pharma Flashcards

1
Q

what are the 4 types of pharmacokinetics?

A

Absorption, Distribution, Metabolism, Excretion

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2
Q

what is bioavailability of an IV drug?

A

1

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3
Q

what factors affect absorption of a drug?

A

motility of GI tract, acid/base balance of drug

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4
Q

why does acidity of a drug affect absorption?

A

ionised form cannot cross membranes and therefore the acidity (equilibrium between ionised and unionised) affects absorption

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5
Q

what are 3 locations drugs can be distributed to?

A

proteins, tissues, effect site

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6
Q

what affect do protein-bound drugs have on the body?

A

no effect while protein bound

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7
Q

what happens to strength of a drug administered with another if both have high protein affinity?

A

strength of drug will be more as they compete for proteins to bind to

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8
Q

what is a common example of an enzyme inducer drug?

A

Alcohol

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9
Q

what happens to slow and fast metabolisers who are administered codine?

A

slow- no effect

fast- very quick … respiratory arrest

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10
Q

warfarin and which type of juice can cause a serious interaction?

A

grapefruit juice

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11
Q

what effect do agonists have on receptors?

A

bind to receptors causing activation

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12
Q

what effect to antagonists have on agonists?

A

reduce effect of agonists

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13
Q

what are the routes of drug administration? (10)

A

orally, subcutaneously, IV, IM, topically, sublingually, intra arterial, rectal, intrathecal, inhalation

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14
Q

which vaccinations make up the 6 in 1?

A

diphtheria, hep B, polio, Hib, tetanus, whooping cough

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15
Q

what is another name for diamorphine?

A

heroin

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16
Q

what is the reverse drug to opioids?

A

naloxone

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17
Q

order the routes of administration from quickest to slowest

A

IV, subcut & IM, oral

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18
Q

what is potency of a drug?

A

how many mg are required to produce a given effect, highly potent drug requires less mg for desired effect

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19
Q

what is efficacy of a drug?

A

the drugs ability to produce a desired effect, what effect do you get when binding occurs

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20
Q

what is tolerance in relation to drugs?

A

down regulation of receptors due to over stimulation therefore higher dose required, subjects get a reduced reaction to drug over long-term usage

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21
Q

what is dependence in relation to drugs?

A

neurones adapt to repeated exposure and individual functions normally only in the presence pf drug, psychological - craving, euphoria, physical effects too

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22
Q

how do opioids produce the euphoric effects?

A

inhibit pain transmitter release at spinal cord and midbrain

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23
Q

which receptors do opioids work on?

A

M receptors

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24
Q

where do opioids act, in addition to the pain system, and what are the consequences?

A

M receptors are found in pain system, gut and respiratory system
constipation and respiratory depression are common side effects

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25
Q

what steps should you take if suspecting someone of opioid induced respiratory depression?

A

call for help, ABC, naloxone IV

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26
Q

what is intrathecal administration?

A

through spinal cord into subarachnoid space

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27
Q

what is pinocytosis?

A

entry of substance into cell cytoplasm by budding

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28
Q

what is the difference between water and lipid solubility in ionised and unionised forms of drugs?

A

ionised-water soluble

unionised-lipid soluble

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29
Q

what is first pass metabolism?

A

drug metabolism can greatly reduce concentration of drug before it reaches circulation, barriers to circulation include: intestinal lumen, intestinal wall, liver, lungs

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30
Q

why is intestinal lumen a barrier to circulation? (1st pass metabolism)

A

bacteria and digestive enzymes may reduce or hydrolyse drugs

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31
Q

why is intestinal wall a barrier to circulation? (1st pass metabolism)

A

cellular enzymes, efflux transporters- transport drug back to lumen

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32
Q

how can liver metabolism of drugs delivered to digestive system be avoided?

A

deliver drugs to area not drained by splanchnic to liver, e.g. mouth and rectum

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33
Q

what are efflux transporters?

A

present in membrane of most cells and move substances out of cell, active process

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34
Q

what is a side effect?

A

an unintended effect related to pharmalogical properties of a drug

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35
Q

what do ABCDEF in Rawlins Thompson classification of adverse drug reactions stand for?

A
Augmented pharmacology
Bizarre
Chronic use
Delayed presentation
End of treatment
Failure of therapy
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36
Q

what is an example for A of Rawlins Thompson classification?

A

Augmented pharmacological: Morphine and constipation

37
Q

what is Rawlins Thompson classification used for?

A

Classifying adverse drug reactions

38
Q

which types of reactions fall into A of the Rawlins Thompson classification?

A

Augmented pharmacological: Predictable, common, dose dependent reactions

39
Q

what is an example for B of Rawlins Thompson classification?

A

Bizarre: Anaphylaxis and Penicillin

40
Q

which types of reactions fall into B of the Rawlins Thompson classification?

A

Bizarre: unpredictable, not dose dependent, idiosyncratic (unique/peculiar)

41
Q

what is an example for C of Rawlins Thompson classification?

A

Chronic use: Osteoporosis and long-term steroid use

42
Q

what types of reactions fall into C of the Rawlins Thompson classification?

A

Chronic use

43
Q

what is an example for D of Rawlins Thompson classification?

A

Delayed presentation: malignancies and immunosuppression drugs

44
Q

what types of reactions fall into D of Rawlins Thompson classification?

A

Delayed presentation, years after exposure

45
Q

what is an example for E of Rawlins Thompson classification?

A

End of treatment: opioid withdrawal

46
Q

which types of reactions fall into E of Rawlins Thompson classification?

A

End of treatment, withdrawal from drugs

47
Q

what is an example for F in Rawlins Thompson classification?

A

Failure of therapy: oral contraceptive pill failure with enzyme inhibitor drug

48
Q

what does DoTS stand for?

A

Dose related
Timing
Susceptibility of patient

49
Q

what is DoTS used for?

A

Classifying adverse drug reactions

50
Q

what are risk factors associated with adverse drug reactions?

A
age- elderly, neonatal
gender- female>male
polypharmacy
genetic predisposition
allergy and hypersensitivity
renal impairment
non adherence
hepatic impairment
51
Q

what are the classic symptoms of acute anaphylaxis in response to drug?

A
rash (in minutes)
vasodilation- red
swelling
urticaria
angioedema
bronchoconstriction
52
Q

what is the difference between allergic anaphylaxis and non-immune anaphylaxis?

A

allergic happens upon second exposure to agent

53
Q

what is treatment for anaphylaxis?

A

ABC

ADRENALIN! (EpiPen or 500mg IM)

54
Q

what effects does adrenalin have on the body?

A

vasoconstriction, bronchodilation, reduces oedema, stimulation of B1 receptors in the heart

55
Q

what category of drug is naproxen?

A

NSAID

56
Q

which enzyme does naproxen inhibit?

A

cyclooxygenase

57
Q

what are contraindications?

A

times when a drug shouldn’t be prescribed due to harmful effects

58
Q

which substances do NSAIDS inhibit synthesis of?

A

prostaglandins

59
Q

what effect do NSAIDS have on patients with asthma?

A

can exacerbate asthma, causing bronchospasms

may cause allergic reaction symptoms

60
Q

what risk factors are important when considering prescribing NSAIDS in a patient?

A
age>65
atherosclerosis
chronic hypertension
renal problems
reduced blood volume
61
Q

what is a common ACE inhibitor?

A

Ramipril

62
Q

what are ACE inhibitors commonly used for?

A

hypertension, heart failure, diabetic nephropathy

63
Q

what are the possible adverse effects of ACE inhibitors?

A
hypotension
acute renal failure
hyperkalaemia
pregnancy- teratogenic effects to foetus
cough- dry and persistent
rash
anaphalactic reactions
64
Q

why is a cough common in patients taking ACE inhibitors?

A

ACE also breaks down bradykinin, so inhibition causes a build up of kinins in respiratory tract

65
Q

where are ACE inhibitors metabolised?

A

kidneys

66
Q

what is the mechanism of ACE inhibitors?

A

competitive inhibitors of ACE which converts angiotensin 1 to angiotensin 2

67
Q

what effect do ACE inhibitors have of angiotensin 2 and therefore what occurs?

A

reduced angiotensin 2 production

BP reduced due to less vasoconstriction

68
Q

what are ARBs?

A

angiotensin 1 receptor blockers

69
Q

which receptors detect angiotensin 2?

A

angiotensin 1 receptors

70
Q

if patients are struggling with ACE inhibitor cough, which drugs can be used in their place?

A

ARBs

71
Q

what are examples of ARBs?

A

candesartan, valsartan

72
Q

what is an example of a calcium channel blocker?

A

amlodipine

73
Q

what type of calcium channels are targeted pharmacologically?

A

L type channels

74
Q

what are the side effects of calcium channel blockers that work on peripheral vasodilation?

A

flushing, headache, oedema, palpitations

75
Q

what is a common side effect of the calcium channel blocker verapamil?

A

constipation

76
Q

what are common examples of beta blockers?

A

bisoprolol, metoprolol

77
Q

what is selectivity of beta blockers?

A

some work on B1 receptors and others work on both B1&2 receptors (non selective)

78
Q

what is the selectivity of Bisoprolol?

A

B1 selective

79
Q

which 2 common resp conditions are worsened by beta blockers?

A

COPD and asthma

80
Q

on which part of the nephron do thiazides work?

A

distal tubules

81
Q

to which 2 groups of patients would you prescribe calcium channel blockers initially for hypertension?

A

age>55

afro-Caribbean

82
Q

which 6 types of drugs are used to manage IHD?

A
calcium channel blockers
antiplatelet
nitrates
beta blockers
statins
ACE inhibitors
83
Q

what is an example of a common nitrate used for IHD or angina?

A

GTN spray

84
Q

which antiplatelet drugs are commonly administered for patients with IHD?

A

LD aspirin & clopidogrel

85
Q

what is an example of a statin commonly used?

A

simvastatin

86
Q

what do statins do?

A

reduce cholesterol

87
Q

what do antiplatelets do?

A

thin blood, reduce clotting

88
Q

what do nitrates do?

A

vasodilation