Forensic Toxicity Flashcards
what is medical examiner system
its headed by a forensic pathologist (MD)
what is a coroner system
it may not be headed by a physician
what are 2 things that you do in clinical toxicology
- emergency screening (overdose)
- therapeutic drug monitoring
when do you do clinical toxicology testing
if it is likely to influence treatment of the patient
why do we do forensic toxicology
for legal purposes
what are 4 examples of forensic toxicology
- postmortem (cause of death)
- impaired driving/sexual assault
- workplace drug testing
- sports
what kind of specimen do you get from veins post mortem + why
whole blood (not serum or plasma) because the blood hemolyzes
what are 6 examples of tissues used for post mortem toxicology
-whole blood
-vitreous (eye)
-liver
-urine
-stomach contents
-hair
etc
what is the main methodology for forensic tox
GC/MS(MS) and LC/(Q)TOF
what are 2 main differences for instrumentation for clinical and forensic tox (so these 2 points are about forensic)
1-does not rely only on immunoassay
2-must use better extraction and chromatography
is blood reliable own its own for assessing the presence of alcohol at the time of death + why
no because postmortem BAC can increase (from bacteria and contamination)
what part of the body is better than blood when it comes to assessing alcohol
the vitreous of the eyeball
what is the main mechanism of postmortem redistribution
release and diffusion from major organs
what 2 things does postmortem redistribution dependent on
time and concentration dependent
what are candidates of postmortem redistribution (2)
high volume of distribution (like 3L/kg)
“basic character”
how much can concentrations increase with postmortem redistribution
2-10 fold
what are the 4 orders of decreased postmortem redistribution
cardiac > subclavian > femoral > antemortem
what is antemortem
when the sample is taken before death
are central or more distant areas more effected by postmortem redistribution
central
what is bad about postmortem redistribution
it can lead to mis-interpretation of toxicological results
what are 4 main difficulties of interpreting postmortem data
- dont know when drug was last taken
- dont know metabolism for person
- increase and decrease conc
- dont know tolerance
can you take a post mortem drug and then figure out the concentration
no, because of metabolism, tolerance… not that easy
why is it much tricker to interpret postmortem levels of opioids
because there is a wide range of tolerance levels
what is the drug that the kid died from (7 yo ADD)
imipramine
how does imipramine get metabolized
CYP2D6 and CYP3A4
what happens when imipramine gets metabolized by CYP2D6
it is metabolized again by CYP3A4 then removed by the body
what happens when imipramine gets metabolized by CYP3A4 (Compound name + rest of pathway)
desipramine => it is metabolized again by CYP2D6 then removed by the body
what is desipramine
when imipramine gets metabolized by CYP3A4, still active
what happens if you are deficient in CYP2D6 and take imipramine
you get a build up of desipramine because it needs CYP2D6 to get excreted
what happens if you are deficient in CYP2D6 and take codeine
it wont be metabolized into morphine
what happens if you are deficient in CYP3A4 and take codeine
nothing, its CYP2D6 that metabolizes it
which enzymes metabolizes codeine into morphine
CYP2D6
which enzymes metabolizes imipramine into desipramine
CYP2D6
what is the half life of THC in blood like
relatively short
what is the half life of THC in brain like
longer than in blood
what is the half life of THC in body like
much longer than blood and brain
with THC, does a certain blood concentration directly correlate to impairment
no, not like alcohol
what are 4 “past wisdom” things about THC that have been debunked
- that blood level of 2-3ng/mL means you used it within the past 6h
- THC drops to near zero a few hours after last smoke
- can use THC:THC-CPPH ratio to estimate time of last use
- little postmortem change
what is the typical baseline blood THC several hours after smoking in light smokers
often less than 2ng/mL
what is the typical baseline blood THC several hours after smoking in heavy smokers
can be more than 5ng/mL
what is the typical baseline blood THC 7 days after smoking in heavy smokers
1.2-5.5 ng/mL 7 days after use
why does THC stay high in the blood
because THC is slowly released into the blood
does THC go through postmortem redistribution
yes
how much can THC levels in femoral blood be diff in cardiac blood with postmortem redistribution
it can be 6 fold higher in femoral blood than cardiac blood
where may THC concentrate before redistributing postmortem
in muscle tissue
why might you get super high levels of THC in the femoral blood post mortem
because there may be fat in the blood draw
what are the 2 main things to interpret when trying to find the manner of death
circumstance of death and investigations (medical history, autopsy, toxicology on multiple specimens)
what shouldnt you do if you dont have enough information
dont offer interpretation or give clear caveats
what is poison hemlock
primary alkaloid coniine
what are the effects of poison hemlock / coniine like
similar to nicotine but more toxic - paralyzes muscle by blocking nACh
what does it look like when you die from hemlock / coniine
(asecnding paralysis, lower limbs affected first) respiratory paralysis leads to cessation of breathing, death from lack of oxygen
is the hemlock tree poison
no
what is the water hemlock poison
yes
what is the toxin in water hemlock
circutoxin
what does circutoxin do
disrupts CNS
what are symptoms of circutoxin
nausea, emesis, abdominal pain, tremors, seizures
what is an example of a poison nut
cerbera odollam
What are the active ingredients in cerbera odollam
cerberin and neriifolin
what are cerberin and neriifolin
potent cardiac glycosides
what are 6 symptoms of cerberin and neriifolin overdose (cardiac glycosides)
nausea, vomiting, hypotension, bradycardia, heart block, arrhythmias
what are some pretty things that can kill you
rosary pea seeds
what is the toxin in rosary pea seeds
abrin
what does abrin do
ribosome inhibiting protein
