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Animal Medicines > pharmacokinetics + pharmacodynamics > Flashcards

pharmacokinetics + pharmacodynamics Flashcards

(79 cards)

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1
Q

define pharmacology

(1 mark)

A

science of chemicals (drugs) that interact within the body

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2
Q

define pharmacokinetics

(1 mark)

A

how the drug moves through the body

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3
Q

define pharmacodynamics

(1 mark)

A

what the drug does to the body

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4
Q

what is therapeutic range?

(1 mark)

A

ideal range of drug concentration in body

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5
Q

what happens if drug dose concentration goes above max effective concentration and below minimum?

(2 marks)

A

above max = toxicity
below min = ineffective

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6
Q

what is steady state?

(1 mark)

A

concentration of drug remins stable from dose to dose

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7
Q

how is steady state achieved?

(1 mark)

A

drug is able to be kept within theraputic range over number of doses

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8
Q

what are the stages of pharmacokinetics?

(4 marks)

A

absorption
distribution
metabolism
excretion

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9
Q

what is absorption?

(1 mark)

A

drug travels from site of administration into systemic circulation

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10
Q

how does absorption vary?

(3 marks)

A

drug quality
drug formulation
route of administration

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11
Q

what are the barriers to absorption?

(4 marks)

A

paracellular = squeezes between cells in membrane
transcellular = passes into cell membrane, travels through and passes out other side

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12
Q

how do drugs pass across the membrane?

(3 marks)

A

direct diffusion
facilitated diffusion
active transport

(facilitaed and active use transmembrane carrier proteins)

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13
Q

difference between lipophilic and hydrophillic?

(6 marks)

A

lipophilic = non-polarised + non-ionised, disolves readily in fat
hydrophilic = polarised + ionisied, dissolves readily in water

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14
Q

importance of lipophilic : hydrophilic?

(3 marks)

A

affects the absorption, distribution and elimination of drug

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15
Q

define direct diffusion

(1 mark)

A

passive diffusion following a concentration gradient

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16
Q

what factors does absorption depend on?

(5 marks)

A
  • concentration gradient
  • molecule size
  • lipophilic nature
  • temperature
  • thickness of membrane
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17
Q

what are carrier proteins?

(1 mark)

A

transmembrane proteins - proteins floating within phosphobilipid layer

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18
Q

types of diffusion allowed by carrier proteins?

(2 marks)

A

passive (facilitated)
active

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19
Q

what does passive diffusion not require?

(1 mark)

A

does not require energy

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20
Q

what does active diffusion require?

(1 mark)

A

requires energy (ATP to ADP)

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21
Q

limiting factor of diffusion allowed by carrier proteins?

(1 mark)

A

number of carriers

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22
Q

factors that affect absorption?

(5 marks)

A
  • route of administration
  • method of crossing membranes
  • lipophilic : hydrophilic nature
  • pH of environment
  • tissue perfusion
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23
Q

what are the routes of administration?

(4 marks)

A

IV
IM
SC
PO

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24
Q

what does a plasma concentration over time graph show?

(2 marks)

A

compare peak / max conc that a drug will reach in circulation and
the time over which it is within the bloodstream

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25
how does IV appear on the graph? ## Footnote (3 marks)
administered straight into circulation 100% absorption plasma conc drops fast because fast absorption into tissues
26
how does the lipophillic : hydrophilic ratio affect acid and basic drugs? ## Footnote (2 marks)
acid drug = more non-ionisied / lipophilic in acidic environments basic drug = more ionisied / hydrophilic in acidic environments
27
how does the pH of the environment affect drugs? ## Footnote (3 marks)
lipophilic : hydrophilic ratio can change depending on pH affects method / rate of membrane crossing ion - trapping
28
what is ion-trapping? ## Footnote (2 marks)
drug becomes trapped due to change in environment build up of drug in one area
29
define bioavailability ## Footnote (1 mark)
proportion of drug that reaches circulation when introduced into body
30
what does AUC work out? ## Footnote (1 mark)
amount of drug absorbed
31
what does concentration max vs time work out? ## Footnote (1 mark)
how effective drug is
32
how is distribution of a drug known? ## Footnote (1 mark)
tissue penetration of drug
33
can drugs pass into fat readily? ## Footnote (1 mark)
no = overweight animals have a reduced tissue penetration therefore volume of distribution
34
what is distribution dependant on? ## Footnote (3 marks)
perfusion capillary wall permeability protein binding
35
structure of the capillary cell wall? ## Footnote (1 mark)
less permeable meaning only small lipophilic molecules can cross
36
examples of capillary wall structures? ## Footnote (3 marks)
blood brain barrier placenta testicles
37
what plasma proteins are produced by the liver? ## Footnote (2 marks)
albumin + globulin
38
what do plasma proteins do? ## Footnote (2 marks)
hold drugs in circulation = inactive and not metabolised / excreted. free : bound ratio.
39
when do you not want a drug to be rapidly absorbed? ## Footnote (3 marks)
slow release tablets and boluses topical meds - work where applied local anaesthetic - desensitive nerves in certain areas
40
benefit of drug redistribution? ## Footnote (1 mark)
the effect of drug can be terminated whilst the drug is still in circulation
41
what is biotransformation? ## Footnote (1 mark)
conversion from one chemical enity to another
42
metabolism aids in? ## Footnote (2 marks)
detoxification elimination
43
how does interference between metabolic pathways affect a drug? ## Footnote (1 mark)
one drug may not be broken down as much and could further impact toxicity in another drug / acumulation of both
44
how are original molecules chemically transformed during phase 1 of metabolic reactions? ## Footnote (3 marks)
oxidation reduction hydrolysis
45
what does the molecule become after the transformation process? ## Footnote (1 mark)
metabolite
46
what happens in phase 2? ## Footnote (3 marks)
the metabolite is combined with another chemical substance - conjucation reduced bioactivity
47
what is excretion? ## Footnote (1 mark)
removal of drug from body
48
what organs are involved in excretion? ## Footnote (6 marks)
* kidney * liver * lungs * hair * milk * saliva
49
stages of renal excretion? ## Footnote (3 marks)
glomerular filtration - filtrate squeezed out passive tubular resorption - some reabsorbed into circulation active tubular secretion - back into filtrate
50
amount of drug excreted is calculated by? ## Footnote (1 mark)
amount filtered from glomerulus - amount reabsorbed + amount secreted back by active secretion
51
how are drugs excreted by the liver? ## Footnote (4 marks)
drug passively diffuses into hepatocytes (liver cells). once here they can either be excreted directly into the bile, unchanged / metabolised by the liver + then produced into the bile. once in the bile, the drug is excreted into/via instestines + then out into faeces.
52
what is enterohepatic circulation? | (in terms of hepatic excretion?) ## Footnote (4 marks)
drug is metabolised in liver but binds to glucuronide, which is excreted into bile where is hydrolysed. this allows drug to be reabsorbed back into portal vein + into body. potential for more drug activity.
53
what is half-life? ## Footnote (1 mark)
amount of time taken for half a drug to be removed
54
how many half-lives does it take to reach 95% steady state concentration? ## Footnote (1 mark)
5 half-lives
55
how can the rate of metabolism and excretion be measured? ## Footnote (1 mark)
how long it takes for the drug conc to be reduced by 50% each time.
56
what ways do drugs work within the body? ## Footnote (3 marks)
* mimic * block * enhance
57
how do endogenous chemical work compared to agonist and antagonist? ## Footnote (3 marks)
endogenous - specific shape + size. fits + causes reaction. agonist - similar in shape. binds but not fully - mimic response antagonist - bind but does not fit perfectly, does not cause response - block
58
what do full and partial agonists do? ## Footnote (1 mark)
full + partial response
59
how do competetive + non-competetice antagonists work? ## Footnote (8 marks)
competitive antagonist binds to same site as normal enzyme - compete for same site - reversible non-competitive bind to site near receptor. normal receptor. normal receptor change shape - enzyme cannot bind - blocks receptor - irreversible
60
what is drug potency? ## Footnote (1 mark)
how well a drug binds + acts
61
what is drug affinity? ## Footnote (1 mark)
how well drug binds to receptor
62
how does high, medium and low affinity work? ## Footnote (3 marks)
high - strong bond medium - partially bound - medium strength (some receptor is open and unbound low - low strength binding as lightly attrached
63
what is EC50? ## Footnote (2 marks)
measure of potency. conc of a drug that induces a response that is halfway between max + min response
64
what is efficiacy? ## Footnote (1 mark)
how effective is the drug at producing a response
65
how is potency determined? ## Footnote (1 mark)
affinity + afficacy
66
what is selectivity? ## Footnote (1 mark)
ability to preferntially bind to one receptor than other
67
what is ideal selectivity? ## Footnote (1 mark)
want drug with high sensitivity to reduce side effects
68
what happens is drug has low selectivity? ## Footnote (1 mark)
drug interacts with lots of different receptors, causing lots of different responses
69
what is specificity? ## Footnote (1 mark)
ability to target the site in which it is required
70
how does binding cause a response? ## Footnote (4 marks)
dependent on type of receptor: 1. ligand-gated ion channel 2. G protein coupled receptor 3. protein kinase receptors 4. intracellular receptor
71
how do ion channels work? ## Footnote (3 marks)
drug binds to receptor changes shape of protein molecule channel opens channel to allow it to move to other side of phosphobilipid layer
72
how do local anaesthetics work? ## Footnote (5 marks)
block receptor nerve depolarisation causes influx of sodium ions into cell blocks nerve transfer bind to receptor + block it channel cannot open - no response
73
how many proteins are in the phosphobilipid layer involved in G-protein coupled receptors? ## Footnote (1 mark)
7
74
how do G-protein coupled receptors work? ## Footnote (4 marks)
* ligand binds to protein * GDP converted into GTP * G-proteins released - triggers cascade of events * GDP to GTP
75
how do protein kinases work? ## Footnote (2 marks)
catalyse effect of variety of different proteins either drug molecule binds to receptor / endogenous chemicals
76
how does insulin use protein kinases? ## Footnote (4 marks)
* insulin = endogenous chemicals * bind to tyrosine kinase receptors * causes the two molecules to join * triggers a cellular cascade in response to insulin binding
77
how do intracellular receptors work? ## Footnote (3 marks)
receptor within cell - inside cytoplasm / nucleus signalling in cytoplasm / pass through + bind in nucleus able to attach to DNA to interrupt transcription
78
what does it mean if the body becomes desensitied? ## Footnote (1 mark)
the desired result is no longer achieved due to change in body / prolonged exposure to drug / ligand
79
how can desensation occur? ## Footnote (5 marks)
* change in receptors - does not achieve same response * loss of receptors - go inside cells * depletion of mediators - reponse is blocked * altered metabolism - quicker = reduction of drug * physiological adaptation - body adapt e.g. insulin resistance

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