BEHAVIOURAL HEALTH Flashcards
recreational sympathomimmetics (cocaine, amphetamines) inhibits …
reuptake from synaptic cleft by MATs
(monoamine transporters)
*terminating stimulation of postsyanptic neurons -> increases NE, serotonin, dopamine in synaptic cleft *
tetrahydrocannabinol has what affect on adenyl cyclase
inhibits
dry mouth
red eyes
impaired reaction time
mydriasis
mild tachycardia
delusion/paranoia
cannabis intoxication
what receptor does LSD activate
5-HT2A in CNS
visual illusions
synesthesia
disortered time perception
mild sympathomimetic
anxiety, aggitation, paranoid delusions (bad trip)
LSD intoxication
lysergic acid diethylamide
formication
sensation of insects crawling on/under skin
cocaine, amphetamines
negative urine screening
bath salts
(stimulant - natural occuring amphetamine) sympathetic stim+ neuropsych
amphetamines can be synthesised from
over the counter pseudoephedrine
(cold & flu meds)
LSD can be synthesised from
ergotamine
GHB (gamma-hydroxybutyrate) can be synthesised from
sodium oxybate
GHB = direct agonist of GABA receptors
cocaine can be used as
a local anaesthetic
(or recreationally - induce euphoria)
binds & inhibits MATs - decreased reuptake NE, dop, ser
anaesthetic properties from Na+ channel blockade
indirect symathomimmetic - pupil dilation from blockade a and b receptors
? should be used with caution in cocaine users
beta blockers
(unopposed a1 stimulation can cause hypertensive crisis)
especially non-selective
Overdose with MDMA (3,4-methylenedioxymethamphetamine) can cause …..
2 things
serotonin syndrome
MDMA induced SIADH
MDMA stimulates ADH (vasopressin) release, leading to water retention and hyponatremia.
This occurs via serotonin activation of the hypothalamus, which controls ADH secretion.
excess serotonin activity, particularly at 5-HT1A and 5-HT2A receptors.
Leads to neuromuscular excitation, autonomic instability, and altered mental status.
thirst, euphoria, confusion, hyperthermia, tachycardia, hypertension, mydriasis, tremor, and hyponatremia
MDMA intoxication
Ecstacy
mood swings (rapid, brief)
irritability
slurred speech
conjunctial injection
ataxia / dysdiadochokinesia
perioral exematous rash
inhalent
MOA similar to nitric oxide - short duration 15-45min
aerosol, glue, show polish, paint
how does PCP (phencyclidine) act on receptors
inhibition NMDA receptors
activation dopaminergic receptors
usually smoked
patients with stimulant intoxication should be treated with
benzodiazapines i.e. midazolam
avoid antipsychotics i.e. hapoperidol in stimulant intoxication - decrease seizure threshold
runny nose
yawn, irritable
leg muscle cramps
diarrhoea, abdo pain
cool, damp skin, piloerection
sympathetic hyperactivity i.e. reflexes
heroin (opiate) withdrawal
To quote John Lennon: “My body is aching, goose-pimple bone, can’t see nobody, leave me alone/ my eyes are wide open, can’t get to sleep, one thing I’m sure of, I’m in at the deep freeze/ cold turkey has got me on the run.”
brains reward pathway is called
mesocorticolimbic pathway
incldues 3 areas: frontal cortex, nucleus accumbens, ventral tegmental
release of doapmine in these areas caused by drug use (strengthens, motivates use)
smoking cessation treatment
nicotine replacement therapy
& varenicline & bupropion
Acute delirium resulting from thiamine deficiency. Triad of cerebellar dysfunction, confusion, and ocular findings.
Wernicke’s encephalopathy
Thiamine cofactor for enzymes in carbohydrate metabolism: α-ketoglutarate dehydrogenase, pyruvate dehydrogenase, and transketolase
*
occular findings - opthalmoplegia, nystagmus, ptosis*
what can precipitate wernickes encephalopathy during treatment of i.e. gastroenteritis
giving IV with glucose prior to thiamine
can further deplete thiamine levels
must give thiamine before treatment
irreversible, late manifestation of confabulations, memory loss/personality change is….
Korsakoff psychosis
manifests after Wernickes encephalopathy
Drug treatment for alcohol withdrawal
benzodiazapines
binding to γ-aminobutyric acid (GABA) type A receptors
conformational change -> increases the frequency of channel opening -> influx of chloride ions.
