Cardia Agents Flashcards

Question

Procainamide Bioisosteric drug design Treats? analog of? Dose adjustment in? Metabolized into?

Answer 1

analog of procain Ventricular arrythmias N-acetyl procainamide is active Unchanges in urine 50% Leukopenia and agranulocytosis

Answer 2

Inamrinone is longer acting - inhibition of PDE Milrinon- Greater selectivity Dose adjustment in renal impairment

Answer 3

Dihydromoeity essential Aromatic ring with ortho or meta required Ester functional group Can increase potency (amlodipine) Free NH at one position is REQUIRED

Answer 4

* Synthetic drug. An amide analog of the local anesthetic Procaine (example of bioisosteric drug design principle!) * Orally bioavailable. Parenteral (IV and IM) formulation also available. * Indicated for the treatment of ventricular arrythmias * Hepatic metabolism. Metabolites include N-acetyl procainamide (active) and p-aminobenzoic acid. Renal excretion of unchanged drug (~50%) and the metabolites. * Might require dose adjustment in hepatic and renal impaired patients * SEs- Drug induced lupus syndrome. Can also cause (0.5%) serious hematological disorders, particularly leukopenia and agranulocytosis.

Answer 5

Quinidine, Procainamide, Disopyramide Phase 0 depol

Answer 6

Tubular excretion of DIgoxin leading to toxic Substrate for CYP3A4 unchanges urine

Answer 7

* Synthetic drug. Cardiac activity similar to Procainamide, Also exhibit weak anticholinergic activity. * Good oral availability. T1/2= 5-7 hr. * Partially metabolized in liver (CYP3A4), mostly to a mono-N-dealkylated product. Renal excretion of unchanged drug (~50%) and metabolites. * Dose adjustment might be required in patients with liver/renal impairment * SEs- are primarily related to anticholinergic activities of the drug, and can include dry mouth, blurry vision, constipation, and urinary retention.

Answer 8

analog of procain Ventricular arrythmias N-acetyl procainamide is active Unchanges in urine 50% Leukopenia and agranulocytosis

Answer 9

* Original use as a local anesthetic (Procaine-like). * Drug of choice for emergency treatment of ventricular arrythmia (IV). Also used parenterally for suppression of arrythmias associated with acute myo cardial infraction and cardiac surgery. * Rapid onset (1-2 min) and short duration of action (T1/2 = \< 30 min). * Liver metabolized (N-Deethylation and amidase hydrolysis). Renal excretion. * SEs- Dizziness, paresthesis and seizure in severe cases.

Answer 10

* Structurally analogous to barbiturates, but does not possess sedative properties. * Long history of use for the treatment of epileptic seizures. * Useful antiarrythmic agent for the treatment of digitalis induced arrythmias. * Orally active. Also available for parenteral (IV) use. * High plasma protein binding (~ 90%). T1/2 = 15 -30 hrs. * Slow hepatic (CYP450) metabolism to mono-p-hydroxyphenyl derivative, followed by glucuronide conjugation and excretion in urine. * Prevention of metabolism, or the presence of other plasma protein bound drugs can cause toxicity.

Answer 11

* Potent antiarrythmic drug with local anesthetic activity. * Orally administered for the treatment of ventricular arrythmias. * Plasma half-life ~14 hrs. * Part of the drug (~50%) is metabolized in liver (CYP2D6). Metabolism involves m-O-dealkylation. Urinary excretion of unchanged drug and the metabolites. * New or worsened arrythmias have been reported with the use of this drug. * Other adverse effects: Dizziness, blurred vision, nausea, and headache etc.

Answer 12

* Structural resemblance to class 1C antiarryhmics, as well as β-blockers * Used primarily for ventricular and supraventricular arrythmias * Oral drug. Metabolized in liver (CYP2D6; CYP3A4; CYP1A2). Dose adjustment might be required with simultaneous use of other drugs interacting with the above metabolic enzymes. * New or worsened arrythmias have been reported with the use of this drug. * Other adverse effects: Agranulocytosis, taste disturbance, dizziness, nausea, and constipation etc.

Answer 13

β-Adneregic blockers. Suppresses sympathomimetic activity. Slows ‘Phase 4’ depolarization. Propranolol

Answer 14

* K+-ion channel blockers. Prolongs ‘Phase 3’ repolarization and duration of action potential. * A quaternary ammonium salt. Originally developed as an antihypertensive. * Use limited for the treatment of emergency life threatening ventricular arrythmias resistant to other therapy. * Usually administered iv or im. * Adverse Effects : Hypotension (most common), nausea, and dizziness etc.

Answer 15

* Antiarrythmic effects similar to Bretylium. Approved for the treatment of life-threatening ventricular arrythmias refractory to other drugs. * Oral and parenteral formulations. Long half-life (several weeks) * Hepatic metabolism involving N-deethylation (active metabolite). * Severe toxicity limits the use of this drug (used in hospital setting only)

Answer 16

* Used orally for tachyarrythmias (esp. AF). T1/2 ~ 10 hr. * Due to the pro-arrhythmic potential of dofetilide, to be prescribe by physicians who have undergone specific training in the risks of treatment with dofetilide. * Hepatic metabolism (20%). Metabolites and unchanged drug excreted in urine. Dose adjustment in renal impairment. * Adverse effects: Induced arrythmia, headache, dizziness, nausea, rash, flu-like syndrome etc.

Answer 17

* Rapid rate of dissociation from Na+-ion channels. Shortens ‘Phase 3’ repolarization and action potential duration. Drug examples include: Lidocaine, and Phenytoin etc.

Answer 18

* Slows rate of dissociation from Na+-ion channels. Markedly slow ‘Phase 0’ depolarization * Flecainide, Propafenone

Answer 19

* Ca2+-ion channel blockers. Slows ‘Phase 4’ depolarization and duration. * Prototypical drug examples are Verapamil, and Diltiazem etc.

Cardia Agents Flashcards

(44 cards)