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47 Cards in this Set
- Front
- Back
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What is the most common source of acute iron poisoning?
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OD'ing on multivitamins
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What are the relevant pharmacodynamics of iron?
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A - only ~10% is absorbed
D - generally bound to transferrin, but following OD this becomes saturated and free iron that is toxic circulates |
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How can the total amount of elemental iron be approximated?
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Number of tablets x fraction of elemental iron
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What levels of acute iron ingestion result in toxicity?
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<20mg/kg / <350mcg/dL - no symptoms
20-60mg/kg / 350-500mcg/dL - mild-moderate symptoms >60mg/kg / >500mcg/dL - severe morbidity |
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Where does iron have its toxic effects?
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The gastric mucosa and cellular metabolism
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What effect does iron have on the gastrointestinal system?
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It causes caustic injury to the mucosa resulting in N/V/D/abd pain, bleeding, perforation and peritonitis
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What effect does iron have on cellular metabolism?
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Damages lipid membranes through peroxidation
Uncouples oxidative phosphorylation - |
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What are the stages of iron poisoning?
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1 - V/D/caustic GI injury (90 minutes)
2 - Apparent recovery (1 day) 3 - Recurrance of GI symptoms, decreased mental status, AGMA, leukocytosis, coagulopathy, renal failure and cardiovascular collapse (1-2 days) 4 - Fulminent hepatic failure (2-5 days) 5 - Pyloric scarring/obstruction; liver recovery |
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What are the lab findings in iron poisoning?
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Phase 1/2 nothing
Phase 3 - lactate AGMA, elevated coags, elevated creatinine, hypoglycemia, leukocytosis Phase 4 - elevated coags, transaminitis |
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When should peak serum iron levels be drawn to quantify the extent of the ingestion?
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3-5 hours
Sustained/enteric coated preparations 6-8 hours |
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What is the efficacy of an abdominal radiograph in iron ingestion?
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Many tablets are radiopaque. The presence of tablets correlates with ingestion severity. Can not rule it out.
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Are activated charcoal, gastric lavage, whole bowel irrigation, chelation or dialysis useful in iron poisoning?
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AC does not bind iron.
GL does not get tabs because they clump together. WBI is indicated Dialysis is not effective secondary to a large Vd Exchange transfusion may be useful in severe OD |
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How can chelation be used to treat iron poisoning?
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Deferoxamine forms a water-soluble, renally excretable compound (ferrioxamine)
100mg = 9.35mg of elemental iron Continuous infusion 15-30mg/kg/h for 24 hours (watch for hypotension, fine in pregnancy) |
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What happens to the urine when deferoxamine is used?
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It becomes a "vin rose" color
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What are the indications for admission for iron poisoning?
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<20mg/kg ingestion or <350mcg/dL peak level (6h observation)
Pills visible on radiograph (requires WBI) |
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Which basic laboratory tests are highly specific for iron levels >300mcg/dL?
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Elevated glucose and WBC
However, these are not sensitive. |
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What are the most common sources of iron poisoning?
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Historically: lead-based paint and gasoline
Moonshine Imported herbs and products |
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When do children present with lead poisoning?
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1 - post ingestion
2 - symptomatic with a compatible history 3 - for management of an elevated lead level |
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When do adults present with lead poisoning?
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Following workplace (smelting, battery manufacture, radiators, bridge/ship construction, weldeing, etc) or hobby (pottery, fishing sinkers, home remodels) exposure.
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How does lead cause toxicity?
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Binds to sulfhydryl groups and interferes with enzymatic reactions.
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What systems does lead affect most prominently?
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Hematopoietic
Neurologic Renal |
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What are the hematopoietic manifestations of lead poisoning?
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Normo or hypochromic anemia due to inhibition of heme synthesis
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What are the neurologic manifestations of lead poisoning?
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Acute - lead encephalopathy and cerebral edema
Demyelination and degeneration of motor axons - peripheral neuropathy, wrist drop, foot drop In children, neuropsychiatric disorders, decreased IQ, hyperactivity, learning disabilities, aggressive behavior and hearing loss. |
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What are the renal manifestations of lead poisoning?
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"Lead nephropathy" characterized by fibrosis of the proximal tubules
Hyperuricemic gout due to increased reuptake of uric acid |
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What are the laboratory findings of lead poisoning?
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Elevated lead level (>10mcg/dL toxic for children)
Also: basophilic stippling on peripheral smear, transaminitis |
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Are activated charcoal, gastric lavage, whole bowel irrigation, chelation or dialysis useful in lead poisoning?
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AC does not bind lead
GL does not get tabs because they clump together WBI is indicated Dialysis is not effective secondary to a large Vd |
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When is chelation indicated for lead poisoning? What agents should be used?
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>70mcg/dL or encephalopathy: parenteral dimercaprol and CaNa2EDTA.
<70mcg/dL: oral DMSA OR Penicillamine Chelation allows renal/hepatic excretion |
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How are the chelation agents dosed in severe lead poisoning?
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-Dimercaprol 3-5mg/kg IM q4h x 2 days, q6h x 2 days, q12h x 2 days
-The 2nd dose of Dimercaprol is followed by Disodium ethylenediaminetetraacetic acid (CaNa2EDTA) 75mg/kg/d IV/IM divided bid-qid. |
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What are the contraindications and side effects to dimercaprol?
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-Contraindicated in peanut allergy
-Relative contraindication in G6PD deficiency (hemolysis) -Side effects are N/V/urticaria/HTN |
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What are the contraindications and side effects to CaNa2EDTA?
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-Have not already given dimercaprol (concern that more lead may cross the BBB and increase toxicity if given first)
-Inadequate renal function (requires concurrent hemodialysis -Renal tubular injury and chelation of other metals (iron and zinc) |
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When should penicillamine be used for lead poisoning?
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Ingestions <70mcg/dL when oral DMSA is not tolerated
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When must adults with occupational lead exposure be removed from work?
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Lead levels >50mcg/dL
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What are the most common sources of arsenic poisoning?
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Historically used in homicide
Smelters/power plants Rodentisides Contaminated drinking water in 3rd world countries |
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How does arsenic cause toxicity?
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Binds to sulfhydryl groups preventing enzyme function (disrupts oxidative phosphorylation). Also causes massive hemolysis (mechanism unknown).
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How does arsenic poisoning present?
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Severely - mortality 25-30%
GI effects initially - N/C/D/abd pain/metallic taste Massive hemolysis and renal tubular injury ARDS, dysrhythmias, cardiovascular collapse May be dx'd as gastroenteritis or sepsis |
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What are the chronic effects of arsenic poisoning?
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Triad: H/O severe GI illness, rash & peripheral neuropathy.
See Mees' lines on nails Painful sensorimotor neuropathy Hyperkeratosis of palms and soles |
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What are the laboratory findings in arsenic poisoning?
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Arsenic level in blood (>5mcg/L) or urine (>50mcg/24h - spot urine lots of false negatives; seafood lots of false positives)
Anemia & basophilic stippling, elevated creatinine, transaminitis |
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How does seafood falsely elevate urinary arsenic levels?
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It contains arsenobetaine which does not result in arsenic toxicity
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How can chronic arsenic poisoning be confirmed?
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Using hair and nail specimens
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Are activated charcoal, gastric lavage, whole bowel irrigation, chelation or dialysis useful in arsenic poisoning?
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-AC will not absorb
-GL or WBI could be considered for recent ingestion/radioopaque material on x-ray -Exchange transfusions should be considered -Chelation with dimercaprol or DMSA -Hemodialysis is useful in context of renal failure |
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What are the most common sources of mercury poisoning?
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Sphygmomanometers
Flourescent lights, batteries Fish |
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What are the different kinds of mercury and how are we exposed to them?
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Metallic mergury - inhaled as a vapor but NOT GI causing resp problems
Inorganic mercury salts - Acute GI absorption/damage and renal toxicity Organic mercury - Chronic GI and dermatologic absorption |
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How does metallic mercury cause toxicity?
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Retained in the lungs causing pneumonitis and ARDS. Also can affect renal and CNS.
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How does inorganic mercury cause toxicity?
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Acute
GI absorption along with corrosive gastroenteritis and hemorrhage Renal toxicity caused by direct and immune damage. Chronic Neurologic(neurasthenia), renal (nephrotic syndrome), GI (gingivostomatitis, loose teeth, burning sensation in mouth) |
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How does organic mercury cause toxicity?
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Has chronic (not acute) toxicity
GI and dermatological absorption result in delayed neurotoxicity with ataxia/tremor/dysarthria/tunnel vision. Carcinogen |
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What are the laboratory findings in mercury toxicity?
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Organic - positive serum levels (>35mcg/L)
For other exposures use urine levels |
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Are activated charcoal, gastric lavage, whole bowel irrigation, chelation or dialysis useful in mercury poisoning?
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AC - absorbs little, not recommended
GL - try for mercury salts with milk/egg whites Chelation - dimercaprol for inorganic mercury but NOT organic mercury; DMSA for organic mercury. |
