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PBL Notes > PBL 8 - Schizophrenia- Psychosis > Flashcards

PBL 8 - Schizophrenia- Psychosis Flashcards

1
Q

What is the prefrontal association cortex?
What are the regions within it?
What is its function?

A
  • The cortical region that receives thalamic input from the dorsomedial nucleus
    • Little or no input from other thalamic nuclei
    • Granular cortex of frontal lobe
    • Region of frontal lobe that does not cause movement when stimulated

Regions:
• Orbitofrontal cortex (approximates limbic prefrontal)
• Medial prefrontal
• Dorsolateral prefrontal

Functions:
	• Planning for voluntary movements
	• Emotional regulation
	• Decision making
	• Working memory
	• Problem solving
	• Inhibition of inappropriate social responses
	• Verbal reasoning
	• Mental flexibility
	• Personality traits
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2
Q

What is the process of feeling fear?

A

• stimulus is presented
• Information is projected to the thalamus
• Amygdala receives information from
○ Hippocampus - about a conditioned stimulus
○ Thalamus- about current stimulus
• Amygdala integrates information and sends it to the hypothalamus
• Behaviour, autonomic, endocrine and inflammatory response occurs

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3
Q

What test can you perform to examine the pre-frontal cortex?

A

• Wisconsin card sorting test

○ Patient will show perseveration- persisting with a response that incorrect because they are unable to adapt

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4
Q

Where are the dopaminergic neurons located?

Where do they project to?

A

Origin:
• substantia nigra
• Ventral tegmental area

Project:
• VTA dopamine neurons project to the prefrontal cortex limbic structures, some basal ganglia components (ventral striatum

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5
Q

What is the target for controlling the psychotic symptoms of schizophrenia?

A

• Dopamine D2R antagonists located in the midbrain

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6
Q

How does the prefrontal cortex module dopaminergic input?

A
  • VTA dopamine cells project to the prefrontal cortex
    • The PFC then inhibits the limbic area (NuAcc) and the VTA dopaminergic cells
    • Feedback loop
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7
Q

What type of receptors does dopamine work on?

What effect do antipsychotics have?

A 
• They are ALL GPCR
	• There are at least 6 of them 
		○ D1 
		○ D2a and D2b
		○ D3-5
	• Two major groups
		○ D1 and D5 
		○ D2-5
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8
Q

What is the function of the different Dopamine receptors?
Where are they located?
What is the clinical function ?

A

D1 = in the striatum
D5 is in the cerebral cortex and hipocampus
Function:
• Coupled to Gs and STIMULATE CAMP
Clinical fx:
• Low affinity for most antipsychotic drugs

D2= In Neurons of the midbrain. Caudate and limbic regions (amygdala, nucleus accumbens, hippocampus and cerebral cortex)

Function:
• D2a = INHIBITS camp
○ Function as inhibitory autoreceptors decreasing firing of AP and dopamine release (feedback loop)
• D2b = stimualtes PKC and increases intracellular CA

Clinical Fx:
• High affinity for typical antipsychotic drugs
• D2 receptors may contribute to extrapyramidal side effects

D3 and D4
Location:
• restricted to the limbic system and cerebral cortex
• Weakly expressed in the basal ganglia

Function:
• atypical antipsychotics bind here and do not give rise to Extrapyramidal side effects

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9
Q

What is the possible link between Dopamine and Schizophrenia?

A

Overactivity of the meso-corticolimbic dopamine system. Depends on the following:
• Overdose of drugs that enhance dopamine release (L-DOPA) can lead to positive symptoms
• Drugs that are effective in treating positive symtpoms are potent blockers of dopamine receptors particularly D2
• The same drugs used for positive symptoms are used for drug induced psychosis
• Brains of patients at autopsy show increased levels of D2 receptors in caudate and nucleus accumbens especially in patients showing positive symptoms
• Negative symptoms resemble defect seen in patients after prefrontal damage

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10
Q

Explain the reward/pleasure pathway:

A

• 5HT neurons are located in the raphe neurons in the midbrain:
○ Activate the DA neurons in the Ventral tegmental area
○ Increased the release of Da in the Nucleus Accumbens
○ Auto inhibits the raphe neurons (where it comes from)
• Dopaminergic neurons
○ Originates in the VTA where it is stimulated by 5HT
○ Releases Dopamine which causes pleasure

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11
Q

What is the neurodevelopmental hypothesis of Schizophrenia?

A
  • Schizophrenia involves a primary lesion in the prefrontal cortex
    • This normally acts to modulate the stress response by inhibiting the amygdala
    • Usually comes online in adolescence and early adulthood
    • In Schizophrenia PFC does not come online to modulate stress
    • PFC deficit causes negative symptoms of ZA
    • PFC deficit reduces feedback inhibition of VTA dopamine neurons
    • Excessive mesolimbic dopamine transmission causes positive symptoms
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12
Q

What is the Glutamate Hypothesis in relation to schizophrenia?

A
  • Phencyclidine induces hallucinations and paranoia
    • Symptoms of intoxication are similar to those in schizophrenia- both positive and negative
    • PC does not affect dopaminergic transmission
    • PCP affects glutamatergic transmission by specifically BLOCKING NMDA receptors
    • VTA neurons require activity of glutamatergic afferent inputs in order to release dopamine in PFC or limbic system
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13
Q

What is Psychosis?

A

• it is a generic term that means a break from reality
• It is a symptom not an illness
• Caused by a variety of conditions that affect the functioning of the brain
• Includes:
○ Hallucinations
○ Delusions
○ Thought disorder

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14
Q

What are some differential diagnosis for Psychosis?

A 
• Dementia 
	• Delirium
	• Medications
	• Substance induced 
	• Mood disorders
		○ Bipolar
		○ Major depression with psychotic features
	• Personality disorders
		○ Paranoid
		○ Borderline
		○ Antisocial 
	• Misc
		○ PTSD
		○ Dissociative disorders
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15
Q

What are the functional causes of psychosis?

A
  • Schizophrenia
    • Biopolar
    • Severe depression
    • Sleep deprivation
    • Epileptic disorders
    • Exposure to traumatic event
    • Stress
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16
Q

What are some organic causes of psychosis?

A 
• Neurological disorders 
		○ Brain tumour 
		○ Dementia with lewy bodies
		○ Multiple sclerosis
		○ Sarcoidosis 
		○ Syphilis
	• Electrolyte disorders 
		○ Hypocalcaemia
		○ Hypernatraemia
		○ Hyponatraemia
		○ Hypokalaemia
	• Hypoglycaemia
	• Lupus
	• Aids
17
Q

How does cannabis effect your risk of developing schizophrenia?

A

• Frequent use doubles the risk of psychosis and schizophrenia

18
Q

What are important diagnostic questions in Psychosis?

A
  • Have organic cause been ruled out?
    • Is there a delirium or dementia (cognitive deficits)?
    • Is the illness episodic or continuous?
    • Are any negative or positive symptoms present
    • Is there a history of substance abuse?
    • What is the duration?
19
Q

What is the workup for someone with new onset psychosis?

A 
• Good clinical history 
	• Physical exam
	• Labs:
		○ Metabolic panel
		○ CBC with differential 
		○ B12, folate
		○ RPR, VDRL
		○ Serum alcohol 
		○ Urinalysis
		○ Thyroid profile
		○ Urine drug screen
		○ CSF/LP
		○ HIV serology
		○ CT-MRI
		○ EEG
20
Q

What Medications cause psychosis?

A
  • Bromocriptine
    • Phenylpropanolamine
    • Vigabatrin (antiepileptic by increasing GABA)
21
Q

What is the prevalence of Schizophrenia?

Epidemiology?

A
  • 1% of population worldwide
    • Lifetime risk equal for males and females
    • Age of onset for males = 18-25 years
    • Age of onset for females = 26-45 years
    • 20% have a second peak at 40-50 years
    • Early aggressive treatment decreases long term problems
22
Q

What is the diagnostic criteria for Schizophrenia?

A 
Must have at least two of the following symptoms
	• Delusions
	• Hallucinations
	• Disorganised speech 
	• Disorganised or catatonic behaviour
	• Negative symptoms

At Least 1 of the symptoms must be the presence of delusion. Hallucinations or disorganised speech.

* Impairment in social or occupational functioning
* Duration of illness for at least 6 months
* Symptoms not due to mood disorder or schizoaffective disorder 
* Symptoms not due to medical, neurological, or substance induced disorder
23
Q

What are the clinical features of Schizophrenia?

A 
•  Formal thought disorders:
		○ Neologisms
		○ Tangentiality
		○ Derailment
		○ Loosening of associations (word salad)
		○ Perseveration
	• Delusions
		○ Paranoid/persecutory
		○ Ideas of reference
		○ External locus of control
		○ Thought broadcasting
		○ Thought insertion, withdrawal
		○ Jealously
		○ Guilt
		○ Grandiosity
		○ Religious delusions
		○ Somatic delusions
	• Hallucinations
		○ Auditory
		○ Visual
		○ Olfactory
		○ Somatic/tactile
		○ Gustatory
	• Behaviour
		○ Bizarre dress/appearance
		○ Catatonia
		○ Poor impulse control
		○ Anger/agitation
		○ Stereotypies
	• Mood and affect
		○ Inappropriate affect
		○ Blunting of affect/mood
		○ Flat affect
		○ Isolation or dissociation affect
		○ Incongruent affect
24
Q

What is the onset and course of Schizophrenia?

A
  • Insiduous onset
    • Chronic course
    • More than 6 months
25
Q

What are the anatomical abnormalities found in patients with schizophrenia?

A

• Enlargement of the lateral ventricles
• Smaller than normal total brain volume
○ Particularly frontal and temporal lobes
• Cortical atrophy
○ Reduction in interneurons that inhibit the pyramidal neurons
○ Less cortical synchronisation
• Widening of third ventricle
• Smaller hippocampus
• Normal global cerebral flow
• Hypofrontality
• Failure to activate dorsolateral prefrontal cortex

26
Q

What are the differences between the dopamine systems?

Cell bodies, projections, functions and implications in schizophrenia?

A 
Nigro striatal:
Cell bodies = substantia Nigra
Projections = Caudate and Putament
Functions = movement 
Clinical implications = EPS, dystonias and Tardive dyskinesia

Mesolimbic:
Cell bodies = Ventral tegmental area, substantia Nigra
Projections = accumbens, amygdala, olfactory tubercle
Funcitons = emotions, affect and memory
Implication = Positive symptoms

Mesocortical:
Cell bodies = VTA
Projections = Prefrontal cortex 
Function = thought, volition, memory
Implications = blockade can worsen negative symptoms
27
Q

What is the psychosocial treatment options for schizophrenia?

A
  • Education and compliance
    • Hospitalise for acute loss of funcitoning
    • Outpatient rehabilitation treatment
    • Cognitive remediation therapy
    • Psychoanalysis - exploratory therapies have limited value
    • Families should be involved
28
Q

What is the role of Genetics in schizophrenia?

A
  • Schizophrenia is estimated to be 80% heritable
    • Monozygotic twins 40-50%
    • Dizygotic twins = 10-15% (same as first degree relatives)
29
Q

What is the medication approach to schizophrenia?

A
  • essential starting point of treatment
    • Minimum effective dosing
    • Avoid large doses if possible
    • Use what has been effective in the past
    • Avoid medications that have had poor side effects
    • First onset start with Atypicals antipsychotics
30
Q

How common is co-occuring disorders?

What risks are increased?

A 
• Occur in 50% of serious mental health disorder
	• Increased risk of:
		○ Relapse and rehospitalisation
		○ Suicide
		○ Financial stress
		○ Violence 
		○ Medical illness
31
Q

What are the positive symptoms of schizophrenia?

A
  • Hallucinations
    • Delusions
    • Bizarre behaviour
    • Positive formal thought disorder
    • Disorganised speech
    • Catatonic behaviour
32
Q

What are the Negative symptoms of Schizophrenia?

A
  • Loss of function
    • Flat affect
    • Alogia (poverty of speech)
    • Avolition and apathy
    • Social withdrawal
    • Lack of grooming and hygiene
33
Q

What are the cognitive deficits found in Schizophrenia?

A

• Poor performance on tasks involved in working memory and attention

34
Q

What are the proposed causes of schizophrenia?

A

• Genetic predisposition
• Developmental abnormality in utero and other developmental insults
• Structural abnormalities have been found in many brain regions
○ Temporal cortex (superior temporal gyrus, parahippocampal gyrus, hippocampus, amygdala)
○ Frontal cortex
• Several neurotransmitters implicated

35
Q

What are the neurotransmitters that are proposed to be involved in schizophrenia?

A
  • Dopamine increase
    • Lack of Glutamate
    • Serotonin increase
36
Q

What dopaminergic pathways are believed to be involved in schizophrenia?

A
  • Reduced activity at the D1 receptors of the mesocortical pathway leads to negative symptoms
    • Hyperactivity at the D2 receptors of the mesolimbic pathway lead to psychosis
    • Nigrostriatal pathway
    • Ventral tegmental area
    • Tuberohypophyseal pathway
37
Q

What is the first line treatment for the first schizophrenic episode?

what is second line?

A

First line =
Second Generation Anti-psychotic OTHER than Sertindole and clozapine and including aripiprazole

Second line =
An alternate second generation Anti-psychotic or a irst generation anti-psychotic

38
Q

How common is co-occuring disorders?

What risks are increased?

A 
• Occur in 50% of serious mental health disorder
	• Increased risk of:
		○ Relapse and rehospitalisation
		○ Suicide
		○ Financial stress
		○ Violence 
Medical illness

PBL Notes (14 decks)

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