE inhibitors
- ARB’s
True/ False:
angiotensinogen is produced continously by the liver
True
True/ False:
Renin is continuously released by the kidneys
false
release in response to stress (diet, emtion, or physiologic)
what is formed by renin reacting with angiotensinogen
angiotensin I
what are the 3 pathways of renin release?
macula densa pathway
intrarenal baroreceptor pathway
beta-adrenergic receptor pathway
where is renin stored
juxtaglomerular cells in kidney
what is the macula densa
cell that signals for renin release if Na levels are low
what activates renin release with a decrease in renal blood flow
intrarenal baroreceptors
ACE has what effect on what other substance other than Angio I?
breaks down bradykinin (a vasodilator)
angiotensin II has what 3 major effects?
- rapid pressor effect
- slow pressor response
- vascualr and cardiac hypertrophy
what is the MOA of angio II’s rapid pressor response
direct vasoconstriction and increased NE release leads to altered peripheral resistance
what is the MOA of angio II’s slow pressor response
- increases sodium reabsorption in proximal tubule
- increases aldosterone release from adrenal cortex
- direct alteration of hemodynamics (renal vasoconstriction)
what is the MOA of angio II’s vascular and cardiac hypertophy and remodeling effect
- encreased expression of proto-oncogenes and growth factors
- increases afterload and vascular wall tension
what bioreaction is stopped by direct renin inhibitors
angiotensinegin to angio I
what type of bioavailability does aliskiren have
very low bioavailability (2.5-3%)
what type of affinity does aliskiren have for renin?
very high affinity
