Use assoc with: hyperthermia, rhabdomyolysis, contraction band necrosis, accelerated atherosclerosis, MI, cerebral hemorrhages, dissecting Ao aneurysms
Deaths usually not dose-related.
Snorted: HCl cocaine (assoc with nasal perforation).
Increases blood levels of norepinephrine; blockage of re-uptake in synapse.
Route of administration most important factor in increasing blood levels.
Cocaine-iduced delerium: not assoc with massive drug levels, due to dopamine receptor binding, associated with hyperthermia and manifested w/psychosis.
Paranoid psychosis: induced by prolonged and heavy use. May die in prolonged struggle.
Increased D1 receptors assoc with hyperthermia; when increased D3 & decreased D1, increased craving & less euphoria with a given dose; dec D2 assoc with psychotic reactions. a receptors on coronaries cause contraction; b1 receptors chronotropic.
Cocaine and cocaethylene both cross blood brain barrier.
Illegal processing: gasoline, acetone, KMg (potassium permanganate), HCl
+ ETOH = cocaethylene, ethylbenzoylecognine
Hydrolysis by water = bezoylecognine
Plasma esterase = methylecognine
Rx intoxication: IV diazepam
Metabolism decreases gluconeogenesis, increases triglycerides in liver.
ETOH converted to acetaldehyde by alcohol dehydrogenase (depleting NAD), predominantly in liver, producing a fruity odor at autopsy.
Elimination shows first order kinetics under 0.2%, zero order 0.2%-03%, Widmark formula can be used.
Peak BAC on empty stomach 1.3 hrs after ingestion; main avsorption is in small intestine.
Post-absorptive phase: equilibration of BAC
Delayed absorption: fatty meal, fear, pain, exercise, amphetamines, decreased GI motility
Increased elimination: fructose, glycine or alanine ingestion, liver adaption to ETOH
Post-mortem concentrations higher in plasma than whole blood, and is not constant throughout brain.
Analysis: gas chromatography
|Ratio of blood to vitreous alcohol is 0.89. Blood ETOH = 0.89 x vitreous ETOH.|
Most common family of drugs in U.S. suicides.
I. amitriptyline, nortriptyline, imipramine, desipramine, doxepin (DAN ID)
II. amoxepine, trazodone, buproprion, maprotiline
III. venlafaxine, nefazodone, mirtazapine
Mechanism of deatg: cardiac, intraventricular conduction abnormalities, widened QRS.
Can also produce: CNS confusion, hallucinations, seizures and coma, hyperpyrexia
* Significant post-mortem redistribution
Enzyme multiplied immunoassay technique (EMIT): used for urine screen. Detects benzoylecgonine not cocaine.
NaF prserves blood at 2.5mg/ml, inhibits bacteria but not fungi (kills neither) & still requires refrigeration.
GC-MS (only specific method):
Immunoassay (EMIT): screen for opiates, salicylates, cocaine, amphetamines, metamphetamines, barbiturates and cannabinoids in urine. Confirm by GC-MS
GC: acetone, isopropyl, ethyl and methyl alcohol, toluene, benzene, trichloroethane and trichloroethylene.
UV spectrophotometry: CO
|Barbiturates: vitreous levels lower than blood.|
|Mushroom poisons: Amanita phalloides (almost all fatalities) from CA, Pacific Northwest and Northeast. Contains cyclopeptide toxins (hepatotoxic) not destroyed by cooking with no taste or smell. One can kill you. No symptoms for several hours. Then, nausea/vominting, cramps, diarrhea. Seem better, then hepatorenal failure. Fulminant hepatic necrosis by day 2. Mortality rate 20-30%|
|Electrolytes you can trust
Vitreous Na > 155 mEq/l or < 130 mEq/l
VUN (parallels BUN and is only slightly off even after 100 hours).
If vitreous humor has glucose, you can R/O hypoglycemia; glucose> 300 mg/100 ml reliable for hyperglycemia if you have ketones, acetone.
Oxalates: laminated sheaf or fan (ethylene glycol or methoxyflurane toxicity)
Magnesium silicate (talc): birefringent, thin pismatic crystals
Starch (amylose): maltese cross, PAS+, used in surgical glove powder
Talwin (pentazocine) or calcium complexed fillers: larger globules and aggregates of birefringent crystals