Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Class one divisions give examples

A

Na + Channel Blockers

Ia Quinidine

Ib Lidocaine

Ic Flecainide Propafenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Class Ia give examples

A

Quinidine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class Ib give examples

A

Lidocaine

Mexiletine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Class Ic give examples

A

Flecainide propafenone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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 🤷‍♀️)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Non-selective Beta Blockers give examples

A

Propranolol

Sotalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

b1

selective blockers
Long acting
Short acting

A

Longer Acting Atenolol Bisoprolol

Shorter Acting Metoprolol Nebivolol Esmolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Mixed

b1 a1 blockers

A

Carvedilol

Labetalol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Class III give examples

A

amiodarone & sotalol , dofitlide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Drug Interactions with amiodarone

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Other Antiarrhythmic Drugs

A

— Adenosine —
Digoxin —
Magnesium

—

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Adenosine mechanism of action
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
26
Digoxin | Mechanism of action
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
Phamacokinetics of digoxin
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
Drug Interactions with digoxin Pharmacokinetic Pharmacodynamic
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
Adverse Effects of digoxin | & Signs & symptoms?
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
Clinical Use of digoxin
Main use is rate control in atrial fibrillation * Heart failure * No mortality benefit
31
Magnesium
* iv Mg 2+ used to treat Torsades de Pointes * Also digoxin toxicity * Mechanism of action unknown * No benefit to chronic administration
32
Spontaneous AF | What drugs best to use
Drug options: Flecainide Propafenone Amiodarone
33
Spontaneous SVT | Drug options ?
Drug options: Adenosine Flecainide Betablocker Calcium Channel Blocker Amiodarone
34
Ischemia – Myocardial Infarction | Drug options
Lidocaine | Amiodarone
35
QT prolongation 2°anti-psychotic drug options ?
Magnesium
36
Classes of diuretics
Carbonic anhydrase inhibitors § Osmotic Diuretics § Loop Diuretics § Thiazides § Potassium sparing diuretics § Aldosterone antagonists § ADH Antagonists
37
Carbonic anhydrase inhibitors give examples
Acetazolamide | Dorzolamide
38
Carbonic anhydrase inhibitors mechanism of action ? | Side effect ?
Sodium bicarbonate diuresis Excretion of Na ,K & PO3 Metabolic acidosis , hypokalemia
39
Osmotic diuretics | Give examples
Mannitol
40
Osmotic diuretics | Mechanism of action
Filtered at glomeuruls increase osmotic gradient throughout nephron , excessive water loss Hypernatremia ( dilution )
41
Loop agents give examples | Site of action ?
Furosemide Bumetanide Thick ascending limb of loop of Henle
42
Loop diuretics mechanism of action ? | Side effect ?
Inhibit Na/Cl reabsorption Concurrent Ca/Mg exception Hypokalemia
43
Thiazides diuretics | Mechanism of action ?
Inhibits Na/Cl reabsorption Promotes Ca reabsorption ( hypercalcemia ) Hypokalemia Hyperurecemia
44
Thiazides side effects ?
Hypercalcemia Hypokalemia Hyperuricaemia
45
Aldosterone antagonist | Give examples
Spironalctone ( canrenone )/ Eplerenone
46
What is the mechanism of action of aldosterone antagonist | Side effect ?
Inhibit Na retention ( Na K ATPase / Na flux ) Blunt K & H secretion Androgenic cross-reactivity Hyperkalemia
47
ADH antagonist | Give examples
Lithium / demeclocyclin
48
ADH antagonist mechanism of action
Reducing concentrating ability of urine in collecting duct
49
Other drugs with Diuretic activity give examples
Digoxin | Amiloride
50
Digoxin mechanism of action as a diuretic ?
Inhibits tubular Na/K-ATPase
51
Amiloride mechanism of action as diuretics ?
Inhibits Na channels in DCT / CD • K+ sparing
52
``` Diuretics: Common Specific ADRs Thiazides Spironalctone Furosemide Bumetanide ```
Thiazide s • Gout • Erectile dysfunction Spironalctone Hyperkalaemia Painful gynecomastia Furosemide Ototoxicity Bumetanide Myalgia
53
ACE Inhibitors / K + - Sparing Diuretics
Increased hyperkalaemia Þ cardiac problems
54
Aminoglycosides / Loop Diuretics
Ototoxicity and nephrotoxicity
55
Digoxin / Thiazide & Loop D.
Hypokalaemia Þ increased digoxin binding & toxicity
56
β- Blockers / Thiazide Diuretics
Hyperglycemia, hyperlipidemia, hyperuricaemia.
57
Steroids / Thiazide & Loop D.
Increased risk of hypokalaemia
58
Carbamazepine / Thiazide Diuretics
Increased risk of hyponatraemia
59
Major Indications Specifically relating to diuretic use
HTN HF Decompensated Liver Disease
60
K sparing diuretics | Give examples
Amiloride
61
Decompensated Liver Disease | Drug options ?
Spironolactone § Loop diuretics
62
Potentially Nephrotoxic Drugs
ACE Inhibitors § Aminoglycosides: e.g: gentamicin § Penicillins § Cyclosporin A § Metformin § NSAIDs § ++ more Double Whammy if renal function is impaired
63
Management of Hyperkalaemia
Identify cause! § ECG § Treatment: * Calcium gluconate * Insulin / Dextrose * Calcium resonium * Sodium bicarbonate * Salbutamol

S6 (20 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions