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
MOA of ezetimibe
1) prevents cholesterol reabsorption at small intestine brush border
26
Gemfibrozil Clofibrate Bezafibrate Fenofibrate
Fibrates 1) Upregulate Lipoprotein lipase 2) Causes increased triglyceride clearance and decreased VLDL formation
27
Vitamin K dependent coagulation factorss
II, VII, IX, X and proteins C and S
28
MOA of Bile acid binding resins (cholestyramine)
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
29
Drug that directly inhibits Na/K ATPase that leads to indirect inhibition of Na/Ca exchanger; results in Increased Ca causing increased inotropy (contractility)
Digoxin
30
MOA of Digoxin
Inhibition of Na/K ATPase leading to indirect inhibition of Na/Ca exchanger leading to increased Ca calcium concentration within the cardiac muscle
31
What factors predispose pt. to a greater chance toxicity of digoxin?
1) Renal failure (decreased excretion) 2) Hypokalemia (Loss of K results in increased binding sites for digoxin) 3) Quinidine (decreased digoxin clerance)
32
How does digoxin affect ECG?
1) Increased PR interval 2) Decreased QT 3) T wave inversion 4) Arrhythmia 5) AV block
33
What is the role of class I Antiarrhythmics?
1) Na channel blockers | 2) Results in decreased slope of phase 0 depolarization (prolonged QT interval)
34
Quinidine Procainamide Disopyramide
think: Queen Proclaims Diso's Pyramid Class 1A Antiarrhythmics 1) Affect both atrial and ventricular arrhytmias 2) SVT and Vtach
35
Toxicity of Procianamide
1) SLE-like syndrome 2) Long QT syndrome 3) Increased risk for torsades de pointes
36
Lidocaine Mexiletine Tocainidine
Class 1B Antiarrhythmics (Think: I'd Buy Lidy's Mexican Tacos) 1) Best used post MI
37
Flecainide Propafenone Morcizine
think: More Fries Please Class 1C antiarrhythmics Think: 1C is Contraindicated in structural heart diseases and post MI
38
What should you not give to a pt. with arrhythmia and a structural heart disease?
Class 1C antiarrhythmics
39
Which class 1 drug causes an increased effective refractory period?
Class 1A antiarrhythmics 1) Quinidine 2) Procainamide 3) Disopyramide
40
``` Metoprolol (beta 1 blocker) Propranolol (Non selective beta blocker) Esmolol (beta 1 blocker) Atenolol (beta 1 blocker) Timolol (Non selective beta blocker) ```
Class II Antiarrhythmics (beta blockers)
41
MOA of Class II antiarrhythmics
1) Decrease activity of beta receptors resulting in decreased cAMP and Ca 2) Decreases slope of phase 4 3) Increase in PR interval
42
Toxicity of Class II antiarrhythmics
1) Impotence 2) Exacerbation of asthma 3) Bradycardia
43
Amiodarone Ibutilide Dofetilide Sotalol
Think AIDS | Class III Antiarrhythmics
44
MOA of Class III Antiarrhythmics
1) K channel blockers 2) Increase action potential duration 3) Increased Effective refractory period 4) Increased QT interval
45
Verapimil | Diltiazem
Class IV Ca channel blockers
46
MOA of Class IV antiarrhthymics
Ca channel blockers 1) Decreased conduction velocity 2) Increase effective refractory period
47
Name the G protein affected by alpha-1 receptor? alpha-2? Beta-1? Beta-2? M1? M2? M3? D1? D2? H1? H2? V1? V2?
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
Location of alpha 1 receptor and effect?
1) Located on vascular smooth muscle | 2) Activates Gq protein
49
What is the MOA of Gq protein?
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
What G protein receptors are involved with Gq protein?
Think: HAVe 1M&M 1) H1 2) alpha-1 3) V1 4) M1 5) M3
51
What G protein receptors are involved with Gi protein?
MAD 2's 1) M2 2) Alpha 2 3) D2
52
What is the MOA of Gi protein?
1) Inhibits adenylyl cyclase causing a decrease in cAMP | 2) Decreased cAMP results in decreased protein kinase A
53
What G protein receptors are involved with Gs protein?
1) B1 and B2 2) D1 3) H2 4) V2
54
What is the MOA of Gs protein?
1) Increases activity of adenylyl cyclase causing an increase in cAMP 2) Increased cAMP results in increased protein kinase A
55
Location of M2
1) Heart | 2) Activates Gi protein
56
Nicotinic location?
Neuromuscular junctions
57
Location of H1 receptors
1) Respiratory tract | 2) Activates Gq protein
58
What drug causes a balanced venous and arterial vasodilation?
Nitroprusside
59
Why do Ca channel blockers not effect skeletal muscles?
1) Skeletal muscles do not depend on extracellular Ca
60
What closes a patent ductus arteriosus?
think: ENDomethacin (Indomethacin) ENDs patency of pda Indomethacin
61
What drugs reduce the mortality of CHF?
1) ACE inhbitors 2) Beta blockers 3) ARBs 4) Spironolactone
62
What drugs improve both mortality and symptoms of CHF?
1) Hydralazine with nitrate therapy
63
Amlodipine | Nifedipine
Vascular selective Ca Channel blockers
64
Adverse effects of Fibrates
1) Myositis | 2) Hepatotoxicity
65
What subtype of Class I antiarrhythmics has the greatest binding strength to Na channels?
1) 1C > 1A > 1B
66
Which drugs Class I antiarrhthmics are selective for ischemic myocardium?
1) 1B (lidocaine, Mexiletine, and tocainide)
67
What is the effect on Effective Refractory period for each of the Class I antiarrhythmics?
1) 1A = Increased ERP 2) 1B = Decreased ERP 3) 1C = no change in ERP
68
Which Class 1 subtype has the strongest inhibition of phase 0?
Class 1C
69
Second line treatment for atrial fibrilation
1) Digoxin 2) Slows AV conduction 3) Increases PNS tone
70
MOA of dobutamine
1) Beta adrenergic agonist (beta-1) | 2) Used for treatment of acute heart failure associated with decrease myocardial contractility
71
``` Inotropic = ? Chronotropic = ? ```
1) Contraction | 2) Heart rate
72
What are adverse effects of thiazides?
1) hyperuricemia 2) Hypercalcemia 3) Hyperglycemia 4) Hyperlipidemia 5) Hypokalemia 6) Hypotension
73
Adverse effect of nitrates
Headaches
74
Adverse effects of digoxin
1) AV block (via increased PNS through vagus) 2) Blurry vision and change in color vision 3) diarrhea 4) Confusion, delirium 5) Bradycardia
75
MOA of Isoproterenol
1) Beta 1 agonist at high doses | 2) Beta 2 at low doses
76
MOA of Clopidogrel
Inhibits ADP induced expression of GpIIb/IIIa
77
What do you use to treat a heparin overdose?
Protamine sulfate- positively charged molecule that binds negatively charged heparin
78
Enoxaparin | Dalteparin
Low molecular weight heparins
79
Lepirudin | Bivalirudin
Anticoagulant derivatives from hirudin (found in leeches)
80
What pathway is inhibited by Warfarin?
1) Extrinsic secondary coagulation pathway (Low PT)
81
Alteplase Reteplase Tenecteplase
Thrombolytics
82
MOA of tPA
1) Activates plasminogen to plasmin | 2) Increases fibrin degredation
83
When is tPA contradindicated
1) Pt with active bleeding 2) Pt with history of intracranial bleed 3) Recent surgery 4) Bleeding diatheses 5) Severe hypertension
84
What do you use to treat a tPA overdose?
aminocaproic acid
85
Clopidogrel Ticlopidine Prasugrel Ticagrelor
Irreversible ADP receptor inhibitors which decreases glycoprotein IIb/IIIa leading to decreased platelet aggregation
86
Abciximab | Eptifibatide
GP IIb/IIIa inhibitors
87
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?
1) Heparin (does not cross placenta) | 2) Warfarin (teratogenic)
88
Treatment for sickle cell anemia?
Hydroxyurea
89
MOA of hydroxyurea?
1) Inhibits ribonucleotide reductase | 2) Increased amount of HbF
90
Treatment for TIA
Aspirin
91
Treatment for Advanced wet age releated macular degeneration?
VEGF inhibitor
92
MOA of celecoxib
Selective COX2 inhibitor
93
What does COX1 play a physiologic role? COX2?
1) Platelets, GI tract | 2) Sites of inflammation
94
Adverse effect of ticlopidine
Mouth ulcers and neutropenia
95
Adverse effects of amiodarone
1) Thyroid dysfunction 2) Corneal deposits 3) Blue grey skin 4) Drug related hepatitis 5) Pulmonary fibrosis
96
Adverse effect of nitroprusside
May cause cyanide poisoning
97
Where is the only place that COX-2 is observed?
Within inflammatory cells
98
Reversible alpha blocker
Phentolamine
99
Irreversible alpha blocker
Phenoxybenzamine
100
What cardio drugs have an adverse effect of aggravated lupus syndrome? What type of metabolism do these drugs go through in the body?
1) Procainamide 2) Hydralazine 3) Acetylation in the liver
101
MOA of cilostazol/dipyridamole
Phosphodiesterase III inhibitor; increases cAMP in platelets inhibiting aggregation; also a vasodilator
102
MOA of argatroban
1) Direct thrombin inhibitor | 2) used for HIT