dyshemoglobinemias Flashcards
1
Q
CO (mechanism, O2 sats, tx)
A
- gains entry/exit through respiration; no metabolism
- binds Hb and myoglobin with greater affinity than O2 –> hypoxemia
- binds mitochondrial cytochrome oxidase –> inhibits cellular respiration
- displaces NO from platelets –> peroxynitrites –> free radical damage
- late/chronic nuerologic effects due to reperfusion injury and lipid peroxidation
- pulse ox falsely normal (can’t distinguish between oxy Hb and carboxy Hb)
- arterial blood gas falsely normal bc pO2 isn’t affected
- tx: hyperbaric O2 prevents lipid peroxidation and neurologic sequelae
- HBO indications = loss of consciousness, CO level >10%, GCS <15, MI, ventricular dysrhythmias
2
Q
CN poisoning (mechanism, tx)
A
- identified by lactate levels (> 10 mmol/L) or PT unresponsive to O2 tx
- binds to cytochrome A3 on electron transport chain
- tx: nitrites, sodium thiosulfate, hydroxycobalamin (vit B12a)
**note: O2 tx doesn’t help CN poisoning like it does for CO poisoning!
3
Q
sodium nitrite
A
- used to treat CN poisoning
- CN likes Fe3+
- turn Hb into Met-Hb –> CN moves from Fe3+ on cytochromes to those in RBCS (but then you need to treat Met-Hb with methylene blue)
- dangerous in concurrent CO poisoning
4
Q
sodium thiosulfate
A
- used to treat CN poisoning
- enhances normal metabolism of CN via rhodanase
5
Q
hydroxycobalamin
A
- used to treat CN poisoning
- binds with CN to make cyanocobalamin
- give concurrently with sodium thiosulfate
- indications: any smoke inhalation victim that is NOT improving despite supportive care and O2, any intentional CN exposure
6
Q
Methemoglobinemia (mechanism, causes, O2 sats, tx)
A
- heme iron oxidized to Fe3+ form
- shifts O2 disassociation curve to the left –> less O2 unloading to tissues
- causes: congenital or acquired via drugs/toxins(nitrites, nitrates in infants)
- O2 sats: pulse ox in mid 80’s (falsely low because it can’t read MetHb), arterial blood gas falsely normal bc pO2 isnt affected
- tx: methylene blue
7
Q
Methylene blue
A
- cofactor of NADPH reducatse, gains electron and donates directly to reduce MetHb to Hb
- indications: MetHb >20-30% or symptoms
- adverse side effects: hemolytic anemia because of weak oxidizing capabilities –> RBC oxidative damage –> hemolysis
- non-responders: Hb M disease, G6PD deficiency (lack generation of NADPH-dependent MetHb reductase), sulfhemoglobinemia, wrong dx