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Pharmacology > Cardiovascular > Flashcards

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
Q

Amiodarone adverse affects

A

1) Pulmonary fibrosis
2) blue pigmentation of the skin (Smurf Skin)
3) Phototoxicity
4) Corneal deposits
5) Hepatic necrosis
6) Thyroid dysfunction

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26
Q

Sotalol mechanism of action

A

Decrease conductance of K channels slowing phase 3

Non - selective Beta blockade - Beta 1 leading to decrease HR, AV conduction

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27
Q

Sotalol adverse affects

A

Torsades (the worst)

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28
Q

Class 3 drus

A

Amiodarone

Sotalol

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29
Q

Class 3 mechanism of action

A

Block K channels decrease phase 3

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30
Q

Verapamil and diltiazem mechanism of action

A

Class 4 antiarrythmics that block Ca Channels

Decrease phae 0 and phase 4

Decrease SA and AV nodal activity

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31
Q

Verapamil adverse affects

A

1) consitpation
2) dizziness
3) flushing
4) hypotension
5) AV block
6) Gingival hypoplasia

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32
Q

Diltiazem adverse affects

A

Same as Verapamil minus constipation

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33
Q

Class 4 drugs

A

Verapamil and Diltiazem

Ca blocks

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34
Q

Class 4 antiarrythmic drug interactions

A

Additive AV block with Beta blockers and Digoxin

Verapamil displaces Digoxin from tissue-binding sites, increasing Digoxin toxicity

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35
Q

How to treat Torsades

A

1) Control HypoK
2) Correct HypoMg
3) Discontinue drug causing prolonged QT
4) attempt to shorten APD with Isoproterenol or electrical paceing

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36
Q

Drugs causing QT prolongation (Torsades)

A

Class 1A and Class 3 drugs

Thioridazine

TCA

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37
Q

Adenosine Action

A

Causes Gi coupled decrease in cAMP

Decrease SA and AV nodal activity

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38
Q

Adenosine is DOC for

A

Paroxysmal supraventricular tachycardia

AV nodal arrhythmia

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39
Q

Adenosine adverse affects

A

1) Flushing
2) Sedation
3) Dyspnea

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40
Q

Adenosine interaction with Methylxanthines

A

Methyxanthines are Theophylline and caffeine

Adenosine antagonized by Methylxanthines

Methylxanthines will decrease affect of Adenosine

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41
Q

Stratagey for antihypertensives

A

Decrease TPR - CCB

Decrease CO - Beta blockers, CCB

Decrease body fluids - Diuretics, ACEI, ARB

Decrease BP

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42
Q

Clonodine and Methyldopa Mechanism of action

A

Alpha 2 agonist that decreases sympathetic outflow

Decreases TPR and HR

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43
Q

Clonodine used for

A

Mild to moderate hypertension

Opiate withdrawl

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44
Q

Methyldopa used for

A

Mild to moderate HT

Hypertensive managment in pregnancy

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45
Q

Issue with Clonodine

A

Can lead to MASSIVE rebound HT if stopped

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46
Q

Reserpine mechanism of action

A

Decreases presynamptic storage levels decreasing CO and TPR because of decreased Norepi, Dopamine and serotonin in CNS

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47
Q

Reserpine adverse affects

A

Depression (severe leading to suicide)

Edema

Increase GI secretion

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48
Q

Guanethidine mechanism of action

A

Inhibit NE release

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49
Q

Adverse affects of Alpha 1 blockers used for HT

A

1) First dose syncope (sudden fall of BP)
2) Orthostatic Hypotension
3) Urinary incontinence

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50
Q

Advantages of using Alpha 1 blockers for HT

A

Good for HT and BPH

Increase HDL and Decrease LDL

51
Q

Adverse affects of using Beta blockers in HT

A

1) CVS depression
2) Fatigue
3) Sexual dysfunction
4) Increase LDL and TG
5) mask DM

52
Q

Hydralazine mechanism of action

A

1 for preganancy induced HT

Decrease TPR via arteriolar dilation

Acts through Nitric Oxide

53
Q

Hydralazine adverse affects

A

1) SLE like syndrome in Slow Acetylators
2) Edema
3) Reflex Tachycardia

54
Q

Nitroprusside Mechanism of action

A

Decrease TPR via dilation of both arterioles and venules

DOC for Hypertensive emergencies via IV

Acting through Nitric oxide

55
Q

Nitroprusside adverse affects

A

Causes cyanide toxicity when co-administered with nitrites and thiosulfates

56
Q

Minoxidil mechanism of action

A

Opens K channels causing HYPERPOLARIZATION of smooth muscle results in ARTERIOLAR vasodilation

57
Q

Minoxidil used for

A

1) severe HT
2) Baldness

58
Q

Diazoxide mechanism of action

A

Opens K channels causing HYPERPOLARIZATION of smooth muscles reults in arteriolar vasodilation

59
Q

Diazoxide used for

A

Hypertensive emergencies

60
Q

Adverse affects of Minoxidil

A

1) Hypertrichosis (Hirsturism)
2) Edema
3) Reflex tachycardia

61
Q

Adverse affects of Diazoxide

A

1) hyperglycemia (decrease insulin release)
2) Edema
3) reflex tachycardia

62
Q

Captopril (-Prils) mechanism of action

A

ACE inhibitors

Block formation of AT 2 resulting in prevention of AT1 - receptor stimulation

Decrease aldosterone and vasodilation

63
Q

Losartan (-Sartan) mechanism of action

A

ARB

Blocks AT1 receptors

Same result as ACEIs on BP mechanisms

64
Q

Aliskiren mechanism of action

A

Directly inhibit Renin

65
Q

ACEI, ARB and Aliskiren used for

A

Mild eot moderate HT

Protective of Diabetic nephropathy (ACEI and ARBS)

CHF (ACEI adn ARBS)

66
Q

ACEI, ARB, and Aliskiren Adverse affects

A

1) Dry cough (ACEI)
2) HyperK
3) Acute renal artery stenosis
4) Angioadema

67
Q

PT has HT with Angina give:

A

Beta blockers and CCB

68
Q

PT has HT and Diabetes give

A

ACEIs and ARBs

69
Q

PT has HT and HF give

A

ACEIs, ARBs, and Beta blockers

70
Q

PT has HT and post MI give

A

Beta Blocker

71
Q

PT has HT and BPH give

A

Alpha 1 selective blocker

72
Q

PT has HT and Dyslipidemia give

A

Alpha blocker, CCBs, ACEIs/ARBs

73
Q

Bosentan mechanism of action

A

Endothelin - 1 receptor antagonist inhibiting ETA action of vasoconstriction Used for pulmonary HT

74
Q

Bosentan adverse affects

A

Headache, flushing, hypotension and is contraindicated in pregnancy

75
Q

Epoprostenol mechansim of action and use

A

Prostacyclin (PGI2) analog

Used via infusion pump to treat pulmonary HT

76
Q

Sildenafil mechanism of action

A

Inhibits type V PDE and increases cGMP causing pulmonary artery relaxation and decreases pulmonary HT

77
Q

Goal for treating HF

A
  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
Q

Digoxin mechanism of action

A

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
Q

Digoxin pharmacokinetics

A

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
Q

Digoxin adverse affects

A
  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
Q

Inamrinone and milrinone mechanism of action

A

Phosphodiesterase inhibitors causing Increase in cAMP in heart muslce resulting int increase inotropy and increase cAMP in smooth muscle resulting in decrease TPR

82
Q

Ranolazine mechanism of action

A

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
Q

Ranolazine adverse affects

A
  1. Constipation and nausea
  2. Increased QT
84
Q

Acetazolamide mechanism of action

A

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
Q

Acetazolamide used for

A

Galucoma, Acute mountain sickness, Metabolic Alkalosis

86
Q

Acetazolamide adverse affects

A
  1. Bicaronaturia and acidosis
  2. HypoK
  3. HyperCl
  4. Paresthesias
  5. Renal stones
  6. Sulonamide hypersensitivity
87
Q

Dorzolamide is

A

Similar to Acetazolamide a CA inhibitor Used Topically for Glaucoma

88
Q

Furosemide mechanism of action

A

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
Q

Furosemide used for

A
  1. Acutue pulomnary edema
  2. HF
  3. HT
  4. Refractory edema
  5. Acute renal faiulre
  6. Anion overdose
  7. HyperCa states
90
Q

Ethacrynic acid is

A

A loop diuretic similar to furosemide with out the sulfonamide allergic reaction. However, causes irreversible ototoxicity

91
Q

Drugs with sulfa allergies

A
  1. CA inhibitors
  2. Furosemide
  3. Thiazides
  4. Sulfa antibiotics
  5. Celecoxib
92
Q

Furosemide adverse affects

A
  1. Sulfa reaction
  2. HypoK and Alkalosis
  3. HypoCa - can cause renal Ca stones
  4. HypoMg
  5. Hyperuricemia
93
Q

Furosimede drug interactions

A

Lithium decreases clearance.

Digoxin in toxicity due to electrolyte disturbances

94
Q

Thiazide mechanism of action

A

Na/Cl transporter inhibition in DCT resulting in:

  1. Increase luminal Na and Cl
  2. Increase diuresis
95
Q

Thiazides used for

A
  1. HT and CHF
  2. Calcium kidney stones
  3. Nephrogenic DI
96
Q

Thiazide adverse affects

A
  1. Sulfa reaction
  2. HypoK and Alkalosis
  3. HyperCa
  4. Hyperuricemia
  5. Hyperglycemia
  6. Hyperlipidemia
97
Q

Indapamide is

A

A thiazide that does not cause Hyperlipidemia

98
Q

Spironolactone mechanism of action

A

K-sparing diuretic that inhibits aldosterone receptors in the basolateral side of Collecting tubules. Causes increase K and decrease Na

99
Q

Spironolactone used for

A
  1. Hyperaldosteronic sstate
  2. Adujunt to K-wasting
  3. Antiandorgenic uses (female hisutism)
  4. CHF
100
Q

Spironolactone adverse affects

A

HyperK and Acidosis

Antiandrogen

101
Q

Eplerenone is

A

A K-sparing that is selective aldosterone receptor blocker

102
Q

Amiloride and mechanism of action

A

Na channel blocker in the luminal area of Collecting tubules

103
Q

Triamterene is

A

Na channel blocker like amiloride

104
Q

Amiloride used for

A

K sparing

Lithium induced nephrogenic DI

105
Q

Amiloride adverse affects

A

HyperK and Acidosis

106
Q

Acetazolamide Urinary Electrolytes

A
  • Increase in Na
  • Increase in K
  • Double increase in HCO

Resulting in Blood ACIDOSIS

107
Q

Furosemide Urinary Electrolytes

A
  • Double increase in Na
  • Increase in K
  • Increase in Ca
  • Increase in Mg
  • Increase in Cl

Resulting in Blood ALKALOSIS

108
Q

Thiazide Urinary Electrolytes

A
  • Increase in Na
  • Increase K
  • Increase Cl
  • Decrease Ca

Resulting in blood ALKALOSIS

109
Q

K-sparing Urinary Electrolytes

A
  • Small Increase in Na
  • Decrease in K

Resulting in Blood ACIDOSIS

110
Q

Lovastatin (-Statins) mechanism of action

A

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
Q

Lovastatin adverse affects

A
  1. Myalgia, Myopathy (check creatine kinase)
  2. Rhabdomyolysis (increase with Gemfibrozil)
  3. Hepatotoxicity (check liver enzymes)
112
Q

Cholestyramine mechanism of action

A

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
Q

Colestipol is

A

Same as cholestyramine a bile acid inhibitor

114
Q

Cholestyramine adverse affects

A
  1. Increase VLDL and Triglycerides (contraindicated in Hypertriglyceridemia)
  2. GI disturbance (steatorrhea)
  3. Vit malabsorption
115
Q

Niacin (Vit B3) mechanism of aciton

A

Inhibits VLDL synthesis resulting in:

  1. Decrease plasma VLDL
  2. Decrease plasma LDL
  3. Increase plasma HDL
116
Q

Niacin (Vit B3) adverse affects

A
  1. Flusing, pruritus, burning pain (use asprin)
  2. Hepatotoxicity
117
Q

Gemfibrozil mechanism of action

A

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
Q

Fenofibrate is

A

Same as gemfibrozil a fibrate

119
Q

Gemfibrozil adverse affects

A

Cholesterol Gallstones

Myositis

120
Q

Ezetimibe mechanism of action

A

Prevents intestinal absorption of cholesterol resulting in Decrease in LDL

121
Q

Antihyperlipidemics that are used when there is an increase in cholesterol

A
  1. Cholestyramine
  2. Colestipol
  3. Ezetimibe
122
Q

Antihyperlipidemic used when there is increase TG

A
  1. Gemfibrozil
  2. Fenofibrate
123
Q

Antihyperlipidemics used when there is increas in Cholesterol and TG

A
  1. Statins
  2. Niacin
  3. Ezetimibe
124
Q

Orlistat mechanism of action

A

Inhibits pancreatic lipase leading to decreas triglyceride breakdown in intestines

Pharmacology (12 decks)

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