Other Flashcards
(35 cards)
Salicylate poisoning symptoms, treatment?
Confusion/agitation, tachypnea, hyperglycemia, anion gap acidosis, seizure
Ingestion of >300 mg/kg can be fatal
Treatment: Increase urinary excretion through alkalinization (drug won’t give up H+ if urine is acidic, nonpolar form gets reabsorbed), activated charcoal, hemodialysis
Sodium bicarb infusion: 0.5 mEq/kg/hr, watch for hypokalemia
Treatment for cyanide poisoning
Hydroxycobalamin
Sodium nitrite or sodium thyosulfate
Sodium nitrite creates methemoglobin, ferric ion binds cyanide liberating it from cytochrome oxidase
Treatment of clonidine overdose?
Naloxone 0.1 mg/kg – reverses neurologic but not cardiovascular effects in some patients
What is most common genetic mutation associated with neonatal familial HLH?
Perforin gene (PRF1)
Perforin is released by cytotoxic T cell and NK cells to perforate target cell membranes; when absent, these cells activity is disrupted and cytokines/activated macrophages are unchecked
Glasgow coma scale
Eyes (4): spontaneous, to speech, to pain, none
Verbal (5): coo and babble, irritable cry, cry to pain, moan to pain, none
Motor (6): spontaneous and purposeful, withdraw to touch, withdraw to pain, abnormal flexion to pain, abnormal extension to pain, none
What is three column model of spine injury?
Spine is made up of anterior column (anterior ligament and anterior 2/3 of vertebral body), middle column (posterior ligament and posterior 2/3 of vertebral body), posterior column (pedicles, facets, lamina, spinous processes)
Need two intact to maintain stability, otherwise likely surgery with hardware
Pediatric burn stabilization
ABCDE
Consider early intubation (airway edema)
Early imaging for other injuries
Depth and surface area:
1. superficial-damage to epidermis but will heal (sunburn)
2. partial thickness-variable damage to dermis, areas of injured cells that will evolve, blisters and moist; deep partial thickness less painful, >50% of dermis is damaged, potential severe scaring, pink to pale white, less edema, all of epidermis and significant portion of dermis
3. full thickness-complete dermal destruction with almost no capacity for skin regeneration, need to excise (bright white, leathery)
Surface area = only count partial and full thickness
Rule of 7s for smaller kids, rule of 9s for older and adults
Burn physiology: loss of skin barrier (fluid loss) with vasoactive mediator release
TBSA>15% develop a systemic inflammatory response, hypermetabolic response with protein needs 3 g/kg/d
Excise early to blunt the global inflammatory response (first postinjury week), get improved healing, decreased infection, and improved survival; best coverage is autograft, in large burns can supplement with cadaver allograft
Parkland formula for burn resuscitation
4mL x TBSA x weight in kg
First half over 8 hours from start of burn, second half over 16 hours
Inhalational injury
Look for: hoarse voice, stridor, wheezing, soot in pharynx or nares, singed nose hairs
Bronchospasm then PARDS
Early bronch to remove carbonaceous material
No role for steroids
How does carbon monoxide impact body?
Cytochrome oxidase system, electron transport chain and production of ATP
Hgb oxygen dissociation curve is shifted left, mild acidosis may actually be helpful
How does cyanide impact the body?
Often co-exists with carbon monoxide poisoning, burning of household materials
Binds with cytochrome a3, a component of the cytochrome c oxidase complex in mitochondria, prevents cells from using oxygen
Antidote is hydroxocobalamin
Snake bite
In the United States, most venomous snakebites are from members of the Crotalinae subfamily, including rattlesnakes, copperheads, and water moccasins.
Crotalid venom contains multiple enzymes and proteins, which can cause hypofibrinogenemia and thrombocytopenia, resulting in persistent coagulopathy.
Coral snake antivenom is no longer commercially available.
What are symptoms of cholinergic toxicity (e.g. organophosphate)?
Cholinergic toxicity
SLUDGE - salivation, lacrimation, urination, defacation, GI cramps, emesis/edema
Bradycardia, miosis, faciculations
What is pralidoxime (2-PAM) used for?
Treat organophosphate toxicity - breaks the bond between oganophosphate and acetylcholinesterase (enzyme that should break down acetylcholine)
What causes damage in acetaminophen toxicity?
Acetaminophen metabolized by glucuronidation, sulfonation, and …
CYP-450 oxidation > N-acetyl-p-benzoquinoneimine (NAPQI) > reduced by glutathione to a clearable metabolite
When glutathione stores are depleted, NAPQI accumulates causing hepatotoxicity
N-acetylcysteine replaces glutathione stores, helpful within 8hrs of ingestion
Toxic dose of acetaminophen?
10x usual dosing
Child: 150 mg/kg
Adult: 10 g
Salicylate poisoning
salicylate toxidrome includes vomiting, tinnitus, tachypnea, and confusion/agitation. Patients may develop hyperreflexia, hypotension, noncardiogenic pulmonary edema, and acute respiratory distress syndrome with severe salicylate intoxication. There is typically a mixed respiratory alkalosis and anion gap metabolic acidosis
30-60-90 rule for salicylate ingestions may be helpful: levels greater than 30 mg/dL require urinary alkalinization; levels greater than 60 mg/dL for chronic use and 90 mg/dL for acute ingestions may be life threatening and require hemodialysis
Thiamine role
Thiamine is important for mitochondrial activity and energy production. Thiamine deficiency affects the entrance of pyruvate into the mitochondria resulting in lactate formation. Decreased levels of thiamine can result in impaired oxidative phosphorylation and carbohydrate metabolism resulting in lactic acidosis and cell death.
Treatment for cyanide toxicity?
Hydroxycobalamin
Combines with cyanide, turns urine red, interferes with lab tests
If unavailable, cyanide antidote kit: sodium nitrite and sodium thiosulfate
sodium nitrite - downside is methemoglobinemia
sodium thiosulfate - give with sodium nitroprusside, serves as a sulfur donor in reaction converting cyanide to thiocyanate (excreted)
Symptoms of hemlock ingestion
Combo of cholinergic and sympathomimetic (selective agonist for nicotinic-type acetylcholine receptors)
Cholinergic: bronchorrhea, bronchospasm, vomiting, salivation, urination
Sympathomimetic: hypertension, tachycardia, tremor, mydriasis, seizure, rhabdo
Other: bronchoconstriction, difficulty walking, hypothermia, coma
What kind of damage is caused by bleach or alkaline ingestion?
Saponification of fats > liquifaction necrosis, high risk of perforation and stricture (more than acidic ingestion)
High dose methylpred can prevent stricture formation
Acid ingestion causes coagulation necrosis
Caustic ingestion and syptomatic should generally get an EGD
Don’t induce emesis - increases mucosal contact
Iron ingestion
Ferrous sulfate tablets are 20% elemental iron (60mg in a tablet)
Ferrous fumarate tabs are 33% elemental (107mg in a tablet)
> 40 mg/kg ingestion requires hospital evaluation; severe toxic effects >60 mg/kg
iron level <300 ok, moderate 500-100 ug/dL, >1000 ug/dL severe
Negative inotrope, inhibits thrombin, interferes with oxidative phosphorylation
Phase 1: N/V/D, intestinal bleeding
Phase 2: metabolic acidosis
Phase 3 (12-24hrs): worsening metabolic acidosis, shock, coagulopathy, hemodynamic instability
Phase 4: hepatotoxicity
Phase 5 (3-6 weeks): GI strictures, fistula formation
Rx: deferoxamine (red urine
Charcoal not effective
Not dialyzable
Marfan Syndrome
FBN1 gene mutation, autosomal dominant
CV: Aortic dilation, risk of dissection, mitral valve prolapse, TV prolapse; most common cause of mortality is Ao root disease leading to aneurysmal dilation, AI, and dissection
Treat with Bblocker and ARB
Signs of cyanide toxicity
shock, neurologic impairment, lactic acidosis and a low arterial-venous oxygen difference
