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Cardiovascular Pharmacology > CV Drugs > Flashcards

CV Drugs Flashcards

1
Q

Mechanism(s) of Centrally-acting Agents

A

Stimulates the A2 receptor on SNS neurons, causing downregulation of norepinephrine release to systemic smooth muscle cells (clonidine)

Acts as a norepinephrine mimic that primarily acts on the brain to limit SNS outflow (methyldopa)

MAJOR EFFECT of both is to decrease systemic vascular resistance

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2
Q

How does increased SNS tone raise BP? There are 4 mechanisms

A

They cause vasoconstriction via A1-adrenergic signaling to smooth muscles, increasing systemic vascular resistance, and thus BP.

They act on B1-adrenergic receptors in the heart to increase CO and contractility, thus increasing BP.

They cause venous constriction via A1-adrenergic signaling to smooth muscles, increasing venous return/preload, causing increases in CO and contractility that lead to increased BP.

They stimulate renin release from the kidney, activating the RAA system, resulting in increased Na and water retention, thus raising BP.

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3
Q

Naming of Centrally-acting Agents

A

Clonidine and methyldopa

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4
Q

Clinical uses of Centrally-acting Agents

A

HTN: good adjunctive therapy (2nd line) due to having very few drug-drug interactions, w/methyldopa primarily used in pregnant women

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5
Q

Side Effects of Centrally-acting Agents

A

Both: sedation, depression, dry mouth (central acting agents can cause CNS problems, like depression)

Methyldopa: hepatotoxicity

Clonidine: bradycardia (unknown mechanism, perhaps due to increased vagal stimulation), clonidine withdrawal symptoms (HTN, headache, tremors, sweat)

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6
Q

Mechanism of A1-receptor Blockers

A

Block A1-adrenergic receptors on smooth muscle, preventing the action of norepinephrine, which normally causes smooth muscle contraction.

MAJOR EFFECT is decreased vascular resistance

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7
Q

Naming of A1-receptor Blockers

A

-zosin suffix (prazosin, terazosin, doxazosin)

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8
Q

Clinical uses of A1-receptor Blockers

A

HTN: adjunctive therapy (2nd line, NEVER a first line drug), good in patients w/enlarged prostates

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9
Q

Side Effects of A1-receptor Blockers

A

Orthostatic hypotension (due to all the vasodilation)

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10
Q

Mechanism(s) of Beta-Blockers

A

Block B1-adrenergic receptors on the heart and kidney, preventing norepinephrine from acting to increase CO/HR and renin release. Results in lower oxygen demand and decreased CO/HR/BP. Also results in greater diastolic filling time

Block B2-adrenergic receptors on smooth muscle cells, preventing epinephrine from acting to cause vasodilation and bronchodilation.

MAJOR EFFECT is to decrease CO/HR, vasoconstriction and bronchoconstriction are minor

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11
Q

Naming of Beta-Blockers

A

-olol suffix

B1-specific drugs: atenolol, metoprolol (LETTERS A-M)

B1 and B2 blocking drugs: propranolol, nadolol (particularly long half-life), timolol (LETTERS N-T)

B1, B2, and A1 blocking drugs: carvedilol, labetalol

B1 blocking and NO-activating drugs: nebivolol

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12
Q

Clinical uses of Beta-Blockers

A

HTN: adjunctive treatment (2nd line), HTN emergencies (labetolol can be administered IV)

HF: first line treatment, improves the heart’s sensitivity to SNS stimulation by inhibiting GPCR recycling via GRK2 and B-arrestin. ONLY THESE 3: metoprolol succinate, bisoprolol, carvedilol

CAD/IHD: acute (reduce ischemia by lowering oxygen demand), chronic (prevent recurrence), post-CABG

Arrhythmias: (FILL THIS IN)

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13
Q

Side Effects of Beta-Blockers

A

Bradycardia

Hyperkalemia (due to blocking of RAAS resulting in less Na/K antiport)

Fatigue (decreased CO)

Cold extremities and bronchospasm (due to B2-blockage causing vasoconstriction and bronchoconstriction)

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14
Q

Mechanism(s) of Ca-channel Blockers

A

Block L-type Ca-channels on smooth muscle, preventing Ca intake, thus inhibiting MLCK activity and smooth muscle contraction.

Block L-type Ca-channels in the heart, lowering HR and decreasing CO.

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15
Q

Naming of Ca-channel Blockers

A

Dihydropyridines (-dipine suffix, amlodipine, nifedipine) act only on VASCULATURE

Phenylalkylamines (verapamil) act only on HEART

Benzothiazepines (diltiazem) act on BOTH

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16
Q

Clinical Uses and Contraindications of Ca-channel Blockers

A

HTN: FIRST LINE drug, also good adjunctive drug; safe in diabetics, asthma, renal insufficiency, and lipid problems

CAD: slow down the HR/CO to decrease oxygen demand; acute (control spasm by inducing vasodilation)

Arrhythmias: (FILL THIS IN)

Contraindications: HF, do not give verapamil or diltiazem if pt is already on another HR slowing drug like a B-blocker

17
Q

Side Effects of Ca-channel Blockers

A

Vasculature acting (dihydropyridines and diltiazem): edema (MOST COMMON SIDE EFFECT)

Central acting (verapamil and diltiazem): bradycardia (MOST COMMON SIDE EFFECT)

All 3: drug-drug interactions due to CYP3A4 metabolism (though dihydropyridines to a lesser extent), dizziness, nausea, headache, constipation

18
Q

Mechanism(s) of Peripheral Vasodilators

A

Hydralizine: relaxes arterial smooth muscle to decrease vascular resistance (exact mechanism unknown)

Minoxidil: K-channel agonist that hyperpolarizes smooth muscle, leading to decreased vascular resistance

Nitroprusside and Nitrates: metabolized into NO, which increases cGMP in smooth muscle cells, activating PKG, resulting in more MLCP activity and less contraction, leading to decreased vascular resistance. This leads to decreased afterload. Nitrates also dilate the coronary arteries to allow for more blood flow.

19
Q

Naming of Peripheral Vasodilators

A

Hydralizine, minoxidil, nitroprusside

Nitrates: “nitro” in the name (nitroglycerin, dinitrate, isosorbide mononitrate)

20
Q

Clinical Uses of Peripheral Vasodilators

A

Hydralizine: HTN when other drugs don’t work due to side effects (can be administered PO or IV), HTN emergencies (IV administration); HF (combined w/isosorbide mononitrate)

Minoxidil: last resort for outpt HTN (PO only administration)

Nitroprusside: HTN emergencies (due to IV only administration)

Nitrates: acute MI (sublingual, control spasm), intermediate onset (topical, oral), long-term (transdermal, sustained release pills); HF (combined w/hydralazine)

21
Q

Side Effects of Peripheral Vasodilators

A

Hydralizine: headache, nausea, dizziness, vomiting; edema, angina/heart failure

Minoxidil: Na/water retention (downregulation of SNS firing in kidney), tachycardia/angina/heart failure (faster repolarization in pacemakers due to increased K-channel activity)

Nitroprusside: hypotension, cyanide/thiocyanate toxicity (manifests as lactic acid, anorexia, fatigue, confusion, psychosis)

Nitrates: headache, nausea, dizziness, vomiting

22
Q

What is the consequence of the body being quick to develop a tolerance for nitric oxide?

A

The dosing of nitrates and nitroprusside has to be spaced out, w/8 hour gaps where no drug is given in between each dose.

23
Q

Mechanism of Ranolazine

A

Blocks the late inward Na-current that is present in ischemic cells. Normally, the increased Na due to this current increases the activity of the Na/Ca exchanger, causing Ca to move into the cell and increasing contractility, and thus increasing oxygen demand and preventing proper relaxation.

Ranolazine prevents all this and reduces oxygen demand in ischemic cells.

24
Q

What is special about Ranolazine compared to anti-ischemic drugs?

A

Ranolazine does not lower BP or change HR since it only acts on ischemic cells. This allows it to be safely used in conjunction with nitrates, beta-blockers, and dihydropyridines

25
Q

Clinical Uses of Ranolazine

A

CAD/IHD: reduces oxygen demand of ischemic cells and helps them relax properly, preventing further damage

26
Q

Side Effects of Ranolazine

A

Potential drug-drug interactions since it is metabolized by CYP3A4

27
Q

Mechanism(s) of Digoxin

A

Positive inotropic effect: blocks Na/K ATPase in the heart, partially dissipating the Na gradient. The lack of gradient prevents the Na/Ca exchanger from functioning, leaving more Ca inside the cell, thus increasing contractile force.

Vagomimetic effect: slows down phase 4 depolarization in pacemaker cells

28
Q

Clinical uses of Digoxin

A

Arrhythmias: (FILL THIS IN)

HF: can help w/HF, but other medications are more popular

29
Q

Side Effects of Digoxin

A

Super low therapeutic window
Nausea, diarrhea
Yellow vision
Pro-arrhythmic

30
Q

How do you counteract the effects of severe Digoxin toxicity?

A

Monoclonal antibody fragments targeting digoxin

31
Q

Mechanism of Ivabridine

A

Slows HR by blocking the inward Na (FUNNY) current in SA node

32
Q

Clinical uses of Ivabridine

A

HF: only indicated if B-blockers have already been used and the pt’s HR is still too high (3rd/4th line drug)

33
Q

Mechanism of B1 Agonists

A

Stimulate the B1 receptor on the heart, causing increased HR and contractility/inotropy/lusitropy

34
Q

Naming of B1 Agonists

A

Dobutamine, norepinephrine, dopamine

35
Q

Clinical uses of B1 Agonists

A

ADHF: inotrope for cold/wet

36
Q

Mechanism of Milrinone

A

Inhibit phosphodiesterase 3 in the heart, preventing it from hydrolyzing cAMP. The increased cAMP results in increased HR and contractility/inotropy/lusitropy

37
Q

Clinical uses of Milrinone

A

ADHF: inotrope for cold/wet

Cardiovascular Pharmacology (5 decks)

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