2015 PEM Boards: Napo Flashcards
Cholinergic poisoning
“SLUDGE” (salivation, lacrimation, urination, diarrhea, gastric emesis)
DUMBBBBELS: Diarrhea, Urination, Miosis, Bradycardia, Bronchorrhea, Bronchospasm, Bradypnea, Emesis, Lacrimation, and Sialorrhea (drooling) are common physical findings.
-due to irreversible inhibition of acetylcholinesterase and excess acetylcholine at the neuromuscular junction
-resulting overstimulation of cholinergic receptors
-Organophosphate exposure
-mainstay of stabilization and treatment for cholinergic poisonings is the administration of atropine
-An easy way to remember which antidote is needed is: if wet (bronchorrhea, diaphoresis, sialorrhea), give atropine, which helps to dry secretions; if weak (fasciculations, weakness, paralysis) give pralidoxime, which will help protect nicotinic skeletal muscle receptors.
Tetanus Tx for un immunized child
TIG +
Tdap, Td, or TT if >7yo
DTaP if 6weeks-6years
Atropine
competes with acetylcholine at the cholinergic receptors
-classified as an anticholinergic drug = antimuscarinic
-competitive antagonist for the muscarinic acetylcholine receptor
-decreases the muscarinic cholinergic effects
-Atropine is given as a treatment for SLUDGE
Pralidoxime aka “2-PAM” = acetylcholinesterase reactivating agent → treats SLUDGE
-“hot as a hare, blind as a bat, dry as a bone, red as a beet, and mad as a hatter”
Physostigmine
agent that may be used in significantly symptomatic anticholinergic (atropine) poisonings
Jimson weed
causes anti-cholinergic effects
causes atropine toxidrome
Asystole or PEA (PALS)
CPR
Epi 0.01 mg/kg (0.1 mL/kg of 1:10,000)
Bradycardia (PALS)
CPR if HR <60
Epi 0.01 mg/kg
Atropine 0.02 mg/kg
Pace em
Tachycardia (PALS)
Unstable = synchronized cardioversion 0.5-1J/kg then 2J/kg
Adenosine 0.1 mg/kg then 0.2mg/kg
Amiodarone 5mg/kg
Malignant hyperthermia
Tx?
Cause?
Treat malignant hyperthermia with dantrolene
sux is usually the offending agent
VFib/Pulseless VT
Defibrillate @ 2J/kg then 4J/kg
then try epi 0.01mg/kg
NMS
Tx?
Cause?
Treat neuroleptic malignant syndrome with bromocriptine (antpsychotics are offenders)
serum osmolality formula
serum osmolality = (serum Na x 2) + (serum glucose/18) + (BUN/2.8)
-elevated osmolar gap= > 10
Metabolic abnormality of Pyloric Stenosis
pyloric stenosis = hypokalemic, hypochloremic metabolic alkalosis due to loss of gastric acid (which contains hydrochloric acid and potassium)
winter’s formula?
P CO2 = (1.5xHCO3)+8+/-2
-used to evaluate respiratory compensation when analyzing acid-base disorders and a metabolic acidosis is present
Fatty Acid Oxidation Disorder
- Hypoglycemia with absence of ketones in urine indicates a problem with mitochondrial oxidation of fatty acids
- MCAD is the most common form
- have low plasma carnitine levels on a acylcarnitine profiles
- high levels of urinary organic acids
- Test with Plasma acylcarnitine profile
- Treat with avoidance of fasting and perhaps carnitine supplementation.
- acidosis with no ketones
Organic acidemia
- disorder involving the metabolic pathway in degradation of the organic amino acids valine, leucine, and isoleucine
- Results in buildup of intermediate organic acids causing profoundly high anion gap metabolic acidosis.
- Presents with lethargy, poor feeding, and convulsions.
- Elevated ammonia levels occur as a result of inhibition of the urea cycle enzymes from the Organic acidemia.
- elevated ammonia levels but not as high as primary urea cycle disorders.
- Also have thrombocytopenia.
- acidosis +ketones
- Maple syrup urine disease is an example
Primary urea cycle disorders
- eg. OTC deficiency
- present with extremely high ammonia levels and encephalopathy with ataxia
- presents during periods of stress or from exposure to a high-protein diet.
- Not associated with metabolic acidosis and will have normal lactate levels, differentiating this from organic acidemia.
- BUN is also typically very low.
- ARGININE ADMINISTRATION IS BENEFICIAL IN THE TREATMENT OF ELEVATED AMMONIA DUE TO UREA CYCLE DISORDERS
- Sodium benzoate and phenylacetate are other agents that can be used for elevated ammonia levels from any cause; they can be added to the regimen to facilitate excretion.
- If that doesn’t work → hemodialysis. Think about it when they say “clumsy” or encephalopathy.
glutaric aciduria Type 1 (GA1)
- inborn error of metabolism most consistent with the presentation of macrocephaly, chronic subdural effusion with an acute decompensation
- caused by a deficiency of glutaryl-CoA dehydrogenase, required in the breakdown of hydroxylysine, lysine, and tryptophan.
- Unlike other organic acidurias, GA1 rarely manifests in the newborn period.
- The diagnosis is usually made during crises, such as intercurrent illnesses, in which patients may present with metabolic acidosis, hyperammonemia and encephalopathy. -Macrocephaly is a common finding in GA1, with 30% associated with subdural effusions. Minor trauma will often lead to acute intracranial bleeding.
- Urine reducing substance and uric acid are expected to be normal.
- Test with urine organic acids.
typical dextrose infusion rate
6-8mg/kg/min
Galactosemia
- excretion of reducing substances in urine due to galactose-1-phosphate uridyltransferase deficiency.
- Will have elevated direct bilirubin.
- High association with cataract formation.
- High association with E. coli sepsis.
Glycogen storage disorder
–presents with lactic acidosis, hepatomegaly, and hypoglycemia.
-Normal ammonia level differentiates this from organic acidemias
Charcot’s triad
= acute ascending cholangitis
= is RUQ pain, jaundice and high fever
-occurs when a gallstone blocks the common bile duct (choledolithiasis) and an infection occurs
Intussusception in patient with HSP
- the most common type is ileal – ileal.
- Because of this, CT scan has better sensitivity for small bowel intussusception, rather than ultrasound
the most lethal of malarias is?
Plasmodium faciparum