Dyshemoglobinemias Flashcards

1
Q

How is CO produced in the environment?

A

Incomplete combustion of carbon containing material

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2
Q

What is the route of entry for CO into the body? What consequences does this have?

A

CO gains entry and exit through direct respiration which means increased respiratory rate equals increased dose

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3
Q

What is the only situation when CO will rise after removal from the source?

A

Methylene chloride exposure

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4
Q

name 4 physiological effects of CO in the body

A

1 Binds to hemoglobin (200-250x affinity of O2) shifts O2 curve to the left, also decreases BPG which further shifts to the left
2 Binds to myoglobulin causing direct cardiotoxicity
3 binds to mitochondrial cytochrome oxidase and inhibits respiration
4 displaces NO from platelets and forms peroxynitrites resulting in free radical mediated damage though to produce CNS symptoms

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5
Q

What are mild acute CO symptoms?

A

HA, N/V, dizziness

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6
Q

What are moderate acute CO symptoms?

A

chest pain, blurred vission, dyspnea, tachycardia, tachypnea, cognitive deficits, myonecrosis, ataxia

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7
Q

What are severe acute CO symptoms?

A

Seizures, coma, dysrythmias, hypotension, MI/ischemia, skin bullae

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8
Q

What are late/chronic CO symptoms?

A

Cognitive dysfunction
dementia, psychosis, amnesia
Parkinsonianism, paralysis chorea, cortical blindness

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9
Q

What is thought to be the mechanism of late/chronic symptoms?

A

delayed lipid peroxidation caused by reperfusion when WBCs adhere to brain microvasculature.

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10
Q

What is the major indicator for late/chronic effects of CO poisoning?

A

Loss of consciousness at the scene (CO level doesnt matter at this point)

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11
Q

What will O2 sat tests show with CO poisoning?

A

Pulse Ox - falsely normal bc carboxyheme shows same as oxyheme
co-ox appropriate
calculation falsely normal bc pO2 is not affected

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12
Q

What is the main treatment from CO poisoning and how does it help?

A

Hyperbaric oxygen. Shortens half life of CO and possibly prevent lipid peroxidation.

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13
Q

What is the standard pressure for HBO in CO treatment?

A

2.8 ATM

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14
Q

What are indications for HBO treatment is CO exposure?

A

loss of consciousness, GCS < 15, CO >10%, myocardial ischemia, ventricular dysrhythmias, neurologic signs

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15
Q

What brain findings are seen in CO poisoning?

A

bilateral low density in areas of globus pallidus, putamen, and caudate nuclei

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16
Q

How does CN fuck your shit up?

A

Binds to Cytochrome A3 on ETC

17
Q

What are 3 treatments fort CN poisoning?

A

1 Nitrites for methemoglobinemia- attract CN away from Fe 3+ on CA3 to Fe3+ on metheme. [CANNOT DO THIS WITH CONCURRENT CO POISONING]
2 Sodium thiosulfate - enhances natural metabolism
3 hydroxycobalamin binds with CN to make cyanocobalamin

18
Q

How can you recognize CN poisoning?

A

Lactate >10mM

pt doesnt respond to supportive care. if CO they will get better with O2, with CN they will not.

19
Q

What is the major cause of formationof methemoglobin?

A

nitrates

20
Q

How does methemoglobin affect binding curve?

A

left shift

21
Q

What do O2 sat tests show with methemoglobin formation?

A

pulse ox- falsely and aberrantly lowered into high 80s
co-ox appropriate
calculation- falsely normal because pO2 not affected.

22
Q

What is the specific antidote to methemoglobin?

A

methylene blue

23
Q

How does methylene blue work?

A

Cofactor for methemoglobin reductase, requires NADPH thus functioning G6PD

24
Q

When is methylene blue indicated?

A

methemoglobin >20-30%

25
Q

What are some reasons why someone wouldnt responds to methylene blue treatment?

A
hemoglobin M disease
G6PD deficiency
CL salts inactivating G6PD
sulfhemoglobinemia
wrong diagnosis
26
Q

How is sulfhemoglobinemia treated?

A

Supportive care only, little toxicity.