FINAL-TOX Flashcards
mechanism(s) of CO toxic action on the body
CO has 220 times greater affinity for Hgb compared to O2
CO + Hgb = carboxyhemoglobin which can not carry O2
tx for CO2
Administer high-flow oxygen with face mask or endotracheal tube
Arterial blood sample for blood gases and CO level
If CO > 50%, then hyperbaric oxygen chamber may be required
Monitor ECG for cardiac arrhythmias
Anticonvulsant drugs if seizures occur
CO CNS damage may be subtle and could last for years
Fetus vulnerable to CO, hyperbaric oxygen therapy may be required based on mother’s blood gases and CO level
pathphys of organophosphates ( like.. Malathion Parathion Diazinon Fenthion Dichlorvos Chlorpyrifos Ethion
Inactivate AChE irreversibly by phosphorylating serine hydroxyl group into a covalent bong
clinical presentation of an overdose or exposure organophosphates
Cholinergic excess
- SLUDGE: salivation, lacrimation, urination, defecation, gastric emptying
- BBB: bradycardia, bronchorrhea, bronchospasm
- Respiratory insufficiency
- Nicotinic effects: fasciculation, paralysis
- Cardiac arrhythmias
Intermediate syndrome
- Bulbar, respiratory, proximal muscle weakness
Organophosphorus Agent-Induced Delayed Peripheral Neuropathy
treatment for organopsphosphate poisoning
how does this tx work
Can use Pralidoxime (2 PAM) which regenerates AchE through hydrolysis of the phosphorylated Ach-organophosphate complex.
atropine, scopolamine (also used for motion sickness), pralidoxime (2-PAM)
atropine for up to a month every day may be required (following overdose, nerve gas in war etc)
Atropine competes with Ach for binding sites on the muscarinic receptor and reverses the effects of excess Ach
atropine is the cure for what type of poison
yes maisa this card is fixed
mushroom poioning
signs of mushroom poisoning toxicity
rapid or delayed (weeks)
Signs of toxicity consistent with muscarinic (Ach) excess.
DUMBELS: diarrhea, sweating, miosis, nausea and urinary urgency.
Muscarine is a potent acetylcholine (Ach) agonist. Muscarine receptors in numerous organs stimulated by muscarin
: HA myalgia, severe CNS disturbance, and severe abd pain in a painter.
think
lead poisoning
how can lead enter the body
absorbed via the respiratory and GI tract.
DX tests for lead poisoning
calcium disodium
basophilic stippling indicates inhibition of enzyme
.
Tx for lead poisoning
chelating agent Ca EDTA or BAL should be considered
” Chelator works by forming two bonds with the metal ion preventing it from binding to tissue proteins and permitting rapid excretion
If the tube is purple it has sodium EDTA
The most common form of lead poisoning is
Inorganic lead
Ceramic dishware not intended for food use (
manifestations of lead poisoning other than CNS effects ( anorexia, fatigue, malaise, headache, developmental delay in children, coma and death)
“saturnine gout” (Lead inhibits ion transport and excretion in the kidney)
Lead induces “lead colic” a spasmodic contraction of the smooth muscles in the intestines.
Gingival lead lines caused by lead combining with the sulfur produced by oral bacteria. Lead sulfide deposits along the gum line.
Bone is the major storage site for lead with slow release into the circulation for years.
6 characteristics of an ideal chealtor
- water soluble
- resistant to biotransformation
- distributed into storage sites where metal is being sequestered.
- forms nontoxic complex with the metal.
- easily excreted in the urine and/or bile.
- low affinity for essential elements (calcium, zinc etc).
- focuses on lead
BAL tx is most effective in what type of toxicity
BAL is more effective in complexing free metals and will not release metals bound to enzymes.
can lead to renal toxicity
beware of peanut sensitivity
ADE of BAL tx for metal poisoning
Most patients respond with up to 50 mm Hg rise in blood pressure.
Nausea, vomiting, headache, burning sensation of the lips, tingling of the hands.
Causes hemolytic anemia in patients with G6PD deficiency of their red cells.
Ca EDTA what type of metal poisoning would you not want to use it in
Ethylenediaminetetracetic acid
EDTA charged at physiological pH and does not enter cells.
Lead binds with high affinity. Not used for mercury due to poor binding in vivo.
tx for iron overdose
deferoxamine
deferasirox
CM of iron poisoning
Nausea, vomiting, abdominal cramps, constipation, epigastric discomfort.
Parenteral dose im, iv.
Isolated from Streptomyces pilosus.
Drug has high affinity for Fe and low affinity for calcium.
deferoxamine
Some allergic reactions are seen (rashes through anaphylaxis)
drug name and ADE of the tx for iron overdose that cna be administered PO
deferasirox
GI disturbance and skin rash, low incidence ADRs.
opioid overdose Tx
naloxone, naltrexone, methyl naltrexone
opioid overdose CM
analegesia euphoria sedation resp depression cough supression miosis tuncal rigidity N/V meperidine induces tachy GI constipation renal function
which receptors fo canaboids act on
Bind to presynaptic cannabinoid receptors which results in inhibition of either excitatory glutamate or GABA.
drugs commonly screened for
Amphetamines Barbiturates Benzodiazepines THC BE (the thing that cocaine becomes) Opiates (morphine) PCP Propoxyphene
For legal action you use a ___ for drug testing
confirmation method (2-3 weeks for results)
Most used confirmation method GC/MS
All States require confirmation
two synthetic analogs of THC
dronabinol and nabilone
most used confirmation method
GC/MS
all states require confirmaton
what are some Causes for False Pos/Negs:2
Cross reacting other drugs with antb Chemical interferences Actual drug not abused Dilution and/or substitution Adulteration
adulterants
adulterants: bleach, visine, urinaid, hoy soap
elimination of ETOH
Alcohol is zero order eliminations like phenytoin and ASA
converts ethanol into acetaldehyde
ADH
Acetaldehyde is converted by ___ into acetate and acetate is turned into CO2 and H20
Acetaldehyde is converted by ALDH into acetate and acetate is turned into CO2 and H20
asians have a deficiency in
” Genetic polymorphism in Asians because of deficiency in ALDH í feel sick
how does disulfiram work
inhibits ALDH
Ethanol acts by enhacing
GABA
EtOH does enhance GABA binding to GABAA receptors (sedative-hypnotic aspects to EtOH)
Ethylene glycol how does it kill you
is converted by the same enzymes as alcohol but is eventually converted to oxalic acid because it leads to kidney failure
Ethylene glycol Tx
flood body with alcohol and the body will metabolize and remove ethylene glycol which will not be metabolized because it will be blockes
LFT w/ greatest sensitivity
GGT
how does Naltrexone work for ETOH abuse
block opioid receptors (opioid receptor antagonist). Makes patient more tolerant to the “high” of EtOH, less inclined to drink more.
Acamprosate
GABAa agonist and NMDA receptor antagonist
Vitamin B1 is used for
alcohols as their absorption is impaired
deficiency is called Beriberi
how does ETOH interact with APAP
increases biotransformation and increased production of toxic metabolite
Ethylene Glycol phases
Excitation followed by CNS depression within a few hours.
At 4-12 hours severe metabolic acidosis from metabolites.
Oxalate crystals in kidney leads to renal failure.
TX for ethylene glycol overdose
Administer EtOH or Fomepizole, treat for acidosis
Tx for acetaminophen overdose
N-acetyl cysteine (NAC)
needed because GSH does not cross the BBB
how does APA overdose work
glutathione is needed to make non toxic is needed to
overdose leads to depletition GSH and leads to liver toxicty
antidote to benzo toxicity
flumazenil
flute-mase-nail
overdose leads to respiratory depression
mechanism of benzo action
Benzo increase FREQUENCY of Cl channel opening by binding to GABA receptor (barbs keep gate open longer).