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44 Cards in this Set
- Front
- Back
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accidents
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-leading cause of mortality til adolescence
-responsible for 50% of all deaths under 25 yrs old -50% of all accidental childhood deaths are in infants <1yrs old -3 millions births/yr – 98% travel home in a car! 200-300 die in this drive yearly |
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top 3 causes of death under 1 yr
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1. inhalation/aspiration (food, safety, pins, small toys, pacifiers, balloons)
2. mechanical suffocation or strangulation 3. motor vehicles |
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top causes 1-4 yrs old
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1. automobile
2. poisoning |
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school age accidents
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-different male:female
-pedestrian deaths -pedestrian injuries have a higher death to injury ratio -falls: 5th leading cause of death -walker falls = 24,000 ER visits/yr -drowning: 5-14 yrs = second leading cause of death -bicycles: 5-14 yrs = 600 deaths/yr -motorcycles: death rate is 15x greater than for cars -pools and tubs |
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poisoning and toxicology incidence
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-10% of pop is <5
-<5 accounts for 2/3 of all poisonings -2 million nonfatal accidental poisoning/year -200 deaths from ingestion per year <5 years of age -<1 yo: poisoning is usually iatrogenic ->5: poisoning is usually a suicide attempt -Peak age of poisoning –1-3 years old male>female |
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poisoning prevention
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-medicine is not candy
-keep inedible products separate from food -keep all products in original containers -always read labels before use -teach to take medicine only from adults -keep hand a 1oz bottle of ipecac -childproof containers -If child swallows a poison, there is a 50% chance of a second attempt |
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nontoxic ingestions
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-usually will not produce sx
-product must be identified -must be single product ingestion -no signal words are on container -danger-poiron-warning-caution-antidote-call a dr |
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nontoxic ingestions
rules |
-vol of a swallow: 18mo-3yrs: 4.5 cc; adults 15 cc
-toxic dose = 5x therapeutic dose (not narcotics) -Documented single tablet ingestion – will not produce toxicity (except opiates) |
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evaluation of an unknown poison
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-bring in container
-spell out name of product -read ingedients -clues: <1yr = therapeutic OD >5 yr = potential suicide -WHAT were they doing, WHERE was child playing, WHEN did sx manifest, HOW much of substance was available |
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evaluation cont
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-examine pt: burns on tongue, lip, mouth
-gasoline odor or breath? -consider poisoning when: abrupt sx, age 1-4 yrs old, hx of prior ingestion |
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acetaminophen
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-<6 rarely toxic amts ingested
->6 yo toxic amts common-suicide -absorption is complete and rapid: 1-2 hrs -in OD absorption is delayed: 4 hrs -toxicity results in hepatocellular necrosis -Toxic dose –children >150 mg/kg adults >7.5gm |
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tylenol clinical manifestations
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-initial: 12-24hrs: Nausea, vomiting, diaphoresis, lethargy
-second: pt is asymtomatic-onset of hepatic dysfunction -third: 28-96 hrs: vomiting, jaundice, RUQ pain, liver failure, hepatic coma, renal failure -fouth-recovery- 7-8 days post ingestion |
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tylenol dx and tx
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-draw acetiminphen level
-tx: ipecac followed by water (throw up) -cathartic: MgSO4 or Mg citrate to quicken transit time and dec absorption -activated charcol -tylenol level: 4hrs post absorption -baseline liver chemistries STAT then q4h -acetylcysteine (mucomist) |
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salicylates
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-rare, 80% of poisonings due to therapeutic OD --> common in infants b/c
1. illnesses with dec fluid intake 2. fever which increases fluid intake 3. both result in inc serum concentration 4. sx may mimic an illness so Dx is missed |
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salicylates- pathology
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-rapidly absorbed in therapeutic doses
-OD: absorption slowed to 24 hrs due to saturation of metabolic pathways -toxic effects: direct stim of CNS resp center, inhibition of Kreb cycle enzyme; uncoupling of phosphorylation thus interferes with glucose metabolism; fluid and electrolyte loss, resp alkalosis, metabolic acidosis -look like daibetic |
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salicylates- clinical manifestation
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-hyperventilation with inc rate and depth = Kussmal breathing
-anorexia, vomiting, sweating, flushed, fever -CNS signs: delerium, tinnitus, coma, convulsions |
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salicylates dx
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-serum salicylate level
-urine: ferric chloride test |
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salicylates tx
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-induce emesis: ipecac, gastric lavage up to 24 hrs
-adequate ventilation, oxygenation -rehydrate with IV fluids -glucose if ketosis present -inc urine output: alkalinize to pH 8-8.5 over first 4-8 hours. Allows salicylates to clear in urine -activated charcoal -diuretics -dialysis |
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Lead- sources
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-drinking water
-lead based paints -fumes from burning batteries, smelting -unglazed pottery exposed to acid fluids -color newsprint |
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lead pathology
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-affects cellular metabolism of every organ/tissue
-interferes with biosynthesis of heme = anemia -affects CNS from mild learning disability to frank enecephalopathy -kidney damage causing proximal tubular damage = Fanconi syndrome -replaced calcium in bone = lead line on x-ray |
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acetaminophen
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-<6 rarely toxic amts ingested
->6 yo toxic amts common-suicide -absorption is complete and rapid: 1-2 hrs -in OD absorption is delayed: 4 hrs -toxicity results in hepatocellular necrosis -Toxic dose –children >150 mg/kg adults >7.5gm |
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tylenol clinical manifestations
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-initial: 12-24hrs: Nausea, vomiting, diaphoresis, lethargy
-second: pt is asymtomatic-onset of hepatic dysfunction -third: 28-96 hrs: vomiting, jaundice, RUQ pain, liver failure, hepatic coma, renal failure -fouth-recovery- 7-8 days post ingestion |
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tylenol dx and tx
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-draw acetiminphen level
-tx: ipecac followed by water (throw up) -cathartic: MgSO4 or Mg citrate to quicken transit time and dec absorption -activated charcol -tylenol level: 4hrs post absorption -baseline liver chemistries STAT then q4h -acetylcysteine (mucomist) |
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salicylates
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-rare, 80% of poisonings due to therapeutic OD --> common in infants b/c
1. illnesses with dec fluid intake 2. fever which increases fluid intake 3. both result in inc serum concentration 4. sx may mimic an illness so Dx is missed |
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salicylates- pathology
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-rapidly absorbed in therapeutic doses
-OD: absorption slowed to 24 hrs due to saturation of metabolic pathways -toxic effects: direct stim of CNS resp center, inhibition of Kreb cycle enzyme; uncoupling of phosphorylation thus interferes with glucose metabolism; fluid and electrolyte loss, resp alkalosis, metabolic acidosis -look like daibetic |
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salicylates- clinical manifestation
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-hyperventilation with inc rate and depth = Kussmal breathing
-anorexia, vomiting, sweating, flushed, fever -CNS signs: delerium, tinnitus, coma, convulsions |
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salicylates dx
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-serum salicylate level
-urine: ferric chloride test |
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salicylates tx
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-induce emesis: ipecac, gastric lavage up to 24 hrs
-adequate ventilation, oxygenation -rehydrate with IV fluids -glucose if ketosis present -inc urine output: alkalinize to pH 8-8.5 over first 4-8 hours. Allows salicylates to clear in urine -activated charcoal -diuretics -dialysis |
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Lead- sources
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-drinking water
-lead based paints -fumes from burning batteries, smelting -unglazed pottery exposed to acid fluids -color newsprint |
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lead pathology
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-affects cellular metabolism of every organ/tissue
-interferes with biosynthesis of heme = anemia -affects CNS from mild learning disability to frank enecephalopathy -kidney damage causing proximal tubular damage = Fanconi syndrome -replaced calcium in bone = lead line on x-ray |
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lead patho- cont
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-more common in spring and summer as:
1. sunlight increasing Vit D production which increases mobilization of lead from bones to blood, then into brain, kidney and other organs replaces Fe in hemoglobin thus mimics iron deficiency |
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lead classification based on lead levels
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I = blood lead level <9
IIA = blood lead level 10-14 IIB = blood lead level 15-19 III = blood lead level 20-44 (begin treatment if symptomatic IV = blood lead level 45-69 – begin immediate treatment V = blood lead level >70 – medical emergency |
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lead clinical manifestations
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-usually no overt sx: diagnosed form screening
-sx indicated serious poisoning -GI: vomiting, abd pain, constipation, PICA -hematology: pallor, anemia, irritability -CNS: lethargy, irritability, projectile vomiting, ataxia, convulsions, dec attention span |
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lead dx
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-suspicion and screening
-serum lead levels -xray of long bones (lead lines) -flat plate of abd- radio opaque substances |
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lead tx
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-remove from environment
-correct enviornmental problem -education of caretakers -test al siblings -BAL = dimercaprol -CaEDTA = edetate disodium calcium -Cuprimine = D-penicillamine -chemet = DMSA = succimer |
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iron intoxication
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-most common source: iron tabs
-ferrrous sulfate: most common form -lethal dose: 300mg/kg -OD rarely results in death |
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iron- patho
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related to:
- local irritating effects on GI mucosa (bleeding) metabolic effects in liver secondary to Fe deposits -occasional CNS effect |
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iron clinical manifestations
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Four clinical stages:
I: 30 min after ingestion; vomiting, bloody diarrhea, subsides in 6-12hrs, may be followed by acidosis, shock and death II: 12-36 hrs; absorbed Fe delivered to liver III: 24-36 hrs; signs of hepatic toxicity, progression to coma, convulsions, shock, death IV: post recovery complications; scarring and stenosis of pyloric area, fibrosis of the liver, 1-2mo post ingesiton |
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iron treatment
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-prompt emsis: ipecac first, will remove large potions of tabs THEN gastric levage with desferrioxamine via NG tube in sodium bicarb
-Desferrioxamine IV – 15mg/kg/hr for 6 hours urine turns brown, continue until urine clears -for renal impairment- dialysis with desferrioxamine |
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hydrocarbons
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-30,000 ingestion/yr
-95% under 5 yo with 100 deaths -Low viscosity hydrocarbons – highly volatile and lead to aspiration at time of ingestion -High viscosity hydrocarbons – less toxic but lead to lipoid pneumonia if aspirated |
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hydrocarbons tx
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-no ipecac or lavage! --> wil inc risk of vomiting and aspiration
-if no aspiration then no problem once stomach is emptied -is aspiration is present: hospitalize to treat PNA |
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barbiturates
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-Accidental overdose = 10% of cases
-suicide most common problem -lethal dose is variable -are respiratory and myocardial depressants -tx is supportive |
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vitamins
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-impt ones are A and D
-presents with manifestations of inc intracranial P (bulging fontanelle) |
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Alkali
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-Lyes (drano)
-if oral burns present, must R/P esophageal burns thus endoscopy -do not induce vomiting --> will result in more burns |
