Overlap of physical and mental health px

Question 1

A BREAK FROM REALITY - CAUSES OF PSYCHOSIS

i) name two iatrogenic causes
ii) name three situations where a patient may be having a transient psychotic experience? how many days of psychosis may indicate this?
iii) name two substances they may be withdrawing from?
iv) name three things that can cause organic psychosis?
v) name two other conditions the person may be suffering from
vi) which NT is imbalanced here? which two pathways are involved
vii) name three substances that can cause psychosis

Answer 1

i) steroids, ADHD, medication

ii) autism, extreme sleep deprivation, personality disorders, anxiety, torture and sensory deprivation
- less than seven days

iii) alcohol, heroin, cocaine
iv) autoimmine encephalitis, wilsons disease, hungtindons chorea, temporal lobe epilepsy
v) bipolar affective disorder, depression

vi) dopamine - too much in the mesolimbic pathway (voices/beliefs) and too little in the mesocortical pathway (reduced ability to plan)
- also get reduced Glu and GABA

vii) cannabis, ketamine, LSD, psylcibin, cocaine, spice, GHB

Question 2

DEPRESSION AND PSYCHOSIS

i) what can all depression affect? (2) what can severe depression cause?
ii) what level of depression can cause psychosis? what is this called? what does that mean?
iii) in this case what is the psychotic state usually preceeded by?
iv) what are three core symptoms of depression? at what age to these peak?
v) name two cognitive and two somatic symptoms of depression

Answer 2

i) all depression can affect concentration and attention
- severe depression can cause cognitive impairment

ii) severe depression > affect congruent = delusional themes are negative or associated with blame, guilt etc (inkeeping with low mood)
iii) preceeded by worsening depressive illness

iv) anhedonia, low mood and tiredeness
- peaks 25-35yrs, more common in women (1:1 <13yrs)

v) cog = hopless, helpless, worthlesss, guilt, poor conoc, poor attention, low motivation
somatic = early am waking, loss of appetite, weight loss, libido

Question 3

DEPRESSION - STRESS VULNERABILITY MODEL

i) is depression strongly genetically determined?
ii) how do stress and vulnerability interact?
iii) dysfunction of which NT can cause progression to major depressive disorder?

Answer 3

i) yes
ii) in those who are vulnerable > the stressor to trigger depression is much less than in those who are not genetically vulnerable
iii) monoamine dysfunction

Question 4

MONOAMINE HYPOTHESIS IN DEPRESSION

i) what are all monoamines derived from? which two things do receptors work downstream of?
ii) what are they all broken down by? give three examples of monoamines? what two fates to monoamines have in the synapse?
iii) which nucleus does serotonin act through? what is its precursor? what transporter recycles it? what happens when there is breakdown in this pathway?

Answer 4

i) all derived from aromatic acids > precusor to monoamine
- all work on aden cyc and PLC

ii) broken down by monoamine oxidase
- serotonin, dopamine, histamine, noradrenaline, adrenaline
- either taken back up into pre syn and recycled or broken down by MAO

iii) main effect is projections from the raphe nucleus
- precursor is tryptophan
- SERT
- bdown = depression

Question 5

SEROTONIN AND DEPRESSION

i) how may tryptophan be implicated in development of depression? how is adenyl cyclase implicated?
ii) which anti hypertensive can cause rapid depletion of 5HT in syn cleft and cause depression? how does it do this?
iii) how do SSRIs work?

Answer 5

i) dietary depletion of tryptophan > relapse of depression in patients with prev dx/FH but not in controls
- inhib of downstream activation of aden cyc > depressive symptoms

ii) reserpine
- stops post receptor reuptake (5HT2) and recycling into presyn neuron (SERT)

iii) block reuptake of 5HT by SERT > more in synapse to active post synaptic receptors

Question 6

NORADRENALINE

i) where does it project from? which two areas does it innervate?
ii) what is the NA precursor?
iii) name two serotonin noradrenaline reuptake inhibtors? which part of the pathway do they work on? when are these drugs given?
iv) how can NA receptors be implicated in depression?

Answer 6

i) from locus coruleus > limbic system and frontal lobe
ii) tyrosine

iii) venlafaxine and duloxetine > block recyc and reuptake by mono amine transporter
- usually given 2md or 3rd line when SSRIs havent worked

iv) some people with variations in NA receptors are more vulnerable to depression

Question 7

ANXIETY DISORDERS

i) name disorders that fall under the anxiety disorder umbrella
ii) which area of the brain do sensory inputs come in to? where does concious information then go? where does unconcious information go?
iii) which area of the brain differentiaties sensory information from the thalamus into threat or no threat?
iv) what happens if a threat is perceived through conc/unconc pwys? how does this manifest?

Answer 7

i) generalised anx disorder, PTSD, social anxiety, phobia, agoraphobia, panic disorder
ii) sensory input to thalamus > concious to frontal lobe (slower) and unconcious to amygdala (quicker)
iii) amygdala
iv) if threat is percieved > physiological response seen in stress reac/anxiety disorder > fight or flight, freeze response, cortisol released through HPA > activates basal forebrain

Question 8

HPA AND ANXIETY

i) what happens to the HPA in anxiety?
ii) which hormone is ultimately released? what can cause high levels of this? what is the consequence?
iii) what can chronic stress exposure therefore lead to?

Answer 8

i) it is overstimulated

ii) release of cortisol >if amygdala is firing a lot = high levels of cortisol
- high cortisol = lose feedback loop > end up with high levels > anxiety disorders

iii) development of anxiety disorders

Question 9

PTSD

i) name four things it is characterised by?
ii) what does it often occur after? in which patients may this not be the cause
iii) what happens to the hippocampus? what happens in childhood trauma?
iv) where does trigger information feed into? what does the hippocampus then do? what does the amygdala then do? what does the PFC do? what does the person then do
v) which therapeutic approach can help this?

Answer 9

i) hypervigilance, flashbacks, nightmares and avoidance

ii) incident that is a threat to life
- those with neurodiverse brains eg autism = dont need life threat to get PTSD

iii) hippocampus never stores the memory correctly
- in PTSD > HV shrinks and is less functional
- chilhood trauma > under developed HC

iv) trigger memory eg smell is identified in the thalamus > HC recalls the fragmented memory eg an image > amygdala reacts to the memory > PFC is unable to rationalise or recognise that the person is safe
- person attempts to avoid or escape

v) EDMR > allows HC to form a memory rather than fragmented