Antihypertensives Flashcards
1
Q
Acetazolamide
A
- diuretic (decrease stroke volume)
- carbonic anhydrase inhibitor - inhibits exchange of H for Na at the proximal tubule
- weak diuretic property because the rest of the tubule will work harder to reclaim things
- uses: HTN (not first-line), mountain sickness (can cause respiratory alkalosis; acetazolamide is used as prophylaxis), glaucoma
- effects: hyperchloremic metabolic acidosis - the only diuretic that does not cause metabolic alkalosis
2
Q
Furosemide
Bumetinide
Torsemide
Ethacrynic acid
A
- diuretic (decrease stroke volume)
- strongest diuretic
- loop diuretic - acts on the thick ascending limb of the loop of Henle
- inhibits Na/K/2Cl co transport
- uses: HTN, pulmonary edema, hypercalcemia
- effects: hypercalciuria (not good for calcium renal stones), hypochloremic metabolic alkalosis, ototoxicity
3
Q
Hydrochlorothiazide
Metolazone
Indapamide
A
- diuretic (decrease stroke volume)
- blocks Na/Cl co transport at the luminal side of the DCT
- uses: HTN, hypercalciuria, nephrogenic diabetes insipidus
- effects: Hyper-GLUC (glycemia, lipidemia, uricemia - avoid in gout patients, calcemia), hypochloremic metabolic alkalosis
- African American population responds most well to thiazide diuretics
4
Q
Spironolactone (generic) aka Aldactone (brand)
A
- diuretic (decrease stroke volume)
- aldosterone blocker
- either an antagonist or a receptor blocker
- prevents the formation of mediator proteins that stimulate the Na/K pump
- uses: HTN, HF, primary hyperaldosteronism (would cause secondary HTN), end stage liver disease
- effects: hyperkalemia (all other diuretics cause hypokalemia), gynecomastia
5
Q
Triamterene
Amiloride
A
- diuretic (decrease stroke volume)
- kidney principal cell blocker - does not require aldosterone
- acts on the collecting duct
- principal cells usually mediate the collecting duct’s influence on sodium and potassium balance via sodium and potassium channels located on the cell’s apical membrane
6
Q
Atenolol Betaxolol Bisoprolol Esmolol Metoprolol Nebivolol
A
- second generation of beta blockers
- beta-1 receptor antagonist (decrease SV and HR)
- beta-1 receptors normally have 2 roles:
1. increase chronotropy (rate)/inotropy (contractility) of the heart and increase dromotropy (AV node conduction velocity)
2. increase renin release from renal JG cells
Beta-1 receptor antagonists decrease inotropy, chronotropy, and dromotropy.
7
Q
Nadolol
Propanolol
Sotalol
Timolol
A
- first generation of beta blockers
- non-selective beta antagonist
- beta-2 receptors normally have 2 roles:
1. bronchodilation of bronchial smooth muscle (–> contraindicated to give a non-selective beta blocker to an asthmatic patient)
2. uterine relaxation of the uterine muscle - side effect: coronary vasoconstriction
Activation of β2‐adrenergic receptors in the coronary
artery normally causes vasodilation.
• Activation of α1‐adrenergic receptors in the coronary
artery normally causes vasoconstriction.
• Blockade of β2‐adrenergic receptors in the coronary
artery may result in predominance of α1‐adrenergic
receptor activity causing vasoconstriction.
• Coronary artery vasoconstriction is not desirable in
angina pectoris, especially in Prinzmetal’s angina.
• β1‐selective adrenergic blockers may not have this side
mechanism of action:
Norepinephrine (NE) binds to beta‐1 adrenergic
receptors. Beta‐1 adrenergic receptors are coupled
to G‐protein (Gs)
• Adenylate cyclase is activated and cAMP is formed
from ATP. Increased levels of cAMP activate proteinkinase‐
A (PK‐A)
• PK‐A phosphorylates L‐type calcium channels and
calcium enters the cell. Calcium is also released
from the sarcoplasmic reticulum (SR).
• Increased levels of calcium in the cell promote
increased contractility of the myocardial tissue
Activation of beta‐adrenergic receptors increases
myocardial contractility.
• Activation of beta‐adrenergic receptors in the
cardiac sino‐atrial node tissue increases the
automaticity of these cells resulting in increase in
heart rate.
• Therefore, blockade of beta‐adrenergic receptors
results in decrease in myocardial contractility and
heart rate.
• Both effects result in decrease in myocardial oxygen demand
8
Q
Carvedilol
Labetalol
A
- non-selective beta antagonist + alpha antagonist
Carvedilol - very effective in heart failure patients
Labetalol - most effective out of all beta blockers in decreasing HTN; increasingly preferred in pregnancy due to reduced side effects
9
Q
Acebutolol
A
- beta-1 antagonist but sympathomimetic (acts as both agonist and antagonist)
10
Q
Penbutolol
Pindolol
A
- non-selective beta antagonist but sympathomimetic (acts as both agonist and antagonist)
11
Q
Diltiazem
Verapamil
A
- nondihydropyridine - works on the heart whereas dihydropyridines work on the peripheral vasculature
- calcium channel blocker
- binds to L type calcium channels and causes a negative inotropic and chronotropic effect –> decreased contractility/SV and HR
- adverse effects: heart block, worsen heart failure, constipation
12
Q
Benazepril Captopril Enalapril Fosinopril Lisinopril Moexipril Perindopril Quinapril Ramipril Trandolapril
A
- ACE inhibitors
[ACE has 2 main functions: the conversion of angiotensin I to angiotensin II and the metabolism of bradykinin, substance P, and enkephalins into inactive fragments] - uses: HTN, especially also with diabetes; systolic heart failure
- adverse effects: hyperkalemia, cough (when bradykinin/substance P/enkephalins are not broken down), angioedema, teratogenic
–> ACE inhibitors are contraindicated for pregnant females - enalapril is used for hypertensive emergencies
13
Q
Aliskiren
A
- Renin inhibitor
14
Q
Angiotensin Receptor Blockers
A
- Angiotensin receptor blockers
- uses: HTN, especially also with diabetes; systolic heart failure
- adverse effects: hyperkalemia, angioedema, teratogenic
- if pt taking ACE inhibitor is having cough, can switch to angiotensin receptor blockers (no effect on bradykinin metabolism)
15
Q
Candesartan Eprosartan irbesartan Losaran Olmesartan Telmisartan Valsartan
A
- Angiotensin II receptor blockers
