topic 28 Flashcards
What are symptoms of ethanol overdose? What is the mechanism of ethanol? How is it treated? Why is the order of treatment important?
• One of the most common ingestants
• CNS depressant causing ataxia, lethargy,
coma, loss of DTRs, hypothermia in overdose,
• Hypoglycemia, especially in children, can
occur and can be delayed in onset
• Can result in ketoacidosis (typically a Board question), causes high AG Gap
• Ethanol augments GABA mediated synaptic
transmission and binds to GABAA
channel leading to CNS depressant effects
• Ethanol also inhibits the NMDA receptor but
in chronic ethanol use, it up-regulates NMDA receptors.
• Supportive care: intravenous fluids, thiamine
first, and then glucose
Thiamine is important for carb metabolism.
• In this setting, an acute glucose load may precipitate acute, severe cerebral thiamine deficiency (Wernicke’s encephalopathy , nystagmus,
ophthalmoplegia, coma.)
• Therefore, prior to giving hypertonic dextrose (D50W) in adults who present in coma, a dose of 100 mg of thiamineis routinely given first.
Where is methanol found? How is it metabolized? How is it toxic? How is it treated?
- Methanol commonly found in windshield washer fluids and gas line antifreeze
- Rapidly absorbed by oral route (also dermal)
• Metabolized by ADH to formaldehyde, formic
acid and CO2 and water
• Formate is the toxic agent (may take 12 to >
24 hours to manifest)
• Basis for treatment is blocking methanol
metabolism by ethanol competition for ADH
• Fomepizole (4-methylpyrazole) used successfully to block ADH. Ethanol is also used to do the same thing, but they should not be used together, and 4 methylpyrazole works better. This should be done quickly.
Where is ethylene glycol found? How is it metabolized? What is its halflife? What are the symptoms of ethylene glycol toxicity?
- Found in radiator antifreeze, brake fluids, etc
- EG half-life in adults 3 - 5 hrs, longer elimination in OD
- Metabolized to glycolic acid, glyoxalate and oxalate with resultant AG metabolic acidosis
• First order probably switches to zero order in
OD; EtOH or 4-MP delays/halts metabolism
- Renal and CNS toxicity predominate
- Hypocalcemia results from oxalate complexing with tissue calcium
Where is isopropanol found? How is it excreted? How is it metabolized? What is its half life and that of its product? What are the symptoms?
- Found in cleaners, perfumes, deicers, and soaps
- Absorbed via oral, dermal and inhalation.
• ~ 20-50% of isopropanol is renally excreted
unchanged
• 50-80% is converted in the liver to acetone, which
is also a CNS depressant
• Elimination half-life of isopropanol is 4-6 hours
and is 16-20 hours for acetone.
• Isopropanol does not cause acidosis but does
cause ketosis from acetone so anion gap is usually not elevated (very likely Board question)
- Osmolar gap is elevated by isopropanol
- Toxicity involves CNS depression, hypotension, cardiac depression, vomiting, gastritis (may be hemorrhagic).
What are the symptoms of aliphatic hydrocarbons and those of halogenated hydrocarbons? What are two types of aromatic hydrocarbons?
- Aliphatic hydrocarbons (kerosene, gasoline, mineral seal oil, etc) risk aspiration and chemical pneumonitis
- Halogenated hydrocarbons (trichloroethane, freons, etc) can sensitize myocardium arrhythmias
• Aromatic hydrocarbons include benzene
(associated with leukemia) and toluene
What are the symptoms of toluene toxicity?
• Toluene (glue sniffing) may result in severe
neurological deficits when used chronically
– other effects are CNS depression, distal renal tubular acidosis, hepatotoxicity, CNS atrophy
What is the mechanism of cyanide? what are two ways its treated? How does one of them work?
• Cyanide toxicity primarily due to inactivation of
cytochrome aa3
• Cellular hypoxia is primary mechanism (boards)
• Treatment is cyanide antidote kit:
• Newer treatment out in 2007 is hydroxocobalamin
– Combines with cyanide to form cyanocobalamin.
How common is envenomation by snakes? What snakes are venomous in MO? What does snake venom consist of? How do they work? What is the antivenin?
• Snakebites common in spring/ summer;
no envenomation ~20 - 30% of time
• Genera of interest in Missouri are the
Copperhead, Cottonmouth, types of rattlesnakes
Snake venom is complex-consists of lots of things
Pit viper and elapidae venom prevent ACh release from nerve endings
• Commercial antivenin has been equine derived polyvalent product but a purified Fab antibody is now available (CroFab®)
Which spider envenomations are of interest? What do they result in?
- Spider bites of particular interest are the brown recluse (Loxosceles reclusa) and black widow (Latrodectus mactans)
- Loxosceles venom: dermonecrotic complex with vasoactive peptides, hyaluronidase, esterase, proteases, hemolysins, sphingomyelinase D, etc.
Black Widow:
• Binds receptors on presynaptic neuronal membranes, opening ion-specific cation channels (Ca++ influx) and release of Ach and NE and motor end plate–>pain and rigidity
