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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

sodium thiosulfate

A
  • used to treat CN poisoning
  • enhances normal metabolism of CN via rhodanase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly