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Definition Deck > More drugs > Flashcards

More drugs Flashcards

1
Q

Codeine difference to morphine

A

methyl group on C3

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2
Q

Naloxone difference to morphine

A

methylation on the amine group

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3
Q

Heroin difference to morphine

A

acetylation of C3/C6 hydroxyl groups

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4
Q

Protein binding fentanyl

A

85%

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5
Q

Protein binding alfentanyl

A

90%

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6
Q

Protein binding morphine

A

35%

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7
Q

Protein binding remi

A

70%

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8
Q

T1/2 B morphine

A

160 mins

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9
Q

T1/2 B fentanyl

A

190 mins

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10
Q

Vd morphine

A

4L/kg

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11
Q

Potency compared to morphine - fentanyl

A

100x

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12
Q

Potency compared to morphine - alfentanyl

A

10-20x

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13
Q

Potency compared to morphine - codeine

A

0.1x

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14
Q

Morphine oral bioavailability

A

25%

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15
Q

Morphine clearance

A

15ml/kg/min

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16
Q

Morphine metabolism

A

Hepatic glucuronidation
M3G, M6G metabolites.
Active
M3G no analgesic property, neurotoxic + seizure
M6G 10x more potent than parent
renal excretion

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17
Q

Pethidine metabolism

A

de-methylation -> norpethidine -> 50% potency
- Convulsant property

Ester hydrolysis -> pethidinic acid -> inactive

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18
Q

Effects of pethidine other than opioid effect

A

anti-cholinergic - tachycardia, dry mouth
LA effect
SSRI - interaction with MAO inhibitors -> serotonin syndrome

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19
Q

Metabolism fentanyl

A

hepatic -> norfentanyl, inactive
also significant first pass pulmonary endothelium uptake

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20
Q

Opioid with highest lipid solubility

A

sufentanyl

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21
Q

Vd alfentanil

A

0.6L/kg

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22
Q

Methadone T1/2B

A

12-60 hours, unpredictable

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22
Q

Methadone

A
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23
Q

Methadone bioavailability

A

75%

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24
Q

Methadone protein binding

A

90%

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25
Q

Methadone side effects

A

QT prolongation
other opioid related side effects

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26
Q

Tramadol enantiomers

A

(+) - SSRI effect
(-) - SNRI effect

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27
Q

Tramadol bioavailability

A

90%

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28
Q

Tramadol metabolism

A

2D6
Demethylation -> glucuronidation
ODMT -> high affinity for opioid receptors, 10x more potent

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29
Q

Tapentadol metabolism

A

Extensive hepatic, no active metabolite

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30
Q

Aspirin - pKa

A

3

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31
Q

Aspirin - PO bioavailability

A

70%

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32
Q

Aspirin - protein binding

A

85%

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33
Q

Aspirin - metabolism

A

rapidly to salicylic acid via intestinal and hepatic esterase’s

active metabolite with longer T1/2B of 3 hours

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34
Q

Aspirin - what is Reye’s syndrome

A

fatty liver, encephalopathy, cerebral oedema

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35
Q

Aspirin - overdose pathophys

A

uncoupling of oxidative phosphorylation

Increased aspirin level -> direct stimulation of resp centre -> resp alkalosis

Anaerobic glycolysis -> metabolic acidosis

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36
Q

Aspirin - overdose Sx

A

sweating, tinnitus, blurred vision
tachycardia
pyrexia
hyperventilation

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37
Q

Parecoxib onset and peak effect

A

15 mins
2 hours

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38
Q

Basic structure of LA

A

Hydrophilic tail - determines degree of ionisation
Lipophilic aromatic ring - determines lipid solubility
Intermediate link - determines type of LA (amide vs. ester

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39
Q

LA binding site on VG NAC

A

domain IV, segment 6

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40
Q

what is frequency dependent blockade

A

LA molecules have greater access to Na channels when they are in activated open state.

increase opening -> increase access to LA binding site of Na channels

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41
Q

Protein binding of lignocaine

A

70%

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42
Q

Protein binding of bupivocaine

A

95%

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43
Q

Ranking of vasodilatory effect of LA

A

Prilocaine > lignocaine > bupivocaine > ropivocaine

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44
Q

LA systemic absorption route in order of decreasing rate

A

Intravenous > intercostal > caudal block > epidural > peripheral nerve > submit infiltration

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45
Q

Metabolite of lignocaine

A

hydroxy-xylidine, active metabolite

46
Q

Lignocaine dose dependent systemic effect

A

1-5ug/ml - analgesia
5-10 - tingling, visual disturbance
10-15 - seizure
15-20 - hypotension, coma
>20 - respiratory depression, CV collapse

47
Q

T1/2 B lignocaine

A

1.5hrs

48
Q

T1/2B bupivocaine

A

2.5hrs

49
Q

T1/2 B ropivocaine

A

2.0 hrs

50
Q

Ropivocaine pharmaceutics

A

Enantiopure, S enantiomer

51
Q

Prilocaine pKa

A

7.7, 33% unionised

52
Q

Protein binding prilocaine

A

50%

53
Q

Define Eutectic

A

A mixture of substances that has a lower melting point than that of its constituents

54
Q

Cocaine max dose

A

1.5mg/kg

55
Q

Cocaine MOA

A

LA + uptake 1 and MAO inhibitor

56
Q

Structure-activity sympathomimetics - requirement for direct activity

A

-OH group on C3 + Beta carbon

57
Q

Structure-activity sympathomimetics - indirect activity

A

non-bulky terminal amine to allow reuptake

58
Q

Structure-activity sympathomimetics - phenylephrine

A

Lacks -OH 4, non-catecholamine
Direct activity due to -OH on C3 and BC
No beta activity

59
Q

Steps of adrenaline synthesis

A

tyrosine -> DOPA -> L-DOPA -> Norad -> adrenaline

60
Q

Classify ionotropes

A

B-1 agonists, catecholamines
Phosphodiesterase inhibitors
Glucagon
Thyroid hormone
Ca2+
Levosimenden
Digoxin

61
Q

Classify a-antagonists

A

Non-selective: phentolamine (short), phenoxybenamine (long)
Selective a1
- a1: prazosin
- a2: yohimbine (indicated for impotence)

62
Q

Classify B-antagonist

A

Non-selective - propranolol
Cardio selective - metoprolol, atenolol, esmolol
Mixed - labetalol

Intrinsic sympathomimetic activity
- Present: pindolol, absent: metoprolol

63
Q

Centrally acting anticholinergics

A

atropine
hyoscine

64
Q

GI effect of atropine

A

reduce LOS tone
Reduce GI acid secretion
Reduce GIT motility

65
Q

Atropine metabolism

A

Extensive hepatic esterases
Renal excretion

66
Q

Timing of action of atropine

A

tachycardia onset 2-4 mins
T1/2B 2.5 hours
Duration of action 3 hours

67
Q

Is atropine racemic?

A

Yes, but only L-isomer is active

68
Q

What are the brand names of hyoscine?

A

buscopan
scopolamine

69
Q

Glycopyrulate metabolism

A

Minimal metabolism
Renal excretion unchanged 85%

70
Q

Class 1a anti-arrhythmic - example and MOA

A

Quinidine, procainamide
Na blockade + increase duration of refractory period and AP

71
Q

Class 1b anti-arrhythmic - example and MOA

A

Lignocaine
NA blockade + decrease duration of refractory period and AP

72
Q

Class 1c anti-arrhythmic - example and MOA

A

flecanide
NA blockade + no change to refractory period

73
Q

Digoxin - PO bioavailability

A

80%

74
Q

Digoxin protein binding

A

25%

75
Q

Digoxin metabolism

A

Minimally metabolised.
Renal excreted

76
Q

Digoxin toxic plasma level

A

> 2.5ng/ml

77
Q

Cardiac toxic effects of digoxin

A

premature ventricular contraction
AV blocks
junctional rhythm
prolonged PR
VT/VF

78
Q

How is dig toxicity treated?

A

Early - gastric lavage
Correct hyper / hypo K, acid-base imbalance
Treat bradycardia
Digoxin-specific Fab (digibind) - for Plasma level > 20ng/ml

79
Q

Contraindication of adenosine

A

asthma
2nd and 3rd degree HB
sick sinus syndrome

80
Q

Amiodarone metabolism and excretion

A

extensive liver metabolism to N-desmethyl amiodarone

Mainly excreted in bile but also lacrymal gland

81
Q

Protein binding amiodarone

A

> 95%, can potentiate effect of highly protein bound drugs like warfarin and phenytoin

82
Q

Mg toxicity levels

A

2-3mmol/L - therapeutic
5 - loss of reflex
7.5 - respiratory depression, heart block
>12 - cardiac arrest

83
Q

GTN metabolism

A

rapid hepatic and RBC hydrolysis to glycerol di-nitrate and NO

80% urine excretion

84
Q

Pathophys cyanide toxicity

A

Free CN- ions can bind to cytochrome oxidase to uncouple oxidative phosphorylation -> histotoxic hypoxia

85
Q

Classify anti-HTN

A

Ace-inhibitor
B-blockers
Ca channel blockers
A2 agonists
A1 antagonists
Nitrites
Hydralazine
Diuretics
Anaesthetic agents

86
Q

MOA methyldopa

A

prodrug - converts centrally to methyl-noradrenaline

Acts as a central A2 agonist - sympatholysis effect

87
Q

Examples of MAO inhibitors

A

Non-selective / irreversible - phenelzine
Selective, reversible MAO-A - Moclobemide
Selective irreversible MAO-B - selegiline

88
Q

MOA of TCA

A

Inhibit reuptake of serotonin, noradrenaline
M-AchR, H1/H2 receptors, A1 receptors, NMDA receptors

89
Q

Compare SSRI with TCA effects

A

Antidepressant - no difference
Less sedation, fewer anti-cholinergic, less cardio toxic

More sexual dysfunction
Higher rate of N/V

90
Q

What is serotonin syndrome

A

Triad of cognitive, autonomic and neuromuscular symptoms due to excess serotonin activity both centrally and peripherally

91
Q

Signs of serotonin syndrome

A

Cognitive: confusion, agitation, hallucination
Autonomic: sweating, hyperthermia, hypertension, tachycardia
Neuro: hyper-reflexia, myoclonus, tremor

92
Q

What does MAO-A break down?

A

deamination of 5HT, noradrenaline, dopamine

93
Q

What does MAO-B break down

A

deamination of dopamine, tyramine, phenyl-ethylamine

94
Q

What happens when MAO inhibitors are mixed with cheese?

A

tyramine -> hypertensive crisis

95
Q

What is neuroleptic malignant syndrome triggered by?

A

All drugs with D2 antagonist properties
Blockade of DA receptors in corpus striatum to cause excessive heat production and spasticity of skeletal muscles

96
Q

How is NMR different to serotonin syndrome?

A

More slow onset
Rigidity, hyporeflexia
Normal pupils
No GI symptoms

97
Q

Phenyltoin bioavailability

A

70-100%

98
Q

Phenyltoin protein binding

A

90%

99
Q

Phenyltoin metabolism

A

Hepatic hydroxylation, saturable process -> zero order kinetics

Enzyme inducer

100
Q

Metabolism of gabapentinoids?

A

negligible metabolism, excreted unchanged in urine

101
Q

How is levodopa administered, and why?

A

Orally with carbidopa, a peripheral decarboxylase inhibitor to increase % of drug crossing into the BBB.

102
Q

Classify drugs acting on the serotonin pathway

A

Agonist - sumatriptan, paracetamol
Antagonist - ondansetron
Reuptake inhibition - SSRI, TCA
Prevention of breakdown - MAO-i

103
Q

How is the MOA of clopidogrel different to ticagrelor

A

Ticagrelor is a reversible P2Y12 antagonist. Also not a prodrug

104
Q

Drug that the IIa/IIIb receptors?

A

Tirofiban

105
Q

Which fluid can be used for their anti-platelet effect?

A

dextran - induces a type 1 VWF deficiency state

106
Q

Classify side effects of heparin

A

Dose-dependent: bleeding, hypotension, osteoporosis, skin necrosis, hyperkalaemia due to reduced aldosterone secretion

Severe: allergy, HITT

107
Q

What is heparin

A

polyanionic polysaccharide derived from bovine or porcine sources

MW 5000-25000Da

108
Q

Advantage of enoxaparin

A

single daily dose due to longer T1/2B
lower risk of bleeding, more predictable effect
Less risk of thromobocytopenia
Monitoring not required
Does not cross the placenta

109
Q

Side effects of protamine

A

histamine release
allergy
pulmonary HTN due to complement activation
anticoagulation in excess
interaction with some insulin formulation

110
Q

What is fondaparinux

A

synthetic anticoagulant that resembles the active site of heparin -> increases ATIII activity by 300x specifically to FXa

111
Q

How is dabigatran metabolised?

A

Prodrug, converts to active drug by liver and plasma esterase’s

112
Q

What is the equivalent dose of 4mg dexamethasone for other steroids?

A

hydrocortisone - 100mg
prednisolone - 25mg
Methylpred - 20mg

Definition Deck (5 decks)

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