WK 3: mental health Flashcards

1
Q

adverse drug reactions=

A

unwanted/ harmful reactions from a drug at normal therapeutic doses

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2
Q

example of adverse drug reaction=

A

anaphylaxis after taking a drug

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3
Q

adverse drug event=

A

untoward occurance after exposure to a drug that is not necessarily caused by the drug

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4
Q

example of adverse drug event

A

having a road accident whilst on medication

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5
Q

type A adverse drug reactions=

A

augmented reactions resulting from exaggeration of a drug’s normal actions at normal therapeutic dose

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6
Q

respiratory depression with opioids or bleeding with warfarin = what type of drug reaction

A

type A

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7
Q

type B adverse drug reactions =

A

bizarre reactions -novel responses not expected from known actions of drug

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8
Q

anaphylaxis with penicillin

skin rashes with antibiotics= what type of drug reaction

A

type B

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9
Q

dry mouth with TCAs = what type of drug reaction

A

type A

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10
Q

type C reactions=

A

continuing reactions, persist for a very long time

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11
Q

osteonecrosis of jaw with bisphosphonates=

A

type C reaction

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12
Q

type D reactions=

A

delayed reactions -become apparent after some time after the use of medicine

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13
Q

leukopenia 6 weeks after a dose of lomustine =

A

type D reactions

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14
Q

type E reactions=

A

end-of-use reactions -withdrawal

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15
Q

BDZ anxiety and perceptual distubances after stopping=

A

type E reaction

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16
Q

most adverse drug reactions=

A

type A

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17
Q

primary effects of type A drug reactions =

A

augmentation of therapeutic action -e.g beta blocker bradycardia

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18
Q

secondary effects of type A drug reactions=

A

can rationalise from pharmacology -e.g beta blocker bronchospasm

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19
Q

constipation with opioids because

A

stimulation of Mu receptor in GI tract

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20
Q

why sedation with antihistamines

A

blockage of central histaminergic receptors

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21
Q

which antihistamines are less sedating (2)

A

2nd gen -
certirizine
Loratadine

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22
Q

which antihistamine is more sedating

A

1st gen

chlorphenamine

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23
Q

why are second generation antihistamines less sedating

A

lipophobic so don’t readily cross blood brain barrier

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24
Q

what drugs induce parkinsonism

A

dopamine antagonists

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25
Q

which class of antipsychotics cause less extrapyramidal SEs

A

atypical antipsychotics

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26
Q

3 atypical antipsychotics (less EPS)

A

clozapine
olanzapine
risperidone

27
Q

why atypical antipsychotics have less EPS

A

less affinity for D2 receptors and more for D4 receptors

28
Q

dopamine effect on prolactin

A

inhibitory effect

29
Q

effect on prolactin from dopamine antagonists

A

hyperprolactinemia –> breast tenderness, amenorrhoea

breast tenderness

30
Q

what are atypical antipsychotics less likely to cause

A

tardive dyskinesia

31
Q

prochlorperazine=

A

dopamine antagonist

32
Q

SE of prochlorperzine and metaclopramide

A

EPS

33
Q

tardive dyskinesia and parkinsonism can occur when after drug

A

after long term use

34
Q

dystonia and akathisia can occur when after drug

A

single dose

35
Q

why do NSAIDs cause GI upset

A

NSAID stop COX –> stopping prostaglandins –> GI mucosal damage

36
Q

COX role in prostaglandin synthesis

A

rate limiting enzyme converts arachidonic acid into PGG2 and then to PGH2

37
Q

what converts PGH2 to prostanoids (prostaglandins and thromboxane)

A

gastric and duodenal mucosa

38
Q

e.g of NSAIDs (5)

A
  • ibuprofen
  • indomethacin
  • naproxen
  • diclofenac
  • aspirin
39
Q

what do Celecoxib and rofecoxib selectively inhibit

A

COX-2

40
Q

downside of selective COX-2 inhibitors

A
  • still block COX-1 -potential for stomach damage

- CV events

41
Q

primary metabolism of paracetamol

A

conjugation with glucuronide and sulphate

42
Q

toxic compound small amounts of paracetamol are oxidised to

A

quinone imine -extremely toxic

43
Q

how is quinone imine inactivated

A

conjugation with glutathione and excreted in urine

44
Q

treatment for paracetamol overdose

A

methionine and N-acetylcysteine

45
Q

methionine and N-acetylcysteine =

A

boost levels of glutathione in liver to prevent liver failure

46
Q

if a patient developed a rash after amoxicillin for tonsillitis=

A

allergic reaction- true drug rash

47
Q

if a patient has infectious mononucleosis and given amoxicillin and develops a rash=

A

not a true allergic reaction

48
Q

when does a rash always develop with IM

A

when given amoxicillin or ampicillin

49
Q

risk factors for anaphylaxis/ allergy

A

history of atopic allergy -hay fever, asthma, eczema

50
Q

what antibiotics to avoid with a rash after penicillin

A

penicillin
cephalosporin
beta lactam
(Tazocin and co-amoxiclav contain penicillin)
(imipenem, meropenem and carbapenem cotnain beta lactam ring)

51
Q

ramipril + naproxen can cause

A

AKI

52
Q

drug related AKI common with (3)

A

antiretroviral
aminoglycoside antibiotics
NSAIDs

53
Q

ACEi cause in the kidney

A

efferent arteriolar vasodilation

54
Q

NSAIDs cause in the kidney

A

afferent arteriolar vasoconstriction (decreased prostacyclin synthesis)

55
Q

levodopa + carbidopa –>

A

benefit - prevents peripheral decrease in Levodopa so more can cross blood-brain barrier

56
Q

amoxicillin + clavulanic acid –>

A

decreased bacterial resistance

57
Q

Carbamazepine and warfarin –>

A

INR decreases upon carbamazepine -more clotting and sub-therapeutic INR levels (close monitoring needed)

58
Q

cytochrome P450 inhibitors (5)

A
fluconazole 
clarithromycin 
erythromycin 
grapefruit juice 
ritonavir
59
Q

cytochrome P450 inducers (4)

A

carbamazepine
rifampicin
rifabutin
St. johns wort

60
Q

enzyme induction leads to

A

-tolerance or decreased effectiveness
-increased doses
-increased metabolism and excretion
-slow development
-

61
Q

combined oral contraceptive and rifampin

A

contraceptive cannot be relied upon whilst on rifampicin

62
Q

enzyme inhibition leads to

A
  • sensitivity
  • decreased dose
  • drug accumulation
  • rapid development
63
Q

e.g enzyme inhibition reactions (2)

A
  • statins and clarithromycin

- warfarin and amiodarone

64
Q

warfarin and amiodarone –>

A

prolonged INR increased bleeding risk