Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

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

ARB receptor blockers dosing

A

1 day orally.

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

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

A

NSAIDs

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

Therapeutic uses for BB

A

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

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

Longest half life of calcium channel blockers

A

Amlodipine

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

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

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

How does minoxidil work

A

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

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

How to treat diabetes insidious symptoms of polyuria and polydipsia?

A

Thiazide

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

Most common diuretic

Most efficacious

A

Common- Thiazide

Loop works best- use in HF

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What drug may reduce effects of loop diuretics

A

NSAIDS

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

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

Thiazide diuretics are derived from

A

Sulfa.

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

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

A

1-3 weeks.

Hyperuricemia= gout

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Aldosterone antag Potassium Sparing diuretics adverse effects

A

Gi upset, peptic ulcer, chemical resembles sex hormones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Resistance is influenced by what 2 things

A

Diameter (Direct)
____
Blood vol (indirect)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

most common cardiovascular disease

A

HTN

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

2 systems that control CO and peripheral resistance

A

Baroreceptors (quick)

RAAS (Slow)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Conversion of angiotensinogen to angiogtension II

A

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

4 tips to manage HF

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Pharmacokinetics of digoxin

A

Little metab- leads body the same

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

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

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

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions