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My Notes > Cardio drugs - easier > Flashcards

Cardio drugs - easier Flashcards

1
Q

Which antiarrhythmics prolong the QT interval?

A

Class IA and Class III

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2
Q

Which antiarrhythmics cause constipation?

A

quinidine (may cause constipation due to antimuscarinic effects or diarrhea due to alpha effects)
amiodarone
Ca2+ channel blockers (verapamil, diltiazem)

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3
Q

Which antiarrhythmics are contraindicated in COPD and asthma?

A 
β-blockers (class II)
(Adenosine may cause bronchospasm)
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4
Q

Which antiarrhythmics may mask signs of hypoglycemia?

A

β-blockers (class II)

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5
Q

Which antiarrhythmic drug may exacerbate vasospasm in Prinzmetal angina?

A

propranolol

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6
Q

Which antiarrhythmic is contraindicated in cocaine users?

A

β-blockers

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7
Q

For overdose of which antiarrhythmic would you give glucagon?

A

β-blockers

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8
Q

Which class is flecainide in?

A

IC

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9
Q

Which class is propafenone in?

A

IC

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10
Q

Which class is mexiletine in?

A

IB

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11
Q

Which class is procainamide in?

A

IA

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12
Q

Which class is ibutilide in?

A

III

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13
Q

Which class is sotalol in?

A

III

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14
Q

Which class is dofetilide in?

A

III

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15
Q

Which class is carvedilol in?

A

II

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16
Q

Which class are K+ channel blockers?

A

III

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17
Q

Describe the curve of IC drugs

A

slope of phase 0 is very decreased

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18
Q

Describe the curve of IB drugs

A

slope of phase 0 is slightly decreased and AP duration is decreased

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19
Q

Describe the curve of IA drugs

A

slope of phase 0 is moderately decreased and AP duration is prolonged

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20
Q

Describe the curve of class III drugs

A

normal phase 0, very prolonged AP

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21
Q

Which drugs work on nodal cells rather than nerve fiber conduction?

A

Class II, IV

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22
Q

Caffeine and theophylline block the effects of which antiarrhythmic drug?

A

Adenosine

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23
Q

Which drug is used for diagnosing/abolishing paroxysmal supraventricular tachycardia?

A

Adenosine

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24
Q

Which antiarrhythmic drug has a duration of action of 15 seconds? Which has a T1/2 of 80 days?

A

15 seconds: adenosine

80 days: amiodarone

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25
Q

Which antiarrhythmic drug hyperpolarizes cells by ↑ K+ outflow? Which blocks K+ inflow thus prolonging repolarization?

A

Adenosine

Class III drugs s.a. amiodarone

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26
Q

What is the treatment for torsades de pointe?

A

Magnesium sulfate

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27
Q

Which drugs cause conduction delay?

A

drugs which affect AV node conduction:

  • Ca2+ channel inhibitors (class IV)
  • Beta blockers (class II)
  • Digoxin
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28
Q

What is the most commonly noted side effect of amlodipine?

A

peripheral edema (it is a vascular-selective Ca2+ channel blocker)

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29
Q

What is the problem with reflex tachycardia? In which patients should vasodilators that cause reflex tachy be avoided?

A

↑ myocardial O2 demand → ischemia in patients with acute coronary syndrome

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30
Q

What is the mechanism of action of digoxin?

A
  1. Na+/K+ ATPase inhibitor → indirect inhibition of Na+/Ca2+ exchanger → ↑ [Ca2+]i → positive inotropy
  2. stimulates vagus nerve → ↓ HR
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31
Q

What two conditions is digoxin used for?

A
  1. CHF (because ↑ contractility)

2. A fib (b/c SA node depression and ↓ AV node conduction, both via vagus)

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32
Q

Does digoxin cause constipation or diarrhea?

A

Diarrhea via cholinergic effects (think about how it stimulates the vagus to ↓ HR; other cholinergic effects: vomiting, nausea, blurry yellow vision)

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33
Q

What is the mechanism of hydralazine? As such, what should be co-administered?

A

(NO donor?) → ↑ cGMP → smooth mm. relaxation, selective for arterioles
Should give beta-blocker to prevent reflex tachycardia and diuretics for edema

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34
Q

Which hypertension drugs act via the NO → cGMP pathway?

A

Hydralaine and nitroprusside

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35
Q

Which drug can cause cyanide toxicity if given for more than 24 -36 hours?

A

Nitroprusside

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36
Q

Which receptor do ARBs block?

A

AT-1 in vascular smooth muscle

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37
Q

What does aliskrein block?

A

Renin (so inhibits formation of AT1 from angiotensinogen)

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38
Q

What are the direct effects of captopril?

A

Blocks ACE → ↓ ATII and ↓ bradykinin breakdown

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39
Q

What are the actions of AT II?

A

Main two actions:

  1. AT I receptor → vasoconstriction → ↑ BP [blocked by ARBs]
  2. Renal cortex → ↑ aldosterone

Other actions:

  1. Efferent arteriole → vasoconstriction → ↑ GFR
  2. Posterior pit → ↑ ADH
  3. Proximal tubule → ↑ Na+/H+ activity → Na, HCO3, and H20 reabsorption (prevent contraction alkalosis)
  4. Hypothalamus → thirst
40
Q

What are the enzymes and their respective inhibitors in the path below:
Angiotensinogen → (enzyme 1) → AT I →(enzyme 2)→ AT II

A
  1. renin, blocked by aliskiren

2. ACE, blocked by ACE inhibitors

41
Q

How do class IA drugs cause a prolonged QT interval?

A

They also inhibit the K+ channel → delay phase 3 repolarization

42
Q

What class of drugs are used to treat hypertensive patients post-MI?

A

β-blockers

43
Q

Drug class used for hypertensive patients with BPH:

A

α-blockers

44
Q

Drugs classes used for hypertensive patients with dyslipidemia:

A

α-blockers (also ↓ lipids), CCBs, ACEi/ARB

anything but β-blockers or thiazides b/c these ↑ blood lipids

45
Q

How do labetolol and carvedilol prolong survival in CHF patients?

A

α-1/β-1 blockade → prevents concentric remodeling (↓HR → ↑ symp → ↑ α1 → vasoconstrict → ↑ afterload → ↑ work → concentric hypertrophy)

46
Q

What drugs are used to ↓ eccentric remodeling in CHF patients, thus prolonging survival?

A

RAAS pathway blockers (to ↓ preload): ACEIs, ARBs, spironolactone; theoretically aliskiren but no data; β-blockers (prevent renin release)

47
Q

When would inotropes be beneficial in CHF management? Which drug is used?

A

acute only to ↑ CO to perfuse body (chronic use would → remodeling); digoxin is the drug of choice for ↑ contractility → ↑ CO

48
Q

What is the strategy in CHF treatment?

A
  1. prevent remodeling via ↓ preload (RAASi) and ↓ afterload (α-blockers)
  2. increase CO in acute cases via ↑ contractility (inotrope=digoxin)
  3. ↓ edema (loop diuretics, spironolactone [also good for #1])
49
Q

What are the pharmacokinetics of digoxin?

A
  1. Long T1/2 → high loading dose → ↑ risk for arrhythmias (b/c digoxin depolarizes cells)
  2. High protein binding → ↑ Vd → ↑ opportunity for displacement by quinidine, verapamil, amiodarone
  3. Renally cleared (and kidneys often underperfused in CHF → ↑ T1/2)
50
Q

Why can’t β-agonists be as inotropes in CHF patients? What are the alternatives?

A

β-receptors rapidly desensitize; alternatives: phosphodiesterase inhibitors (inamrinone, milirinone) and digoxin

51
Q

How would you treat arrythmia caused by digoxin toxicity?

A

Class IB - blocks inactivated Na channels in cells depolarized by digoxin; examples: lidocaine and phenytoin

52
Q

What are the direct activities of digoxin?

A

Na+/K+ ATPase inhibition → depolarizes nerve cell membranes → ↑ vagal activity → ↑ ACh release onto nodal cells → ↓ HR
Related side effect:
- depol → other NT’s released → disorientation (drunk appearance)

53
Q

What are the indirect activities of digoxin?

A

Na+/K+ ATPase inhibition → ↑ [Na+]i → inhibition of Na+/Ca2+ exchanger → ↑ [Ca2+]i → positive inotropy

54
Q

Which drugs should you be careful about administering with digoxin?

A
  1. Drugs that → hypokalemia: loop and thiazide diuretics (K+ competes with digoxin for site on Na+/K+ ATPase so too little K+ → exaggerated activity of digoxin)
  2. Drugs that compete for renal clearance and displace digoxin from its protein binding sites: verapamil, amiodarone, quinidine
55
Q

What is the antidote for digoxin overdose?

A
  1. slowly normalize K+ (digoxin can → hyperkalemia)
  2. cardiac pacer
  3. anti-digoxin Fab fragments
  4. Mg2+
    (5. class IB drugs for arrhythmia)
56
Q

What is the treatment strategy for prinzmetal angina?

A
  1. ↑ O2 delivery to heart by ↓ vasospasm: nitrates, CCBs
  2. ↓ O2 demand by ↓ TPR (α-block + β-block to prevent reflex tachy), CO (β-blockers), or both (β-blockers, nitrates, CCBs)
57
Q

Where is NO normally synthesized? from what? which enzyme?

A

Endothelial cells convert L-Arginine to NO using NO synthase (which is activated by Gq in many inflamm. pathways) → release NO into blood

58
Q

How does NO work?

A

synth in endothelial cells → enters smooth mm. cells of large veins from blood → activates guanylyl cyclase to convert GTP to cGMP → relaxation

59
Q

What AA is required in the breakdown of nitroglycerine to NO?

A

cysteine as GSH

60
Q

Why is nitroglycerine primarily used acutely in response to angina episodes?

A

rapidly acting, and can → acute tolerance (tachyphylaxis) due to GSH depletion (req’d to → NO)

61
Q

What drug do you want to make sure patients aren’t taking when you give nitroglycerine?

A

sildenafil (PDE5 inhibitor) b/c it also ↑ cGMP and can → massive vasodilation → ↓ BP → reflex tachy → ischemia

62
Q

What is isosorbide?

A

an oral extended release nitrate

63
Q

How does angioedema usually manifest clinically?

A

edema of the lips and larynx

64
Q

What CHF drug can cause angioedema?

A

ACE-I

65
Q

What is the suffix for ARBs?

A

-sartan (e.g. Losartan)

66
Q

What are the 3 side effects of adenosine?

A

flushing, hypotension, chest pain

67
Q

What is the diagnosis and treatment of a patient with palpitations come and go suddenly?

A 
paroxysmal SVT (if pacemaker is atrial tissue or AV node)
adenosine
68
Q

What activates and deactivates MLCK in smooth muscle?

A

Activation: Ca2+Calmodulin complex (M3/α1→Gq→↑Ca2+)

Deactivation (phosphorylation): PKA (β2 → Gs→adenylyl cyclase → ↑cAMP→ PKA)

69
Q

Which smooth muscle receptors ↑ [Ca2+]i (i.e. → contraction)?

A

Bronchial, GI, eye: M3
Vessels: α-1
Both are coupled to Gq

70
Q

Which receptors and what enzyme → ↑ NO?

A

Gq coupled M3, bradykinin, H1 receptors on endothelium → stimulate nitric oxide synthase (NOS) → NO production

71
Q

What enzyme does NO activate?

A

guanylyl cyclase

72
Q

What reaction does guanylyl cyclase catalyze?

A

GTP → cGMP

73
Q

What does cGMP activate?

A

protein kinase G

74
Q

What does protein kinase G activate? What does the activated enzyme do?

A

phosphatase - dephosphorylates myosin light chain so that it can’t interact with actin (relaxes smooth muscle)

75
Q

How do the final targets of cAMP and cGMP differ?

A

cAMP → → phosphorylation of MLCK (becomes inactive)
cGMP → → dephosphorylation of MLC
Both lead to relaxation of smooth muscle

76
Q

What are two examples of drugs that cause selective arteriolar dilation? When are they used?

A

hydralazine, minoxidil; severe HTN refractory to other tx b/c → reflex tachy & edema (use w/ sympatholytic and diuretic)

77
Q

What doe HMG-CoA reductase produce?

A

mevalonic acid (mevalonate), a precursor to cholesterol

78
Q

What are the two mechanisms of statins?

A
  1. block HMG-CoA reductase → ↓ mevalonic acid → ↓ cholesterol synthesis
  2. ↓ hepatic VLDL synthesis → ↓ triglycerides
79
Q

What drug besides statins ↓ VLDL synthesis, therefore reducing plasma triglycerides?

A

niacin (B3)

80
Q

Why are statins especially good for diabetics?

A

diabetics usually have high cholesterol and triglycerides, and statins work to ↓ both

81
Q

Why do statins cause rhabdomyolysis?

A

inhibition of HMG-CoA reductase → ↓ Coenzyme Q, a product of the cholesterol pathway and component of ETC → ↓ ATP → ↓ Na+/K+ pump → ↑ Na+ intracell → cell swelling and rupture

82
Q

Why do statins cause hepatotoxicity?

A

↓ VLDL synthesis → ↓ ability for liver to eliminate fat produced

83
Q

What do we monitor with statins?

A

LFTS: ALT/AST
Rhabdo: muscle CK

84
Q

Would chronic or acute EtOH users have a higher risk of toxicity with statin use?

A

acute → inhibits p450 → ↑ [statin]

85
Q

Why can’t you combine statins with the other lipid lowering drugs niacin and fibrates?

A

↑ risk for rhabdomyolysis: fibrates ↓ elimination of drug at kidney through competition

86
Q

What are two drugs that sequester bile acid in the gut?

A

cholestyramine and colestipol

87
Q

What effect do cholesterol lowering drugs have on LDL? Why?

A

↓ LDL b/c ↓ cholesterol → ↑ LDL receptor production in liver → ↑ liver sequestration of LDL from blood stream

88
Q

What lipid-lowering drugs ↑ risk of bleeding?

A

bile acid sequestrants b/c ↓ absorption of fat soluble vitamins (so will also have risk of osteomalacia, night blindness, etc..)

89
Q

What interactions do bile acid resins s.a. cholestyramine have with other drugs?

A

Any orally administered drug will have ↓ absorption because the lipid soluble portion of drugs is what we absorb, which requires bile salts to absorb

90
Q

Why do VLDL and TG ↑ with the use of bile acid resins?

A

compensatory mechanism for loss of LDL: liver has to make more VLDL → IDL → LDL; TGs are synthesized along with VLDL

91
Q

What is the clinical use for bile acid resins?

A

only in pure hypercholesterolemia b/c it causes ↑/exacerbation of hypertriglyceridemia and ↑ VLDL

92
Q

What is the primary side effect of niacin in it’s high-dose use as a lipid-lowering agent? How can we treat the side effect?

A

hypersensitivity → facial flushing; the fact that we can prevent it with an asprin a day indicates that the mechanism of the side effect is mediated by prostaglandins, NOT histamine

93
Q

What side effect does niacin have on the liver?

A

fatty liver b/c blocked VLDL production → buildup of fat

94
Q

What is the mechanism of fibrates (e.g. gemfibrozil)? What patients are they used for?

A

Induces lipoprotein lipases → causes TG to be taken up into cells (and stored as fat) → ↓↓↓ triglyceride levels; can only be used in patients with triglyceride imbalance (causes ↑ LDL in pts. w/ hypercholesterolemia)

95
Q

Recap on antihyperlipidemics:

  1. drug used ONLY in ↑ cholesterol and NOT if pt has ↑ TG?
  2. drug used ONLY in ↑ TG and NOT in pt. w/ ↑ cholesterol?
  3. drug used if combined ↑ TG and ↑ cholesterol?
A
  1. Cholestyramine, cholestipol
  2. Gemfibrozil
  3. Statins (can synergize with ezetimibe) and niacin

My Notes (23 decks)

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