case 8 Flashcards
with SZ non adherence is predicted by
not seeing a medical benefit, not predicting relapse, not liking the medication, poor insight into their condition
cognitive remediation
restorative or compensative. strategy based instructions.
SZ
inc DA in nigrostriatal pathway. Knock on effects from abnormalities in glutamate or GABA systems. Dec DA in DLPFC. psychosis-loss contact with reality. hallucinations, delusions, dosorganised speech and behaviour, flattened effect, cog deficits, occupational social dysfunction. 1% prevalence. more common men. higher in lower socioeconomic classes. age onset 20-30 in woman, 15-25 men.
dopamine
hormone-catecholamine and phenthylamine. motivation reward and reinforcement. tyrosine - tyrosine hydroxylase - LDOPA - DOPA decarboxylase - Dopamine. Reuptake Na ion dependent DA transporter DAT. MOA and COMT catabolise. Activate G protein coupled receptors. D1 type (D1 and D5) D2 type (D2,3,4). D1 coupled to G protein GSalpha activated adenylyl cyclase inc cAMP. D2 coupled G protein Gialpha inhibits formation cAMP.
nigrostriatal dopamine pathway
projects from substantia nigra to basal ganglia or striatum. Extrapyramidal nervous system. controls motor function and movement. hyperactivity is associated with pos symptoms, delusions and hallucinations. pleasure, hyperkinetic movement. SZ occurs in associative striatum of NS pathway. can be detected 3 yrs before first episode.
mesocortical dopamine pathway
from ventral tegmental area of brainstem to prefrontal cortex. cog symptoms in DLPFC, neg symptoms in DLPFC and VMPFC. deficit of DA. may be consequence of neurodevelopmental abnormalities in NMDA glutamate system.
mesolimbic dopamine pathway
ventral tegmental area to limbic areas, mainly nucleus accumbens in ventral striatum. deficient in this area leads to anhedonia and lack of pleasure.
tuberoinfundibular dopamine pathway
from hypothalamus to anterior pituitary gland. inhibit prolactin release. When pregnant Da neurons dec so prolactin levels rise for breast feeding. This can occur with antipsychotics that block D2.
3 functional pathways of striatum
sensorimotor-input from SNc, D1/2 receptors. Associative-learning, memory, attention, emotion, input from DLPFC, DA from SNc. D1/2/3. Limbic-reward. DA from VTA. D1/2/3.
causes and risk factors
thought to have a biological basis as enlarged ventricles, thinning of cortex, dec hippocampus, changes in DA and glutamate. Genetic componant. environmental-stressers can cause reacurance but not causative. neurodevelopment vulnerability, substance abuse. cannabis doubles the risk. cocaine can give psychotic sympt.
signs and symptoms
abnormal ideas-delusion. abnormal perceptions-hallucinations in all semses, auditory most prominent. motor and behavioural disorders-stereotypies(purposeless acts repetitivly) strange mannerisms, bizzare behaviour, catatonia, catalepsy(limbs can be manipulated) hyperactivity, impuslive behavious. thought disorders-unintelligible speech, neologism. emotional disorders-affective flattening, innapropriate affect.
types of delusions
persecution-somones trying to harm them. reference-everythings directed at and about them. control-something else is controling them. grandiose-divine purpose. hypochondrical-body is rotten. delusional mood.
positive symptoms
delusions, hallucinations, thought disorder, bizarre behavious. acute episodes
Negative symptoms
absence or reduction in normal function. apathy, affective blunting, poverty of speech, anhedonia, lack of desire for relationships, social withdrawl, avolition, impaired cog. chronic sympt.
phases
premorbid-may show no symptoms. predromal-symptoms. middle phase, late illness phase.