Flashcards in Valentovic: Poisoning & OD (2) - Leah :) Deck (49):
Two goals when taking an H/P in the case of acute poisoning
What is the main cause of death imposed by most poisons?
-what toxins/ what dose?
-respiratory and cardio status
(MAIN CAUSE OF DEATH: cardio/ pulmonary failure-- find out: do they need respiratory support/ ventilation?)
Most common ages of poisoning in children?
Four main sources of toxicity in children?
-under 5, especially 1-2 year old toddlers
-iron in vitamins, OTC meds, cleaning substances, pesticides
Most common sources of poisoning in adults?
#1 in US: carbon monoxide!!
Here.... opiates more common.
But also think of:
analgesics, illicit drugs, antidepressants, sedatives, anti-anxiety agents, alcohol, and usually a COMBINATION of these things in addicts.
MOST COMMON thing you will need to do in the ER for poisoned patients in WV?
-Maintain respiratory status because:
opiates (i.e. oxycodone, fentanyl, heroin & combos) are very common here (cause respiratory depression)
-also probably: NALOXONE (although she didn't mention this.)
effect the circulatory system?
-Cocaine: tachycardia --> clot --> MI
-CO: lowers O2 carrying ability of the blood --> hypoxia
-Opiates: cause low BP (and respiratory depression) = massive hypoxia
When are rates of CO poisoning expected to be high?
winter time, kerosine heaters
**also common during massive power outages
How is CO poisoning treated?
1. get them to fresh air if mild
2. get them to 100% O2 if moderate
3. get them to 100% O2 + hyperbaric O2 if severe
Three ways to terminate exposure to a toxin:
1. remove source
2. enhance elimination
(alkalinize urine to remove acidic toxin; emesis etc)
3. use antidote/ antagonist
(i.e. naloxone. flumazinil)
By what drug can emesis be induced?
How does it work? (2)
Most common toxin we use this for?
Syrup of Ipecac
1. stimulates CTZ + direct effect on stomach
**Very effective for many drugs but esp for paraquat (Pot!)
Why is syrup of ipecac not widely available? (2)
1. abused by bulimics
2. parents gave their kids the whole bottle when they got really nervous about an ingestion.
(1/2 bottle = ADULT dose)
When shouldn't syrup of ipecac/ removal of toxin by emesis be used? (5)
1. Ingestion of CORROSIVE agents
(do not want to re-expose the esophagus)
(drain cleaner, ammonia, electric dishwasher cleaner)
2. Loss of GAG reflex/ comatose patients
3. Sharp objects
4. Drugs assc with SEIZURES (strychnine, TCAs, GHB)
5. Ingestion of HYDROCARBONS (furniture polish)
(risk aspiration pnuemonitis worse than systemic tox)
How does activated charcoal remove toxins?
What kinds of toxins does it typically remove?
-charcoal absorbs drugs --> charcoal removed by lavage and rest in feces
(prevents absorption of toxin)
-common drugs (OTC), nicotine gum OD, malathion (insecticide), too much ipecac
List four cases in which charcoal absorption should not be used to remove a toxin.
-acids/alkali (won't bind)
When is it used?
How is it given?
-competitive reversible antagonist of the mu receptor
-reverses respiratory depression in opiate OD
(--codeines, morphine, heroin)
-IV, short t1/2, so usually multiple times
-competitive reversible antagonist at BDZ receptor
-reverses respiratory depression in BDZ OD
-muscarinic antgonist --> reduces parasympathetic fx
-organophospate and carbamate insecticide poisoning
(should also use 2PAM for organophosphate)
How is excretion of acidic drugs enhanced? (2)
Does similar methodology work to facilitate excretion of basic counterparts?
1. Administer sodium bicarb to alkalinize urine
-Acidic drugs ionized at the tubular filtrate --> not reabsorbed into blood --> excreted as ions
**Cannot generally use acid to remove basic toxin.
-age group usually poisoned
-common souce of toxin
- two "classic" sources for test?
-most detrimental effect
-kids 1-3 yoa
-kerosine stored in poor container (orange, looks like soda)
-***gasoline v. mineral oil
-causes chemical pneumonitis if aspirated!!!
Risk of aspiration in petroleum distillate toxicity is dependent on what three things?
Which is MOST important?
**#1 VISCOSITY**, volatility, and surface tension
LOW viscosity, LOW ST, HIGH volatility = ^^^ risk
Example of a low viscosity pertroleum distillate?
How is viscosity expressed?
-low viscosity: gasoline, ^^ aspiration risk
-high viscosity: mineral oil, low aspiration risk
SUS units: high number = unlikely to aspirate
How does volatility of petroleum distillates determine their toxicity?
Which is more volatile: gasoline or mineral oil?
^^ volatility --> displaces O2 in lungs --> hypoxia
gasoline more volatile and more dangerous!
How does surface tension effect the toxicity of petroleum distillates?
Which has lowest surface tension: gasoline or mineral oil?
-LOW ST = easy spread from mouth --> trachea --> lungs = chemical pneumonitis
-Gasoline has LOW surface tension = more dangerous!
When do we see increased incidence of gasoline/ pertrolleum distillate toxicity in the US?
-when gas prices rise --> ^^ incidence of "siphoning" gasoline using mouth!
What are the deleterious effects of "huffing" paint/ glue/ etc. ?
How common is this seen?
What is the classic sign that a kid has been huffing?
-cardiac arrest, hypoxia acutely
-permanent brain damage or cancer long term
-over 1 million US teens have tried at least once
-"huffers rash"-- red ring around mouth
Long term effects of inhaling toluene?
anything during pregnancy?
Toluene: blindness, deafness (TOLtally deaf and blind)
Pregnancy: low birth weight, neural damage, fetal death
-what age group
-whats the toxic dose
(she says you do actually need to know this NUMBER)
-leading cause of fatal OD in kids
(vitamins are like candy)
-more than 20 mg/ Kg "elemental" iron
What is the difference between ferrous sulfate/ gluconate and elemental iron?
-sulfate/ gluconate are not 100% elemental iron.
-only 30-50% of a ferrous sulfate/ gluconate formula is actual elemental iron
(takes more of these than elemental iron to induce toxicitiy)
-first stage symptoms
-6-24 hrs/ second stage symptoms
-12-24 hr/ third stage symptoms
-4th phase symptoms
-1st stage: vomiting/ diarrhea
-2nd stage: iron absorbed --> "apparent recovery"
-3rd stage: organ failure
-4th stage: pyloric obstruction
Three methods for treating iron tox
-chelation w/ DEFEROXAMINE
(antidote given IV for systemic iron tox = UWORLD QUESTION!!!) de"FE"roxamine
target organs for damage (2)
what is the effect on each of these organs?
-liver (centrilobular necrosis)
-kidneys (proximal tubular necrosis)
..damage at each organ by a DIFFERENT metabolite and a DIFFERENT mechanism
In what two ways is acetaminophen removed from the body? (major path vs. minor path)
1. MAJOR: conjugated (glucuronidated and sulfated) = no toxicity
2. metabolized by CYP450 in liver --> toxic metabolite NAPQI (a quinone)
- Must be detoxified by reduced glutathione
- ^^ Concentrations--> glutathione depleted--> NAPQI binds proteins --> centrilobular necrosis of the liver
What is the acetaminophen antidote?
When does acetaminophen antidote need to be administered in cases of OD?
When do symptoms appear?
When does hepatic damage begin?
Antidote: N-acetylcysteine (precursor for glutathione synth)
--> ^ Glutathione
-administer antidote w/in 6-12 hours
-24 hours minor symptoms (N/V)
-24-48 hours hepatic damage*** (delayed hepatotoxicity)
How is risk of liver damage post acetaminopen ingestion determined?
-Get blood level of acetaminophen (not NAPQI, to unstable)
-Get time of ingestion
Using time + level, can determine risk of liver damage using a chart called a "nomogram".
In what ways can acetaminophen toxicity be reversed? (3)
-lavage with activated charcoal
-antidote: n-acetyl cysteine (oral or IV)
How does n-acetyl cysteine work?
Problem with n-acetyl cysteine?
-provides cysteine for glutathione synthesis
-oral NAC smells like rotten eggs --> patient pukes up the antidote OR kids just wont take it.
-can use IV NAC in these cases but oral is more effected.
What three amino acids make up glutathione?
What is the rate limiting step of glutathione synthesis?
Why cant IV glutathione be administered?
-Addition of Cys to the peptide
-IV glutathione itself will not enter the cell.
When can therapeutic levels of acetaminophen cause liver damage? Why? (3) ****
***Consumed with ALCOHOL.
2 Alcoholic beverages + 1 normal acetaminophen dose = LIVER DAMAGE!!!!! BAD.
-Alcohol activates CYP2E1 --> increased NAPQI
-Alcohol decreases glutathione --> dont clear NAPQI
-Alcohol decreases NADPH/ ^^ NADH -->further decreases reduced glutathiones!
"Remember this, they ask it on step one"
What is the major path for aspirin metabolism?
Always starts with aspirin --> salicylic acid
CYP450- salicylic acid --> gentistic acid
conjugation with glucuronides or glycine
Salicylates (aspirin/ methyl salicylates in sports cream):
Describe the kinetics with one dose vs many doses (i.e. arthritis, OD):
-first order with one dose
(constant FRACTION of elimination, enzymes not saturated, 2-4 hr t1/2)
-zero order with ^^ doses; i.e. arthritis or OD
(saturated enzymes, constant AMOUNT of elimination, minor CYP 450 path takes over, 18-20 hr t1/2)
Describe the findings in ASA OD:
-ox-phos uncoupling = ^^ CO2 and HIGH FEVER
-medullary stimulation = hyperventilation
-headache, TINNITUS, etc
Describe the acid-base disturbances assc with aspirin OD:
1. respiratory alkalosis (hyperventilation)
2.respiratory acidosis (kids, caused by respirator inhibition)
3. metabolic acidosis w/ anion gap
(uncoupling oxphos= ^^ ketones, lactic acid, pyruvic acid)
How is aspirin toxicity excreted?
What can be administered to increase salicylate excretion? What is a common electrolyte imbalance associated with ASA toxicity?
What should we correct immediately?
(4 bullets total)
-emesis, lavage, or charcoal
-*IV* bicarb increases salicylate excretion
-correct fluid imbalance + electrolye imbalances (usually HYPOkalemia)
To predict aspirin toxicity risk, a nomogram is used, as in acetaminophen tox.
What information is needed for this nomogram? (2)
-blood levels of salicylate (NOT aspirin)
-time since ingestion
-How does it compare to ethanol in terms of inebriation?
-How is it metabolized?
-Key feature in toxicity?
-Greater CNS depressant and drying effect than ethanol
-converted by alcohol dehydrogenase + aldehyde dehydrogenase --> *acetone*
-smells like "fruit" just like in DKA because = ^^ ketones/ ketoacidosis
Two Toxic metabolites?
What does each metabolite cause?
-converted to formaldehyde and then formic acid
-BLINDNESS** due to **formic acid**
-GI symptoms due to **formaldehyde**
(also causes inebriation)
-found in what substance?
-What are the metabolites? (3)
-What is the main toxicity?
-ethylene glycol --> glycoaldehyde --> glycolic acid --> oxalate
= *oxalate* crystal in lumen of kidney, olgiuric renal failure
What three treatment options are available for alcohol toxicities?
-emesis or lavage if less than 3 hours
-administer IV ethanol to compete for alcohol dehydrogenase
-fomepizole- inhibits alcohol dehydrogenase
2 y/o w/ pain, nausea chills.
X ray show ovals.
Kid says he ate some "colored candy he found in mom's bathroom".
What tests do you run? Whats the most likely substance involved? What would you give?
-Tox screens for most common drugs in bathroom
-Prob not prescription because it was colorful
-Check for acetaminophen, aspirin, and esp *iron*
-If Fe ^^^, give kiddo deferoxamine (chelate)