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69 Cards in this Set
- Front
- Back
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what are the options available for gastric decontaminoation?
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emesis with syrup of ipecac
gastric lavage whole bowel irrigation activated charcoal cathartics |
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what is the efficacy of emesis with syrup of ipecac?
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i. Use is declining, efficacy is less than other methods.
ii. It is only useful if used within 30-60 minutes of exposure. iii. It removes 20-30% of gastric contents at the time of administration. |
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what is the efficacy of gastric lavage
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i. Use is declining.
ii. Only useful in older children and adults (can’t use in young children). iii. Only useful if it is used within 30-60 minutes after exposure. iv. It removes about 25-35% of gastric contents at the time of administration. |
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what is the efficacy of whole bowel irrigation?
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c. Whole bowel irrigation
i. Involves the gastric administration of 1-2 or more liters of a mixed electrolyte solution, such as Golytely. ii. It is useful for slowly absorbed materials including sustained release products, iron preparations, and drug packets. iii. It is often used with activated charcoal. |
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what is the efficacy of activated charcoal?
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i. Probably the most efficacious method.
ii. The product is charcoal made with a very large surface area. iii. It absorbs most toxins except: 1. Metals (Pb, Li, Fe, etc.) 2. Low molecular weight alcohols/glycols 3. Aliphatic hydrocarbons 4. Caustics |
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what is the most effective gastric decontaminoation technique?
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activated charcoal
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what is the efficacy of cathartics?
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i. Produces that induce stool
ii. Slower working |
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how is respiratory exposures decontaminated?
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a. Respiratory exposure: remove patient to fresh air and give oxygen if needed.
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how is dermal exposure decontaminated?
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b. Dermal exposure: remove exposed clothing and wash with soap and water. The time required for washing depends on the toxin.
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how is ocular exposure decontaminated?
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c. Ocular exposure: flush with water or saline. The time required for flushing depends on the toxin, but is generally 10 minutes at minimum.
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when is extra corporeal removal of toxins used?
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a. Extracorporeal removal of toxins is uncommonly used and reserved for treatment of certain toxins. It is not a first-line treatment.
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what are the examples of extra corporeal removal?
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b. The modalities for extracorporeal removal include:
i. Hemodialysis ii. Peritoneal dialysis iii. Hemoperfusion (e.g. charcoal) iv. Ultra filtration techniques |
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what toxins are usefully removed by extra corporeal removal?
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c. Only useful for methanol, ethylene glycol, salicylate, theophylline, lithium.
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what are the sources of lead in teh US
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a. Old paint (pre-1977)
b. Leaded gasoline (phased out in 1970-80’s) c. Ceramic glazes/crystal d. Batteries e. Solder f. Ethnic medicinals g. Bullets |
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what are the two mechanisms of lead toxicity?
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binding to nucleophils groups
acting as a calcium substitute |
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what is the effect of lead binding to nucleophilic groups?
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a. Lead binds to nucleophilic groups (SH, NH, CO2H) in many tissues, causing:
i. Enzyme inhibition (e.g. heme synthesis). ii. Cell membrane damage. iii. Inhibition of Na+/K+-ATPase. |
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what are the effects of lead acting as a calcium substitue?
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b. Lead acts as a calcium substitute (it is also a bivalent cation) and functions as a second messenger.
i. Activates proteinkinase C altering neural cell development. ii. Alters neural cell adhesive molecules leading to poor development of neural cell interactive pathways. |
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what are the neuro symptoms of lead poisen?
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c. Neurological symptoms of lead poisoning:
i. Anorexia, irritability, coma, and seizures, which are more commonly seen in occupational exposure in adults. ii. Neurodevelopmental defects, such as decreased IQ and behavioral problems (ADHD, ODD) in children. |
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what are the GI symptoms of lead poisen
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d. Gastrointestinal symptoms of lead poisoning:
i. Abdominal pain ii. Constipation iii. Nausea/vomiting iv. Metallic taste in mouth |
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what are the miscellaneous symptoms of lead poisen?
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e. Miscellaneous symptoms:
i. Anemia ii. Hypertension iii. Limb pain iv. Reproductive problems (spontaneous abortion, decreased sperm count) v. Bradycardia |
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what is the main stratagy for preventing lead poisen
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a. Primary: identify and remove sources before exposure occurs.
b. Secondary: screen at-risk populations and remove children from potential exposures. c. Tertiary: treat identified cases and remove other children from exposure to prevent more people from getting exposed. |
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what is the treatment for lead poisen?
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a. The most important thing is to remove the patient from the source. Treatment with chelation is possible, but is not done as often as it used to be.
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what is the downside of treatment for lead poisen?
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b. Treatment does not reverse neurologic injury, but it may prevent further injury.
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when is chelation used?
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c. Chelation is used when the patient is symptomatic or levels >50 mcg/dl.
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what are the chelators
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i. BAL
ii. EDTA iii. 2,3-dimercaptosuccinic acid (DMSA or succimer) 1. This is the chelator most commonly used because it can be given orally. iv. D-penicillamine |
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what is the most common chelator used?
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2,3 dimercaptosuccinic acid(DMSA or succimer)
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what are the most common classes of pesticides?
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a. Organophosphates, carbamates, organochlorines, chlorphenols, pyrethrins, arsenicals, fumigants.
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what is MOA of organophosphates?
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a. Organophosphates are irreversible inhibitors of both acetylcholinesterase and pseudo-cholinesterase
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what is MOA of carbamates?
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Carbamates reversibly inhibit these same enzymes. Clinical symptoms associated with exposure to these agents relate to the accumulation of acetylcholine at nerve junctions.
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what is the MOA of organochlorine
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b. Organochlorine compounds include agents such as DDT, chlordane, and lindane. They primarily affect the brain by interfering with axonal transmission. They may also cause myocardial irritability and some members of the group stimulate hepatic enzymes.
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what are some examples of organochlorines?
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b. Organochlorine compounds include agents such as DDT, chlordane, and lindane
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how are teh cholinesterase inhibitor toxins treated?
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a. Treatment includes stabilizing the patient and appropriate decontamination. After this is achieved, atropine and pralidoxime can be used and supportive care administered.
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what are the cholinesterase inhibitor toxins?
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organophosphates, carbamates
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what is atropines effect in treatment of cholinesterase inhibitor toxins?
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i. Works by blocking the acetylcholine receptor at the nerve ending.
ii. Large and repeated doses are often necessary, and may need to be administered over several days. |
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what is pralidozime(2--PAM) used for?
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secondary antidote, used mainly for treating organophosphate poisonings rather than carbamate poisonings.
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how does pralidoxime(2-PAM) work?
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i. Works by reversing the binding of organophosphate to cholinesterases. It may also have some atropine-like action and also chemically degrades some organophosphates.
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how long after exposure should 2-PAM be used?
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ii. The irreversible binding of organophosphates to cholinesterase takes a few hours, so administration of 2-PAM should be used early in the course of treatment before this process is complete.
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what are the symptoms seen in the cholinesterase inhibitors?
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a. Life threatening symptoms: respiratory failure, cardiac dysrhythmias, seizures.
b. Others: lacrimation, salivation, diarrhea, urinary incontinence, pinpoint pupils |
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what is the acronym DUMBELS
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DUMBELS:
i. Diarrhea ii. Urination iii. Miosis iv. Bronchospasm v. Emesis vi. Lacrimation vii. Salivation symptoms of cholinesterase inhibitors |
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which cholinesterase inhibtor exposure symptoms is generally more severe?
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c. Symptoms following carbamate exposure are generally less severe than those following organophosphate exposure, although there is wide variability depending on the exact agent involved and the route and extent of exposure.
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how are patients with exposure to cholinesterase inhibitors usually evaluated?
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d. Evaluation of the severity of the exposure depends upon an assessment of the history and clinical appearance of the patient. Levels of acetyl- or pseudo-cholinesterase generally correlate with the severity of symptoms but are seldom readily available.
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what is most important first assessment in any emergency situation?
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ABC
airway breathing cardiac |
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who is gastric lavage countraindicated in?
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children can't get big enough tube to really get out what needs to be removed
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what won't activated charcoal remove
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metals(Pb, Li, Fe,)
low molecular weights(alcohol/glycols) aliphatic hydrocarbons(kerasene, gasoline) caustics(acids and alkalis) |
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what are some adverse effects of activated charcoal?
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constipation, vomiting, aspiration
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what is important consideration in use of NG tube to administer activated charcoal?
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make sure its in the stomach and not the lungs dont want to dump charcoal into someones lungs
aspirating Gastric contents or hearing bowel sounds is good for placement if not should get xray to make sure. best way push 20cc water through first if in lung will get cough response |
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what is the main drug used in whole bowel irrigations?
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golytely
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what is the antedote for digoxin/digitalis?
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digibind
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what is digibind?
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antibody antidote new wave of antidotes being developed
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what is the leading preventable public health problem in children in the industrialized world?
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lead poison
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what is the most rapid way lead is absorbed?
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rapid absorption of vapor from lung
slow, partial and saturable absorption from small bowel. so people who do certain things where where they work with lead in art/handicrafting where it may be aerosolized and inhaled may be prone to lead poisen. |
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what is the half life of lead?
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plasma/soft tissue-half life 35-40days
retained in bone half life 30-40years |
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how is lead eliminated from the body?
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75% urine
25% bile/sweat/nails/hair |
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what is the most alarming effect of lead poisen?
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neurodevelopmental defects in children definite damage done can't be reversed
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how is lead poisening diagnosed
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blood level(gold standard)
x-ray fluorescence of bone for total body burden x-ray bone-lead lines or abdomen (paint chips) delta-aminolevulinic acid in blood or coproporphyrins in urine(not used anymore) |
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what are the two groups of affects brought on by cholinesterase inhibitors?
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muscarinic effects(parasympathetic)
nicotinic effects(sympathetic) |
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what is probably going to kill someone in cholinesterase inhibitor exposure before they reach the hostpital?
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pulmonary edema from muscarinic effects
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what is a general picture of presentation for cholinesterase inhibitor exposure?
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fluid pouring out every hole, eye, nose, mouth, urine, bowel, lungs
pin point pupil-miosis |
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what are cardiovascular effects of cholinesterse inhibitors?
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can go either way depending on predominance of the muscarinic or nicotinic effects.
can have bradycardia and hypotension or tachycardia and hypertension |
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what is the main respiratory issues in cholinesterase inbhitiors?
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muscarinic effects causes pulmonary edema
nicotinic causes respiratory muscle paralysis. sooo yea don't hang out near pesticides they will @#$$ you up |
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what are some treatments for organochlorine compounds?
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mainly just treat symptoms after decontamination
cholestyramine might be useful in chronic exposures, not really acute ones |
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what are some examples of chlorophenols?
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pentachlorophenol(PCP,not the street drug) which is used as an herbicide,wood preservative, germicide, fungicide, and molluscicide
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what is the norma route of PCP exposure?
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inhalation from chonic exposure, dermal and GI exposures can occur in industial settings
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what is the MOA of PCP
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pcp is an irritant to mucous membranes. it also uncouples oxidative phosphorylation leading to stimulation of cellular oxidative metabolism
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what are pyrethrins?
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bug sprays
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what is the MOA of pyrethrins?
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only issue in humans is idiosyncratic allergic reactino exhibited by some individuals
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what are the fumigants?
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gasses or liquids used on soils to kill pests before planting.
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what are some examples of fumignts?
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methyl bromide, ethylene oxide, carbon disulfide, formaldehyde,
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what is a common presentation for chronic fumigant exposure
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works on farm
comes in with unexplained neurologic problems find out they keep fumigants in contianer could be leaking and constantly exposing them |
