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Cardio > Lecture 27: Cardio Pharm > Flashcards

Lecture 27: Cardio Pharm Flashcards

1
Q

What is ISA activity?

A

Intrinsic sympathomimetic activity

Blocks strong stimulation of beta receptors by endogenous EPI and NE but act as weak agonists at beta receptors

Useful for patients who need beta blocker but get adverse cardiac effects from too much beta receptor blockade

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2
Q

What are drugs with ISA activity?

A

Beta blockers:

Pindolol (nonselective)

Acebutolol (beta1 selective)

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3
Q

What are therapeutic uses for beta blockers?

A

Angina

HF

MI

Some cardiac arrhythmias

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4
Q

Explain angina pectoris

A

Chest pain triggered by O2 supply demand imbalance

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5
Q

What are determinants of MVO2 (oxygen demand)?

A

HR

IS

AL

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6
Q

How might some angina patients have low oxygen supply?

A

Some patients have low coronary blood flow from underlying coronary artery disease

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7
Q

What is the most likely explanation for efficacy of beta blockers in treatment of angina?

A

Beta blockers decrease HR

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8
Q

How do beta blockers decrease AL?

A

Decrease afterload by decreasing BP

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9
Q

How do beta blockers help with angina?

A

Dec. oxygen demand
Dec. HR, IS, BP (which dec. AL)

Inc. oxygen supply indirectly
Dec. HR = longer diastole (more filling time) = inc. CBF

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10
Q

How do beta blockers help with HF?

A

Dec. bad effects from sympathetic activation = dec. oxygen demand, dec. cardiac hypertrophy + remodeling

Antiarrhythmic effects

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11
Q

How do beta blockers help with cardiac arrhythmias?

A

Dec. conduction = inc. refractoriness in AV node

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12
Q

What are beta blocker AEs?

A

HF, sinus bradycardia, AV block

Inc. airways resistance in patients with asthma/COPD

DM + hypoglycemia episodes

Impaired peripheral circulation in patients with PVD (beta2 vasodilation blocked)

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13
Q

Only which beta blockers have established efficacy for HF?

A

Metoprolol

Carvedilol

Bisoprolol

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14
Q

What is phentolamine?

A

Nonselective alpha blocker

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15
Q

What are prazosin and tamsulosin?

A

Alpha1 blockers

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16
Q

What are therapeutics for alpha 1 blockers?

A

HPT (for strong)

Block vasoconstriction = dec. SVR = dec. BP

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17
Q

What are alpha1 blocker AEs?

A

Orthostatic hypotension

Less reflex tachycardia than nonselective alpha blocker

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18
Q

What is phenylephrine and midodrine?

A

Alpha1 selective agonists

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19
Q

What is clonidine and alpha-methyldopa?

A

Alpha2 selective agonists

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20
Q

What are therapeutic uses for alpha2 agonists?

A

HPT (not first line)

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21
Q

What is the MOA of alpha 2 agonists?

A

Act at alpha2 receptors in medulla oblongata to dec. sympathetic tone to CV system

Act at presynaptic alpha2 receptors to decrease NE release

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22
Q

What are alpha 2 agonists AEs?

A

Sedation

Xerostomia

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23
Q

What are DRIs and what do they act on?

A

Direct renin inhibitors

Act on renin

“Kirens”

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24
Q

What are ACEIs and what do they block?

A

ACE inhibitors

Block ACE enzyme

“Prils”

25
Q

What are ARBs and what do they act on?

A

Angiotensin receptor blockers

Act at AT1 receptors

“Sartans”

26
Q

Identify drug class for Aliskiren, Captopril, Losartan

A

Aliskiren = DRI

Captopril = ACE inhibitor

Losartan = ARB

27
Q

What are major indications for ACE inhibitors?

A

HPT (1st-line)

HF

MI

28
Q

What are major adverse effects of ACE inhibitors?

A

Cough

Angioedema

29
Q

What are indications for ARBs?

A

HPT (1st line)

HF

MI

30
Q

What are major indications for DRIs?

A

HPT

31
Q

What is another potential adverse effect of ACEIs, ARBs, and DRIs???

A

HYPERkalemia

32
Q

Differentiate between MOA of ACEIs and ARBs

A

ACEIs block synthesis of Ang II

ARBs block effects of Ang II

33
Q

Where are L-type calcium channels (LTCCs) found?

A

Vascular SM

Cardiac myocytes

SA node

AV node

34
Q

What are effects of LTCCs at vascular SM, cardiac myocytes, and pacemaker cells

A

Vascular SM = vasoconstriction

Cardiac myocytes = Inc. IS

SA node = inc. HR

AV node = inc. AV conduction

35
Q

Describe effect of calcium influx through each LTCC

A

Vascular SM
Inc. Ca-calmodulin activation of MLCK = inc. phosphorylation of MLC = inc. SM contraction

Cardiac myocytes
Inc. Ca release from SR = inc. binding of calcium to TnC = inc. contractile force

SA node
Inc. phase 4 slope (automaticity) = inc. firing rate

AV node
Inc. Phase - slope/amplitude = inc. conduction velocity

36
Q

Compare non-DHPs vs. DHPs

A

Non-DHPs = slower recovery of LTCCs in heart

DHPs result in more vasodilation

37
Q

What are examples of DHPs

A

Nifedipine

Little effect on IS, HR or AV conduction

38
Q

What are examples of non-DHPs?

A

Verapamil

Diltiazem

39
Q

What are therapeutic uses of CCBs?

A

HPT (1st line, especially DHPs)

Particularly for patients with angina or cardiac arrhythmias

Cardiac arrhythmias

40
Q

How do CCBs help angina?

A

CCBs dec. AL (by causing vasodilation which decreases BP) and inc. CBF

Non-DHPs will also dec. HR and IS

41
Q

What are AEs of CCBs?

A

Vasodilation = hypotension, headache, peripheral edema (DHPs**)

Constipation (verapamil **)

Bradycardia, AV block, cardiac depression/HF (non-DHPs **)

42
Q

What are examples of organic vs. inorganic nitrates?

A

Organic = nitroglycerin, isosorbide dinitrate

Inorganic = nitroprusside

43
Q

How do organic nitrates help with angina?

A

Inc. oxygen supply via vasodilation (and inc. CBF)

Dec. oxygen demand
Vasodilation = dec. AL
Arteriole dilation = dec. BP + AL
Venodilation = dec. venous return = dec. AL

44
Q

What are AEs of organic nitrates?

A

Vasodilation = hypotension, headache, flushing, reflex tachycardia

Tolerance

45
Q

How is vasospastic angina treated?

A

CCBs or organic nitrates

Avoid Beta blockers because we don’t want to block vasodilation!!

46
Q

What are therapeutic uses of nitroprusside?

A

Hypertensive emergencies

Acute HF

Production of controlled hypotension during surgery

47
Q

What are AEs of nitroprusside?

A

Hypotension

Cyanide toxicity

48
Q

What are examples of PDE inhibitors and how do they work?

A

Sildenafil

Inhibit PDE = dec. degradation of cGMP = inc. effects of endogenous NO

49
Q

What are indications for PDE5 inhibitors?

A

ED

Pulmonary HTN

50
Q

What are AEs of PDE5 inhibitors?

A

Headache, flushing

Back pain

Vision loss

Hearing loss

Dec. BP in patients taking anti-HPT drugs (most likely a problem with alpha1 blockers)

51
Q

What is Riociguat and how does it work?

A

SGC activator - stabilizes binding of NO to sGC

52
Q

What are major indications for Riociguat?

A

Pulmonary HPT

53
Q

What are major AEs for Riociguat?

A

Headache, GI effects

Contraindicated in patients taking organic nitrates or PDE5 inhibitors, pregnancy

54
Q

What drugs are good for pulmonary HPT?

A

Endothelin receptor antagonists

PGI2 analogs

PDE5 inhibitors

sGC activator

CCBs (especially DHPs)

55
Q

What is digoxin?

A

Cardiac glycoside = inotropic drug

56
Q

How does digoxin work?

A 
Inhibits NCX (sodium-K ATPase)
=
Dec. electrochemical gradient for sodium
=
Dec. calcium extrusion by NCX
=
Inc. intracellular calcium
=
Inc. IS
57
Q

What is the effect of digoxin’s increased parasympathetic and decreased sympathetic tone to heart?

A

Dec. AV conduction

Useful for re-entrant supraventricular tachycardia (AVNRT) and control of ventricular rate in atrial fibrillation

58
Q

What is dobutamine?

A

Beta1 agonist that leads to increased IS

59
Q

What is dobutamine used for?

A

Short term acute HF

Cardio (8 decks)

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