Schizophrenia

Question 1

What is the first antipsychotic called

Answer 1

Chlorpromazine

Question 2

What was the first antipsychotic actually developed for

Answer 2

Anti histamine

Question 3

What does the first antipsychotic do

Answer 3

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

Question 4

Chemical classses of typical neuroleptics

Answer 4

Phenothiazine
Butyrophenones
Thioxanthines

Question 5

What makes these drugs dirty drugs

Answer 5

The act on many receptors

Question 6

What receptors do these drugs act

Answer 6

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

Question 7

What does interacting with many receptor cause

Answer 7

Lots of SE

Question 8

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

Answer 8

Dopamine receptors - dopamine hypothesis

Question 9

When are atypical neuroleptic used

Answer 9

As a second generation when the typical don’t work

Question 10

When were they developed

Answer 10

More recent than typical

Question 11

What makes them atypical drugs

Answer 11

Block dopamine

If they treat negative symptoms they are atypical

Question 12

Distinction from typical on the basis of

Answer 12

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

Question 13

Clozapine facts

Answer 13

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

Question 14

Risperidone, zotepine, sertindole

Answer 14

Serotonin, dopamine antagonists

Question 15

Quetiapine

Answer 15

Novel type - first line for newly diagnosed

Question 16

Clozapine used with who and why

Answer 16

First line for TR patients

Due to the potentially fatal SE

Question 17

Aripiprazole is a

Answer 17

Partial D2 antagonists

Question 18

Typical neuroleptics 3 key facts

Answer 18

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

Question 19

Atypical 3 key facts

Answer 19

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

Question 20

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

Answer 20

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

Question 21

What area is said to be involved with the negative symptoms

Answer 21

Mesocortical pathway

Question 22

Positive symptoms

Answer 22

Mesolimbic symptoms

Question 23

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

Answer 23

Hypofunction

Question 24

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

Answer 24

Hyperfunction

Question 25

What types of SE are there

Answer 25

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

Question 26

What are the main types of SE

Answer 26

Anti emetic Increased prolactin release Motor disturbances

Question 27

How does the ant emetic effect happen

Answer 27

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

Question 28

Happens with the increased prolactin release

Answer 28

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

Question 29

Happens with the motor disturbances

Answer 29

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

Question 30

SE that are not dopamine caused

Answer 30

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

Question 31

SE of atypical neuroleptics

Answer 31

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

Question 32

Is it all about dopamine

Answer 32

No | As another receptors are effected too

Question 33

MARTAs what does they block

Answer 33

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

Question 34

Problems with the dopamine hypothesis

Answer 34

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