First aid Pharm Flashcards

0
Q

Which CCBs are dihydropyridines? Where do they work best?

A

Amlodipine, nifedipine “dipine”. Vascular smooth muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
1
Q

Mechanism of Calcium Channel Blockers

A

Block voltage dependent L type calcium channels to decrease contractibility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

Diltiazem, verapamil. Heart.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Side effects of CCB?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

MOA of Hydralyzine?

A

Inc cGMP leads to muscle relaxation of arterioles > veins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Toxicity of Hydralyzine?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Use, MOA, and toxicity of nitroprusside?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

MOA and use of fenoldopam?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

MOA of nitrates?

A

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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Toxicity of nitrates?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

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

A
  • Decreases LDL
  • inhibits conversion of HMG-CoA to mevalonate (cholesterol precursor)
  • hepatotoxicity, myopathy (elevated CK, worse when taken with fibrates)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Effect, MOA, side effects of bile acid resins?

A

Names: cholestyramine, colestipol, colesevelam

  • prevent intestinal reabsorption of bile acids (making liver use cholesterol to reproduce)
  • GI upset
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Effect, MOA, toxicity of ezetimibe?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Niacin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Prazosin

A

Selective alpha 1 adrenergic blocking causing peripheral vasodilation.

16
Q

Causes of drug-induced long QT syndrome?

A
AntiArrythmics (class 1A and 3)
AntiBiotics (macrolides)
Anti"C"ychotics: haloperidol 
AntiDepressants: TCAs
AntiEmetics: ondansetron
17
Q

Mechanism and toxicity of digoxin? How is toxicity treated?

A

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+

18
Q

In general, what do class I antiarrhythmics do?

A

They are sodium channel blockers. They slow or block conduction

19
Q

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

A

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

20
Q

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

A

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

21
Q

What is class 1C? Mechanism? Toxicity?

A

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

22
Q

What is the general effect of class II antiarrhythmics?

A

Beta blockers!

23
Q

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

A

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

24
Q

What do class III antiarrhythmics do in general?

A

Potassium channel blockers

25
Q

Names, effect, and toxicity of class III antiarrhythmics?

A

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

26
Q

What do class IV antiarrhythmics do? Toxicity?

A

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

27
Q

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

A

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

  • blunted by caffeine and theophylline
  • flushing, hypotension, bronchospasm, sense of impending doom
28
Q

When is Mg used in cardiac disease?

A

Torsades and dig toxicity

29
Q

What happens when both nitrates and PDEs are used?

A

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

30
Q

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

A

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)

31
Q

How does norepinephrine extravasation present? What is the antidote?

A

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