Lecture 16. Depression and Schizophrenia Flashcards
What are the symptoms required to diagnose major depressive disorder and its definition
Symptoms required
1 of Depressed mood, apathy/loss of interest
4+ of
- Weight/appetite change, sleep disturbance, psychomotor, fatigue, worthlessness, executive dysfunction, suicidal ideation
Defined by occurrence of at least a single major depressive episode (mo) - although recurrent episodes common
Compare dysthymia and double depression
Dysthymia is less severe form of depression that is long lasting (2yr+) and often unremitting.
Whereas Double depression is where patients with unremitting dysthymia also have 1+ major depressive episodes - poor interepisode recovery.
Compare origin of pathway, production and breakdown of dopamine, norepinephrine, and serotonin
Origin
D: sub nigra and ventral tegmental area,
Ne: locus coeruleus in brainstem.
5HT: Raphe nuclei in brainstem
Prod:
- NE is made from Dopamine made from tyrosine which is converted to -> dopa.
- Serotonin made in neuron from dietary Tryptophan, via two reactions
Term:
Transporter
or Monoamine oxidase. for all. NE can also be destroyed via cathecol o methyltransferase (COMT)
What is monoamine theory of depression and what is wrong with it
Depression is due to deficiency of monoamine neurotransmitters - due to observations of antidepressant effects.
However:
- effect is seen 2-4 weeks after immediate rise in serotonin levels
- Reducing serotonin doesn’t cause depression, increased synaptic serotonin is associated with increased depressive symptoms.
- Other treatments like ketamine, ECT, TMS,Psychotherapy cannot be explained by this theory
What is the Neurotrophic hypothesis of depression
Depression may be caused by reduced synthesis of proteins involved in neurogenesis and synaptic plasticity.
eg. Brain Derived Neurotrophic Factor gene which has increased transcription by monoamine binding.
The gene may be turned off by environmental stressors (high levels of cortisol) leading to neural death and less synapses. prefrontal cortex, hippocampus and amygdala particularly susceptible due to involvement in stress response
How can depression be treated- specific drugs
- Psychotherapeutic
- Psychopharmacological: after one treatment fails go onto next but risk of having treatment resistant depression increases
a) SSRIs ^sero
b)SNRIs ^sero, NE
c)MAOI: ^ s, n, d
….
g) TCA: ^sero,NE, most effective but more side effects
What are the 3 types of psychoses
Psychosis is set of symptoms associated with many psychiatric disorders
- Paranoid: paranoid projections, hostile belligerence and grandiose expansiveness
- Disorganised/excited: conceptual disorganisation, disorientation, excitement
- Depressive psychosis: psychomotor retardation, apathy, anxious self punishment and blame.
Compare the epidemiology of schizophrenia with depression
Schiz: most common psychotic illness. more common in males, southeast asia, low SES.
Dep: higher prev in women and young people. leading cause of years lived with disability in NZ
What is the dopamine hypothesis of schizophrenia and how does it cause positive, negative and cognitive effects of schizophrenia
Overactivation of Mesolimbic pathway (midbrain ventral tegmental area to nuc. accumbens) by dopamine via D2 receptors causes Positive symptoms for schizophrenia (psychosis, auditory hallucinations, delusions)
Underactivation of Mesocortical pathway (ventral tegmental area to dorsolateral prefrontal cortex) causes
Negative symptoms ( alogia, apathetic social withdrawal, avolition, blunted affect)
Cognitive symptoms
(attentional resources, problem solving, modulating behaviour based on social cues)
How do anti-psychotic drugs work (eg. chloropromazine) , what are the side effects- and difference between atypical (newer) drugs vs conventional one
Both types of drugs will have D2 receptor antagonist actions which reduce Positive symptoms by blocking mesolimbic dopamine activity. Atypical ones will also have serotonin2A antagonist/inverse agonist actions. Therefore less side effects.
Side effects: reduce dopamine leading to tardive dyskinesia (parkinsons)
Risk of side effects steadily increases with duration of treatment not good for life long disease. CVS symptoms and makes negative symptoms worse
What are the risk factors for schizophrenia development
- Strong genetic component: family history being highest risk factor but each gene adds a small amount of risk. Genes related to glutamine, GABA, dopamine systems + synapse formation etc.
- Environmental stressors eg, strong cannabis exposure during vulnerable synaptic pruning age 18m,25f, CNS damage, Prenatal bereavement, Rubella infection can trigger maladaption in susceptible individuals leading to Sz.
