Hematology
Blood is a suspension of particles in an aqueous
colloidal solution containing electrolytes.
The Plasma acts as a transport medium.
Red Blood Cells (RBC) - function is to transport or exchange O2 and CO2. The rate of RBC production is under hormonal
control. Erythropoietin is
produced by the kidney and its production is apparently stimulated by
hypoxia. Erythropoietin acts to
increase the number of immature red blood cells precursors in the Bone Marrow. In the adult. hematopoiesis (formation and
maturation of blood cells) occurs in marrow of skull, pelvis, sternum,
vertebrae, ribs and the proximal epiphyses of the long bones. Marrow stem cells
are targets for the erythropoietin and initiate proliferation and maturation of
RBCs. This process is dependent upon
adequate amounts of B12, Folic Acid, Fe, Copper,
and ascorbic acid.
The breakdown and removal of the RBC involves Bilirubin metabolism.
Breakdown of hemoglobin to heme and globin. Globin is further broken down to enter the amino acid pool. Iron is
released and carried by binding proteins.
However, the heme is converted to biliverdin which is rapidly converted to "free" or
unconjugated bilirubin ( the pigment of bile) which is insoluble in plasma. It attaches to plasma proteins, and travels
to the liver where it is conjugated
with either glucuronic acid or glucuronic sulfate, and excreted as a
constituent of bile. It is responsible
for the dark color of stool. The bilirubin is converted to urobilinogen by
intestinal microorganisms. A portion of
the urobilinogen is reabsorbed and excreted in urine. Urobilinogen is
responsible for the yellow color of urine.
Direct bilirubin is conjugated.
Indirect bilirubin is unconjugated.
Anemia
Classified by morphology
1)
Normocytic
normochromic - decreased number of cells - Bone CA, renal
disease, hemorrhage.
2)
Macrocytic normochromic
- MCV is increased. - decrease in B12, or Folic acid.
3)
Microcytic
hypochromic - MCV decreased and MCHC
decreased - decreased iron.
Etiology of anemias
1)
Increased RBC loss -
bleeding - decreased number (Reticulocytes -
increased number indicate bone marrow is trying to keep up with loss by
releasing less mature form
2)
Decreased production or
defective cell (Cancer or Chronic Disease such as Aplastic Anemia)
Clinical
Picture in Anemia
|
Neuro |
H/A, vertigo, fatigue, irritability |
|
Resp |
Dyspnea, Increased Resp
rate, Bibasilar Rales |
|
CV |
Increased heart rate, palpitations,
increased pulse pressure, edema, congestion of neck veins |
|
GI |
Nausea, Anorexia,
constipation, diarrhea |
|
GU |
Menstrual disturbances,
proteinuria |
|
Mus/skel |
Pallor of mucous membranes, palpebral conjunctiva,
gums |
Sickle Cell
Anemia
It is a recessive autosomal hemoglobinopathy
associated with abnormality in hemoglobin structure. Exacerbation by infection
or dehydration. It occurs in the homozygous recessive state. There is Amino Acid substitution in the
formation of the hemoglobin (Hgb) molecule. (Valine replaces Glutamic acid)
This results in a change in shape of the Hgb molecule when is O2 decreased.
Cells elongate and become rigid.
This causes clumping of the cells, vascular occlusion, pain, and organ
infarctions. Recurrent episodes cause
hemolysis. The number of red cells is
decreased increased the demand. More
strain is placed on bone marrow.
It is possible that the defective gene has persisted
since the heterozygous sickle cell trait provides resistance to malaria.The
illness is not a problem in newborns since fetal hgb doesn't have Sickling
tendency. Experimental work being done
to extend the production of fetal hgb.
When there is an increase in the breakdown of RBCs, this can overload
the system, and cause - jaundice and an increase in urobilinogen and bilirubin
in the urine. The plasma carrier for unconjugated bilirubin is a binding
protein called haptoglobin. With severe hemolytic anemias, the amount of
circulating hemoglobin from destroyed RBCs may exceed the binding capacity of
the haptoglobins. When this
happens the hemoglobin is excreted in
the urine -hemoglobinuria. - May
indicate a positive blood, not RBCs, on urinalysis.
Treatment is with fluids, pain management, blood
transfusions.
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