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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
DDI of Amiodarone
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
Dronedarone, PK, Thera
- 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
Sotalol and its PK
- 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
Thera of Sotalol
- Life threatening ventricular arrhythmias and Maintenance of sinus rhythm in pts with AF Pediatric arrhythmias - WPW syndrome
29
AE and DDI of Sotalol
AE Incidence of torsades de pointes, Can cause serious ventricular arrhythmia DDI Drugs that prolong QT interval
30
Dofetilide
- Pure class 3 - Blockade of Ikr increases in hypokalemia - Moderate reverse use dependence
31
PK of Dofetilide
- 100% bioavailable - Metabolites inactive - Cimetidine increases level and increases chance of torsades - Dose adjustment based on renal function
32
Thera and CI of Dofetilide
Thera Second choice to Amiodarone in arrhythmia with HF CI QT prolongation, bradycardia, hypokalemia
33
Ibutilide
IV route Rapid metabolism by liver
34
Ca++ Channel blockers
- 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
MISC agents (MIRA)
Magnesium, Ivabradine, Ranolazine, Adenosine, Atropine
36
Magnesium
- Used for digitalis-induced arrhythmias if hypomagnesemia is present, Patients with torsades even if magnesium levels are normal - Influences many channels
37
Ivabradine
- 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
Ranolazine MOA
- 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
PK / AE / CI of Ranolazine
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
Adenosine MOA and PK
Activates GPCR in heart, Gi-coupled (decrease cAMP), Activation of inward rectifier K current IV bolus only
41
Thera and DI of Adenosine
Thera Acute termination of reentrant supraventricular arrhythmias DI Potentiation by dipyridamole
42
Atropine / PK / Thera / AE
- Parasympatholytic (anticholinergic) - PK- IV admin - Thera- Symptomatic bradycardia, bradycardia with escape rhythms - AE- Paradoxical decrease in HR
43
Receptor affinities
- 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
Norepinephrine
- 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
PK and AE of NE
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
DDI of NE and what drugs does this apply to
- 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
Phenylephrine
- 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
Thera / AE / CI /
- Thera - Second line to NE for septic shock - AE - Hypertension, stinging, lacrimation - CI - Narrow angle glaucoma (wide is fine)
49
DDI of Phenylephrine and precautions
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
Epinephrine
Response is dose related: a1- VC (high dose)-> treats vascular shock, b1- cardiac stimulant (low dose)-> treats cardiogenic shock, b2- vasodilator (low dose)
51
PK / Thera / AE / DDI
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
Vasopressin MOA
ADH analogue- retains water, posterior pituitary hormone, vesicant, VC at high doses
53
Vasopressin PK / Thera / AE
- 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
Desmopressin MOA
- Retains water and is a VC at high doses - Elevates factor 8 and Von Willebrand factor
55
Desmopressin thera
Hemostatic in Hemophilia, Von Willebrand disease, Thrombocytopenia Diabetes insipidus
56
Desmopressin AE and DDI
- AE - Facial flushing, Dizziness, Headache, Abdominal cramps, pain at injection site - DDI - Decreased ADH effects- Lithium, Democlocycline Increased ADH effects- Fludrocortisone, Chlorpropamide
57
AT-II
Septic and Vasodilatory shock
58
Dopamine type of compound and what it is considered
Natural compound Considered a weak EPI with positive inotropic and VC effects
59
MOA of Dopamine
Inotropic action (b1)- Increases contractility at low dose Chronotropic (b1)- Increases HR at low dose Vasopressor (a1)- VC at high dose
60
Dopamine thera / AE / CI / DDI
- Thera - Cardiogenic and Vascular shock - AE - Hyperglycemia, Extravasation Ischemia - CI - Tachyarrhythmias, Pheochromocytoma, VF - DDI - same as NE
61
What is Dobutamine and its MOA and its DDI
- Synthetic ISO deriv (isoproterenol analogue) and a1 - MoA - Potent b1 agonist with + inotrope and chronotrope - Vasodilator -DDI- same as NE All hypertensive drugs
62
Milrinone MOA and PK
- 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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