antidepressants

Question 1

emotional and biological symptoms of depression

Answer 1

low confidence/motivation, and loss of libido/appetite

Question 2

unipolar depression, and to who it occurs

Answer 2

mood swings in same direction, with late onset

Question 3

types of unipolar depression- include genetics

Answer 3

reactive ie due to stressful events- NO genetic component or endogenous (from within)- genetic component

Question 4

bipolar depression: how common, how early, genetic?

Answer 4

back and forth between mania (lots of energy) and depression- less common and occurs earlier: also genetic component

Question 5

monamine theory of depression/mania, and why valid

Answer 5

idea that depression due to less monoamines in the brain ie NA and 5-HT (seretonin), and mania opposite- still valid as based on pharmacological evidence ie antidepressants increase monoamines

Question 6

TCAs- mechanism and example+ delayed effects with significance

Answer 6

EQUAL inhibition of reuptake of both NA and 5HT- also leads to delayed down-regulation of 5HT and beta adrenoreceptors, hence delayed effects- amitriptyline

Question 7

pharmacokinetics of TCA’s: absorption, how bound, metabolism

Answer 7

rapid absorption but BOUND HEAVILY in blood: metabolised into ACTIVE metabolites

Question 8

side effects at therapeutic dosage

Answer 8

atropine-like effects, drowsiness and postural hypotension

Question 9

side effects at toxic soage

Answer 9

CNS- seizures, respiatory depressiob: CVS- arrhythmias: often used to try and commit suicide

Question 10

how other drugs can affect dose of TCA’S

Answer 10

drugs that are heavily PPB or metabolised by P450 enzymes displace TCA’s from PP/enzyme= greater effect

Question 11

how TCAS relate to alcohol

Answer 11

they add to depressant effect of alcohol

Question 12

TCAS and antihypertensives

Answer 12

when given together, BP must be monitored more closely

Question 13

MAO receptors

Answer 13

either MAO-A (breaks down NA+ 5HT) or MAO-B (breaks down dopamine)

Question 14

MAO inhibitors- selectivity, type of inhibition + delayed effects+ example

Answer 14

mostly non selective, and cause IRREVERSIBLE inhibiton= long duration: delayed effects are down-regulation of B adrenoreceptors+ 5 H-T receptors, thus clinical response delayed- phenelzine

Question 15

pharmacokinetics- absorption, half life

Answer 15

rapid absoprtion as well, shorter half life than TCA’s, BUT longer duration (as irreversible)

Question 16

side effects of MAOI’s

Answer 16

atropine-like effects (LESS than TCAS’s), postural hypotension+ sedation, LIVER TOXIICITY, and WEIGHT GAIN (makes you hungry)

Question 17

cheese reaction of MAOI’S+ other cause of hypertension

Answer 17

tyramine containing foods eg cheese increase NA, and if combined with MAO’s can lead to hypertension- MAOIs and TCAS together can do this too

Question 18

what other drug should not be combined with MAOI’s

Answer 18

pethidine= hyperpyrexia (increase B.P)

Question 19

alternative MAO inhibitor

Answer 19

MOCLOBEMIDE- selective for MAO-A, and REVERSIBLE ie lower duration

Question 20

SSRIs- example and mechanism

Answer 20

fluoxetine- selective 5HT reuptake inhibition ONLY

Question 21

comparision with TCAS/MAOI’sq

Answer 21

less side effects and safer if overdose, but less effective

Question 22

pharmacokinetics- half life, and delayed or not

Answer 22

longest half life, delayed action

Question 23

what fluoxetine not given with

Answer 23

TCAS and MAO’s as compete for hepatic enzymes= enhanced effects

Question 24

side effects

Answer 24

less libido, insomnia, and diarrhoea

Question 25

other drugs

Answer 25

venlafaxine- dose-dependent reuptake inhibitor ie first inhibit 5HT, then NA: 2nd line treatmnet: mirtazapine- a2 receptor antagonist less -feedback of NA and 5HT

Question 26

arguments against monoamine theory

Answer 26

effects of anti-depressants delayed, and drugs like cocaine increase NA, but are NOT anti-depressants