WK 3: mental health

Question 1

adverse drug reactions=

Answer 1

unwanted/ harmful reactions from a drug at normal therapeutic doses

Question 2

example of adverse drug reaction=

Answer 2

anaphylaxis after taking a drug

Question 3

adverse drug event=

Answer 3

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

Question 4

example of adverse drug event

Answer 4

having a road accident whilst on medication

Question 5

type A adverse drug reactions=

Answer 5

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

Question 6

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

Answer 6

type A

Question 7

type B adverse drug reactions =

Answer 7

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

Question 8

anaphylaxis with penicillin

skin rashes with antibiotics= what type of drug reaction

Answer 8

type B

Question 9

dry mouth with TCAs = what type of drug reaction

Answer 9

type A

Question 10

type C reactions=

Answer 10

continuing reactions, persist for a very long time

Question 11

osteonecrosis of jaw with bisphosphonates=

Answer 11

type C reaction

Question 12

type D reactions=

Answer 12

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

Question 13

leukopenia 6 weeks after a dose of lomustine =

Answer 13

type D reactions

Question 14

type E reactions=

Answer 14

end-of-use reactions -withdrawal

Question 15

BDZ anxiety and perceptual distubances after stopping=

Answer 15

type E reaction

Question 16

most adverse drug reactions=

Answer 16

type A

Question 17

primary effects of type A drug reactions =

Answer 17

augmentation of therapeutic action -e.g beta blocker bradycardia

Question 18

secondary effects of type A drug reactions=

Answer 18

can rationalise from pharmacology -e.g beta blocker bronchospasm

Question 19

constipation with opioids because

Answer 19

stimulation of Mu receptor in GI tract

Question 20

why sedation with antihistamines

Answer 20

blockage of central histaminergic receptors

Question 21

which antihistamines are less sedating (2)

Answer 21

2nd gen -
certirizine
Loratadine

Question 22

which antihistamine is more sedating

Answer 22

1st gen

chlorphenamine

Question 23

why are second generation antihistamines less sedating

Answer 23

lipophobic so don’t readily cross blood brain barrier

Question 24

what drugs induce parkinsonism

Answer 24

dopamine antagonists

Question 25

which class of antipsychotics cause less extrapyramidal SEs

Answer 25

atypical antipsychotics

Question 26

3 atypical antipsychotics (less EPS)

Answer 26

clozapine olanzapine risperidone

Question 27

why atypical antipsychotics have less EPS

Answer 27

less affinity for D2 receptors and more for D4 receptors

Question 28

dopamine effect on prolactin

Answer 28

inhibitory effect

Question 29

effect on prolactin from dopamine antagonists

Answer 29

hyperprolactinemia --> breast tenderness, amenorrhoea | breast tenderness

Question 30

what are atypical antipsychotics less likely to cause

Answer 30

tardive dyskinesia

Question 31

prochlorperazine=

Answer 31

dopamine antagonist

Question 32

SE of prochlorperzine and metaclopramide

Answer 32

EPS

Question 33

tardive dyskinesia and parkinsonism can occur when after drug

Answer 33

after long term use

Question 34

dystonia and akathisia can occur when after drug

Answer 34

single dose

Question 35

why do NSAIDs cause GI upset

Answer 35

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

Question 36

COX role in prostaglandin synthesis

Answer 36

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

Question 37

what converts PGH2 to prostanoids (prostaglandins and thromboxane)

Answer 37

gastric and duodenal mucosa

Question 38

e.g of NSAIDs (5)

Answer 38

- ibuprofen - indomethacin - naproxen - diclofenac - aspirin

Question 39

what do Celecoxib and rofecoxib selectively inhibit

Answer 39

COX-2

Question 40

downside of selective COX-2 inhibitors

Answer 40

- still block COX-1 -potential for stomach damage | - CV events

Question 41

primary metabolism of paracetamol

Answer 41

conjugation with glucuronide and sulphate

Question 42

toxic compound small amounts of paracetamol are oxidised to

Answer 42

quinone imine -extremely toxic

Question 43

how is quinone imine inactivated

Answer 43

conjugation with glutathione and excreted in urine

Question 44

treatment for paracetamol overdose

Answer 44

methionine and N-acetylcysteine

Question 45

methionine and N-acetylcysteine =

Answer 45

boost levels of glutathione in liver to prevent liver failure

Question 46

if a patient developed a rash after amoxicillin for tonsillitis=

Answer 46

allergic reaction- true drug rash

Question 47

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

Answer 47

not a true allergic reaction

Question 48

when does a rash always develop with IM

Answer 48

when given amoxicillin or ampicillin

Question 49

risk factors for anaphylaxis/ allergy

Answer 49

history of atopic allergy -hay fever, asthma, eczema

Question 50

what antibiotics to avoid with a rash after penicillin

Answer 50

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

Question 51

ramipril + naproxen can cause

Answer 51

AKI

Question 52

drug related AKI common with (3)

Answer 52

antiretroviral aminoglycoside antibiotics NSAIDs

Question 53

ACEi cause in the kidney

Answer 53

efferent arteriolar vasodilation

Question 54

NSAIDs cause in the kidney

Answer 54

afferent arteriolar vasoconstriction (decreased prostacyclin synthesis)

Question 55

levodopa + carbidopa -->

Answer 55

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

Question 56

amoxicillin + clavulanic acid -->

Answer 56

decreased bacterial resistance

Question 57

Carbamazepine and warfarin -->

Answer 57

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

Question 58

cytochrome P450 inhibitors (5)

Answer 58

``` fluconazole clarithromycin erythromycin grapefruit juice ritonavir ```

Question 59

cytochrome P450 inducers (4)

Answer 59

carbamazepine rifampicin rifabutin St. johns wort

Question 60

enzyme induction leads to

Answer 60

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

Question 61

combined oral contraceptive and rifampin

Answer 61

contraceptive cannot be relied upon whilst on rifampicin

Question 62

enzyme inhibition leads to

Answer 62

- sensitivity - decreased dose - drug accumulation - rapid development

Question 63

e.g enzyme inhibition reactions (2)

Answer 63

- statins and clarithromycin | - warfarin and amiodarone

Question 64

warfarin and amiodarone -->

Answer 64

prolonged INR increased bleeding risk