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2A content- Sameera > 3. PHARMACOLOGY > Flashcards

3. PHARMACOLOGY Flashcards

1
Q

what r the two main routes of administration

A

enteral and parenteral

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2
Q

define enteral administration

A

through gastro-intestinal tract

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3
Q

define parenteral administration

A

not through GI tract

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4
Q

two examples of enteral administrations

A

oral and rectal suppositary

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5
Q

5 examples of parenteral administration

A

subcutaneous, intramuscularr, intravenous, sublingual, inhalers

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6
Q

what routes of administration have a systemic effect

A

enteral and parenteral

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7
Q

what two administrations have a local effect

A

transdermal (patches) and topical creams

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8
Q

define agonist using the terms affinity, efficacy and what does it do to the receptor

A

full affinity
full efficacy
ligand that increases activation of the receptor

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9
Q

define antagonist using the terms affinity, efficacy and what does it do to the receptor

A

full affinity
zero efficacy
ligand that decreases activation of the receptor

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10
Q

define inverse agonist and compare it to an antagonist

A

binds to receptor and always has an opposite response to agonist
antagonist= can have a neutral response (not necessarily opposite)

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11
Q

define affinity

A

how well a ligand binds to a receptor

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12
Q

define efficacy (in terms of ligand and receptor and in terms of drug)

A

how successful a ligand ACTIVATES its receptor
maximum effect a drug can have on the body

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13
Q

compare graph shape for log conc and conc

A

log conc= sigmoidal, conc= linear

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14
Q

what is EC50

A

value of 50% response on log conc graph

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15
Q

what is Emax

A

maximal efficacy

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16
Q

define potency

A

relative strength of the drug

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17
Q

if a drug is more potent what happens to its dose

A

more potent drugs require lower doses for a response

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18
Q

define selectivity and give an example

A

acts on a subtype of a target
selective beta blocker bisoprolol only acts on B1 heart receptors (not B2 in lungs)

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19
Q

define specificity and what does low specificity cause

A

receptors ability to response to a single ligand
low= side effects

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20
Q

what 4 things can affect drug response

A

efficacy, affinity, number of receptors, signal amplification

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21
Q

where do competitive inhibitors bind and how do they affect affinity and efficacy

A

binds at the active site
decreases efficacy reversibly
affinity is unchanged

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22
Q

where do non-competitive inhibitors bind and how do they affect affinity and efficacy

A

binds away from the active site which changes its shape
decreases efficacy irreversible
affinity is reduced

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23
Q

explain the Dose/response curve for competitive inhibitors (shift direction and use affinity, potency and efficacy to describe the changes)

A

curve shifts right
drug has less affinity and less potency and less efficacy

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24
Q

explain the Dose/response curve for non-competitive inhibitors (shift direction and use affinity, potency and efficacy to describe the changes)

A

curve shifts right and down
drug has less affinity, less potency and less efficacy

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25
Q

what is bioavailability and what route has 100% of this

A

how much drug is uptake systemically for effect
IV

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26
Q

what is therapeutic range and what does a narrow range mean

A

upper and lower bounds of safe doses of a drug
the narrower the range, the more care is required in dispensing the drug (more likely to over or underdose)

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27
Q

what are the 2 names type of receptors in cholinergic pharmacology and what type of receptors r they

A

nicotinic= ion channel
muscarinic= G-protein couples

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28
Q

what r the 4 drug targets

A

receptors
enzymes
ion channels
transporters

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29
Q

give an example of a G-protein coupled receptor and how it works

A

beta adrenoreceptor
muscarinic receptors within proteins produce 2nd messenger cAMP which produce further reactions

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30
Q

what can an imbalance of NTM/ receptors lead to and give an example

A

pathology
decreased dopamine causes Parkinson’s

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31
Q

give an example of a ligand gated receptor and how it works

A

nicotinic ACh
binding opens pores to allow cations to move into cells

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32
Q

give an example of a drug that targets receptors (2)

A

beta blockers, angiotensin receptor blockers

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33
Q

explain the selectivity of aspirin and celecoxib

A

non selective as it acts on COX 1 and 2, celecoxib is more selective as it only acts on COX 2

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34
Q

what is another example of a drug that targets enzymes

A

ACE inhibitor

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35
Q

give two examples of NSAIDs
explain how NSAIDs work (ending with what 3 symptoms it reduces) and what type of inhibition is this

A

NSAIDs eg aspirin/ ibuprofen: inhibit COX 1 to inhibit breakdown of arachnoid acid to prostaglandin H2 which acts as a painkiller and reduces fever/ inflammation
NSAIDs= competitive inhibition

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36
Q

give an example of a drug that targets ion channels

A

calcium channel blocker

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37
Q

how does lidocaine target ion channel

A

local anaesthesia eg lidocaine
blocks Na+ channels so no action potential is generated for pain transmission

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38
Q

how do calcium channel blockers target ion channels, give an example and what it is prescribed for what is their overall effect

A

calcium channel blocker eg amlodipine for HPT
blocks voltage Ca2+ channels in muscle to prevent influx of calcium ions and an action potential, stopping muscle vasoconstriction

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39
Q

what drug targets transporters, give an example and how does it work

A

proton pump inhibitors eg lansoprazole
inhibit parietal cells H+/K+ATPase pump to decrease stomach acid

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40
Q

define pharmacodynamics

A

the effect of the drug on the body

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41
Q

define pharmacokinetics

A

the effect of the body on the drug

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42
Q

what r the three aspects of Pharmacodynamics

A

affinity, potency and efficacy

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43
Q

explain ADME in brief detail

A

absorption: route of entry, bioavailability of drug
distribution: based on chemical properties eg hydrophilicity can it cross barriers eg BBB
metabolism: via kidney or phase 1&2 in liver
excretion: as urine/ faeces

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44
Q

what r the 4 aspects of pharmacokinetics

A

absorption, distribution, metabolism, excretion (ADME)

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45
Q

name 4 factors that affect distribution in pharmacokinetics

A

affected by blood flow, molecular weight, how lipophillic/phobic a drug is, natural barriers in body eg BBB

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46
Q

what r the 3 locations of metabolism

A

GI tract, hepatic or renal

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47
Q

what is metabolised in the GI tract and how

A

food
mechanical and physical digestion

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48
Q

what is metabolised in renal metabolism

A

simple, already soluble molecules which r easily to pee out directly

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49
Q

what is metabolised in hepatic metabolism and how

A

complex, hydrophobic molecules
undergo phase 1 and/or phase 2 reactions

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50
Q

what type of reaction is phase 1 metabolism, what is its aim and what enzyme foes it involve

A

non-conjugation
aims to slightly increase hydrophilicity
requires microsomal enzymes eg CYP 450

51
Q

what type of reaction is phase 2 metabolism and what is its aim

A

conjugation
adds functional groups eg glucuronidation to massively increase hydrophilicity

52
Q

what r the three types pf neurotransmission systems

A

parasympathetic, sympathetic and motor

53
Q

is parasymp autonomic or somatic, name the neurotransmitter at post and pre synaptic neurone, name the final receptor

A

autonomic (self-governing)
presynaptic acetylcholine
postsynaptic acetylcholine
muscarinic Ach receptor

54
Q

is symp autonomic or somatic, name the neurotransmitter at post and pre synaptic neurone, name the final receptor

A

autonomic (self-governing)
presynaptic acetylcholine
postsynaptic noradrenaline
Noradrenaline receptor

55
Q

give an example of motor NS, is it somatic or voluntary, what neurotransmitter is involved and name the final receptor

A

skeletal msucle
somatic
Ach post and presynaptic
nicotinic ACh receptor

56
Q

what are the two main receptors in cholinergic pharmacology and where r these usually found

A

nicotinic- usually presynaptic
muscarinic-usually postsynaptic

57
Q

location of M1, M2, M3 receptors and what pharmacology is this

A

M1= brain
M2= heart
M3= lungs
cholinergic

58
Q

name the 5 steps in the cycle of the ACh neurotransmitter lifecycle

A

synthesis of neurotransmitter
storage in vesicles
release into synapse
breakdown
reuptake

59
Q

what 3 drugs can act at the NMJ

A

curare, botulinum toxin, ACh-ase inhibitor

60
Q

what is curare’s action at the NMJ

A

curare: antagonist to nicotinic ACh receptor and prevents ACh from binding so it relaxes muslces

61
Q

what is botulinum toxin’s action at the NMJ

A

binds to presynpatic vesicles and inhibits ACh release= paralysis

62
Q

what is ACh-ase inhibitors action at NMJ and what is this used for

A

causes less breakdown of ACh so increased ACh concentration at NMJ
used in dementia medication

63
Q

what can excessive ACh stimulation cause and what r the symptoms of this

A

cholinergic crisis
salivation, lacrimation, urination, defecation, GI distress, emesis (vomiting)- SLUDGE

64
Q

what is the issue in myasthenia gravis and how does the treatment work

A

disrupted Ach transmission at NMJ
Tx: acetylcholinase inhibitors eg rivastigmine (stops breakdown of acetylcholine)

65
Q

what 4 receptors r involved in adrenergic pharmacology

A

alpha 1&2 receptors and beta 1&2 receptors

66
Q

what do alpha 1 receptors do

A

on vessel sphincters for vasoconstriction
cause bladder constriction
cause pupil dilation

67
Q

what is an example of a alpha 1 blocker, what is it first line med for and what is its mechanism of action

A

alpha 1 blocker= tamsulosin= 1st line medication for benign prostatic hyperplasia
mechanism of action: relaxes bladder neck, allowing easier urine flow

68
Q

where r alpha 2 receptors found and what do they do

A

receptors in brainstem and periphery
inhibit sympathetic activity so they reduce BP

69
Q

where r beta 1 receptors found

A

heart

70
Q

what is the effect of beta 1 receptors agonists and give an example

A

increase inotropy and chronotropy of cardiac contraction
eg dobutamine

71
Q

what is the effect of beta 1 receptors antagonists and give an example

A

decrease inotropy and chronotropy
eg bisoprolol (beta blocker)

72
Q

when r beta blockeres contraindicated

A

asthma

73
Q

where r beta 2 receptors found

A

lungs

74
Q

what do beta 2 receptor agonists cause and give 2 examples

A

bronchodilation of airways
eg SABAs (salbutamol) prescribed for COPD and asthma
eg LABA in asthma

75
Q

give an example of a cardioselective drugs and define this

A

beta blocker drugs that only act on cardiac tissue

76
Q

what types pf hypersensitivity r immediate and delayed

A

1,2,3 r all immediate
4 is delayed

77
Q

explain the ABCDE of adverse drug reactions

A

A- augmented (common/ expected eg ACE-I cough)
B- bizzarre
C- chronic use
D- delayed (type 4 hypersensitivity)
E- end of use (eg opioid withdrawal)

78
Q

what should be done if a patient has an adverse drug reaction

A

report to MHRA using the Yellow Card Scheme

79
Q

differentiate between tolerance and dependance

A

tolerance is physiological craving (body wants it because its receptors have been desensitised to it so thee need a higher dose)
dependance is psychological craving (craving euphoria)

80
Q

examples of opiates (4)

A

morphine, diamorphine (heroin), codeine, pethidine

81
Q

where r opioid receptors found (4)

A

spinal cord, midbrain, GI tract, breathing centre

82
Q

how do opiates work (3)

A
  1. binds to opiate receptors in spinal cord and midbrain
  2. this inhibits release of pain neurotransmitters
  3. this blocks the descending pain transmission
83
Q

when r opiates used (2) and give an example

A

used in chronic sever pain relief eg cancer pain

84
Q

3 main side effects of opiates

A

respiratory depression, constipation and vomiting

85
Q

what is the oral bioavailability of morphine and how does this relate to IV vs oral doses

A

morphine has 50% oral bioavailability (oral dose is twice as much as an IV dose)

86
Q

list potency of three opiates in regard to one another and their dose

A

potency: 5mg diamorphine= 10mg morphine= 100mg pethidine

87
Q

what can opiate overdose cause and what is treatment for this and how is this administered

A

respiratory DEPRESSION
treatment: naloxone by IV

88
Q

what is typically prescribed for severe pain

A

opioid analgesia eg morphine and diamorphine

89
Q

what is typically prescribed for moderate pain

A

tramadol or moderate opiates eg codeine

90
Q

what is typically prescribed for mild pain

A

weak analgesics eg paracetamol NSAIDs (ibuprofen/ naproxen)

91
Q

what are the 4 types of pain

A

acute (nociceptive)
cancer
neuropathic (nerve pain)
chronic non cancer (pain 3+ months eg fibromyalgia)

92
Q

what r the 2 main complications with paracetamol overdose

A

rapidly acute liver failure
shutdown of basic physiological systems eg shock which can lead to death

93
Q

What is the acute ascending pain pathway

A
  1. nociceptors detect pain
  2. impulse through C or A delta fibres to dorsal root ganglion in spinal cord
  3. second order neurone to thalamus via ascending lateral spinothalamic tract
94
Q

what is the acute descending pain pathway

A
  1. cortex to thalamus
    to periaqueductal grey in midbrain
  2. to rostral ventral medulla
  3. signal to spinal cord and activation of the opiate system to suppress pain
95
Q

what are the 4 physiological processes regarding pain

A

transduction
transmission
modulation (excitation or inhibition of pain)
perception

96
Q

explain paracetamol metabolism and what is significant about the 5%

A

undergoes phase 2 hepatic metabolism 95%, phase 1 for 5%
the 5% that undergoes CYP450 metabolism in phase 1 reaction is still hepatotoxic

97
Q

explain paracetamol metabolism in an overdose

A

in cases of overdose, phase 2 is too saturated so paracetamol is shunted down the phase 1 pathway= build up of NAPQI (product of phase 1 metabolism of paracetamol)
this leads to hepatotoxicity and can cause liver failure

98
Q

what are the indications for anticoagulant drugs (5)

A

DVT/ PE (deep vein thrombosis/ pulmonary embolism)
atrial fibrillation
prosthetic valves
bleeding disorders
ischaemic stroke/ MI

99
Q

mechanism of DOACs, 2 examples and what do they stand for

A

Direct acting oral anticoagulants
inhibit factor 10a
eg apixiban, rivaroxaban

100
Q

mechanism of warfarin

A

inhibit 10, 9, 7, 2 (vitamin K dependant factors)

101
Q

mechanism of alteplase

A

fibrinolytic, activates plasmin to digest the fibrin mesh

102
Q

mechanism of antiplatelets and 2 examples

A

inhibits P2Y12 which affects the primary platelet plug
eg clopidogrel and ticagrelor

103
Q

mechanism of LMWPs and what do they stand for

A

inhibit factor 10 and thrombin
Low molecular weight heparins

104
Q

NAID 2 examples

A

eg ibuprofen, naproxen

105
Q

what r NSAIDs prescribed for generally

A

weak analgesics for mild pain

106
Q

mechanism of NSAIDs

A

inhibits arachidonic acid pathway COX1 and COX 2

107
Q

what is COX 1 pathway involved in and what is a side effect of inhibiting COX 1

A

involved in prostaglandin synthesis
side effect is peptic ulcer disease (gastric ulcers) because prostaglandin protects the gastric mucosa

108
Q

what is COX 2 pathway involved in and give an example of a specific COX 2 drug

A

pathway causes inflammation when activated
eg celeoxib

109
Q

how do diuretics work

A

reduce the volume of water reabsorbed in the kidneys

110
Q

what r the three types of diuretic drugs

A

loop diuretic, aldosterone antagonist and thiazide diuretic (LooT AlAn)

111
Q

where do loop diuretics act, what does it inhibit and give an example

A

acts on ascending loop of Henle
inhibits Na-K-Cl co transporter= prevents their uptake= water doesn’t move with them
eg furosemide

112
Q

what r aldosterone antagonists also known as

A

K+ sparing diuretic

113
Q

where do aldosterone antagonist diuretics act, what does it cause and give an example

A

acts on aldosterone receptors of the collecting duct
inhibits reabsorption of sodium and water in distal convoluted tubules which increases sodium excretion and retains potassium
eg spironolactone

114
Q

side effect of spironalactone

A

can cause hyperkalamia

115
Q

where do thiazide diuretics act, what does it do and give two examples

A

acts on distal convoluted tubules
inhibits Na-Cl cotransporter causes less sodium to be absorbed which absorbs less water
eg bendroflumethiazide and indapamide

116
Q

name two side effect of ACE inhibitors and why they occur

A

main side effect= dry cough due to bradykinin accumulation
other side effect= worsens kidney function because it dilates afferent glomerular arteriole

117
Q

action of ACE inhibitor, mechanism of action and 1 example

A

anti-hypertensive by blocking conversion of angiotensin 1 to 2 which prevents aldosterone production eg ramipril

118
Q

action of calcium channel blockers, 2 examples and side effect

A

anti-hypertensive eg amlodipine, verapamil
side effect= ankle swelling (can be mistaken for heart failure)

119
Q

action of proton pump inhibitor and example

A

reduces acidity of GI lumen by reducing acids secretion by irreversibly inhibiting H+/K+ ATPase pump in gastric parietal cells eg lansoprazole

120
Q

side effect of antihistamines and beneficial side effect of antihistamines

A

side effects: older ones can cross the BB and cause sedation
many H1 receipts in the vomitign centres so they can acts as anti-emetics

121
Q

action of antihistamines

A

H1 receptors antagonist
prevent release of histamine from storage granules in mast cells

122
Q

side effect of long term PPI use

A

increase risk of fractures in the elderly

123
Q

Effect of sympathetic NS (7) (think heart, lungs, GI, mouth, bladder, skin, arteries)

A

increased heart rate and cardiac output
vasoconstriction
bronchodilation
reduce GI motility and reduced GI secretions
reduced bladder detrusor activity
increased sweating
reduced salivation

124
Q

Effect of parasympathetic NS (5) (think heart, arteries, lungs, GI, bladder)

A

decreased heart rate and cardiac output
vasodilation
bronchoconstriction
increased digestion
increased bladder detrusor

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