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pharmacology Flashcards

1
Q

what are the 2 concepts of pharmacology

A

pharmacokinetics and pharmacodynamics

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2
Q

define pharmacokinetics and why is it important

A
  • how drugs/substances move around body
  • allows to get right dosage/frequency for specific drug and patient
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3
Q

what are the 4 stages of pharmacokinetics

A

1) absorption
2) distribution
3) metabolism
4) elimination

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4
Q

(pharmacokinetics)
what is ‘absorption’ and what 3 things can influence it?

A

the movement of a drug into the body affecting a targeted area

1) type of administration (route)
2) particle size
3) solubility

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5
Q

(pharmacokinetics -> absorption)
effect of food in stomach is vital to absorbing certain medication. what medication is absorbed better without food in the stomach?

A

(flucloxacillin) antibiotic

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6
Q

(pharmacokinetics -> absorption)
why are some medications given topically rather than orally?

A

good way to avoid gastro-intestinal tract and enzymes that may destroy medication or react negatively

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7
Q

(pharmacokinetics)
define ‘distribution’ and what 2 categories are drugs divided into solubility wise?

A

process of dispersion/dissemination of drugs throughout the fluids and tissues of body

divided into fat or water soluble

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8
Q

(pharmacokinetics -> distribution)
some tissues are less accessible to drugs if the drugs are unable to cross the blood-brain barrier centre- what type of medication is this an example of and explain the mechanism

A

non-sedative antihistamines
if they cross the barrier, may cause drowsiness eg chlorophenamine which binds to histamine receptors in the brain

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9
Q

define blood brain barrier

A

semi-permeable membrane separating blood from cerebrospinal fluid, creating passage barrier for cells/particles/large molecules

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10
Q

(pharmacokinetics -> distribution)
during distribution, some drugs bind to protein due to lower ________ levels

A

albumin

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11
Q

(pharmacokinetics -> distribution)
during distribution, some drugs bind to protein due to lower albumin levels
what are 2 examples of this drug/its effect and how do they interact with each other on plasma proteins

A

warfarin anti-coagulant and sodium valproate, person may bleed more easily

effect of sodium valproate displaces warfarin that’s bound on the plasma proteins

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12
Q

(pharmacokinetics -> metabolism)
where does this occur and what does it ensure

A
  • occurs in liver
  • ensures drugs are more water soluble, means it can be easily excreted by kidneys
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13
Q

(pharmacokinetics -> metabolism)
how many phases does metabolism have

A

2

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14
Q

(pharmacokinetics -> metabolism)
explain the first stage of metabolism

A

reduction, oxidation or hydrolysis reactions (intramolecular modifications) via use of cytochromes p450 enzymes

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15
Q

(pharmacokinetics -> metabolism)
what are cytochromes p450 and what do they do

A

family of enzymes responsible for metabolites, to oxidise drugs

-> hormone synthesis/breakdown, vitamin D metabolism, cholesterol synthesis

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16
Q

(pharmacokinetics -> metabolism)
phase 1: some medicines are enzyme inducers eg Carbamazepine.
what does this drug do and how does it interact with contraceptive pills?

A

anticonvulsant medication used in treatment of epilepsy, neuropathic pain and certain mental disorders like bipolar 1/mania

decreases bioavailability of contraceptive pill therefore larger dose of pill needed to control fertility

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17
Q

(pharmacokinetics -> metabolism)
what effect does grapefruit have on cytochromes p450

A

reduces action of p450 therefore affecting metabolism of statins/other drugs

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18
Q

define statin drugs

A

drugs reducing illness and mortality of those at high risk of cardiovascular disease -> most commonly described cholesterol-lowering medication

drug names end in ‘-statin’

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19
Q

(pharmacokinetics -> metabolism)
describe phase 2 of metabolism

A

-conjugation -> large ionised molecule added to drug, increasing drugs water solubility
-results in metabolites (this varies according to age and individual)
-liver main site for metabolism but some metabolised in gastro-intestinal, in plasma, and in lungs

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20
Q

(pharmacokinetics -> metabolism)
do all drugs undergo both phases of metabolism

A

no -> some only undergo phase 1, some only phase 2, some both

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21
Q

(pharmacokinetics -> metabolism)
whilst liver is main metabolism site, where else are drugs metabolised?

A
  • gastro-intestinal
  • plasma
  • lungs
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22
Q

(pharmacokinetics)
rate of metabolism is a significant factor governing what

A

the oral bioavailability of a drug

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23
Q

(pharmacokinetics -> metabolism)
describe the pathway a drug takes

A

absorption/gut metabolism:
- bolus dose into small intestine
- drug travels to liver via hepatic portal vein

hepatic metabolism/excretion (bile):
- metabolised in liver
- biliary clearance (toxin removal, prevents toxicity) from gall bladder back to small intestine
- drug travels further via hepatic veins to inferior vena cava

distribution/extrahepatic metabolism/ excretion (renal):
- once in inferior vena cava, bioavailability circulating drug and metabolites leads to pharmacodynamic effect and renal clearance

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24
Q

(pharmacokinetics -> metabolism)
where and how is morphine metabolised

A

metabolised in mucosal cells of small intestine as well as liver

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25
Q

(pharmacokinetics -> metabolism)
what is a pro-drug, name an example

A

inactive precursor that’s converted to active drug by metabolism -> codeine

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26
Q

(pharmacokinetics -> metabolism)
what is codeine metabolised into and where

A

morphine, in liver

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27
Q

(pharmacokinetics -> metabolism)
why is codeine advised only in certain situations for children

A

children metabolise codeine rapidly in some cases, meaning children under 12 are more susceptible to respiratory depression

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28
Q

(pharmacokinetics -> elimination)
what is the most common excretion route and what is excreted

A

by kidneys in urine, water soluble drugs and metabolites

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29
Q

(pharmacokinetics -> elimination)
name all excretion routes

A

urine (kidneys), sweat, bile, tears, breathe

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30
Q

(pharmacokinetics -> elimination)
what is eGFR and what does it measure

A

Estimated Glomerular Filtration Rate, measures creatinine concentration from which the filtration rate is worked out

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31
Q

(pharmacokinetics -> elimination)
define bioavailability

A

how much of a drug reaches the systemic circulation

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32
Q

(pharmacokinetics -> elimination)
what % bioavailability of intravenous drugs reach the circulation

A

100%

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33
Q

(pharmacokinetics -> elimination)
what % bioavailability is reached with oral drugs and why

A

60-70% as some drug is lost in digestion and so, not absorbed

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34
Q

(pharmacokinetics -> elimination)
what may cause bioavailability to decreases

A
  • degradation in gastric acid
  • first pass effect
  • gastric mucosa -> barrier
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35
Q

(pharmacokinetics -> elimination)
changing what will effect the bioavailability of a drug

A

formula -> elixir vs pill

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36
Q

(pharmacokinetics -> elimination)
name 3 drugs with a narrow therapeutic index

A
  • gentamicin
  • lithium
  • digoxin
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37
Q

(pharmacokinetics -> elimination)
how do you ensure drugs with a narrow therapeutic index are working effectively

A

often blood tests to check levels of drugs and right dose is given

38
Q

(pharmacokinetics -> elimination)
define plasma half life

A

how long on eravgd drug stays in system (amount of time is takes for a drug to decrease by 50% within the system)

39
Q

(pharmacodynamics)
define pharmacodynamics and what it entails

A

how drugs affect the body, deals with drug action, clinical side effect and adverse effects

40
Q

(pharmacodynamics)
define affinity

A

tendency for a drug to bind to a receptor

41
Q

(pharmacodynamics)
define efficacy

A

tendency for a drug to produce a response when bound to a receptor

42
Q

(pharmacodynamics)
define potency

A

amount of drug required to produce a defined level response

43
Q

(pharmacodynamics)
define specificity

A

how selectively a drug binds to a particular receptor

44
Q

(pharmacodynamics)
what are agonists

A

chemical binding to receptor, activating it to produce response

45
Q

(pharmacodynamics)
what are antagonists

A

bind to receptor to block its activation by agonists

46
Q

(pharmacodynamics)
what are partial agonists

A

agonists that cause response that’s less than the maximum

47
Q

(pharmacodynamics)
name example of an agonist and explain how it acts

A

adrenaline -> binds to beta receptors on heart muscle, leading to increased pulse

48
Q

(pharmacodynamics)
name example of antagonist and explain how it works

A

propranolol -> beta blocker, slows heart rate by blocking beta cells from adrenaline

49
Q

(pharmacodynamics)
is an anti-histamine an agonist or antagonist

A

antagonist

50
Q

(pharmacodynamics)
name an example of a partial agonist (opioid) and what its use

A

buprenorphine -> prevents withdrawal symptoms when someone stops using heroin

51
Q

explain the difference of a histamine binding to a H1 receptor vs H2 receptor and what their subsequent effects are

A

histamine binds to H1 receptor -> mucus hyper-secretion (cells in the stomach produce more acid) (H1 receptor responsible for allergic reaction)

histamine binds to H2 receptor -> inflammation of mucous membranes eg runny nose, itchy eyes (produces allergic response as H2 is predominantly responsible for acid-peptide disease)

52
Q

what do cyclo-oxygenases (COX) create

A

prostoglandins

53
Q

explain the pathway of an NSAID drug from the moment of injury til the suppression of pain

A

injury/irritation → arachidonic acid released → COX catalyse oxygenation of AA to create prostaglandins → ibuprofen administered → pain and inflammation decrease, suppress prostaglandins synthesis

54
Q

what 2 effects do prostaglandins have on body

A

-reduce acid production and increase mucus in stomach
-increase blood flow to kidneys

55
Q

what are 2 side effects of long term use of NSAIDs

A

-peptic ulceration
-salt and water retention -> hypertension

56
Q

what are the 3 main effects of adrenaline on the body and why do they differ

A

-speeds up heart and pumps faster
-constricts arteries and increases blood pressure
-dilates bronchioles -> open airways

effects due to interaction with different subtypes of adrenergic receptors

57
Q

what happens when propranolol blocks B1 and B2 receptors

A

makes asthma worse

58
Q

atenolol is best avoided with what condition due to blocking some B2 receptors

A

asthma

59
Q

what effect will occur after salbutamol stimulates some B1 receptors

A

heart rate increases

60
Q

what are anticholinergics

A

class of drugs that blocks binding of neurotransmitter acetylcholine in central and peripheral nervous system

61
Q

what are antimuscarinics

A

antagonists that block muscarinic receptors and act as anti-emetics

62
Q

what is an example of an antimuscarinic, how does it work and what effects does it have

A

hyoscine hydrobromide (scopolamine) -> inhibits parasympathetic nerve impulses

useful for managing nausea/motion sickness, cause dry mouth, constipation and urinary retention

63
Q

what are the consequences of antimicrobial resistance?

A
  • infections harder to treat
  • drugs more expensive
  • infection remains contagious
  • increased hospital stays
  • increased cost to healthcare
64
Q

how do bacteria become resistant to antibiotics

A
  • neutralise antibiotic before it has ‘killing effect’
  • pump out antibiotic from cells
  • change site/receptor where antibiotic works
  • share genetic material with other bacteria to also make them resistant
65
Q

what are the causes of antibiotic resistance?

A
  • over-prescribing antibiotics
  • patients not finishing treatment
  • over-use of antibiotics in livestock and fish farming
  • poor infection control in hospitals/clinics
  • lack of hygiene/poor sanitation
  • lack of new antibiotics developed
66
Q

what is the first line of action for syphilis

A

benzathine bencylpenicillin

67
Q

what are the key points to effective antibiotic stewardship

A
  • right drug/dose/time/duration
  • microbiology samples where appropriate
  • avoid unnecessary lengthy durations of antibiotics and avoid broad spectrum
  • discuss switching IV to oral
68
Q

what does AMR stand for

A

antimicrobial resistance

69
Q

explain the importance of vaccinations

A
  • negates need for antibiotics by preventing illness, herd immunity further prevents spread of resistant strains
  • use of second-line antibiotics may promote emergence of new antibiotic resistant isolates
70
Q

name some broad spectrum antibiotics

A
  • carbapenams
  • chloramphenicol
  • 2nd 3rd 4th gen cephalosporiins
  • 3rd gen fluoroquinolones
  • broad spectrum penicillins
  • tetracyclines
71
Q

name some narrow spectrum antibiotics

A
  • penicillin V and G
  • lincosamides (clindamycin)
  • glycopeptides (Vance and teicoplanin)
  • streptogramins
  • rifamycins
  • daptomycin
72
Q

what is empiric antimicrobial therapy

A

directed against anticipated likely cause of infectious disease -> antimicrobials given before specific bacterium/fungus causing infection is known

73
Q

what is targeted antimicrobial therapy

A

possible when microbiology samples identify the bacteria causing the infection and appropriate antibiotics can be recommended

74
Q

what is prophylactic antimicrobial therapy

A

may be given proper to surgeries to reduce post-op infection, as ongoing treatment to avoid recurring infections (eg UTI’s) but not as common due to risk of AMR’s

75
Q

define adverse drug event (ADE)

A

any untoward medical occurrence that may present during treatment with a pharmaceutical product which doesn’t necessarily have casual relationship with this treatment (eg inappropriate drug dosing side effects/ OD)

76
Q

define adverse drug reaction (ADR)

A

an ‘adverse event’ which is noxious, unintended and occurs after normal therapeutic range/dose has been administered -> ADR is a type of ADE

77
Q

what are the characteristics of a Type A (augmented) adverse drug reaction and provide examples

A
  • pharmacologically predictable
  • dose related therefore reduce dose -> reduce reaction
  • common
  • bradycardia due to propranolol
  • drowsiness to anti-histamines
  • dry mouth with tricyclic antidepressants
78
Q

what are the characteristics of a Type B (bizarre) adverse drug reaction and provide examples

A
  • pharmacologically unpredictable
  • not dose related
  • rare
    -NEED TO STOP DRUG
  • anaphylaxis to penicillin
79
Q

what are the characteristics of a Type C (chronic) adverse drug reaction and provide examples

A
  • dose related and time related
  • uncommon
  • related to cumulative dose
  • osteonecrosis of the jaw with biphosphates (alendronate)
80
Q

what are the characteristics of a Type D (delayed) adverse drug reaction and provide examples

A
  • time related
  • uncommon
  • usually dose related
  • occurs some time after the use of the drug
  • teratogenic effects of thalidomide, isotretinoin and primodos pregnancy hormonal test
  • sodium valporate syndrome from sodium valporate
81
Q

what are the characteristics of a Type E (end of use) adverse drug reaction and provide examples

A
  • MAKE PLAN TO STOP
  • uncommon
  • occurs soon after withdrawal of drug
  • withdrawal symptoms of opiates/benzodiazepines eg insomnia, anxiety
82
Q

older people are more sensitive to what 3 types of drugs

A

psychotropics (antipsychotics), diuretics, NSAID’s

83
Q

what is a patient group direction

A

written direction allowing supply/administration of specified medicines by authorised health professionals to well-defined group of patients requiring treatment of specific condition

84
Q

what can you NOT supply under a PGD

A
  • unlicensed medicines
  • dressings, appliances, devices
  • radiopharmaceuticals
  • abortifacients
85
Q

what are patient specific directions

A

instructions from doctor/dentist/other independent prescriber for medicine to be supplied/administered to named patient after prescriber assessed patient on individual basis

86
Q

what factors affect a drugs half life

A

age, ethnicity, renal and liver function, drug interactions, if drugs inhibit/induce liver enzymes

87
Q

define ‘maintenance dose’

A

dose given to keep plasma drug concentration in therapeutic range

88
Q

define ‘loading dose’

A

high conc. of medication given to prime blood stream with significant levels to quickly induce therapeutic effect

89
Q

potency vs efficacy

A

potency- dose of drug required for particular response
efficacy- relates to magnitude of maximal response

90
Q

define drug affinity

A

competition and reversibility of drug- high affinity= good relationship with receptor= binds strongly

91
Q
A

therapeutic interventions (3 decks)

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