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PCOL2 > Antidepressants and Antipsychotics > Flashcards

Antidepressants and Antipsychotics Flashcards

1
Q

Five (out of seven) of these must be present for a diagnosis of depression, and be present for 2 weeks.

A 
Depressed mood
Loss of interest/pleasure
Appetite changes; weight loss or gain
Feelings of worthlessness or guilt
Fatigue
Problems with thinking and concentration/indecisiveness
Sleep problems - insomnia or hypersomnia
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2
Q

4% have had X in the last month; 43% of them have Y.

A

Depressive episode; severe disability.

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3
Q

Depression recurs in 40% or 99% of people?

A

40%.

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4
Q

Main feature of bipolar?

A

Distinct manic and depressive episodes.

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5
Q

Some bipolar patients have only manic episodes. How many?

A

10%

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6
Q

Which are the monoamine transmitters?

A

5HT (Seratonin) and NAd (Noradrenaline) and DA (dopamine).

5HT and NAd are the main drug targets though.

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7
Q

Which molecules are in that big Rang and Dale slide?

A

5-HT, NAd, BDNF (brain-derived neurotrophic factor) and glutamate. Those second two aren’t monoamines.

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8
Q

Sort into good/bad guys for neurogenesis and protection from neuroapoptosis:
BDNF, NAd, Cortisol, Seratonin, Glutamate

A

BDNF, NAd 5HT are good.

Glutamate and cortisol are bad.

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9
Q

Think glutamate, think…

A

excitotoxic effects on hippocampal glutamatergic neurons, with poorly understood influence by antidepressants.
Skipping the detrimental transcription and going straight for the neuroapoptotis in the hippocampus.

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10
Q

Think hypothalamus-pituitary-adrenal cortex axis, think…

A

cortisol enhancing transcription of detrimental (pro-apoptotic or anti-protective) genes in the hippocampus and/or prefrontal cortex.
NAd, 5HT and BDNF counteract this transcription.

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11
Q

Cortisol release by the adrenal glands is stimulated by X from the Y, which is stimulated by B release by the A, stimulated by stress.

A

adrenocorticotrophic hormone (ACTH); pituitary; corticotrophin releasing hormone (CTH); hypothalamus

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12
Q

-pramines and -triptylines are all what?

A

TCAs.

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13
Q

TCAs all end in either…

A

-pramine or -triptyline

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14
Q

Two things to remember about TCAs - one relates to a neurotransmitter it may or may not influence greatly, the other relates to onset of something.
A bonus third is about their effectiveness.

A
  1. little to no effect on DA uptake.
  2. Takes 2-3 weeks for mood elevation to kick in.
  3. They are equieffective; choice of TCA relates to differing unwanted sedative and anticholinergic effects.
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15
Q

Three uses of TCAs.

A
  1. against depression symptoms (70% success rate)
  2. bipolar depression
  3. 2nd line for anxiety
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16
Q

What adverse effects of TCAs tend to develop tolerance?

A

hypotension and anticholinergic effects.

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17
Q

What are “anticholinergic effects”?
AKA “atropine-like” effects?
(i.e. pro-sympathetic or pro-parasympathetic?)

A

Block parasympathetic signalling -> leads to sympathetic effects. Blocks acetylcholine transmission.
Also called atropine-like effects.
Also called muscarinic blockade.
Also called antimuscarinic effects.

Bonus details: pupil dilation, far vision, dry mouth, inhibited digestion, blood goes to muscles, vasodilation, higher heart rate, bronchodilation.

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18
Q

What are common anticholinergic side effects of a drug?

A

Dry-mouth, constipation, blurry vision.

Also called atropine-like effects.
Also called muscarinic blockade.
Also called antimuscarinic effects.

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19
Q

Name the big four side effect headings of TCAs.

A
  1. alpha blockade (makes you fat, dizzy and bad in bed - not very alpha. Alpha is muscular, a beast in the sack and can change positions without fainting).
  2. histamine blockade (H is a monoamine)
  3. antimuscarinic effects
  4. Misc (overdose/change in dose)
20
Q

Think alpha blockade (side effect), think…

A

TCA side effect. Fat, dizzy, bad in bed.

21
Q

Think histamine blockade, think…

A

TCA side effect - causes sleepiness. Remember Ken’s advice about plane travel.

22
Q

Do TCAs have a low therapeutic index?

A

Yes

23
Q

TCA dose changes risk two problems. What are they and what who do you have to watch out for?

A

SEIZURES and HEART PROBLEMS.
Increasing dose can lower the seizure threshold and cause arrhythmias. Cardiotoxicity can kill the human.
Watch out for epileptics and people with heart conduction problems.

24
Q

TCAs can kill the human in two main situations. What are they?

A

Overdose/dose change - cardiotoxicity.

In combination with MOAIs.

25
Q

Name six SSRIs.

PROMPT: Fluo, fluvo, Sir. Trampoline, parrot, sitting metallic baby, e-sittingmetallicbaby

A

fluoxetine, fluvoxamine, paroxetine, citalopram, escitalipram, sertraline

26
Q

Name six SSRIs (no prompts)

A

fluoxetine, fluvoxamine, paroxetine, sertraline, citalopram, escitalopram

27
Q

Pro of SSRIs compared to TCAs

A

Less anticholinergic effects

28
Q

Pro of SSRIs compared to MOAIs

A

No “cheese reactions”

29
Q

Con of SSRIs compared to TCAs

A

Not as good at treating severe depression.

Equieffective for moderate

30
Q

What are three irreversible MOAIs?

PROMPT: fish herb magazine, Noz in Cyprus being mean, isolated cardboard box with a pimple.

A

tranylcypromine, phenelzine, isocarboxazid

31
Q

What is the reversible MOAI?

PROMPT: mock bam bam

A

Moclobemide

32
Q

MOAb is good for oxidising DA. What’s MOAa good for and in what order?

A

5HT > NAd > DA

33
Q

Three side effects of MAOIs unrelated to cheese

A

Insomnia, weight gain, peripheral oedema.

34
Q

Lotta foods contain tyramine. MOAIs block tyramine metabolism in the gut wall. What’s the problem here?

A

Massive andrenergic stimulation - hypertensive crisis. Because tyramine enhances sympathetic catelcholamine release into adrenal medulla.

35
Q

Why does moclobemide have less of a tyramine reaction?

A

Because moclobemide is selective for MOAa (hence 5HT > NAd > DA), and tyramine can be metabolised by MOAb.

36
Q

Apart from no tyramine reaction, why is moclobemide better than phenelzine, tranylcypromide or isocarboxazid?

A

Few CV effects,

much harder to overdose on.

37
Q

What are two reasons SSRIs are better than TCAs for people with CV problems?

A

Less H1 antagonism means no sedation.

Less atropine-like symptoms

38
Q

So out of TCAs, SSRIs, irreversible MOAIs and reversible MOAIs, which two are hard to overdose on?

A

SSRIs and reversible MOAIs.

BUT SSRIs can cause seratonin syndrome in combination.

39
Q

What two headings are big for SSRI unwanted effects?

Other than seratonin syndrome, which is an adverse effect

A

Like teenage Snake from the Simpsons, 1. aggression and 2. suicidal thoughts among children and adolescents.

40
Q

What does seratonin syndrome look like? List four symptoms.

A
  1. Febrility (temp and shivering), 2. me-in-iso mentally, 3. sweating, 4. clonus (flailing), 5. hyperreflexia
41
Q

Different antidepressant classes are similar in X but different in Y.

A

X: efficacy
Y: side effects

42
Q

How long should an effective antidepressant regimen go for?

A

Two years or more.

43
Q

Human is mildly depressed. Give human drugs?

A

No - only from moderate depression and up.

44
Q

How effective are antidepressants as mood stabilisers?

A

NOT AT ALL never do it, this will fuck up the human.

-results include mood elevation, cycle acceleration and mixed episodes.

45
Q

Lithium is more selective for the A and the B because sodium channels are more active there.

A

Brain and kidney.

46
Q

Lithium has neuroprotective effects (antiapoptotic and anti-oxidative).
What does IP3-related signal inhibition got to do with it?

A

Inhibits Glu activation
Inhibits DA activation (mania)
Facilitates GABA.

47
Q

Does lithium have a narrow or a wide therapeutic index?

A

Narrow. Blood levels must be monitored.

PCOL2 (24 decks)

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