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Cardio/Renal 2 Final > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Rank the class 1A drugs in order of most to least anticholinergic effect

A

Disopyramide> Quinidine> Procainamide

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2
Q

What does the reverse use dependence of class 1A drugs lead to

A

Higher arrhythmia rate (at lower heart rate, action of the heart is lower leading to QT prolongation and Torsade de pointes)

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3
Q

Procainamide

A

effective against most atrial and ventricular arrhythmias
-Cardia effects are slows upstroke of AP, directly depresses SA/AV nodes, slows conduction (anticholinergic effect), causes hypotension

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4
Q

PK of Procainamide

A

Oral, IV (slow infusion), IM
Hepatic metabolism - produces NAPA
NAPA has class 3 effects and can cause torsades de pointes
Renal elimination so adjust dose for renal and heart failure

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5
Q

AE of Procainamide

A

Cardiotoxicity - QT prolongation, torsades de pointes, syncope, immune lupus erythematosus, blood dycrasias, pulmonary toxicity

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6
Q

Quinidine and its PK

A

Same cardiac effects as Procainamide
Tablet / injection (rare)
eliminated by hepatic metabolism

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7
Q

AE of Quinidine

A

QT-interval prolongation, Torsades de pointes, excessive Na blockade with slowed conduction, Cinchonism, tinnitus, Immune- thrombocytopenia, hepatitis, edema, fever

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8
Q

DDI of Quinidine

A

CYP3A4 strong inhibitors and Inducers

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9
Q

Disopyramide and its PK

A

used for life threatening arrhythmia and same cardiac effects as procainamide

Capsules and metabolized by CYP3A4

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10
Q

AE and CI of Disopyramide

A

AE are atropine like (dryness of mouth and focusing issues)
CI is may cause or worsen CHF

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11
Q

What class is Lidocaine in and its MOA

A

Class 1B and
- Exerts antiarrhythmic effects by increasing the electric stimulation threshold
- Effective in arrhythmias associated with acute MI
- Greater effects on Purkinje and ventricular cells compared to atrial cells

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12
Q

PK of Lidocaine

A
  • Extensive first pass metabolism so IV route
  • Metabolized in liver (CYP3A4)
  • Adjust dose in Acute MI
  • High binding to alpha acid glycoprotein-> need higher dose
  • Decrease dose for Liver disease and CHF
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13
Q

Thera of Lidocaine

A

Ventricular arrhythmias

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14
Q

AE of Lidocaine

A

Hypotension, keep levels below 9 ug/ml to avoid side effects

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15
Q

Mexiletine, PK, and AE

A
  • Similar effects to Lidocaine
  • Used for life threatening ventricular arrhythmias
  • Orally active
  • Hepatic metabolism (CYP2D6)

AE - neurologic

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16
Q

When can class 1C not be given and what drugs are in this class

A

Cannot be given to previous MI or ventricular tachyarrhythmia

  • Flecainide
  • Propafenone
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17
Q

Flecainide and PK

A
  • Potent blocker of sodium and potassium
  • Proarrhythmogenic
  • Tablet
  • Hepatic metabolism (CYP2D6)
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18
Q

Thera of Flecainide

A

Life threatening Ventricular tachycardia, PSVT (Paroxysmal Supraventricular Tachycardia), PAF (Paroxysmal Atrial Fibrillation)

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19
Q

Propafenone AE/CI

A
  • Prolongs time to recurrence of AF with patients who do not have structural heart disease
  • Similar to propranolol-> weak Beta-blocking action

Provokes HF

Avoid use with CYP2D6/CYP3A4 inhibitor

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20
Q

What do class 3 drugs do ? and what are the drugs in this class

A
  • K+ channel blocker in phase 3 and multi channel blockers-> increase in ADP and ERP
  • Reverse Use Dependence- at lower heart rate, QT prolongation very low and causes torsades

Amiodarone / Dronedarone / Sotalol / Dofetilide / Ibutilide

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21
Q

Whats Amiodarones cardiac effects

A

Cardiac effects- No reverse use dependence, also blocks Na+ channels, slows heart rate and AV node conduction, causes QT prolongation (low incidence of torsades)

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22
Q

PK of Amiodarone

A
  • Oral (prevent arrhythmia) and IV (Acute treatment-> achieving rapid effects )
  • Long onset of action
  • Increased absorption with food
  • Lipophilic, high Vd (volume of distribution)
  • Desethylamiodarone metabolite is bioactive
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23
Q

Thera of Amiodarone

A
  • Used against most arrhythmias
  • Recurrent ventricular fibrillation
  • Unstable ventricular tachycardia (decreases frequency)
  • Atrial Fibrillation
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24
Q

AE of amiodarone

A

Pulmonary Toxicity, Thyrotoxicosis (blocks conversion of T4 to T3), Loss of vision

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25
Q

DDI of Amiodarone

A

CYP3A4 inducers (decrease efficacy of amiodarone)- Rifampin, Misc (substrates)
Amiodarone and these drugs both cause QT prolongation and increase risk of Torsades- macrolide antibiotics, Azoles

26
Q

Dronedarone, PK, Thera

A
  • Iodine removed, methanesulfonyl group on benzofuran
  • Similarities with Amiodarone: Cardiac effects, Liver toxicity
  • Differences with Amiodarone: No pulmonary toxicity
  • Half life- 24 hours
  • Useful for AF

DO NOT USE IN HF PATIENTS

27
Q

Sotalol and its PK

A
  • Beta-adrenergic blocking action (class 2), and class 3 actions
  • Max- beta blocking effect at doses below max APD effect
  • No metabolism
  • Eliminated unchanged in urine (kidney issues, not liver)
28
Q

Thera of Sotalol

A
  • Life threatening ventricular arrhythmias and Maintenance of sinus rhythm in pts with AF
    Pediatric arrhythmias
  • WPW syndrome
29
Q

AE and DDI of Sotalol

A

AE
Incidence of torsades de pointes, Can cause serious ventricular arrhythmia

DDI
Drugs that prolong QT interval

30
Q

Dofetilide

A
  • Pure class 3
  • Blockade of Ikr increases in hypokalemia
  • Moderate reverse use dependence
31
Q

PK of Dofetilide

A
  • 100% bioavailable
  • Metabolites inactive
  • Cimetidine increases level and increases chance of torsades
  • Dose adjustment based on renal function
32
Q

Thera and CI of Dofetilide

A

Thera
Second choice to Amiodarone in arrhythmia with HF

CI
QT prolongation, bradycardia, hypokalemia

33
Q

Ibutilide

A

IV route
Rapid metabolism by liver

34
Q

Ca++ Channel blockers

A
  • All increase ERP
  • Non-DHP (use these)- Verapamil, DIltiazem
  • DHP do not share antiarrhythmic efficacy
  • Blocks active and inactive L-type Ca channels (control conduction velocity)
  • Hypotension can cause reflex increase in SA rate (not useful)
35
Q

MISC agents (MIRA)

A

Magnesium, Ivabradine, Ranolazine, Adenosine, Atropine

36
Q

Magnesium

A
  • Used for digitalis-induced arrhythmias if hypomagnesemia is present, Patients with torsades even if magnesium levels are normal
  • Influences many channels
37
Q

Ivabradine

A
  • Decreases heart rate and oxygen demand
  • Used for stable angina and tachycardia
  • Selective blocker of hyperpolarization-activated HCN ion channels (class 0 action)
  • SA node function is regulated
38
Q

Ranolazine MOA

A
  • Inhibits late inward sodium current leading to reductions in intracellular Ca levels which leads to reduced tension in heart wall and oxygen requirements
  • Increased glucose oxidation, Increased cardiac ATP production, Decreases fatty acid oxidation, removes lactate
  • Balances Na/Ca channels and is anti-edema
39
Q

PK / AE / CI of Ranolazine

A

PK
Extended-release tablets
Metabolism: mainly CYP3A4 and a little CYP2D6

AE
QT prolongation but no torsades

CI
P-gp inhibitors (cyclosporine)- increase absorption (more toxicities), Liver Cirrhosis

40
Q

Adenosine MOA and PK

A

Activates GPCR in heart, Gi-coupled (decrease cAMP), Activation of inward rectifier K current

IV bolus only

41
Q

Thera and DI of Adenosine

A

Thera
Acute termination of reentrant supraventricular arrhythmias

DI
Potentiation by dipyridamole

42
Q

Atropine / PK / Thera / AE

A
  • Parasympatholytic (anticholinergic)
  • PK- IV admin
  • Thera- Symptomatic bradycardia, bradycardia with escape rhythms
  • AE- Paradoxical decrease in HR
43
Q

Receptor affinities

A
  • Phenylephrine: a1>a2»»>b,
  • Norepinephrine: a1=a2; b1»b2
  • Epinephrine: a1=a2; b1=b2 - Dobuatamine: b1>b2»»>a
  • Isoproterenol: b1=b2»»»a
  • Dopamine: D1=D2»b»a
  • Any drug that increases HR and force (positive inotropic drugs) are CI in HF
44
Q

Norepinephrine

A
  • Vasopressor of choice- septic/cardiogenic shock
  • Used in the treatment of cardiac arrest and extreme hypotension (elevates both systolic and diastolic BP)
  • Reverses vascular shock with Bradycardia
45
Q

PK and AE of NE

A

PK - IV
COMT- active metabolite, MAO- inactive metabolite

  • AE
    Extravasation ischemia (use S.C alpha blockade->phentolamine?), Use large central veins to administer vasoconstrictors
46
Q

DDI of NE and what drugs does this apply to

A
  • Increase pressor response- Tricyclic antidepressants, BB, Ergot vasoconstrictors, Atropine (blocks reflex bradycardia)
  • Decrease pressor response- Alpha blockers, Sodium bicarbonate (acid-base inter.), Diuretics
  • Cyclopropane- enhance arrhythmia liability

Applies to all other agents in this drug class

47
Q

Phenylephrine

A
  • Nose drops, eye drops, and cough preps (PE) as a decongestant
  • 99% alpha-1
  • Used systemically to elevate PR in vascular shock
  • Dilates the pupils of the eye
48
Q

Thera / AE / CI /

A
  • Thera - Second line to NE for septic shock
  • AE - Hypertension, stinging, lacrimation
  • CI - Narrow angle glaucoma (wide is fine)
49
Q

DDI of Phenylephrine and precautions

A

DDI- same as NE
Do not use if discolored because forms adrenochrome (inactive)

  • Precautions -
    Causes severe hypertension, Diabetes-increase glucose, Hyperthyroidism, Elderly, Severe ASHD,Cardiac disease, Infants, Extravasation Ischemia
50
Q

Epinephrine

A

Response is dose related: a1- VC (high dose)-> treats vascular shock, b1- cardiac stimulant (low dose)-> treats cardiogenic shock, b2- vasodilator (low dose)

51
Q

PK / Thera / AE / DDI

A

PK - IV- quick onset and short diffusion
IM- injection in thigh

  • Thera - Cardiac Arrest, Hemostasis, anaphylaxis (IM), ophthalmic/nasal (decongestant), Asthma
  • AE - Convulsive seizures, ENT, Palpitations, Tachycardia, Hypertension, Chest pain Dysrhythmias
    DI- same as NE
52
Q

Vasopressin MOA

A

ADH analogue- retains water, posterior pituitary hormone, vesicant, VC at high doses

53
Q

Vasopressin PK / Thera / AE

A
  • PK - V2 Gs coupled (kidneys)
    Vasopressin agonists: Desmopressin- control bleeding, Terlipressin- VC
  • Thera - Esophageal varices with GI bleed
  • AE - Increased BP, Venous thrombosis, VC with high doses
54
Q

Desmopressin MOA

A
  • Retains water and is a VC at high doses
  • Elevates factor 8 and Von Willebrand factor
55
Q

Desmopressin thera

A

Hemostatic in Hemophilia, Von Willebrand disease, Thrombocytopenia
Diabetes insipidus

56
Q

Desmopressin AE and DDI

A
  • AE - Facial flushing, Dizziness, Headache, Abdominal cramps, pain at injection site
  • DDI - Decreased ADH effects- Lithium, Democlocycline
    Increased ADH effects- Fludrocortisone, Chlorpropamide
57
Q

AT-II

A

Septic and Vasodilatory shock

58
Q

Dopamine type of compound and what it is considered

A

Natural compound
Considered a weak EPI with positive inotropic and VC effects

59
Q

MOA of Dopamine

A

Inotropic action (b1)- Increases contractility at low dose
Chronotropic (b1)- Increases HR at low dose
Vasopressor (a1)- VC at high dose

60
Q

Dopamine thera / AE / CI / DDI

A
  • Thera - Cardiogenic and Vascular shock
  • AE - Hyperglycemia, Extravasation Ischemia
  • CI - Tachyarrhythmias, Pheochromocytoma, VF
  • DDI - same as NE
61
Q

What is Dobutamine and its MOA and its DDI

A
  • Synthetic ISO deriv (isoproterenol analogue) and a1
  • MoA - Potent b1 agonist with + inotrope and chronotrope
  • Vasodilator

-DDI- same as NE
All hypertensive drugs

62
Q

Milrinone MOA and PK

A
  • Inhibits PDE 3 and degrades cyclic AMP
  • Increases inotropic (good) and chronotropic activity (oxygen wasting and can cause anginal pain)
  • Causes Vasodilation
  • Decreases blood viscosity
  • PK - IV
    Reduce dose based on CrCl

Cardio/Renal 2 Final (1 decks)

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