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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
(pharmacokinetics -> metabolism) what is a pro-drug, name an example
inactive precursor that's converted to active drug by metabolism -> codeine
26
(pharmacokinetics -> metabolism) what is codeine metabolised into and where
morphine, in liver
27
(pharmacokinetics -> metabolism) why is codeine advised only in certain situations for children
children metabolise codeine rapidly in some cases, meaning children under 12 are more susceptible to respiratory depression
28
(pharmacokinetics -> elimination) what is the most common excretion route and what is excreted
by kidneys in urine, water soluble drugs and metabolites
29
(pharmacokinetics -> elimination) name all excretion routes
urine (kidneys), sweat, bile, tears, breathe
30
(pharmacokinetics -> elimination) what is eGFR and what does it measure
Estimated Glomerular Filtration Rate, measures creatinine concentration from which the filtration rate is worked out
31
(pharmacokinetics -> elimination) define bioavailability
how much of a drug reaches the systemic circulation
32
(pharmacokinetics -> elimination) what % bioavailability of intravenous drugs reach the circulation
100%
33
(pharmacokinetics -> elimination) what % bioavailability is reached with oral drugs and why
60-70% as some drug is lost in digestion and so, not absorbed
34
(pharmacokinetics -> elimination) what may cause bioavailability to decreases
- degradation in gastric acid - first pass effect - gastric mucosa -> barrier
35
(pharmacokinetics -> elimination) changing what will effect the bioavailability of a drug
formula -> elixir vs pill
36
(pharmacokinetics -> elimination) name 3 drugs with a narrow therapeutic index
- gentamicin - lithium - digoxin
37
(pharmacokinetics -> elimination) how do you ensure drugs with a narrow therapeutic index are working effectively
often blood tests to check levels of drugs and right dose is given
38
(pharmacokinetics -> elimination) define plasma half life
how long on eravgd drug stays in system (amount of time is takes for a drug to decrease by 50% within the system)
39
(pharmacodynamics) define pharmacodynamics and what it entails
how drugs affect the body, deals with drug action, clinical side effect and adverse effects
40
(pharmacodynamics) define affinity
tendency for a drug to bind to a receptor
41
(pharmacodynamics) define efficacy
tendency for a drug to produce a response when bound to a receptor
42
(pharmacodynamics) define potency
amount of drug required to produce a defined level response
43
(pharmacodynamics) define specificity
how selectively a drug binds to a particular receptor
44
(pharmacodynamics) what are agonists
chemical binding to receptor, activating it to produce response
45
(pharmacodynamics) what are antagonists
bind to receptor to block its activation by agonists
46
(pharmacodynamics) what are partial agonists
agonists that cause response that's less than the maximum
47
(pharmacodynamics) name example of an agonist and explain how it acts
adrenaline -> binds to beta receptors on heart muscle, leading to increased pulse
48
(pharmacodynamics) name example of antagonist and explain how it works
propranolol -> beta blocker, slows heart rate by blocking beta cells from adrenaline
49
(pharmacodynamics) is an anti-histamine an agonist or antagonist
antagonist
50
(pharmacodynamics) name an example of a partial agonist (opioid) and what its use
buprenorphine -> prevents withdrawal symptoms when someone stops using heroin
51
explain the difference of a histamine binding to a H1 receptor vs H2 receptor and what their subsequent effects are
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
what do cyclo-oxygenases (COX) create
prostoglandins
53
explain the pathway of an NSAID drug from the moment of injury til the suppression of pain
injury/irritation → arachidonic acid released → COX catalyse oxygenation of AA to create prostaglandins → ibuprofen administered → pain and inflammation decrease, suppress prostaglandins synthesis
54
what 2 effects do prostaglandins have on body
-reduce acid production and increase mucus in stomach -increase blood flow to kidneys
55
what are 2 side effects of long term use of NSAIDs
-peptic ulceration -salt and water retention -> hypertension
56
what are the 3 main effects of adrenaline on the body and why do they differ
-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
what happens when propranolol blocks B1 and B2 receptors
makes asthma worse
58
atenolol is best avoided with what condition due to blocking some B2 receptors
asthma
59
what effect will occur after salbutamol stimulates some B1 receptors
heart rate increases
60
what are anticholinergics
class of drugs that blocks binding of neurotransmitter acetylcholine in central and peripheral nervous system
61
what are antimuscarinics
antagonists that block muscarinic receptors and act as anti-emetics
62
what is an example of an antimuscarinic, how does it work and what effects does it have
hyoscine hydrobromide (scopolamine) -> inhibits parasympathetic nerve impulses useful for managing nausea/motion sickness, cause dry mouth, constipation and urinary retention
63
what are the consequences of antimicrobial resistance?
- infections harder to treat - drugs more expensive - infection remains contagious - increased hospital stays - increased cost to healthcare
64
how do bacteria become resistant to antibiotics
- 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
what are the causes of antibiotic resistance?
- 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
what is the first line of action for syphilis
benzathine bencylpenicillin
67
what are the key points to effective antibiotic stewardship
- 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
what does AMR stand for
antimicrobial resistance
69
explain the importance of vaccinations
- 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
name some broad spectrum antibiotics
- carbapenams - chloramphenicol - 2nd 3rd 4th gen cephalosporiins - 3rd gen fluoroquinolones - broad spectrum penicillins - tetracyclines
71
name some narrow spectrum antibiotics
- penicillin V and G - lincosamides (clindamycin) - glycopeptides (Vance and teicoplanin) - streptogramins - rifamycins - daptomycin
72
what is empiric antimicrobial therapy
directed against anticipated likely cause of infectious disease -> antimicrobials given before specific bacterium/fungus causing infection is known
73
what is targeted antimicrobial therapy
possible when microbiology samples identify the bacteria causing the infection and appropriate antibiotics can be recommended
74
what is prophylactic antimicrobial therapy
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
define adverse drug event (ADE)
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
define adverse drug reaction (ADR)
an 'adverse event' which is noxious, unintended and occurs after normal therapeutic range/dose has been administered -> ADR is a type of ADE
77
what are the characteristics of a Type A (augmented) adverse drug reaction and provide examples
- pharmacologically predictable - dose related therefore reduce dose -> reduce reaction - common - bradycardia due to propranolol - drowsiness to anti-histamines - dry mouth with tricyclic antidepressants
78
what are the characteristics of a Type B (bizarre) adverse drug reaction and provide examples
- pharmacologically unpredictable - not dose related - rare -NEED TO STOP DRUG - anaphylaxis to penicillin
79
what are the characteristics of a Type C (chronic) adverse drug reaction and provide examples
- dose related and time related - uncommon - related to cumulative dose - osteonecrosis of the jaw with biphosphates (alendronate)
80
what are the characteristics of a Type D (delayed) adverse drug reaction and provide examples
- 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
what are the characteristics of a Type E (end of use) adverse drug reaction and provide examples
- MAKE PLAN TO STOP - uncommon - occurs soon after withdrawal of drug - withdrawal symptoms of opiates/benzodiazepines eg insomnia, anxiety
82
older people are more sensitive to what 3 types of drugs
psychotropics (antipsychotics), diuretics, NSAID's
83
what is a patient group direction
written direction allowing supply/administration of specified medicines by authorised health professionals to well-defined group of patients requiring treatment of specific condition
84
what can you NOT supply under a PGD
- unlicensed medicines - dressings, appliances, devices - radiopharmaceuticals - abortifacients
85
what are patient specific directions
instructions from doctor/dentist/other independent prescriber for medicine to be supplied/administered to named patient after prescriber assessed patient on individual basis
86
what factors affect a drugs half life
age, ethnicity, renal and liver function, drug interactions, if drugs inhibit/induce liver enzymes
87
define 'maintenance dose'
dose given to keep plasma drug concentration in therapeutic range
88
define 'loading dose'
high conc. of medication given to prime blood stream with significant levels to quickly induce therapeutic effect
89
potency vs efficacy
potency- dose of drug required for particular response efficacy- relates to magnitude of maximal response
90
define drug affinity
competition and reversibility of drug- high affinity= good relationship with receptor= binds strongly
91

therapeutic interventions (3 decks)

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