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Sarahs Pharmacology > Drugs > Flashcards

Drugs Flashcards

1
Q

Describe a wash in curve

A

X axis time
Y axis FA/FI
Negative exponential
Related to BGPC where lowest reach FA/FI first

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2
Q

Factors which increase speed of onset of volatiles

A

Equipment - FiVO, FGF
Patient - high MV, low FRC (large FRC dilutes volatile), low CO, CBF

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3
Q

What is the blood gas partition coefficient?

A

Solubility of agent in the blood compared to the pp it exerts in its gaseous phase at same T and vol at equilibrium

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4
Q

What is the oil gas partition coefficient

A

Measure of lipid solubility, inversely related to MAC (high O:GPC = low MAC = more potent)

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5
Q

How does the blood gas coefficient effect offset of volatiles

A

Low BGPC have faster offset

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6
Q

Describe wash out curve for volatiles

A

X axis time
Y axis FA/FAE (pp in alveoli when gas turned off)
Lowest BGPC washed out first

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7
Q

What is the context sensitive half time

A

Time taken for plasma concentration to fall by 1/2 of its value after stopping administration at steady state

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8
Q

MAC definition

A

Dose required at steady state to prevent 50% of subjects reacting to standard surgical stimulus

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9
Q

Factors which increase MAC

A

Young
Chronic alcohol
Hyperthermia
Hyperthyroid

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10
Q

Factors which decrease MAC

A

Neonate/ old
Acute intoxication
Sedatives
Hypothermia
Hypothyroid

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11
Q

Why is halothane more lipid soluble
OGPC? MAC?

A

Smaller molecule than ether volatiles. Most potent
OG:PC 224 MAC 0.75

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12
Q

Why is halothane more blood soluble than ether volatiles

A

Can form stronger hydrogen bonds
BGPC 2.4

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13
Q

What is the difference between isoflurane and enflurane
BGPC of each

A

Structural isomer
Due to positions of flouride atoms iso is less blood soluble therefore has a quicker onset
Isoflurane BGPC 1.4
Enflurane BGPC 1.8

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14
Q

Why is desflurane least blood soluble

A

Has 6x fluoride atoms therefore more electronegative.

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15
Q

What is the unique metabolite of sevoflurane

A

Hexa-flouro-iso-propanolol

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16
Q

Which volatile is metabolised the most

A

Halothane

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17
Q

Which CYP450 enzyme Mx volatiles and is the same enzyme which is induced by chronic alcohol use

A

CYP2E1

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18
Q

Pharmacodynamics of volatiles

A

Brain - increase ICP?
Excitatory phenomenon
Decrease GCS

Resp - Decrease TV, increase RR
Bronchodilator

Cardiac - Decrease MAP/ SVR
Des/ sevo - increase heart rate
Sevo - increase QTc

GU - relaxes uterus (sevo)

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19
Q

Ideal phsyical properties of vapour

A

Stable liquid at room temp
Inert
Cheap
Non flammable
High SVP, low latent heat of vaporisation

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20
Q

Ideal pharmacological properties of vapour

A

Pleasant non irritating smell
Low BGPC
High OGPC
Cardiovascularly stable
No toxic metabolites

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21
Q

Pathophysiology of MH

A

Uncontrolled release of calcium from SR in skeletal muscle due to RYR1 receptor mutation

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22
Q

Symptoms of MH

A

Tachycardia
High O2 requirement
Hypercapnia
Hyperthermia (late)
Rigidity

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23
Q

Mx of MH

A

Dantrolene 2.5mg/kg bolus, repeat 1mg/kg up to 10mg/kg

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24
Q

How is nitrous oxide made

A

Heating ammonium nitrate to 250 degrees

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25
Q

What colour cylinders is N2O stored in

A

Blue

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26
Q

How does N2O work

A

Inhibits glutamate at NMDA receptor

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27
Q

Negative effects of N2O

A

Increase CBF/ CMRO2
Decreases TV, increases RR
B12/ bone marrow suppression

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28
Q

What is the concentration effect

A

Disproportionate rise of FA/FI when high concentrations of N20 used. Due to large concentration gradient large amount diffused into pulmonary vessels leads to concentration of remaining gases

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29
Q

What is diffusion hypoxia

A

N2O more soluble than N2
N2O leaves the blood into the alveoli quicker than N2 can travel in the opposite direction which dilutes gases to a hypoxic mixture in the alveoli

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29
Q

What is the second gas effect

A

Concentration of volatiles increases quicker in the presence of N20

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30
Q

Pharmacological properties of xenon
BGPC
OGPC/ MAC
CT

A

0.1
1.9/ 71
16.6

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31
Q

Pharmacodyanmics of xenon

A

Brain - neuroprotective
Lungs - apnoea at high concentrations
CVS - no effect

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32
Q

Describe the inhibitory pathways in the CNS

A

Glycine
GABA

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33
Q

How does GABA receptor work

A

5 subunits
Ligand gated ion channel to chloride
Influx of chloride hyper polarises membrane therefore harder to generate AP

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34
Q

Excitatory pathways in CNS

A

nACh (ionotropic receptor)
5HT
Glutamate (metabotropic GPCR)

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35
Q

Proposed mechanism of induction agents

A

Enhance GABA/ glycine
Inhibit glutamate

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36
Q

Structure of propofol

A

Phenol derivative
Aromatic group with 1x OH and 4x CH3 attached

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37
Q

Mechanism of propofol

A

Increases GABA A
Also works at NMDA rec

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38
Q

pKa of propofol

A

11

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39
Q

Vd of propofol

A

4L

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40
Q

Pharmacodynamics of propofol

A

Brain - Sedative/ anticonvulsant
Decrease ICP and CMRO

Eyes - decrease IOP

Airway - obtunds laryngeal reflexes

Resp - Bronchodilates

Cardiac - decrease BP/ SVR

GI - antiemetic

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41
Q

pKa of thiopentone

A

7.6
Weak acid

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42
Q

Pharmacokinetics of propofol

A

A - rapid lipid soluble
D - large Vd (4L), 98% protein bound
M - Liver 60% quinol (repsonsible for green urine)
40% gluconoride
E- renal
Elimination 1/2 life 5-12 hours

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43
Q

Formulation of thiopenton

A

Racemic mixture of keto and enol form
Yellow powder
Dissolved in water pH 10-11 in more soluble enol form
At body pH is becomes more unionised

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44
Q

Vd of thio

A

2.2

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45
Q

Mechanism of thiopentone

A

Mimics chloride at GABA rececptor
Also works at NMDA receptor

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46
Q

What kinetics does thio display at repeat doses

A

Zero order

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47
Q

Pharmacodynamics of thiopentone

A

Brain - decrease ICP/ CBF
Anticonvulsant

Airway - DOES NOT suppress airway reflexes

CVS - decreases BP/ CO

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48
Q

Pharmacokinetics of thio

A

A - highly lipid soluble

D - Vd 2.2L, highly protein bound

M - P450

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49
Q

pKa and acid/base status of ketamine

A

Weak base
pKa 7.5

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50
Q

What is ketamine a derivative of

A

Phencyclidine

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51
Q

Mechanism of action of ketamine

A

Non competitive antagonist at NMDA receptor
Agonist at opiate receptor
Also acts on both ACh receptors and adrenergic receptor

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52
Q

Sedative dose of ketamine

A

0.2-0.75 mg/kg IV
2-4 mg/kg IM

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53
Q

Induction dose of ketamine

A

1-2 mg/kg IV
5-10 mg/kg IM

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54
Q

Pharmacodynamics of ketamine

A

Brain - dissociation, increase CMRO

Eyes - increases IOP

Airway - DOES NOT affect laryngeal reflex, increases secretions

Resp - increases RR, bronchodilates

CVS - Increases HR, increase BP (direct negative inotropy counteracted by catecholamine release)

GI - N+V

Renal - fibrosis, ketamine bladder syndrome

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55
Q

Pharmacokinetics of ketamine

A

A - poor oral BF

D - Vd 3L
20-50% protein bound

M - CYP450 to norketamine

E - Renal
Elimination 1/2 life 2-3 hours

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56
Q

Phases of peripheral nerve action potential

A

Phase 1 - Na/K/ATPase pump maintains resting potential of -80mv

Phase 2 - -60mV is threshold for AP generation. Na influx to +30mV

Phase 3 - K efflux through voltage gated channel restores potential

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57
Q

LA are weak acids or bases?

A

Weak bases

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58
Q

Mechanism of action of LA

A

Block Na channel intracellularly to stop AP

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59
Q

Factors which affect quicker speed of onset of LA

A

Smaller and myelinated fibres
Vasodilated area

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60
Q

Structure of LA

A

Lipophilic ring (responsible for lipid solubility)
Hydrophilic tertiary amine

Ester or amide linkage

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61
Q

Which LA are esters
What is their risk

A

Procaine
Cocaine

Mx to PABA which carries risk of anaphylaxis

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62
Q

Pharmacokinetics of LA

A

A - Depends on blood flow
intercostal> caudal> epidural > brachial plexus > sc in order of risk

D - More protein bound - longer duration of action

M - Esters - pseudocholinesterase (rapid)
Amides - liver

E - 5% unchanged really

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63
Q

pKa of bupivicane and ropivicane

A

8.1

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64
Q

Order of LA protein binding

A

Bupivicine/ ropivicane
Lidocaine
Prilocaine
Procaine

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65
Q

Why does lidocaine/ prilocaine have the quickest onset

A

pKa is 7.7 / 7.9 respectively
Therefore less ionised drug as closer to physiological pH

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66
Q

Which LA has the slowest onset, what is its pKa

A

Procaine
pkA 8.9

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67
Q

Mx of LA toxicity

A

Intralipid
1.5ml/kg over 1 min
15ml/kg/hr infusion
Repeat dose at 5 mins if no improvement and increase infusion to 30ml/kg/hr

Cumulative dose 12ml/kg

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68
Q

Mechanism of paracetamol

A

COX3 inhibitor
Possibly increases cannabinoid receptor

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69
Q

Pharmacokinetics of paracetamol

A

A - PO 80%

D - 1/2 half 2 hours

M - 90% glucuronidation
10% CYP450 to NAPQI
NAPQI conjugated to glutathione which is non toxic

E - Renal

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70
Q

Mechanism of NAC

A

Stimulates glutathione production
Directly binds to NAPQI
Reduces NAPQI back to paracetamol

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71
Q

Describe the arachidonic acid pathway

A

Membrane phosophilds metabolised to Arachidonic acid by phospholipase A2

Arachidonic acid Mx to
1) Leukotrienes by lipoxygenase
2) Prostaglandins and thromboxane A2 by COX 1
3) Prostaglandin (PGE2) and prostacyclin by COX 2

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72
Q

Function of prostaglandins made by COX 1

Function of TXA2

A

GI protection
Renal blood flow
Uterine contraction
Platelet aggregation

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73
Q

Function of induced prostaglandins made by COX 2

A

Pain/ inflammation
Vasodilation

Prostacyclin - platelet relaxatiob

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74
Q

Mechanism of aspirin

A

Irreversible non selective COX inhibitor

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75
Q

Formulation of aspirin

A

Aromatic ester of acetic acid

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76
Q

Mechanism of aspirin overdose

A

Uncouples oxidative phosphorylation

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77
Q

Pharmacodynamics of aspirin

A

Brain - stimulates CTZ –> n+V

Resp - respiratory alkalosis

GI - irritation

Renal - metabolic acidosis, hypoglycaemia.
Decrease renal blood flow

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78
Q

Pharmacokinetics of aspirin

A

A - BF 70%

D - Lasts 7/7 (life of pet)

M - Esterases to salicylate

E - Renal

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79
Q

Pharmacokinetics of NSAIDs

A

A - Rapid

D - Highly protein bound (can displace other highly protein bound drugs to increase their effect ie warfarin)

M - Limited first pass Mx, liver

E - Renal

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80
Q

Are opiates weak acids or bases

A

Weak bases

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81
Q

Opiate receptors and ligands

A

Mu - endorphins
Delta - enkephalins
Kappa - dynorphins

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82
Q

Describe how a GPCR works for opiates

A

Ligand attaches to receptor
G alpha inhibits adenyl cyclase to prevent ATP conversion to cAMP

G beta blocks calcium channel to prevent influx to presynaptic membrane

G gamma stimulates potassium efflux to hyperpolarise post synaptic membrane

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83
Q

pKa of
Morphine
Fentanyl
Alfentanyl
Remifentanyl

A

8
8.4
6.5
7.1

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84
Q

Why does alfentanyl have a quicker action of onset than fentanyl

A

Fentanyl is more lipid soluble however alfentanyls pKa means that it is 90% unionised at a pH of 7.4

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85
Q

Which opiates have no active Mx

A

Fent and alf

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86
Q

Vd of morphine and fentanyl

A

3-5L

87
Q

Metabolism of codeine

A

60% Codeine 6 gluconorate
20% CYP3A4 to norcodeine
10% CYP2D6 to morphine

88
Q

Features of dihydrocodeine

A

Semi synthetic derivative of codeine, more potent

89
Q

Mechanism of buprenorphine

A

Partial agonist of mu receptor
Antagonist at D/K receptor
Higher affinity to receptor > morphine therefore can precipitate acute withdrawal

90
Q

Pharmacokinetics of buprenorphine

A

A - variable
D - 10 hour duration
M - CYP3A4
E - biliary

91
Q

Pharmacokinetics of morphine

A

A - PO BF 25%

D - Low lipid solubility
Vd 3-5L

M - 70% M3G (inactive
M6G (active, more potent)
Normorphine

E - Urine and bile

92
Q

Features of diamorphine

A

Prodrug
More lipid soluble therefore able to cross BBB
Mx by esterases to 6MAM which is mx to morphine

93
Q

Pharmacodynamics of opiates

A

Brain - analgesia, euphoria, sedation

Eyes - miosis

Airway - suppresses cough reflex

Resp - decreased RR, wooden chest at high doses, histamine release

CVS - decreases HR and BP

GI - N+V/ constipation/ Oddi spasm

Renal - retention

Other - itch, tolerance, dependance

94
Q

Physiology of neuromuscular junction

A

AP propagates to pre synaptic terminal
Stimulates Ca2+ influx through N type channels
Ca2+ stimulates Act release from vesicles in cytoplasm and attached to membrane

ACh binds to NAChR at 2x alpha subunits on post synaptic membrane
Stimulates conformational change of ligand gated sodium channel to allow Na influx to continue propagation of AP

AChE in clefts of post synaptic membrane Mx ACh to acetyl coA and choline

95
Q

Structure of ACh

A

Single ester linkage
Ammonium ion

96
Q

Structure of AChE

A

Anionic site cleaves choline
Esteratic site Mx ester linkage

97
Q

Why does neostigmine require glycopyrolate

A

Acetylcholinesterase inhibitors are non selective therefore also block muscarinic receptors

98
Q

Structure and dose of suxamethonium
Water of lipid sol?

A

2x Ach molecules
1mg/kg
Water sol due to ammonium ion

99
Q

Metabolism of suxamethonium

A

PLASMA cholinesterase (therefore neostigmine will prolong block by inhibiting theses enzymes)

100
Q

Phases of depolarising NMB block

A

Phase 1 - NAchR agonist and depolarises membrane then renders inactive

Phase 2 - Characteristics of NDNMB

101
Q

Side effects of suxamethonium

A

Increase ICP
Increase IOP
Decrease HR
Myalgia
Hyperkalaemia

102
Q

Mechanism of ND NMBs

A

Competitive antagonist of NAChr

103
Q

Which drugs are benzylisoquinoloniums

A

Atracurium
Cisatracurium
Mivacurium

104
Q

How is atracurium/ cisatracurium Mx

A

1) Non specific esterases
2) Hoffman degradation

105
Q

How is mivacurium Mx - what is the implication

A

Mx by plasma cholinesterase therefore can’t give to someone with sux apnoea

106
Q

Pharmacokinetics of NMBD

A

A - highly ionised and polar therefore water over lipid soluble

D - Small Vd
Limited crossing of BBB and placenta

M - see separate

E - Urine and biliary (mono quaternary compounds (vec/roc) more biliary)

107
Q

Factors that will prolong NMB

A

Pt - hypothermia, acidotic
Mg, hypoK

Anaesthetic - TCA/ aminoglycoside

108
Q

Which NMBD are aminosteroids

A

Pancuronium (most potent)
Vecuronium
Rocuronium

109
Q

Methods of monitoring NMB

A

Mechanomyography - tension of contraction
Acceleromyography - acceleration of thumb twitch
Electromyography - current of AP

110
Q

Describe reversal of NMBD

A

Drug is cleared from the plasma which creates a concentration gradient so that drug dissociates from NAChR.

111
Q

Mechanism of AChi

A

Non selective binding of AChE at nicotinic and muscarinic.
Binds to ACh enzyme at same sites of ACh so it can’t bind, thereby increasing concentration of ACh over drug at membrane

112
Q

Organophosphates mechanism

A

Irreversible binding to enzyme

113
Q

Mechanism of suggamadex

A

Cyclodextrin ring, lipophilic centre and hydrophilic outer ring. Attracted to ammonium ion on NMBD to encapsulate drug. Excreted as whole complex renally.

114
Q

Patient risk factors for PONV

A

Female
Non smoker
Previous
Prolonged fast

115
Q

Surgical risk factors for PONV

A

ENT
Eye
Gynae
Neuro
Laparoscopic

116
Q

Anaesthetic factors for PONV

A

Volatiles
Opiates
Neostigmine
N2O

117
Q

Inputs to the vomiting centre

A

1) Higher centre
2) GI - 5HT3 and ACh rec
3) Vestibular - ACh and H1 rec
4) CTZ - 5HT3 and D2 rec

118
Q

Where is the CTZ

A

Dorsal surface of medulla on floor of 4th ventricle

119
Q

Structure of ondansetron and receptor

A

Synthetic carbazole
Serotonin rec in GI and CTZ

120
Q

Pharmacodynamics of ondansetron

A

constipation, prolonged QTc

121
Q

Pharmacokinetics of ondansetron

A

A - 60% BO
B - 75% protein bound
M - liver to inactive Mx
E - renal

122
Q

Structure of cyclizine and receptor

A

Piperazine derivative
H1 antagonism, some antimuscarinic

123
Q

SE’s of cyclizine

A

Woozy, dry mouth, tachycardia

124
Q

Prochlorperazine receptor

A

D2 antagonist in CTZ
Some H1
Some antimuscarinic

125
Q

SE’s of prochlorperazine

A

Decrease seizure threshold
Exacerbate PD
NMS

126
Q

Metoclopramide receptor

A

D2 antagonist in CTZ
Some 5HT3 antagonism

127
Q

SE’s metoclopramide

A

Oculogyric crisis
EPSE/ dystonia
Prokinetic

128
Q

Which antiemetic works on antimuscarinic receptors in vestibular system

A

Hyoscine

129
Q

SE’s of hyoscine

A

Sedation, dry mouth, anticholinergic syndrome

130
Q

Action of oxytocin (syntocinon)

A

Acts on GPCR to stimulate uterine contraction and breast milk ejection

131
Q

Pharmacokinetics of synt

A

A - immediate
D - 30% protein bound, crosses placenta
M - hepatic
E - bile/ urine

132
Q

What conditions require cautious use of oxytocin

A

Cardiomyopathies
Decreases BP/ increases HR

133
Q

What is the second line uterotonic? What is its action

A

Ergometrine
Alpha adrenergic receptor antagonist

134
Q

SE’s of ergometrine

A

Increases BP
Reflex Brady
Headache
N+V

135
Q

What is the action of carboprost
When is it contraindicated

A

Prostaglandin rec
CI - asthmatics

136
Q

Dose of carboprost

A

250 mcg IM
Repeat every 15 mins to 2mg

137
Q

What is the most important factor dictating IOP

A

CVP via episcleral vessels - if increased causes decreased drainage of aqueous humour

138
Q

Which drugs decrease production of aqueous humour

A

Timolol
Alpha agonists
Acetozolamide

139
Q

Which drugs increase drainage of aqueous humour

A

Musc. agonists - pilocarpine
Latanoprost

140
Q

Which drugs can increase IOP

A

Ketamine, N2O, Sux

141
Q

Which drugs affect cell wall of bacteria (5)

A

Penicillins
Cephalosporins
Carbapenems
Monobactams
- inhibit cross linking of chains
Vancomycin - inhibits NAG/NAM binding

142
Q

Which drug prevents 50S ribosome to move along mRNA
Is it bacteriostatic or bactericidal?

A

Erythromycin
Bacteriostatic

143
Q

Which drugs acts on 30S ribosome to misread mRNA
Is it bacteriostatic or bactericidal?

A

Gentamicin
Bacteriocidal

144
Q

Which drugs acts on 30S ribosome to inhibit tRNA?

A

Tetracyclines

145
Q

Which drug inhibits dihydrofolate reducates

A

Trimethoprim

146
Q

Which class of drug inhibits DNA gyrase in bacteria with examples

A

Quinolones
Ciprofloxacin
Levofloxacin

147
Q

How does increasing generation of cephalosporin affect cover of organisms

A

Decreasing G positive
Increasing G negative

148
Q

Examples of gram positive cocci and appropriate Abx

A

Staph/ strep

Pencillins, cephalosporins, linezolid

149
Q

Examples of gram positive rods

A

Clostridium
Listeria

150
Q

Poor staining bacteria

A

Mycoplasma
Listeria

151
Q

Gram negative cocci?
Example of appropriate Abx

A

Neisseria
Higher generation cephalosporins

152
Q

Gram negative rods?
Examples of appropriate Abx

A

E. coli
Klebsiella
Pseudomonas

Co-amox/ Taz
Cipro
Gent

153
Q

How do azole drugs work? Give examples

A

Inhibit enzyme that makes ergosterol
Fluconazole

154
Q

How do polyene drugs work
Give an example

A

Binds to ergosterol in cell wall and makes holes
Amphotericin

155
Q

How do echinocandins work
Give an example

A

Inhibit Beta gluten synthesis
Caspofungin

156
Q

Which receptors does salbutamol work on

A

B2 agonist
Some B1 agonist activity

157
Q

SE’s of salbutamol

A

Arrythmias/ Tachycardia
Hypokalaemia
Increased lactate
Uterus relaxation

158
Q

How does ipratropium work
What is its structure

A

Antimuscarinic therefore blocks parasympathetic driven bronchoconstriction
Quaternary structure –> doesn’t cross BBB

159
Q

Mechanism of aminophyline (3)?

A

Non selective PPD inhibitor
(PPD is responsible for breakdown of cAMP)
Increased cAMP levels decrease Ca2+ release to cause muscle contraction –> bronchodilator smooth muscle

NA release
Stabilises mast cells

160
Q

How is aminophyline metabolised

A

CYP450 - narrow therapeutic index
Zero order kinetics

161
Q

SE’s of aminophyline

A

Decrease seizure threshold
Positive ionotropy/ chronotropy
Arrythmias
Hypokalaemia

162
Q

Site of action of loop diuretics

A

Binds of Cl binding site of NKCC2 carrier in thick ascending limb to inhibit reabsorption of filtrate

163
Q

Structure of furosemide

A

Sulphonamide derivative

164
Q

Pharmacokinetics of furosmide

A

Highly protein bound
Hepatic Mx
Really excreted unchanged

165
Q

SE’s of furosemide

A

Electrolye disturbance
Increase uric acid –> gout
Hearing loss

166
Q

Structure and mechanism of thiazide diuretics

A

Sulphonamide
Acts on Na/Cl co transporter in early DCT preventing passage into tubular cell

167
Q

SE’s of thiazide diuretics

A

Hypokalaemia, hypochloraemic metabolic alkalosis
Hyperglycaemia
Gout
Impotence

168
Q

Site of action of potassium sparing diuretics

A

Competitive antagonist for aldosterone at MR in late DCT and collecting duct

169
Q

SE’s of MRA

A

Metabolic acidosis
Gynaecomastia

170
Q

Pharmacokinetics of MRA

A

A - slow onset - max 3-4 days
D - highly protein bound
M - Mx in gut and liver to active Mx
E - Urine and bile

171
Q

Classes of antiepileptics

A

Na channel blockers - phenytoin/ carbamazepine/ lamotrigine
GABA enhancers - Keppra, SoVal, Benzos
Glutamate blockers - Topiramate

172
Q

Pharmacokinetics of benzodiazepines

A

A - Good PO bioavailability
D - Strongly protein bound, lipid soluble –> crosses BBB
M - Active Mx, some with long half lives
E - urine

173
Q

Pharmacodynamics of benzodiazepines

A

CNS - Anxiolytics, sedation, anti convulsant

Resp - Obtunds laryngoscopy response, resp depression

CVS - Decreases CO

Renal - decreases blood flow

174
Q

Possible adverse effects of vancomycin

A

Red man syndrome (histamine release)

175
Q

SE’s of quinolones (cipro/ levo)

A

C.diff
Tendonitis
Seizures

176
Q

Difference between tertiary and quaternary antimuscarinic

A

Tertiary crosses BBB

177
Q

Examples of tertiary antimuscarinic

A

Atropine, hyoscine

178
Q

PD of atropine/ glyco

A

CNS - agitation/ confusion (atropine)
Eyes - increases IOP
Resp - bronchodilates
CVS - increases HR
GI - increases secretions, lower LOS tone

179
Q

Pd of noradrenaline

A

Cardiac - increased SVR ++
Reflex Brady, increased O2 consumption

Resp - increased PVR

GI - decreased blood flow

Uterus - fetal Brady

Other - necrosis

180
Q

Pk of noradrenaline

A

A - 1/2 life 2 mins
M - COMT - inactive Mx
E - Urine

181
Q

Receptor site of dobutamine

A

B1 >B2

182
Q

Cardiac effect of dobutamine

A

Increased HR and contractility
B2 usually decreases SVR however BP usually maintained

183
Q

CI of dobutamine

A

Fixed CO - AS, tamponade

184
Q

Pd of adrenaline

A

Resp - bronchodilator

CVS - Increased CO and O2 consumption
decreased SVR at low doses, increased at high doses

Renal - decreased flow

Metabolic - glucose and lactate rise

185
Q

Pk of adrenaline

A

A - IM > SC

M - MAO/ COMT to inactive Mx

E - Urine 1/2 life mins

186
Q

Which volatile interacts with adrenaline

A

Halothane

187
Q

Effect of ephedrine

A

Direct - alpha and beta
Indirect - NA release from sympathetic nerves

188
Q

Pk of ephidrine

A

A - 100%
D - Rapid
M - Hepatic therefore half life
E - 65% excreted unchanged in urine

189
Q

Class 1a antiarrythmics

A

Quinidine
Procainamide

190
Q

Class 1b antiarrythmics

A

Lidocaine/ phenytoin

191
Q

Class 1c antiarrythmics

A

Flecainide

192
Q

Class 2 anti arrythmics

A

B blockers
Propanolol
Metoprolol

193
Q

Class 3 antiarrythmics

A

Amiodarine

194
Q

Class 4 antiarrythmics

A

Verapamil
Diltiazem

195
Q

Action of clopidogrel

A

Irreversible ADP P2Y12 antagonist
Prevents fibrinogen binding

196
Q

Mx of clopidogrel

A

Prodrug, hepatically Mx to active form

197
Q

Ticagrelor action

A

Reversible allosteric inhibition of ADP receptor

198
Q

Dipyradimole action

A

PDE receptor - inhibits platelet adhesion

199
Q

G1b/G3a rec action and examples

A

Inhibits adhesion of fibrinogen binding
Tirofiban
Eptifbatide

200
Q

Action of heparin/LMWH

A

Wraps around anti-thrombin-thrombin complex so can’t act
LMWH is smaller molecule (<8000 daltons) which wraps around X10

201
Q

Time frame of HIT vs non immune thrombocytopenia

A

4-14 vs <4

202
Q

Do heparins cross placenta/ BBB

A

No

203
Q

Pk of DOACs

A

A - 60-80%
M - CYP3A4
E - Renal (apixaban least therefore better in renal failure)

204
Q

Action of dabigatran
Mx of dabigatran

A

Prodrug, 2a antagonist
Hepatic and plasma esterase

205
Q

Pd Sodium nitroprusside

A

CVS - Aterio and veno dilator by producing NO
Decreases SVR –> BP
Decreases preload
Reflex tachycardia

RS - Increased shunt

CNS - cerebral vasodilation increases ICP

206
Q

Pk of sodium nitroprusside

A

A - No PO BF, duration 10 mins
M - RBCs, hepatic, renal, creates cyanide
E - Urine

207
Q

Action of GTN

A

Ventilator by producing NO
Activates granulate cyclase to increase cGMP. Decreases cytoplasmic Ca –> vasodilation

208
Q

Pd GTN

A

CVS - Decreases preload, O2 demand
Increase flow to subendocardial tissues
Decreases SVR and tachy in high dose

CNS - headache

209
Q

Pk GTN

A

A - dependent
D - not protein bound
M - 1st pass Mx (nicorandil), denitration
E - 20% of metabolite excreted in urine

210
Q

pKa of lidocaine

A

7.8

211
Q

Calculate max dose of bupivicaine

A

0.5% = 0.4 x wt
0.25% = 0.8 x wt

212
Q

Which LA’s can ppt metHb

A

EMLA and prilocaine

213
Q

Which LA need to be avoided in sux apnoea

A

Procaine

214
Q

Which LA can be motor sparing

A

Ropivicaine

Sarahs Pharmacology (2 decks)

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