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34 Cards in this Set
- Front
- Back
Contraindications of vomiting induction
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unconsciousness, caustic and volitile susbstances, rapid poison
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Gastric lavage: risks
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esophageal perforation, aspiration
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Activated charcoal: uses
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adsorbs organic lipid-soluble compounds
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Alkalinization of urine: use what? for what?
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Use NaHCO3, acteazolamide
Increases excretion of acidic compounds (e.g. barbiturates, salicylates) |
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Acidification of urine: use what? for what?
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Use NH4Cl
Use to increase excretion of basic compounds (e.g. amphetamines) |
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Dialysis: clears substances with what characteristics?
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water-soluble, low MW, not protein bound
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4 components of the evaulation of the poisoned patient
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1. Identity of the poison.
2. Time of exposure 3. Route of exposure 4. Amount of exposure |
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Opiod toxicity: antidote
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Pharmacological antagonist: Naloxone (Narcan)
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Beta-blocker overdose: antidote
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Give a physiological antagonist (beta-agonist)
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Acetaminophen overdose: antidote
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Give a chemical antidote (N-acetylcysteine)
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CO poisoning sx
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10%: mild HA, vasodil
20%: throbbing HA 30%: severe HA, dizziness, visual changes 40%: unconsciousness, inc HR, RR 50%: intermittent seizures 60%: hypotension, vent dep 70%: death |
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Carbon monoxide: attributes
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Affinity for Hb > 200x that of O2
Displaces oxygen from binding to Hb Shifts O2 dissociation curve to the LEFT Binds to cytochrome oxidase |
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CO poisoning: txt
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Eliminate source of CO
Give 100% O2 Consider mechanical vent, paralysis (?) Consider hyperbaric therapy Consider barbiturate coma (?) |
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CO: half-life
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4-6 hr in room air
40-80 min in 100% oxygen 15-30 min in 100% oxygen at 3 atm |
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Aspirin: CP of early and late OD
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Aspirin uncouples oxidative phosphorylation.
Initially: respiratory alkalosis, compensatory metabolic acidosis Later: combined respiratory and metabolic acidosis Lethal dose: 10-30 g |
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Acetaminophen: management of OD
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Decrease absorption: vomiting, charcoal
Inc elimination: inc urinary pH (NaHCO3, acetazolamide) Correct acid/base, consider mech vent, dialysis Theraputic window for N-acetylcysteine (NAC) is about 36 hrs after ingestion Acetaminophen metabolism: Glucuronide (60%), Sulfate (35%), Mercapturic acid (5%) |
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Cyanide sources, chemistry
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HCN gas use as pesticide, photography, ore extraction, fruit pits.
Binds tightly to Fe3+ Major target is cytochrome oxidase Lactic acidosis Lethal dose: KCN, about 200 mg HCN, about 50 mg |
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Cyanide: detox chemistry
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CN(-) + S2O3(2-) --rhodanase--> SCN(-) + SO3(2-)
cyanide + thiosulfate --rhodanase--> thiocyanate + sulfate |
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Cyanide: management of poisoning
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Intentional converstion of Hb(2+) to Hb(3+) via amyl nitrate (inhaled), sodium nitrate (IV)
Sodium thiosulfate IV: supply of S2O3(2-) is rate limiting 100% oxygen Consider gastric lavage Very often fatal. |
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Steps of ethanol metabolism vs. steps of methanol metabolism
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Ethanol --alcohol dehydrogenase--> acetaldehyde --aldehyde dehydrogenase--> acetic acid (vinegar)
Methanol --alcohol dehydrogenase--> formaldehyde --aldehyde dehydrogenase--> formic acid |
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Signs of methanol OD
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Severe metabolic acidosis
Formic acid toxic to the retina 15 mL causes blindness 100 mL is a fatal dose txt: ehtanol or fomepizole prevents methanol conversion to formic acid (by inhibiting alcohol dehydrogenase) MECH? |
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Pesticides: type, toxicity, management
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Types:
Organophosphates: Malathion, Parathion, Diazinon Carbamates: Carbaryl, Baygon Pesticide tox: Inc muscarinic effects (N, V, inc pulmonary secr, sweating, salivation, miosis, bradycardia) Inc nicotinic effects: (hypertension, muscle weakness, twitching) CNS Effects:(anxiety, restlessness, sz, coma) Management: Prevent additional absorption (skin-bathing, GI - gastric lavage, charcoal. Atropine to dry secretions. Pralidoxime. |
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Lead: environmental sources, lead kinetics, lead toxicity in adults, lead tox in children, management
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Env sources: house dust (used in paint until 1978). in dirt (tetraethyllead was an additive in gasoline until 1970s), lead pipes, lead solder to join copper pipes, batteries, radiators, acidic fruits
Kinetics: after GI absorp circulates bound to hemoglobin, then redistributes to bone. Half life in circ = 2 months. Half life in bone = 30 years. Lead tox in adults: Vague GI effects (anorexia, constipation, metallic taste, later painful intestinal spasms) Renal (proteinuria, hematuria, cell casts) Hematopoietic (microcytic, hypochromic anemia) Neuro (periph neuropathy, hypertension) Lead tox in children: CNS (HA, irritability, ataxia, lowered IQ, behavioral problems) Abdominal pain, anemia Screen routinely [Pb] > 10 mcg/dL --> change environment [Pb] > 25 mcg/dL --> chelation therapy Management: CaNa(2)EDTA: Pb displaces Ca. Must be given IV or IM Causes proximal tubule damage. Also chelates essential metals (Cu, Zn, Fe) Dimercaprol: Solution in peanut oil Must be given IM Used in combination with EDTA in Pb poisoning Inc HR, BP Requires an alkaline urine Penicillamine Metabolite of penicillin Effective orally Useful in long-term outpt txt of Pb poisoning Also used in Wilson's dz Tox: autoimmune phenomena Succimer: Effective orally Less toxic than dimercaprol, penicillamine Does not chelate essential heavy metals (Cu, Zn, Fe) Only approved in Pb poisoning Toxicity: chemical hepatitis |
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Mercury: characteristics, tox, management
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Characteristics:
Elemental Hg is a vapor at room temp. Found in pressure meters, switches. Hg salts: Used in medicine through the 1970s, used in many industries, converted to methylmercury by bacteria Methylmercury: Poisons sulfhydryl enzymes, rises in the food chain. Mercury poisoning: Primarily CNS sx, visual and hearing loss, ataxia Management: Chelation therapy: dimercaprol, penicillamine, succimer (not approved, only for Pb) CNS damage may not be reversible. |
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Arsenic: characteristics, sources, management
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Characteristics:
As(5+): least toxic form, AsO4(3-) competes with PO4(3-). Converted in vivo to As(3+) As(3+): inhibits sulfhydryl enzymes, esp Krebs cycle. Early signs are neurological (weakness, aching), late signs include hepatic cirrhosis. GaAs are used in LEDs AsH3: denatures hemoglobin, used to make silicon chips Sources: usually ingested in drinking water. Natural constituent of ground water (esp that contaminated with agricultural runoff) Very occasionally used in medications (e.g. Trypanosomiasis) Management: Dimercaprol initially Chronic therapy: penicillamine, succimer (not approved, only for Pb) |
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Cadmium: sources, tox, management
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Common uses:
NiCd batteries, many alloys, paint (cadmium yellow) Routes of exposure: foods (esp grains), tobacco smoke, inhalation of dust Inhalation: acute: pneumonitis chronic: emphysema, fibrosis Ingestion: renal damage (tubule and glomerulus) carcinogen Management: Acute: chelation therapy, drug of choice unknown Chronic: half-life is 10-30 years, ? effectiveness. |
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Which gov org monitors public water supplies, private wells, and air?
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The EPA (Environmental Protection Agency)
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Which gov org monitors the safety of the workplace?
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OSHA (occupational safety and health administration)
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What are some of the parameters used to monitor drinking water?
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Maximum containment level goal (MCLG)
Maximum containment level (MCL) MCLG < or = to MCL |
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What are some of the parameters for monitoring workplace exposure?
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Permisible exposure lmits (PEL): time-weighted average (TWA), acceptable ceiling, maximum peak.
PEL's not established for most organics. a CIH (certified industrial hygenist) determines if workplaces are "safe" |
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Tricholorethylene (TCE)
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Used for: volatile anesthetic until 1977, industrial drycleaning solvent, decaffinating coffee
Metabolism: Via the glutathione-S-transferase pathway, then beta-lyase TCE in drinking water: MCLG = 0 MCL = 5 ppb Removing TCE from water: aeration, activated charcoal filtration Industrial exposure to TCE: TWA (8 hr day) = 100 ppm Acceptable ceiling = 200 ppm Max peak = 300 ppm, 5 min Tox: Acute: anesthetic effect (MAC = about 1% = 10,000 ppm) drowsiness, ataxia, dizziness Chronic: carcinogenic kidney, liver, esophagus, leukemia, NHL |
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Benzene
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Sources:
present in most fuels, common industrial solvent, used to separate out foods in making veggie burgers Tox: bone marrow supression, carcinogen Metabolism: via CYP to an epoxide Benzene in drinking water: MCLG = 0 MCL = 5 ppb Removing benzene from water: aeration, activated charcoal filtration Industrial exposure to benzene: TWA (8 hr day) = 10 ppm Acceptable ceiling = 25 ppm Max peak = 50 ppm, 10 min |
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TCDD (Dioxin)
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Sources:
from burning organic matter low volatility, high lipid solubility persists in the env conc rises in the food chain Kinetics: binds to AChR? Induces CYP1A1 metabolizes PAH not metabolized itself half-life is about 8 years Tox: Acute: chloracne Chronic: diabetes mellitus inc female births (60-62%) CNS, PNS damage endometriosis hypothyroidism immunosuppression |
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Polychlorinated biphenyl (PCB)
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Characteristics:
Many isomers Insulators in transformers, capacitators Low volatility, high lipid sol Almost inert Conc rise in the food chain Acute: chloracne Chronic: Cancer: melanoma, non-Hodgkin lymphoma, brain, liver, gall-bladder, bile duct Neuro: Parkinson's disease, ALS |