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Acem Primary > ACEM Pharmacology > Flashcards

ACEM Pharmacology Flashcards

1
Q

Mechanism of action of atropine

A

a competitive reversible muscuranic ACh receptor agonist
Anticholinergic activity
equally powerful at M1 M2 M3 receptors
minimal effect of nicotinic receptors

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2
Q

Pharmacokinetics of atropine

A

Administration: IV oral topical nebulized/inhaled
Distribution: wide Vd including into CNS
Metabolism and excretion: Half life is 2 hours, 60% is excreted unchanged via kidneys. 40% undergoes phase I and phase II metabolism and then renally excreted

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3
Q

Organ effects of atropine

A

Eye - mydriasis and cycloplegia
CNS delerium decreased tremor in parkinsons
CVS tachycardia
Resp bronchodilation and decreased secretions
GIT decreased saliva decreased gastric acid secretion decreased mucin production delayed gastric emptying decreased gut motility
Urinary relaxes ureteric and bladder wall smooth muscle urine retention
Skin decreased sweating

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4
Q

Clinical use of atropine

A

Treatment of symptomatic bradycardia or bradyarrhythmias
in opthalmology for mydriasis (dilate pupils)
occasionally used in RSI in paediatrics
drying of secretions in palliative patients
travellers diarrhoea

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5
Q

Atropine toxicity effects

A

Agitation, delirium
raised temperature
blurred vision, mydriasis
flushed skin
dry mouth
tachycardia
(mad as a hatter, blind as bat, red as a beet, dry as a bone)

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6
Q

What is the mechanism of action of indirectly acting cholinomimetics

A

(acetylcholinesterase inhibitors)
inhibit acetylcholinesterase enzyme
increasing concentration of Ach in the vicinity of cholinoreceptors
action on both nicotinic and musarinic receptors

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7
Q

what type of indirectly acting cholinomimetics (acetylcholinesterase inhibitors) are there ?

A

Reversible - neostigmine, physostigmine, pyridostigmine
Irreversible - organophosphates and insecticides

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8
Q

Cardiovascular effects of Indirectly acting cholinomimetics (acetylcholinesterase inhibitors)

A

Both sympathetic and parasympathetic ganglia can be activated
Parasympathetic effects generally predominate -
bradycardia, decreased CO, decreased contractility
OVerdose may cause tachycardia and hypotension

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9
Q

Pharmacokinetics of Adrenaline?

A

Administration; IV, IM, subcut, nebulised. Poor oral absorption
Distribution: Crosses the placenta, does not cross blood brain barrier. 50% protein bound. Onset within seconds, duration 2 mins
Metabolism: terminated by metabolism in sympathetic nerve terminals by COMT and MAO. Circulating adrenaline metabolised by COMT
Elimination: metabolites excreted in urine

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10
Q

Pharmacodynamics of adrenaline?

A

Equal effects on alpha and beta receptors
Alpha - vasoconstriction
Beta1 - positive inotropic and chronotropic effects
Beta2 - smooth muscle relaxation in airways and skeletal muscle

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11
Q

Effects of adrenaline on other organs?

A

Respiratory - bronchodilation
Eyes - pupil dilation, decreased IOP and production of aqueous humour
Gastric smooth muscle - relaxation
Genitourinary - bladder smooth muscle relaxation
Liver - enhanced glycolysis
Increased production of sweat at apocrine glands

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12
Q

What receptors does noradrenaline act on ?

A

Predominantly alpha 1 - vascular smooth muscle constriction
some alpha 2 beta 1 and beta 2

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13
Q

How does noradenaline increase blood pressure?

A

Increase in both systolic and diastolic blood pressure
Alpha 1 activity - vasoconstriciton, increased peripheral resistance = increased diastolic pressure
Beta 1 activity - increased myocardial contractility = increased systolic BP

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14
Q

What effect does noradrenaline have on heart rate ?

A

Minimal change
Beta 1 increases heart rate
however,
compensatory baroreceptor reflex causes decrease in HR

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15
Q

Mechanism of action metaraminol ?

A

Direct alpha 1 agonist - vascular smooth muscle constriction

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16
Q

Classes of local anaesthetics

A

Aminoamides - Lignocaine, Bupivocaine, prilocaine
Aminoesters - procaine, benzocaine, tetracaine

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17
Q

Mechanism of action of lignocaine

A

Sodium channel blocker
Class 1B antiarrhytmic
Local anaesthetic
Blocks voltage gated sodium channels without altering the resting membrane potential

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18
Q

Toxic effects of Lignocaine

A

CNS; perioral or tongue numbness, metallic taste > nystagmus, tinnitus, muscle twitching, nausea, vomiting > seizures, sedation
CVS; arrhythmias, hypotension, worsening CCF
GIT; vomiting anorexia nausea
Haem; methaemoglobinaemia (increase in MetHb, become blue), most often with prilocaine

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19
Q

Mechanism of action of nitrous

A

Modulates GABA-A recetpors
Increased dynorphin release
NMDA agonist
low solubilty in the blood so reaches arterial tension rapidly, rapid equilibrium in the brain, fast onset and fast recovery

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20
Q

Organ effects of nitrous

A

CNS; analgesia amnesia increased cerebral blood flow
Renal; decrease GFR increased renal vascular resistance
CVS; dose dependent mycardial depression
Resp; reduced response to CO2 and hypoxia
GI; nausea, vomiting

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21
Q

Pharmacokinetics of propofol

A

Administration; IV only
Distribution; rapid onset and recover is driven by redistribution of the drug from the brain to other areas. Half life 2-4 minutes, elimination half life up to 25 mins
Metabolism; rapidly metabolised in the liver
Elimination; Excreted in the urine as inactive metabolites

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22
Q

Usual induction dose of propofol

A

1-2.5mg/kg in adults
2.5-3.5mg/kg in paediatrics

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23
Q

Clinical effects of propofol

A

Anaesthesia/sedation
no analgesia
Transient apnoea
Decreased BP
anti-emetic properties

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24
Q

Adverse effects of Propofol

A

Hypotension
Apnoea
pain on injection
allergy/anaphylaxis
propofol infusion syndrome (a metabolic acidosis)

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25
Q

Pharmacodynamics of Ketamine

A

NMDA receptor antagonist
Inhibits reuptake of serotonin and catecholamines
Potent short acting sedative

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26
Q

Pharmacokinetics of Ketamine

A

Absorption; Highly lipid soluble so rapid onset
Distribution; Effect is terminated by redistribution to inactive tissue sites. Low protein binding
Metabolism; Metabolised in the liver via the P450 enzymes to inactive metabolites
Elimination; metabolites are excreted in the urine

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27
Q

System effects of Ketamine

A

CNS; dissociative anaesthesia, profound analgesia, Cerebral vasodilation. Potential anticonvulsant properties
CVS; haemodynamically stable, increase HR, BP, CO and myocardial oxygen consumption
Respiratory; Maintains airway reflexes, minimal respiratory depression, bronchodilator effects. Can cause lacrimation and laryngospasm in children
Ocular; nystagmus

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28
Q

Adverse effects of ketamine

A

CNS - emergence phenomenon, dysphoria, hallucinations
GI - nausea, vomiting
Respiratory - latyngospasm, increased salivation

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29
Q

Pharmacokinetics of Thiopentone

A

Administration; IV bolus
Rapidly crosses BBB, highly lipid soluble, redistributes to muscle and fat
metabolised in the liver
excreted by the kidney

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30
Q

Advantages of Thiopentone

A

rapid onset
amnesic
reduction in ICP
anitconvulsant

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31
Q

Adverse effects of thiopentone

A

hypotension
reduced stroke volume and cardiac output
apnoea

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32
Q

Mechanism of Action of Suxamethonium

A

Deploarizing neuromuscular blocker
2 acetylcholine molecules linked end to end
2 phases;
1. depolarising
- reacts with nicotinic receptor to open channel
- depolarises the motor endplate which spread to adjacent membranes
- causes fasiculations
2. desensitising
- continued repeat exposure to sux
end plate depolarisation increases
membrane repolarizes but cannot depolarise
unresponsive to subsequent impulses
causes a flaccid paralysis

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33
Q

Pharmacokinetics of suxamethonium

A

Administration; IV
Distribution; rapid onset 30-60 seconds, short duration 2-8 minutes
Metabolism - Hydrolysed rapidly by plasma pseudocholinesterase

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34
Q

Adverse effects of suxamethonium

A

Muscle pain and fasiculations
Bradycardia
release of potassium - especially in burns and trauma
raised IOP and raised ICP
risk of malignant hyperthermia
risk of prolonged paralysis in cases of reduced or abnormal cholinesterase

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35
Q

Mechanism of action of Rocuronium

A

A non deploarizing neuromuscular blocker
a competitive inhibitor of acetylcholine at the nicotinic receptors
In large doses it can enter the pore of the ion channel and cause a stronger block

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36
Q

Pharmacokinetics of Rocuronium

A

Administered; IV bolus 1.2mg/kg onset 40/60 seconds
Distribution ; Rapid, highly ionized, small Vd. Duration of 20-75 minutes
metabolised in the liver, short half life
Eliminated the urine

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37
Q

How does suxemethonium differ from rocuronium?

A

Duration of suxamethonium is shorter - 5-10 mins
Suzamethonium is depolarising NMB
Rocuronium is non depolarising
Suxamethonium metabolised in the plasma
Rocuronium in the liver

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38
Q

Pharmacodynamics of ethanol

A

CNS; sedation, disinhibition, impaired judgement, impaired motor skills, ataxia, slurred speech, coma, respiratory depression
CVS; decreased contractility
Smooth muscle vasodilation = hypothermia

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39
Q

Pharmacokinetics of ethanol

A

Absorption; rapidly absorbed from the GIT (water soluble)
Distribution; Rapid, Vd is total body water
Metabolism; mostly in the liver by alcohol dehydrogenase via zero order kinetics
Excretion; lung and urine

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40
Q

What is zero order kinetics

A

Elimination occurs at a constant rate independent of drug concentration

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41
Q

What drugs have zero order kinetics

A

phenytoin, theophylline, warfarin, salicylate, heparin, ethanol

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42
Q

Mechanism of action of benzodiazepines

A

Binds to components of the GABA-A receptor in neuronal membranes in the CNS
This receptor is a chloride channel
Enhance GABAs effects without directly activating the channel
causes an increased frequency of channel opening

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43
Q

Organ effects of Diazepam

A

Sedation - calming effect, anxiolysis
Hypnosis and anaesthesia at higher doses
anticonvulsant effect
muscle relaxation
respiratory and cardiovascular depression

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44
Q

Mechanism of action of carbamazepine

A

Sodium channel blockers
Binds to those in an inactive state and stabilises them there
Inhibits high frequency repetitive firing neurones

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45
Q

Pharmacokinetics of carbamazepine

A

100% oral bioavailability
Peak level 6-8 hours
70% protein bound
low clearance, 36 hours half life
induces its own metabolism via _450 system effect so dose increase required in the first few weeks of treatment

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46
Q

Adverse effects of of carbamazepine?

A

ataxia
diplopia
sedation
blood dyscrasias - aplastic anaemia, agranulocytosis
skin rash
drug interactions with p450 metabolised drugs

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47
Q

Pharmacokinetics of phenytoin

A

Administration; Oral, IV
high oral bioavailabiliity
Peak serum concentration 3-12 hours
Highly plasma protein bound with moderate volume of distribution
Metabolised in the liver to an inactive metabolites and then renal excretion
Elimination is dose dependent
lower dose is first order kinetics but at higher doses enzymes become saturated and shifts to zero order kinetics
Half life is variable

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48
Q

What is the mechanism of action of Phenytoin

A

Sodium channel blockade
Prolongation of the inactive state of the Na channel
enhances GABA release
Work to inhibit the generation of rapidly repetitive action potentials

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49
Q

Why use a loading dose of phenytoin

A

Need 4 half lives to reach a steady state, so to reach target concentration rapidly

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50
Q

Risks of IV phenytoin

A

Hypotension and bradycardia with rapid infusion
local necrosis if there is extravasation
Purple glove syndrome - black discolouration distal to the IV site

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51
Q

Adverse effects of phenytoin

A

Nystagmus and loss of smooth pursuits is normal with therapeutic levels and not concerning
Anyone with ataxia and diplopia need a decrease in their dose
Ginigival hyperplasia and hirsutism can occue over long term use
Osteolmalacia, abnormal rashes, low vitamin D
Foetal abnormalities
Sedation, coma, cerebellar toxicity

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52
Q

Mechanism of action of levetiracetam

A

Binds the SV2 synaptic vessel protein
Undergoes endocytosis and binds in the vesicle
Prevents release of glutamine during increased frequency activity

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53
Q

Pharmacokinetics of levetiracetam

A

Given orally or IV , rapid oral absorption just over 1 hour
Low protein binding
Half life 6-8 hours so BD dosing
2/3 excreted in urine
1/3 deaminated in the blood
No liver metabolism = mineral interactions compared to other antiepileptics

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54
Q

Side effects of levetiracetam

A

Mild; drowsiness, ataxia, dizziness
severe; behavioural or mood changes - aggression/anxiety

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55
Q

What is the dose of levetiracetam in status epilepticus

A

Paeds 40mg/kg IV/IO up to 3g
Adults 60mg/kg IV/IO up to 4.5g

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56
Q

Mechanism of action of sodium valproate

A

Unknown

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57
Q

What are the adverse effects of Sodium Valproate

A

Mild; nausea, vomiting, abdominal pain
Severe; Cerebral oedema and coma
Hepatic toxicity including acute liver failure
Thrombocytopaenia and bruising from bone marrow depression
Neural tube defects if used in pregnancy
Hyperammonaemia leading to sedation
Inhibits metabolism of p450 enzyme system
Directly displaces phenytoin from plasma proteins
Increases level of carbomazapine
Decreases the clearance of lamotrigine

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58
Q

Mechanism by which serotonin syndrome occurs

A

Excessive stimulation of serotonin receptors in the CNS due to overdose of a single drug or concurrent use of several drugs
Predictable rather than idiosyncratic

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59
Q

How do drugs cause excessive stimulation of serotonin receptors

A

Inhibition of serotonin metabolism - amphetamines
Prevention of serotonin reuptake in nerve terminals - fluoxetine, sertraline, venlafaxine, tramadol, TCAs
serotonin release or increased intake of serotonin precursors - tryrophan, lithium

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60
Q

Mechanism of action of tricyclic antidepressants?

A

Inhibition of serotonin and noradrenaline reuptake
Increases the amount of serotonin and noradrenaline in certain parts of the brain and spinal cord
Also block sodium channels, potassium channels, M1 receptors, Histamine 1 receptors, post synaptic alpha 1 adrenergic receptors

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61
Q

Pharmacokinetics of tricyclics antidepressants

A

Well absorbed orally
Bioavailability 40-50%
long half life
high first pass metabolism
high protein binding
high lipid solubility
large volume distribution
metabolism in the liver with active metabolites

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62
Q

Effects of overdose in TCAs

A

Cardiac; tachycardia, hypotension, prolonged PR, wide QRS, long QT, VT , VF
CNS; Drowsiness, delerium, seziures, coma
Anticholinergic effects; agitation, mydriasis, warm dry flushed skin, urinary retention, ileus

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63
Q

Pharmacokinetics of lithium

A

Administration; orally, rapid and near complete absorption, peak concentration at 1-2 hours but complete 6-8 hours
Volume distribution is in total body water - very slow distribution from extra to intracellular compartments
No protein binding
No metabolism
Excreted unchanged in urine 20% of the creatinine clearance
Plasma half life is 20 hours

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64
Q

Some drug interactions with lithium

A

Thiazide diuretics - cause reduction in lithium clearance
Newer NSAIDS reduce clearance
Osmotic or loop diuretics actually increase clearance

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65
Q

Why is levodopa used in combination of carbidopa

A

Carbidopa is a peripheral dopa carboxylase inhibitor.
It doesn’t cross the BBB, reduces the peripheral metabolism of levodopa which leads to increased half life and more dopa being available to enter the CNS to exert its effects

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66
Q

What are the adverse effects of levodopa ?

A

GIT; anorexia, nausea, vomiting is common due to stimulation of emetic centre in the brain
CVS; arrhythmias
Dyskinesis
Behavioural changes
Gout, abnormal LFTs

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67
Q

How do sumatriptans work in treatment in migraines?

A

Triptans are selective agonists for 5HT-1 receptors found on these vessels
Cause vasoconstriction, preventing symptoms

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68
Q

Pharmacokinetics of Triptans?

A

Bioavailability is a low/varied 10-70%
So given subcut or intranasal more often than orally
Half life is 2-3 hours

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69
Q

Pros and cons to sumatriptan use?

A

Pros; only usually mild side effects, tingling weakness
Cons; contraindicated in patients with IHD, expensive

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70
Q

Pharmacodynamics of adenosine

A

Slow conduction through the Av node
Blocks specific adenosine receptors
Mechanism is increased K+ conductance and decreased cAMP induced calcium influx
ECG = increased PR interval

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71
Q

Pharmacokinetics of adenosine

A

Administration: IV with rapid absorption
Distribution to most cells
Metabolism : rapidly degraded by cells, deaminated and phosphorylated
Half life is 10 seconds

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72
Q

Indication of Adenosine

A

SVT
Diagnostic tachyarrhythmias
Adjunct to thallium scanning

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73
Q

Pharmacodynamics of adrenaline

A

Binds to alpha and beta receptors
Act through G proteins
Beta stimulates cAMP
Alpha leads to inhibition cAMP
- relaxes smooth muscle of bronchi
- cardiac stimulation
- skeletal muscular vascular dilation

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74
Q

Structure/class amiloride

A

Potassium sparing diuretic
Not an aldosterone antagonist

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75
Q

Pharmacodynamics of amiloride

A

Reduces Na+ absorption in collecting tubules and ducts and inhibits tubular secretion of K+

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76
Q

Pharmacokinetics of amiloride

A

Administration: orally 5-20mg daily dose
Absorption: excreted unchanged by kidneys
Peak plasma levels in 3-4 hours
Half life 6-9 hours

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77
Q

Indication of amiloride

A

Used to spare potassium when other diuretics are the main agents
Congestive heart failure and HTN
Hepatic cirrhosis with ascites

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78
Q

Indication of aminophylline

A

Bronchospasm

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79
Q

Pharmacodynamics of aminophylline

A

Bronchodilator in reversible airways obstruction
Also causes diuresis, cns and cardiac stimulation and gastric acid secretion by blocking phosphodiesterase.
Increases tissue concentrations of cAMP which promotes catecholamines stimulation of lipolysis, glycogenolysis and gluconeogenesis
Induces release of adrenaline from adrenal medulla

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80
Q

Pharmacokinetics of aminophylline

A

Administration: injection, tablet, suppository
Can be 100% orally absorbed
Loading dose needed
Metabolised in the liver by demethylation and oxidation
Half life variable
10% excreted unchanged in urine

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81
Q

Mechanism of action of Promethazine

A

first generation H1 receptor antagonist
Competitively blocks histamine at the H1 receptor

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82
Q

Pharmacokinetics of Promethazine

A

Absorption; well absorbed orally but has significant first pass effect - bioavailabilty 25%
Distribution; widely distributed throughout the body, enters CNS
Metabolised in the liver, excreted in the urine

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83
Q

Organ effects of Promethazine

A

CNS - sedation, anxiolytic, reduces motion sickness
Respiratory - bronchodilation, reduction in secretions, suppress cough

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84
Q

Toxicity of Promethazine

A

Anticholinergic side effects
Extrapyramidal reactions in high doses
sedation confusion

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85
Q

Example of 2nd generation H1 antagonists

A

Loratadine, cetirizine

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86
Q

Mechanism of action of Cimetidine

A

A second generation H2 receptor antagonist
Competitively inhibits histamine at H2 receptors on parietal cells in the stomach, decrease gastric secretion

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87
Q

Pharmacokinetics of Cimetidine

A

Absorption; Rapid absorption but significant first pass effect, oral bioavailability approximately 50%
Distribution; 20% protein bound
metabolism; liver cytochrome p450
excretion 40-55% unchanged by kidneys

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88
Q

Clinical use of Cimetidine

A

Peptic ulcer disease
GORD
Reflux oesophagitis
Zollinger-Ellison syndrome
Non-ulcer dyspepsia

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89
Q

mechanism of action of sumatriptan

A

selective 5-HT1B and 5-HT1D receptor agonist
Vasoconstriction in cerebral and meningeal vessels

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90
Q

Pharmacokinetics of Sumatriptan

A

Absorption; oral, nasal spray, SC, low oral bioavailability
Distribution; 15-20% protein bound , large volume distribution, crosses BBB
Metabolism; by MAO locally and in the liver
Excretion 60% urine 40% faeces
half life 2 hours

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91
Q

Mechanism of action of ondansetron

A

a 5-HT receptor antagonist
used as an antiemetic

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92
Q

Pharmacokinetics of ondansetron

A

Absorption; rapidly oral absorption, oral bioavailability 60%
Distribution; 76% protein bound
Metabolism; Extensive hepatic metabolism
Excretion; renal and hepatic excretion, serum hlaf life 4-9hours

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93
Q

Adverse effect of ondansetron

A

prolongation of QT interval

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94
Q

Mechanism of action of Ergotamine

A

Agonist, partial agonist and antagonist effects of alpha adrenoreceptors and serotonin (5-HT1A and 5-HT1D) receptors

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95
Q

Pharmacokinetics of ergotamine

A

Absorption; Variable oral dose is about 10 mins larger than IM dose, can be PR, buccal cavity, inhaled
speed of absorption and peak blood levels can be increased by administration with caffeine
Distribution; crosses BBB
extensive metabolism

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96
Q

Clinical application of ergotamine

A

migraine
hyperprolactinaemia
postpartum haemorrhage

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97
Q

Toxic effects of Nifedipine

A

hypotension, tachycardia
peripheral oedema, constipation, flushing, dizziness, nausea, headache

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98
Q

mechanism of action of nifedipine

A

a calcium channel blocker
a dihydropyridine
predominantly vasodilating effects

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99
Q

pharmacokinetics of nifedipine

A

complete oral absorption, bioavailability 50%
highly protein bound
metabolised by the liver
excreted in the urine

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100
Q

clinical use of nifedipine

A

angina
htn
raynauds
coronary artery spasm
preterm labour

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101
Q

mechanism of action of captopril

A

ACEi
binds to ACE with 30000x affinity of ATI preventing formation of ATII

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102
Q

pharmacokinetics of captopril

A

rapid absorption, bioavailability 65%
35% protein bound
renally excreted

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103
Q

toxic effects of captopril

A

hypotension
hyperkalaemia
angioedema
dry cough (bradykinens)
precipitates renal failure

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104
Q

what are the 4 classes of antiarrhythmics

A

Class 1; Sodium channel blockers

Class 2; Sympatholytics, reduce beta adrenergic activity

Class 3; AP duration prolongers, blocking K channels

Class 4; Ca channel blockers

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105
Q

What is the mechanism of action of Amiodarone

A

Class 3 antiarrhythmic
properties of class 1, 2 and 4
Blocks K channels, marked prolongation of AP duration
blockade of inactivated Na channels
weak B blocker
weak ca channel blocker

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106
Q

Pharmacokinetics of amiodarone

A

Administered; orally, IV
98% protein bound, accumulates in many tissues
long half life, large Vd
excreted in bile and faeces
half life has 2 phases, rapid component has half life of 3-10 days, remainder eliminated over weeks.

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107
Q

Amiodarone interactions

A

A substrate for CYP3A4
- conc decreased by inhibitors eg Cimetidine
- conc increased by inducers eg Rifampicin

Inhibits warfarin metabolism

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108
Q

examples of Beta blockers with Intrinsic Sympathomimetic activity/partial agonist activity

A

Cartelol, Acebutolol, Pindolol, Pnebutolol, Labetolol

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109
Q

When are Beta Blockers with ISA used?

A

when non-ISA beta blockers are contraindicated, eg sinus bradycardia, sick sinus syndrome, raynauds , COPD

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110
Q

what is the half life of sotolol

A

12 hours

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111
Q

nitroglycerine relieves exertional angina by ?

A

reduced oxygen consumption

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112
Q

is substance P a vasodilator or vasoconstrictor?

A

potent vasodilator
dependent on NO release

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113
Q

what is the elimination half life of sotalol

A

12 hours

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114
Q

Pharmacokinetics of Sotalol

A

well absorbed orally
bioavailability 100%
not metabolised in the liver
not bound to plasma proteins
excretion via kidneys unchanged
half life 12 hours

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115
Q

mechanism of action of labetaolol

A

mixed alpha/beta adrenergic antagonist

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116
Q

mechanism of action of esmolol

A

selective beta1 antagonist

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117
Q

what is streptokinase

A

non fibrin selective fibrinolytic

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118
Q

streptokinase reduces mortality from MI by what %

A

25%

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119
Q

what is Vigabactrins anticonvulsant property due to?

A

Irreversible inhibition of GABA aminotransferase

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120
Q

mechanism of action of propafenone

A

class 1C antiarrhythmic
weak beta blocking and calcium channel blocking activity

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121
Q

mechanism of action labetalol

A

mixed alpha/beta adrenergic antagonist used to treat high blood pressure

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122
Q

Organ effects of GTN;
CVS, Respiratory, GIT, GU, Haematological

A

Vasodilation (veins first), increase venous capacity, decrease preload, decrease pulmonary pressure, decrease heart size , reflexive tachycardia
widespread smooth muscle relaxation in resp, GI, GU
Decrease Platelet aggregation

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123
Q

Mechanism of action of GTN

A

stimulates NO release, increases cGMP, dephosphorylation of myosin LC and causes smooth muscle relaxation

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124
Q

Pharmacokinetics of GTN

A

sublingual
rapidly absorbed, high first pass metabolism
oral availability <10%
60% protein bound
duration of action 10-20 minutes
metabolised in liver by organic nitrate reductase
excreted renally

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125
Q

Name the 2 Calcium channel blockers in the non-dihydropiridine group

A

Diltiazem
Verapamil

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126
Q

Mechanism of action of the non-dihydropyridine calcium channel blockers

A

L type alpha 1 subunit calcium channel in cardiac and smooth muscle
reduces frequency of calcium channel opening, decreasing calcium channel influx, decrease transmembrane calcium current

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127
Q

dihydropyridine calcium channel blocker effects on smooth muscle

A

relaxation, arterioles > veins

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128
Q

non-dihydropyridine calcium channel blocker effects on cardiac muscle

A

decreases contractility

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129
Q

non- dihydropyridine calcium channel blocker effects on SA node

A

sodium channel blockade, decrease pacemaker potential rate
verapamil has most effect

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130
Q

non - dihydropyridine calcium channel blocker effects on AV node

A

decrease conduction velocity
verapamil has most effect

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131
Q

what type of beta blocker is sotalol

A

beta 1 and beta 2 adrenergic receptor blocker

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132
Q

pharmacokinetics of sotalol

A

well absorbed orally
bioavailability 100%
not metabolised in the liver, not bound to protein
excretion via kidneys unchanged
half life 12 hours

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133
Q

what type of antiarrhythmic is sotalol

A

class II and class III

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134
Q

where is noradrenaline released

A

postganglionic sympathetic fibers

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135
Q

how does methyldopa reduce blood pressure

A

reduces peripheral vascular resistance, central alpha-receptor agonist
centrally acting sympathoplegic agent
an analogue of L-dopa

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136
Q

Pharmacokinetics of methyldopa

A

Absorption; variable absorption of oral dose, extensive first pass effect, bioavailability 25%
Distribution; 50% protein bound
Metabolism; Conjugated to sulphate in intestinal mucosa, metabolised in liver
Excretion 20-40% urine, 2/3 unchanged
half life 2 hours

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137
Q

Clinical application of methyldopa

A

HTN during pregnancy
pre-eclampsia

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138
Q

mechanism of action of Clonidine

A

A centrally acting sympathoplegic agent
Causes direct stimulation of alpha-adrenorecptors both centrally and peripherally
when reaches the medulla decreases SNS and increases PNS

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139
Q

Pharmacokinetics of Clonidine

A

Absorption; rapid oral absorption bioavailability 95%
Lipophilic and readily crosses BBB
65% excreted unchanged in urine, 20% faeces
half life 8-12 hours

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140
Q

Clinical applications of Sodium Nitroprusside

A

Hypertensive emergencies
Severe heart failure
Aortic Dissection
Intraoperative production of hypotension

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141
Q

Mechanism of action of Sodium Nitroprusside

A

a powerful vasodilator
releases NO and increases cGMP
a complexe of iron, cyanide groups and nitroso moiety

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142
Q

Pharmacokinetics of sodium nitroprusside

A

IV administration, onset of action within 1-2 minuts
confined to plasma
Metabolised; uptake into RBCs, excreted renally

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143
Q

Organ effects of sodium nitroprusside

A

CVS; vasodilation of arteries and veins, reflex tachycardia so no change in CO
Respiratory; decrease hypoxic vasoconstriction
CNS; cerebral vasodilation, raised ICP

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144
Q

precautions of sodium nitroprusside

A

Toxicity related to cyanide accumulation
Thiocyanate can accumulate
methaemoglobinaemia

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145
Q

Mechanism of action of Hydralazine

A

Vasodilator that acts on arterioles
A donor of NO that increases cGMP and decreases IP3 which leads to decreased calcium availability

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146
Q

Pharmacokinetics of Hydralazine

A

well absorbed, high first pass extraction, bioavailability 25%
half life 2-4 hours
highly protein bound crosses the placenta
metabolites excreted in urine and faeces

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147
Q

Clinical uses of Hydralazine

A

Chronic moderate to severe HTN
Pre eclampsia
congestive heart failure

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148
Q

Clinical use of Minoxidil

A

HTN

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149
Q

Mechanism of action Minoxidil

A

Orally active vasodilator
Active metabolite opens K+ channels in smooth muscle

150
Q

What does antithrombin III inhibit

A

factors IIa IXa Xa XIIA

151
Q

What does protein C and S inhibit

A

Factors Va and VIIA

152
Q

Describe Class 1 antiarrhythmics

A

Na channel blockers
1A prolong AP duration
1B shorten AP
1C Minimal AP effect, prolongs QRS

153
Q

Examples of 1A anti-arrhythmic

A

Disopyramide, Quinidine, Procainamide
prolong AP and QRS

“Double quarter pounder’

154
Q

Examples of 1B anti-arrhythmic

A

Lignocaine, Phenytoin
shortens the refractory period
shorten AP

155
Q

Examples of 1C anti-arrhythmic

A

Flecainide
increase QRS duration

156
Q

mechanism of action of digoxin

A

inhibits action of Na/K ATPase
increases intracellular Na
this alters the Na/Cl pump
causes displacement of Ca in SR
overal increases Ca which increases contractility
positive inotrope
increases ventricular excitability, contraction, ejection, cardiac output

157
Q

Pharmacokinetics of Digoxin

A

administered oral or IV
Loading dose IV
65-80% oral absorption
long half life 36-40 hours
2/3 excreted in kidney
rate is proportional to Cr clearance

158
Q

which drugs reduce digoxin clearance

A

Verapamil
Amiodarone
Quinidine

159
Q

which drugs potentiate digoxin effect

A

quinidine
NSAIDs
CCB
Furosemide

160
Q

Mechanism of action of adenosine

A

acts on a specific adenosine receptor that inhibits adenylyl cyclase and reduces cAMP
Inward K+, marked hyprpolarisation, calcium channel inhibition and suppress Ca
Delay the action potential in the SA node

161
Q

Cardiac effects of adnosine

A

Inhibits AV node
Increases Av node refractory period

162
Q

What are Class 2 anti arrhythmics

A

Sympatholytics
reduced beta adrenergic activity
eg B-blockers

163
Q

What are Class 3 antiarrhythmics

A

AP duration prolongers
block K channels
eg sotolol

164
Q

What are class 4 antiarrhythmics

A

Ca channel blockers
eg verapamil

165
Q

mechanism of action of verapamil

A

blocks active and inactive L type Ca channels
prolongs the refractory period
reduces conduction through SA and AV node
increases the refractory period
negative inotropic

166
Q

Calcium channel blockers from quickest to slowest acting

A

Nifedipine - 5-20 mins
Verapamil - 30 mins
Diltiazem - >30 mins
Felodipine - 2-5 hours

167
Q

mechanism of action of prazosin

A

competitive piperazinyl quinazoline
management of HTN
highly selective alpa 1 receptor blocker on vascular smooth muscles in arterioles and venules
reduces afterload and preload

168
Q

where do thiazide diuretics work

A

proximal part of Distal convoluted tubule

169
Q

where does spironolactone work?

A

DCT and CT

170
Q

where does furosemide work?

A

Loop of Henle

171
Q

where does acetazolamide work

172
Q

Mechanism of action of GTN

A

releases NO
NO activates guanylyl cyclase and increase in cGMP
causes vasodilation

173
Q

what is GTN tolerance to

A

decrease in sulfhydral groups

174
Q

what type of beta blocker is propanolol

A

non selective beta blocker

175
Q

what can happen in propanolol overdose

A

because of its Na channel blocking activity if can cause prolonged QRS and VF arrest
can cause seizures as it crosses the BBB
Treatment is bicarb

176
Q

why does nitroglycerine relieve angina

A

reduced oxygen consumption
decreased venous return to the heart

176
Q

regarding nitrates what do they do to collateral flow

A

increase collateral flow even in fixed constriction

177
Q

how do ACEi cause cough

A

block conversion of ANGI to ANGII
inhibit degradation of bradykinen substance P and enkephalins
inhibiting bradykinin causes cough and angiooedma

178
Q

where does mannitol work in the kidney?

A

inhibits H2O absroption in proximal tubule, loop of henle, collecting tubule

179
Q

mechanism of action of clonidine

A

stimulates CENTRAL alpha 2-adrenoceptors which inhibits sympathetic nervous system providing the anti-hypertensive effects.
Initial hypertensive effect is due to direct stimulation of alpha 1-receptors in arterioles following parenteral use

180
Q

mechanism of action of labetalol

A

competitive selective alpha 1 antagonist and a competitive non selective beta 1 (B1) and 2 (B2) antagonist

181
Q

half life of metoprolol

182
Q

which antihypertensive can cause necrotizing pancreatitis

A

thiazides
cause hypercalcaemia and hyperlipidaemia which can predispose to pancreatitis

183
Q

which cardiac drug should not be used with sildenafil

A

GTN
as both drugs cause vasodilation

184
Q

does sotalol have any anaesthetic action

185
Q

what class of antiarrhythmic is sotalol

A

class II and class III
a non selective Beta 1 and Beta 2 adrenergic blocker

186
Q

side effects of nifedipine

A

peripheral oedema and constipation

187
Q

administration of nifedipine

A

usually orally

188
Q

alpha 1 receptors display the following potency series in decreasing potency

A

Noradrenaline >adrenaline > isoprenaline

189
Q

which calcium channel blocker is predominantly excreted in faeces

A

nifedipine

190
Q

drug class and indication for Amitriptyline

A

Tricyclic antidepressant
Depression
Nocturnal enuresis
Chronic pain/migraine/trigeminal neuralgia/phobic anxiety

191
Q

Pharmacodynamics of Amitriptyline

A

Inhibits;
Sodium-dependent noradrenaline transporter
Sodium-dependent serotonin transporter
5-HT receptor
has anticholinergic effects

192
Q

Pharmacokinetics of Amitriptyline

A

Administrated; PO 75mg up to max 300mg
IM/IV 20-30mg
Absorption; orally
half life ~25 hours
95% protein bound
wide volume distribution
metabolised in the liver
excreted in urine 60% and faeces

193
Q

Toxicology of Amitriptyline

A

> 1000mg is toxic
can prolong QRS and ST
agitation, delerium, seixure, coma, arrhythmia, metabolic acidosis, bladder and bowel paralysis

194
Q

Pharmacodynamics of Amoxycillin

A

Selective inhibitors of bacterial cell wall synthesis
Binds to cell receptors on bacteria, inhibiting transpeptidation and peptidoglycon synthesis is blocked
Bectericidal agents

195
Q

Pharmacokinetics of Amoxicillin

A

Administration - PO, IV, IM
Absorption - oral bioavailability 93%
best taken one hour before or after food
half life 1-2 hours
86% excreted in the kidneys unchanged

196
Q

Indication and class of drug of Amphetamine

A

Narcolepsy, Attention deficit, obesity

197
Q

Pharmacodynamics of Amphetamine

A

Alpha and Beta effects from release of neurotransmitter from synaptic vesicles NOT direct stimulation receptors

198
Q

Pharmacodynamics of Aspirin

A

COX -1 and COX -2 inhibitor
inhibit platelet aggregation by COX-1 inhibiting thromoxane A2 for about 7-10 days

199
Q

side effects of suxamethonium

A

tachycardia
muscle fasiculations
excess salivation

200
Q

phase 1 reactions

A

hydrolysis, oxidation and reduction.

201
Q

Phase 2 reactions

A

glucuronidation, acetylation, glutathione conjugation, glycine conjugation, sulfate conjugation, methylation, and water conjugation

202
Q

calculation of volume distribution

A

mount of drug in the body/ concentration of the drug in blood or plasma

203
Q

how to calculate half life

A

T1/2 = (0.7 x Vd ) / CL
this means Vd is proportional to half life

204
Q

half life of lignocaine

A

120 minutes

205
Q

what is the bioavailablity of digoxin

206
Q

mechanism of action of naloxone

A

pure antagonist
has high affinity to mu receptors

207
Q

Define potency

A

how much of a drug that is required to produce an effect
dose required to bring about 50% of drugs maximal effect

208
Q

Define Affinity

A

how tight the drug binds to its receptors.

209
Q

Define efficacy

A

the maximum response produced by a drug regardless of dose

210
Q

Define TD50

A

the dose required to produce toxic effects in 50% of patients.

211
Q

The Beta 2 sympathomimetic with the longest duration of action is?
A. Terbutaline
B. Salmeterol
C. Isoprotenerol
D. Sotalol

A

Salmeterol >12 hours

212
Q

How does Cromolyn reduce bronchial reactivity?

A

Inhibiting mediated mast cell degranulation

213
Q

what does ASPAC stand for

A

anisoylated plasminogen streptokinase activator complex

214
Q

Half life of warfarin

215
Q

bioavailability of warfarin

217
Q

% of warfarin that is protein bound

218
Q

with regards to clotting what does streptokinase do

A

forms a complex with endogenous plasminogen;
the plasminogen in this complex undergoes a conformational change that allows it to rapidly convert free plasminogen into plasmin.

219
Q

Heparin induced mild thrombocytopenia is caused by?

A

antibodies that bind to complexes of platelet factor 4 (PF4) and heparin. This immune reaction leads to a hypercoagulable state that can cause thrombosis

220
Q

LMWH levels are not generally measured except in the setting of

A

renal insufficiency
obesity
pregnancy

221
Q

what does ticlopidine do

A

It reduces platelet aggregation by the irreversible inhibition of the ADP-receptor

222
Q

mechanism of action of isoprenalin

A

pure beta agonist
potent vasodilator

223
Q

side effects and overdose of carbamazepine

A

diplopia
ataxia
seizure
foetal aplastic anaemia
agranulocytosis

224
Q

mechanism of action of pilocarpine

A

ciliary muscle contraction
acts on subtype of muscarinic receptor M3 found on the iris sphincter muscle
results in pupil constriction (miosis)

225
Q

mechanism of action of timolol

A

decreases aqueous secretion

226
Q

mechanism of action Acetazolamide

A

decreases aqueous secretion due to a lack of HCO3

227
Q

mechanism of action of latanoprost

A

increased outflow of aqueous

228
Q

how is Vecuronium excreted

A

by the liver 85%
renal 15%

229
Q

regarding sodium valproate what % is protein bound

229
Q

what is the most common adverse effect of procainamide

A

Hypotension

230
Q

which muscle relaxant lasts the longest

A

pancuronium 35-45 mins

231
Q

At low dose, which of the muscle relaxants is most commonly associated with tachycardia?

232
Q

mechanism of action of moclobemide

A

MAO inhibition
Used for depression

233
Q

what class of drug is Imipramine

234
Q

In a patient with widespread burns who develops shock, what is the underlying mechanism?

A

Increased vascular permeability

235
Q

Which of the opiates is associated with seizures when given in high dose to patients with renal failure?

236
Q

Of the following antipsychotics, which is most likely to cause extrapyramidal side effects?

A

haloperidol

236
Q

What is the correct order of catecholamine synthesis?

A

tyrosine
dopa
dopamine
noradrenaline
adrenaline

237
Q

how is atracurium eliminated

A

hofmann - non renal non liver elimination

238
Q

duration of action of pancuronium and compared vecuronium

A

> 35min
longer then vecuronium

239
Q

what does phenytoin cause in the gums

A

hyperPLASIA

240
Q

Which local anaesthetic causes methaemoglobinaemia?

A

prilocaine

241
Q

Which of the cholinoceptor blocking drugs is the least absorbed by the brain?

A

ipatropium
it is a quarternary amine charged

242
Q

what complication can stemetil cause

A

It can cause neuroleptic malignant syndrome

243
Q

what is pralidoxime used for

A

to reactivate acetylcholinesterase inhibited by organophosphates

244
Q

what is diazepam metabolised to

245
Q

Dantrolene is used in malignant hyperthermia. Which statement best describes it’s mechanism of action?

A

It decreases calcium release from sarcoplasmatic reticulum

246
Q

Sulphonamides are a structural analogues of which of the following?

247
Q

AZT half life

A

1.1 hours - short

248
Q

A patient with impetigo would be most likely to respond to which drugs?

A

cephalexin

249
Q

Live attenuated vaccines

A

Measles, mumps, rubella
Chickenpox
Zoster
Rotavirus
Yellow fever
Oral typhoid
Bacillus Calmette-Guerin

250
Q

2nd generation cephalosporin

A

cefoxitin
cefaclor
cefotetan, cefuroxime, cefprozil, cefmetazole, loracarbef and cefonicid

251
Q

The cephalosporin with the highest activity against gram positive bacteria is?

A

Cephalothin
1st generation cephalosporins are very active against gram positive cocci

252
Q

Which class of antibiotics listed below does not possess a beta-lactam ring?

A

Fluoroquinolones

253
Q

Which of the following antibiotics does not exert its action by inhibiting cell wall synthesis?

A

erythromycin
it inhibits formation of 50s ribosomal subunit

254
Q

Penicillins reach high concentrations in what organ

A

tubular fluid in kdineys

255
Q

Acyclovir has therapeutic action against

A

HSV 1 HSV 2 VZV

256
Q

mechanism of action of cephlasporins

A

cell wall inhibitor

257
Q

mechanism of action of tetracyclines

A

inhibit protein synthesis

258
Q

mechanism of action of aminoglycoside (genatmicin)

A

Inhibit protein synthesis

259
Q

mechanism of action of fluroquinolones (ciprofloxacine)

A

DNA gyrase inhibition, thereby inhibiting cell division

260
Q

which antibiotics are resistant to staphlococcal beta lactamase?

A

Isoxazolyl penicillins (eg cloxacillin, oxacillin, dicloxacillin)
nafcillin
methicillin

261
Q

complications of penicillin other than allergy

A

hypernatraemia - if in high doses with renal or cardiovascular disease
seizure - in patients with renal failure

262
Q

what does amikacin do to bacteria

A

inhibits 30s ribosome subunit (protein synthesis)

263
Q

what does erythromycin do to bacteria

A

inhibits protein synthesis
bacteriastatic and at higher concentrations is bactericidal

264
Q

what does vancomycin do to bacteria

A

inhibits cell wall synthesis

265
Q

what does amphotercin B do to fungus

A

inhibits cell membrane function
binds to ergosterol and alters the permeability of the cell membrane forming pores

266
Q

what is pentamidine and what is it used for

A

an antiPROTOZOAL drug
interferes with nuclear metabolism.
used as an agent for prophylaxis against pneumocystosis in immune compromised patients

267
Q

what is a complication of pentamidine

A

it can cause iatrogenic diabetes
cant be toxic to the beta cells in the pancreas

268
Q

which cephlasporins can cause hypoprothrombinaemia and bleeding disorders?
and how is this preventable?

A

cephlasporins containing a methylthiotetrazole group
eg Cefotetan , cefamandole, cefmetazole, cefoperzone
administer vitamin K twice weekly

269
Q

antihistamines have signficant effect on what receptors

A

alpha
serotonin
muscarinic
anaesthetic

270
Q

which is more potent prednisone or hydrocortisone

A

prednisone is 4 times more potent

271
Q

examples of sulphonylureas

A

tolbutamide
tolazamide
acetohexamide
chlorpropamide
glyburide
glipizide
glimepiride

272
Q

examples of buguanides

A

metformin
phenformin
buformin

273
Q

mechanism of action cisapride

A

5HT4 agonist
used in treatment of GORD and motility disorder
It raises lower oesophageal sphincter pressure

274
Q

what happens to excretion of aspirin if the urine is alkalinised

A

increase excretion of aspirin

275
Q

What effects do kappa receptors mediate?

A

slow GI transit
supraspinal analgesia
spinal analgesia
psychotomimetic effect
inhibit ADH release
miosis
sedation
dysphoria

276
Q

what is dextropoxyphene

A

a centrally acting, synthetic, opioid analgesic
structurally related to methadone

277
Q

naloxone half life

278
Q

what happens with ethylene glycol toxicity

A

severe metabolic acidosis
secondary to accumulation of glycolic acid and lactate
calcium oxalate crystals form in the tissues
causes hypocalcaemia, acute renal failure

279
Q

treatment of ethylene glycol toxicity

A

haemodialysis is definitive
temporising antidote is ethanol or fomepizole

280
Q

mechanism of action of alendronic acid (fosamax)

A

suppresses the activity of osteoclasts

281
Q

what receptor does morphine affect

A

Mu receptor for analgesic effects
also is an agonist to kappa and delta

282
Q

Inhibitors of CYP450 enzymes

A

DRSICCKFACES.COM + Grapefruit
diltiazem,
ritonavir, Sodium valproate; Isoniazid (noting current text states inducer); Clarithromycin, Cimetidine; Ketoconazole; Fluconazole; Alcohol (binge); Chloramphenicol; Erythromycin; Sulphonamides; Ciproflox; Omeprazole; Metronidazole.

283
Q

Inducer of the CYP450 enzyme

A

CRAP GP’S
Carbamazepine
Rifampicin
Alcohol (chronic)
Phenytoin
Griseofulvin
Phenytoin
Sulphonylureas, St Johns wort
+
Barbiturates,
glucocorticoiDs,
charcoal broiled foods,

284
Q

A patient taking isoniazid for the a TB infection can become susceptible to the following vitamin deficiency

285
Q

A patient requires ongoing muscle relaxation during a lengthy operation. His past medical includes renal and liver impairment form alcohol. Which of the non depolarising blocking drugs can be used?

A

Atarcurium
- it is cleared from circulation via Hofmann elimination

286
Q

Thiopentone is a “short-lasting” barbiturate because?

A

It is rapidly distributed throughout the body

287
Q

Mnemonic for resuscitation drugs that may be given down the ET tube is NAVEL

A

Naloxone
Atropine
Vasopressin
Epinephrine
Lignocaine

288
Q

Which receptor action is required for an antiemetic to be effective?

A

Dopamine receptor antagonism

289
Q

The anti-hypertensive effects of clonidine occur due to

A

alpha 2 receptor activation

290
Q

Labetalol has the following pharmacodynamic effect

A

alpha 1 + B1 +B2 antagonism

291
Q

How many mmols of Sodium does a litre of normal saline contain?

292
Q

does atropine cross the bloodbrain barrier

A

yes - it is a tertiary compound

293
Q

with atropine how long are the mydriatic effects on the iris

294
Q

stool softeners

A

docusate
glycerin suppository
mineral oil

295
Q

laxative stimulants

A

senna
aloe, cascara, biscodyl

296
Q

what is ergotamine and when is it used

A

ergotamine is used solely for the third stage of labour- for the control of late uterine bleeding and must never be used before delivery.

297
Q

The order of blockade by local anaesthetics is?

A

Sympathetic
pain
temperature
touch
propioception

298
Q

Which receptors do the tricyclic antidepressants NOT block?

299
Q

After treatment for hyperthyroidism a patient has fever and neutropenia, which is the likely drug?

A

propylthiouracil

300
Q

Which drug causes severe hypotension in patient with dehydration?

301
Q

with use of magnnesium in preeclampsia what is a sign of toxicity

A

decreased tendon reflexes

302
Q

use and mechanism of action of moxonidine

A

centrally acting antihypertensive drug
alpha 2 selective recpetor agonist

303
Q

Which of the following best describes the mechanism of action of ciprofloxacin?

A

DNA gyrase inhibitor

303
Q

toxicity of theophylline

A

seizures and arrhythmias

304
Q

Antipsychotics exert their function by antagonising which receptor?

A

D2 - dopamine

305
Q

Which dopaminergic systems are important for the understanding of schizophrenia

A

mesolimbic - mesocortical pathway

306
Q

Which NSAID is best AVOIDED in patients with a history of gastro-oesophageal reflux disease?

A

Indomethacin
has higher selectivity of Cox-1

307
Q

Administration of tetanus toxoid provides what type of immunity?

A

Artificial active

308
Q

A patient who is now day 4 stay in ICU with airway burns, requires intubation. Which of the following muscle relaxant drugs is CONTRAINDICATED?

A

SUccinylcholine
due to risk of hyperkalaemia

309
Q

Which of the drug classes interact dangerously with Monoamine Oxidase Inhibitors (MAOI)

A

SSRIs
life threatening serotonin syndrome can develop

310
Q

Which of the following induction anaesthetics are contraindicated in a patient allergic to eggs?

A

propofol
contains egg yolk

311
Q

What is the treatment of choice for Trichomoniasis

A

metronidazole

312
Q

Hypoprothrombinaemia and bleeding disorders can be caused by cephalosporins that contain a methylthiotetrazole group. These include:

A

cefamandole,
cefmetazole,
cefotetan
cefoperazone.

313
Q

what factor does rivaroxaban bind to

314
Q

what factor does Argatroban and Digabatron bind to

A

IIa (thrombin)

315
Q

The risk of transient neurological symptoms is most likely to occur with which local anaesthetic?

A

lignocaine
TNS is a syndrome of transient pain and or dysaesthesia.

316
Q

Which of the following local anaesthetics is recommended for procedures during labour?

A

bupivocaine
regarded as a very safe spinal anaesthetic agent

317
Q

Which pharmacological agent is best prescribed for motion sickness

A

anti-muscarinic agents

318
Q

Which of the following analgesic medications is relatively contraindicated in patients who have a history of seizure activity?

A

tramadol
central acting analgesia
MoA serotonin reuptake
toxicity associated with seizures

318
Q

A patient presents with cardiac sounding chest pain, tachycardia and hypertension- 220/130. Which drug is the safest and most efficacious to this in this situation?

A

Nitroglycerin

319
Q

Which of the following metabolites of benzodiazepines are INACTIVE?

A

lorazepam
has inactive metabolites

320
Q

This short acting muscle relaxant is eliminated by hydrolysing cholinesterases

A

succinylcholine

321
Q

75 year old man presents to the ED with central chest pain which radiates to the back and has a tearing like quality. Diagnosis of aortic dissection is made. The patient is hypertensive, heart rate 100/min. Your choice of drug for the management of hypertension is?

A

metoprolol

322
Q

90yr old female undergoes a laparotomy for peritonitis. She is slow to regain muscle strength post-operative. Which drug is responsible?

A

Gentamicin
Gentamicin increases the effect of the neuromuscular blocking agents (including suxamethonium)

323
Q

A patient with Parkinson’s disease presents to the ED with profuse vomiting. Which is the anti-emetic of choice?

A

domperidone
well tolerated
does not cross BBB

323
Q

An elderly patient with chronic renal impairment develops a lower respiratory tract infection. Which antibiotic as a single agent is best suited for her?

A

moxifloxacin - fleuroquinolone
it is non renally cleared

324
Q

Which of the following stages of a drug trial examines the effects and side effects of a drug in a population with the disease?

325
Q

On which organ does progesterone have a stimulatory effect?

325
Q

A patient with renal failure presents in severe pain. Which opioid is recommended?

A

fentnayl
Hepatic oxidative metabolism is the primary route of degradation of the phenylpiperidine opioids (fentanyl)
no active metabolites

326
Q

Which of the following eye drops are useful to dilate the eye in the emergency department?

A

Tropicamide

326
Q

What medication is used to decontaminate the body following a toxic iron ingestion?

A

desferioxamine

327
Q

What is the effect of intravenous phenylephrine on heart rate and blood pressure?

A

Increased blood pressure, decreased heart rate

327
Q

Which NSAID is a COX-2 selective inhibitor?

328
Q

An elderly man is commenced on tamsulosin for symptoms of urinary retention and hesitancy. He experiences begins to experience symptoms consistent with postural hypotension. What is the mechanism behind this?

A

alpha 1 receptor antagonism

329
Q

Which cephlasporins have Pseudomonas cover?

A

cefepime (4th generation)
ceftazidime (3rd generation)
cefoperazone (3rd generation)

330
Q

What is the action of benzodiazepines at their receptor site?

A

allosteric modulators at the GABA A receptor
increase chloride channel opening frequency

331
Q

What is meant by the term therapeutic index?

A

The ratio of the median toxic dose to the median effective dose

332
Q

A 23-year-old epileptic has drug concentrations measured and is found to be sub-therapeutic. Her dose is minimally increased and two weeks later on re-testing they are supratherapeutic. Which drug is she likely taking?

333
Q

In a patient on an anti-seizure medication, hyponatraemia is most likely a potential side effect with administration of which of the following medications?

A

carbamazepine

334
Q

What is the mechanism of action of aminophylline in asthma?

A

inhibition of PDE enzyme, inhibition of adenosine receptors, and enhanced histone deacetylation

335
Q

A 33-year-old man develops an arrhythmia after administration of a medication used to treat asthma. Which of the following is most likely responsible?

A

aminophylline

336
Q

A 40-year-old man with chronic renal failure is intubated. Which neuromuscular blocking agent is most appropriate to maintain sedation?

A

Atracurium
undergoes hepatic metabolism and Hoffman elimination

337
Q

Loop diuretics such as Frusemide can cause hypokalemic metabolic alkalosis. What is the mechanism behind this?

A

Increased Na reabsorption in the collecting duct in exchange for H and K secretion

338
Q

What is the mechanism of action of tetracycline antibiotics?

A

Reversible binding to the 30S ribosomal subunit inhibiting protein synthesis

339
Q

Buprenorphine is a partial agonist. Which of the following may occur if it is given to a patient on long-term morphine treatment?

A

It may precipitate a withdrawal syndrome

339
Q

A medication that is an antagonist at the mu receptor, produces little respiratory depression is:

A

naltrexone

340
Q

What is the principle mechanism of NAC in paracetamol toxicity?

A

provision of glutathione
Increased glutathione availability (sulfhydryl donor)
Direct binding to NAPQI
Provision of inorganic sulphate
Reduction of NAPQI back to paracetamol.

341
Q

Sodium phosphate is a laxative medication that can cause which of the following electrolyte abnormalities?

A

hypernatraemia

342
Q

A healthcare worker suffers a needlestick injury from an HIV+ patient and requires prophylaxis.

A

zidovudine

343
Q

Azithromycin has been reported to cause which of the following cardiac arrhythmias?

A

VT
macrolides prolong QT
can lead to TdP

344
Q

A 50-year-old man has develops increasing size of his joints, deepening of his voice and a change in shoe size over the past six months. Which medication is most likely to be effective in treating his condition?

A

Octreotide
a long-acting somatostatin analogue that inhibits endocrine and paracrine factor secretion, including insulin, glucagon, gastrin, GH and TSH.

345
Q

symptoms of neuroleptic malignant syndrome

A

initial symptom is marked muscle rigidity- a lead pipe rigidity. Muscle type creatine kinase are usually elevated, reflecting muscle damage.

346
Q

Which drug should not be used in conjunction with Sildenafil?

347
Q

What is the equivalent dose of dexamethasone and prednisolone compared to 200mg hydrocortisone?

348
Q

Which drug has both a greater anti-inflammatory and salt-retaining effecting than hydrocortisone?

A

fludrocortisone

349
Q

Which antidepressant has an active metabolite?

A

fluoxetine

349
Q

Adrenaline causes skeletal muscle relaxation via which adrenoreceptor?

350
Q

Noradrenaline reduces the production of cAMP via which adrenoreceptor?

351
Q

Which anti-thyroid treatment should be used for a pregnant woman in her 1st trimester?

A

Propylthiouracil

352
Q

A patient with known liver cirrhosis presents with hepatic encephalopathy. He is on acetazolamide, digoxin, ACE-I and frusemide. Which medication is the most likely cause of his encephalopathy?

A

Azetazolmide

353
Q

An effect of sotalol is to prolong the QT. Which receptor is involved with this effect?

354
Q

A patient with ESRF (end stage renal failure) presents with constipation. You are worried about fluid shifts and electrolyte disturbances. Which laxative should not be used?

A

Sodium phosphate is an osmotic laxative that can cause hyperphosphataemia, hypocalcaemia, hypernatraemia and hypokalaemia

355
Q

Which neuromuscular blocker is primarily metabolised in the plasma

A

Succinylcholine

356
Q

Sugammadex has NO affinity for which non-depolarising neuromuscular blocker

357
Q

Heparin exerts its anticoagulant effect primarily by

A

Enhancing the activity of antithrombin III
increasing its ability to inactivate coag factors including thrombin and Xa

358
Q

Heparin’s elimination from the body is best described as

A

Complex, involving a saturable protein-binding phase followed by dose-dependent elimination

359
Q

Which oral anti-diabetic drug can cause B-12 deficiency

A

Metformin
interferes with the calcium-dependent absorption of vitamin B12-intrinsic factor complex in the terminal ileum, and vitamin B12 deficiency can occur after many years of metformin use

360
Q

Diuretics and site of action

A

“MALTS”
Mannitol - PCT
Acetazolamide - PCT
Loop diuretics - ascending loop of henle
Thiazide - DCT
Spironalactone - collecting ducts

Acem Primary (6 decks)

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