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Cardiovascular Flashcards

1
Q

Quinidine mechanism of action

A

Blocks fast Na channels in open or active state

Increases Action potential duration and effective refractory period

Blocks K channels causing prolonged repolarization

Muscarinic receptor blockade which can increase HR and AV conduction

Vasodilation via Alpha block and possible reflex tachycardia

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2
Q

Quinidine used for

A

Orally effective used for many arrhythmias and atrial fibrillation

Need INITIAL DIGITALIZATION to slow AV conduction

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3
Q

Quinidine adverse affects

A

1) Cinchonism (GI, tinnitus, ocular dysfunction, CNS excitation)
2) Hypotension
3) Prolongation of QRS and increase in QT interval associated with Syncope (torsades)
4) Black water Fever

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4
Q

Quinidine drug interactions

A

Hyper K enhances effects and Hypo K decreases affects

Displaces Digoxin from tissue binding sites enhancing toxicity

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5
Q

Procainamide mechanism of action

A

Blocks fast Na channels that are open or activated

Incarease action potential duration and effective refractory period

Blocks K channels

Has less Muscarinic receptor block

Metabolized via N-acetyltransferase to N-acetyl procainamide, an active metabolite

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6
Q

Procainamide used for

A

Antiarrhythmia

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7
Q

Procainamide adverse affects

A

SLE - like syndrome in slow acetylators

Hematotoxicity causing thrombocytopenia and agranulocytosis

Torsades

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8
Q

Class 1A antiarrythmics drugs

A

1) Quinidine
2) Procainamide

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9
Q

Class 1A antiarrhythmics MOD

A

1) block fast, active Na Channels
2) Block K channels
3) Some Muscarinic receptor blockade

Increases APD and ERP

Affect Phase 0

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10
Q

Disopyramide action

A

Class 1A antiarrythmic with the most M blockade

Not used for arterial arrythmia

Used for VENTRICULAR arrhythmia

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11
Q

Drugs that cause SLE- like disease

A

1) Procainamide
2) Isoniazid
3) Hydralazine

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12
Q

Lidocaine mechanism of action

A

Block fast Na channels in inactivated state (damaged tissue)

Decrease APD due to block of SLOW Na “window” currents - increases diastole and extends the time for recovery

Give in IV to prevent First Pass metabolism

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13
Q

Lidocaine used for

A

Arrythmias due to:

1) post MI
2) Open-heart surgery
3) Digoxin toxicity

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14
Q

Lidocaine adverse affects

A

CNS toxicity causing seizures

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15
Q

Mexiletine mechanism of action

A

Blocks fast Na channels in inactivated state

Given orally

Same as Lidocaine

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16
Q

Tocainide mechanism of action

A

Blocks fast inactivated Na channels

Same as Lidocaine

Given orally

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17
Q

Tocainide adverse affects

A

can lead to agranulocytosis and decrease on other blood cells

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18
Q

Class 1B drugs

A

Lidocaine

Mexiletine

Tocainide

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19
Q

Class 1B drugs Mechanism of action

A

Blocks fast, inactivated Na channels

Blocks slow Na channels

Found in Ischemic tissue

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20
Q

Flecainide mechanism of action

A

Blocks fast Na channels in His-Purkinje tissue

Has no effect on APD

No ANS effect

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21
Q

Flecainide adverse affects

A

can cause sudden death post MI

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22
Q

Class 2 drugs

A

Beta blockers:

1) Propranolol (B1=B2)
2) acebutolol (B1)
3) Esmolol (B1 short acting for SVT)

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23
Q

Class 2 antiarrythmics mechanism of action

A

Prevent Beta receptor activation decreasing cAMP

Decrease SA and AV nodal activity

Decrease slope of phase 4 (diastolic current) in AP in Pacemaker

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24
Q

Amiodarone mechanism of action

A

Decreases K channel slowing phase 3 (repolarization) of AP

Increase APD and ERP

Mimics class 1, 2, 3, and 4 antiarrythmics

Large VD and multiple effects

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25
Amiodarone adverse affects
1) Pulmonary fibrosis 2) blue pigmentation of the skin (Smurf Skin) 3) Phototoxicity 4) Corneal deposits 5) Hepatic necrosis 6) Thyroid dysfunction
26
Sotalol mechanism of action
Decrease conductance of K channels slowing phase 3 Non - selective Beta blockade - Beta 1 leading to decrease HR, AV conduction
27
Sotalol adverse affects
Torsades (the worst)
28
Class 3 drus
Amiodarone Sotalol
29
Class 3 mechanism of action
Block K channels decrease phase 3
30
Verapamil and diltiazem mechanism of action
Class 4 antiarrythmics that block Ca Channels Decrease phae 0 and phase 4 Decrease SA and AV nodal activity
31
Verapamil adverse affects
1) consitpation 2) dizziness 3) flushing 4) hypotension 5) AV block 6) Gingival hypoplasia
32
Diltiazem adverse affects
Same as Verapamil minus constipation
33
Class 4 drugs
Verapamil and Diltiazem Ca blocks
34
Class 4 antiarrythmic drug interactions
Additive AV block with Beta blockers and Digoxin Verapamil displaces Digoxin from tissue-binding sites, increasing Digoxin toxicity
35
How to treat Torsades
1) Control HypoK 2) Correct HypoMg 3) Discontinue drug causing prolonged QT 4) attempt to shorten APD with Isoproterenol or electrical paceing
36
Drugs causing QT prolongation (Torsades)
Class 1A and Class 3 drugs Thioridazine TCA
37
Adenosine Action
Causes Gi coupled decrease in cAMP Decrease SA and AV nodal activity
38
Adenosine is DOC for
Paroxysmal supraventricular tachycardia AV nodal arrhythmia
39
Adenosine adverse affects
1) Flushing 2) Sedation 3) Dyspnea
40
Adenosine interaction with Methylxanthines
Methyxanthines are Theophylline and caffeine Adenosine antagonized by Methylxanthines Methylxanthines will decrease affect of Adenosine
41
Stratagey for antihypertensives
Decrease TPR - CCB Decrease CO - Beta blockers, CCB Decrease body fluids - Diuretics, ACEI, ARB Decrease BP
42
Clonodine and Methyldopa Mechanism of action
Alpha 2 agonist that decreases sympathetic outflow Decreases TPR and HR
43
Clonodine used for
Mild to moderate hypertension Opiate withdrawl
44
Methyldopa used for
Mild to moderate HT Hypertensive managment in pregnancy
45
Issue with Clonodine
Can lead to MASSIVE rebound HT if stopped
46
Reserpine mechanism of action
Decreases presynamptic storage levels decreasing CO and TPR because of decreased Norepi, Dopamine and serotonin in CNS
47
Reserpine adverse affects
Depression (severe leading to suicide) Edema Increase GI secretion
48
Guanethidine mechanism of action
Inhibit NE release
49
Adverse affects of Alpha 1 blockers used for HT
1) First dose syncope (sudden fall of BP) 2) Orthostatic Hypotension 3) Urinary incontinence
50
Advantages of using Alpha 1 blockers for HT
Good for HT and BPH Increase HDL and Decrease LDL
51
Adverse affects of using Beta blockers in HT
1) CVS depression 2) Fatigue 3) Sexual dysfunction 4) Increase LDL and TG 5) mask DM
52
Hydralazine mechanism of action
Decrease TPR via arteriolar dilation #1 for preganancy induced HT Acts through Nitric Oxide
53
Hydralazine adverse affects
1) SLE like syndrome in Slow Acetylators 2) Edema 3) Reflex Tachycardia
54
Nitroprusside Mechanism of action
Decrease TPR via dilation of both arterioles and venules DOC for Hypertensive emergencies via IV Acting through Nitric oxide
55
Nitroprusside adverse affects
Causes cyanide toxicity when co-administered with nitrites and thiosulfates
56
Minoxidil mechanism of action
Opens K channels causing HYPERPOLARIZATION of smooth muscle results in ARTERIOLAR vasodilation
57
Minoxidil used for
1) severe HT 2) Baldness
58
Diazoxide mechanism of action
Opens K channels causing HYPERPOLARIZATION of smooth muscles reults in arteriolar vasodilation
59
Diazoxide used for
Hypertensive emergencies
60
Adverse affects of Minoxidil
1) Hypertrichosis (Hirsturism) 2) Edema 3) Reflex tachycardia
61
Adverse affects of Diazoxide
1) hyperglycemia (decrease insulin release) 2) Edema 3) reflex tachycardia
62
Captopril (-Prils) mechanism of action
ACE inhibitors Block formation of AT 2 resulting in prevention of AT1 - receptor stimulation Decrease aldosterone and vasodilation
63
Losartan (-Sartan) mechanism of action
ARB Blocks AT1 receptors Same result as ACEIs on BP mechanisms
64
Aliskiren mechanism of action
Directly inhibit Renin
65
ACEI, ARB and Aliskiren used for
Mild eot moderate HT Protective of Diabetic nephropathy (ACEI and ARBS) CHF (ACEI adn ARBS)
66
ACEI, ARB, and Aliskiren Adverse affects
1) Dry cough (ACEI) 2) HyperK 3) Acute renal artery stenosis 4) Angioadema
67
PT has HT with Angina give:
Beta blockers and CCB
68
PT has HT and Diabetes give
ACEIs and ARBs
69
PT has HT and HF give
ACEIs, ARBs, and Beta blockers
70
PT has HT and post MI give
Beta Blocker
71
PT has HT and BPH give
Alpha 1 selective blocker
72
PT has HT and Dyslipidemia give
Alpha blocker, CCBs, ACEIs/ARBs
73
Bosentan mechanism of action
Endothelin - 1 receptor antagonist inhibiting ETA action of vasoconstriction Used for pulmonary HT
74
Bosentan adverse affects
Headache, flushing, hypotension and is contraindicated in pregnancy
75
Epoprostenol mechansim of action and use
Prostacyclin (PGI2) analog Used via infusion pump to treat pulmonary HT
76
Sildenafil mechanism of action
Inhibits type V PDE and increases cGMP causing pulmonary artery relaxation and decreases pulmonary HT
77
Goal for treating HF
1. Decrease preload: Diuretics, ACEI, ARB, venodilators 2. Decrease afterload: ACEI, ARB, arteriodilators 3. Increase contractility: Digoxin, beta agonist 4. Decrease remodeling of cardiac muscle: ACEI, ARB, spironolactone, beta blockers
78
Digoxin mechanism of action
Inhibition of cardiac Na/K ATPase cuases increas intracellular Na. Increase in Na decreases Na/Ca exchange causing an increase in intracellular Ca resulting in increase Ca release from Sarcoplasmic reticulum. Increase in Ca causes increase actin-myosin interaction and increase in contractile force Also, increase vagal activity resulting in parasympathetic actions
79
Digoxin pharmacokinetics
Long t 1/2: needs LD Cleared by kidneys so take caution in renal failure Large VD because it binds to tissue, caution in displacement via Verapamil and quinidine
80
Digoxin adverse affects
1. Anorexia, nausea 2. **Prolonged PR** 3. **Shortened PT** 4. **Depressed ST or inverted Twave** 5. Visual defects, halos 6. In toxic doses causes: **Arrhythmia and heart block**
81
Inamrinone and milrinone mechanism of action
Phosphodiesterase inhibitors causing Increase in cAMP in heart muslce resulting int increase inotropy and increase cAMP in smooth muscle resulting in decrease TPR
82
Ranolazine mechanism of action
Blocks late inward Na current in cardiac myocytes causing decrease in Ca accumulation resulting in decreased end diastolic pressure and improvement of diastolic coronary flow
83
Ranolazine adverse affects
1. Constipation and nausea 2. Increased QT
84
Acetazolamide mechanism of action
Carbonic Anhydrase inhibitor resulting in: 1. Decrease H formation inside PCT 2. Decrease Na/H antiport 3. Increase Na dn HCO3 in lumen 4. Increase Diuresis
85
Acetazolamide used for
Galucoma, Acute mountain sickness, Metabolic Alkalosis
86
Acetazolamide adverse affects
1. Bicaronaturia and acidosis 2. HypoK 3. HyperCl 4. Paresthesias 5. Renal stones 6. Sulonamide hypersensitivity
87
Dorzolamide is
Similar to Acetazolamide a CA inhibitor Used Topically for Glaucoma
88
Furosemide mechanism of action
Loop diuretic inhibiting Na/K/Cl transporter in TAL resulting in: 1. Decrease intracellular K in TAL 2. Decrease back diffusion of K 3. Decrease positive potential 4. Decrease reabsorption of Ca and Mg 5. Increase diuresis
89
Furosemide used for
1. Acutue pulomnary edema 2. HF 3. HT 4. Refractory edema 5. Acute renal faiulre 6. Anion overdose 7. HyperCa states
90
Ethacrynic acid is
A loop diuretic similar to furosemide with out the sulfonamide allergic reaction. However, causes irreversible ototoxicity
91
Drugs with sulfa allergies
1. CA inhibitors 2. Furosemide 3. Thiazides 4. Sulfa antibiotics 5. Celecoxib
92
Furosemide adverse affects
1. Sulfa reaction 2. HypoK and **Alkalosis** 3. HypoCa - can cause renal Ca stones 4. HypoMg 5. Hyperuricemia
93
Furosimede drug interactions
Lithium decreases clearance. Digoxin in toxicity due to electrolyte disturbances
94
Thiazide mechanism of action
Na/Cl transporter inhibition in DCT resulting in: 1. Increase luminal Na and Cl 2. Increase diuresis
95
Thiazides used for
1. HT and CHF 2. Calcium kidney stones 3. Nephrogenic DI
96
Thiazide adverse affects
1. Sulfa reaction 2. HypoK and **Alkalosis** 3. HyperCa 4. Hyperuricemia 5. **Hyperglycemia** 6. **Hyperlipidemia**
97
Indapamide is
A thiazide that does not cause Hyperlipidemia
98
Spironolactone mechanism of action
K-sparing diuretic that inhibits aldosterone receptors in the basolateral side of Collecting tubules. Causes increase K and decrease Na
99
Spironolactone used for
1. Hyperaldosteronic sstate 2. Adujunt to K-wasting 3. Antiandorgenic uses (female hisutism) 4. CHF
100
Spironolactone adverse affects
HyperK and **Acidosis** Antiandrogen
101
Eplerenone is
A K-sparing that is selective aldosterone receptor blocker
102
Amiloride and mechanism of action
Na channel blocker in the luminal area of Collecting tubules
103
Triamterene is
Na channel blocker like amiloride
104
Amiloride used for
K sparing Lithium induced nephrogenic DI
105
Amiloride adverse affects
HyperK and **Acidosis**
106
Acetazolamide Urinary Electrolytes
* Increase in Na * Increase in K * Double increase in HCO Resulting in Blood **ACIDOSIS**
107
Furosemide Urinary Electrolytes
* Double increase in Na * Increase in K * Increase in Ca * Increase in Mg * Increase in Cl Resulting in Blood **ALKALOSIS**
108
Thiazide Urinary Electrolytes
* Increase in Na * Increase K * Increase Cl * Decrease Ca Resulting in blood **ALKALOSIS**
109
K-sparing Urinary Electrolytes
* Small Increase in Na * Decrease in K Resulting in Blood **ACIDOSIS**
110
Lovastatin (**-Statins**) mechanism of action
HMG-CoA reductase inhibition results in: 1. Decrease liver cholesterol 2. Increase LDL receptor expression 3. Decrease plasma LDL 4. Decrease VLDL synthesis causing Decrease Triglyceridemia *Inhibits conversion of HMC CoA to Mevalonic acid then cholesterol*
111
Lovastatin adverse affects
1. Myalgia, Myopathy (check **creatine kinase**) 2. **Rhabdomyolysis** (*increase with **Gemfibrozil***) 3. Hepatotoxicity (check liver enzymes)
112
Cholestyramine mechanism of action
Complexation of bile salts in the gut results in: 1. Decrease enterohepatic recirculation of bile salts 2. Increase synthesis of new bile salts by the liver 3. Decrease liver cholesterol 4. Increase LDL receptor expression 5. Decrease blood LDL
113
Colestipol is
Same as cholestyramine a bile acid inhibitor
114
Cholestyramine adverse affects
1. Increase VLDL and Triglycerides (**contraindicated in Hypertriglyceridemia**) 2. GI disturbance (steatorrhea) 3. Vit malabsorption
115
Niacin (**Vit B3**) mechanism of aciton
Inhibits VLDL synthesis resulting in: 1. Decrease plasma VLDL 2. Decrease plasma LDL 3. **Increase plasma HDL**
116
Niacin (**Vit B3**) adverse affects
1. Flusing, pruritus, burning pain (*use **asprin***) 2. Hepatotoxicity
117
Gemfibrozil mechanism of action
Fibrate that bind to PPARalpha and increase expression of lipoprotein lipase resulting in: 1. Decrease VLDL and IDL 2. Modest decrease in LDL 3. **Increase in HDL**
118
Fenofibrate is
Same as gemfibrozil a fibrate
119
Gemfibrozil adverse affects
Cholesterol Gallstones Myositis
120
Ezetimibe mechanism of action
Prevents intestinal absorption of cholesterol resulting in Decrease in LDL
121
Antihyperlipidemics that are used when there is an increase in cholesterol
1. Cholestyramine 2. Colestipol 3. Ezetimibe
122
Antihyperlipidemic used when there is increase TG
1. Gemfibrozil 2. Fenofibrate
123
Antihyperlipidemics used when there is increas in Cholesterol and TG
1. Statins 2. Niacin 3. Ezetimibe
124
Orlistat mechanism of action
Inhibits pancreatic lipase leading to decreas triglyceride breakdown in intestines

Pharmacology (12 decks)

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