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pharmacology of antipsychotics Flashcards

1
Q

what causes positive symptoms in schitzophrenia?

A

Positive symptoms are caused by too much dopamine in the mesolimbic pathway

(subcortical dopamine hyperactivity)

Mesolimbic pathway is from:
Ventral Tegmental Area (VTE) -> Nucleus Accumbens (NA)

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2
Q

what is the mesolimbic dopamine pathway?

A

from the Ventral Tegmental Area (VTA) -> Nucleus Accumbens (NA)

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3
Q

What causes negative symptoms in schitzophrenia?

A

Negative symptoms are caused by a reduction of dopamine in the mesocortical pathway

(frontal dopamine hypoactivity)

Mesocortical pathway is from:
Ventral Tegmental Area (VTE) -> Cortex

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4
Q

what is the mesocortical pathway?

A

from the Ventral Tegmental Area -> Cortex

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5
Q

what is used to treat positive symptoms?

A

Dopamine antagonist antipsychotics
-because positive symptoms are due to dopamine hyperactivity in the subcortical area (mesolimbic pathway from VTA-> nucleus acumbens)

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6
Q

what dopamine pathway is involved in movement?

A

Nigrostriatal pathwy
Substantia Nigra -> Striatum (caudate + putamen)

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7
Q

What is the nigrostriatal pathway?

A

Dopamine pathway controlling movement

From Substantia Nigra -> Striatum (caudate + putamen)

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8
Q

What affect can antipsychotics have on the nigrostriatal pathway and how may it present?

A

Antipsychotics decrease dopamine levels in the nigrostriatal pathway and can induce Parkinsonism (extrapyramidal motor symptoms)

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9
Q

What is the tuberoinfindibular pathway?

A

Hypothalamus -> Pituitary gland

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10
Q

what releases prolactin?

A

pituitary gland

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11
Q

what is the relationship between dopamine and prolactin?

A

inverse relationship

increase in dopamine leads to a decrease in prolactin

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12
Q

what affect can antipsychotics have on the tuberoinfundibular pathway and how may this present?

A

Antipsychotics decrease levels of dopamine in Hypothalamus causing increase levels of Prolactin in Pituitary

Increase Prolactin:
-Decrease FSH and lead to Amenorrheoa
-Galactorrhoea

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13
Q

examples of typical/ first generation antipsychotics?

A

-Haloperidol
-Chlorpromazine
-Zuclopenthixol
-Flupentixol
-Trifluoperazine
-Prochlorperazine

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14
Q

MofA of antipsychotics?

A

Antagonists of:
-Dopamine (D2) Receptor
-Histamine (H1) Receptor
-Adrenoceptors (alpha 1) Receptor
-Muscarinic (M1) Receptor

Dopamine - most obvious

HAM- these people be going ham so give them an antipsychotic!

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15
Q

SE of histamine (H1) receptor antagonist?

A

weight gain + sedation

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16
Q

SE of adrenoceptor (alpha 1) receptor antagonist?

A

-hypotension
-priapism (prolonged erection)

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17
Q

SE of muscarinic (M1) receptor antagonist?

A

anticholinergic SE:
-dry mouth
-constipation
-dilated pupils

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18
Q

What type of antipsychotics are more likely to give you extrapyramidal symptoms?

A

1st generation AKA typical

Examples:
-Haloperidol
-Chlorpromazine
-Zuclopenthixol
-Flupentixol
-Trifluoperazine
-Prochlorperazine

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19
Q

what type of antipsychotics are more likely to cause Neuroleptic Malignant Syndrome?

A

1st generation AKA typical

Examples:
-Haloperidol
-Chlorpromazine
-Zuclopenthixol
-Flupentixol
-Trifluoperazine
-Prochlorperazine

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20
Q

examples of 2nd generation AKA atypical antipsychotics?

A

-Clozapine
-Olanzapine
-Quetiapine
-Risperidone
-Paliperidone
-Lurasidone
-Ariprazole

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21
Q

what receptors do second generation drugs bind to that first generation drugs dont?

A

they bind to both:
-Dopamine (D2) receptors
-Seretonin 2a Receptor (5HT2a)

First generation drugs do not bind to serotonin 2a receptors

22
Q

what SE is risperidone (2nd generation) likely to cause?

A

hyperprolactinaemia

23
Q

what SE is Clozapine (2nd generation) more likely to cause?

A

Agranulocytosis

24
Q

what antipsychotic needs monitored closely and why?

A

Clozapine as it can cause agranulocytosis
-need to routinely check bloods

25
Q

what is the most effective antipsychotic and why is it not first line?

A

Clozapine= most effective antipsychotic

-Not first line as risk of agranulocytosis

26
Q

what are examples of Extrapyramidal symptoms?

A

-Dystona
-Akathisia
-Parkinsonism
-Tardive Dyskenesia

27
Q

How does Dystonia present?

A

-Involuntary movement of head/face
-often sustained muscle contraction e.g. eyes stuck looking up or neck stuck in one place
-commonly in young men
-usually happens straight after treatment (antipsychotic)

28
Q

who usually experiences dystonia after being given antipsychotic?

A

-young men

29
Q

when after administering antipsychotic would people normally experience dystonia?

A

-soon after treatment

30
Q

what is the management for dystonia?

A

IM anticholinergics

31
Q

what is akathasia? (EPSE)

A

unpleasant restlessness

32
Q

when will akathasia occur in relation to antipsychotic ? (ESPSE)

A

within 2 weeks of taking antipsychotic

33
Q

treatment for akathasia? (EPSE)

A

-reduce dose (beta bloxker/ benzodiazepine)

34
Q

presentation of Parkinsonism? (EPSE)

A

-bradykinesia, rigidity and tremor

35
Q

how long after taking an antipsychotic will parkinsonism occur ?

A

months after taking antipsychotic

36
Q

management of Parkinsonism? (EPSE)

A

antiparkinson medication

37
Q

presentation of Tardive dyskensia (EPSE)?

A

-face and extremities make involuntary movements

38
Q

when does Tardive dyskenisia occur in relation to antipsychotics? (EPSE)

A

-with prolonged use

39
Q

what is the managment of tardive dyskenesia?

A

stop the drug

40
Q

how does neuroepilelptic malignant syndrome present?

A

-motor, mental and autonomic dysfunction with hyperpyrexia

41
Q

when would neuroepileptic malignant syndrome occur in relation to taking an antipsychotic?

A

within a few weeks

42
Q

management of neuroepileptic malignant syndrome?

A

-stop drugs
-supportive
(10% mortality)

43
Q

what is monitored for antpsychotics?

A

Fasting blood glucose, prolactin, ECG, FBC

44
Q

why is fasting blood glucose monitored for antipsychotics?

A

-Antipsychotics act on glucose and insulin homeostasis
-they impair glucose tolerance and increase the risk of T2DM

45
Q

why is prolactin monitored for antipsychotics?

A

-Antipsychotics decrease dopamine in the tuberoinfindibular pathway (Hypothalamus -> pituitary)

-Dopamine and prolactin have an inverse relationship (decrease dopamine increase prolactin)

46
Q

why is an ECG used to monitor antipsychotics?

A

-as they can cause QT prolongation

47
Q

why is a FBC done to monitor antipsychotics?

A

-Clozapine can cause agranulocytosis
(would appear as decreased neutrophils on FBC)

48
Q

why should a patient make you aware if they smoke- antipsychotics?

A

smoking increases the levels of clozapine
-so patient should let doctor know if they are stopping smoking too

49
Q

which antipsychotic has best SE profile?

A

Aripiprazole

50
Q

what antipsychotic has highest T2DM risk and why?

A

Olanzapine has
-it causes most weight gain

51
Q

what antipsychotic should be given to someone with Parkinsons?

A

-No antipsychotics should be given to someone with Parkinsons
-Give Lorazepam instead

52
Q

SE clozapine?

A

-agranulocytosis (1%), neutropaenia (3%)

-reduced seizure threshold - can induce seizures in up to 3% of patients

-constipation

-myocarditis: a baseline ECG should be taken before starting treatment

-hypersalivation

psych (18 decks)

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