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Drugs > Cardiovascular drugs > Flashcards

Cardiovascular drugs Flashcards

1
Q

MOA of Statin

A

1) HMG CoA Reductase Inhibitor
2) Results in the decreased production of cholesterol
3) Low cholesterol production results in the expression of more LDL receptors which increases uptake

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2
Q

MOA of Heparin

A

1) Increases the rate of anti-thrombin III- thrombin binding

2) Inhibits coagulation factors Xa, IXa, Xa, and XIIa (causes a prolongation in PTT- intrinsic pathway)

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3
Q

Adverse effect of Heparin

A

1) HIT (Heparin induced thrombocytopenia) - due to formation of an autoantibody for platelet factor-4

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4
Q

MOA of Warfarin (Coumadin)

A

1) Inhibits blood clotting by interfering with the hepatic syntehsis of vitamin K dependent clotting factors
2) Inhibits the enzyme Vitamin epoxide reductase (carboxylates glutamate residues)
3) Vitamin K dependent clotting factors (II, VII, IX, X and anti-coagulant protein C and S)

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5
Q

MOA of Aspirin

A

1) Covalently modifys and irreversibly inhibits COX-1
2) Leads to the blocking of TXA2 from platelets with low dose (decreases coagulation)
3) Leads to inhibition in the formation of prostacylcin (PGI2)
4) No effect on PT or PTT

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6
Q

Toxicity of Statins

A

1) Hepatic Damage
2) Rhabdomyolysis
3) Peripheral neuropathies

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7
Q

What are Beta-1 selective blockers?

A

Think: A BEAM

1) Acebutolol
2) Betaxolol
3) Esmololo
4) Atenolol
5) Metoprolol

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8
Q

What are non-selective beta blockers

A

Think: Please Try Not to be Picky

1) Propanolol
2) Timolol
3) Nadolol
4) Pindolol

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9
Q

What drugs are used to treat Essential hypertension?

A

1) Diuretics
2) ACE or ARBs
3) Ca channel blockers

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10
Q

What drugs are used in Diabetes to protect the kidneys?

A

ACE/ARB

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11
Q

Nifedipine
Verapamil
Diltiazem
Amlodipine

A

Calcium channel blockers

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12
Q

Cardio selective Calcium channel blockers

A

1) Verapamil (ventricle=verapamil)

2) Diltiazem

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13
Q

Toxicity of Ca channel blockers

A

1) Cardiac depression
2) AV block
3) Peripheral edema
4) Constipation

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14
Q

MOA of Calcium channel blockers

A

1) Block voltage dependent L-type calcium channels of cardiac and smooth muscle
2) Results in reduced muscle contractility

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15
Q

MOA of Hydralazine

A

1) Arteriodilator
2) Increases cGMP
3) Causes smooth muscle relaxation

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16
Q

What is the treatment for malignant hypertension?

A

1) Nitroprusside

2) Fenoldopam

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17
Q

MOA of nitropruside

A

1) Increases cGMP via direct release of NO

2) Arterial and venous dilator

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18
Q

MOA of fenoldopam

A

1) Dopamine D1 receptor agonist resulting in coronary, peripheral, renal, and splanchnic vasodilation
2) Only IV agent that improves renal perfusion while lowering blood pressure

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19
Q

MOA of nitroglycerine

A

1) Vasodilation by releasing NO in smooth muscle, causing increased cGMP and smooth muscle relaxation
2) vasodilation reduces preload (major importance)

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20
Q

What should not be given to a person on nitroglycerin?

A

Do not give the phosphodiesterase inhibitors (fils) drug class (used for erectile dysfunction)

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21
Q

MOA of Niacin

A

1) inhibits lypolysis

2) reduces VLDL secretion and increases HDL

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22
Q

Adverse effects of niacin

A

1) red, flushed face
2) long term hyperglycemia
3) hyperuricemia

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23
Q

Cholestyramine
Colestipol
Colesevelam

A

Bile acid resins

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24
Q

MOA of cholestyramine, colestipol, colesevelam

A

1) Prevent intestinal reabsorption of bile acids

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25
Q

MOA of ezetimibe

A

1) prevents cholesterol reabsorption at small intestine brush border

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26
Q

Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate

A

Fibrates

1) Upregulate Lipoprotein lipase
2) Causes increased triglyceride clearance and decreased VLDL formation

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27
Q

Vitamin K dependent coagulation factorss

A

II, VII, IX, X and proteins C and S

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28
Q

MOA of Bile acid binding resins (cholestyramine)

A

1) Bind to bile acids interfering with enterohepatic circulation of bile acids
2) Results in the production of new bile acids which involves the use of liver cholesterol stores

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29
Q

Drug that directly inhibits Na/K ATPase that leads to indirect inhibition of Na/Ca exchanger; results in Increased Ca causing increased inotropy (contractility)

A

Digoxin

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30
Q

MOA of Digoxin

A

Inhibition of Na/K ATPase leading to indirect inhibition of Na/Ca exchanger leading to increased Ca calcium concentration within the cardiac muscle

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31
Q

What factors predispose pt. to a greater chance toxicity of digoxin?

A

1) Renal failure (decreased excretion)
2) Hypokalemia (Loss of K results in increased binding sites for digoxin)
3) Quinidine (decreased digoxin clerance)

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32
Q

How does digoxin affect ECG?

A

1) Increased PR interval
2) Decreased QT
3) T wave inversion
4) Arrhythmia
5) AV block

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33
Q

What is the role of class I Antiarrhythmics?

A

1) Na channel blockers

2) Results in decreased slope of phase 0 depolarization (prolonged QT interval)

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34
Q

Quinidine
Procainamide
Disopyramide

A

think: Queen Proclaims Diso’s Pyramid
Class 1A Antiarrhythmics
1) Affect both atrial and ventricular arrhytmias
2) SVT and Vtach

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35
Q

Toxicity of Procianamide

A

1) SLE-like syndrome
2) Long QT syndrome
3) Increased risk for torsades de pointes

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36
Q

Lidocaine
Mexiletine
Tocainidine

A

Class 1B Antiarrhythmics (Think: I’d Buy Lidy’s Mexican Tacos)
1) Best used post MI

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37
Q

Flecainide
Propafenone
Morcizine

A

think: More Fries Please
Class 1C antiarrhythmics
Think: 1C is Contraindicated in structural heart diseases and post MI

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38
Q

What should you not give to a pt. with arrhythmia and a structural heart disease?

A

Class 1C antiarrhythmics

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39
Q

Which class 1 drug causes an increased effective refractory period?

A

Class 1A antiarrhythmics

1) Quinidine
2) Procainamide
3) Disopyramide

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40
Q 
Metoprolol (beta 1 blocker)
Propranolol (Non selective beta blocker)
Esmolol (beta 1 blocker)
Atenolol (beta 1 blocker)
Timolol (Non selective beta blocker)
A

Class II Antiarrhythmics (beta blockers)

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41
Q

MOA of Class II antiarrhythmics

A

1) Decrease activity of beta receptors resulting in decreased cAMP and Ca
2) Decreases slope of phase 4
3) Increase in PR interval

42
Q

Toxicity of Class II antiarrhythmics

A

1) Impotence
2) Exacerbation of asthma
3) Bradycardia

43
Q

Amiodarone
Ibutilide
Dofetilide
Sotalol

A

Think AIDS

Class III Antiarrhythmics

44
Q

MOA of Class III Antiarrhythmics

A

1) K channel blockers
2) Increase action potential duration
3) Increased Effective refractory period
4) Increased QT interval

45
Q

Verapimil

Diltiazem

A

Class IV Ca channel blockers

46
Q

MOA of Class IV antiarrhthymics

A

Ca channel blockers

1) Decreased conduction velocity
2) Increase effective refractory period

47
Q

Name the G protein affected by alpha-1 receptor? alpha-2? Beta-1? Beta-2? M1? M2? M3? D1? D2? H1? H2? V1? V2?

A

THINK: QISS and QIQ till your’e SIQ of SQS (super quinky sex)

1) alpha-1 = Gq protein
2) alpha-2 = Gi protein
3) beta-1 = Gs protein
4) beta-2 = Gs protein
5) M1 = Gq protein
6) M2 = Gi protein
7) M3 = Gq protein
8) D1 = Gs protein (remember nigra striatal)
9) D2 = Gi protein (remember nigra striatal)
10) H1 = Gq protein
11) H2 = Gs protein
12) V1 (vasopressin) = Gq protein
13) V2 = Gs protein

48
Q

Location of alpha 1 receptor and effect?

A

1) Located on vascular smooth muscle

2) Activates Gq protein

49
Q

What is the MOA of Gq protein?

A

1) Gq protein causes activation of PIP2 to break into DAG and IP3
2) Results in increased Ca concentration and activation of protein kinase C

50
Q

What G protein receptors are involved with Gq protein?

A

Think: HAVe 1M&M

1) H1
2) alpha-1
3) V1
4) M1
5) M3

51
Q

What G protein receptors are involved with Gi protein?

A

MAD 2’s

1) M2
2) Alpha 2
3) D2

52
Q

What is the MOA of Gi protein?

A

1) Inhibits adenylyl cyclase causing a decrease in cAMP

2) Decreased cAMP results in decreased protein kinase A

53
Q

What G protein receptors are involved with Gs protein?

A

1) B1 and B2
2) D1
3) H2
4) V2

54
Q

What is the MOA of Gs protein?

A

1) Increases activity of adenylyl cyclase causing an increase in cAMP
2) Increased cAMP results in increased protein kinase A

55
Q

Location of M2

A

1) Heart

2) Activates Gi protein

56
Q

Nicotinic location?

A

Neuromuscular junctions

57
Q

Location of H1 receptors

A

1) Respiratory tract

2) Activates Gq protein

58
Q

What drug causes a balanced venous and arterial vasodilation?

A

Nitroprusside

59
Q

Why do Ca channel blockers not effect skeletal muscles?

A

1) Skeletal muscles do not depend on extracellular Ca

60
Q

What closes a patent ductus arteriosus?

A

think: ENDomethacin (Indomethacin) ENDs patency of pda

Indomethacin

61
Q

What drugs reduce the mortality of CHF?

A

1) ACE inhbitors
2) Beta blockers
3) ARBs
4) Spironolactone

62
Q

What drugs improve both mortality and symptoms of CHF?

A

1) Hydralazine with nitrate therapy

63
Q

Amlodipine

Nifedipine

A

Vascular selective Ca Channel blockers

64
Q

Adverse effects of Fibrates

A

1) Myositis

2) Hepatotoxicity

65
Q

What subtype of Class I antiarrhythmics has the greatest binding strength to Na channels?

A

1) 1C > 1A > 1B

66
Q

Which drugs Class I antiarrhthmics are selective for ischemic myocardium?

A

1) 1B (lidocaine, Mexiletine, and tocainide)

67
Q

What is the effect on Effective Refractory period for each of the Class I antiarrhythmics?

A

1) 1A = Increased ERP
2) 1B = Decreased ERP
3) 1C = no change in ERP

68
Q

Which Class 1 subtype has the strongest inhibition of phase 0?

A

Class 1C

69
Q

Second line treatment for atrial fibrilation

A

1) Digoxin
2) Slows AV conduction
3) Increases PNS tone

70
Q

MOA of dobutamine

A

1) Beta adrenergic agonist (beta-1)

2) Used for treatment of acute heart failure associated with decrease myocardial contractility

71
Q 
Inotropic = ?
Chronotropic = ?
A

1) Contraction

2) Heart rate

72
Q

What are adverse effects of thiazides?

A

1) hyperuricemia
2) Hypercalcemia
3) Hyperglycemia
4) Hyperlipidemia
5) Hypokalemia
6) Hypotension

73
Q

Adverse effect of nitrates

A

Headaches

74
Q

Adverse effects of digoxin

A

1) AV block (via increased PNS through vagus)
2) Blurry vision and change in color vision
3) diarrhea
4) Confusion, delirium
5) Bradycardia

75
Q

MOA of Isoproterenol

A

1) Beta 1 agonist at high doses

2) Beta 2 at low doses

76
Q

MOA of Clopidogrel

A

Inhibits ADP induced expression of GpIIb/IIIa

77
Q

What do you use to treat a heparin overdose?

A

Protamine sulfate- positively charged molecule that binds negatively charged heparin

78
Q

Enoxaparin

Dalteparin

A

Low molecular weight heparins

79
Q

Lepirudin

Bivalirudin

A

Anticoagulant derivatives from hirudin (found in leeches)

80
Q

What pathway is inhibited by Warfarin?

A

1) Extrinsic secondary coagulation pathway (Low PT)

81
Q

Alteplase
Reteplase
Tenecteplase

A

Thrombolytics

82
Q

MOA of tPA

A

1) Activates plasminogen to plasmin

2) Increases fibrin degredation

83
Q

When is tPA contradindicated

A

1) Pt with active bleeding
2) Pt with history of intracranial bleed
3) Recent surgery
4) Bleeding diatheses
5) Severe hypertension

84
Q

What do you use to treat a tPA overdose?

A

aminocaproic acid

85
Q

Clopidogrel
Ticlopidine
Prasugrel
Ticagrelor

A

Irreversible ADP receptor inhibitors which decreases glycoprotein IIb/IIIa leading to decreased platelet aggregation

86
Q

Abciximab

Eptifibatide

A

GP IIb/IIIa inhibitors

87
Q

Pregnant woman has a dvt. what do you give her? what would you give a normal pt., but can’t give to a pregnant woman?

A

1) Heparin (does not cross placenta)

2) Warfarin (teratogenic)

88
Q

Treatment for sickle cell anemia?

A

Hydroxyurea

89
Q

MOA of hydroxyurea?

A

1) Inhibits ribonucleotide reductase

2) Increased amount of HbF

90
Q

Treatment for TIA

A

Aspirin

91
Q

Treatment for Advanced wet age releated macular degeneration?

A

VEGF inhibitor

92
Q

MOA of celecoxib

A

Selective COX2 inhibitor

93
Q

What does COX1 play a physiologic role? COX2?

A

1) Platelets, GI tract

2) Sites of inflammation

94
Q

Adverse effect of ticlopidine

A

Mouth ulcers and neutropenia

95
Q

Adverse effects of amiodarone

A

1) Thyroid dysfunction
2) Corneal deposits
3) Blue grey skin
4) Drug related hepatitis
5) Pulmonary fibrosis

96
Q

Adverse effect of nitroprusside

A

May cause cyanide poisoning

97
Q

Where is the only place that COX-2 is observed?

A

Within inflammatory cells

98
Q

Reversible alpha blocker

A

Phentolamine

99
Q

Irreversible alpha blocker

A

Phenoxybenzamine

100
Q

What cardio drugs have an adverse effect of aggravated lupus syndrome? What type of metabolism do these drugs go through in the body?

A

1) Procainamide
2) Hydralazine
3) Acetylation in the liver

101
Q

MOA of cilostazol/dipyridamole

A

Phosphodiesterase III inhibitor; increases cAMP in platelets inhibiting aggregation; also a vasodilator

102
Q

MOA of argatroban

A

1) Direct thrombin inhibitor

2) used for HIT

Drugs (13 decks)

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