Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

MSII Pharmacology > Unit 2 - Dyshemoglobinemia > Flashcards

Unit 2 - Dyshemoglobinemia Flashcards

1
Q

explain what hemoglobin is and its purpose

A

conjugated protein (64,500 D)

  • two pairs of polypeptide chains (4 heme molecules attached total)
  • for tissue perfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is heme’s structure?

A

Fe complexed at the center of a porphyrin ring

  • ferrous state (2+) of the Fe carries O2, CO
  • globin chain protects Fe moiety from inappropriate oxidation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

difference between carboxyhemoglobin, oxyhemoglobin, and methemoglobin?

A 
carboxy = CO
oxy = O2
met = O2, but heme Fe in +3 form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what are sources of CO?

A
  1. incomplete combustion of carbon containing material
    - gasses: methane VS coal VS gasoline
  2. internal production (minimal, only if ingest/inhale methyline Cl)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

explain the entry/exit of CO (pharmacokinetics)

A
  1. absorption/excretion
    - CO gains entry through respiration
    - methylene cloride is converted to CO in vivo only
  2. distribution
    - via hemoglobin, myoglobin, etc.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

explain CO pharmacology?

A

binds to Hb (200-250 x O2)

  • shifts O2 dissociation curve to the left
  • decrease in RBC 2,3-DPG
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

explain the mechanism of CO?

A
  1. mitochondrial cytochrome oxidase binding
    - increased with hypoxia and hypotension
  2. NO displaced from platelets from peroxynitrites
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

explain the mild, moderate, and severe effects of CO?

A

mild: HA, nausea/vomiting, dizziness
moderate: cheset pain, blurred vision, dyspnea on exertion, tachycardia, tachypnea, cognitive deficits, myonecrosis, ataxia
severe: seizures, coma, dysrhythmias, hypotension, MI/ischemia, skin bullae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are “late/chronic effects” of CO? when do they occur?

A
  • cognitive dysfunction
  • dementia, psychosis, amnesia
  • parkinsonism, paralysis chorea, cortical blindness, apraxia, agnosias, peripheral neuropathy, incontinence

these are preceded by a “lucent” period of 2-40 days, meaning it can seem like a patient got better, but then has these effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

what is the theory behind the mechanism of late effects of CO?

A

reperfusion injury

  • during recovery, WBC are attracted and adhere to brain microvasculature due to cyclooxygenase dysfunction (?)
  • WBCs release proteases, convert xanthine dehydrogenase to xanthine oxidase, promoting FR formation, leading to delayed lipid peroxidation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

at what ages are adults at greatest risk?

A

> 30 yo

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

how should one evaluate CO poisoning?

A

look for end-organ manifestations of toxicity

  • CNS, cardiac, perfusion
  • CO level is of relative importance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

what is pulse oximetry in CO poisoning?

A

falsely normal

-carboxyhemoglobin is read as oxyhemoglobin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what is arterial blood gas in CO poisoning?

A

co-oximeter will be appropriate

calculation will be falsely normal b/c pO2 is not affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

what is treatment for CO poisoning?

A
  1. ABC’s, O2 to shorten CO half-life (from 2-7 hr to 30-150 min)
  2. hyperbaric O2 under pressure (HBO)
    - shortens half-life to 4-86 minutes, increases O2
    - prevents lipid peroxidaiton in animal models
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

what are indications for HBO?

A
  1. loss of consciousness
    - syncope, coma, seizures
  2. GCS < 15 on presentation
  3. CO level > 10%
  4. MI, ventricular dysrhythmias
  5. neurologic signs 2-4 hours out
17
Q

what are some neuroanatomical side effects of CO?

A

bilateral low density areas of globus pallidus, putamen, and caudate nuclei
-rarely seen

18
Q

how does one “pick out” cyanide poisoning?

A
  1. lactate > 10 mmol/L

2. patient doesn’t respond to supportive care

19
Q

what are the forms of cyanide?

A
  1. gas (usually chemical warfare/industrial accidents)
  2. crystal (requires mucous membranes or po exposure)
    - jewelers, electroplating, other industries, house fires
20
Q

where does cyanide bind?

A

cytochrome A3 on ETC

-rapid onset of multi-system organ failure (no ATP)

21
Q

what is treatment for cyanide?

A
  1. ABCs, supportive care, ACLS, largely not successful
  2. cyanide antidote kit/package (sodium/amyl nitrite)
  3. hydroxocobalamin
    - binds with cyanide to make cyanocobalamin (B12)
  4. HBO +/0
22
Q

when and how should one treat with hydroxocobalamin?

A
  1. any smoke-inhalation victim that is NOT improving despite supportive care including O2
  2. any intentional cyanide exposure
    - 5 g dose, can be repeated x1
    - give concurrently with sodium thiosulfate
    - may cause increased BP
23
Q

what is the mechanism of sodium/amyl nitrite in cyanide poisoning?

A

sodium/amyl nitrite makes met-Hb, so the CN (and H2S, if any) bind to met-Hb instead of cytochromes

  • these cyanomet-Hb or SHmet-Hb are then excreted
  • -cyanometHb needs thiosulfate to be excreted
24
Q

define what methemoglobin is?

A

heme Fe oxidized to ferric (+3) form

-normal amounts 1-3%

25
Q

what is the mechanism of methemoglobinemia?

A
  1. rate of heme oxidation increases
  2. reduction of heme is limited
  3. structural abnormalities of heme
26
Q

what are causes of methemoglobinemia?

A
  1. congenital
  2. infantile disposition
  3. external causes
27
Q

how does methemoglobin exert its toxicity?

A
  1. incapacitates O2 transport

2. shifts O2 dissociation curve to left

28
Q 
what are symptoms of methemoglobin at:
0-10%
10-20%
20-50%
>50%
>70%
A 
0-10%: asymptomatic
10-20% apparent cyanosis
20-50% dizziness, fatigue, HA, exertional dyspnea
>50% lethargy/stupor
>70% coma/death
29
Q

what is pulse oximetry in methemoglobin?

A

falsely and aberrantly lowered

-measured as both oxy and deoxyhemoglobin, will fall rapidly into high 80s

30
Q

what is arterial blood gas in methemoglobin?

A
  1. co-oximeter will be appropriate

2. calculation will be falsely normal b/c pO2 is not affected

31
Q

what are drugs that give methemoglobinemia?

A
  1. nitrites (major)
  2. nitrates in infants (major)
  3. sulfonamides
  4. phenazopyridine
  5. dapsone
  6. local anesthetics

these cause oxidant stress

32
Q

what are toxins that give methemoglobinemia?

A
  1. nitrites (major)
  2. nitrates in infants (major)
  3. aniline dye
  4. potassium chlorate
  5. diarrheal illness in infants (make nitrites; major)
33
Q

what is treatment for methemoglobinemia?

A
  1. ABC’s
  2. decontamination
  3. methylene blue (tetramethyl tionine chloride; specific antidote)
    - minor antidotes and in non-responders to methylene blue
    - -N-acetylcysteine
    - -exchange transfusion
    - -hyperbaric O2
34
Q

explain the mechanism of methylene blue

A

used in treatment of methemoglobinemia

  • cofactor of NADPH reductase
  • gains electron, then donates directly to methemoglobin
  • methemoglobin reduction to (Fe 2+)
35
Q

when is methylene blue treatment indicated?

A

if methemoglobin level >20-30%, or symptoms

36
Q

what are cautions in using methylene blue?

A
  1. hemolytic anemia from weak oxidizing capability
  2. painful at injection site (dysuria)
  3. higher doses can cause dyspnea, restlessness, tremor, precordial pain, apprehension
37
Q

what are possible reasons for methylene blue non-responders?

A
  1. hemoglobin M disease
  2. G6PD deficiency - lack generation of NADPH dependent methemoglobin reducase
  3. CL salts inactivating G6PD
  4. sulfhemoglobinemia
    - more benign, levels up to 10 g/dL don’t cause cyanosis
  5. wrong diagnosis
38
Q

what is sulfhemoglobinemia?

A

symptoms similar to methemoglobinemia

  • methemoglobin levels will be elevated
  • laboratory can “tease out” by adding cyanide to blood
  • treatment is supportive only
39
Q

what are causes of sulfhemoglibnemia?

A

acetanilid, phenacitin, nitrites, trinitrotoluene, sulfur

MSII Pharmacology (43 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions