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Basic Pharmacology > 18. Antidepressants and Antipsychotics > Flashcards

18. Antidepressants and Antipsychotics Flashcards

1
Q

Depression and schizophrenia are associated with …

A

dysregulation of monoamine neurotransmitter function

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2
Q

Give the monoamine neurotransmitters
What are they involved in?

A
  • 5-hydroxytryptamine (5-HT, serotonin) - depression, anxiety
  • dopamine - schizophrenia
  • noradrenaline - depression and anxiety
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3
Q

What’s the dopamine theory of SZ?

A
  • that SZ is associated with increased dopamine/DA function
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4
Q

Give 3 main dopamine pathways in the brain

A
  • nigrostriatal
  • mesolimbic and memocortical projections
  • tuberoinfundibular
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5
Q

Explain the nigrostriatal dopamine pathway

A
  • substantia nigra go to dorsal striatum
  • controls fine movement (EPS)
  • linked to Parkinson’s in dysfunction
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6
Q

Explain mesocortical/mesolimbic dopamine pathway

A
  • VTA to frontal cortex/ventral striatum
  • for cognition/mood (cortex) and reward/addiction (ventral striatum)
  • linked to SZ in dysfunction
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7
Q

Role of dopamine in regulation of prolactin secretion

A
  • suckling
  • sensed in hypothalamic nuclei
  • dopamine (prolactin releasing inhibiting factor) and prolactin releasing factor released from here
  • affects the anterior pituitary to inhibit prolactin release to mammary tissues
  • mammary tissue can’t produce milk and no differentiation of mammary tissue during pregnancy during maternal behaviour
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8
Q

Explain tuberoinfundibular pathway

A
  • hypothalamus to pituitary stalk
  • tonic inhibition of prolactin secretion
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9
Q

How do dopamine receptors affect SZ?

A
  • use D2 antagonists to counteract increase of dopamine function in SZ
  • D2 antagonists are effective antipsychotics
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10
Q

D2 antagonism in nigrostriatal DA pathway causes what?
Explain

A
  • extrapyramidal side effects (EPS)
  • Parkinson’s syndrome - tremor, muscle rigidity, loss of facial expression
  • tardive dyskinesia - repetitive rhythmical involuntary movement, lip smacking, chewing etc, rocking rotation of ankles, legs, marching in place etc, humming, grunting
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11
Q

D2 antagonism in tuberoinfundibular DA pathway causes …

A
  • hyperprolactinaemia
  • can be galactorrhoea or gynaecomastea
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12
Q

Antipsychotics have an affinity for …
List some

A
  • nondopaminergic receptors
  • histamine receptors
  • muscarinic receptors
  • adrenergic reeptors
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13
Q

Antipsychotics which are H1 mediated cause what?

A
  • sedation
  • weight gain
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14
Q

Antipsychotics which are M1 mediated cause what?

A
  • dry mouth
  • blurred vision
  • constipation
  • urinary retention
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15
Q

Antipsychotics are classified on basis of …

A

side effects

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16
Q

There are … groups of phenothiazines

A

3

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17
Q

Group 1 penothiazines are …
Group 2?
Group 3?

A
  • chlorpromazine
  • thioridazine
  • fluphenazine
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18
Q

Side effect profile of the phenothiazine classification of antipsychotics

A
  • sedation (affinity for H1)
  • anticholinergic (affinity for M1)
  • EPS (mainly D2)
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19
Q

List the antipsychotic classfiications

A
  • phenothiazine
  • thioxanthenes
  • butyrophenones
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20
Q

Fluphenazone is … times more potent than other phenothiazines

A

50

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21
Q

Side effect profile of thioxantheses is similar to …
Give an example of one

A
  • phenothiazines
  • flupenthixol
22
Q

Give an example of a butyrophenone

A

haloperidol

23
Q

Side effect profile of butyrophenones

A
  • selective to D2
  • lack muscarinic and antihistamine activity (no sedation)
  • but EPS a problem
24
Q

Limitations of classical antipsychotics

A
  • around 1/3 of SZ patients fail to respond
  • limited efficacy against negative symptoms
  • high proportion of patient relapse
  • side effects and compliance issues
25
Q

How to improve classic antipsychotics?

A
  • find drugs that are low in extrapyramidal side effects
26
Q

Positive symptoms of SZ

A
  • disorders of thought/disorganised behaviour
  • hallucinations (aural and visual)
  • paranoia
27
Q

Negative symptoms of SZ

A
  • blunted emotions/anhedonia
  • social withdrawal
  • apathy/loss of energy
28
Q

List atypical antipsychotics

A
  • clozapine
  • olanzapine
  • risperidone
  • amisulpiride
  • quetiapine
29
Q

Positives to atypical antipsychotics

A
  • better EPS side effect profile without loss of antipsychootic efficacy
  • better at treating negative symptoms (lower affinity for D2 receptor, higher for D3, D4 (D2 family) and 5-HT2a receptor
  • effective in treatment resistant patients?
30
Q

Negatives to atypical antipsychotics

A
  • clozapine associated with agranulocytosis
  • high incidence of metabolic syndrome, weight gain in risperidone and olanzapine
31
Q

Hypothesis for mechanism of action of atypical antipsychotics

A
  • do have affinity for D2 but much faster dissociation rate from it (Koff) (loose binding)
  • so these drugs can be displaced by physiological phasic bursts of DA transmission (important in DA striatal pathways)
  • results in less distortion of physiological DA signalling in striatal pathways
32
Q

Types of antidepressants

A
  • tricyclic antidepressants (TCA)
  • selective serotonin reuptake inhibitor (SSRI)
  • monoamine oxidase inhibitors
33
Q

Examples of TCAs

A
  • amitriptyline
  • imipramine
  • lofepramine
34
Q

How do TCAs work?

A
  • inhibit 5-HT and NA uptake
35
Q

Negatives to TCA in regards to receptors

A
  • block M1 receptors (cause dry mouth, blurred vision, constipation, urinary retention)
  • block H1 receptors (sedation, weight gain)
  • block alpha 1 receptors (postural hypotension)
36
Q

TCAs are not used in …

A
  • elderly
  • cardiac patients
  • hepatic insufficiency
  • suicidal patients (overdose)
  • drivers and workers (sedations)
37
Q

Why are TCAs not used for cardiac patients?

A
  • increase chance of conduction abnormalities
38
Q

TCAs are useful for …

A
  • severe treatment resistant depression
  • where sedation is also required
  • where disease history indicates efficacy and tolerance
  • CHEAP
39
Q

What are
- SNRI?
- NARI?
Give examples

A
  • serotonin/noradrenaline reuptake inhibitors like venlafaxine
  • noradrenaline reuptake inhibitor like reboxitine
40
Q

SSRI, SNRI and NARI are …
How do they work?

A
  • 2nd generation antidepressants
  • selective for 5-HT and NA transporter and don’t have affinity for postsynaptic receptors
41
Q

Why do 2nd generation antidepressants have less sidde effects?

A
  • don’t have affinity for postsynaptic receptors
42
Q

SSRIs and TCAs have … antidepressant efficacy

A

equivalent

43
Q

SSRIs have a … adverse side effect profile than TCAs

A

better

44
Q

SSRI side effects

A
  • sexual dysfunction/impotence
  • gastrointestinal
  • precipitate anxiety
  • no sedation or anticholinergic
45
Q

Other uses of SSRI

A
  • effective in treating panic disorder, OCD and eating disorders
46
Q

Explain the 2 isoforms of monoamine oxidases

A
  • MAOa breaks down 5-HT and a bit of DA
  • MAOb breaks down DA
47
Q

Compare old and new monoamine oxidases

A
  • old ones blocked both isoforms irreversably like tranylcypromine, phenelzine - caused stimulant effects and dangerous in overdose
  • new ones are selective for MAOa - reversable inhibitors of monoamine oxidase A like moclobemide
  • less stimulant and safer
48
Q

Explain MAOI and cheese effect

A
  • hypertensive crisis
  • results from excess of dietary tyramine
  • either activates sympathetic nervous system itself or displaces endogenous amines from vesicles and indirectly activates sympathetic nervous system
49
Q

How do MAOI and SSRI’s interact?

A
  • serotonin syndrome
  • hyperthermia, confusion, hypertensive crisis
50
Q

Antiparkinson drugs lead to …

A

severe hypertension

Basic Pharmacology (16 decks)

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