Dyshemoglobinemias Flashcards
Name four places CO binds in the body.
- binds Hgb - shifts oxygen dissociation curve, decreases 2,3-BPG
- binds myoglobin - myocardial tox.
- binds mitochondrial cytochrome oxidase - inhibits cellular respiration
- displaces NO from platelets - forms peroxynitrites
Which symptoms of acute CO effects are mild, moderate, severe?
chest pain, SOB on exertion, HA, coma, seizures, dysrhythmias, N/V, blurred vision, tachycardia, tachypnea, MI, ischemia, hypotension, dizziness, nyonecrosis, ataxia, cognitive deficits, skin bullae
mild - HA, N/V, dizziness
moderate - chest pain, blurred vision, SOB on exertion, tachycardia, tachypnea, cognitive deficits, myonecrosis, ataxia
severe - seizures, coma, dysrhythmias, hypotension, MI, ischemia, skin bullae
What are the late/chronic effects of CO?
cognitive dysfunction, dementia, psychosis, amnesia, parkinsonism, apraxia, peripheral neuropathy, incontinence
How long after CO exposure will late effects manifest?
2-40 days later
What is believed to be the theory behind late CO effects?
reperfusion injury - delayed lipid peroxidation
Who is at greatest risk for late CO effects? Adult or child? Associated acute symptoms?
adult over 30 who had a loss of consciousness
How will pulse ox read in CO poisoning?
falsely normal - carboxyHgb read as oxyHgb
How will an ABG read in CO poisoning?
co-oximeter - appropriate
calculation - falsely normal because pO2 normal
What is the appropriate treatment for CO poisoning?
ABCs (airway, breathing, circulations)
oxygen - shortens CO T1/2
consider hyperbaric O2 - shortens CO T1/2 further; prevents lipid peroxidation and neurologic sequelae
When are people exposed to cyanide?
jewelers, electroplating (mucus membrane or po exposure)
mostly - house fires
How does CN cause toxicity?
binds cytochrome A3 in ETC - no ATP!!
How does a CN patient differ from CO poisoning?
won’t be responding to supportive care, ABCs
lactate >10 associated with CN poisoning
What are the two components of the antidote for CN?
sodium thiosulfate and hydroxocobalamin (Vit B12a)
What is the MOA of sodium thiosulfate in CN poisoning?
enhances normal metabolism of CN through rhodenase enzyme
What is the MOA of hydroxocobalamin in CN poisoning?
binds with cyanide to make cyanocobalamin (Vit B12)
When should CN antidote be given?
any smoke inhalation victim not responding to supportive care and O2 therapy;
and any intentional CN exposure
What is methemoglobin?
heme iron is oxidized to ferric (Fe+3) form
What four ways is methemoglobin normally reduced back to normal? Which one can be exploited for therapeutic use?
- NADH met-Hb Reductase
- Ascorbate
- Glutathione
- NADPH met-Hb Reductase - can be increased with methylene blue
What drugs and toxins lead to methemoglobin production?
Drugs - nitrites, nitrates in infants, sulfonamides, phenazopyridine, dapsone, local anesthetics
Toxins - nitrites, nitrates in infants, aniline dye, potassium chlorate, diarrheal illness in infants (makes nitrites)
How does methemoglobin cause toxicity?
shifts O2 dissociation curve left - less willing to give up O2 in tissues
Match the percent met-Hb to the symptoms:
0-10, 10-20, 20-50, >50, >70
apparent cyanosis; coma and death; dizziness, fatigue, HA, exertional SOB; asymptomatic; lethargy/stupor
0-10 asymptomatic 10-20 apparent cyanosis 20-50 dizziness, fatigue, HA, exertional SOB >50 lethargy/stupor >70 coma and death
What is the antidote for methemoglobin?
methylene blue
What’s the MOA for methylene blue in treating methemoglobinemia?
cofactor for NADPH reductase; gains electrons and donates them to methemoglobin
What is the indication for using methylene blue?
met-Hb >20-30% or symptoms
