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S6 > Pharmacology S10 > Flashcards

Pharmacology S10 Flashcards

1
Q

Vaughan Williams Classification of antiarrythmia

A

Class I

Na + Channel Blockers

Class II

Beta Blockers

Class III

Prolong Action Potential

Class IV

Calcium Channels Blockers

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2
Q

Class one divisions give examples

A

Na + Channel Blockers

Ia Quinidine

Ib Lidocaine

Ic Flecainide Propafenone

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3
Q

Class Ia give examples

A

Quinidine

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4
Q

Class Ib give examples

A

Lidocaine

Mexiletine

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5
Q

Class Ic give examples

A

Flecainide propafenone

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6
Q

Class I mechanism of action

A
  • Mainly block fast Na + channels
  • Weak K + channel block (1a) — ¯C onduction velocity — ¯D epolarisation amplitude — ¯A utomaticity — ¯P hase 4 slope ( decreases all )
  • ­ increase Depolarisation threshold
  • Alter duration of action potential
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7
Q

Effect on Action Potential
Class la
Class lb
Class lc

A

Class Ia e.g. Quinidine

Intermediate Na + Block
Action Potential Duration Effective Refractory Period ( increased in both )

Class Ib e.g. Lidocaine
Weak Na+ Block
¯Action Potential Duration ¯E ffective Refractory Period ( decreased in both )

Class Ic e.g. Flecainide
Strong Na+ Block

Action Potential Duration « Effective Refractory Period ( no change maybe 🤷‍♀️)

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8
Q

Lidocaine

Pharmacokinetics

Adverse effects

Clinical use

A

Class Ib agent

  • Rapid dissociation half life ~ 0.1s
  • Binds open & inactive Na + channels
  • Pharmacokinetics
  • Adverse effects
  • Clinical use

Extensive first pass metabolism iv administration Short half life

Negatively ionotropic Seizures Nystagmus

Ventricular tachycardia post MI

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9
Q

Flecainide

Pharmacokinetics

Clinical Use
CI

A

Class 1c agent

  • Also blocks outward K + channels
  • Long dissociation half life ~ 10 s
  • Binds open Na + channels only
  • ­ PR, QRS and QT intervals at normal rates
  • ­ action potential in atrial tissue at fast rates
  • Pharmacokinetics
  • Clinical Use
  • Adverse effects

Well absorbed orally Metabolised by CYP2D6 & renal elimination Elimination t 1/2 10-18 hours

Prophylaxis and treatment of SVT/PAF

Contraindicated with history of IHD/HF – Causes lethal dysrhythmias

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10
Q

Non-selective Beta Blockers give examples

A

Propranolol

Sotalol

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11
Q

b1

selective blockers
Long acting
Short acting

A

Longer Acting Atenolol Bisoprolol

Shorter Acting Metoprolol Nebivolol Esmolol

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12
Q

Mixed

b1 a1 blockers

A

Carvedilol

Labetalol

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13
Q

Adverse Effects & Clinical Use of beta blockers

A

Adverse effects

• Clinical Use

Heart failure Bradycardia Bronchospasm Peripheral limb ischaemia Loss of hypoglycaemic symptoms Fatigue

Rate control of AF/Atrial flutter Cardioversion AVRT/AVNRT 2°prevention VT/VF Heart failure Hypertension Ischaemic Heart Disease

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14
Q

Class III give examples

A

amiodarone & sotalol , dofitlide

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15
Q

Class III mechanism of action

A

­ action potential duration

  • Block slow outward K + channels
  • ­ refractory period
  • ­ QT interval ( increased all )
  • Suppress re-entry circuits
  • However can ­ risk of early after depolarisation leading to torsade de pointes
  • Most commonly used are amiodarone & sotalol
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16
Q

Amiodarone mechanism of action

A

Acute

Blocks fast Na + and Ca 2+ channels – Class I & IV action Use dependent Blocks acetylcholine gated K + channels - Class II action Less negatively ionotropic than Class I/II/IV agents

Chronic
Blocks outward K + channels – Class III action Inhibits cell-cell coupling Prolongs action potential duration & refractory period Slows AV node conduction Prolongs QT interval

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17
Q

Pharmacokinetics of amiodaron

A
  • 30% bioavailability
  • Large V d » 66 L/kg (approx 5000L in a 70kg individual!)
  • I.v. or oral loading dosing required
  • Elimination t 1/2 10-100 days
  • Hepatic metabolism by CYP450 3A4 to Desethyl-amiodarone (DEA)
  • Dose adjustments not required in renal/hepatic/cardiac dysfunction
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18
Q

Adverse Effects of amiodaron
Short term
Long term

A

Phlebitis & hypotension with iv administration Requires central access when given iv

Pulmonary fibrosis Hypo/hyperthyroidism Hepatic dysfunction Corneal microdeposits Slate grey skin/photosensitivity Peripheral neuropathy Proximal myopathy Increases defibrillation threshold for ICDs

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19
Q

Drug Interactions with amiodarone

A

Inhibits CYP3A4 and CYP2C9 & P-glycoprotein Dose reductions of warfarin, digoxin and flecainide may be required

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20
Q

Clinical Use of amiodarone
Acute indications
Chronic indications

A

Acute indications

Atrial Fibrillation Atrial Flutter Ventricular Tachycardia When other antiarrhythmics contraindicated

Chronic indications
2°prevention of VT/VF When other antiarrhythmics not tolerated

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21
Q

Sotalol

A

— Racemate

  • d-sotalol pure class III agent
  • l-sotalol has b blocker and class III action
  • Blocks outward K + channels
  • Reverse use dependence
  • Lowers defibrillation threshold for ICDs
  • Doses < 120mg bd has mainly b blocker action
  • Higher doses have class III action
  • Adverse effects
  • Clinical use

b blocker adverse effects Torsades de pointes

Paroxysmal AF

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22
Q

Class IV

A
  • Diltiazem & verapamil block slow inward Ca 2+ channels on SAN and AVN
  • Slow phase 4 depolarization
  • Slow conduction velocity
  • Increase refractory period on AVN
  • Dihydropyridine calcium channel blockers (eg nifedipine, amlodipine) act on vascular smooth muscle & have no antiarrhthymic effects
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23
Q

Verapamil & Diltiazem

Adverse Effects
Clinical uses

A

Verapamil

  • Diltiazem
  • Adverse Effects
  • Clinical use

iv or oral Sustained release preparations Negatively ionotropic Drug interactions with digoxin & amiodarone

Less negatively ionotropic than verapamil Sustained release preparations

Bradycardia Heart failure Constipation

Rate control of AF Cardioversion of AVRT/AVNRT Antianginal/antihypertensive

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24
Q

Other Antiarrhythmic Drugs

A

— Adenosine —
Digoxin —
Magnesium

—

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25
Q

Adenosine mechanism of action

A

Main action as an AV node blocker

  • Activates A 1 receptors in the heart
  • A 1 receptors are G i linked ® Inhibits adenylate cyclase ® ¯cAMP levels
  • Activates Ach K + channels in SAN and AVN ® Hyperpolarises cells
  • Reduces automaticity, increases AVN refractory period
  • t 1/2 » few seconds
  • Associated with transient chest tightness
  • Used as an iv bolus to diagnose/treat SVTs
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26
Q

Digoxin

Mechanism of action

A

Inhibits Na+/K +ATPase

  • Direct cardiac effects
  • CNS mediated effects
  • Combined effect

+ve ionotrope
Decrease ¯SNS outflow ­ increase PNS outflow Sensitizes baroreceptor reflex ¯decrease Automaticity of SAN and AVN ­
Increase Refractory period of AVN ¯decrease Conduction velocity of AVN

27
Q

Phamacokinetics of digoxin

A

Oral biovailability 70-80%

  • Large V d » 4-7 L/kg
  • 20-30% protein bound
  • Loading dose required for rapid onset of action
  • 2 compartment model kinetics
  • Elimination t 1/2 36-48 hours with normal renal function
  • Renal excretion unchanged by P-glycoprotein
  • Digoxin clearance µ GFR
  • Reduce dose in elderly & renal impairment
  • Loading usually in 2 divided doses to minimise risk of toxicity
  • Plasma digoxin levels checked 6-8 hours after dosing
28
Q

Drug Interactions with digoxin

Pharmacokinetic

Pharmacodynamic

A

Pharmacokinetic:

• Pharmacodynamic:

­ Digoxin Levels Propafenone, quinidine, amiodarone verapamil, spironalatone, cyclosporine Likely mediated by P-glycoprotein

­ Digoxin Levels Erythromycin, tetracycline

Beta blockers, verapamil, diltiazem, flecainide

Diuretics

29
Q

Adverse Effects of digoxin

& Signs & symptoms?

A

Narrow therapeutic index » plasma level 1-2.6 nmol/L

  • Toxicity enhanced with ¯plasma K+
  • Cardiac toxicity
  • Signs & symptoms

Bradycardia Atrial/ventricular/junctional ectopics AVN block Atrial tachycardia with AVN block Accelerated idioventricular tachycardia

Delerium, fatigue, confusion, nausea, vomiting anorexia, diarrhoea, blurred & yellow vision (xanthopsia)

• Severe toxicity can be treated with antibody fragment therapy (Digibind)

30
Q

Clinical Use of digoxin

A

Main use is rate control in atrial fibrillation

  • Heart failure
  • No mortality benefit
31
Q

Magnesium

A
  • iv Mg 2+ used to treat Torsades de Pointes
  • Also digoxin toxicity
  • Mechanism of action unknown
  • No benefit to chronic administration
32
Q

Spontaneous AF

What drugs best to use

A

Drug options: Flecainide Propafenone Amiodarone

33
Q

Spontaneous SVT

Drug options ?

A

Drug options: Adenosine Flecainide Betablocker Calcium Channel Blocker Amiodarone

34
Q

Ischemia – Myocardial Infarction

Drug options

A

Lidocaine

Amiodarone

35
Q

QT prolongation 2°anti-psychotic drug options ?

A

Magnesium

36
Q

Classes of diuretics

A

Carbonic anhydrase inhibitors § Osmotic Diuretics § Loop Diuretics § Thiazides § Potassium sparing diuretics § Aldosterone antagonists § ADH Antagonists

37
Q

Carbonic anhydrase inhibitors give examples

A

Acetazolamide

Dorzolamide

38
Q

Carbonic anhydrase inhibitors mechanism of action ?

Side effect ?

A

Sodium bicarbonate diuresis
Excretion of Na ,K & PO3

Metabolic acidosis , hypokalemia

39
Q

Osmotic diuretics

Give examples

A

Mannitol

40
Q

Osmotic diuretics

Mechanism of action

A

Filtered at glomeuruls increase osmotic gradient throughout nephron , excessive water loss
Hypernatremia ( dilution )

41
Q

Loop agents give examples

Site of action ?

A

Furosemide
Bumetanide

Thick ascending limb of loop of Henle

42
Q

Loop diuretics mechanism of action ?

Side effect ?

A

Inhibit Na/Cl reabsorption
Concurrent Ca/Mg exception
Hypokalemia

43
Q

Thiazides diuretics

Mechanism of action ?

A

Inhibits Na/Cl reabsorption
Promotes Ca reabsorption ( hypercalcemia )
Hypokalemia
Hyperurecemia

44
Q

Thiazides side effects ?

A

Hypercalcemia
Hypokalemia
Hyperuricaemia

45
Q

Aldosterone antagonist

Give examples

A

Spironalctone ( canrenone )/ Eplerenone

46
Q

What is the mechanism of action of aldosterone antagonist

Side effect ?

A

Inhibit Na retention ( Na K ATPase / Na flux )
Blunt K & H secretion
Androgenic cross-reactivity

Hyperkalemia

47
Q

ADH antagonist

Give examples

A

Lithium / demeclocyclin

48
Q

ADH antagonist mechanism of action

A

Reducing concentrating ability of urine in collecting duct

49
Q

Other drugs with Diuretic activity give examples

A

Digoxin

Amiloride

50
Q

Digoxin mechanism of action as a diuretic ?

A

Inhibits tubular Na/K-ATPase

51
Q

Amiloride mechanism of action as diuretics ?

A

Inhibits Na channels in DCT / CD

• K+ sparing

52
Q 
Diuretics: Common Specific ADRs
Thiazides 
Spironalctone
Furosemide
Bumetanide
A

Thiazide s
• Gout
• Erectile dysfunction

Spironalctone
Hyperkalaemia
Painful gynecomastia

Furosemide
Ototoxicity

Bumetanide
Myalgia

53
Q

ACE Inhibitors / K + - Sparing Diuretics

A

Increased hyperkalaemia Þ cardiac problems

54
Q

Aminoglycosides / Loop Diuretics

A

Ototoxicity and nephrotoxicity

55
Q

Digoxin / Thiazide & Loop D.

A

Hypokalaemia Þ increased digoxin binding & toxicity

56
Q

β- Blockers / Thiazide Diuretics

A

Hyperglycemia, hyperlipidemia, hyperuricaemia.

57
Q

Steroids / Thiazide & Loop D.

A

Increased risk of hypokalaemia

58
Q

Carbamazepine / Thiazide Diuretics

A

Increased risk of hyponatraemia

59
Q

Major Indications

Specifically relating to diuretic use

A

HTN
HF

Decompensated Liver Disease

60
Q

K sparing diuretics

Give examples

A

Amiloride

61
Q

Decompensated Liver Disease

Drug options ?

A

Spironolactone § Loop diuretics

62
Q

Potentially Nephrotoxic Drugs

A

ACE Inhibitors § Aminoglycosides: e.g: gentamicin § Penicillins § Cyclosporin A § Metformin § NSAIDs § ++ more Double Whammy if renal function is impaired

63
Q

Management of Hyperkalaemia

A

Identify cause! § ECG § Treatment:

  • Calcium gluconate
  • Insulin / Dextrose
  • Calcium resonium
  • Sodium bicarbonate
  • Salbutamol

S6 (20 decks)

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