First aid Pharm

Question 0

Which CCBs are dihydropyridines? Where do they work best?

Answer 0

Amlodipine, nifedipine “dipine”. Vascular smooth muscle

Question 1

Mechanism of Calcium Channel Blockers

Answer 1

Block voltage dependent L type calcium channels to decrease contractibility

Question 2

What are the non-dihydropyridine CCBs? Where do they work?

Answer 2

Diltiazem, verapamil. Heart.

Question 3

Side effects of CCB?

Answer 3

Cardiac depression, AV block (non-dihydropyridines), hyperprolactinemia (verapamil),
Verapamil: constipation, gingival hyperplasia.
Amlodipine: flushing, ankle swelling

Question 4

MOA of Hydralyzine?

Answer 4

Inc cGMP leads to muscle relaxation of arterioles > veins.

Question 5

Toxicity of Hydralyzine?

Answer 5

Compensatory tachycardia (not used in angina/CAD), lupus-like syndrome.

Question 6

Use, MOA, and toxicity of nitroprusside?

Answer 6

Hypertensive emergency; short acting inc in cGMP for direct release of NO, can cause cyanide toxicity.

Question 7

MOA and use of fenoldopam?

Answer 7

Dopamine D1 receptor agonist: vasodilator coronary, peripheral, renal, splanchnic beds. Dec BP, and inc naturesis.

Question 8

MOA of nitrates?

Answer 8

Vasodilates by inc NO in vascular smooth muscle, which inc cGMP, which dec Ca, leading to myosin de phosphorylation, and smooth muscle relaxation. Greater effect on veins.

Question 9

Toxicity of nitrates?

Answer 9

Reflex tachycardia, hypotension, “Monday disease” loss of tolerance over the weekend (tachycardia, dizziness, headache)

Question 10

Effect, MOA, side effects of HMG-CoA reductase inhibitors?

Answer 10

• Decreases LDL
• inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
• hepatotoxicity, myopathy (elevated CK, worse when taken with fibrates)

Question 11

Effect, MOA, side effects of bile acid resins?

Answer 11

Names: cholestyramine, colestipol, colesevelam

• prevent intestinal reabsorption of bile acids (making liver use cholesterol to reproduce)
• GI upset

Question 12

Effect, MOA, toxicity of ezetimibe?

Answer 12

Dec LDL, prevents cholesterol absorption, rare side effects: inc LFTs and diarrhea

Question 13

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

Answer 13

Dec TG by up regulating LDL to inc TG clearance, also induces HDL synthesis through PPAR-alpha. Risk of myopathy, cholesterol gallstones

Question 14

Niacin

Answer 14

Inhibits lipolysis, reduces hepatic VLDL
Can cause red flushed face, hyperglycemia and hyperuricemia
-Can also cause vasodilation

Question 15

Prazosin

Answer 15

Selective alpha 1 adrenergic blocking causing peripheral vasodilation.

Question 16

Causes of drug-induced long QT syndrome?

Answer 16

AntiArrythmics (class 1A and 3)
AntiBiotics (macrolides)
Anti"C"ychotics: haloperidol 
AntiDepressants: TCAs
AntiEmetics: ondansetron

Question 17

Mechanism and toxicity of digoxin? How is toxicity treated?

Answer 17

Inhibits NaK ATPase, which decreases NaCa2+ exchanger
Cholinergic: nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias and AV block. Can lead to hyper K
Risk factors: quinidine dec dig clearance
Treatment: normalize K, anti-dig fragments, Mg+

Question 18

In general, what do class I antiarrhythmics do?

Answer 18

They are sodium channel blockers. They slow or block conduction

Question 19

What are the names, mechanism, and toxicity of Class IA?

Answer 19

Quinidine, Procainamide, Disopyamide
Inc AP duration, inc ERP, inc QT interval
Thrombocytopenia, torsades from QT
Quinidine: cinchonism (headache, tinnitus), Procainamide: reversible SLE like syndrome, Diso: HF

Question 20

What are the names of class 1B? MOA? Toxicity?

Answer 20

Lidocaine, mexiletine, phenytoin
Dec AP duration, used post-MI
Toxicity: CNS stimulation/depression, CV depression

Question 21

What is class 1C? Mechanism? Toxicity?

Answer 21

Flecainide, Propafenone
Prolong ERP, minimal AP effect
Toxicity: proarrhythmic esp in post-MI

Question 22

What is the general effect of class II antiarrhythmics?

Answer 22

Beta blockers!

Question 23

What are the beta blocker names? How do they work? What’s the toxicity?

Answer 23

Metoprolol, propranolol, esmolol (short acting), atenolol, timilol, carvedilol
MOA: dec SA and AV node (inc or interval) by dec cAMP, dec Ca currents
Toxicity: impotence, COPD exacerbation, Brady, AV block, HF, sedation, sleep problems.
Metoprolol: dyslipidemia, propranolol: exacerbates prinzmetal angina. Treat with saline, atropine, glucagon

Question 24

What do class III antiarrhythmics do in general?

Answer 24

Potassium channel blockers

Question 25

Names, effect, and toxicity of class III antiarrhythmics?

Answer 25

Inc AP duration, ERP, and QT interval
Sotalol (excessive B blockade) and Ibutilide- torsades. Amiodarone- pulm fibrosis, hepatotoxicity, thyroid, neurological, constipation, Brady, heart block, H
-Dofetilide

Question 26

What do class IV antiarrhythmics do? Toxicity?

Answer 26

CCB, dec conduction velocity, inc ERP and PR interval
Toxicity: constipation, flushing, edema, HF, AV block, sinus node depression
Contraindicated in HF, negative inotrope

Question 27

What is the effect of adenosine? What drugs blunt it’s effect? What are the side effects?

Answer 27

Hyperpolarizes cells by inc K+ release, dec Ca current.

• blunted by caffeine and theophylline
• flushing, hypotension, bronchospasm, sense of impending doom

Question 28

When is Mg used in cardiac disease?

Answer 28

Torsades and dig toxicity

Question 29

What happens when both nitrates and PDEs are used?

Answer 29

Cyclic GMP accumulates and causes profound hypotension (dizziness and confusion). Phosphodiesterase inhibitors block cGMP degradation while nitrates enhance synthesis

Question 30

What is streptokinase? When is it used? What are the side effects?

Answer 30

Streptokinase is a protein that makes a complex with plasminogen to cleave plasmin, which cleaves fibrin and dissolves thrombi. Most common side effect is hemorrhage (intracerebral-dec consciousness, asymmetric pupils, irregular breaths, or in GI)

Question 31

How does norepinephrine extravasation present? What is the antidote?

Answer 31

the tissues surrounding the site become cold, hard, and pale from alpha 1 vasoconstriction. Prompt treatment with phentolamine, an alpha blocker, does the trick.