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Anemia
1. ANEMIA
Submitted to: Mrs. Manisha Mistri Ma’m
Medical surgical DPT, Nursing Teacher
of Scon
Submitted By:
Bhagyashri P.
PBBsc 1st year Scon.
2. Introduction
Anemia is defined as a below-normal plasma hemoglobin
concentration resulting from a decreased number of
circulating red blood cells.
4. 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 CELLANEMIA
Hydroxyurea
Pentoxifylline
5. IRON
Iron is stored in the intestinal mucosal
cells, liver, spleen, and bone marrow as
ferritin (an iron–protein complex) until
needed by the body.
Iron is delivered to the marrow for
hemoglobin production by a transport
protein, namely transferrin.
6. IMPACT 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
7. 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
8. ORAL PREPARATIONS PARENTERAL
PREPARATIONS
Ferrous sulfate Iron dextran
Ferrous fumarate Sodium ferric gluconate
Ferrous gluconate Iron sucrose
Polysaccharide–iron complex
Carbonyl iron formulations
9. 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
10. 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 acid—also known as
leucovorin calcium—available as oral and parenteral formulations)
11. Content
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
12. CYANOCOBALAMIN &
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.
13. SIGNS AND SYMPTOMS
May cause tingling (pins and needles) in the
hands and feet,
Difficulty Walking
Dementia
In extreme cases, hallucinations, paranoia, or
schizophrenia.
14. Undiagnosed or untreated iron-deficiency
anemia may cause the following
complications:
Depression.
Heart problems. ...
Increased risk of infections.
Motor or cognitive development delays in children.
Pregnancy complications, such as preterm
delivery or giving birth to a baby with low birth
weight
15. Content
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
16. Content
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.
17. 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
18. Content
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.
19. Content
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.
21. AGENTS USED FOR
NEUTROPENIA
Myeloid growth factors or granulocyte colony stimulating factors
(G-CSF)
Filgrastim
Tbo-filgrastim
Pegfilgrastim
Granulocyte–macrophage colony–stimulating factors (GM-CSF)
Sargramostim
22. Content
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
23. SICKLE CELLANEMIA
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
24. Content
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