Dyshemoglobinemias Flashcards Preview

Pharm Unit 2 MJC > Dyshemoglobinemias > Flashcards

Flashcards in Dyshemoglobinemias Deck (26)
1

How is CO produced in the environment?

Incomplete combustion of carbon containing material

2

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

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

3

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

Methylene chloride exposure

4

name 4 physiological effects of CO in the body

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

5

What are mild acute CO symptoms?

HA, N/V, dizziness

6

What are moderate acute CO symptoms?

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

7

What are severe acute CO symptoms?

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

8

What are late/chronic CO symptoms?

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

9

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

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

10

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

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

11

What will O2 sat tests show with CO poisoning?

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

12

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

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

13

What is the standard pressure for HBO in CO treatment?

2.8 ATM

14

What are indications for HBO treatment is CO exposure?

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

15

What brain findings are seen in CO poisoning?

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

16

How does CN fuck your shit up?

Binds to Cytochrome A3 on ETC

17

What are 3 treatments fort CN poisoning?

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

How can you recognize CN poisoning?

Lactate >10mM
pt doesnt respond to supportive care. if CO they will get better with O2, with CN they will not.

19

What is the major cause of formationof methemoglobin?

nitrates

20

How does methemoglobin affect binding curve?

left shift

21

What do O2 sat tests show with methemoglobin formation?

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

22

What is the specific antidote to methemoglobin?

methylene blue

23

How does methylene blue work?

Cofactor for methemoglobin reductase, requires NADPH thus functioning G6PD

24

When is methylene blue indicated?

methemoglobin >20-30%

25

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

hemoglobin M disease
G6PD deficiency
CL salts inactivating G6PD
sulfhemoglobinemia
wrong diagnosis

26

How is sulfhemoglobinemia treated?

Supportive care only, little toxicity.