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Flashcards in Antihypertensives Deck (22):
1

Acetazolamide

- 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

Furosemide
Bumetinide
Torsemide
Ethacrynic acid

- 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

Hydrochlorothiazide
Metolazone
Indapamide

- 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

Spironolactone (generic) aka Aldactone (brand)

- 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

Triamterene
Amiloride

- 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

Atenolol
Betaxolol
Bisoprolol
Esmolol
Metoprolol
Nebivolol

- 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

Nadolol
Propanolol
Sotalol
Timolol

- 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

Carvedilol
Labetalol

- 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

Acebutolol

- beta-1 antagonist but sympathomimetic (acts as both agonist and antagonist)

10

Penbutolol
Pindolol

- non-selective beta antagonist but sympathomimetic (acts as both agonist and antagonist)

11

Diltiazem
Verapamil

- 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

Benazepril
Captopril
Enalapril
Fosinopril
Lisinopril
Moexipril
Perindopril
Quinapril
Ramipril
Trandolapril

- 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

Aliskiren

- Renin inhibitor

14

Angiotensin Receptor Blockers

- 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

Candesartan
Eprosartan
irbesartan
Losaran
Olmesartan
Telmisartan
Valsartan

- Angiotensin II receptor blockers

16

alpha 1 receptor antagonists

[alpha1 receptors normally increase smooth muscle contraction --> peripheral arterial vasoconstriction --> increase SVR --> increase MAP]
- uses: HTN, benign prostatic hyperplasia
- adverse effects: dizziness, orthostatic hypotension

17

Methyldopa
Clonidine

- alpha 2 receptor agonists
[alpha2 receptors normally act as negative feedback inhibitors. When stimulated, it inhibits alpha1 receptors and smooth muscle contraction]
- methyldopa: useful in pregnancy, can cause a hemolytic anemia

18

Clonidine

- alpha 2 receptor agonists
[alpha2 receptors normally act as negative feedback inhibitors. When stimulated, it inhibits alpha1 receptors and smooth muscle contraction]
- decreases HR, rebound HTN after sudden withdrawal from a high dose

19

Hydralazine

- direct arteriolar vasodilator
- used for HTN and heart failure
- causes lupus like syndrome as a side effect as seen also in isoniazid and procainamide
- used for hypertensive emerges

20

Minoxidil

- directly vasodilates arterial smooth muscle
- opens potassium channels, results in hyper polarization and relaxation
- causes hypertichosis - hair growth everywhere

21

Sodium Nitroprusside

- direct vasodilator (mixed)
- used for hypertensive emergencies, along with Nitroglycerin (venodilator)
- can cause cyanide toxicity (bad for people with renal disease)
- similar mechanism to Sildenafil (side effect = erection): increases intracellular GMP pathways to promote relaxation
cannot combine vasodilators and sildenafil - risk of orthostatic HTN

22

Amlodipine
Felodipine
Isradipine
Nicardipine sustained release
Nifedipine long-acting
Nisoldipine

- dihydropyridines - work on the peripheral vasculature (vasodilator) whereas non-dihydropyridines work on the heart
- calcium channel blockers
- Nicardipine used for hypertensive emergencies
- long term treatment of typical angina, prinzmetal's angina, HTN, cardiac arrhythmias
- adverse effects: peripheral edema, orthostatic hypotension

Prolong the time to onset of angina during
exercise
• Decrease frequency of anginal attacks
• Decrease the need to administer nitroglycerin
• Combined treatment with a calcium channel
blocker and a nitrate or a beta‐blocker has an
additive effect
• Calcium channel blocker alone is not effective in
the treatment of unstable angina

They reduce the amount of calcium entering the
smooth muscle cells of the systemic and
coronary vasculature. This effect results in:
• Relaxation of coronary arteries and therefore
increase in blood supply to the myocardium
• Relaxation of systemic arterioles and therefore
decrease in systemic blood pressure, decrease in
after‐load on the heart and decrease in
myocardial oxygen demand (MVO2).
They reduce the amount of calcium entering the
cardiac muscle cells. This effect results in
negative inotropic effect and decrease in
myocardial oxygen demand (MVO2).
• They reduce automaticity of sinoatrial node cells
in the heart and decrease heart rate. Decrease in
heart rate (negative chronotropic effect) is likely
to decrease MVO2