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BRS Y2 > pharmacology > Flashcards

pharmacology Flashcards

1
Q

what are the 4 drug targets

A

enzyme
receptor
ion channel
transport protein

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2
Q

what are the 4 ways drug can react with receptors through chemical reactions

A

electrostatic interactions
hydrophobic interactions
covalent bonds
stereospecific interactions

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3
Q

what do u call full affinity but 0 efficacy drug

A

antagonist

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4
Q

what is the standard measure of potency

A

determine concentration or dose of a drug required to produce 50% tissue response

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5
Q

which is related to dose, potency or efficacy

A

potency

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6
Q

in ionised form, will the acid donate or accept protons

A

donate

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7
Q

in ionised form, will the base donate or accept protons

A

accept

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8
Q

what determines whether the drug is ionised or not

A

pH
pKa

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9
Q

what happens when pKa of drug and pH of tissue is equal

A

drug 50% ionised 50% unionised

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10
Q

for weak acid, when pH decreases which form will start to dominate

A

unionised form

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11
Q

for weak base, when pH increase, which form starts to dominate

A

unionised form

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12
Q

for weak base when pH decreases which form dominates

A

ionised form

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13
Q

different forms of drug administration

A

oral
inhalational
dermal(percutaneous)
intra-nasal

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14
Q

what affects diffusion of drug

A

lipid solubility

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15
Q

what influence tissue distribution

A

regional blood flow
plasma protein binding
capillary permeability
tissue localisation

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16
Q

factors affecting amount of drug that is bound

A

free drug conc
affinity of protein binding sites
plasma protein conc

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17
Q

what are the different types of capillary structure

A

continuous
fenestrated
discontinuous
BBB

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18
Q

which enzyme is responsible for drug metabolism

A

P450 enzymes

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19
Q

what are the phases of drug metabolism

A

phase 1 – introduce a reactive grp to a drug
phase 2 – add a conjugate to reactive grp

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20
Q

what are the main aims of the 2 stages in drug metabolism

A

decrease lipid solubility to aid excretion and elimination

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21
Q

what are the major excretion methods for drug via kidney

A

glomerular filtration
active tubular secretion (or reabsorption)
passive diffusion across tubular epithelium

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22
Q

what is the drug target of metformin

A

AMPK (5′-AMP-activated protein kinase (AMPK)

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23
Q

where is the primary site of metformin action

A

hepatocyte mitochondria

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24
Q

mechanism of action of metformin

A

inhibits gluconeogenesis and hence glucose output
metformin activates AMPK to inhibit ATP production to block gluconeogenesis, block adenylate cyclase to promote fat oxidation to restore insulin sensitivity

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25
Q

side effects of metformin

A

GI (abdominal pain, reduced appetite, diarrhoea, vomit)

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26
Q

why metformin can accumulate in liver and GIT

A

it’s high polar and need organic cation transporter-1 (OCT-1) to access tissue

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27
Q

when is metformin most effective in a patient

A

with presence of endogenous insulin / functioning pancreatic islet cells

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28
Q

example of DPP-4 inhibitors

A

sitagliptin

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29
Q

what is the primary site of DPP-4 inhibitors

A

vascular endothelium

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30
Q

main action of DPP-4 inhibitors

A

reduce break down of insulin / increase insulin production

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31
Q

mechanism of action of DPP-4 inhibitors

A

DPP-4 metabolise incretins in plasma which incretins help to stimulate production of insulin and reduce production of glucagon by liver
by inhibiting DPP-4, can let incretin remain to stimulate insulin production

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32
Q

side effects of DPP-4

A

upper respiratory tract infections (flu like symptoms)
allergic reaction

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33
Q

which patients shd avoid DPP-4 inhibitors

A

patients with pancreatitis

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34
Q

main benefit of DPP-4 inhibitors compared to other anti-diabetic drug

A

no weight gain

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35
Q

when is DPP-4 inhibitors effective

A

when residual pancreatic beta-cell activity is present

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36
Q

examples of sulphonylurea

A

gliclazide

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37
Q

target of sulphonylurea

A

ATP sensitive K+ channel

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38
Q

primary site of sulphonylurea

A

pancreatic Beta cells

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39
Q

main action of sulphonylurea

A

stimulate insulin production

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40
Q

mechanism of action of sulphonylurea

A

inhibit K+ ATP channel on pancreatic beta cell
cause depolarisation and stimulate Ca2+ influx and hence insulin vesicle exocytosis

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41
Q

side effects of sulphonylurea

A

wight gain
hypoglycaemia

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42
Q

when is sulphonylurea most effective

A

when residual pancreatic beta cell activity is present

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43
Q

risk of sulphonylurea

A

hypoglycaemia

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44
Q

examples of SGLT-2 transporter inhibitors

A

dapaglifozin

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45
Q

target site of SGLT-2 inhibitors

A

PCT

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46
Q

mechanism of action of SGLT-2 inhibitors

A

inhibit SGLT-2 in PCT to reduce glucose reabsorption and increase urinary glucose excretion

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47
Q

side effects of SGLT-2 inhibitors

A

uro-genital infections due to increase glucose load
decrease in bone formation
worsen diabetic ketoacidosis

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48
Q

physiological changes of SGLT-2 inhibitors

A

reduce weight
reduce BP

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49
Q

in which patients are SGLT-2 inhibitors less effective

A

renal impairment

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50
Q

what to administer when HbA1c > 48

A

standard release metformin

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51
Q

what to administer when HbA1c > 58

A

metformin + one of below
DPP-4 inhibitors
Pioglitazone
Sulphonylurea
SGLT-2 inhibitor

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52
Q

which transporter does metformin use

A

organic cation transporter -1 (OCT-1)

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53
Q

where is OCT-1 found in body

A

hepatocytes (liver) allow it to be absorbed
enterocytes (Small bowel) to be distributed to site of action
PCT (kidney) help excretion

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54
Q

risk of pioglitazone

A

heart failure

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55
Q

mechanism of pioglitazone

A

reduces peripheral insulin resistance, leading to a reduction of blood-glucose concentration.

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56
Q

why metformin may lead to lactic acidosis

A

accumulate metformin in bloodstream
block pyruvate carboxylase
inhibit gluconeogenesis and pyruvate build up
cause lactic acidosis

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57
Q

what are examples of dopamine precursors

A

levodopa, fos-levodopa

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58
Q

main goal of dopamine precursors

A

This compensates for the loss of endogenous dopamine in nigrostriatal neurones.

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59
Q

mechanism of dopamine precursors eg levodopa

A

Levodopa is taken up in the terminals of nigrostriatal neurones.
Then decarboxylated into dopamine by dopa decarboxylase (useful to think of levodopa as a prodrug for dopamine).

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60
Q

are there any drug target for levodopa

A

no, once converted into dopamine then the targets will be dopamine receptors

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61
Q

side effects of dopamine precursors

A

N+V
dizziness
headache
GI discomfort
dyskinesias
somnolence

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62
Q

relationship between levodopa and fos-levodopa

A

fos-levodopa is a phosphate pro drug of levodopa
more water soluble than levodopa so more suitable for sub-cutaneous infusion

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63
Q

what can rapid withdrawal if levodopa lead to

A

neuroleptic malignant syndrome

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64
Q

drugs to treat diabetes

A

metformin
SGLT-2 inhibitors
Sulfonylurea
DPP4-inhibitors

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65
Q

examples of dopa decarboxylase inhibitors

A

carbidopa
benserazide

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66
Q

target of dopa decarboxylase inhibitor

A

dopa decarboxylase

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67
Q

main target of dopa decarboxylase inhibitor

A

dopa decarboxylase

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68
Q

mechanism of dopa decarboxylase inhibitor

A

Dopa decarboxylase inhibitors block the dopa decarboxylase enzyme and prevent the conversion of dopa to dopamine.

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69
Q

why dopa decarboxylase inhibitors only hv peripheral side effects

A

these drugs cannot enter brain

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70
Q

side effects of dopa decarboxylase inhibitors

A

dyskinesias (facial twitching, head bobbing)
vitamine deficiencies
peripheral monoamine depletion

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71
Q

why carbidopa (dopa decarboxylase inhibitor) is rarely administered alone

A

there will be no antiparkinsonian effect

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72
Q

examples of dopamine receptor agonists

A

rotigotine
ropinorole

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73
Q

target of dopamine receptor agonists

A

dopamine receptors (D2/D3 receptors esp in parkinson’s)

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74
Q

mechanism of dopamine receptor agonist

A

Dopamine receptor agonists bind to post-synaptic dopamine receptors (i.e. independently of dopaminergic neurone activation).

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75
Q

side effects of dopamine receptor agonists

A

Nausea and vomiting
Dizziness
Headache
Gastrointestinal discomfort
Somnolence
Hallucinations
Dyskinesias

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76
Q

examples of lcoal anaethetics

A

lidocaine

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77
Q

target site of local anaethetics

A

voltage gated na+ channels

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78
Q

mechanism of local anaesthetics

A

Uncharged form of local anaesthetics diffuse through the neurone to bind to the sodium channel from the inside.
This locks them in the open state and prevents nerve depolarisation.

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79
Q

side effects of local anaethetics

A

mild: redness, swelling at site of injection, numbness
severe toxicity: fear, anxiety, anaphylaxis

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80
Q

where will lidocaine’s efficacy be reduced

A

sites of inflammation

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81
Q

is pH higher or lower in site of inflammation

A

lower

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82
Q

what happen to lidocaine in site of inflammation

A

pH is lower at these sites, so basic lidocaine exists in a more polarised (charged) state so less can diffuse across neurones.

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83
Q

what is lidocaine for another disease

A

Lidocaine is also classified as a class 1b anti-arrythmic – slows conduction in the heart due to decreasing permeability of sodium channel to sodium

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84
Q

how is dopamine agonsist differ from levodopa

A

less potent than carbidopa-levodopa

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85
Q

what are off effects when treating parkinson’s

A

the fewer nigrostriatal dopaminergic neurones present, the less neurones present to store dopamine and maintain tonic activation

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86
Q

what drug classes are to treat depression (5)

A

Sertraline
Citalopram
fluoxetine
venlafaxine
mirtazapine

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87
Q

drug classes to treat parkinson’s (4)

A

dopamine precursors
dopa decarboxylase inhibitors
dopamine receptor agonists
local anaethetics

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88
Q

drug target for sertraline

A

serotonin transporter

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89
Q

mechanism of sertraline

A

inhibition of serotonin reuptake
accumulation of serotonin in CNS to regulate mood, personality, wakefulness

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90
Q

side effects of sertraline

A

GI (nausea, diarrhoea) sexual dysfunction, anxiety, insomnia

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91
Q

sertraline cause mild inhibition in what

A

dopamine transporter

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92
Q

drug target of citalopram

A

serotonin transporter

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93
Q

main action of citalopram

A

inhibit serotonin reuptake
accumulation of serotonin in CNS to regulate mood, personality, wakefulness

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94
Q

side effects of citalopram

A

GI (nausea, diarrhoea)
sexual dysfunction, anxiety, insomnia
prolong QT interval

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95
Q

citalopram is mild antagonist of what

A

muscarinic and histamine receptors

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96
Q

what is sertraline partial inhibiting

A

CYP2D6 at high dose

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97
Q

what is citalopram metabolised by

A

CYP2C19

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98
Q

drug target of fluoxetine

A

serotonin transporter

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99
Q

main action of fluoxetine

A

inhibit serotonin reuptake
accumulation of serotonin in CNS to regulate mood, personality, wakefulness

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100
Q

side effects of fluoxetine

A

GI (nausea, diarrhoea)
sexual dysfunction, anxiety, insomnia

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101
Q

fluoxetine is mild antagonism of what 2 receptor

A

5HT2A
5HT2C

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102
Q

drug target of venlafaxine (2)

A

serotonin and noradrenaline receptor

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103
Q

mechanism of venlafaxine

A

inhibit serotonin and noradrenaline reuptake

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104
Q

does venlafaxine inhibit serotonin or noradrenaline better

A

serotonin

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105
Q

role of noradrenaline in CNS

A

regulate emotions and cognition

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106
Q

side effects of venlafaxine

A

GI (nausea, diarrhoea)
sexual dysfunction
anxiety
insomnia
hypertension (at higher dose)

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107
Q

when administer fluoxetine, which drug has to be used with caution

A

warfarin (anticoagulant)
increase GI bleeding

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108
Q

drug target of mirtazapine (2)

A

Histamine (H1) receptor
alpha-2 receptor
5-HT2 receptor
5-HT3 receptor

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109
Q

main action of mirtazapine

A

increase release of serotonin and nordrenaline

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110
Q

mechanism of mirtazapine

A
  1. antagonises central presynaptic alpha-2-adrenergic receptors
  2. increase release of serotonin and noradrenaline
  3. antagonises central 5HT2 receptors which leave 5HT1 receptors unopposed causing anti-depressant effects
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111
Q

side effects of mirtazapine

A

weight gain
sedation
sexual dysfunction (low probability)
may exacerbate REM sleep behavior disorder

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112
Q

what are the 3 common SSRI

A

citalopram
sertraline
fluoxetine

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113
Q

mechanism of SSRI

A

target 5HT receptors in presynaptic knob
block 5HT receptors
reduce reuptake of serotonin
increase serotonin in synapse

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114
Q

Why do we slowly cut off sertraline first before starting the new anti-depressant?

A

Caution is required when switching from one antidepressant to another due to the risk of drug interactions, serotonin syndrome, withdrawal symptoms, or relapse.
Washout required before starting new drug

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115
Q

how does mirtazapine affect sleep

A

Mirtazapine modestly suppressREMsleep whilst still having a beneficial impact on sleep continuity and duration due to its anti-histaminergic effects.

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116
Q

drugs to treat Hypertension (4)

A

ACEi
calcium channel blockers
Thiazide / thiazide - like diuretics
angiotensin receptor blockers

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117
Q

drug target of ACEi

A

ACE

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4
5
Perfectly
118
Q

mechanism of ACEi

A

Inhibit the angiotensin converting
enzyme.
Prevent the conversion of
angiotensin I to angiotensin II
by ACE.

119
Q

examples of ACEi

A

ramipril
lisinopril
perindopril

120
Q

side effects of ACEi

A

cough
hypotension
hyperkalaemia
foetal injury (so need avoid in pregnant women)
renal failure

121
Q

why most ACEi need hepatic activation

A

mostly are pro drugs

122
Q

what has to be regularly monitored when prescribing ACEi (2)

A

eGFR
serum potassium

123
Q

examples of calcium channel blockers (2)

A

amlodipine
felodipine

124
Q

target of calcium channel blockers to treat HTN

A

L-type calcium channel

125
Q

where do calcium channel blockers block the channel at

A

vascular smooth muscle

126
Q

mechanism of calcium channel blocker

A

Block L-type calcium channels on vascular smooth muscle.
decrease in calcium influx, with downstream inhibition of myosin light chain kinase and prevention of cross-bridge formation. The resultant vasodilation reduces peripheral resistance.

127
Q

side effect of calcium channel blocker (4)

A

ankle oedema
constipation
palpitations
flushing/headaches

128
Q

which type of calcium channel blocker has a higher degree of vascular activity

A

Dihydropyridine

129
Q

examples of thiazide

A

bendro-flumethiazide

130
Q

example of thiazide like diuretic

A

indapamide

131
Q

target of thiazide / thiazide like diuretics

A

sodium/chloride cotransporter

132
Q

mechanism of thiazide

A

block Na+/Cl- co transporter in early DCT
reduce Na+ and Cl- reabsorption
increase osmolarity of tubular fluid
reduce osmotic gradient for water reabsorption in collecting duct

133
Q

side effects of thiazide

A

hypokalaemia
hyponatremia
metabolic alkalosis (increased H+ excretion)
hypercalcemia
hyperglycaemia
hyperuricemia

134
Q

how long does Thiazide and thiazide-like diuretics lose their diuretic effects

A

within 1-2 weeks of treatment.

135
Q

target of angiotensin receptor blocker

A

angiotensin receptor

136
Q

examples of angiotensin receptor blockers

A

losartan
irbesartan
candesartan

137
Q

mechanism of angiotensin receptor blockers

A

non competitive antagonists at angiotensin I receptor
on kidney and on vasculature

138
Q

side effects of angiotensin receptor blockers

A

hypotension
hyperkalaemia
foetal injury (avoid in pregnant women)
renal failure (in pt with renal artery stenosis)

139
Q

as Losartan and candesartan are pro-drugs what do they require

A

They require hepatic activation to generate the active metabolites required for therapeutic effects.

140
Q

what do we use to measure how the ability of body to eliminate of drug

141
Q

what is elimination half-life

A

time required for concentration of a drug to decrease to half of its starting dose in body

142
Q

what is time to peak plasma level:

A

time required for a drug to reach peak conc in plasma
faster the absorption rate, lower the time to peak plasma level

143
Q

does ACEi cause vasodilation or constriction

A

vasodilation

144
Q

does ACEi cause aldosterone secretion

145
Q

does ACEi cause salt and water secretion or retention in kidney

146
Q

which group of patient use angiotensin 2 receptor blocker instead of ACEi

A

african or caribbean descent

147
Q

Why might ACE inhibitors have a negative effect on eGFR

A

ACE inhibitors can dilate efferent arterioles, which reduces intraglomerular pressure and potentially decreases the filtration rate in the kidneys.

148
Q

Why might ACE inhibitors cause increase in serum potassium level

A

Normally, angiotensin II acts on the adrenal glands to stimulate aldosterone secretion, which promotes potassium excretion in the kidneys. ACE inhibitors block the production of angiotensin II, reducing aldosterone secretion and thereby decreasing potassium excretion.

149
Q

effect of thiazide like diuretics

A

reduced blood volume
reduce venous return
reduce cardiac output

150
Q

how to diuretic travel from blood to access sodium chloride transporters and inhibit them

A

from blood, to basolateral side, then to apical side of DCT facing the lumen

151
Q

does thiazide lead to hyper or hypokalaemia

A

hypokalaemia

152
Q

how thiazide cause hypokalaemia

A

inhibit Na+ from reabsorbed from the DCT
more sodium reaches the collecting duct, the epithelial sodium channels (ENaC) in principal cells reabsorb more sodium.
sodium enters the principal cells through ENaC, the electrical gradient favors potassium secretion into the urine via potassium channel

153
Q

what activates raas system

A

there is a drop in blood pressure (reduced blood volume)
to increase water and electrolyte reabsorption in the kidney

154
Q

what are the drugs to treat asthma (5)

A

salbutamol
fluticasone
mometasone
budesonide
montelukast

155
Q

drug target for salbutamol

A

beta 2 adrenergic receptor

156
Q

main target of salbutamol

A

prevents smooth muscle contraction

157
Q

mechanism of salbutamol

A

Agonist at the β2 receptor on airway smooth muscle cells
Activation reduces Ca2+ entry
this prevents smooth muscle contraction.

158
Q

side effects of salbutamol

A

palpitations
agitation
tachycardia
arrythmias
hypokalaemia

159
Q

type of drug of salbutamol

A

beta agonist

160
Q

is salbutamol long or shor acting beta agonist

A

short acting beta agonist (SABA)

161
Q

can salbutamol be administered with corticosteroids

162
Q

why salbutamol cannot be administered with corticosteroids

A

will exacerbate hypokalaemia and have cardiac effect due to non absolute selectivity in beta2 agonist

163
Q

drug target for fluticasone

A

glucocorticoid receptor

164
Q

mechanism of fluticasone

A

directly decrease inflammatory cells eg eosinophils, dendritic cells, macrophages, mast cells, monocytes
hence reduce number of cytokines they produce

165
Q

main target of fluticasone

A

anti-inflammatory

166
Q

local side effects of fluticasone

A

sore thora
hoarse voice
opportunistic oral infections

167
Q

systemic side effects of fluticasone

A

growth retardation in children
hyperglycaemia
reduced Bone mineral density
immunosuppression
effects on mood

168
Q

why administer fluticasone, budesonide and mometasone through pulmonary vasculature instead of oral

A

oral bioavailbility only <1%

169
Q

drug target of mometasone

A

glucocorticoid receptor

170
Q

mechanism of mometasone

A

directly decrease inflammatory cells eg eosinophils, dendritic cells, macrophages, mast cells, monocytes
hence reduce number of cytokines they produce

171
Q

local side effects of mometasone

A

sore thora
hoarse voice
opportunistic oral infections

172
Q

systemic side effects of mometasone

A

growth retardation in children
hyperglycaemia
reduced Bone mineral density
immunosuppression
effects on mood

173
Q

drug target of budesonide

A

glucocorticoid receptor

174
Q

mechanism of budesonide

A

directly decrease inflammatory cells eg eosinophils, dendritic cells, macrophages, mast cells, monocytes
hence reduce number of cytokines they produce

175
Q

local side effects of budesonide

A

sore thora
hoarse voice
opportunistic oral infections

176
Q

systemic side effects of budesomide

A

growth retardation in children
hyperglycaemia
reduced Bone mineral density
immunosuppression
effects on mood

177
Q

montelukast drug target

A

CysLT1 leukotriene receptor

178
Q

mechanism of montelukast

A

Antagonism of CysLT1 leukotriene receptor on eosinophils, mast cells and airway smooth muscle cells decreases eosinophil migration, broncho-constriction and inflammation induced oedema

179
Q

key goal of montelukast

A

inhibit broncho-constriction

180
Q

side effects of montelukast

A

diarrhoea
fever
headaches
N+V
mood changes
anaphylaxis

181
Q

when shd Montelukast be administered before initiate exercise

A

at least 2 hrs before

182
Q

can we diagnose asthma in children under 5yo

183
Q

B2 agonist mechanism to treat asthma

A

bronchodilators.
bind to receptors in your lungs. This relaxes the muscles in your airways, allowing them to open up.

184
Q

Why nebulizer was the best method for delivering the salbutamol in the emergency situation?

A

can deliver many drug combinations
minimal patient cooperation required
all ages
concentration and dose can be modified
normal breathing pattern

185
Q

why only small amount of inhaled drugs can penetrate deep enough to lung, where are the others (5)

A
  1. exhaled
  2. absorption from lungs
  3. mucociliary clearance
  4. oral swallowed portion
  5. absorbed across mucous membrane in oral cavity and pharynx
186
Q

how viral infection/ pollutants/ allergens exacerbates asthma conditions

A

they trigger IL-5, trigger IgE-mediated immune responses, eosinophil maturation, migration, recruitment leading to histamine release, airway inflammation, and bronchoconstriction.

187
Q

Like salbutamol, a significant proportion of inhaled fluticasone is actually swallowed. Despite this, the oral bioavailability (i.e. the proportion of drug that reaches the plasma VIA the gastrointestinal tract) is less than 1%. Why is this the case?

A

first pass inactivation (liver metabolize and inactivate/eliminate the drug before it reaches the systemic circulation)

188
Q

which enzyme does NSAIDs block

A

cyclooxygenase (COX)

189
Q

why is montelukast particularly useful for NSAID (Non-steroidal anti-inflammatory drug)-induced asthma?

A

NSAIDs inhibit COX pathway, so arachidonic acid cannot convert to prostaglandin H2.
Arachidonic acid is redirected to lipoxigenase pathway to increase leukotriene synthesis, which trigger triggering severe bronchospasm, airway inflammation, and nasal congestion
as montelukast targets CysLT1 receptor,Montelukast competitively blocks the binding of leukotrienes to the CysLT1 receptor, reducing their effects eg bronchoconstriction and inflammation

190
Q

how leukotrienes contribute to asthma symptoms

A

leukotrienes cause bronchoconstriction, airway inflammation, mucus secretion, and increased vascular permeability

191
Q

drugs to treat GORD or peptic ulcer disease (4)

A

NSAIDS
PPIs
Histamine (H2) receptor antagonists
paracetamol

192
Q

examples of NSAID

A

ibuprofen, naproxen, diclofenac

193
Q

drug target of NSAIDs

A

Cyclo-oxygenase enzyme (COX)

194
Q

main goal of NSAIDs

A

anti-inflammatory

195
Q

mechanism of NSAIDs

A

NSAIDS inhibit the COX enzyme, which is the rate-limiting step for the production of all prostaglandins & thromboxane from the arachidonic acid.
Inhibit prostaglandin pathway (which triggers inflammation) and go along with leukotriene pathway

196
Q

side effects of NSAIDS

A

Common: gastric irritation, ulceration and bleeding and, in extreme cases, perforation; reduced creatinine clearance and possible nephritis; and bronchoconstriction in susceptible individuals (contraindicated in asthma). Skin rashes & other allergies, dizziness, tinnitus.
Adverse cardiovascular effects (hypertension, stroke, MI) may occur following prolonged use or in patients with pre-existing CV risk.
Prolonged analgesic abuse over a period of years is associated with chronic renal failure.
Aspirin has been linked with a rare but serious post-viral encephalitis (Reye’s syndrome) in children.

197
Q

main function of NSAIDs

A
  1. analgesics
  2. antipyretics (reduce fever)
  3. anti-inflammatory
  4. anti-aggregatory (inhibit platelet aggregation for stroke/MI pt)
198
Q

PPIs example

A

omeprazole
lansoprazole

199
Q

drug target of PPIs

A

H+/K+ ATPase (‘proton pump’)

200
Q

main goal of PPIs

A

inhibit basal and stimulate gastric acid secretion

201
Q

mechanism of PPIs

A

Irreversible inhibitors of H+/K+ ATPase in gastric parietal cells.
Proton pump inhibitors inhibit basal and stimulated gastric acid secretion by >90%.

202
Q

are PPIs strong or weak bases

203
Q

where do PPIs accumulate in human

A

acid environment of canaliculi of parietal cells

204
Q

why PPIs accumulate in acidic environment in parietal cells canaliculi

A

prolongs their duration of action
(omeprazole plasma half-life approx. 1 h but single daily dose affects acid secretion for 2-3 days).

205
Q

side effects of PPIs

A

Unwanted effects are uncommon but may include headache, diarrhoea, bloating, abdominal pain & rashes.

206
Q

which cancer may PPIs mask the symptoms of

A

gastric cancer

207
Q

method of administration of PPI

208
Q

why PPIs given as capsules

A

degrade rapidly in oral so administered as capsules containing enteric-coated granules

209
Q

drug target of Histamine (H2) receptor antagonsits

A

Histamine H2 receptors

210
Q

examples of Histamine H2 receptors
antagonsits

A

ranitidine

211
Q

main goal of Histamine H2 receptors
antagonists

A

inhibit gastric acid secretion

212
Q

mechanism of Histamine H2 receptors
antagonists

A

H2 antagonists are competitive antagonists of H2 histamine receptors (structural analogues of histamine). They inhibit the stimulatory action of histamine released from enterochromaffin-like (ECL) cells on the gastric parietal cells.
hence inhibit gastric acid secretion by approximately 60%.

213
Q

side effects of Histamine (H2) receptor antagonists

A

Incidence of side-effects is low. Diarrhoea, dizziness, muscle pains & transient rashes have been reported.

214
Q

which Histamine receptor antagonsits inhibit cytochrome P450

A

cimetidine
will retard metabolism and potentiate effects of other drugs eg oral anticoagulants and TCA

215
Q

example of paracetamol

A

acetaminophen

216
Q

drug target of paracetamol

A

unclear

5HT3 receptors/Cannabinoid reuptake proteins/Peroxidase

217
Q

mechanism of paracetamol

A

Still not totally clear.

At peripheral sites, may inhibit a peroxidase enzyme which is involved in the conversion of arachidonic acid to prostaglandins (1st step in this pathway involves the enzyme, cyclooxygenase). The ability of paracetamol to inhibit peroxidase can be blocked if excessive levels of peroxide build up (as is commonly seen in inflammation)

Activation of descending serotonergic pathways possibly via 5HT3 receptor activation.

Inhibits reuptake of endogenous endocannabinoids, which would increase activation of cannabinoid receptors - this may contribute to activation of descending pathways.

218
Q

side effects of paracetamol

A

Relatively safe drug with few common side effects.

OVERDOSE:
Liver damage and less frequently renal damage.

Nausea and vomiting early features of poisoning (settle in 24h).

Onset of right subcostal pain after 24hindicates hepatic necrosis.

219
Q

main function of paracetamol

A

analgesic
anti-pyretic

220
Q

is paracetamol anti-inflammatory

221
Q

is naproxen (NSAIDs) selective

A

no, inhibit both COX 1 and COX 2

222
Q

what are COX 1 and COX 2 pathway for respectively

A

COX-1: platelet function
COX-2: pain relief and anti-pyretics

223
Q

do COX 2 directly cause pain

A

no
they sensitise peripheral nociceptors mediators (eg bradykinin and histamine) which cause pain

224
Q

what is the unintended effect of naproxen

A

target to inhibit COX-2 but inhibits COX-1 as well, causing side effects

225
Q

where is side effects of naproxen to treat joint pain

A

gastric mucosal cells that cause stomach injury

226
Q

why naproxen cause gastric injury side effects

A

inhibit Prostaglandin production and hence inhibit prostaglandin mediated protection of gastric mucosa

227
Q

how prostaglandin protect gastric mucosal cells from acid (3)

A

increase bicarbonate release
increase mucus protection
increase blood flow

228
Q

why cannot take both oral naproxen and topical diclofenac together

A

increase risk risk of stomach injury

229
Q

what to do if administered both oral naproxen and topical diclofenac together accidentally

A

stop gel
switch to ibuprofen
stop NSAIDs completely

230
Q

for pt with OA and RA, what should administer with naproxen

A

PPIs with NSAIDs

231
Q

for pt with low back pain, psoriatic arthritis, axial spondyloarthritis, what to administer with naproxen

A

gastroprotection with NSAIDs

232
Q

for pt with high risk of GI side effects, which NSAID to administer

A

COX-2 selective NSAID
co prescribe PPI

233
Q

for pt with moderate risk of GI side effects, which NSAID to administer

A

COX-2 inhibitor
or NSAID + PPI

234
Q

for pt with low risk of GI side effects, which NSAID to administer

A

non selective NSAID

235
Q

why need coprescribe NSAID + PPI

A

NSAID leave stomach wall exposed to effect of acid which causes pain
PPI help reduce acid production

236
Q

why in osteoporosis/OA patient, GP will prescribe Histamine receptor antagonist instead of PPI

A

PPI increase risk of fracture (cause change in pH and reduce calcium absorption available for bone, reduce bone turnover, adverse to bone)

237
Q

drug target of statin

A

Hydroxymethylglutaryl-CoA (HMG-CoA) reductase

238
Q

main goal of statin

A

reduce cholesterol level

239
Q

mechanism of statin

A

selective, competitive inhibitor of hydroxymethylglutaryl-CoA (HMG-CoA) reductase, which is the enzyme responsible for converting HMG-CoA to mevalonate in the cholesterol synthesis pathway
By reducing hepatic cholesterol synthesis, an upregulation of LDL-receptors and increased hepatic uptake of LDL-cholesterol from the circulation occurs.

240
Q

side effects of statin

A

muscle toxicity
constipation
diarrhoea
GI symptoms

241
Q

what should be regularly checked for using statin

A

hyperkalaemia
acute renal failure

242
Q

drug target of aspirin

A

Cyclo-oxygenase

243
Q

mechanism of aspirin

A

Irreversible inactivation of COX enzyme. Prevents oxidation of arachidonic acid to produce prostaglandins.
Reduction of thromboxane A2 in platelets reduces aggregation.
Reduction of PGE2 (i) at sensory pain neurones reduces pain and sensation and (ii) in the brain decreases fever
(iii) antiplatelet

244
Q

main goal of aspirin

A

pain relief
anti-inflammatory

245
Q

side effects of aspirin

A

dyspepsia
haemorrhage

246
Q

what does aspirin need to administer in patients with peptic ulcer

247
Q

drug target of trimethoprim

A

Dihydrofolate reductase

248
Q

mechanism of trimethoprim

A

Direct competitor of the enzyme dihydrofolate reductase. Inhibits the reduction of dihydrofolic cid to tetrahydrofolic acid (active form) – a necessary component for synthesising purines required for DNA and protein production.

249
Q

main goal of Trimethoprim

A

antibiotic
manage UTI in CKD

250
Q

side effects of Trimethoprim (2)

A

diarrhoea
skin infection

251
Q

what is Trimethoprim co-administered with

A

sulfamethoxazole (co-trimoxazole)

252
Q

why Trimethoprim need to administer with sulfamethoxazole

A

they block two steps in bacterial biosynthesis of essential nucleic acids and proteins.

treat a variety of infections of the urinary tract, respiratory system, and gastrointestinal tract

253
Q

drug target of gentamicin

A

30s ribosomal subunit

254
Q

mechanism of gentamicin

A

target gram negative cell membrane
Binds to the bacterial 30s ribosomal subunit disturbing the translation of mRNA leading to the formation of dysfunctional proteins.

255
Q

main goal of gentamicin

A

antibiotic

256
Q

side effects of gentamicin

A

Ototoxicity (hearing/balance problems)
nephrotoxicity

257
Q

is gentamicin administered orally or IV

258
Q

which disease are gentamicin used to treat in hospital

A

More likely to be administered intravenously (in hospital) for endocarditis, septicaemia, meningitis, pneumonia or surgical prophylaxis.

259
Q

what is proteinuria a marker of

A

glomerular dysfunction

260
Q

drugs to treat proteinuria

A

ACEi
SGLT-2 inhibitor

261
Q

how trimethoprim affects creatinine secretion

A

inhibits active secretion of creatinine making GFR equation invalid

262
Q

how ibuprofen affects prostaglandin

A

inhibits PG synthesis, reduce PG-induced vasodilation and hence reduce renal blood flow, damage kidney

263
Q

how ACEi affects perfusion in glomerulus

A

reduces perfusion pressure in glomerulus

264
Q

what to consider when prescribe drugs for a patient with reduced renal function

A
  1. will drug damage kidney (eg ibuprofen)
  2. is the drug elimated by kidney (we dun wna let drug accumulate in blood) (eg metformin, morphine)
265
Q

drug to treat pain (2)

A

paracetamol
opioids

266
Q

drug target of paracetamol

A

Unclear.
5HT3 receptors/Cannabinoid reuptake proteins/Peroxidase

267
Q

mechanism of paracetamol

A

Still not totally clear.

At peripheral sites, may inhibit a peroxidase enzyme which is involved in the conversion of arachidonic acid to prostaglandins (1st step in this pathway involves the enzyme, COX). The ability of paracetamol to inhibit peroxidase can be blocked if excessive levels of peroxide build up (as is commonly seen in inflammation)

Activation of descending serotonergic pathways possibly via 5HT3 receptor activation.

Inhibits reuptake of endogenous endocannabinoids, which would increase activation of cannabinoid receptors - this may contribute to activation of descending pathways.

268
Q

side effects of paracetamol

A

Relatively safe drug with few common side effects.

OVERDOSE:
Liver damage and less frequently renal damage.

Nausea and vomiting early features of poisoning (settle in 24h).
Onset of right subcostal pain after 24h indicates hepatic necrosis.

269
Q

drug target of opioids

A

opioid receptor

270
Q

examples of opioids (both weak and strong)

A

Weak – codeine, tramadol
Strong – morphine, fentanyl, (heroin)

271
Q

mechanism of opioids

A

depressant effect
on cellular activity
Multiple sites within pain pathway, where activation of the opioid receptor leads to decreased perception or increased tolerance to pain.
Anti-tussive (cough suppressants) effect due to decreased activation of afferent nerves relaying cough stimulus from airways to brain

272
Q

side effects of opioids

A

Mild – nausea & vomiting (increase activity in chemoreceptor trigger zone) and constipation (opioid receptors in GIT can reduce gut motility)

OVERDOSE - respiratory depression (direct and indirect inhibition of respiratory control centre.)

273
Q

drug target of co-amoxiclav

A

Amoxicillin = penicillin binding proteins
Clavulanate = beta lactamase

274
Q

mechanism of co-amoxiclav

A

amoxicillin: binds to bacterial penicillin binding proteins to prevent transpeptidation
clavulanate: inhibit beta lactamase (Beta lactamase is a bacterial enzyme that degrades beta lactam Abx and confer resistance to these Abx)

275
Q

side effects of co-amoxiclav

A

Amoxicillin is well tolerated. Most common side effects are nausea and diarrhoea.

276
Q

is amoxicillin broad or narrow spectrum Abx and bactericidal or bacteriostatic

A

bactericidal
broad spectrum

277
Q

drug target of lactulose

A

no drug target

278
Q

mechanism of lactulose

A

Lactulose is a non-absorbable disaccharide.
It reaches the large bowel unchanged. This causes water retention via osmosis and an easier to pass stool. It can also be metabolised by colonic bacteria. The colonic metabolism of sugars has an additional laxative effect.

279
Q

side effects of lactulose

A

Abdominal pain, diarrhoea, flatulence, nausea.

280
Q

how long does lactulose take to have effect

A

begins working in 8-12 hrs but may take up to 2 days to improve constipation

281
Q

main goal of lactulose

A

improve constipation

282
Q

difference in effects between NSAIDs and paracetamol

A

NSAIDs: anti-inflammatory, anti-pyretic, analgesia
paracetamol: anti-pyretic, analgesia

283
Q

compare and contrast in terms of mechanism of paracetamol and NSAIDS

A

both inhibit production of prostaglandins from arachidonic acid
difference: NSAIDs inhibits COX(first step); paracetamol inhibits peroxidase activity (2nd step)

284
Q

surgical treatment for acute appendicitis

A

surgery: open laparoscopy and appendectomy

285
Q

medical treatment for appendicitis

A

analgesia
antibiotics
hydration (IV crstalloids)

286
Q

in periaqueductal gray (PAG), how GABAergic neurone make us feel pain

A

GABA is inhibitory, it inhibits descending pain-inhibitory neurons

287
Q

how opioid has analgesia effetcs

A

opioids inhibit adenyl cyclase and calcium channels, open K+ channel for hyperpolarisation of GABAergic neurones, reduce GABA neurones cause less inhibition of descending pain-inhibitory pathway

288
Q

why opioid may cause shallower breathing

A

they act on respiratory control centre on brain, cause reduce stimulus to lungs and reduce respiratory rate –> hypoxia -> suffocate/die

289
Q

is naloxone opioid receptor agonist or antagonist

A

antagonist

290
Q

pro-drug of morphine

291
Q

what will codeine metabolised into (2)

A

norcodeine (inactove metabolite) and morphine (active)

292
Q

which enzyme helps to metabolise codeine to norcodeine and morphine respectively

A

CYP3A4 for fast metabolism to norcodeine
CYP2A6 for slow metabolism to morphine

BRS Y2 (10 decks)

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