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Pharm Fall 2020 > Test 1 > Flashcards

Test 1 Flashcards

1
Q

What ace inhibitors have long 1/2 life, which is not a pro drug like all others

A

Fosinopril and ramipril have long 1/2 lives

Captopril is not a pro rug

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2
Q

ARB receptor blockers dosing

A

1 day orally.

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3
Q

Renin inhib. What other drug reduces it’s efficiency?

A

NSAIDs

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4
Q

Therapeutic uses for BB

A

HTN patients with arrhythmia, prev heart attack, agnina, chronic heart failure, migraine, anxiety, glaucoma.

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5
Q

Longest half life of calcium channel blockers

A

Amlodipine

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6
Q

Adverse effects/contra for calcium channel blockers

A

Most AE due to hypotension- dizzy, peripheral edema, reflex tachycardia, headache, fatigue.

Contra in HF patient

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7
Q

Hydrazaline usually take what with it

A

Vasodilator. Usually take BB to help with reflex tachycardia (prevent adverse effects of arrhythmia and angina) and a diuretic to help with reflex water retention.

Monotherapy in pregnancy ok

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8
Q

How does minoxidil work

A

Hyperpolarizes K+ channels. Oral admin for severe, non responsive HTN.

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9
Q

How to treat diabetes insidious symptoms of polyuria and polydipsia?

A

Thiazide

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10
Q

Most common diuretic

Most efficacious

A

Common- Thiazide

Loop works best- use in HF

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11
Q

CAI location of action and what are they used for

Avoid in pts with

A

PCT.
used to tx glaucoma, mountain sickness and pseudotumor cerebri.

Acetazolamide- 2 250 tablets for glaucoma.

Avoid in pts with liver problems.

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12
Q

What drug may reduce effects of loop diuretics

A

NSAIDS

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13
Q

Loop diuretic DOC

Adverse effects

A

Used to reduce acute pulmonary edema due to HF.
Also treats hyperglycemia and hyperkalemia.

Adverse effects: ototoxicity and hyperuricemia, hypovolemia (shock)

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14
Q

Thiazide diuretics are derived from

A

Sulfa.

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15
Q

How long does it take thiazide diuretics to work? Adverse effects

A

1-3 weeks.

Hyperuricemia= gout

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16
Q

Aldosterone antag Potassium Sparing diuretics adverse effects

A

Gi upset, peptic ulcer, chemical resembles sex hormones.

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17
Q

Resistance is influenced by what 2 things

A

Diameter (Direct)
____
Blood vol (indirect)

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18
Q

most common cardiovascular disease

A

HTN

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19
Q

How do baroreceptors control CO and peripheral resistance

A

Fall in BP causes baroreceptors to send fewer impulses to cardiovascular centers in the spinal cord. Reflex response of increase sympathetic and decrease parasympathetic. Vasoconstriction and inc erase CO

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20
Q

2 systems that control CO and peripheral resistance

A

Baroreceptors (quick)

RAAS (Slow)

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21
Q

Conversion of angiotensinogen to angiogtension II

A

Angiotensinogen converted by renin to angiotensin 1. Then converted by ace to angiotensin II

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22
Q

Role of angiotensin II

A

Vasoconstrictor
Increases levels of aldosterone, which causes reabsorption of sodium and water= increasing blood volume.
Induces cardiac hypertrophy. Causes myocardial stiffness and fibrosis and apoptosis

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23
Q

How do baroreceptors increase sympathetic activity

A

When they sense a decrease in blood pressure, they stimulate B1 to increase heart rate and force of contraction.

They also stimulate alpha 1 to cause vasoconstriction.

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24
Q

4 tips to manage HF

A

Decrease activity
Decrease Na intake
Treat co-morbid conditions
Avoid NSAIDS, alcohol, calcium channel blockers

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25
Q

Pharmacokinetics of digoxin

A

Little metab- leads body the same

Long 1/2 life bc accumulates in muscle. High Vd.

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26
Q

Digoxin adverse effects

A

Toxicity- arrhythmia, Gi probs, HA, confusion, fatigue

**blurred vision, halos, color distortion. Flashes, yellow vision.

Drug/drug interactions with other drugs that also decrease K+ levels in blood: erythromycin, tetracycline, verapamil, quinidine

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27
Q

Milrinone MOA and admin

A

PDE 5 inhibitor- cannot break down cAMP, which results in an increased level of calcium inside cell.
IV

28
Q

Aldosterone antagonists. Why are these good to use in HF and which one has less side effects

A

Good to use in HF because HF patients have increased levels of aldosterone.

Sprironolactone has more side effects due to sex hormones.
Epelerone has less.

29
Q

Vasodilators

A

Hydrazaline
Minoxidil
Isosorbide dinitrate and isosorbide mononitrate release NO (also organic nitrates)

30
Q

2 BB approved for chronic HF

A

carvedilol and metoprolol. Only use in chronic

31
Q

What drugs to use for high risk/no symptoms to lots of symptoms of HF patients

A

High risk/no symptoms

Risk factor reduction and inform patient
ACE or ARB
ACE + BB
Digoxin + diuretic + diet restriction

Lots of symptoms

32
Q

Quinidine adverse effects

A

Na channel blocker Type IA
Increase concentration of digoxin
GI
blurred vision due to anticholinergic activity

33
Q

Procainide adverse effects

A 
Lupus, CNS side effects 
Metabolites show class III activity
34
Q

Disopyramide adverse effects

A

Dry mouth, urine retention, blurred vision, constipation. Similar to anticholinergic.

35
Q

Flecainide and propafenone (1C) adverse effects

A

Metallic taste, constipation, induce arrhythmia

36
Q 
How does each class affect the heart contraction?
Class I thru 4
A

1: Na blocker. Slows phase 0, also affects phase 3
2: BB. Slows AV node. Slows phase 4.
3: K+. Prolongs phase 3 and QT interval (4)
4. Refractory period prolonged (phase 4) AV and SA node prolonged. Slows depol (phase 0)

0 and 3
4
3 and 4
0 and 4

37
Q

Potassium channel blocker drugs

A

Amiodarone long half life, lots of side effects, Whorl keratopathy, NAION.

Dronedarone- short half life, less side effects
Ibutalide-
Dofetilide
Sotalol- BB but high Class III activity

38
Q

Amiodarone

A 
Complex- has class 1-4 actions
DOC for atrial fib and anti anginas 
Long half life and lots of side effects
-pulmonary fibrosis 
-GI 
-CNS: dizzy, tremor 
-Blue skin
NAION
Whorl keratopathy
39
Q

4 other anti-arrhythmic drugs

A

Adenosine- caffeine decreases effectivity
Digoxin- Positive inotropic? ocular toxicity!
Magnesium- unknown MOA
Potassium- balance

40
Q

Arrhythmias have disfunction of

A
  1. Impulse generation
  2. Impulse conduction
    Both cause CO to decrease
    Worsened by ischemia, acidosis, electrolyte imbalances

tricky to treat!

41
Q

phases of heart contraction

A

phase 0: depol. Na+ flows into cell.
Phase 1: K+ channels open, then quickly close. Na+ channels inactivated.
Phase 2: Ca++ channels open and Ca++ enters cell, K+ leaks out. Plateau
Phase 3: Ca++ channels cost. K+ opens and K+ exits cell causing repol.
Phase 4: gradual increase in Na+ permeability. Na+ can start entering cell, causing depol.

42
Q

Force of contraction is directly related to unbound intracellular calcium levels. Sources of intracellular calcium.

A
  1. Voltage sensitive channels that cause calcium to move into cell
  2. Exchange with sodium
  3. Release from SR and mitochondria
43
Q

Abnormal automaticity causing arrhythmia

A

When sites other than SA show enhanced automaticity. Ex: Damaged myocardial cells may remain partially depolarized, allowing them to reach threshold sooner.
Tx with drugs that decrease calcium or sodium

44
Q

Abnormal impulse conduciton

A

Blocked nerve impulse may cause short circuit= premature contraction and re-entry defect.

Tx: Slow conduction or increase refractory period. Converts unidirectional block that may cause flutter into bidirectional block.

45
Q

How to treat angina

A

Decrease myocardial O2 requirements by decreasing cardiac work or increase 02 delivery with vasodilators.

46
Q

Determinants of cardiac O2 demand

A

Wall stress
HR
Contractility

Any increase = increase 02 demand. Often during physical activity

47
Q

Determinants of coronary blood flow

A

Perfusion pressure (diastolic)
Duration of diastole
Coronary vascular resistance

48
Q

Determinants of vascular tone

A

Arteriole tone (controls peripheral vascular resistance, systolic wall stress)

Venous tone (controls amount of blood returning to heart. Diastolic wall stress)

49
Q

3 types of angina

A
  1. Stable/classic/typical. usually due to blockage of coronary artery. Short lasting, happens during activity. Treat with rest or nitroglycerin.
  2. Variant/vasospastic. Occurs at rest. Unrelated to activity or HR. Respond well to vasodilators and calcium channel blockers.
  3. Unstable. (maybe due to plaque rupture) Classic angina getting worse- attacks with less exertion. Rest and nitroglycerin do not work.
50
Q

Organic nitrates

  • 3 types
  • Admin
A

Nitroglycerin
Isosorbide di- and mono nitrate

Admin sublingual or patch (first pass inactivates)
Tolerance develops quickly- do 12 hours on/12 off.

51
Q

DOC for acute angina

A

nitroglycerin.

52
Q

Nitroglycerine adverse effects

A

HA, tachycardia due to vasodilation, orthostatic hypotension, 12 hours on/12 off to avoid tolerance. Do to combine with PDE type 5 inhibitor.

53
Q

Preferred BB for angina

A

Atenolol, metoprolol

54
Q

What type of angina is BB not helpful for

A

Vasospastic angina because BB is not a vasodilator.

55
Q

DOC for chronic angina

A

BB or Ranolzaine (Sodium channel blocker)

56
Q

MOA of ranolzaine

A

Sodium channel blocker. Tx chronic angina. Inhibits late phase of Na+ current during depol.

Improves diastolic function and increases O2 supply

57
Q

3 type 5 PDE inhibitors

A

Sildenafil
Tadalafil - more selective to PDE 5, not 6.
Vardenafil

58
Q

MOA and side effects of PDE 5 inhibitors

A

MOA: Prevents inactivation of cGMP. No increases cGMP inside the cell, which leads to vasodilation.

Type 5 usually breaks it down.
Ocular side effects bc similar to PDE 6 inside the eye, a phototransductor. Causes mild impairment of color vision- blue/yellow/pink tinge. Last mins to hours.
Also causes blurred vision.

Do not take with organic nitrates= severe vasodilation.

59
Q

ADP receptor blockers have what side effects

A

Severe bruising, life threatening TTP

PP bound, 450 met

60
Q

What anti-thrombin med is excreted by the liver

A

Argatroban.

61
Q

DOC for dabigitran

A

prevent stroke because atrial fib

62
Q

administration for Xa inhibiting drugs

A

Apixiban and rivaroxaban are oral

Fondaparinux is Sub Q

63
Q

What thrombolytic drug is only approved for pulmonary emboli and is produced naturally by the liver

A

Urokinase.

64
Q

What thrombolytic agent is fibrin selective and a DNA recombinate

A

Alteplase

65
Q

What additional meds should you take with thrombolytic agents?

A

Aspirin. As it breaks down clot, may induce more clotting.

Pharm Fall 2020 (17 decks)

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