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1
Q

Nifedipine

A

Ca++ channel blocker

  • block voltage gated L-type Ca++ channels
    • cardiac + smooth muscle
  • Reduce muscle contractility
  • Vascular smooth muscle *
    • vasodilation
  • Use:
    • HTN
    • Angina
    • Prinzmetal’s angina
    • Raynaud
    • prevent vasospam post subarachnoid hemorrage
  • Toxicity
    • cardiac depression
    • AV bock
    • Peripheral edema
    • Flushing
    • Dizziness
    • Constipation
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2
Q

Verapamil

A

Class IV Antiarr

  • Ca++ channel blocker
  • block voltage gated L-type Ca++ channels
    • cardiac + smooth muscle
  • Reuce muscle contractility
  • **Cardiac smooth muscle * **
    • Decrease heart contractility + rate
  • Use:
    • HTN
    • Angina
    • Prinzmetal’s angina
    • Raynaud
    • Prevent nodal arrhythmias (SVT)
    • rate control in a-fib
  • Toxicity
    • CV:
      • bradycardia
      • 1st, 2nd, 3rd degree AV block
      • Esp if combined with beta blocker!
    • Constipation
    • Gingival hyperplasia
    • Peripheral edema
    • Flushing
    • Dizziness
      *
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3
Q

Diltiazem

A

Class IV Antiarrhythmic

  • MOA
    • Ca++ channel blocker
    • block voltage gated L-type Ca++ channels
      • cardiac + smooth muscle
    • Cardiac smooth muscle
      • Reduce muscle contractility
      • reduce rate
      • increase PR
    • increases effective refractory period
  • Use:
    • HTN
    • Angina
    • Prinzmetal’s angina
    • Raynaud
    • Prevent nodal arrhythmias (SVT)
    • rate control in A-fib
    • prevent vasospasm post subarachnoid hemorrhage
  • Toxicity
    • CV: CHF, AV block, sinus node depression
    • Peripheral edema
    • Flushing
    • Dizziness
    • Constipation
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4
Q

Amlodipine

A

Ca++ channel blocker

  • block voltage gated L-type Ca++ channels
  • Reduce muscle contractility
  • vascular smooth muscle
    • vasodilation
  • Use
    • HTN
    • Angina
    • Arrhythmias
    • Prinzmetal’s angina
    • Raynaud
    • prevent vasospasm post subarachnoid hemorrhage
    • isolated reduction in systolic BP
  • Toxicity
    • cardiac depression
    • AV bock
    • Peripheral edema
    • Flushing
    • Dizziness
    • Constipation
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5
Q

Hydralazine

A

Vasodilator

  • increases cGMP = smooth muscle relaxation
  • Vasodilation
    • arteries > veins
    • decrease afterload
  • Use
    • severe HTN
    • CHF
    • HTN in prego (With methylodopa)
  • Can give with B-blocker to prevent reflex tachycardia
  • Toxcitiy
    • compensatory tachycardia
    • fluid retention
    • nausea
    • headache
    • angina
    • SLE (lupus)
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6
Q

Malignant HTN

A
  • Nitroprusside
    • short acting
    • increase cGMP = release NO
    • Cyanide toxicity
  • Fenoldopam
    • dopamine DI receptor agonist
    • vasodilation: coronary, peripheral, renal, splanchnic
    • decrease BP
    • increase natriuresis
  • Nitroglycerin + Isosorbide Dinitrate
    • vasodilate veins > arteries
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7
Q

Nitroglycerine

A

Vasodilate

  • Release NO = increase cGMP = decrease intracellular Ca+ = myosin dephosphorylation = smooth muscle relaxation
  • Need period without drug in system each day to avoid tolerance
  • Vasodilate
    • Veins > arteries
    • decrease preload
  • ​Use
    • angina
    • pulmonary edema
    • malignant HTN
  • Toxicity
    • reflex tachycardia
    • hypotension
    • flushing, headache
    • monday disease = tolerance of vasodilators during work week but loss of tolerance over weekend
      • dizziness, headache, tachycardia upon reexposure
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8
Q

Isosobide dinitrate

A

Vasodilate

  • Release NO = increase cGMP = decrease intracellular Ca+ = myosin dephosphorylation = smooth muscle relaxation
  • Need period each day where drug is not in system to avoid tolerance
  • Vasodilate
    • Veins > arteries
    • decrease preload
  • Use
    • angina
    • pulmonary edema
  • Toxicity
    • reflex tachycardia
    • hypotension
    • flushing
    • headache
    • monday disease: tolerance of vasodilators during work week but loss of tolerance during weekend
      • tachycardia, dizziness, headache upon reexposure
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9
Q

Angina therapy

A
  • Reduce myocardial O2 consuption by decreasing
    • end diastolic volume
    • blood pressure
    • heart rate
    • contractility
    • ejection time
  • Nitrates
    • preload
    • decrease EDV
    • decrease BP
    • increase contractility (reflex)
    • increase heart rate (reflex)
    • decrease ejection time
    • decrease MVO2
  • B- blockers
    • afterload
    • increase EDV
    • decrease BP
    • decrease contractility
    • decrease heart rate
    • increase ejection time
    • decrease MVO2
  • Together
    • no effect on EDV
    • decrease BP
    • no effect on contractility
    • decrease HR
    • no effect on ejection time
    • decrease MVO2
  • ​Ca++ channel blocker
    • nifedipine = nitrate
    • verapamil = b blocker
  • Partial Beta blockers
    • Pindolol and acebutol = dont use
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10
Q

Niacin

(B3)

A

Niacin

  • Effect
    • Decrease LDL (xx)
    • Increase HDL (^^^)
    • Decrease triglucerides (x)
  • Mechanism
    • inhibit VLDL release from hepatocyte
    • inhibit lipolysis in adipose tissue
  • Toxicity
    • Red, flushed face (due to prostaglandins)
      • decreased by aspirin
    • Hyperglycemia
      • acanthos nigricans
    • Hyperuricemia
      • gout
    • Potentiate effects of hypertensive drugs b/c vasodilatory
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11
Q

Cholestyramine

A

Bile acid resin

  • Effect
    • Decrease LDL (xx)
    • Increase HDL (^)
    • Increase Triglycerides (^)
  • Mechanism
    • prevent bile acid reabsorption from intestine
    • increase hepatic cholesterol synthesis
  • Toxicity
    • Most hated by patients
      • bad taste
      • GI discomfort
    • Decrease fat soluble vit absorption
      • DAKE
    • Cholesterol gallstones
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12
Q

Colestipol

A

Bile acid resin

  • Effect
    • Decrease LDL (xx)
    • Increase HDL (^)
    • Increase Triglycerides (^)
  • Mechanism
    • inhibit bile acid reabsorption from intestine
    • increase hepatic cholesterol synthesis
  • Toxicity
    • patients hate
      • bad taste
      • GI discomfort
    • Decreases absorption of fat soluble vit
      • DAKE
    • Cholesterol gallstones
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13
Q

Colesevelam

A

Bile acid resin

  • Effects
    • Decrease LDL (xx)
    • Increase HDL (^)
    • Increase Triglycerides (^)
  • Mechanism
    • Inhibit bile acid reabsorption from gut
    • Increase hepatic cholesterol synthesis
  • Toxicity
    • Patients hate it
      • bad taste
      • GI discomfort
    • Decreases absorption of fat soluble vit
      • DAKE
    • Cholesterol gallstones
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14
Q

Ezetimibe

A

Cholesterol absorption blocker

  • Effect
    • Decreases LDL (xx)
  • Mechanism
    • prevent cholesterol reabsorption from small intestine
  • Toxicity
    • Increase LFT (rare)
    • Diarrhea
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15
Q

Gemfibrozil

A

Fibrate

  • Effect
    • Decrease LDL (x)
    • Increase HDL (^)
    • Decrease Triglycerides (xxx)
  • Mechanism
    • upregulate lipoprotein lipase (LPL)
      • VLDL –> IDL
    • increase TG clearance
    • increase hepatic cholesterol synthesis*
    • Suppresses 7-alpha hydroxylase
      • decreased cholesterol –> bile acids
      • increased gallstone formation
  • Toxicity
    • Myositis (muscle inflammation)
    • Hepatotoxicity (increase LFT)
    • Cholesterol gallstones
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16
Q

Clofibrate

Bezafibrate

Fenofibrate

A

Fibrates

  • Effect
    • Decrease LDL (x)
    • Increase HDL (^)
    • Decrease Triglycerides (xxx)
  • Mechanism
    • Upregulate lipoprotein lipase (LPL)
    • Increase TG clearance
    • Increase hepatic cholesterol synthesis
    • Suppress 7-alpha hydroxylase
      • decrease cholesterole –> bile conversion
      • increase cholesterol gallstones
  • Toxicity
    • Myositis (muscle inflammation)
    • Hepatotoxicity (increase LFT)
    • Cholesterol gallstones
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17
Q

Digoxin

A

Cardiac Glycoside

  • 75% bioavailable
  • Urinary excretion
  • Antagonised by actions of K+
  • Mechanism
    • Directly inhibits Na+/K+ ATPase
      • indirections inhibits Na+/Ca+ exchanger
      • inceases incracellulat Ca++
      • Positive ionotropy
    • Stimulates CN X
      • decrease heart rate
    • ​​Increases refractoriness in AV node
  • Toxicity
    • Cholinergic (DUMBBELSS)
      • Diarrhea, Urination, Miosis, Bradycardia, Bronchospasm, Excitation of skeletal m and nervous system, Lacrimation, Salivation, Sweating
    • Changes in color perception
    • occurs with decreased renal function b/c renally cleared
  • ECG:
    • increase PR
    • decrease QT
    • ST scooping
    • T wave inversion
    • Arrythmia
    • AV block
  • Hyperkalemia (poor prognostic factor)
  • Digitalis induced tachycardia = increased Ca+ = Delayed Afterdepolarization
    • most serious and potentially fatal effects
  • Factors predisposing to toxicity
    • renal failure, hypokalemia, quinidine use
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18
Q

Na+ / K+ ATPase

Na+ / Ca+ Exchanger

A
  • Na+ / Ka+ ATPase
    • Na+ out
    • K+ in
  • –> decreases intracellular Na+ turning on exchanger
  • Na+ / Ca+ Exchanger
    • Na+ in
    • Ca+ out
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19
Q

Quinidine

A

Class 1A antiarrhythmic

  • double, quarter, pounder
  • Medium Na+ binding strength
  • Mechanism
    • Na+ block
      • preferentially active and inactive channels in pacemaker cells
    • K+ block
  • Effect
    • Prolong action potential
    • increase effective refractory period
    • increase QT interval
  • Use
    • atrial + ventricular arrhythmias
    • esp: reentract + ectopic supraventricular and ventricular tachycardias
  • Toxicity
    • Thrombcytopenia
    • Torsades de pointe
    • Q: headache, tinnitus
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20
Q

Procainamide

A

Class **1A **Antiarrhythmic

  • double quarter pounder
  • medium Na+ binding strength
  • Mechanism
    • Na+ block
      • preferentially block active and inactive channels in pacemaker cells
    • K+ block
  • Effect
    • Prolong action potential
    • Increase effective refractory period
    • Increase QT interval
  • Use
    • atrial + ventricular arrhythmias
    • esp: ectopic supraventricular and ventricular tachycardia
  • Toxicity
    • thrombocytopenia
    • torsades de pointe
    • P: SLE
21
Q

Disopyramide

A

Class 1A Antiarrhythmic

  • double, quarter, pounder
  • Medium Na+ channel binding affinity
  • Mechanism
    • Na+ block
      • preferentially block active and ianctive Na+ channels in pacemaker cells
    • K+ block
  • Effect
    • Prolong action potential
    • increase effective refractory period
    • Increase QT interval
  • Use
    • atrial and ventricular arrhythmias
    • esp: reentrant supraventricular and ventricular tachycardia
  • Toxicity
    • thrombocytopenia
    • torsades de pointe
    • D: heart failure
22
Q

Lidocaine

A

Class 1B antiarrhythmic

  • Lettuce, mayo, tomato
  • Weakest Na+ channel blocker
    • rapid dissociation
    • minimal cumulative effect over many selectives
  • Mechanism
    • Na+ channel blocker
    • Shortens AP
    • Selective for ischemic or depolarized Purkinje ventricular tissue
  • Use
    • Post MI - acute ventricular arrhythmias
    • Digitalis induced arrhythmias
  • Toxicity
    • local anesthetic
    • CNS stimulation/ depression
    • CV depression
23
Q

Mexiletine

A

Class IB antiarrhythmic

  • lettuce, tomato, mayo
  • Weakest Na+ block
    • rapidly dissociate from Na+ channels
    • minimal cumulative effect over time
  • Mechanism
    • Na+ channel block
    • **Shorten AP **
    • Selective for ischemic or depolarized Purkinje and ventricular tissue
  • Use
    • Post MI
      • acute ventricular arrhythmias
    • Digitalis induced arrhythmias
  • Toxicity
    • local anesthetic
    • CNS stimulation/ depression
    • CV depression
24
Q

Tocainide

A

Class IB antiarrhythmic

  • lettuce, tomato, mayo
  • Weaknest Na+ channel blocker
    • rapid dissociation from channel
    • minimal cumulative effect over time
  • Mechanism
    • Na+ channel blocker
    • Shorten AP
    • Selective for ishcmeic or depolarized Purkinje and ventricular tissue
  • ​Use
    • Post MI​
      • acute ventricular arrhythmias
    • Digitalis induced arrhythmias
  • Toxicity
    • Local anesthetic
    • CNS stimulation/ depression
    • CV depression
25
Fenoldopam
Malignant HTN Fenoldopam * Dopamine D1 receptor agonist * Arteriol Vasodilator: * coronary * peripheral * renal * splanchnic * Decrease BP * increase natriuresis dopamine DI receptor agonist vasodilation: coronary, peripheral, renal, splanchnic decrease BP increase natriuresis
26
CHF
* _Decrease mortality_ * **ACE inhibitors** * captopril * enalapril * lisinopril * **B- blockers** * **ARBs ** * (sartans) * **Spironolactone** * _Decrease symptoms_ * **thiazide diuretic** * hydrochlorathiazide * **loop diuretic ** * furosamide
27
Flecainide MOA? AP effect? Uses?
Class IC antiarrythmic * MOA: Na+ blocker * binds strongly * slow dissociation * **Use dependence**= na+ block increases as heart rate increases (prolong QRS with faster rate) * blocking accumulates b.c less time between action potentials for drug to dissociate * No effect on AP * Use: * ventricular tachycardia that progresses to VF * intractable SVT * Last resport in refractory tachyarrythmias * \*\*\* NO structural abnormalitites * Toxicity * proarrythmias if post MI * prolonges refractory period in SA node *
28
Propafenon MAO? AP effect? Use?
Class IC antiarrhythmic * MOA: Na+ inhibitor * binds tightly * slow dissociation * **Use dependence** = sodium blocking effect increases with heart rate (prolong QRS with faster rate) * blocking effect accumulates b/c less time between action potentials for medicine to dissociate from receptor * AP effect * no effect on duration * Use * ventricular tachycardias that progress to VF * intractable SVT * last resport in refractory tachyarrhythmias * \*\* no structural abnormalities * Toxicity * proarrhythmic post MI * prolongs refractory period in AV node
29
Metoprolol Selective nonselective? MOA? Use Toxicity
Class II antiarrhythmic * B-blcoker * B1 selective = heart (ABEAM) * MOA: * decrease SA + AV node activity * decrease cAMP * decrease Ca++ currents * suppress abnormal pacemakers * decrease phase 4 slope * Decrease heart rate * decrease ionotropy * decrease conduction velocity * Use * ventricular tachycardia * SVT * a-fib * slow ventricualr rate * a-flutter * CHF * Toxicity * impotence * CV = bardycardia, av block, chf * CNS = sedation, sleep alterations * Mask signs of hypoglycemia \*\*\* * Do not use in cocaine users = unopposed alpha-adrenergic receptor agonists * **dislipidemaia** * treat with glucagon
30
Propranolol Selective? MAO? Use? Toxicity
Class II Antiarrhythmic * B-blocker * Non- selective * MAO * decrease SA and AV node activity * decrease cAMP * decrease Ca++ * suppress abnormal pacemakers * decrease slope of phase 4 * decrease HR * decrease ionotropy * decrease conduction velocity * Use * v-tach * SVT * a-fib + a-flutter * slow ventricular rate * CHF * Toxicity * impotence * exacerbation of asthma * prevent brochodilation * CV = bradycardia, AV block, CHF * CNS = sedation, sleep alteration * Mask signs of hypoglycemia \*\*\* * Do not give to cocaine users = unooposed alpha adrenergic receptor agonist * **Exacerbate vasospasm in Prinzmetal's angina**
31
Esmolol Selective? MOA? Use? Toxicity
Class II Antiarrhythmic * B-blocker * B1 selective = heart (A BEAM) * Shortest acting * MOA * decrease SA and AV node activity * decrease caMP * decrease Ca++ * supress abnormal pacemakers * decrease slope of phase 4 * decrease ionotropy * decrease HR * Decrease conduction velocity * Use * v-tach * SVT * a-fib and a-flutter * slow ventricular rate * CHF * Toxicity * CV = bradycardia, AV block, chf * CNS = sedation, sleep alteration * mask signs of hypoglycemia \*\*\* * done give to cocaine users = unopposed alpha adrenergic receptor agonists
32
Atenolol Selective? MOA? Use? Toxicity
Class II antiarrhythmic * B-blocker * B1 selective = heart (A BEAM) * MOA * decrese SA + aV node activity * decrease cAMP * decrease Ca++ * suppress abnormal pacemakers * decrease slope phase 4 * decrease ionotropy * decrease HR * decrease conduction velocity * Use * v-tach * SVT * a- fib + a-flutter * slow ventricular rate * Toxicity * CV = bradycardia, AV block, CHF * CNS = sedation, sleep alteration * Mask signs of hypoglycemia\*\*\* * dont give to cocain users = unopposed alpha adrenergic receptor agonists
33
Timolol Selective MOA Use Toxicity
Class II antiarrhythmic * B-blocker * Non selective * MOA * decrease SA + AV node activity * decrease caMP * decrease Ca++ * suppress abnormal pacemakers * decrease slope phase 4 * decrease ionotropy * decrease HR * decrease conductionv velocity * Use * v-tach * SVT * a-fib + a-flutter * slow ventricular rate * CHF * Toxicity * impotence * exacerbation of asthma (no bronchodilation) * CV = bradycardia, AV block, CHF * CNS = sedation, altered sleep * Mask signs of hypoglycemia\*\* * dont give to cocaine users = unopposed alpha adrenergic receptor agonist
34
Amiodarone MAO Use Toxicity
Class III antiarrhythmic (AIDS) * K+ channel blocker * also has class I, II, IV effects * Na+, B-blocker, K+, Ca+ block * MOA * increase AP duration * increase effective refractory period * increase QT interval * but low risk torsades de pointes * fail when used with other antiarrhythmics * Use * A-fib + left ventricle dysfunction * A-flutter * V-tach * Toxicity * Pulm: **pulmonary fibrosis** (most common) * **​**amiodarone interstitial pneumonitis * dyspnea, cough, fever, pulm infiltrate * reversible * Endo**: hypothyroid**( no T4--\> T3 conversion) + hyperthyroid * 40% iodine by weight * GI/ Hepatic: * constipation * elevated transaminases * Cardiac: bradycardia, heart block, QT prolongation, torsades de pointes * Neuro: peripheral neuropathy * Ocular: optic neuropathy, corneal microdeposits * Derm: blue gray skin discoloration
35
Sotalol MAO Use Toxicity
Class III antiarrhythmic (AIDS) * K+ channel blocker * B blocker * MOA * increase AP duration * increase effective refractory period * increase QT interval * decrease HR (b block) * Use * A-fib * A-flutter * V-tach * Toxicity * torsades de pointes * excess beta block
36
Dofetilide MAO Use Toxicity
Class III antiarrhythmic (AIDS) * K+ channel blocker * MOA * increase AP duration * increase effective refractory period * increase QT interval * Use * A-fib * A-flutter * V-tach * Toxicity * torsades de pointes
37
Ibutilide MAO Use Toxicity
Class III antiarrhythmic (AIDS) * K+ channel blocker * MOA * increase AP duration * increase effective refractory period * increase QT interval * Use * A-fib * A-flutter * V-tach * Toxicity * torsades de pointes (prolonged QT)
38
Lovastatin Pravastatin Simvastatin Atorvastatin Rosuvasatin
HMG-Co-A Reductase inhibitors * LDL: xxx * HDL: ^ * TG: x * MOA: * inhibit HMG-CoA --\> mevalonate * cholesterol precursor * **Increase surface LDL receptors on hepatocytes ** * Increase LDL uptake * Use * commonly prescribed post MI (lower cholesterol adn satbilize plaques) * Toxicity * hepatotoxicty * increased LFT * Rhabdomyolysis (muscle tissue breakdown) * Myalgia = low dose, no rise in CK * Myositis = high dose, rise in CK * Risk of myopathy is increased when used with **fibrates**
39
Nitroprusside Use MOA Toxicity
Malignant HTN * Use: emergency setting when you need to control blood pressure quickly * MOA: mixed arterial + venous dilation * inceases cGMP via release of NO * Toxicity: **Cyanide poisoning** * metabolized to CN + NO * Signs: altered mental status + lactic acidosis * Treatment: **sodium thiosulfate **
40
Adenosine MOA Use Toxicity Block effect
* MOA: Decreases If * increases K+ out of cell --\> hyperpolarize cell and decrease Ca++ * Use: * diagnose and abolish supraventricular tachycardia * very short acting (15 sec) * Toxicity * flushing * hypotension * chest pain * Block effects with * theophylline * caffeine
41
Mg2+ Use
* Use: * torsades de pointe * digoxin toxicity
42
Isoproterenol
* Isolated beta agonist * increase contractility of heart * decrease systemic vascular restistance * use * torsades de pointes (tachycardia decrease QT interval) * braduarrhythmias (worsen ischemia) * rarely used due to AV block
43
Atropine
* Muscarine receptor bocker * blocks vagal influence on SA + AV node * increases heart rate * Use: bradycardia * most inferior MI * Toxicity * normal antimuscarinic effects * acute closed angle glaucoma * unilateral severe ye pain and visual disturbance (halos)
44
Phosphodiesterase 3 Inhibitors
* MOA: Increase contractility in heart * inhibit phosphodiesterase = no metabolism of cAMP * increased cAMP --\> inceased conductance of Ca+ channels in SR --\> strengthen contraction * Use: CHF * Toxicity * vasodilation * do not use in hypotension
45
Dobutamine
* MOA: B1 receptor agonist * increased production of cAMP causing * positive ionotropic efffect * increased heart rate = weak chronotropic effect * increased myocardial O2 consumption * increased cardiac conduction velocity * Use: heart failure * cardiac stress test
46
47
Essential HTN
* Diuretics * ACE inhibitors * prevent unfavorable heart remodeling * Angiotensin II receptor blocler (ARB) * Ca+ channel blocker
48
CHF
* Diuretics * ACE inhibitors * Angiotensin II receptor blockers (ARBs) * B-blockers (compensated) * use cautiously * do not use in cardiogenic shock * K+ sparing diuretics
49
Diabetes Mellitus
* ACE inhibitors * protect against diabetic nephropathy * Angiotensin II receptor blocker (ARB) * calcium channel blocker * diuretics * B-blocker * A-blocker

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