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
What can you combine Niacin with to increase it's effect on lowering LDL?
A bile acid sequestrant (aka resin) or resin + statin (decrease up to 70% of LDL)
26
A common SE of Niacin is flushing. What is the mechanism of flushing? What can the pt take to prevent this SE?
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
When giving niacin w/ a statin, what risk is increased?
rhabdomyolysis
28
Why should you be cautious when giving niacin to a diabetic? | What other SE does niacin have?
b/c it increases plasma glucose. | it increases uric acid levels→↑ risk of gout attack
29
What drugs are used to treat Type III (familial dysbetalipoproteinemia: a mutant apoE causing an ↑ in IDL → ↑s TG & cholesterol)?
Fibric Acid Derivatives (Fenofibrate & Gemfibrozil)
30
When Gemfibrozil and statins are co-administered levels of both drugs may ↑↑. Why does this NOT happen when you give Fenofibrate w/ statins?
different glucuronidation
31
What is the BBW for Lomitapide?
BBW=Hepatotoxicity | Microsomal Triglyceride Transfer Protein (MTP) Inhibitors
32
What is the BBW for Mipomersen?
BBW=Hepatotoxicity and increased hepatic fat (hepatic steatosis) (Oligonucleotide Inhibitor)
33
Class I (Na+ channel blockers) decrease which phase of the AP? What do they do to nodal cells?
Decrease phase 0 slope. | Decrease slope of phase 4 and increase the threshold for firing.
34
What are the two serious SE of Quinidine?
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
What are the 2 serious SE of Procainamide?
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
What do Class IA drugs do to ERP and the slope of Phase 0?
increase the ERP; intermediate effect on reducing slope of phase 0.
37
What do Class IB drugs do to ERP and the slope of Phase 0?
decrease the ERP (↓ AP duration); smallest effect on reducing slope of phase 0.
38
What do Class IC drugs do to ERP and the slope of Phase 0?
no effect on ERP; greatest effect on reducing slope of phase 0.
39
Why should you reserve use of Class IC drugs to only life-threatening arrhythmias?
Assoc. w/ mortality and cardiac arrest! (MOST potent Na+ channel blockers) Do NOT use in pt post MI.
40
What are Class II (β blockers) proven to prevent?
Recurrent infarction and sudden death post MI.
41
If your pt has asthma, which class of antiarrhythmic drugs should you use FIRST?
Class II CARDIOSELECTIVE β blockers | Atenolol, Metoprolol, Acebutolol, Bisoprolol, Esmolol
42
What major SE are Class III (K+ channel blockers) assoc. w/?
Increase the likelihood of developing early after depolarization and torsade de pointes (“reverse use-dependency”).
43
What does Amiodarone (Class III antiarrhythmic) contain? What is it structurally similar to? What are its MOA?
``` Contains iodine and is structurally related to thyroid hormones. MOA: has class I-IV effects + blocks alpha receptors and induces vasodilation ```
44
What SE are assoc. w/ Amiodarone (Class III antiarrhythmic)?
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
What antiarrhythmic drug should you avoid using in pts w/ acute decompensation or advances heart failure? Why?
Dronedarone (Class III antiarrhythmic). | Assoc. w/ increased risk of stroke, heart failure and death.
46
What are the two classes/mechanisms assoc. w/ Sotalol (antiarrhythmic)? What serious SE is it assoc. w/?
β-adrenoreceptor-blocking (Class II) and cardiac action potential duration prolongation (Class III) properties. SE: torsade de pointes.
47
Ibutilide (pure class III antiarrhythmic agent with no other class effects) is assoc. w/ what serious SE?
SE: torsade de pointes
48
Verapamil and Diltiazem (o Class IV – Calcium channel blockers) are assoc. w/ what serious SE?
AV nodal block (can be reversed by atropine and b-receptor stimulant)
49
What are all of the antiarrhythmic drugs associated w/ torsade de pointes?
1. Quinidine (Class IA) 2. Procainamide (Class IA) 3. Class III drugs (Sotalol, Dofetilide, Ibutilide)