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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

81
Q

Mechanism of action of Promethazine

A

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

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

83
Q

Organ effects of Promethazine

A

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

84
Q

Toxicity of Promethazine

A

Anticholinergic side effects
Extrapyramidal reactions in high doses
sedation confusion

85
Q

Example of 2nd generation H1 antagonists

A

Loratadine, cetirizine

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

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

88
Q

Clinical use of Cimetidine

A

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

89
Q

mechanism of action of sumatriptan

A

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

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

91
Q

Mechanism of action of ondansetron

A

a 5-HT receptor antagonist
used as an antiemetic

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

93
Q

Adverse effect of ondansetron

A

prolongation of QT interval

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

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

96
Q

Clinical application of ergotamine

A

migraine
hyperprolactinaemia
postpartum haemorrhage

97
Q

Toxic effects of Nifedipine

A

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

98
Q

mechanism of action of nifedipine

A

a calcium channel blocker
a dihydropyridine
predominantly vasodilating effects

99
Q

pharmacokinetics of nifedipine

A

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

100
Q

clinical use of nifedipine

A

angina
htn
raynauds
coronary artery spasm
preterm labour

101
Q

mechanism of action of captopril

A

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

102
Q

pharmacokinetics of captopril

A

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

103
Q

toxic effects of captopril

A

hypotension
hyperkalaemia
angioedema
dry cough (bradykinens)
precipitates renal failure

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

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

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.

107
Q

Amiodarone interactions

A

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

Inhibits warfarin metabolism

108
Q

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

A

Cartelol, Acebutolol, Pindolol, Pnebutolol, Labetolol

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

110
Q

what is the half life of sotolol

A

12 hours

111
Q

nitroglycerine relieves exertional angina by ?

A

reduced oxygen consumption

112
Q

is substance P a vasodilator or vasoconstrictor?

A

potent vasodilator
dependent on NO release

113
Q

what is the elimination half life of sotalol

A

12 hours

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

115
Q

mechanism of action of labetaolol

A

mixed alpha/beta adrenergic antagonist

116
Q

mechanism of action of esmolol

A

selective beta1 antagonist

117
Q

what is streptokinase

A

non fibrin selective fibrinolytic

118
Q

streptokinase reduces mortality from MI by what %

A

25%

119
Q

what is Vigabactrins anticonvulsant property due to?

A

Irreversible inhibition of GABA aminotransferase

120
Q

mechanism of action of propafenone

A

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

121
Q

mechanism of action labetalol

A

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

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

123
Q

Mechanism of action of GTN

A

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

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

125
Q

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

A

Diltiazem
Verapamil

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

127
Q

dihydropyridine calcium channel blocker effects on smooth muscle

A

relaxation, arterioles > veins

128
Q

non-dihydropyridine calcium channel blocker effects on cardiac muscle

A

decreases contractility

129
Q

non- dihydropyridine calcium channel blocker effects on SA node

A

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

130
Q

non - dihydropyridine calcium channel blocker effects on AV node

A

decrease conduction velocity
verapamil has most effect

131
Q

what type of beta blocker is sotalol

A

beta 1 and beta 2 adrenergic receptor blocker

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

133
Q

what type of antiarrhythmic is sotalol

A

class II and class III

134
Q

where is noradrenaline released

A

postganglionic sympathetic fibers

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

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

137
Q

Clinical application of methyldopa

A

HTN during pregnancy
pre-eclampsia

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

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

140
Q

Clinical applications of Sodium Nitroprusside

A

Hypertensive emergencies
Severe heart failure
Aortic Dissection
Intraoperative production of hypotension

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

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

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

144
Q

precautions of sodium nitroprusside

A

Toxicity related to cyanide accumulation
Thiocyanate can accumulate
methaemoglobinaemia

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

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

147
Q

Clinical uses of Hydralazine

A

Chronic moderate to severe HTN
Pre eclampsia
congestive heart failure

148
Q

Clinical use of Minoxidil

A

HTN

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

A

PCT

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

A

3-4 hours

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

A

no

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

Acem Primary (5 decks)

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