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Cardio Exam 1 > Pharm Need to Knows (Anti-HTN, Anti-Hyperlipidemics & Arrhythmics) > Flashcards

Pharm Need to Knows (Anti-HTN, Anti-Hyperlipidemics & Arrhythmics) Flashcards

1
Q

How does Angiotensin II raise BP?

A

Systemic vasoconstriction (effect seen w/n 10 sec. of exogenous injection, acts on resistance arterioles)

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2
Q

What is the MOST important class of Angiotensin antagonists?

A

ACE inhibitors (end in -pril)

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3
Q

What are the BEST drugs to use for HTN in pts w/ chronic kidney disease, diabetes and heart failure post MI?

A

ACE inhibitors

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4
Q

What is the MOST common SE of ACE inhibitors? What causes it? What is the other main SE we need to know?

A
  1. Dry cough (d/t ↑ bradykinin which is usually metabolized by ACE)
  2. angioedema
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5
Q

What drugs were we told to remember reduce renin secretion?

A

β-Blockers!

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6
Q

What drug has the common SE of a cough that is NOT mediated by bradykinin?

A

Aliskiren (one and only approved Renin inhibitor)

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7
Q

What drug is associated w/ “Lupus Erythematous-like” SE?

A

Hydralazine (oral vasodilator)

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8
Q

What vasodilator drug dilates arterioles ONLY w/ no effect on veins?

A

Minoxidil

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9
Q

What is a common SE of Minoxidil? Who should you not give this drug to?

A

Hypetrichosis (increased hair)- (FYI: Minoxidil is the main ingredient in Rogaine)

CAUTION in heart failure

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10
Q

What drug has a SE profile of hypotension, metabolic acidosis, arrhythmias, death (assoc. w/ the release of cyanide)? What is the antidote?

A

Nitroprusside (parenteral vasodilator)

Antidote=thiosulfate and hydroxocobalamin

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11
Q

All calcium channel blockers inhibit which calcium channel?

A

L-type and cause relaxation of arterial smooth muscle (not venous)

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12
Q

What calcium channel blocker has the common SE of constipation?

A

Verapamil

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13
Q

What centrally acting sympathoplegic agent is SAFE to use during pregnancy?

A

Methyldopa

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14
Q

Why does Clonidine (centrally acting sympathoplegic agent) initially cause an increase in BP when given IV?

A

It stimulates vascular a2b

discontinue slowly to avoid hypertensive crisis

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15
Q

What is the MOST important SE of propranolol?

A

bronchospasm (induces asthma)

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16
Q

What drugs’ cardioselectivity makes them good for treating pts w/ HTN and asthma, diabetes or peripheral vascular disease?

A

Metoprolol and Atenolol

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17
Q

What is the BEST drug to use in hypertensive emergencies assoc. w/ tachycardia? Why?

A

Esmolol (IV)
Because it is a β1 selective blocker that is rapidly metabolized. Once crisis is over, stop infusion and normal heart function resumes almost immediately.

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18
Q

What should you always give in combo w/ α1-adrenergic antagonists (Prazosin, Terazosin, Doxazosin)? Why?

A

Common SE is salt and water retention= give in combo w/ β-blocker or diuretic.

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19
Q

Random: What is a common secondary cause of HTN Fuchs told us to remember?

A

Licorice

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20
Q

Why should you give any HMG CoA Reductase inhibitor w/ a t(1/2)<4hrs as a single dose at bedtime?

A

b/c max rate of cholesterol synthesis from 12-2am

21
Q

ALL STATINS are candidates for drug-drug interactions w/ drugs that alter what 2 enzymatic activities?

A

CYP3A4 or OATP1B1 (less true for pravastatin)

22
Q

What 2 statins are NOT administered as β-hydroxy acid form? Why?

A

lovastatin and simvastatin (because they are pro-drugs).

23
Q

Why don’t bile acid sequestrants have systemic SE?

A

b/c the resins are NOT absorbed from the gut

24
Q

What should you caution your pt about when giving a bile acid sequestrant? How do you prevent this SE?

A

Impaction: blockage of digestive tract – minimized w/ fluids, fiber in diet or Metamucil as a stool softener.

25
Q

What can you combine Niacin with to increase it’s effect on lowering LDL?

A

A bile acid sequestrant (aka resin) or resin + statin (decrease up to 70% of LDL)

26
Q

A common SE of Niacin is flushing. What is the mechanism of flushing? What can the pt take to prevent this SE?

A

Stimulating HM74A receptors on epidermal Langerhans cells ↑s intracellular Ca2+ →activation of Ca2+ sensitive PLA2 → liberates arachidonic acid from membrane phospholipids.
Arachidonic acid is acted on by COX-1 to form PGs → ↑’d synthesis/release of PGD2/E2 from epidermal Langerhans.
Aspirin helps prevent flushing by inhibiting COX.

27
Q

When giving niacin w/ a statin, what risk is increased?

A

rhabdomyolysis

28
Q

Why should you be cautious when giving niacin to a diabetic?

What other SE does niacin have?

A

b/c it increases plasma glucose.

it increases uric acid levels→↑ risk of gout attack

29
Q

What drugs are used to treat Type III (familial dysbetalipoproteinemia: a mutant apoE causing an ↑ in IDL → ↑s TG & cholesterol)?

A

Fibric Acid Derivatives (Fenofibrate & Gemfibrozil)

30
Q

When Gemfibrozil and statins are co-administered levels of both drugs may ↑↑. Why does this NOT happen when you give Fenofibrate w/ statins?

A

different glucuronidation

31
Q

What is the BBW for Lomitapide?

A

BBW=Hepatotoxicity

Microsomal Triglyceride Transfer Protein (MTP) Inhibitors

32
Q

What is the BBW for Mipomersen?

A

BBW=Hepatotoxicity and increased hepatic fat (hepatic steatosis)
(Oligonucleotide Inhibitor)

33
Q

Class I (Na+ channel blockers) decrease which phase of the AP? What do they do to nodal cells?

A

Decrease phase 0 slope.

Decrease slope of phase 4 and increase the threshold for firing.

34
Q

What are the two serious SE of Quinidine?

A
  1. QT prolongation (toxicity), by delaying repolarization, can precipitate torsade de pointes
  2. Cinchonism: blurred vision, tinnitus, headache, disorientation, psychosis.
    Class I (Na+ channel blockers)
35
Q

What are the 2 serious SE of Procainamide?

A
  1. Excessive action potential prolongation, QT-interval prolongation and induction of torsade de pointes
  2. Lupus-like syndrome: arthralgia and arthritis, pleuritis, pericarditis reversible by stopping drug administration.

Class I (Na+ channel blockers)- side note: can use these post-MI when arrhythmias appear.

36
Q

What do Class IA drugs do to ERP and the slope of Phase 0?

A

increase the ERP; intermediate effect on reducing slope of phase 0.

37
Q

What do Class IB drugs do to ERP and the slope of Phase 0?

A

decrease the ERP (↓ AP duration); smallest effect on reducing slope of phase 0.

38
Q

What do Class IC drugs do to ERP and the slope of Phase 0?

A

no effect on ERP; greatest effect on reducing slope of phase 0.

39
Q

Why should you reserve use of Class IC drugs to only life-threatening arrhythmias?

A

Assoc. w/ mortality and cardiac arrest! (MOST potent Na+ channel blockers)
Do NOT use in pt post MI.

40
Q

What are Class II (β blockers) proven to prevent?

A

Recurrent infarction and sudden death post MI.

41
Q

If your pt has asthma, which class of antiarrhythmic drugs should you use FIRST?

A

Class II CARDIOSELECTIVE β blockers

Atenolol, Metoprolol, Acebutolol, Bisoprolol, Esmolol

42
Q

What major SE are Class III (K+ channel blockers) assoc. w/?

A

Increase the likelihood of developing early after depolarization and torsade de pointes (“reverse use-dependency”).

43
Q

What does Amiodarone (Class III antiarrhythmic) contain? What is it structurally similar to? What are its MOA?

A 
Contains iodine and is structurally related to thyroid hormones. 
MOA: has class I-IV effects + blocks alpha receptors and induces vasodilation
44
Q

What SE are assoc. w/ Amiodarone (Class III antiarrhythmic)?

A
  1. Thyroid dysfunction(hyper and hypo)
  2. Pulmonary toxicity (fibrosis) possibly fatal
  3. Liver toxicity
  4. Photodermatitis and blue-skin discoloration
  5. Asymptomatic microdeposits in the cornea
45
Q

What antiarrhythmic drug should you avoid using in pts w/ acute decompensation or advances heart failure? Why?

A

Dronedarone (Class III antiarrhythmic).

Assoc. w/ increased risk of stroke, heart failure and death.

46
Q

What are the two classes/mechanisms assoc. w/ Sotalol (antiarrhythmic)? What serious SE is it assoc. w/?

A

β-adrenoreceptor-blocking (Class II) and cardiac action potential duration prolongation (Class III) properties.
SE: torsade de pointes.

47
Q

Ibutilide (pure class III antiarrhythmic agent with no other class effects) is assoc. w/ what serious SE?

A

SE: torsade de pointes

48
Q

Verapamil and Diltiazem (o Class IV – Calcium channel blockers) are assoc. w/ what serious SE?

A

AV nodal block (can be reversed by atropine and b-receptor stimulant)

49
Q

What are all of the antiarrhythmic drugs associated w/ torsade de pointes?

A
  1. Quinidine (Class IA)
  2. Procainamide (Class IA)
  3. Class III drugs (Sotalol, Dofetilide, Ibutilide)

Cardio Exam 1 (5 decks)

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