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integrated studies in mental health > SCHIZOPHRENIA > Flashcards

SCHIZOPHRENIA Flashcards

1
Q

what characterizes anxiety disorders?

A

Characterised by the inappropriate expression of fear

e.g. Panic attacks (sudden, intense feeling of terror);
Generalised Anxiety Disorder (at least 6 months of persistent and excessive anxiety or worry); PTSD (re-experiencing of an extremely traumatic event; various phobias

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2
Q

what characterizes affective disorders?

A

Affect =mood. = Disordered emotions

e.g. Major depression (symptoms everyday for at least 2 weeks)

Bipolar Disorder (repeated episodes of mania and depression)

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3
Q

epidemiology of schizophrenia

________ risk in general population
Typically starts in ____________
Men (______) are at a slightly greater risk of developing SZ
Women (___________) are at a greater risk of bipolar disorder
Higher incidence associated with________ and ____________
In all cultures, similar incidence across continents

fill in the blanks

A

1/100 lifetime risk in general population
Typically starts in late adolescence or early adulthood
Men (15-25) are at a slightly greater risk of developing SZ
Women (20-30) are at a greater risk of bipolar disorder
Higher incidence associated with urbanicity and migration
In all cultures, similar incidence across continents

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4
Q

what are the positive symptoms of schizophrenia?

A

Delusions
Hallucinations
Disorganised speech
Grossly disorganized or catatonic behaviour

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5
Q

what are the Negative symptoms of schizophrenia?

A

Reduced expression of emotion
Poverty of speech
Difficulty in initiating goal-directed movements
Cognitive/Memory impairment

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6
Q

list the types of schizophrenia?

A

Paranoid schizophrenia

Disorganised schizophrenia

Catatonic schizophrenia

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7
Q

what characterizes Paranoid schizophrenia

A

delusions and hallucinations are present

thought disorder, disorganized behaviour, and mood flattening are absent

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8
Q

what characterizes disorganoized schizophrenia?

A

thought disorder and mood flattening are present

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9
Q

what characterizes Catatonic schizophrenia?

A

exhibits agitated, purposeless movement

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10
Q

what is the Aetiology (Causes) of schizophrenia?

A

Environmental factors

genetics

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11
Q

what are the Environmental factors that cause schizophrenia?

A

Social stress
Prenatal infection and famine
Obstetric and perinatal complications
Older paternal age
Cannabis use

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12
Q

how do genetics affect schizophrenia?

A
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13
Q

Pathophysiology of Schizophrenia

what are the core features of schizophrenia?

A

The core features of schizophrenia include deficits in cognitive processes mediated by the circuitry of the dorsolateral prefrontal cortex (DLPFC).

These deficits are associated with a range of molecular and morphological alterations in the DLPFC,

Could be a cause, consequence, or compensation in relation to other changes

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14
Q

what are the number of hypotheses based pathophysiology of schizophrenia?

A

Pharmacology
Genetics
Neurochemistry

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15
Q

which neurotransmitters are hypothetically involved in schizophrenia?

A

Dopamine hypothesis

Glutamate hypothesis

GABA hypothesis

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16
Q

in the dopamine hypothesis of schizophrenia

which brain structures are involved?

A

Substantia Nigra (SN)

Ventral tegmental area (VTA)

Tuberohypophyseal system

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17
Q

how is the substantia nigra involved in schizophrenia?

what does it do normally?

A

Projects to the striatum (Facilitates the initiation of voluntary movements (Parkinson’s Disease)

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18
Q

how is the Ventral tegmental area (VTA) involved in schizophrenia?

what does it do normally?

A

Innervates frontal cortex and limbic system

Called Mesocorticolimbic dopamine system

Involved in reward/motivation; psychiatric disorders

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19
Q

how is the Tuberohypophyseal system involved in schizophrenia?

what does it do normally?

A

Connects Arcuate & Paraventricular neurons to Hypothalamus and Pituitary

Dopamine release inhibits prolactin secretion

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20
Q

what is the Most widely considered neurochemical hypothesis of schizophrenia

A

The dopamine hypothesis of schizophrenia

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21
Q

The dopamine hypothesis of schizophrenia Postulates ___________________

A

Postulates that symptoms of schizophrenia may result from excess dopaminergic neurotransmission particularly in mesolimbic and striatal brain regions

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22
Q

list 5 evidence for The dopamine hypothesis of schizophrenia

A

Many antipsychotic drugs strongly block D2 receptors, especially in mesocorticolimbic system

Drugs that increase dopaminergic activity such as levodopa (precursor) ; amphetamine (releases dopamine); apomorphine (direct agonist) either aggravate schizophrenia or produce psychosis

D receptor number increased in post-mortem brains of schizophrenics

PET scans show increased D receptor density in schizophrenics

Successful treatment of schizophrenics changes the levels of homovanillic acid (a metabolite of dopamine)

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23
Q

list 3 evidence against The dopamine hypothesis of schizophrenia

A

Antipsychotic drugs only partially effective for most (ineffective for some) patients

NMDA receptor (glutamate receptor) antagonists (phencyclidine) more potent in inducing schizophrenic symptoms than dopamine agonists

Dopamine receptors. Which D receptors are involved?

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24
Q

what are the evidence for the The glutamatergic hypothesis of schizophrenia

A

NMDA receptor antagonists (phencyclidine; ketamine; MK-801)
 potent activators of dopamine release
 cause marked psychotic symptoms in healthy human volunteers and
exacerbation of symptoms in schizophrenic patients
Treatment of schizophrenia with D-Serine, glycine, and sarcosine:
 modulate NMDA receptors
 has therapeutic benefit, particularly with regard to negative symptoms

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25
Q

what is the evidence for the The glutamatergic hypothesis of schizophrenia

in reference to NMDA Receptor agonist

A

NMDA receptor antagonists (phencyclidine; ketamine; MK-801)
🡺 potent activators of dopamine release
🡺 cause marked psychotic symptoms in healthy human volunteers and
exacerbation of symptoms in schizophrenic patients

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26
Q

what is the evidence for the The glutamatergic hypothesis of schizophrenia

in reference to Treatment of schizophrenia with D-Serine, glycine, and sarcosine

A

Treatment of schizophrenia with D-Serine, glycine, and sarcosine:

  🡺 modulate NMDA receptors
   🡺 has therapeutic benefit, particularly with regard to negative symptoms
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27
Q

what is the glutamatergic hypothesis of schizophrenia?

A

Hypofunction of the NMDA receptor, possibly on critical GABAergic interneurons

Less inhibition onto Principal Glutamatergic cells 🡺 excessive activity of Glutamatergic cells

This activates Dopamine expressing cells

🡺 More Dopamine released

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28
Q

what is the evidence for The GABAergic hypothesis of schizophrenia

A

Inhibitory interneurons are essential for controlling the activity of the excitatory pyramidal cells
Deficiency in signalling through the TrkB neurotrophin receptor
 leads to reduced GABA synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia
Death of a sub-population of these neurons
 decreased GABA production
 enhanced excitability of pyramidal neurons
 Enhanced activation of DA neurons  more DA release

R

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29
Q

how does “Deficiency in signalling through the TrkB neurotrophin receptor” provide evidence for The GABAergic hypothesis of schizophrenia

A

🡺 leads to reduced GABA synthesis in the parvalbumin-containing subpopulation of inhibitory GABA neurons in the dorsolateral prefrontal cortex of individuals with schizophrenia

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30
Q

how does “Death of a sub-population of these neurons” provide evidence for The GABAergic hypothesis of schizophrenia

A

🡺 decreased GABA production
🡺 enhanced excitability of pyramidal neurons
🡺 Enhanced activation of DA neurons 🡺 more DA release

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31
Q

what are the drug therapies used for schizophrenia?

A

Antipsychotic drugs

Dopamine

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32
Q

dopamine is one of the therapies for schizophrenia?

this principle takes advantage of major dopamine pathways in the CNS

Any drug affecting Dopamine activity has the potential to act in any/all of these pathways
🡺 Diverse adverse effects

describe the different dopamine pathways in the CNS?

A

Meso-cortical-limbic pathway: VTA to limbic and neocortex

Nigro-striatal pathway: Substantia Nigra to Striatum

Tuberoinfundibular system: Hypothalamus to Pituitary

Medullary-Periventricular pathways: Neurons in the motor nucleus of the vagus

Incertohypothalamic pathway: From Zona incerta to hypothalamus and amygdala.

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33
Q

all the dopamine pathways affect something in the brain

which pathway is mostly related to behaviour?

A

Meso-cortical-limbic pathway

34
Q

all the dopamine pathways affect something in the brain

which pathway is involved in the cordination of voluntary movement?

A

Nigro-striatal pathway

35
Q

all the dopamine pathways affect something in the brain

which pathway is involved in the inhibition of of prolactin release?

A

Tuberoinfundibular system

36
Q

all the dopamine pathways affect something in the brain

which pathway might be involved in feeding behaviour but the real projections are unknown?

A

Medullary-Periventricular pathways

37
Q

all the dopamine pathways affect something in the brain

which pathway is involved in fear conditioning?

A

Incertohypothalamic pathway

38
Q

dopamine Generally exerts _____________

A

Generally exerts slow inhibitory action in CNS (depends on the specific D receptor)

39
Q

The functions of dopaminergic pathways divide broadly into?

list 3

A

motor control (nigrostriatal system)

behavioural effects (mesolimbic and mesocortical systems)

endocrine control (tuberohypophyseal system).

40
Q

state features of Dopamine Receptors

A

5 Dopamine receptors (D1 to 5)

Functionally 2 families: D1-like (D1 & D5) + D2-like (D2; D3;D4)

All are metabotropic (G-protein coupled

41
Q

function of D1 receptor?

A

increases cAMP by Gs-coupled activation of adenylyl cyclase
expressed mainly in Putamen; Nucleus Accumbens; Olfactory tubercle

42
Q

function of D1 receptor?

A

increases cAMP expressed in hippocampus and hypothamus

43
Q

function of D5 receptor?

A

increases cAMP expressed in hippocampus and hypothamus

44
Q

Therapeutic potency of Antipychotic drugs does not ________________

A

Therapeutic potency of Antipychotic drugs does not correlate with their affinity for binding the D1 receptor

45
Q

function of D2 receptor?

A

decreases cAMP by Gi-coupled inhibition of adenylyl cyclase

inhibits calcium channels

opens potassium channels

expressed both pre- and post-synaptically on neurons caudate-putamen; nucleus accumbens; olfactory tubercle

46
Q

Activation of D2 receptors 🡺 increased ___________ in rats. 🡺 Model for screening antipsychotic drugs

A

Activation of D2 receptors 🡺 increased motor activity and stereotypes behaviour in rats. 🡺 Model for screening antipsychotic drugs

47
Q

Antipsychotic agents _________

A

Antipsychotic agents block D2

48
Q

Binding affinity to dopamine receptor strongly correlated with ______ and _______effects

A

Binding affinity strongly correlated with antipsychotic potency and extrapyramidal effects

49
Q

function of D3 receptor?

A

decreases cAMP frontal cortex; medulla; midbrain

50
Q

function of D4 receptor?

A

decreases cAMP

51
Q

Classification of antipsychotic drugs

what are they?

A

first-generation (‘typical’) antipsychotics

second-generation (‘atypical’) antipsychotics

52
Q

list different examples of first-generation (‘typical’) antipsychotics

list 5

A

chlorpromazine, haloperidol, fluphenazine, flupenthixol, clopenthixol

53
Q

list different examples of second-generation (‘atypical’) antipsychotics

A

clozapine, risperidone, sertindole, quetiapine, amisulpride, aripiprazole, zotepine

54
Q

state differences between typical and atypical groups pf antipsychotics

A

receptor profile

incidence of extrapyramidal side effects (less in atypical group)

efficacy (specifically of clozapine) in ‘treatment-resistant’ group of patients

efficacy against negative symptoms

55
Q

Antipsychotic drugs
First generation

what are the classes?

A

Phenothiazine class

Butyrophenone class

56
Q

Phenothiazine class has 3 groups what are they?

A

group1: chlorpromazine; levomepromazine; promazine

group 2: pericyazine; pipotiazine

group 3: fluphenazine; prochlorperazine

57
Q

what are the features of group 1 of phenothiazine class?

A

First to be developed#

Binding affinities for different receptors (D2;adrenergic > H1; mACh; 5-HT2)
🡺 Marketed under the name Largactil

Pronounced sedative effects which wear off with repeated administration

Moderate anti-muscarinic and extrapyramidal side effects

Also endocrine;hypotensive S/E

Relatively inexpensive

Low clinical potency (chlorpromazine)

58
Q

what are the features of group 2 of phenothiazine class?

A

Moderate sedative effects
Severe anti-muscarinic but fewer extrapyramidal side effects

59
Q

what are the features of group 2 of phenothiazine class?

A

Moderate sedative effects
Severe anti-muscarinic but fewer extrapyramidal side effects

60
Q

what are the features of group 3 of phenothiazine class?

A

Fewer sedative and anti-muscarinic effects
Pronounced extrapyramidal side effects

61
Q

what are the features of haloperidol in the Butyrophenone class

these are typically why it is worse than second generation antipsychotics?

A

Use is limited due to severe EPS

High D2 receptor affinity

Potent antipsychotic

More severe EPS though less anticholinergic; hypotensive S/E

62
Q

which dopamine receptors are really important in dopamine drug therapy?

A

D2, D3, AND D4

63
Q

which drug is under the butyrophenone class?

A

Haloperidol

64
Q

what is the features of clozapine

this is a second generation

why is it better than first generation?

A

Greater affinity for 5HT2 receptors than D2

Potent antagonist at D4-receptors

Efficacy in treatment-resistant patients

Effective against negative and positive symptoms

No EPS

Risk of agranulocytosis (2%):regular blood counts required

Lowers seizure threshold 🡺

Weight gain

Clozapine licensed for use in treatment of Schiz only in patients unresponsive to or intolerant of conventional therapy 🡺 patient monitoring

Olanzapine is similar, without risk of agranulocytosis

65
Q

what are the features of risperidone?

this is also a second generation

what advantage does it offer?

A

Greater affinity for 5HT2 receptors than D2
Broad efficacy and more potent than clozapine
Little or no EPS, ANS and Cardiac side effects at low dose

66
Q

what are the features of Aripiprazole ?

this is also a second generation

what advantage does it offer?

A

Fairly new
Partial agonist at D2 receptor
Limited S/E effect profile (Maybe not known yet)
Long half life

67
Q

what are the Advantages of 2nd generation agents over 1st

A

Little or no EPS
Treating positive and negative symptoms
Treatment resistant patients

68
Q

what are 7 NICE guidelines on the use of atypical antipsychotics.

A

Considered when choosing “newly diagnosed” psychotic patients.

For management of an acute schizophrenic episode when discussion with the patient is not possible.

Considered for a patient experiencing unacceptable S/E of conventional antipsychotics

Considered for a patient in relapse whose symptoms were previously inadequately controlled.

No need to change to atypical antipsychotics if patient stabilised and no SE with 1st generation

Clozapine introduced if schizo inadequately controlled despite the sequential use of 2 or more antipsychotics (one of which should be 2nd generation) each for 6-8 weeks

If symptoms do not respond to optimised dose of clozapine, measure clozapine plasma levels before adding 2nd antipsychotic to augment clozapine.

69
Q

what are the Non-psychiatric indications for antipsychotics

A

Anti-emetics

Sedatives

70
Q

how do antipsychotics act like anti-emetics?

A

Act by blocking dopamine receptors centrally and peripherally in the stomach
E.g. Prochlorperazine used solely for this purpose

this happens mainly with older agents

71
Q

how do antipsychotics act like sedatives?

A

Block Histamine 1 receptor e.g. Promethazine

72
Q

what are the adverse effects of Antipsychotics

A

1 Extrapyramidal Reaction:
Acute dystonia (Parkinsonian movements)

  Tardive dyskinesia

2 Seizures

73
Q

what adverse effects of antipsycotics called extrapyramidal reaction?

A

(part of the Motor System involved in the co-ordination of movement)

74
Q

what is the onset of Acute dystonia (Parkinsonian movements)?

is it reversible?

A

Early onset: (dopamine receptor blockade in Nigrostriatal pathway)
Often reversible.

75
Q

what is the onset of Tardive dyskinesia ?

also what is it?

is it reversible?

A

(involuntary, repetitive movements)

Late onset: (dopamine receptor supersensitivity)

More serious. Very debilitating. Often irreversible. Most serious/debilitating S/E

76
Q

what decreases the threshold for seizures as an adverse effects?

A

Mainly Chlorpromazine. Sometimes Clozepine

77
Q

what are the Autonomic Nervous System Effects as Adverse Events of Antipsychotics

A

Anti-muscarinic effects:
Loss of accommodation; dry mouth; difficulty urinating; constipation

  1. Adreno-receptor blocking effects:
    Othostatic hypotensions; impotence
78
Q

what are the Metabolic and Endocrine Effects as Adverse Events of Antipsychotics

A

Weight gain (esp clozapine; olanzapine) (5HT2 blockade)
Hyperglycaemia secondary to insulin resistance
Hyperprolactinaemia (Dopamine normally blocks prolactin secretion)

79
Q

what are the cardiac Effects as Adverse Events of Antipsychotics

A

Thioridazine (first generation): ventricular arrythmias; cardiac conduction block; sudden death

Ziprasidone (2nd generation): carries greatest risk of ECG effects (QT prolongation)

80
Q

what are the toxic or allergic reactions as Adverse Events of Antipsychotics

A

Agranulocytosis: Clozapine; life threatening 🡺 regular blood tests

Jaundice; skin eruptions

81
Q

what are the behavioural Effects as Adverse Events of Antipsychotics

A

Older agents are unpleasant to take
Pseudodepression
Toxic confusional state

integrated studies in mental health (20 decks)

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