ANAEMIA
Background: Anemia, like a fever, is a symptom of
disease that requires investigation to determine the
underlying etiology
Anemia is strictly defined as a decrease in red blood cell
(RBC) mass. In practice however; anemia is usually
discovered and quantified by measurement of the RBC
count, hemoglobin (Hb) concentration, and hematocrit
(Hct).In kenya defined as Hb below 10g/dl.WHO
definition Hb below 12g/dl.
Changes in plasma volume. eg, dehydration elevates these
values, and increased plasma volume in pregnancy can
diminish them without affecting the RBC mass.
Pathophysiology:
Erythroid precursors develop in bone marrow at rates
usually determined by the requirement for sufficient
circulating Hb to oxygenate tissues adequately. Erythroid
precursors differentiate sequentially from stem cells to
progenitor cells to erythroblasts to normoblasts in a
process requiring growth factors and cytokines. This
process of differentiation requires several days. Normally,
erythroid precursors are released into circulation as
reticulocytes.
-Reticulocytes remain in the circulation for approx. 1 day
before reticulin is excised by reticuloendothelial cells with
the delivery of the mature erythrocyte into circulation.
-The mature erythrocyte remains in circulation for about
120 days before being engulfed and destroyed by
phagocytic cells of the reticuloendothelial system.
-Because erythrocytes have no nucleus, they lack a Krebs
cycle and rely on glycolysis via the Embden-Meyerhof
and pentose pathways for energy
-Basically, only 3 causes of anemia exist:
1) Blood loss
2) Increased RBC destruction (hemolysis)
3) Decreased production of RBCs.
-Each of these 3 causes includes a number of etiologies
that require specific and appropriate therapy.
-Often, the etiology can be determined if the RBCs are
altered in either size or shape or if they contain certain
inclusion bodies. For example, Plasmodium falciparum
malaria is suggested by the presence of more than one ring
form in an RBC and produces pan-hemolysis of RBCs of
all ages.
Prevalance
Although geographic diseases, such as
 sickle cell anemia
 Thalassemia
 malaria
 Hookworm
 Chronic infections, are responsible for a portion
of the increase
- nutritional factors with iron deficiency and, to a lesser
extent, folic acid deficiency play major roles in the
increased prevalence of anemia.
Populations with little meat in the diet have a high
incidence of iron deficiency anemia because heme iron is
better absorbed from food than inorganic iron
History:
Primary symptoms result from tissue hypoxia and might
include the following:
- Fatigue, weakness, irritability
- Headache, Dizziness, especially postural
- Vertigo ,Tinnitus ,Syncope
- Dyspnea, especially with increased physical
activity (exercise intolerance)
- Chest pain, palpitations
- Difficulty sleeping or concentrating
- Thirst ,Anorexia, Decreased urine output/bowel
irregularity
Mortality/Morbidity:
-The morbidity and mortality of anemias vary greatly
depending on the etiology.
-Acute hemorrhage has variable mortality depending on
the site of bleeding (80% with aortic rupture, 30-50% with
bleeding esophageal varices, approximately 1% with
benign peptic ulcers).
-Anemia from gastrointestinal bleeding may be the first
evidence of an intestinal malignancy.
-Sickle cell disease may be associated with frequent
painful crises and a shortened lifespan, or patients with
sickle cell disease may remain relatively asymptomatic
with a nearly normal lifespan.
-Most patients with beta-0 homozygous thalassemia die
during the second or third decade of life unless they
undergo bone marrow transplantation.
-Hereditary spherocytosis either may present with a severe
hemolytic anemia or may be asymptomatic with
compensated hemolysis.
-Similarly, glucose-6-phosphate dehydrogenase (G-6-PD)
deficiency may manifest as chronic hemolytic anemia or
exist without anemia until the patient receives an oxidant
medication.
-The 2-year fatality rate for severe aplastic anemia is 70%
without bone marrow transplantation or a response to
immunosuppressive therapy.
-In addition, tolerance of anemia is proportional to the
anemia's rate of development. Symptoms and mortality
associated with rapidly developing anemia are more
profound than in slowly developing anemia.
Sex:
Overall, anemia is twice as prevalent in females as in
males.
-This difference is significantly greater during the
childbearing years due to pregnancies and menses.
-Approximately 65% of body iron is incorporated into
circulating Hb.
-Women have a markedly lower incidence of anemia from
X-linked anemias, such as G-6-PD deficiency and sex-
linked sideroblastic anemias.
Age:
-Severe genetically acquired anemias (eg sickle cell
disease, thalassemia, Fanconi syndrome) are more
commonly found in children because they do not survive
to adulthood.
-During the childbearing years, women are more likely to
become iron deficient.
-Neoplasia increases in prevalence with each decade of life
and can produce anemia from bleeding, from the
replacement of bone marrow with tumor, or from the
development of anemia associated with chronic disorders.
-Use of aspirin, nonsteroidal anti-inflammatory drugs
(NSAIDs), and Coumadin increases with age and can
produce gastrointestinal bleeding.
-Folate deficiencies may have a sore tongue, cheilosis, and
symptoms associated with steatorrhea
-Color, bulk, frequency, and odor of stools and whether the
feces float -malabsorption. In steatorrhea whether the toilet
needs to be flushed more than once to rid it of stool and
whether an oily substance is floating on the water surface
after the first flush.
-Fever because infections, neoplasm, and collagen
vascular disease can cause anemia.
-Occurrence of purpura, ecchymoses, and petechiae
suggest the occurrence of either thrombocytopenia or other
bleeding disorders; this may be an indication either that
more than one bone marrow lineage is involved or that
coagulopathy is a cause of the anemia because of bleeding