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Revision Theme 3 Flashcards

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1
Q

What is psychosis?

A

A loss of boundaries with reality, a loss of insight, with primary features of hallucinations and delusions.

A psychotic episode = 1 week duration of symptoms at significant severity

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2
Q

What is a delusion?

A

A belief held firmly but on inadequate grounds, not affected by rational argument or evidence to the contrary. Not shared by someone of a similar cultural, age, social, religious or educational background.

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3
Q

Salience of attribution

A

Excess dopamine (reward and motivation) could lead to the world seeming pregnant with significance.

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4
Q

Hallucination

A

Perception experienced in the absence of external stimulus.

Any sensory modality but auditory is most common.

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5
Q

Schneider’s first rank symptoms

A
  • auditory hallucinations (Thoughts spoken aloud, 3rd person hallucinations, running commentary)
  • somatic/ tactile hallucinations
  • Thought insertion, broadcast or withdrawal
  • Passivity phenomena
  • delusional perception
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6
Q

Differential

A

Affective psychosis

  • Bipolar
  • Depressive psychosis
  • Schizoaffective disorder

Organic

  • epilepsy
  • infections
  • trauma
  • cerebrovascular disease
  • demyelination
  • velocardiofacial syndrome
  • endocrine
  • metabolic
  • immunological
  • acute drug intoxication
  • toxins e.g. lead
  • dementias

personality disorders

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7
Q

Side effects of anti-psychotics

A
  • Parkinsonian like symptoms
  • Tardive dyskinesia
  • weight gain
  • skin discolouration
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8
Q

Mental state examination

A
  • appearance/behaviour
  • speech
  • mood/affect
  • thought form
  • thought content
  • hallucinations
  • insight
  • cognition
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9
Q

Onset of schizophrenia

A 
Male = 21-26
Female = 25-32
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10
Q

Neuropathology of schizophrenia : Structural changes

A
  • Ventricular enlargement
  • Reduced brain volume ( less gray matter)
  • cytoarchitectural differences in cortex and hippocampus
  • Decreased length paracingulate sulcus
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11
Q

Neurodevelopment of schizophrenia

A
  • during adolescence gray matter is lost due to synaptic pruning and myelination
  • May speed up early onset schizophrenia
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12
Q

Neurophysiology: Schizophrenia

A
  • Hypofrontality during periods of high cognitive load (Wisconsin card sorting - cognitive flexibility). Leads to negative and cognitive symptoms
  • Increased activity in dlPFC seen in healthy volunteers but absent in schizophrenia
  • Hyper-excitable sensory cortex e.g. auditory cortex activation during hallucinations
  • Abnormal neural oscillations
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13
Q

Dopamine (psychopharmacology schizophrenia)

A
  • Dopamine cell bodies in midbrain > project to forebrain
  • Nigrostriatal system
  • Mesolimbic + Mesocortical = Mesocorticalimbic pathway (involved in reward, reinforcement, stimulus salience)
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14
Q

Dopamine hypothesis evidence (schizophrenia)

A
  • Typical antipsychotics ( D2 receptor antagonists) prevent positive symptoms.
  • Dopamine agonists (cocaine, amphetamine) can produce positive symptoms e.g. psychosis
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15
Q

Dopamine receptors

A

D1 (1 & 5) = gs coupled

D2 (2,3,4) = Gi coupled.

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16
Q

Extrapyramidal side effects

A
  • Caused by typical antipsychotics (e.g. chlorpromazine, haloperidol)
  • Parkonsonian like (inhibition of dopamine action in caudate)
  • Tardive dyskinesias (up regulation of d2 =supersensitivity)

Atypical antipsychotics e.g. Clozapine = selective to d4 without EPS

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17
Q

Clozapine

A
  • Atypical antipsychotics
  • D4 receptor antagonist
  • improves positive and negative symptoms

side effects:

  • weight gain
  • sedation
  • hypersalivation
  • neutropenia
  • tachycardia
  • hypotension
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18
Q

Atypical antipsychotics

A
  • Clozapine
  • Olanzapine
  • Risperidone
  • seem to increase dopamine in PFC
  • decrease dopamine in Nacc
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19
Q

Glutamate hypothesis = evidence

A
  • NMDA receptor/ glutamate antagonist PCP causes positive and negative symptoms
  • Mice with fewer NMDA = schizophrenia symptoms

1) glutamate antagonism in PFC
2) Less glutamate firing to GABA neurons in VTA
3) Less inhibition of VTA -Nacc neurons
4) increased dopamine release Nacc
5) Less activation of VTA-PFC dopamine neurons - less glutamate = hypofrontality

Hyperactive Nacc
Hypoactive PFC

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20
Q

Neurocognitive deficits schizophrenia

A
  • Typical = no improvement
  • Atypicals = some improvements
  • lower iq
  • attentional deficits - stroop task
  • working memory ( wisconsin)
  • planning and informational processing deficits
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21
Q

Affective episodes

A
  • Manic episode
  • Hypomanic episode
  • depressive episode
  • mixed affective episode
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22
Q

Symptoms of depression

A
  • depressed mood
  • anhedonia
  • psychomotor retardation
  • agitation/ restlessness
  • weight loss/ gain
  • diurnal variation of mood
  • insomnia
  • feelings of guilt/worthlessness
  • suicidical ideation
  • somatic symptoms
  • hypochondriasis
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23
Q

Atypical depression

A
  • reactivity
  • weight gain
  • hypersomnia
  • leaden paralysis
  • interpersonal rejection sensitivity
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24
Q

Manic episode symptoms

Study These Flashcards
A
  • abnormally and persistently elevated, expansive or irritable mood
  • Symptoms lasting almost all day, every day for a week
  • inflated self esteem/grandiosity
  • decreased need for sleep
  • more talkative than usual
  • flights of ideas/ racing thoughts
  • distractibility
  • psychomotor agitation
  • increased goal-directed activity
  • excessive involvement in high risk activities
  • psychosis
  • delusions and hallucinations
  • significantly severe to cause marked functional impairment or necessitate hospitalisation.
25
Hypomanic episode
- lasting at least 4 days - symptoms as per manic episode - but not severe enough to cause functional impairment or hospitalisation.
26
Features associated with depression and mania
- anxiety - catatonia - psychotic symptoms eg delusions/ hallucinations
27
Mixed affective episodes
- full criteria met for manic/hypomanic or depression plus at least 3 symptoms of opposite polarity present
28
Major depressive disorder
- onset - 25 - 35 - females more than males - 1 in 5 lifetime prevalence - 8-19% die by suicide
29
Bipolar disorder
- Bipolar 1 = at least 1 manic episode - Bipolar 2 = at least one hypomanic episode + one depressive episode - peak onset = 15-24 - females and males equally affected - 10 x higher risk in 1st degree relative
30
Neurobiology of major depression
- adverse childhood experience, current stress, genetics factors > HPA axis > increased cortisol > decreased serotonin and NA = depressive syndrome
31
Monoamine dysfunction in depresssion
- all antidepressants affect serotonin and NA systems
32
Serotonin dysfunction in depression evidence
- decreased serotonin (tryptophan depletion studies) = depression - decreased serotonin receptors in post mortem - reduced serotonin transporters in depression (PET)
33
Monoamine theory of depression
- deficiency in synaptic serotonin and NA underlies depression - 5-HT (Raphe) and NA (LC) project to PFC (executive functions), limbic system (behaviour, motivation, emotion) such as hippocampus, cingulate cortex, amygdala, hypothalamus).
34
1st generation antidepressants
- MAOI's e.g. phenelzine inhibit breakdown of monoamines | - Tricyclics e.g. amitryptilline - inhibit repute of monoamines
35
Second generation antidepressants
- SSRI's = Fluoxetine, citalopram, sertraline = - SNRI's = NA reuptake inhibitors = Venlafaxine - alpha2 and 5-HT antagonist modulate NA and serotonin release e.g. mirtazipine - Dopamin-noadrenaline reuptake inhibitors e.g. buproprion
36
SSRIs
- efficacy equal to tricyclics - large spectrum of action = depression, OCD, PTSD, Panic, GAD, - low toxicity and safe in overdose - initial treatment = side effects prevail over benefits (slow titration) ``` side effects = Gi symptoms (nausea diarrhea) headache irritability anxiety reduction of libido sexual dysfunction ```
37
Tricyclics side effects
- constipation - orthostatic hypotension - dry mouth - drowziness - cardiac toxicity in overdose
38
MAOI side effects
- Dry mouth - GI symptoms - headache - drowziness - insomnia - food interactions (hypertensive crisis)
39
Venlafaxine (SNRI)
- nausea - vertigo - headache - insomnia
40
HPA axis dysfunction in mood disorders
- increased cortisol levels associated with primary depression - depression in cushing's disease
41
Inflammation
- High commodity between depression and inflammation - administration of cytokines promotes depression - microglial activation in depression patients - raised plasma cytokines and inflammatory markers in depression
42
Neural systems in depression
- increased activity of amygdala and PFC to negative stimuli | - bias of attention towards negative stimuli and away from positive emotional and reward stimuli
43
Bipolar disorder treatment
Anti-psychotics: - D2 receptor antagonists - atypical have some effect on serotonin - long term adverse effects = weight gain, glucose regulation, lipids. EPS. Lithium: - anti-suicidal - mood stabiliser - strongest evidence for prevention of relapses of any polarity - narrow therapeutic index - risk of toxicity - adverse long term effects on kidney function Anticonvulsants: - Valporate = anti manic - lamotrogine = prevention of depressive episodes - Carbamazepine may be used if lithium ineffective. Effective against manic relapse.
44
Treatment of depressive episodes
- Antipsychotics (Quetiapine, lurasidone) - Fluoextine/ olanzapine combinations - antidepressants to be co prescribed with anti manic drug - consider lamotrigine (for depressive episode) + anti manic
45
Treatment acute manic episodes
- antipsychotic (dopamine antagonists) e.g. Haloperidol, olanzapine, risperidone, quetiapine) - valporate
46
Long-term treatment for prevention of new episodes
- lithium > kidney and thyroid dysfunction - valporate > liver damage - dopamine antagonists (ant-psychotics) > weight gain, metabolic syndrome - Carbamazepine
47
Amygdala
- Emotion and fear - Detect threats and prepares us - Threat detection and survival Sensory cortex, thalamus > Lateral nucleus Hippocampus> basolateral nucleus > central nuclei and basal nucleus also output to ventral striatum and thalamus Central nuclei > Hypothalamus, midbrain, pons, medulla Basal Nuclei > PAG Olfactory> Medial nucleus > medial basal forebrain and hypothalamus.
48
Fearful stimuli elicit stress response
- sensory info channeled to amydala - amydala excites locus ceoreleus and hypothalamus Acute stress response HPA axis (hypothalamus, pituitary, adrenal axis) - Hypothalamus released CRH ( corticotropin releasing hormone) - Pituitary releases ACTH (adrenocorticotropic hormone) - Adrenal cortex releases cortisol Also... Locus coereleus releases NA = fight or flight
49
Push-pull regulation of HPA axis
Amydala + Hypothalamus = increased cortisol | Hippocampus - Hypothalamus = increased cortisol feedback to hippocampus to stop HPA producing more cortisol
50
Chronic stress
- chronic activation of glucocorticoid receptors in hippocampus leads to increased ca2+ > excitotoxic - Hippocampus can't feedback to limit cortisol production - Therefore, some anxiety disorders may result from diminished activity of hippocampus, loss of feedback to amygdala, inappropriate fear responding. Evidence - hippocampus volume in PTSD patients is reduced.
51
Diffuse modulatory systems
- Serotenergic = Mood, emotion - Noadrenergic = arousal, attention - thought to balance one another > serotonin inhibits LC firing. - dysregulation may result in inappropriate fear and anxiety
52
Panic disorder symptoms
- SOB - Irregular heart heart beat - fear of impending death - clammy sweat - dizziness - faintness - often leads to agoraphobia - often associated with depression, alcoholism, drug abuse
53
Treatment - anxiety/panic disorders - benzos
Benzos indirect gaba (a) agonist anxiolytic, sedation, sleep inducing, reduced muscle tone benzo antagonists eg flumazanil produce anxiety and panic attacks - perhaps result from fewer bento receptors? - work well in panic and GAD - Not so well in OCD and PTSD
54
Treatment for anxierty/ panic
SSRI'S and CBT ssris efefctive: OCD, PTSD, GAD and panic can be anxiogenic in short term. anxiolytic after a few weeks. Buspirone - 5-HT receptor agonist = GAD
55
Treatment anxiety
Drugs that increase GABA reduce anxiety - Alcohol - Benzos - Barbituates Drugs that decrease GABA induce anxiety - Flumazenil (benzo antagonist) GABA(a) ionotropic chloride channel (hyper polarisation)
56
Evidence for GABAergic dysfunction in anxiety
Patients with panic disorder have fewer bento binding sites (receptors)! Panic disorder patient lack inhibitory control in cortical and limbic regions to suppress inappropriate fear response
57
SSRI'S
- take a few weeks to produce anxiolytic effect - neuroplasticity downstream from antidepressant action - Intracellular signalling downstream from serotonin receptor can lead to changes in neuronal plasticity and morphology - Reversal of stress induced changes may restore function e.g hippocampus
58
Panic disorder
Serotonin and NA have opposing functions in hippocampus, amydala, hypothalamus. Shifted balance between pathways to NE may manifest in panic attacks. By increasing serotonin, it restores balance.
59
OCD
- disorder of basal ganglia? repeated behaviours, associated with tourettes. - imbalance between indirect and direct pathways - direct pathway controlling previously learned behaviour becomes automatic = overactivity of direct pathway without being able to switch it off. SSRIs are best drugs for treating OCD Caudate hyperactivity??

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