12 - Pshchiatry intro 4 lectures Flashcards

1
Q

organic vs functional in psychiatry

A
Functional – neurotic disorders (e.g.
depression, anxiety, phobias) or psychotic
disorders (e.g. schizophrenia, bipolar
disorder)
we may all experience for a while

Organic- e.g. dementia, psychiatric
manifestations of epilepsy or Parkinson’s or
stroke, acquired or traumatic brain injury,
Huntington’s disease, drug-induced states,
etc.

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2
Q

define anxiety, what are its symptoms

A

a feeling of worry about an uncertain outcome

  • Palpitations
  • Sweating
  • Trembling or shaking
  • Dry mouth
  • Difficulty breathing
  • Chest pain or discomfort
  • Nausea or abdominal distress (e.g. butterflies in stomach)
  • Feeling dizzy, unsteady, faint or light-headed

anxiety is a normal response of the limbic system stimulating the sympathetic NS in response to a threat

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3
Q

outline how the limbic system responds to stressors

A

o This response is mediated primarily by the limbic system, which has neural and endocrine targets

Neural elements of the stress response (limbic system)
• Hippocampus
o Receives inputs from many parts of the cortex and
processes their emotional content
o Ultimately projects to the thalamus and also to the
hypothalamus
(causing autonomic features of
emotional responses, since the hypothalamus send
projections down through the cord to autonomic
preganglionic neurones – the hypothalamospinal tract.
This will lead to sympathetic nervous system activation,
as well as release of adrenaline from the adrenal
medulla – the acute stress response)

• Amygdala
o Almond shaped structure sitting near the tip of the
hippocampus
o Receives many inputs from the sensory system
o Major outputs to cortex and hypothalamus

Endocrine elements of the stress response
• The limbic system is able to act on the hypothalamus to
stimulate the secretion of stress hormones
o Via the familiar hypothalamo-pituitary-adrenal axis
o Release of cortisol from the adrenal cortex is part of
the ‘chronic’ stress response

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4
Q

key facts on the hippocampus

A

Folded into medial surface
of temporal lobe

Occupies floor of temporal
horn of lateral ventricle

Three parts: subiculum,
hippocampus proper,
dentate gyrus

Involved in memory and
expressions of emotion

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5
Q

key facts on the amygdala

A

Buried in the roof of lateral ventricle
Collection of nuclei
Inputs of sensory information, brainstem, thalamus, cortex
Outputs to cortex, brainstem and hypothalamus

Drive related behaviours and processing of associated emotions

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6
Q

anxiety pathologically is when we gain a stress response to a threat that cannot be ran away from ie work ect

A

bonus

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7
Q

what are the key anxiety disorders ?

A

PTSD
OCD
Panic and socail disorders
generalised anxiety

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8
Q

briefly outline the 3 stages of the general adaptation syndrome to stress

A

The general adaptation syndrome refers to three stages that the body goes through
during prolonged exposure to stressors
o Stage 1: The alarm reaction
Release of adrenaline and cortisol as well as sympathetic activation
(described above)
o Stage 2: Resistance (effect of adrenaline starts to wear off)
Chronic stress response, prolonged release of cortisol
o Stage 3: Exhaustion (when you cannot escape an ongoing stressor)
Chronic side effects of prolonged cortisol secretion start to occur
o The stress response can become pathological when you cannot escape a
stressor(s), or when ‘trivial’ stressors elicit a strong stress response.
However, patients with anxiety disorders may go through all of the stages
above

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9
Q

what is GABA and its role in stress

A

it is the main inhibitory neurotransmitter
it is lower in patients with panic disorders
we can treat with benzodiazepines(short term only) to increase gaba transmission decreasing anxiety
long term we also can increase seretonin with ssri’s
and give patient CBT

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10
Q

outline OCD

A

obsessions - they dominate the thoughts and are unpleasant
compulsions - are motor acts to neutralise the obsessive impulse

the patient acknowledges the obsession is unreasonable or excessive but cannot stop it

repetitive and unpleasant

side fact - PANDAS - a strep infection in a child can trigger OCD symptoms due to antibody cross reaction with neurons of basal ganglia - kinda mad

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11
Q

treatment of OCD is …

A
o Treatment
 Biological
• SSRIs +/- antipsychotics - help block basal ganglia re entry loops ? 
• Deep brain stimulation?
 Psychological
• CBT and variety of other interventions
 Social
• Family support
• Groups etc
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12
Q

outline PTSD

A

o Features
Can occur within six months following an exceptionally severe traumatic event (e.g. rape, battlefield trauma)

Causes repetitive, intrusive recollection or re-enactment of the event in memories, daytime imagery, or dreams

There is conspicuous emotional detachment, numbing of feeling, and avoidance of stimuli that might arouse recollection of the trauma
o Pathophysiology
 Unclear
• Evidence of amygdala hyperactivity causing exaggerated behavioural responses
• However, low levels of cortisol!

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13
Q

PTSD treatment

A
Treatment
 Biological
• SSRIs
• Maybe short term benzodiazepines
 Psychological
• CBT
• Eye movement desensitization reprocessing therapy
 Social
• Charities are particularly active, such as ‘Help for Heroes’
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14
Q

what are the features of Depression

A

more than two weeks

core of low mood, low energy, lack of enjoment in anything

depressive throughts
may stop eating
some somatic biological symptoms
most severe - psychotic symptoms possible

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15
Q

depression vs adjustment reaction

A
in a ADR - energy is not low
time is limited
onset sudden after event not gradual 
no sleep disturbance pattern
anger is common unlike depression
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16
Q

outline the features of mania / a mainic episode

A
Elated Mood
• Increased energy
• Pressure of speech
• Decreased need for sleep
• Flight of ideas
• Normal social inhibitions are lost
• Attention cannot be sustained
• Self esteem is inflated, often grandiose
• May have psychotic symptoms
17
Q

how do we diagnose bipolar affective disorder

2 types

A

• Diagnosis is made following 2 episodes of a mood disorder at least one of which is mania or hypomania.

  • Bipolar 1 – discrete episodes of mania only or mania and depression
  • Bipolar 2 – discrete episodes of hypomania or hypomania and depression.
18
Q

dont need all of this - give some examples of physical differentials that may look like mania or depression

A

Physical health differentials: depression
• Hormone disturbance such thyroid dysfunction
• Vitamin deficiencies such as vitamin B12
• Chronic disease e.g. renal, CVS & liver failure
• Anaemias
• Substance misuse e.g. alcohol, cannabis & stimulants
• Hypoactive delirium

Physical health differentials: Mania
• Iatrogenic e.g. steroid induced
• Hyperthyroidism
• Delirium
• Infection e.g. encephalitis, HIV, syphyllis
• Head injury
• (intoxication with stimulants)
19
Q

3 brain structures involved in a mood disorder are

elaborate on their roles

A

limbic system - runs emotion, some memory with hippocampus and motivation - all of these are reduced in depression

frontal lobe - The ventromedial prefrontal cortex – is thought to be involved in the
generation of emotions.
• While the orbital prefrontal cortex is thought to be involved in emotional responses – possibly via connection with the amygdala.

basal ganglia - Motor function; malfunction of the basal ganglia are implicated in neurological illnesses such as
- Parkinson's disease
- Wilson’s disease
- Huntington's disease
• Psychological function:
- Emotion
- Cognition
- Behaviour
The main hypothesis is that mood is determined by functional circuits between these brain areas. E.g. the frontal lobe projects to parts of the limbic system which in turn connects to the basal ganglia and the brainstem. 
This affects:
• Cognitive processed (thoughts)
• Sympathetic output
• Parasympathetic output
• Motor systems
20
Q

bonus info

A

Overall – involvement several circuits could
account for symptoms
• For depression:
• Prefrontal cortex: Slowing of thought, executive dysfunction.
Altered emotional processing.
• Amgydala: Abnormal emotional processing
• Basal ganglia: Impaired incentive behaviour. Psychomotor changes

21
Q

the 2 main neurotransmitters affected in depressive diorders are …

A
seretonin
 Produced in the brain stem (Raphe nuclei) and transported to cortical
areas and limbic system
• Thought to have roles in:
– Sleep
– Impulse control (link with suicide)
– Appetite
– Mood
thought to be low in depression - hence we use ssri's

Noradrenaline
• Produced in the locus coeruleus (pons) and projects to limbic system and the cortex

Functions in the brain:
• Mood
• Suggests a role in behaviour (arousal and attention) – fight or flight response
• Implicated in memory functions

NA is thought to be lowered in depression

22
Q

outline the treatment for depression

think biopshycosocial

A

Treatment of Depression

• Biological - First line = Selective Serotonin Reuptake inhibitors.
Other options: SNRI’s, TCA’s etc
Life threatening/treatment resistant: ECT

  • Psychological – First line treatment for depression: CBT
  • Social – Help with e.g. isolation, social stressors (including housing,finances)
23
Q

treatment of bipolar

biopshycosocial

A

difficult
aim for a steady maintinance state
treat the mania then the depression then mania ect

treat the maina

Biological – First line: antipsychotics
Alternatively: mood stabiliser

• Psychological – Acutely unlikely to be helpful, longer term – psychoeducation re. BPAD, triggers and signs of relapse.

• Social – Treat in a place of safety – where risk to self and others is
minimal. Consideration of implications of mania e.g. debts
(excessive spending).

treat the bipolar depression

Biological – Can use antidepressant – but ONLY with mood stabiliser cover.
ECT
Lithium
• Psychological – CBT
• Social – as for unipolar depression

Maintaining stability in bipolar disorder
• Biological – Mood stabilisers e.g. lithium, sodium valproate
Antipsychotic (used as a mood stabiliser e.g.Quetiapine)

• Psychological – Psychoeducation re. bipolar affective disorder.
CBT – to help prevent relapses
• Social – Consideration of BPAD on employment e.g. shift work.
Involvement of family, education of family etc.

24
Q

define psychosis

A

the presence of halluscinations or dellusions - mostly auido or sometimes visual

a hallucination is a perception without a stimulus

a delusion is a fixed false belief which is unshakeable.

25
Q

what are the key (first rank symptoms) of schizophrenia

A

• Auditory hallucinations - ie a third person - he brushes his teeth
• Passivity experiences - patient belives an external force (MI5) causes an action - put chip in tooth
• Thought withdrawal, broadcast or
insertion - the adding, removing of your thoughts by others
• Delusional perceptions
• Somatic hallucinations

26
Q

what are some positive and negative symptoms ?

A

Positive symptoms:
Delusions, hallucinations, thought disorder, lack of
insight
Added symptoms

Negative symptoms:
Underactivity, low motivation, social withdrawal,
emotional flattening,
Self neglect
Symptoms that take away from the patient

bad idea to just remove all the + and leave the -, then then are mega depressed

27
Q

outline the pathology of schizophrenia

just outline this, not the details

A

Dopamine (DA) theory of Schizophrenia
• Drugs e.g. amphetamines which
cause the release of DA induces
psychotic symptoms.

• All medications that antagonise DA
receptors, help treat psychosis &
those with the strongest affinity to
D2 receptions are most clinically
effective.

• 4 DA pathways in the brain.
Mesolimbic pathway
From Ventral tegmental area To Limbic structures
(amygdala, septal area, hippocampal formation)
and
Nucleus accumbens
both Thought to be overactive in schizophrenia

Mesocortical pathway
From Ventral tegmental area To Frontal cortex
and
Cingulate cortex

both Thought to be underactive in schizophrenia

Brain changes
Enlarged ventricles
Reduced grey matter (with reduced brain weight)
Decreased temporal lobe volume
Reduced hippocampal formation, amygdala, parahippocampal gyrus and prefrontal cortex

Neuropathology of Schizophrenia
• Decreased pre-synaptic markers
• Decreased oligodendroglia
• Fewer thalamic neurons
• Together these changes have led to a theory of “aberrant connectivity” causing schizophrenia.
28
Q

outline how we may treat schizophrenia

A

Typical antipsychotics
• Block D2 receptors in all CNS dopaminergic pathways
• Main action as antipsychotics is on mesolimbic and mesocortical pathways.
But side effects come from antagonising D2 receptors in other pathways

Atypical antipsychotics
• Lower affinity for D2 receptors
• Milder side effects as dissociate rapidly from D2 receptor
• Also block 5HT2 receptors

29
Q

bonus

A

if we block DA receptors - we are blocking the basal ganglia - Sub niagra - putamen ect loop

this leads to movement inhibition increase and stimuli decrease

causing parkinsonism

30
Q

what are some side effects of antipsycotics

A

Hyperprolactinaemia & antipsychotics
• Dopamine normally inhibits prolactin release from the pituitary.
• DA antagonists, which lower DA lead to loss of DA’s inhibitory function, and therefore increased prolactin levels.
• This can lead to: amenorrhoea, galactorrhoea, decreased fertility, reduced libido and long term can lead to osteopenia/osteoporosis

31
Q

what is a key issue of treating schizophrenic patients?

A

due to the nature of the disease they do not trust health professionals , so will often try and hide and not take medications

give in many forms to avoid this -ie in food, liquid ect

32
Q

outline prognosis for schizophrenia

A
  • Earlier someone is treated the better the prognosis.
  • Moderately good long term global outcome in about 50%

• Mortality is twice as high as in general
population
• Shorter life expectancy
• Higher incidence of CVS disease, respiratory
disease and cancer
• Suicide risk is 9x higher than in general
population
• Death from violent incidents in 2x as high
• About 50% have a substance misuse
problem
• Higher rate of cigarette smoking