general addiction Flashcards
Basal Ganglia
striatum (putamen, caudate and nucleus accumbens)- movement/reward
substantia nigra (dopaminergic neurons)-movement
globus pallidus (movement)
sub thalamic nucleus (receives input from striatum-movement)
reward system: which are the main pathways
mesolimbic dopamine pathway:
VTA (midbrain structure rich in dopaminergic neurones) and Nucleus nucleus accumbens.
mesocortical dopamine pathway: connects the VTA with the cortex, many connection with frontal cortex
Cannabis (11-hydroxy-delta9THC) receptors
CB1: responsible of psychoactive effects. Are central (striatum, hippocampus and cerebellum, less cortex)
CB2: periferic
cannabis intox:
poor coordination, euphoria, anxiety, slowing of time, social isolation, judgment affected.
red conjunctiva, more appetite, dry mouth, tachycardia.
can also give hypertension, constipation, mydriasis, low libido.
medical indications for cannabis:
chronic pain
anti nausea in chemotherapy
for spasticity in MS
which enzymes are involved in ROH metabolism?
which order of elimination?
ADH: alcool deshydrogenase
ALDH: aldeide desydrogenase (blocked by Disulfiram)
Zero order of elimination
marker for ROH use
most sensitive: CDT (used in research)
GGT (most clinical sensitive)
VGM, uric acid, AST, ALT, LDL, TG, alcool level,
LDH is not a marker.
ROH
which neurotransmitters are involved in ROH intox
which are involved in ROH wd
ROH intox: GABA agonist, NMDA antagonist
ROH wd: glutamate.
criteria for hospital admission ROH detox
Hx of delirium tremens or seizure Hospital: moderate-severe wd Sx comorbid psychiatric Dx or comorbid medical condition pregnant more than 60 yo dangerosity for self others heavy use failure of previous outpatient detox Residential: living conditions focused on substance poor support system poor social skills
what is ROH hallucinosis?
develops during or after ROH intox. not disconnected from reality mainly visual hall, also auditory and tactile paranoid delusions can respond to antipsychotic depression and anxiety (no OCD)
Wernicke encephalopathy triad
ataxia, confusion, ophthalmoplegia
WACO acronym
Wernicke prevention vs treatment
prevention: thiamine B1 100 mg IV/IM for 3 days, then P
treatment: thiamine IM-IV 500 mg TID for 3-5 days
replete thiamine before glucose (thiamine is required for glucose metabolism)
complications of Wernicke
mortality if not treated 15-20%
complete remission 40%
80% develop Korsakoff
Korsakoff syndrome
caused by thiamine depletion
mammillary body affected
it’s a permanent condition in more than 50%
20% remission
symptoms: anterograde amnesia, retrograde amnesia, poor rappel, preserved working memory, confabulation, poor insight, possible hallucinations. ataxia, aphasia, agnosia and impaired executive functioning.
which are the stages on ROH wd
6-8 hrs: tremors, anxiety increased HR, HTN, diaphoresis.
8-12 hrs: visual hallucinations (5X auditory hallucinations). can last 1-3 days
12-24 hrs: seizures usually generalized, no aura, tonic clonic and short post ictal.
24-96 hrs delirium tremens: usually starts 5-14 days after the last drink. Can last up to 5 days. confusion, tremors, agitation, anxiety, hallucinations, delirium, diaphoresis, low grade fever, dehydration, autonomic lability.
