Brainscape's Knowledge GenomeTM

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


See full index

M2 Pharmacology Jen > Antianginal > Flashcards

Antianginal Flashcards

1
Q

Nitroglycerin: class

A

organic nitrate

Antianginal, vasodilator, venodilator

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

Nitroglycerin: PD

A

reacts directly with nitrate receptor on SM cell; sulfhydryl groups in receptor reduce organic nitrate (R-ONO2) to NO2 and then NO; NO crosses into SM cells, activates guanylate cyclase, leading to production of cGMP from GTP; cGMP acts to relax SM cells (probably by dephosphorylation of myosin light chains, making them less likely to react with Actin); then produces venodilation and vasodilation

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

Nitroglycerin: PK

A

well absorbed po, but very high first pass effect; prompt onset (1-2 min) when taken as SL tablet or spray; also can be given transdermally or iv

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

Nitroglycerin: tox

A

excessive hypotension, esp if patient is volume depleted; throbbing headache; flushing

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

Nitroglycerin: special issues

A

remove transdermal patch before defibrillation; use only fresh TNG tablets; tolerance can develop quickly (give 8 h holiday each night)

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

Nitroglycerin: interactions

A

excessive hypotension with other vasodilators; severe hypotension if taken with Viagra™ (sildenafil)[why is that???]

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

Nitroglycerin: indications

A

angina

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

Isosorbide dinitrate: class

A

organic nitrate, Venous vasodilator

Antianginal, CHF, antihypertensive

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

Isosorbide dinitrate: PD

A

same as nitroglycerin?:
reacts directly with nitrate receptor on SM cell; sulfhydryl groups in receptor reduce organic nitrate (R-ONO2) to NO2 and then NO; NO crosses into SM cells, activates guanylate cyclase, leading to production of cGMP from GTP; cGMP acts to relax SM cells (probably by dephosphorylation of myosin light chains, making them less likely to react with Actin); then produces venodilation and vasodilation

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

Isosorbide dinitrate: PK

A

same as nitroglycerin?:
well absorbed po, but very high first pass effect; prompt onset (1-2 min) when taken as SL tablet or spray; also can be given transdermally or iv

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Isosorbide dinitrate: tox

A

same as nitroglycerin?:

excessive hypotension, esp if patient is volume depleted; throbbing headache; flushing

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

Isosorbide dinitrate: special issues

A

same as nitroglycerin?:
remove transdermal patch before defibrillation; use only fresh TNG tablets; tolerance can develop quickly (give 8 h holiday each night)

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

Isosorbide dinitrate: interactions

A

same as nitroglycerin?:

excessive hypotension with other vasodilators; severe hypotension if taken with Viagra™ (sildenafil)[why is that???]

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

Isosorbide dinitrate: indications

A

angina

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

Atenolol: class

A 
Beta blocker (relatively beta1 specific)
Antihypertensive, antianginal, antiarrhythmic, anti-MI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Atenolol: PD

A

binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system via reduced renin release); recent evidence suggests less effective in preventing strokes than other drugs

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

Atenolol: PK

A

available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)

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

Atenolol: tox

A

excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Atenolol: special issues

A

may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal; may no longer be “first line” drug unless other indications exist (recent data)

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

Atenolol: interactions

A

additive effects with most other antihypertensives, additive AV block with CEB’s

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

Atenolol: indication

A

HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Atenolol: monitor

A

BP, HR, exercise tolerance. You cannot stop this drug cold turkey: you will have rebound angina/rearrythmias.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Metoprolol: class

A 
Beta blocker (relatively beta1 specific)
Antihypertensive, antianginal, antiarrhythmic, CHF
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Metoprolol: PD

A

binds directly to beta-receptors, with a preference for beta-1 over beta-2, leading to lower blood pressure via several potential mechanisms (less cardiac output, less activation of the RAA system via reduced renin release); recent evidence suggests less effective in preventing strokes than other drugs

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

Metoprolol: PK

A

available po or iv; variable oral F; onset 1-2 hours h, duration 12-24 h; can be given once per day; renally excreted (longer half-life)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Metoprolol: tox

A

excessive hypotension; bradycardia; heart block can worsen severe CHF (but indicated for mild to moderate CHF); worsen bronchospasm in severe asthmatics (bc not perfectly B1 selective, will block 10% of B2s)

27
Q

Metoprolol: special issues

A

may be especially useful in HTN patients with exertional angina, MI, atrial fibrillation; watch out for abrupt withdrawal
from lect: pts have to be compliant with taking it 3x/day OR take a more expensive brand name

28
Q

Metoprolol: interactions

A

additive effects with most other antihypertensives, additive AV block with CEB’s

29
Q

Metoprolol: indication

A

HTN

30
Q

Metoprolol: monitor

A

BP, HR, exercise tolerance. You cannot stop this drug cold turkey: you will have rebound angina/rearrythmias.

31
Q

Verapamil: class

A

pharmacologic class–calcium entry blocker; therapeutic class– antihypertensive, antianginal, antiarrhythmic CLASS IV

32
Q

Verapamil: PD

A

reduces BP by inhibiting influx of calcium through “slow channels”, thereby dilating peripheral arterioles; produces negative inotropic effect as well; for angina, reduces afterload, thus decreasing oxygen consumption; also, inhibits spasm of coronary arteries in vasospastic angina; blocks reentry paths through AV nodes in paroxysmal SVT.
From Rang/Dale: Blocks Ca2+ channels in both cardiac and smooth muscle so has negative inotropic and smooth muscle relaxant actions. prolongs plateau in action potential.

33
Q

Verapamil: PK

A

absorbed rapidly, but F ~30%; also available in SR tablets; cleared by kidney and liver (produces active metabolites); onset 2 h po, 1-5 min iv; half-life 6-12 h; may be given po or iv

34
Q

Verapamil: tox

A

hypotension, AV block (because slows action potential in SA and AV nodes), worsening of CHF, bradycardia

35
Q

Verapamil: interactions

A

additive effects with most other antihypertensives; additive toxic effects on heart when given with beta-blockers

36
Q

Verapamil: special

A

use reduced doses in patients with both renal and hepatic disease; short-acting nifedipine (and similar CEBs) can increase risk of MI (unclear why); Pregnancy C

37
Q

Verapamil: monitor

A

weight, edema, BP

38
Q

Diltiazem: class

A

Ca entry blocker

Antihypertensive, antianginal, antiarrhythmic

39
Q

Diltiazem: class representative?

A

Verapamil

40
Q

Aspirin: class

A

Pharm class–salicylate, COX inhibitor

Therapeutic class–analgesic, anti-inflammatory, antiplatelet, antipyretic, prevention of MI

41
Q

Aspirin: PD

A

at low doses (<325 mg/day), tends to irreversibly inhibit COX (1) in platelets, leading to decreased formation of TBX A2 (vasocontrictor, platelet aggregator), and transiently inhibit COX(2) in endothelium, leading to transient decreased formation of prostacyclin (PGI2) (vasodilator, inhibitor of platelet aggregation)

42
Q

Aspirin: PK

A

F~60%, Tmax variable (e.g. AlkaSeltzer), metabolized to salicylate, half-life 3-4 h, duration 4-24+ h, 90% excreted as salicylate metabolites in urine

43
Q

Aspirin: tox

A

especially at high doses can cause ulceration of GI tract, bleeding disorders, tinnitus

44
Q

Aspirin: interactions

A

inhibit tubular secretion of methotrexate, potentiate bleeding from warfarin

45
Q

Aspirin: special

A

avoid in patients with nasal polyps and asthma; regular, buffered, enteric coated

46
Q

Aspirin: indications

A

antiplatelet, arthritis

47
Q

Clopidogrel: class

A

pharmacologic; ADP receptor blocker

therapeutic class–platelet aggregation inhibitor

48
Q

Clopidogrel: PD

A

Inhibits platelet aggregation by irreversibly blocking ADP receptors. Inhibits fibrinogen binding by preventing glycoprotein IIb/IIIa from binding to fibrinogen.
useful in primary or secondary prevention of TIA, stroke, angina, MI, angioplasty, stent placement, ACS, etc

49
Q

Clopidogrel: PK

A

well absorbed, onset 1-2 h after oral dose, hepatic metabolism, half-life ~8h
bc irreversible, effects last several days until platelets are replaced

50
Q

Clopidogrel: tox

A

hemorrhage at virtually any site;

51
Q

Clopidogrel: special

A

Careful risk/benefit assessment in each patient, AND it’s quite expensive

52
Q

Clopidogrel: interactions

A

may inhibit CYP 3A4

53
Q

Clopidogrel: indications

A

ACS. often given with aspirin

54
Q

Abciximab: class

A

pharmacologic class–Fab fragment chimeric monoclonal antibody, IIb-IIIa inhibitor
therapeutic class: adjunct to PCI to prevent ischemic complications; treatment of MI; Antiplatelet

55
Q

Abciximab: PD

A

noncompetitive inhibitor of the GP IIb/IIIa receptor, prevents binding of fibrinogen, vWF, and other adhesive ligands to the receptor on activated platelets. Need to block >80% of these receptors to maximially inhibit platelet

56
Q

Abciximab: PK

A

IV bolus followed by IV infusion; half-life about 30 min. Bleeding time declines to <12 min within 12 h of stopping infusion

57
Q

Abciximab: tox

A

contraindicated in presence of aneurysm, AV malformation, bleeding, coagulopathy, GI bleed, intracranial mass, retinal bleeding, stroke, surgery, low platelets, trauma, vasculitis

58
Q

Abciximab: special

A

Exact role is still being defined, and evolves over time; cost is a big factor

59
Q

Abciximab: interactions

A

Additive effects with aspirin, clopidogrel, heparin, low dose t-PA

60
Q

Abciximab: indication

A

when PCI is planned to treat ACS

61
Q

Tirofinab: class

A

IIb-IIIa inhibitor

Antiplatelet

62
Q

Tirofinab: class rep

A

Abciximab

63
Q

Eptifibatide: class

A

IIb-IIIa inhibitor

Antiplatelet

64
Q

Eptifibatide: class rep

A

Abciximab

M2 Pharmacology Jen (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions