Cardio Unit 1 Flashcards
What are the 3 types of drugs that reduce cardiac remodeling?
- Aldosterone antagonists
- ACE inhibitors & ARBs
- β-blockers
Are loop diuretics K wasting or sparing?
Wasting
What is the mechanism of loop diuretics?
They block the Na+-K+-2Cl cotransporter (NKCC2 on the luminal side) in thick ascending limb loop of Henle.
What other ions, besides Na, are excreted during the use of loop diuretics?
Mg++ and Ca++
Loop diuretics cause excess K intercellularly, which diffuses back out to lumen and drives reabsorption of Mg++ and Ca++ back into blood.
What are 2 potential negative effects of loop diuretics?
1) They can cause a hypokalemic metabolic acidosis
2) They can cause hyperuricemia –> gout
For #2 –> the same transporter handles both the diuretic drug and uric acid. If too much drug is going out, not enough uric acid :(
What are the different loop diuretics?
Furosemide, bumetanide, torsemide
What are the differences among the loop diuretics?
Furosemide has shortest duration of effect (2-3 hours), followed by torsemide (4-6 hours), then bumetanide (6 hours).
Are thiazide diuretics K wasting or sparing?
Wasting
What is the mechanism of thiazide diuretics?
They inhibit the Na/Cl co-transporter in the distal convoluted tubule. Prevent reabsorption of Na.
What is one added benefit of thiazide diuretics?
They promote re-uptake of Ca. There is less Na intracellularly, which drives the Na/Ca exchanger on the interstitial/vessel side of the cell and promotes Ca entry into the blood.
What are the thiazide diuretics, and how are they different?
Hydrochlorothiazide and chlorthalidone
HCTZ is bid, chlorthalidone is 1x daily (longer duration)
What is the major potential toxicity with thiazide diuretics?
Hypokalemia –> can result in weakness, paresthesias, cardiac sensitization (predisposition to ectopic pacemakers), thus use not advisable in patients with arrhythmias, history of MI, pre-infarction angina
What else can go wrong with thiazide diuretics?
Gout attacks and hyperglycemia :(
Are aldosterone antagonists K wasting or sparing?
Sparing
Are Na-channel blockers K wasting or sparing?
Sparing
What are the names of the K-sparing diuretics?
Spironolactone, eplerenone, triamterene, and amiloride
What is the mechanism of spironolactone and eplerenone?
They block the aldosterone receptor –> block aldosterone from ↑ gene transcript of Na+ and K+ channels in collecting tubule –> net effect is to decrease Na+ reabsorption and K+ secretion
Thus, they’re named aldosterone antagonists
What is the mechanism of triamterene and amiloride?
They block the Na+ channels in the lumen of the collecting duct –> prevent both Na+ reabsorption & K+ loss
Thus, they’re named Na-channel blockers
What are the doses and duration of actions of all of the K-sparing diuretics?
Spironolactone + eplerenone = 1-2x daily
Triamterene + amiloride = 1-3 days to max effect.
Tri –> liver metab
Ami –> excreted unchanged (need to be careful)
What is one rather less desirable effect of spironolactone and eplerenone?
Gynecomastia ( . )( . )
What is another danger of all the K-sparing agonists? (…Think about it…)
Hyperkalemia (–> conduction abnormalities, arrhythmias)
What does angiotensin II do in the body?
(1) Increases BP (TPR)
Stimulates Gq protein in vascular SM cells –> IP3 –> ↑ intracellular Ca –> contraction
(2) Stimulates thirst at hypothalamus
(3) Acts to ↑ aldosterone secretion at adrenal cortex –> increased Na reabsorption –> ↑ blood volume
(4) Acts on CNS to ↑ sympathetic activity –> ↑ in CO, arterial constriction
What do ACE-inhibitors do besides inhibiting ACE?
Decrease the inactivation of bradykinin, leading to vasodilation (and a bad COUGH :(_
How can you tell by a drug’s name if it’s an ACE-inhibitor?
-pril
