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BDS2 bams > pharmacology > Flashcards

pharmacology Flashcards

1
Q

drug definition

A

external substance that acts on living tissue to produce a measurable change in the fct of that tissue

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2
Q

2 ways drugs work

A

stimulate/interrupt normal body communications
OR
act on non-host organisms to aid body defences

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3
Q

autonomic drugs

A

epinephrine - B agonist
atenolol - B blocker
pilocarpine - cholinergic agonist
atropine - cholinergic blocker

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4
Q

3 components drugs act on

A

receptors
enzymes
ion channels

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5
Q

what do drugs have their effects on?

A

proteins

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6
Q

receptors

A

transmembrane protein

coupled to ion channels, G proteins, enzymes, gene transcription

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7
Q

drug receptor interaction

A

agonist stimulates receptor, G-protein interacts directly with and changes the open probability of the ion channel

agonist stimulates receptor - G-protein activates or inhibits enzyme that gives rise to 2nd messengers

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8
Q

affinity

A

attraction of drug to receptor

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9
Q

occupancy

A

time drug stays stuck to receptor for

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10
Q

efficacy

A

how well combination of drug and receptor works

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11
Q

law of mass action

A

more drugs in vicinity of receptor = likely to get more efficacy

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12
Q

types of drug actions

A

agonists
partial agonists
antagonists

competitive/non-competitive
reversible/irreversible

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13
Q

agonists

A

bind to receptor and produce effect

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14
Q

partial agonists

A

more difficult to produce effect

increased conc might improve efficacy

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15
Q

antagonists

A

binds to receptor but nothing happens

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16
Q

drug phases

A

absorption
clinical effect
metabolism
excretion

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17
Q

routes of administration

A

enteral - oral

parenteral

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18
Q

enteral - oral advantages

A

socially acceptable

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19
Q

enteral - oral disadvantages

A 
slow onset
variable absorption
gastric acid
FPM
also: lipid solubility and ionisation, drug formulation, GI motility, interactions with other substances in gut, GIT disease
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20
Q

parenteral routes of administration

A 
IV
IM
SC
inhalation
intra-osseous
topical
sublingual/buccal
rectal
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21
Q

parenteral advantages

A

predictable plasma levels

no FPM

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22
Q

parenteral disadvantages

A

more severe allergic reactions
access difficulties
drug cost higher

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23
Q

FPM

A

GIT (except sublingual and rectal)
HPV
liver

metabolises - inactivates/activates

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24
Q

abnormal liver fct causes

A

extremes of life
drug interactions
disease

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25
Q

bioavailability

A

proportion of an ingested drug that is available for clinical effect
FREE not bound

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26
Q

what affects bioavailability?

A

dosage form
destruction in gut
poor absorption
FPM

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27
Q

causes of poor absorption

A

molecule size
lipid solubility (easy absorbed)
degree of ionisation (very ionised not as easily absorbed)

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28
Q

3 aspects of drug distribution

A

compartments - dilution
lipid binding - slow release from accumulation
drug binding to plasma proteins

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29
Q

drug distribution - compartments

A

dilution

vascular, tissues, CNS

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30
Q

drug distribution - lipid binding

A

slow release from accumulation

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31
Q

drug distribution - drug binding to plasma proteins

A

bound = inactive = reservoir
interactions by competitive binding
e.g. aspirin higher affinity than Warfarin

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32
Q

excretion

A

renal, liver (bile), lungs, sweat, saliva

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33
Q

what organ can modify drug excretion secretions?

A

kidney

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34
Q

drug metabolism

A

phase 1 - inactivation

phase 2 - conjugation

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35
Q

drug metabolism phase 1

A

inactivation
change shape - doesn’t bind to receptor
oxidation, reduction, hydrolysis

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36
Q

drug metabolism phase 2

A

conjugation

glucuronidation, sulphation, methylation, acetylation, glutathione

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37
Q

where does drug metabolism happen?

A

liver

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38
Q

factors affecting drug metabolism

A

liver/kidney disease
interactions
some drugs increase activity of liver enzymes - increase rate
age - extremes have slower metabolisms and less plasma proteins
genetic factors

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39
Q

pharmacokinetics

A

what body does to drug - drugs don’t distribute evenly

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40
Q

pharmacokinetics - “body compartments”

A

single - behaves as if evenly distributed

2 compartment model - in equilibrium with different tissues in body

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41
Q

pharmacokinetics - more blood flow

A

tissue exposed to bigger doses

eventually - distribution equilibrium

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42
Q

drug clearance

A

removal of a drug from plasma

depends on 1/2 life

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43
Q

plasma half life

A

period of time required for conc/amount of drug in body to be reduced by half

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44
Q

what is the most common type of drug clearance?

A

1st order

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45
Q

1st order clearance

A

elimination/absorption by passive diffusion
drug removal proportional to drug conc
higher conc - moves quicker into urine/bile
curved graph

46
Q

0 order clearance

A

active process - can be saturated by high drug conc
linear graph - straight line
enzyme system
think - ice cream scoop - fixed rate

47
Q

2 examples of 0 order clearance

A

blood-alcohol elimination

paracetamol toxicity

48
Q

drug accumulation

A

how plasma conc build if repeated doses of a drug are given

drug trial - dosing schedule

49
Q

hazards of drug use

A

death - allergy/toxicity of drug

interactions - effect on absorption/metabolism of other essential meds

50
Q

paracetamol

A 
mechanism of action?
anti-pyretic
analgesic
little anti-inflammatory action
few SEs
1g x4 daily
51
Q

LAs mechanism of action

A

1 - membrane expansion - forces pore closed

2 - acts on 2 gates- binds just under halt gate reversibly - stops Na+ getting in

52
Q

esters metabolised in?

A

plasma

53
Q

amides metabolised in?

A

liver

54
Q

pH and LAs

A

pH sensitive in tissues

55
Q

aspirin dose

A

300-600mg up to x4

56
Q

aspirin kinetics

A

rapid absorption from GIT

1st order kinetics - unless overdose - enzyme saturation

57
Q

aspirin mechanism of action

A

inhibits COX 1 prostaglandins
quick acting
anti-pyretic
analgesic

58
Q

aspirin SEs

A 
gastric irritation
inhibits platelet fct
bronchospasm (exacerbate asthma)
allergic reactions
drug interactions: significant protein binding, Warfarin potentiation
association with problems in children
59
Q

what can aspirin be used to reduce the risk of?

A

bowel cancer
stroke
cardiac problems

60
Q

salicylates

A

aspirin

61
Q

propionic acid derivatives

A

ibuprofen

62
Q

phenylacetic acid derivatives

A

diclofenac

63
Q

mechanism of action of NSAIDs

A

reduce inflammatory mediators
- inhibit prostaglandin synthesis
COX enzyme inhibition
- converts arachidonic acid - prostaglandins

change PGE1 and PGE2 balance - anti-inflammatory

  • COX1 inhibitors
  • COX2 inhibitors - reduce 1 SEs (caution with heart issues) e.g. celecoxib
64
Q

what can NSAIDs cause GIT?

A

peptic ulcers

65
Q

ibuprofen

A

same actions as aspirin

less SEs - safer

66
Q

diclofenac

A

POM - more powerful inhibitor of enzyme pathway
- higher risk of gastric problems, asthma triggering, allergic reactions (rash)
more effective anti-inflammatory

67
Q

diclofenac dose

A

50mg x3 daily

68
Q

ibuprofen dose

A

200-600mg x3 daily

69
Q

CS structure

A

ring

70
Q

how do CSs reduce inflammation?

A

they inhibit:

  • capillary permeability
  • formation of bradykinin
  • migration of WBC
  • reduce eicosanoid synthesis

suppress inflammation features not cause
- don’t inhibit COX pathways

71
Q

topical steroid tx for mouth ulcers

A

beclomethasone inhalers
hydrocortisone adhesive tablets
betamethasone solutions

72
Q

systemic steroids - prednisolone

A

prevent transplant rejection

tx immunological diseases

73
Q

systemic steroids - dexamethasone

A

injection

reduce swelling after surgery

74
Q

SEs of steroids

A 
high bp
weight gain (fluid)
centripetal obesity and 'buffalo hump'
gastric ulceration
adrenal suppression
osteoporosis
diabetes
75
Q

BZDs mechanism of action

A

GABA agonists
- inhibitory neurotransmitter in CNS
anxiolytics

76
Q

advantages of nitrous oxide

A

metabolised as soon as stop
no needle
amount of effect can be adjusted during procedure
no organ metabolism issues - excreted unchanged as gas

77
Q

disadvantage of nitrous oxide

A

interferes with folic acid metabolism - avoid in pregnancy

78
Q

oral anxiolytic

A

diazepam

79
Q

IV sedation drug

A

midazolam

80
Q

BZD metabolism

A

phase 1 - convert to metabolites

phase 2 - conjugation, convert to inactive metabolites

81
Q

medical emergencies - adrenaline

A

1ml ampoules or prefilled syringes of 0.5ml of 1:1000 solution for IM injection

82
Q

medical emergencies - aspirin

A

300mg dispersible tablets

83
Q

medical emergencies - glucagon

A

1mg IM

84
Q

medical emergencies - GTN spray

A

sublingual

400mcg per metered dose

85
Q

medical emergencies - midazolam

A

oromucosal solution 5mg/ml

topical buccal administration

86
Q

medical emergencies - oral glucose

A

non-diet fizzy drinks
glucose gel
powdered glucose
sugar lumps

87
Q

medical emergencies - O2 cylinder

A

15l/min, enough for 30min supply

2 size D/CD or 1 size E

88
Q

medical emergencies - salbutamol

A

inhaler 100mcg per actuation

89
Q

what determines whether excreted in liver or kidney?

A

size of molecule with metabolites attached

90
Q

drug graphs - oral

A

upside down U

91
Q

drug graphs - IV

A

curve from top

92
Q

drug graphs - IM

A

increases a little then curve from top

93
Q

what do drug graphs give info for?

A

repeated timed doses to keep at therapeutic levels

94
Q

routes of administration - ABs

A

oral
topical
IM
IV

95
Q

mechanisms of action of ABs

A

bactericidal - kill bacteria
bacteriostatic - stop them growing, then host defences kill
1 - inhibit cell wall synthesis
2 - interfere with nucleic acids/metabolites
3 - inhibits protein synthesis
4 - cell membrane

96
Q

vertical resistance

A

mutation

passed on in reproduction/replication

97
Q

horizontal resistance

A

one species becomes resistant

pass it on via plasmids to own/other species

98
Q

mechanisms of resistance

A 
1 - reduce permeability
2 - inactivate antibiotic
3 - alter receptor site
4 - develop different metabolic pathway that drug doesn't act on
6 - can increase elimination
99
Q

combating resistance

A

overexposure

  • sort, correct doses
  • targeted specific antibiotics not broad spectrum ones
100
Q

penicillin mechanism of action

A

bactericidal - inhibits final step in cell wall synthesis

narrow/broad range

101
Q

penicillin resistance

A

penicillinase (bacteria can sometimes produce it, inactivates and increases elimination)

102
Q

metronidazole mechanism of action

A

acts on DNA of bacteria - inhibits protein synthesis

103
Q

peripherally acting analgesics

A

aspirin

paracetamol

104
Q

central acting analgesics

A

receptors in CNS

codeine, morphine

105
Q

where are NSAIDs mostly absorbed?

A

stomach and SI

106
Q

where are NSAIDs mostly excreted and what can be a consequence of this?

A

urine

could damage kidney if not drinking much - not a lot of fluid

107
Q

where are opioids metabolised?

A

liver

108
Q

where are opioids excreted?

A

urine

109
Q

groups affecting safety

A 
liver/kidney disease
v elderly/young
immunocompromised
pregnant
lactation
110
Q

reducing risk of interactions

A

MH, check BNF
WARFARIN
alcohol - up regulates liver enzymes up to a point then liver disease
some ABs affect OCP

BDS2 bams (6 decks)

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