ANEMIA

Prescilla Diana L. Montances

ANEMIA
Anemia - hemoglobin level <130 g/L (13
g/dL) in men and <120 g/L (12 g/dL) in
women.

The functional classification of anemia has
three major categories.
1) marrow production defects
(hypoproliferation)
2) red cell maturation defects
(ineffective erythropoiesis)
3) decreased red cell survival (blood
loss/hemolysis).
Hypoproliferative Anemias
most common anemias, 70%
IRON-DEFICIENCY ANEMIA
Anemia of Acute and Chronic
Inflammation/Infection-most common
Anemia of Chronic Kidney Disease
(CKD)
Anemia in Hypometabolic States
ANEMIA IN LIVER DISEASE
IRON-DEFICIENCY ANEMIA
Stages of Iron Deficiency
Negative Iron Balance
demands for iron exceed the body's ability to
absorb iron from the diet (ex. blood loss,
pregnancy adolescent, or inadequate dietary
iron intake)
Iron-Deficient Erythropoiesis
-transferrin saturation falls to 1520%,
hgb synthesis becomes impaired.
Iron-Deficiency Anemia
hemoglobin and hematocrit begin to fall. The
transferrin saturation at this point is 1015%.
Differential Diagnosis of Hypochromic
Microcytic Anemia
Treatment: Iron-Deficiency
Anemia
RED CELL TRANSFUSION
Transfusion therapy is reserved for
individuals who have symptoms of anemia,
cardiovascular instability, continued and
excessive blood loss

ORAL IRON THERAPY
In the asymptomatic patient
Anemia of Acute and Chronic Inflammation
one of the most common forms of
anemia seen clinically
serum ferritin values increase threefold
over basal levels
Interleukin 1 (IL-1) directly decreases
EPO production in response to anemia.

Anemia of Acute and Chronic
Inflammation
IL-1, acting through accessory cell
release of interferon (IFN-y ), suppresses
the response of the erythroid marrow to
EPO
(TNF), acting through the release of IFN-
by marrow stromal cells, also suppresses
the response to EPO.
Hepcidin, made by the liver, is increased
in inflammation and acts to suppress iron
absorption and iron release from storage
sites

Anemia of Chronic Kidney
Disease (CKD)
anemia is primarily due to a failure of
EPO production by the diseased kidney
and a reduction in red cell survival.

Patients with the anemia of CKD usually
present with normal serum iron, TIBC,
and ferritin levels.
Treatment: Hypoproliferative
Anemias
TRANSFUSIONS
Patients without serious underlying cardiovascular or
pulmonary disease can tolerate hemoglobin levels
above 8 g/dL and do not require intervention until the
hemoglobin falls below that level.
Patients with more physiologic compromise may
need to have their hemoglobin levels kept above 11
g/dL.
A typical unit of packed red cells increases the
hemoglobin level by 1 g/dL.
ERYTHROPOIETIN (EPO)
CKD, the usual dose of EPO is 50150 U/kg three
times a week intravenously.
cancer is higher, up to 300 U/kg three times a week
MEGALOBLASTIC ANEMIAS
are a group of disorders characterized
by the presence of distinctive
morphologic appearances of the
developing red cells in the bone marrow.

The marrow is usually cellular and the
anemia is based on ineffective
erythropoiesis.

The cause is usually a deficiency of
either cobalamin (vitamin B12) or folate
Causes of Cobalamin Deficiency
Sufficiently Severe to Cause Megaloblastic
Anemia

Nutritional : Vegans
Malabsorption: Pernicious anemia
Gastric causes: Congenital absence of intrinsic
factor or functional abnormality ,Total or partial
gastrectomy
Intestinal stagnant loop syndrome: jejunal
diverticulosis, ileocolic fistula, anatomic blind loop,
intestinal stricture,
Ileal resection and Crohn's disease
Selective malabsorption with proteinuria
Tropical sprue
Transcobalamin II deficiency
Fish tapeworm
HEMATOLOGIC FINDINGS
Oval macrocytes, usually with
considerable anisocytosis and
poikilocytosis, are the main feature.
The MCV is usually >100 fL unless a
cause of microcytosis (e.g., iron
deficiency or thalassemia trait) is
present.
Some of the neutrophils are
hypersegmented (more than five nuclear
lobes).
Treatment: Megaloblastic Anemia
COBALAMIN DEFICIENCY
lifelong regular cobalamin injections.
FOLATE DEFICIENCY
Oral doses of 515 mg folic acid daily are
satisfactory, as sufficient folate is absorbed from
these extremely large doses even in patients
with severe malabsorption. a
Pregnancy
Folic acid, 400 g daily, should be given as a
supplement before and throughout pregnancy.
In women who have had a previous fetus with a
neural tube defect, 5 mg daily is recommended
HEMOLYTIC ANEMIAS
primary etiology is due to increased destruction of
red cells which may be inherited or acquired
essential pathophysiologic process common to all
HAs is an increased red cell turnover.
The gold standard for proving that the life span of
red cells is reduced (compared to the normal
value of about 120 days) is a red cell survival
study, which can be carried out by labeling the
red cells with 51Cr and measuring residual
radioactivity over several days or weeks
if hemolysis is recurrent or persistent, the
increased bilirubin production favors the
formation of gallstones.
If a considerable proportion of hemolysis takes
place in the spleen, as is often the case,
splenomegaly