Hemoglobin Derivatives

Almira Coleen · 28問 · 1年前

通報

問題一覧

Formed due to the high affinity of Hb for carbon monoxide (CO) than for O2 (240x).

Carboxyhemoglobin

The manifestations associated with CO poisoning or increase in carboxyhemoglobin are related to tissue?

 Hypoxia or Cyanosis

It is present in blood in very concentration attributed to breakdown of Hb, heme to bilirubin. When heme is converted to bilirubin, CO is liberated and that accounts for 2% of COHb in the blood under normal conditions

Endogenous Production

Found in the blood of tobacco smokers in concentrations of 1 to 15% (5% per pack of cigarettes).

Carboxyhemoglobin

Smokers may have a higher hematocrit and polycythemia to compensate for hypoxia.

True

In response to tissue hypoxia, the _________ produces more RBCs to compensate by increasing oxygen delivery.

Bone Marrow

In response to tissue hypoxia, the bone marrow produces more RBCs to compensate by increasing oxygen delivery.  Symptoms of headache, nausea, dizziness, and muscular weakness will occur at levels of 20 to 30%.  40%: loss of consciousness (due to severe hypoxia), coma, seizure, cardiac arrhythmia and rapid death.  It gives blood a __________, which is sometimes imparted to the skin of victims.

Cherry Red Color

What type of poisoning which is a fetal condition because it is known as a “silent killer,” being an odorless and colorless gas.

Carbon Monoxide

Formed by the reversible oxidation of heme iron to the ferric state (Fe3+).

Ferrihemoglobin

Hemoglobin bound to ferric iron (Hgb + Fe3+). Ferrous iron is oxidized to the ferric state resulting in the inability to combine reversibly with O2.

Ferrihemoglobin

Small amount (1% of total Hb) is normally formed in our? But is reduced by enzyme systems within the erythrocyte.

Blood

Increased amount is termed? Causes chocolate brown discoloration of blood that can lead to cyanosis, and functional anemia

Methemoglobinemia

When that enzyme is lacking, the individual is suffering from ↓ propensity for reduction of Hemiglobin (Hi) back to Hb

NADH methemoglobin reductase enzyme system

Asymptomatic

<25% of Methemoglobin

Cyanosis/Hypoxia

<30% of Methemoglobin

Coma/Death

>50% of Methemoglobin

Too much carboxy & methemoglobin can lead to fetal condition because hemoglobin will not be able to transport oxygen that can lead to cyanosis/hypoxia and death.

True

Acquired: Occurs in normal individuals after exposure to an exogenous oxidant, such as nitrites, primaquine, dapsone, or benzocaine

Toxic methemoglobinemia

If the level of methemoglobin increases to 30% or more of total hemoglobin? it is administered.

intravenous methylene blue

Inherited: The methemoglobin produced is called? It is not depleted by methylene blue Not treatable with methylene blue

M hemoglobin or Hb M

Results in the incorporation of sulfur into the heme rings of Hb producing a green hemochrome (incorporation of sulfur in Hi first then to SHb)

Sulfhemoglobin (SHB)

Methemoglobin first then to Sulfhemoglobin formation is irreversible; further oxidation results in the denaturation and precipitation of Hb as Heinz bodies

True

Due to abnormal substitution of amino acid.

Abnormal Hemoglobin

Due to amino acid substitution specifically the substitution of Valine for a glutamic acid at the 6th position of beta chain.  6th position is crucial to the structure of hemoglobin.

HB s (α2β26val)

- Under conditions of reduced O2 concentration. - Confined to the black race

Sickle of RBC (Sickle cells)

Sickle cell anemia

Homozygous state

Sickle cell trait

Heterozygous state

Substitution of Lysine for a glutamic acid at the 6th position of beta chain.  Target cells are commonly seen and rarely, precipitated Hb C crystals.  Often seen in association with HbS and causes mild hemolytic anemia (caused by condensation of Hb forming crystals that may lead to eventual rupture of RBC cells).

Hb c (α2β26Lys)

121st position Glycine.  Composed of many variants, the most common being Hb D Los Angeles (Punjab).

Hb D (α2β2121Gln)

Less clinically significant than Hb S.  • Not associated with significant clinical abnormality except for a few target cells among homozygotes.

Hb D

Los Angeles (Punjab)

Hb D

Substitution of Lysine for Asparagine (Asn) at the 68th position of alpha chain.  Most common α-chain variant in black people.  The homozygosity and heterozygosity exhibit no clinical or hematologic abnormalities.

Hemoglobin G philadelphia (α268Lysβ2)

Substitution of Lysine for a glutamic acid at the 26th position of beta chain.  2nd most common hemoglobinopathy in US other than S and C.  Most common in the Philippines and Southeast Asia.

HB E (α2β226Lys)

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