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ANEMIA

Anemia is defined as a below-normal plasma


hemoglobin concentration resulting from a
decreased number of circulating red blood
cells.

GENERAL SIGNS AND SYMPTOMS

Fatigue
Rapid heartbeat
Shortness of breath
Pale skin
Dizziness
Insomnia.

DRUGS FOR TREATMENT OF ANEMIA


TREATMENT OF ANEMIA
Cyanocobalamin (B12)
Darbepoetin
Epoetin alfa
Folic acid
Iron
TREATMENT OF NEUTROPENIA
Filgrastim
Peglgrastim
Sargramostim
Tbo-lgrastim
TREATMENT OF SICKLE CELL ANEMIA
Hydroxyurea
Pentoxifylline

IRON
Iron is stored in the intestinal mucosal cells, liver,
spleen, and bone marrow as ferritin (an ironprotein
complex) until needed by the body.
Iron is delivered to the marrow for hemoglobin
production by a transport protein, namely transferrin.

CAUSES OF IRON DEFICIENCY ANEMIA


Acute or chronic blood loss,
From insufficient intake during periods of
accelerated growth in children, and in
Heavily menstruating or pregnant women

Iron deficiency anemia may cause


Pica (hunger for ice, dirt, paper, etc.)
Koilonychias (upward curvature of the finger
and toe nails)
Soreness and cracking at the corners of the
mouth

Acidic conditions in the stomach keep iron in


the reduced ferrous form, which is the more
soluble form. Iron is then absorbed in the
duodenum
Daily iron requirements in patient with iron
deficiency anemia is 150 -180 mg /day

ORAL PREPARATIONS

PARENTERAL PREPARATIONS

Ferrous sulfate

Iron dextran

Ferrous fumarate

Sodium ferric gluconate

Ferrous gluconate

Iron sucrose

Polysaccharideiron complex
Carbonyl iron formulations

Abdominal pain, constipation, diarrhea and dark


stools are the most common adverse effects of
oral iron supplements.
Fatal hypersensitivity and anaphylactoid
reactions can occur in patients receiving
parenteral iron (mainly iron dextran
formulations).
Excessive iron can cause toxicities that can be
reversed using chelators such as deferoxamine

FOLIC ACID (FOLATE)


Folate deficiency may be caused by
Increased demand (for example, pregnancy and lactation
Poor absorption caused by pathology of the small intestine
Alcoholism
Treatment with drugs that are dihydrofolate reductase
inhibitors (for example, methotrexate, pyrimethamine, and
trimethoprim) & treated by folinic acid
Reduced or active form of the vitamin (folinic acidalso
known as leucovorin calciumavailable as oral and
parenteral formulations)

A primary result of folic acid deficiency is


megaloblastic anemia (large-sized red blood
cells)
Folic acid is well absorbed in the jejunum
unless pathology is present.
If excessive amounts of the vitamin are
ingested, they are excreted in the urine and
feces. Oral folic acid administration is nontoxic

CYANOCOBALAMIN AND
HYDROXOCOBALAMIN (VITAMIN B12)
Deficiencies of vitamin B12 can result from
either low dietary levels
Poor absorption of the vitamin due to the
failure of gastric parietal cells to produce
intrinsic factor (as in pernicious anemia),
which is required for vitamin B12 absorption.

SIGNS AND SYMPTOMS


May cause tingling (pins and needles) in the
hands and feet,
Difficulty Walking
Dementia
In extreme cases, hallucinations, paranoia, or
schizophrenia.

The vitamin may be administered orally (for dietary


deficiencies), intramuscularly, or deep subcutaneously (for
pernicious anemia)
Folic acid administration alone reverses the hematologic
abnormality and, thus, masks the vitamin B12 deficiency, which
can then proceed to severe neurologic dysfunction and disease
Therefore, megaloblastic anemia should not be treated with folic
acid alone but, rather, with a combination of folate and vitamin
B12.
Therapy must be continued for the remainder of the life of a
patient suffering from pernicious anemia

In patients with bariatric surgery (surgical


treatment for obesity), vitamin B12
supplementation as cyanocobalamin is
required in large oral doses, sublingually or
once a month by the parenteral route.
Intramuscular hydroxocobalamin is now
preferred since it has a rapid response, is highly
protein bound, and maintains longer plasma
levels.

ERYTHROPOIETIN AND DARBEPOETIN


Peritubular cells in the kidneys work as sensors
that respond to hypoxia and mediate synthesis
and release of erythropoietin
Erythropoietin stimulates stem cells to
differentiate into proerythroblasts and promotes
the release of reticulocytes from the marrow and
initiation of hemoglobin formation
Erythropoietin thus, regulates red blood cell
proliferation and differentiation in bone marrow

Human erythropoietin (epoetin alfa), produced


by recombinant DNA technology
Effective in the treatment of anemia caused by
End-stage renal disease,
Anemia associated with HIV
Anemia in bone marrow disorders,
Anemias in some cancer patients.

Darbepoetin is a long-acting version of


erythropoietin
It differs from erythropoietin by the addition of
two carbohydrate chains, which improves its
biologic activity.
Darbepoetin has decreased clearance and has a
half-life about three times that of epoetin alfa.

ADVERSE EFFECT
ERYTHROPOIETIN/EPOETIN
ALFA

DARBEPOETIN ALFA

Edema

Edema

Thrombosis

Thrombosis

Nausea/Vomiting

Dyspnea

Hypertension

cerebrovascular accident

Pruritus

Hypertension

cerebrovascular accident

AGENTS USED FOR NEUTROPENIA


Myeloid growth factors or granulocyte colony
stimulating factors (G-CSF)
Filgrastim
Tbo-filgrastim
Pegfilgrastim
Granulocytemacrophage colonystimulating
factors (GM-CSF)
Sargramostim

Stimulate granulocyte production in the marrow to


increase the neutrophil counts and reduce the duration
of severe neutropenia.
They are typically used prophylactically to reduce risk
of neutropenia following chemotherapy and bone
marrow transplantation.
Filgrastim and sargramostim can be dosed either
subcutaneously or intravenously,
Tbo-filgrastim and pegfilgrastim are dosed
subcutaneously only

SICKLE CELL ANEMIA


Hydroxyurea can reduce the frequency of painful sickle cell crises
Hydroxyurea is also used off-label to treat chronic myelogenous
leukemia and polycythemia vera.
In sickle cell disease, the drug apparently increases fetal
hemoglobin levels, thus diluting the abnormal hemoglobin S
(HBS). This process takes several months
Polymerization of HBS is delayed in treated patients, so that
painful crises are not caused by sickled cells blocking capillaries
and causing tissue anoxia.
Side effects include bone marrow suppression and cutaneous
vasculitis

Pentoxifylline increases the deformability of red blood


cells (improves erythrocyte flexibility) and reduces the
viscosity of blood.
This decreases total systemic vascular resistance,
improves blood flow, and enhances tissue oxygenation
in patients with peripheral vascular disease
It is available in extended-release tablets and is taken
three times a day with food.
Adverse reactions are mainly GI in nature and are
lessened by administration with food