Cardiovascular drugs Flashcards
MOA of Statin
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
MOA of Heparin
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)
Adverse effect of Heparin
1) HIT (Heparin induced thrombocytopenia) - due to formation of an autoantibody for platelet factor-4
MOA of Warfarin (Coumadin)
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)
MOA of Aspirin
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
Toxicity of Statins
1) Hepatic Damage
2) Rhabdomyolysis
3) Peripheral neuropathies
What are Beta-1 selective blockers?
Think: A BEAM
1) Acebutolol
2) Betaxolol
3) Esmololo
4) Atenolol
5) Metoprolol
What are non-selective beta blockers
Think: Please Try Not to be Picky
1) Propanolol
2) Timolol
3) Nadolol
4) Pindolol
What drugs are used to treat Essential hypertension?
1) Diuretics
2) ACE or ARBs
3) Ca channel blockers
What drugs are used in Diabetes to protect the kidneys?
ACE/ARB
Nifedipine
Verapamil
Diltiazem
Amlodipine
Calcium channel blockers
Cardio selective Calcium channel blockers
1) Verapamil (ventricle=verapamil)
2) Diltiazem
Toxicity of Ca channel blockers
1) Cardiac depression
2) AV block
3) Peripheral edema
4) Constipation
MOA of Calcium channel blockers
1) Block voltage dependent L-type calcium channels of cardiac and smooth muscle
2) Results in reduced muscle contractility
MOA of Hydralazine
1) Arteriodilator
2) Increases cGMP
3) Causes smooth muscle relaxation
What is the treatment for malignant hypertension?
1) Nitroprusside
2) Fenoldopam
MOA of nitropruside
1) Increases cGMP via direct release of NO
2) Arterial and venous dilator
MOA of fenoldopam
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
MOA of nitroglycerine
1) Vasodilation by releasing NO in smooth muscle, causing increased cGMP and smooth muscle relaxation
2) vasodilation reduces preload (major importance)
What should not be given to a person on nitroglycerin?
Do not give the phosphodiesterase inhibitors (fils) drug class (used for erectile dysfunction)
MOA of Niacin
1) inhibits lypolysis
2) reduces VLDL secretion and increases HDL
Adverse effects of niacin
1) red, flushed face
2) long term hyperglycemia
3) hyperuricemia
Cholestyramine
Colestipol
Colesevelam
Bile acid resins
MOA of cholestyramine, colestipol, colesevelam
1) Prevent intestinal reabsorption of bile acids
MOA of ezetimibe
1) prevents cholesterol reabsorption at small intestine brush border
Gemfibrozil
Clofibrate
Bezafibrate
Fenofibrate
Fibrates
1) Upregulate Lipoprotein lipase
2) Causes increased triglyceride clearance and decreased VLDL formation
Vitamin K dependent coagulation factorss
II, VII, IX, X and proteins C and S
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
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
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
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)
How does digoxin affect ECG?
1) Increased PR interval
2) Decreased QT
3) T wave inversion
4) Arrhythmia
5) AV block
What is the role of class I Antiarrhythmics?
1) Na channel blockers
2) Results in decreased slope of phase 0 depolarization (prolonged QT interval)
Quinidine
Procainamide
Disopyramide
think: Queen Proclaims Diso’s Pyramid
Class 1A Antiarrhythmics
1) Affect both atrial and ventricular arrhytmias
2) SVT and Vtach
Toxicity of Procianamide
1) SLE-like syndrome
2) Long QT syndrome
3) Increased risk for torsades de pointes
Lidocaine
Mexiletine
Tocainidine
Class 1B Antiarrhythmics (Think: I’d Buy Lidy’s Mexican Tacos)
1) Best used post MI
Flecainide
Propafenone
Morcizine
think: More Fries Please
Class 1C antiarrhythmics
Think: 1C is Contraindicated in structural heart diseases and post MI
What should you not give to a pt. with arrhythmia and a structural heart disease?
Class 1C antiarrhythmics
Which class 1 drug causes an increased effective refractory period?
Class 1A antiarrhythmics
1) Quinidine
2) Procainamide
3) Disopyramide
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)
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
Toxicity of Class II antiarrhythmics
1) Impotence
2) Exacerbation of asthma
3) Bradycardia
Amiodarone
Ibutilide
Dofetilide
Sotalol
Think AIDS
Class III Antiarrhythmics
MOA of Class III Antiarrhythmics
1) K channel blockers
2) Increase action potential duration
3) Increased Effective refractory period
4) Increased QT interval
Verapimil
Diltiazem
Class IV Ca channel blockers
MOA of Class IV antiarrhthymics
Ca channel blockers
1) Decreased conduction velocity
2) Increase effective refractory period
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
Location of alpha 1 receptor and effect?
1) Located on vascular smooth muscle
2) Activates Gq protein
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
What G protein receptors are involved with Gq protein?
Think: HAVe 1M&M
1) H1
2) alpha-1
3) V1
4) M1
5) M3
What G protein receptors are involved with Gi protein?
MAD 2’s
1) M2
2) Alpha 2
3) D2
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
What G protein receptors are involved with Gs protein?
1) B1 and B2
2) D1
3) H2
4) V2
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
Location of M2
1) Heart
2) Activates Gi protein
Nicotinic location?
Neuromuscular junctions
Location of H1 receptors
1) Respiratory tract
2) Activates Gq protein
What drug causes a balanced venous and arterial vasodilation?
Nitroprusside
Why do Ca channel blockers not effect skeletal muscles?
1) Skeletal muscles do not depend on extracellular Ca
What closes a patent ductus arteriosus?
think: ENDomethacin (Indomethacin) ENDs patency of pda
Indomethacin
What drugs reduce the mortality of CHF?
1) ACE inhbitors
2) Beta blockers
3) ARBs
4) Spironolactone
What drugs improve both mortality and symptoms of CHF?
1) Hydralazine with nitrate therapy
Amlodipine
Nifedipine
Vascular selective Ca Channel blockers
Adverse effects of Fibrates
1) Myositis
2) Hepatotoxicity
What subtype of Class I antiarrhythmics has the greatest binding strength to Na channels?
1) 1C > 1A > 1B
Which drugs Class I antiarrhthmics are selective for ischemic myocardium?
1) 1B (lidocaine, Mexiletine, and tocainide)
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
Which Class 1 subtype has the strongest inhibition of phase 0?
Class 1C
Second line treatment for atrial fibrilation
1) Digoxin
2) Slows AV conduction
3) Increases PNS tone
MOA of dobutamine
1) Beta adrenergic agonist (beta-1)
2) Used for treatment of acute heart failure associated with decrease myocardial contractility
Inotropic = ? Chronotropic = ?
1) Contraction
2) Heart rate
What are adverse effects of thiazides?
1) hyperuricemia
2) Hypercalcemia
3) Hyperglycemia
4) Hyperlipidemia
5) Hypokalemia
6) Hypotension
Adverse effect of nitrates
Headaches
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
MOA of Isoproterenol
1) Beta 1 agonist at high doses
2) Beta 2 at low doses
MOA of Clopidogrel
Inhibits ADP induced expression of GpIIb/IIIa
What do you use to treat a heparin overdose?
Protamine sulfate- positively charged molecule that binds negatively charged heparin
Enoxaparin
Dalteparin
Low molecular weight heparins
Lepirudin
Bivalirudin
Anticoagulant derivatives from hirudin (found in leeches)
What pathway is inhibited by Warfarin?
1) Extrinsic secondary coagulation pathway (Low PT)
Alteplase
Reteplase
Tenecteplase
Thrombolytics
MOA of tPA
1) Activates plasminogen to plasmin
2) Increases fibrin degredation
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
What do you use to treat a tPA overdose?
aminocaproic acid
Clopidogrel
Ticlopidine
Prasugrel
Ticagrelor
Irreversible ADP receptor inhibitors which decreases glycoprotein IIb/IIIa leading to decreased platelet aggregation
Abciximab
Eptifibatide
GP IIb/IIIa inhibitors
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)
Treatment for sickle cell anemia?
Hydroxyurea
MOA of hydroxyurea?
1) Inhibits ribonucleotide reductase
2) Increased amount of HbF
Treatment for TIA
Aspirin
Treatment for Advanced wet age releated macular degeneration?
VEGF inhibitor
MOA of celecoxib
Selective COX2 inhibitor
What does COX1 play a physiologic role? COX2?
1) Platelets, GI tract
2) Sites of inflammation
Adverse effect of ticlopidine
Mouth ulcers and neutropenia
Adverse effects of amiodarone
1) Thyroid dysfunction
2) Corneal deposits
3) Blue grey skin
4) Drug related hepatitis
5) Pulmonary fibrosis
Adverse effect of nitroprusside
May cause cyanide poisoning
Where is the only place that COX-2 is observed?
Within inflammatory cells
Reversible alpha blocker
Phentolamine
Irreversible alpha blocker
Phenoxybenzamine
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
MOA of cilostazol/dipyridamole
Phosphodiesterase III inhibitor; increases cAMP in platelets inhibiting aggregation; also a vasodilator
MOA of argatroban
1) Direct thrombin inhibitor
2) used for HIT
