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Mixed revision > Revision Theme 3 > Flashcards

Revision Theme 3 Flashcards

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

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
Q

Hypomanic episode

A
  • lasting at least 4 days
  • symptoms as per manic episode
  • but not severe enough to cause functional impairment or hospitalisation.
26
Q

Features associated with depression and mania

A
  • anxiety
  • catatonia
  • psychotic symptoms eg delusions/ hallucinations
27
Q

Mixed affective episodes

A
  • full criteria met for manic/hypomanic or depression plus at least 3 symptoms of opposite polarity present
28
Q

Major depressive disorder

A
  • onset - 25 - 35
  • females more than males
  • 1 in 5 lifetime prevalence
  • 8-19% die by suicide
29
Q

Bipolar disorder

A
  • 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
Q

Neurobiology of major depression

A
  • adverse childhood experience, current stress, genetics factors > HPA axis > increased cortisol > decreased serotonin and NA = depressive syndrome
31
Q

Monoamine dysfunction in depresssion

A
  • all antidepressants affect serotonin and NA systems
32
Q

Serotonin dysfunction in depression evidence

A
  • decreased serotonin (tryptophan depletion studies) = depression
  • decreased serotonin receptors in post mortem
  • reduced serotonin transporters in depression (PET)
33
Q

Monoamine theory of depression

A
  • 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
Q

1st generation antidepressants

A
  • MAOI’s e.g. phenelzine inhibit breakdown of monoamines

- Tricyclics e.g. amitryptilline - inhibit repute of monoamines

35
Q

Second generation antidepressants

A
  • 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
Q

SSRIs

A
  • 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
Q

Tricyclics side effects

A
  • constipation
  • orthostatic hypotension
  • dry mouth
  • drowziness
  • cardiac toxicity in overdose
38
Q

MAOI side effects

A
  • Dry mouth
  • GI symptoms
  • headache
  • drowziness
  • insomnia
  • food interactions (hypertensive crisis)
39
Q

Venlafaxine (SNRI)

A
  • nausea
  • vertigo
  • headache
  • insomnia
40
Q

HPA axis dysfunction in mood disorders

A
  • increased cortisol levels associated with primary depression
  • depression in cushing’s disease
41
Q

Inflammation

A
  • 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
Q

Neural systems in depression

A
  • increased activity of amygdala and PFC to negative stimuli

- bias of attention towards negative stimuli and away from positive emotional and reward stimuli

43
Q

Bipolar disorder treatment

A

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
Q

Treatment of depressive episodes

A
  • Antipsychotics (Quetiapine, lurasidone)
  • Fluoextine/ olanzapine combinations
  • antidepressants to be co prescribed with anti manic drug
  • consider lamotrigine (for depressive episode) + anti manic
45
Q

Treatment acute manic episodes

A
  • antipsychotic (dopamine antagonists) e.g. Haloperidol, olanzapine, risperidone, quetiapine)
  • valporate
46
Q

Long-term treatment for prevention of new episodes

A
  • lithium > kidney and thyroid dysfunction
  • valporate > liver damage
  • dopamine antagonists (ant-psychotics) > weight gain, metabolic syndrome
  • Carbamazepine
47
Q

Amygdala

A
  • 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
Q

Fearful stimuli elicit stress response

A
  • 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
Q

Push-pull regulation of HPA axis

A

Amydala + Hypothalamus = increased cortisol

Hippocampus - Hypothalamus = increased cortisol feedback to hippocampus to stop HPA producing more cortisol

50
Q

Chronic stress

A
  • 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
Q

Diffuse modulatory systems

A
  • Serotenergic = Mood, emotion
  • Noadrenergic = arousal, attention
  • thought to balance one another > serotonin inhibits LC firing.
  • dysregulation may result in inappropriate fear and anxiety
52
Q

Panic disorder symptoms

A
  • 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
Q

Treatment - anxiety/panic disorders - benzos

A

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
Q

Treatment for anxierty/ panic

A

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
Q

Treatment anxiety

A

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
Q

Evidence for GABAergic dysfunction in anxiety

A

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
Q

SSRI’S

A
  • 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
Q

Panic disorder

A

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
Q

OCD

A
  • 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??

Mixed revision (3 decks)

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