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Drug Action I > Block 3 - Antiarrhythmics Med Chem > Flashcards

Block 3 - Antiarrhythmics Med Chem Flashcards

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1
Q

What are pharmacology properties of having a more lipophilic drug?

A
  1. Bind to plasma proteins
  2. High volumes of distribution
  3. Longer duration
  4. Long half life
  5. Rapidly absorbed
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2
Q

What are pharmacology properties of having a more basic drug?

A
  1. Amines with pKa of 8-10 is charged at physiological pH
  2. Low bioavailability
  3. Charged can’t cross membranes easily
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3
Q

What are arrhythmias?

A

Alteration in normal sequence of electrical impulse rhythm that leads to contraction of myocardium

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4
Q

What abnormalities does arrhythmias affect?

A
  1. Rate
  2. Impulse origination site
  3. Conduction through myocardium
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5
Q

What are the Antiarrhythmic drug classes?

A
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6
Q

Compare the 3 Class I?

A
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7
Q

What is the APD and Kinetics of Class IA? Drug class?

A

Prolonged APD; intermediate dissociation kinetics

Slow phase 0 depolarization

Na+ channel blockers

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8
Q

What are Class IA?

A
  1. Quinidine
  2. Procainamide
  3. Disopyramide
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9
Q

What is the physiological properties of quinidine?

A
  1. Basic nitrogens (pKa 11)
  2. Water soluble salt (sulfate or gluconate)
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10
Q

Which has better IV and PO/IM capabilities?

A

Gluconate more water soluble → better for emergenies (injectable), sulfate usually oral or IM

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11
Q

What are DDIs of quinidines?

A
  1. P-gp substrate -> inhibits renal tubular secretion of digoxin
  2. Increases plasma levels of digoxin
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12
Q

What is the contaminate that contributes to quinidine’s effectiveness?

A

Dihydroquinidine

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13
Q

How does Dihydroquinidine contribute to quinidines activity?

A
  1. Reduction of vinyl group to an ethyl
  2. More potent as an anti arrhythmic, but more toxic
  3. Commercial preps can vary based on levels of contaminant
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14
Q

How was procain modified for better efficacy? What was the new drug called?

A

Procainamide replaces an ester with an amide which is more resistant to esterase hydrolysis

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15
Q

How is procainamide metabolisized and why is this significant?

A

N-acetyltrasferase has genetic variations

Slow acetylators → elevated levels → drug induced lupus syndrome

Metabolite also implicated in torsades de pointes

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16
Q

How does disopyramide differ from procainamide?

A

Has anti-cholinergic effects due to its struccutral similarities

Receptors prefer a tertiary amine with a 2-4 carbon distance from 2 different rings

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17
Q

What is the APD and kinetics of Class IB?

A

Shortens (or no effect) APD; rapid dissociation from sodium channels

Shortens Phase 3 repolarization

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18
Q

What are the drugs in IB?

A
  1. Lidocaine
  2. Tocainide
  3. Mexiletine
  4. Phenytoin
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19
Q

How is lidocaine dosed? What happens if its given PO?

A
  1. Given as an IV
  2. Emergency treatment of ventricular arrhythmia → rapid on set
  3. Rapid first-pass metabolism (hydrolysis) by CYP3A4 and 2D6
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20
Q

ADRS of lidocaine?

A
  1. CNS (DZ, paresthesia, seizures)
  2. GI
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21
Q

In order to have a longer half-life, how does tocainide differ from lidocaine? ADRs?

A

a-methyl → slows metabolism, increased half-life

GI and CNS

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22
Q

How is mexiletine more effective than lidocaine and tocainide? Do the ADRs differ?

A

Amide → ether

Drug can be PO due to slow metabolism and longer half-life

No

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23
Q

What is unique about phenytoin metabolism?

A

Induces CYP3A4/UGT including its own therefore its half-life is quite high

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24
Q

What is route for phenytoin?

A

IV dissolved in a pH of 12 (weakly acidic)

Can’t do IM → tissue necrosis and erratic absorption

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25
In addition to arrhythmias, what is another indication for phenytoin?
Seizures
26
What is the APD and kinetics of Class IC?
No effect to APD; slow dissociation from sodium Slow Phase 0 depolarization Slows conduction
27
What are the drugs of IC?
1. Flecainide 2. Encainide 3. Propafenone 4. Moricizine
28
What is important to note about flecainides metabolism? ADRs?
Metabolized by the genetic variable CYP2D6 Cna aggravate existing arrhythmias or induce new ones
29
How does encainide differ from flecainide?
Less negative inotropic effect
30
What is unique about propafenone structure?
1. Related to b receptor blockers 2. S enantiomer produce b blocking 3. Both enantiomers are anti arrhythmic
31
Describe the PK properties of propafenone? How is it significant?
Good absorption, but low bioavailability due to metabolism by CYP2D6 (genetic variability) → PD effect variation
32
How is Moricizine metabolized?
Short half-life due to **CYP1A2** metabolism but duration of action for many hours
33
What class of drug is considered b-receptor blockers?
Class 2
34
What are the rate control classes?
II and IV
35
What is the MOA of Class II?
Depress enhanced calcium influx, work best on SA and AV nodes
36
What the kinetics of Class II?
1. Slow Phase 4 depolarization 2. Prolong repolarization
37
Describe how Class II has anesthetic properties at high doses?
1.. Decreased excitability 2. Decreased conduction velocity 3. Prolonged effective refractory period
38
What drugs are considered Class II?
1. Propanalol 2. Sotalol
39
What kind of b-blocker is propranolol?
Nonselective
40
What is unique about sotalol?
Class II/III Given as an enantiomer mixture Nonselective
41
Describe the activity of sotalol enantiomers?
Both block potassium channels but ultimately produce different effects on the heart L(-) enantiomer has β-blocking activity
42
Why is sotalol considered a good drug?
1. Good F 2. Not metabolized by the liver 3. Not bound to plasma proteins 4. Excreted unchanged in kidneys 5. Very few DDIS
43
What is the APD and kinetics of Class III? Drug class?
Prolong APD → prolongs refractory period Rhythm control Prolong Phase 3 repolarization K+ channel blockade
44
Describe how Class III affect action potential **Figure**
45
Drugs in Class III?
1. Bretylium Tosylate 2. Ibutilide 3. Amiodarone (Cordarone, Pacerone) 4. Dronedarone
46
How is bretylium tosylate used?
Quaternary ammonium (Nitrogen) salt for HTN but can cause hypotension Erratic PO absorption due to permanent charge
47
Describe the activity of ibutilide? Dosage forms?
Affinity for Na+ channels IV fumarate salt PO is dofetilide
48
What is the unique MOA of amiodarone?
1. Alters lipid membrane where ion channels and receptors are located 2. Acts as an all class drug 3. Very toxic → agent of last choice
49
How does the PK properties of amiodarone contribute to its toxicity?
1. Half life is 58 day (lipophilic from iodines and rings) 2. Slow onset (several days) 3. Large Vd **Thyroid hormones accounting for some of its adverse effects**
50
What was the improved solution to decrease amiodarone toxicity?
Dronedarone contains: 1. Methysulfonamido group (Decrease lipophilicity and neurotoxicity) 2. Dibutyl substitution on Nitrogen 3. Removal of Iodines 4. Increased F with high fat foods, heavy protein binding
51
How is dronedarone metabolized?
It is a substrate and inhibitor of CYP3A4
52
What is Class IV?
CCB that blocks inward current carried by Ca2+ → Best for Ca2+ dependent cells → rate control Slows phase 4 depolarization
53
What are the Class IV drugs?
1. Verapamil 2. Diltiazem
54
Describe the PK of Verapamil? Any DDIs?
Long onset (2hr) AUC increase in digoxin
55
What are the forms of Diltiazem? How is it metabolized?
PO and IV for A fib Fast onset CYP3A4 metabolite → mechanism based inhibition of CYP3A4
56
What is mechanism based inhibition?
Drug generates a metabolite that inhibits metabolizing enzyme
57
Identify the class and activity?
Class IA Increase ERP Increased AP duration
58
Identify the class and activity?
Class II Increased PR interval
59
Identify the class and activity?
Class IV Increased PR interval Increased ERP
60
Identify the class and activity?
Class IB Decreased ERP Decreased AP duration
61
Identify the class and activity?
Class III Increased ERP Increased AP duration
62
Identify the class and activity?
Class IC Normal ERP Normal AP duration
63
What is the MOA of adenosine?
1.Endogenous nucleoside 2. Slows conduction time through AV node 3. Can restore normal sinus rhythm in patients with paroxysmal supraventricular tachycardia
64
DDIs of Adenosine?
Antagonized by caffeine/theophylline (adenosine receptor blockers)
65
PK and ADRs of adenosine?
Half-life in blood less than 10 seconds -> Given as rapid intravenous bolus (6 mg administered over a 1 – 2 second period) 1. Facial flushing 2. SOB 3. Sweating 4. Nausea
66
Why does adenosine have such a short half-life?
Endogenous compounds get metabolized very fast → short half-lives/duration of action IF they even absorb
67
Match
68

Drug Action I (32 decks)

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