Schizophrenia Flashcards

1
Q

What is the first antipsychotic called

A

Chlorpromazine

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2
Q

What was the first antipsychotic actually developed for

A

Anti histamine

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3
Q

What does the first antipsychotic do

A

It attentuates positive symptoms without excessive sedation
Not depressant - preserves intellectual function
Classical/ typical/ first generation neuroleptic. Had a profound impact on treatments allowed people to be released from institutions - symptom control

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4
Q

Chemical classses of typical neuroleptics

A

Phenothiazine
Butyrophenones
Thioxanthines

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5
Q

What makes these drugs dirty drugs

A

The act on many receptors

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6
Q

What receptors do these drugs act

A
Dopamine D1 and D2 receptor families 
Ach muscarinic 
Histamine H1 
Noradrenaline alpha adrenoreceptor 
5HT serotonin
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7
Q

What does interacting with many receptor cause

A

Lots of SE

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8
Q

What receptor out of the ones the drugs act on has been implicated as the causation from this efficacy of the drug to the receptors

A

Dopamine receptors - dopamine hypothesis

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9
Q

When are atypical neuroleptic used

A

As a second generation when the typical don’t work

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10
Q

When were they developed

A

More recent than typical

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11
Q

What makes them atypical drugs

A

Block dopamine

If they treat negative symptoms they are atypical

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12
Q

Distinction from typical on the basis of

A

Pharmacological profile - higher dopamine selectivity
Fewer pyramidal side effects - motor
More effective against the negative symptoms
More effective in the treatment resistant group
Sulpiride, amisulpride- selective dopamine antagonists D2/D3 receptors

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13
Q

Clozapine facts

A
Best example of an atypical neuroleptic 
More effective antipsychotic 
But it is a dirty dirty drug binding to many receptors 
Fewer motor SE 
And can control the negative symptoms
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14
Q

Risperidone, zotepine, sertindole

A

Serotonin, dopamine antagonists

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15
Q

Quetiapine

A

Novel type - first line for newly diagnosed

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16
Q

Clozapine used with who and why

A

First line for TR patients

Due to the potentially fatal SE

17
Q

Aripiprazole is a

A

Partial D2 antagonists

18
Q

Typical neuroleptics 3 key facts

A

Control the positive symptoms
Neg symptoms not well controlled
SE are problematic

19
Q

Atypical 3 key facts

A

Better for negative symptoms
Less marked SE
Some efficacy in the treatment resistant group

20
Q

What is the current thinking about why there are positive and negative symptoms

A

Due to different areas in the brain affected causing the positive symptoms and the negative symptoms

21
Q

What area is said to be involved with the negative symptoms

A

Mesocortical pathway

22
Q

Positive symptoms

A

Mesolimbic symptoms

23
Q

What is thoughts to happen to the mesocortical pathway to cause the negative symptoms

A

Hypofunction

24
Q

What is thought to happen to the mesolimbic system to cause the positive symptoms

A

Hyperfunction

25
Q

What types of SE are there

A

1 type is due to the direct effects of the action of the drugs on dopaminergic receptors
And the other type is due to the activation of other receptors

26
Q

What are the main types of SE

A

Anti emetic
Increased prolactin release
Motor disturbances

27
Q

How does the ant emetic effect happen

A

Dopamine receptor block in the chemoreceptor trigger zone
This done is dopaminergic so responds to the treatment D2 is blocked
H1 receptors block is also important
Neural SE

28
Q

Happens with the increased prolactin release

A

released from the pit gland
Its release is normally inhibited by dopamine
D2 receptor mediated
Neuroleptics block the inhibition
Causes breast swelling, pain, location - males and females
SE can effect the compliance and schiz can reemerge

29
Q

Happens with the motor disturbances

A

Acute: dystonias - due to blockade of the dopamine receipts in striatum nigra
Dystonias- involuntary movements - face, tongue and neck
Parkinsonian- tremor at rest, muscle rigidity and decreased mobility
Developed relatively rapidly
Reversible - reduce dose
Chronic: tardive dyskinesia
Severely disabling motor disturbance
Involuntary movements to face and tongue, limbs and trunk
Slowly developing -tardive
Generally irreversible
Not produced by all neuroleptics
Don’t know when this SE will emerge could. E taking The drug years and will suddenly appear
Drugs that don’t produce this are used as cirstvline treatment

30
Q

SE that are not dopamine caused

A

Related to blockade of other receptor sites
Anti muscarinic effects - dry mouth, constipation, visual disturbances
Postural hypotension due to alpha adrenoreceptor block
Sedation due to the histamine H1 receptor block

31
Q

SE of atypical neuroleptics

A

Better SE profiles
Mainly due to greater selectivity
Lower incidence of motor disturbances
Increased likelihood of compliance

32
Q

Is it all about dopamine

A

No

As another receptors are effected too

33
Q

MARTAs what does they block

A

D2, D4, 5HTA, Ach muscarinic unique and effective pharmacology
Pharmacology decreased likelihood of tardive dyskinesia
More effect for the negative symptoms so not just about dopamine
Clozapine has serious SE - agranulocytosis and myocarditis

34
Q

Problems with the dopamine hypothesis

A

Neuroleptics take weeks to work therefore secondary effects are important
Less effective on neg symptoms so are too simplistic
Dysfunction of dopaminergic systems may not be primary cause could be secondary to other causes