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CVD > 02b: Pharmacology (MI and antithrombotics) > Flashcards

02b: Pharmacology (MI and antithrombotics) Flashcards

1
Q

Myocardial oxygen demand/supply: (increased/decreased) oxygen (demand/supply) in pneumonia.

A

Decreased supply

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2
Q

Myocardial oxygen demand/supply: (increased/decreased) oxygen (demand/supply) in sympathomimetic toxicity (i.e. cocaine).

A

Both increased demand and decreased supply

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3
Q

Myocardial oxygen demand/supply: (increased/decreased) oxygen (demand/supply) in aortic stenosis.

A

Increased demand

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4
Q

T/F: B-blockers, nitrates, and CCBs are disease-modifying agents used for MI.

A

False - non-disease modifying agents used for MI

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5
Q

List the B-blocker prototype used for MI.

A

Metroprolol

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6
Q

List the Ca channel blockers (CCBs) prototypes used for MI.

A

Diltiazem, verapamil, amlodipine

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7
Q

List the nitrate prototypes used for MI. What’s the difference between them?

A
  1. Nitroglycerin (short-acting)

2. Isosorbide dinitrate (intermediate-acting) and mononitrate (long-acting)

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8
Q

First-line therapy in symptom control for patients with exertional angina.

A

B-blockers

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9
Q

T/F: B-blockers have been shown to decrease mortality following acute MI.

A

True

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10
Q

List the three main disease states that B-blockers are used/indicated for.

A
  1. Angina/post-MI
  2. HT
  3. CHF
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11
Q

Metroprolol has (weak/moderate) lipid solubility and is mainly excreted via (bile/renal).

A

Moderate;

renal (95%)

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12
Q

Atenolol is (selective/non-selective) antagonist with (moderate/weak) lipid solubility and mainly excreted via (bile/renal).

A

Beta-1 selective;

Weak; renal

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13
Q

Propranolol is (selective/non-selective) antagonist with (moderate/weak) lipid solubility and mainly excreted via (bile/renal).

A

Non-selective;
HIGH lipid solubility;
50% bile, 50% renal

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14
Q

Labetolol is (selective/non-selective) antagonist with (moderate/weak) lipid solubility and mainly excreted via (bile/renal).

A

Non-selective (like Carvedilol);
Weak;
renal

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15
Q

(X) beta-antagonist is ONLY given by IV. Why?

A

X = esmolol

Relative potency is very low (not given for maintenance)

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16
Q

List some important side effects to consider with beta-blockers.

A
  1. Bradycardia and bronchoconstriction
  2. Fatigue/CNS stuff (depression, nightmares, insomnia)
  3. Erectile dysfunction
  4. Worsen PVD (ex: Raynaud’s)
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17
Q

β-antagonists should be used with caution in combination with (X) drugs. Both types can (increase/decrease) myocardial contractility and AV nodal conduction, possibly causing (Y).

A

X = nondihydropyridine CCBs (ex: Diltiazem/verapamil)
Decrease;
Y = heart failure or AV conduction block

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18
Q

CCBs block (inward/outward) Ca current through which specific cardiac channels?

A

Inward;

L-type Ca channel (responsible for maintaining plateau phase)

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19
Q

T/F: CCBs dilate all coronary and peripheral vessels.

A

False not veins

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20
Q

Which CCB prototype would you choose for vasodilation?

A

Amlodipine - specific target tissue is vascular SM cell

second choice: diltiazem

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21
Q

Which CCB prototype would you choose for slowing HR?

A

Verapamil - target nodal tissue

second choice: diltiazem

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22
Q

Which CCB prototype would you choose for reducing wall tension?

A

Verapamil - target cardiac myocyte

second choice: diltiazem

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23
Q

T/F: Verapamil, Diltiazem, and amlodipine are all eliminated via renal mechanisms.

A

False - all hepatic

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24
Q

T/F: Most common side effects of CCBs include nausea, HA, constipation, hypotension.

A

True

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25
Q

(Beta-blockers/CCBs/nitrates) are contraindicated for patients with heart failure.

A

Nondihydropyridine CCBs (i.e. Diltiazem, verapamil)

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26
Q

Which side effects of CCBs are potentially most worrisome?

A
  1. Erectile dysfunction

2. Liver dysfunction (rare)

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27
Q

T/F: Nitrates dilate all coronary and peripheral vessels.

A

True (venodilators, coronary vasodilators, and arteriolar dilators0

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28
Q

T/F: CCBs are usually administered orally, once-a-day.

A

True

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29
Q

The main physiologic action of nitrates is (X), particularly targetted to (Y).

A 
X = vasodilation
Y = systemic veins (decrease myocardial oxygen demand)
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30
Q

T/F: Nitrates have a mortality benefit nearly equal to that of beta-blockers.

A

False - no mortality benefit

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31
Q

What’s the mechanism of action of nitrates/nitroglycerin?

A
  1. Converted to NO at cell membrane
  2. Induces cGMP formation by guanylyl cyclase
  3. cGMP decreases intracellular Ca
  4. SM relaxation
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32
Q

Nitrates are very (hydrophilic/lipophilic) compounds. This is why (X) forms of the drug are used in the treatment of acute angina attacks.

A

Lipophilic;

X = sublingual tablets or sprays (rapidly absorbed via oral mucosa!)

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33
Q

T/F: Nitroglycerin is effective when taken prophylactically.

A

True

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34
Q

List the main side effects of nitrates.

A

HA, postural hypotension, flushing, reflex tachycardia

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35
Q

T/F: Tolerance has not yet been an issue in chronic nitrate use.

A

False

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36
Q

If administered concurrently with (X) drug, Sildenafil, a(n) (Y) drug, can cause severe hypotension.

A 
X = nitrates;
Y = PDE5 inhibitor (used to treat erectile dysfunction)
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37
Q

Nitrates are contraindicated in which diseases/patients?

A
  1. Severe aortic stenosis
  2. Acute RV infarction
  3. Hypertrophic cardiomyopathy
  4. Sildenafil use (within 24 h)
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38
Q

Aspirin used as antithrombotic agent for its (stimulatory/inhibitory) action on (X), thus impacting (Y) step of (primary/secondary) hemostasis.

A

Inhibitory
X = COX (synthesizes TXA2 from arachidonic acid);
Y = vasoconstriction and platelet activation
Primary hemostasis

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39
Q

List the classes of antiplatelet agents used for antithrombotic therapy.

A
  1. COX inhibitors (aspirin)
  2. P2Y12 (ADP)-R antagonists (Clopidogrel)
  3. Glycoprotein IIb/IIIa inhibitors (abciximab)
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40
Q

How does the integrin IIb/IIIa receptor play a role in (primary/secondary) hemostasis?

A

Primary hemostasis;

Conformational change causes fibrinogen binding

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41
Q

Platelet granule release of (X) is important in (primary/secondary) hemostasis.

A

X = ADP, TXA2, and Ca

Primary

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42
Q

Final active protease is (X), activated in (primary/secondary) hemostasis.

A

X = thrombin (cleaves fibrinogen)

Secondary

43
Q

Oral contraceptives (increase/decrease) thrombosis risk via which mechanism?

A

Increase;

Increase in hepatic synthesis of clotting factors

44
Q

At present all anti-thrombotic agents have increased (X) as their principle toxicity.

A

X = bleeding risk (hemorrhage)

45
Q

(X) class of antithrombotic drugs prevent primary hemostastic plug formation.

A

X = antiplatelet

46
Q

(X) class of antithrombotic drugs inhibit clotting cascade to ultimately prevent (Y) formation.

A 
X = anticoagulant
Y = fibrin clot
47
Q

(X) class of antithrombotic drugs dissolve an existing clot by digesting (Y).

A 
X = thrombolytic
Y = fibrin
48
Q

Which antiplatelet drugs are especially beneficial in treatment/prevention of ACS and the prevention of thromboembolic events?

A

P2Y12 (ADP) receptor antagonists

49
Q

Which antiplatelet drugs are administered IV, are effective during percutaneous coronary intervention (PCI).

A

Glycoprotein IIb/IIIa antagonists

50
Q

T/F: Patients are given high dose aspirin post-MI to inhibit COX synthesis of TXA2.

A

False - low dose! (325 mg/day)

51
Q

Higher dose aspirin leads to inhibition of (X) production and reduced clinical efficacy of therapy.

A

X = prostacyclin

52
Q

T/F: Aspirin inactivation of COX is irreversible.

A

True - effect persists for life of

platelet (7-10d)

53
Q

(X) drug was found superior to clopidogrel and aspirin combination therapy in stroke prevention in (Y) patients.

A 
X = warfarin
Y = Atrial Fibrillation
54
Q

Clopidogrel (reversibly/irreversibly) (stimulates/inhibits) (X). What is the effect of this?

A

Irreversibly inhibits;
X = P2Y12 (ADP) receptor

Inhibits activation of GPIIb/IIIa (final common) pathway for platelet aggregation

55
Q

T/F: Clopidogrel action persists for life of platelet.

56
Q

(X) antiplatelet drug has black box warning that (Y) patients are at high risk of (Z).

A 
X = Clopidogrel
Y = poor CYP metabolizers
Z = treatment failure

Since clopidogrel is prodrug that requires CYP metabolism

57
Q

(X) antiplatelet drug is Fab fragment of humanized monoclonal Ab directed against the (Y).

A 
X = abciximab
Y = GIIb receptor
58
Q 
Anticoagulant drugs typically reduce global clotting factor
activity by (X)% at therapeutic doses.
A

X = 30-50 (need to strike balance!!)

59
Q

Anticoagulant drug classes act by (stimulating/inhibiting) (pro/anti)-clotting factors.

A

Simulating anti- and inhibiting pro-

60
Q

Heparin is typically given (orally/IV/subQ) and has (short/long) half-life.

A

IV or subQ; short (1h)

61
Q

Heparin mechanism of action: greatly enhances (X) activity, thus inhibiting (Y).

A 
X = antithrombin
Y = clotting factors (IXa, Xa, thrombin)
62
Q

Drug of choice for anticoagulation during pregnancy.

A

Heparin (doesn’t cross placenta)

63
Q

Contraindications for heparin therapy.

A
  1. Hemorrhage (esp intracranial)
  2. Thrombocytopenia
  3. HT
  4. Renal/hepatic disease
64
Q

One of the most dangerous potential side effects of heparin is (X), a systemic (hyper/hypo)-coagulable state.

A

X = heparin-induced thrombocytopenia (HIT)

Hypercoagulable

65
Q

T/F: Osteoporosis and bone fractures are adverse effects of heparin therapy.

66
Q

(X) is an antagonist to heparin. They form a stable complex, devoid of anticoagulant activity.

A

X = protamine sulfate

67
Q

Heparin-induced thrombocytopenia (HIT) occurs (X) days after therapy initiated. There is (Y)% (increase/decrease) in platelets. Which patients at most risk?

A

X = 5-14
Y = 50
decrease;

Women and surgical patients

68
Q

Heparin-induced thrombocytopenia (HIT): what’s the mechanism behind this complication?

A
  1. Immune system generates Ab against heparin bound to platelet factor 4
  2. IgG-heparin-PF4 complex binds platelet receptor and activates platelet
  3. Systemic hypercoagulation
69
Q

T/F: The first thing to do if patient has Heparin-induced thrombocytopenia (HIT) is to give heparin antagonist, protamine sulfate.

70
Q

T/F: Patient develops Heparin-induced thrombocytopenia (HIT) so it’s crucial to administer/transfuse platelets.

71
Q

Heparin-induced thrombocytopenia (HIT): in addition to stopping all heparin, what would you administer to patient?

A
  1. Alternative anticoagulant

2. Irreversible thrombin inhibitor (Hirudin)

72
Q

T/F: Only IV, not SubQ, heparin therapy needs to be monitored via aPTT.

73
Q

Heparin monitored by measuring (X). Typical reference range is (Y) and therapeutic range is (Z) times (Y).

A 
X = activated partial thromboplastin time (aPTT)
Y = 25-39 seconds
Z = 2-2.5
74
Q

If long-term anticoagulation therapy needed, (X) drug is used until (Y) drug takes effect.

A 
X = heparin
Y = warfarin
75
Q

List the prototype drugs for low MW heparin.

A
  1. Enoxaparin

2. Fondaparinux

76
Q

T/F: Low MW Heparin works by the same mechanism of action as unfractionated heparin

A

False - only long enough to bind antithrombin and inhibit Factor Xa (not thrombin)

77
Q

T/F: Neutralization by protamine sulfate is more complete for unfractionated heparin than low MW heparin.

78
Q

T/F: Low MW heparin is contraindicated for pregnancy and obesity.

A

False - but Xa activity is monitored in these patients (as well as renal pts)

79
Q

(Unfractionated/LMW) Heparin has faster absorption. (Unfractionated/LMW) Heparin has longer half-life.

A

LMW; LMW (4hrs)

80
Q

T/F: LMW Heparin requires more frequent monitoring than Unfractionated heparin.

A

False - predictable pharmacokinetic response and no effect on aPTT (so less monitoring)

81
Q

(X) is the most widely used oral anticoagulant with (Y) hour half-life. What is directly (stimulated/inhibited) by this drug?

A 
X = warfarin
Y = 36

Inhibits vit K epoxide reductase (thus inhibiting the reduction of vit K epoxide into active form)

82
Q

Warfarin prevents activation of (X), thus (stimulating/inhibiting) (Y) of which clotting factors?

A

X = vit K epoxide
Inhibiting
Y = gamma carboxylation (of glutamate)

Prothrombin, factors VII, IX, X

83
Q

Warfarin onset of action is (X) hours/days and max effect is (Y) hours/days after administration

A 
X = 8-12 hours (SLOW)
Y = 3-5 days
84
Q

T/F: Like LMW Heparin, Warfarin must be frequently monitored in pregnant and obese patients.

A

FALSE B/C CANNOT GIVE TO PREGNANT PTS (crosses placenta)

85
Q

Why is patient history extra important when prescribing warfarin?

A

DRUG INTERACTIONS

86
Q

List some drugs that increase the effects of warfarin (if taken simultaneously).

A
  1. Aspirin
  2. Anabolic steroids
  3. Oral hypoglycemics
  4. Tamoxifen (for breast cancer)
87
Q

Patient with vit K deficiency. Which anticoagulant would you be worried about administering?

A

Warfarin (effects will be increased since it’s a vit K antagonist)

88
Q

List some drugs that decrease the effects of warfarin (if taken simultaneously).

A
  1. Oral contraceptives
  2. Corticosteroids
  3. Cholestyermine (binds warfarin in intestine and reduces bioavailability)
89
Q

Patient with chronic alcoholism. Which anticoagulant would you be worried about administering?

A

Warfarin (effects will be decreased)

90
Q

(X) is administered to reverse warfarin-associated bleeding.

A

Phytonadione (vit K1)

91
Q

T/F: Warfarin is metabolized by CYP enzymes.

92
Q

Monitoring warfarin requires calculating (X). What’s the formula and the normal value?

A

X = INR (international normalized ratio)

PT (pt)/PT (normal)
where PT is prothrombin time;
Normal INR = 1.0

93
Q

What’s the therapeutic INR for warfarin?

A

2-3 times normal

94
Q

Patient on warfarin has INR of 5. What do you do?

A

Lower warfarin dose (therapeutic window is 2-3)

95
Q

Dabigatran is in (X) class of drugs. What’s its mechanism of action?

A

X = direct thrombin inhibitor (anticoagulant)

Binds thrombin and prevents cleavage of fibrinogen to fibrin

96
Q

Dabigatran adverse effects.

A
  1. Hemorrhage
  2. Heartburn
  3. GI upset
  4. Increased MI risk
97
Q

T/F: Unlike heparin and warfarin, Dabigatran doesn’t require monitoring.

98
Q

What are some key issues with Dabigatran?

A
  1. Costly

2. No antagonist

99
Q

Rivaroxaban is in (X) class of drugs. What’s its mechanism of action?

A

X = Direct Xa inhibitors (anticoagulant)

Inhibits factor Xa

100
Q

T/F: Unlike heparin and warfarin, Rivaroxaban doesn’t require monitoring.

101
Q

T/F: Both direct thrombin and direct Xa inhibitors are given orally with slow onset of action.

A

False - both given orally but RAPID onset of action

102
Q

Alteplase is in (X) class of drugs. What’s its mechanism of action?

A

X = plasminogen activator (fibrinolytic)

Directly converts plasminogen to plasmin (preferentially activates plasminogen bound to fibrin already)

103
Q

T/F: Fibrinolytics, such as Alteplase/tPA, have long half-life.

A

False - short (3-8 min)

CVD (8 decks)

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