pharmacology Flashcards
(110 cards)
1
Q
drug definition
A
external substance that acts on living tissue to produce a measurable change in the fct of that tissue
2
Q
2 ways drugs work
A
stimulate/interrupt normal body communications
OR
act on non-host organisms to aid body defences
3
Q
autonomic drugs
A
epinephrine - B agonist
atenolol - B blocker
pilocarpine - cholinergic agonist
atropine - cholinergic blocker
4
Q
3 components drugs act on
A
receptors
enzymes
ion channels
5
Q
what do drugs have their effects on?
A
proteins
6
Q
receptors
A
transmembrane protein
coupled to ion channels, G proteins, enzymes, gene transcription
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
8
Q
affinity
A
attraction of drug to receptor
9
Q
occupancy
A
time drug stays stuck to receptor for
10
Q
efficacy
A
how well combination of drug and receptor works
11
Q
law of mass action
A
more drugs in vicinity of receptor = likely to get more efficacy
12
Q
types of drug actions
A
agonists
partial agonists
antagonists
competitive/non-competitive
reversible/irreversible
13
Q
agonists
A
bind to receptor and produce effect
14
Q
partial agonists
A
more difficult to produce effect
increased conc might improve efficacy
15
Q
antagonists
A
binds to receptor but nothing happens
16
Q
drug phases
A
absorption
clinical effect
metabolism
excretion
17
Q
routes of administration
A
enteral - oral
parenteral
18
Q
enteral - oral advantages
A
socially acceptable
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
20
Q
parenteral routes of administration
A
IV IM SC inhalation intra-osseous topical sublingual/buccal rectal
21
Q
parenteral advantages
A
predictable plasma levels
no FPM
22
Q
parenteral disadvantages
A
more severe allergic reactions
access difficulties
drug cost higher
23
Q
FPM
A
GIT (except sublingual and rectal)
HPV
liver
metabolises - inactivates/activates
24
Q
abnormal liver fct causes
A
extremes of life
drug interactions
disease
25
bioavailability
proportion of an ingested drug that is available for clinical effect
FREE not bound
26
what affects bioavailability?
dosage form
destruction in gut
poor absorption
FPM
27
causes of poor absorption
molecule size
lipid solubility (easy absorbed)
degree of ionisation (very ionised not as easily absorbed)
28
3 aspects of drug distribution
compartments - dilution
lipid binding - slow release from accumulation
drug binding to plasma proteins
29
drug distribution - compartments
dilution
| vascular, tissues, CNS
30
drug distribution - lipid binding
slow release from accumulation
31
drug distribution - drug binding to plasma proteins
bound = inactive = reservoir
interactions by competitive binding
e.g. aspirin higher affinity than Warfarin
32
excretion
renal, liver (bile), lungs, sweat, saliva
33
what organ can modify drug excretion secretions?
kidney
34
drug metabolism
phase 1 - inactivation
| phase 2 - conjugation
35
drug metabolism phase 1
inactivation
change shape - doesn't bind to receptor
oxidation, reduction, hydrolysis
36
drug metabolism phase 2
conjugation
| glucuronidation, sulphation, methylation, acetylation, glutathione
37
where does drug metabolism happen?
liver
38
factors affecting drug metabolism
liver/kidney disease
interactions
some drugs increase activity of liver enzymes - increase rate
age - extremes have slower metabolisms and less plasma proteins
genetic factors
39
pharmacokinetics
what body does to drug - drugs don't distribute evenly
40
pharmacokinetics - "body compartments"
single - behaves as if evenly distributed
| 2 compartment model - in equilibrium with different tissues in body
41
pharmacokinetics - more blood flow
tissue exposed to bigger doses
| eventually - distribution equilibrium
42
drug clearance
removal of a drug from plasma
| depends on 1/2 life
43
plasma half life
period of time required for conc/amount of drug in body to be reduced by half
44
what is the most common type of drug clearance?
1st order
45
1st order clearance
elimination/absorption by passive diffusion
drug removal proportional to drug conc
higher conc - moves quicker into urine/bile
curved graph
46
0 order clearance
active process - can be saturated by high drug conc
linear graph - straight line
enzyme system
think - ice cream scoop - fixed rate
47
2 examples of 0 order clearance
blood-alcohol elimination
| paracetamol toxicity
48
drug accumulation
how plasma conc build if repeated doses of a drug are given
| drug trial - dosing schedule
49
hazards of drug use
death - allergy/toxicity of drug
| interactions - effect on absorption/metabolism of other essential meds
50
paracetamol
```
mechanism of action?
anti-pyretic
analgesic
little anti-inflammatory action
few SEs
1g x4 daily
```
51
LAs mechanism of action
1 - membrane expansion - forces pore closed
| 2 - acts on 2 gates- binds just under halt gate reversibly - stops Na+ getting in
52
esters metabolised in?
plasma
53
amides metabolised in?
liver
54
pH and LAs
pH sensitive in tissues
55
aspirin dose
300-600mg up to x4
56
aspirin kinetics
rapid absorption from GIT
| 1st order kinetics - unless overdose - enzyme saturation
57
aspirin mechanism of action
inhibits COX 1 prostaglandins
quick acting
anti-pyretic
analgesic
58
aspirin SEs
```
gastric irritation
inhibits platelet fct
bronchospasm (exacerbate asthma)
allergic reactions
drug interactions: significant protein binding, Warfarin potentiation
association with problems in children
```
59
what can aspirin be used to reduce the risk of?
bowel cancer
stroke
cardiac problems
60
salicylates
aspirin
61
propionic acid derivatives
ibuprofen
62
phenylacetic acid derivatives
diclofenac
63
mechanism of action of NSAIDs
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
what can NSAIDs cause GIT?
peptic ulcers
65
ibuprofen
same actions as aspirin
| less SEs - safer
66
diclofenac
POM - more powerful inhibitor of enzyme pathway
- higher risk of gastric problems, asthma triggering, allergic reactions (rash)
more effective anti-inflammatory
67
diclofenac dose
50mg x3 daily
68
ibuprofen dose
200-600mg x3 daily
69
CS structure
ring
70
how do CSs reduce inflammation?
they inhibit:
- capillary permeability
- formation of bradykinin
- migration of WBC
- reduce eicosanoid synthesis
suppress inflammation features not cause
- don't inhibit COX pathways
71
topical steroid tx for mouth ulcers
beclomethasone inhalers
hydrocortisone adhesive tablets
betamethasone solutions
72
systemic steroids - prednisolone
prevent transplant rejection
| tx immunological diseases
73
systemic steroids - dexamethasone
injection
| reduce swelling after surgery
74
SEs of steroids
```
high bp
weight gain (fluid)
centripetal obesity and 'buffalo hump'
gastric ulceration
adrenal suppression
osteoporosis
diabetes
```
75
BZDs mechanism of action
GABA agonists
- inhibitory neurotransmitter in CNS
anxiolytics
76
advantages of nitrous oxide
metabolised as soon as stop
no needle
amount of effect can be adjusted during procedure
no organ metabolism issues - excreted unchanged as gas
77
disadvantage of nitrous oxide
interferes with folic acid metabolism - avoid in pregnancy
78
oral anxiolytic
diazepam
79
IV sedation drug
midazolam
80
BZD metabolism
phase 1 - convert to metabolites
| phase 2 - conjugation, convert to inactive metabolites
81
medical emergencies - adrenaline
1ml ampoules or prefilled syringes of 0.5ml of 1:1000 solution for IM injection
82
medical emergencies - aspirin
300mg dispersible tablets
83
medical emergencies - glucagon
1mg IM
84
medical emergencies - GTN spray
sublingual
| 400mcg per metered dose
85
medical emergencies - midazolam
oromucosal solution 5mg/ml
| topical buccal administration
86
medical emergencies - oral glucose
non-diet fizzy drinks
glucose gel
powdered glucose
sugar lumps
87
medical emergencies - O2 cylinder
15l/min, enough for 30min supply
| 2 size D/CD or 1 size E
88
medical emergencies - salbutamol
inhaler 100mcg per actuation
89
what determines whether excreted in liver or kidney?
size of molecule with metabolites attached
90
drug graphs - oral
upside down U
91
drug graphs - IV
curve from top
92
drug graphs - IM
increases a little then curve from top
93
what do drug graphs give info for?
repeated timed doses to keep at therapeutic levels
94
routes of administration - ABs
oral
topical
IM
IV
95
mechanisms of action of ABs
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
vertical resistance
mutation
| passed on in reproduction/replication
97
horizontal resistance
one species becomes resistant
| pass it on via plasmids to own/other species
98
mechanisms of resistance
```
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
combating resistance
overexposure
- sort, correct doses
- targeted specific antibiotics not broad spectrum ones
100
penicillin mechanism of action
bactericidal - inhibits final step in cell wall synthesis
| narrow/broad range
101
penicillin resistance
penicillinase (bacteria can sometimes produce it, inactivates and increases elimination)
102
metronidazole mechanism of action
acts on DNA of bacteria - inhibits protein synthesis
103
peripherally acting analgesics
aspirin
| paracetamol
104
central acting analgesics
receptors in CNS
| codeine, morphine
105
where are NSAIDs mostly absorbed?
stomach and SI
106
where are NSAIDs mostly excreted and what can be a consequence of this?
urine
| could damage kidney if not drinking much - not a lot of fluid
107
where are opioids metabolised?
liver
108
where are opioids excreted?
urine
109
groups affecting safety
```
liver/kidney disease
v elderly/young
immunocompromised
pregnant
lactation
```
110
reducing risk of interactions
MH, check BNF
WARFARIN
alcohol - up regulates liver enzymes up to a point then liver disease
some ABs affect OCP
