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Abnormal Hemoglobin Pigments/ Methemoglobin

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  • Abnormal Hemoglobin Pigments/ Methemoglobin

    [ :sm199: COLOR="magenta"]
    hello all
    this is very important topic in hematology and u must know :sm200: it and understand it
    i hope it's simple and useful for all :sm199:
    [/COLOR]



    Abnormal Hemoglobin Pigments/ Methemoglobin




    ***HEMOGLOBIN****

    In its role as a respiratory pigment, hemoglobin combines
    with oxygen to form oxyhemoglobin.
    The oxygenation of hemoglobin
    in the lungs is an extremely efficient process, and at the
    partial pressure of oxygen in alveolar air (100 mm Hg),
    almost
    all hemoglobin is converted to oxyhemoglobin.

    The diffusion of
    oxygen through the red cell membrane is rapid, and the total
    surface of erythrocytes exposed to this exchange in the lungs is
    about 80 square meters each second.

    Oxygen is given up in the
    tissues, and oxyhemoglobin becomes reduced hemoglobin, effecting
    a release of base that binds incoming carbon dioxide.

    The efficiency of this mechanism is reduced when an abnormal
    hemoglobin with altered oxygen affinity is present or when
    hemoglobin is converted to abnormal hemoglobin pigments that are
    not capable of transporting oxygen
    .


    The ones of clinical
    importance are

    carboxyhemoglobin,
    methemoglobin and
    sulfhemoglobin.


    A high concentration of any one may produce
    hypoxia or cyanosis.


    Hypoxia is proportional to the diminished
    concentration of hemoglobin, and cyanosis is proportional to the
    concentration of abnormal hemoglobin pigment.


    ***Carboxyhemoglobin***

    Carboxyhemoglobin is formed when hemoglobin is exposed to
    carbon monoxide.
    The affinity of hemoglobin for carbon monoxide
    is 218 times greater than for oxygen at 37 degrees C and is not
    affected if helium is substituted for nitrogen as the inert gas.
    If toxic levels of carbon monoxide are present in the air and
    carboxyhemoglobin is formed, the amount of oxyhemoglobin is
    decreased. Since carboxyhemoglobin is not capable of
    transporting oxygen, hypoxia results. Carboxyhemoglobin produces
    a cherry red color of the blood, both the patient's skin and the
    blood obtained by venipuncture showing this typical color.

    ***Methemoglobin***

    Methemoglobin differs from oxyhemoglobin in that it contains
    ferric rather than ferrous iron,
    the O2 being replaced by OH.
    Methemoglobin is therefore oxidized hemoglobin, or
    ferrihemoglobin. Because it is unable to act as an oxygen
    carrier, methemoglobin in sufficiently high concentration causes
    hypoxia and cyanosis. The symptoms of hypoxia are usually not so
    severe as in carboxyhemoglobinemia, nor is methemoglobinemia as
    dangerous. Methemoglobin is present in small amounts in normal
    blood, 0.3% to 3.1% of the total blood pigment.
    Methemoglobinemia is classified into two major groups,
    hereditary and acquired


    Hereditary methemoglobinemia: Hb M variants.

    The hemoglobins designated M are variants that, because of a
    substitution of an amino acid in either the alpha or the
    beta chain, have altered heme globin binding. They account for
    one of the forms of methemoglobinemia and are only rarely
    associated with diminished erythrocyte survival.
    In four of the variants, the substitution involves the
    proximal or distal histidines of the globin polypeptide chains.
    The substitution of tyrosine for these histidines brings about
    the stabilization of the heme iron in the ferric state. In this
    state hemoglobin is unable to bind oxygen reversibly. When the
    heme iron is in the ferric form, methemoglobin, sometimes also
    called hemiglobin, is the respiratory pigment that is formed.
    Clinically, affected persons show bluish slate gray or brown
    cyanosis of the skin, lips, and nail beds. Transmission is
    autosomal dominant. Affected persons are heterozygous and the
    homozygous state is probably lethal in utero. The cyanosis is
    present from birth in the a chain variants, whereas in the a
    chain variants it may not appear until some months later.
    Affected individuals lead normal lives, the only danger being
    that the etiology of the cyanosis may be misdiagnosed. There is
    no hemolytic disease.


    Hereditary methemoglobinemia:

    Deficient reducing systems

    Methemoglobinemia caused by a deficiency of NADH methemoglobin
    reductase within the red cells is an inherited disease
    transmitted as an autosomal recessive trait.

    Hereditary methemoglobinemia:
    Excessive oxidative activity
    Acquired methemoglobinemia.


    Most cases of methemoglobinemia fall into the acquired
    group.

    The most common cause of acquired methemoglobinemia is the
    toxic effect of drugs such as aniline dyes, aniline derivatives,
    sulfonamides, nitrates and nitrites, acetanilid, acetophenetidin,
    and chlorates.
    The exposure to these agents is sometimes not
    obvious. For example, methemoglobinemia has been described as
    the result of eating Polish sausage, which is rich in nitrite and
    nitrate.
    Methemoglobinemia presents a special problem in pediatric
    practice.
    Because Hb F is more readily converted to
    methemoglobin than Hb A, infants are susceptible to
    methemoglobinemia when exposed to toxic agents in doses that
    would not affect an older child or an adult.
    Furthermore, the
    erythrocytes of newborn infants are relatively deficient in
    methemoglobin reducing enzymes.
    An example is the
    methemoglobinemia of infants caused by the ingestion of well
    water having a high nitrate or nitrite content.
    Water having a
    high nitrate is content surface contaminants is a common
    offender.
    When such water is used to prepare an infant's
    formula, the nitrate is converted to nitrite in the bowel and
    causes methemoglobinemia.

    The methemoglobin concentration in hereditary
    methemoglobinemia seldom exceeds 40%, but the concentration in
    acquired methemoglobin emia may be very high if there has been
    severe exposure to the toxic agent.
    Cyanosis is manifest at a
    concentration of about 15%. Symptoms of hypoxia occur at a
    concentration of 60% and higher.
    If there are symptoms of
    hypoxia, acquired methemoglobinemia should be treated with
    methylene blue.

    ***Sulfhemoglobin***

    Sulfhemoglobin is a stable compound of hemoglobin and
    sulfur. Sulfhemoglobin, once formed, is so stable that it
    disappears from the circulation only after the erythrocytes
    containing it are naturally destroyed.
    The normal concentration of sulfhemoglobin in blood is 0% to
    2.2% of total hemoglobin.

    *** Methemalbumin***

    Methemalbumin consists of hematin bound to serum albumin.
    It has been found in various hemolytic diseases, hemoglobinuria,
    liver disease, and pernicious anemia. Methemalbumin is formed
    after the haptoglobin binding capacity for free hemoglobin is
    exceeded. This may occur with a type of hemolysis known as
    "intravascular" where there is destruction of red cells within
    the vessels, rather than phagocytic destruction by the RE system.
    With intravascular hemolysis, free hemoglobin released from
    the red cells binds immediately with a plasma transport protein
    known as haptoglobin. Only after the available haptoglobin has
    been eliminated does the free hemoglobin bind to albumin.


    if u like it wish to me something nice plez
    التعديل الأخير تم بواسطة soma; الساعة 01-04-2008, 05:54 PM.
    ان عشت فعش حرا أومت كالاشجار وقوفا


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  • #2
    thanx you so much soma
    مهندسة جينات المستقبل:sm182:

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    • #3
      شكراsoma معلومات جميلة جدا

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      • #4
        بسم الله الرحمن الرحيم ---موضوع حلو ومفيد--- بس كان يضوجنا اثناء الدراسه ----- التنفس احدى العمليات الحيويه التي يقوم بها جسم الانسان للاستمرار في الحياة حيث يقوم الانسان البالغ ب25 الف :sm170: عمليه شهيق وزفير يسحب خلالها 180 متر مكعب من الهواء بضمنها 6.5 متر مكعب من الاوكسجين يتحد مع الصبغه المسماة الهيموكلوبين ليكون الاوكسي هيمو كلوبين-------سبحان الله:sm196:
        .http://www.arb-up.com/files/arb-up-2008-6/Znn17028.jpg

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        • #5
          الله يعطيك العافيه على هذه المعلومات الجميله

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          • #6
            thank u all for ur nice passing

            my best regard to all
            ان عشت فعش حرا أومت كالاشجار وقوفا


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