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27 Cards in this Set

  • Front
  • Back

RAAS

series of protein hormones that regulate BP, blood volume and electrolyte balance by affecting the kidneys and vascular smooth muscle

Renin (rate limiting step)

Catalyzes the formation of angiotensin 1 from angiotensinogen


Synthesized and secreted by the juxtaglomerular cells

Factors increasing renin release

decreased Blood volume


low BP


stimulation of beta 1 receptor

ACE

converts inactive angiotensin 1 into the active angiotensin 2

Angiotensin 2 mechanism of action

vasoconstrics by binding to AT1 receptor


simulates release of aldosterone from adrenal cortex to increase sodium retention


acts on post. pituitary to release ADH causing water retention

Why obesity is thought to cause HTN

increased insulin secretion causing Na reabsorption


increased activity of the SNS

What should pts taking ACE inhibitors avoid

High K+ diet

Loop Diuretic

Block Na and Cl reabsorption in the ascending limb


Used for edema, severe HTN and severe renal failure


Adverse effects of Loop Diuretics

Hypokalemia


hyponatremia


dehydration


hypotension

Thiazine Diuretic

Block Na and Cl reabsorption in the distal tubule


Decrease vascular resistance

Adverse effects of Thiazine Diuretics

Hypokalemia


Dehydration


Hyponatremia

Potassium Sparing Diuretics/Aldosterone Antagonists

Inhibit aldosterone receptors in the collecting duct thus blocking the re-uptake of Na and K+ secretion


Main use is to counteract hypokalemia


Do not use with ACE inhibitors or renin inhibitors


Adverse effect: hyperkalemia

Beta Blockers (suffix OLOL)

Block cardiac beta 1 receptor to decrease CO


Block juxtaglomerular beta 1 receptor to decrease renin release

1st generation beta blockers

produce non selective blockage and inhibit betas 1 and 2 (lung)

2nd generation beta blockers

only block beta 1

Adverse effects of selective beta blockers

bradycardia


decreased CO


HF


rebound HTN if withdrawn

Adverse effects of non-selective beta blockers

same as selective


bronchoconstriction


inhibition of hepatic and muscle glycogenolysis

ACEI (suffix- pril)

decreases the production of angiotensin II


inhibits the breakdown of bradykinin (elevated levels cause vasodilation)

Adverse effects of ACEI

1st dose hypotension


hyperkalemia


persistant cough


angioedema

ARBs (suffix- sartan)

decrease actions of angiotensin II by blocking the AT1 receptor and cause vasodilation and decreased aldosterone release therefore increased sodium and water excretion

Direct Renin Inhibitors

Bind to renin to block the conversion of angiotensinogen to angiotensin 1

Adverse effects of DRIs

hyperkalemia


persistent cough and angioedema


diarrhea

Calcium Channel Blockers

block the bringing of calcium from outside the cell to the inside, which is essential for contraction of the heart and smooth vasculature

Kinds of Calcium Channel Blockers

Dihydropyridine and non-dihydropyidine

Dihydropyridine (suffix- dipine) mechanism of action and adverse effects

decrease calcium influx into smooth muscle of arteries


Adverse: flusing, dizziness, headache, peripheral edema, reflex tachycardia, rash

non-dihydropyridine mechanism of action and adverse effects

block calcium channels in both the heart and smooth muscle therefore also decreased CO


adverse effects: constipation, dizziness, flushing, headache, edema, compromised cardiac function

Centrally Acting Alpha 2 Agonists

bind and activate alpha 2 receptors in the brainstem to decrease sympathetic outflow therefore decrease CO and peripheral resistance


adverse effects: drowsiness, dry mouth, rebound HTN