anti anemic preparations summarized description

1. Anti anaemic Drugs

2. Anti anaemic Drugs
Haematopoiesis: it is the production of erythrocytes,
platelets, and leukocytes from undifferentiated stem cells.
The haemtopoietic machinary reside in the bone marrow in
adults.
It requires a constant supply of essential nutrients – iron,
cyanocobalamine, folic acid and presence of hematopoietic
growth factors

3. Anti anaemic Drugs
Anemia:
anemia is a common clinical condition that is caused by an
acquired or hereditary abnormality of RBCS or its precursor,
or it may be a manifestation of an underlying non hematologic
disorder.
anemia is defined as a decrease in the circulating RBC mass;
the usual criteria are a Hb of less than 11.5 G/dl in women and
less than 14 G/dl in men.

4. Anti anaemic Drugs
Signs and Symptoms:
Patients with a Hb less than 7G/dl will have symptoms of
tissue hypoxia (fatigue, headache, dyspnea, pallor, angina,
tachycardia, visual impairment, syncopy, lymphadenopathy,
hepatic and or splenic enlargement, bone tenderness, blood
loss in feces, neurologic symptoms.

5. Anti anemic Drugs
Classification of anemia:
1.anemia associated with decrease RBC production for e.g..
A) iron deficiency anemia,
B) megaloblastic anemia
C) Thalassemia
D) anemia due to chronic disease and renal failure.
2. Anemia due to increased RBC destruction:
Haemolytic anemia
 sickle cell anemia

6. Anti anaemic Drugs
1- Iron:
Total quantity of iron in the body is 4-5G
 65-70% in the form of Hb in RBC
 4% in myoglobin
 1% in various heme compound
 15-30% stored in the form of ferritin and hemosiderin in RE
system, liver, spleen, intestinal mucosa and bone marrow


7. Anti anaemic Drugs
Iron is required for Hb production.
 in the absence of adequate iron, small red cells with insufficient
Hb are formed, giving rise to microcytic hypochromic anemia.
Iron deficiency occur due to:
(a) inadequate dietary intake as in vegetarians, malnourished pts.
(b) due to blood loss a in women in heavy menstruation
(c) when iron requirement is increased as in pregnancy and in
growing children.
(d) acute or chronic blood loss
.

8. Anti anaemic Drugs
2, 3- cyanocoblamine and folic acid:
 are required for normal DNA synthesis.
Deficiency of either of these vitamins results in
impaired production and abnormal maturation of
RBCS giving rise the characteristic blood and bone
marrow picture known as megaloblastic anemia
4- Erythropoeitin and colony stimulating factors
are hormones that regulate blood cell development and
proliferation in the bone marrow.

9. Anti anaemic Drugs
1- Iron preparation:
Oral iron
Parenteral iron
A- oral iron
A) Ferrous sulfate - 325mg - 65mg elemental iron
B )Ferrous gluconate - 320mg -37mg elemental iron
C) Ferrous fumarate - 325mg - 106mg elemental iron
B- Parenteral iron: iron dextran 50mg elemental iron/ml

10. Anti anaemic Drugs
Pharmacokinetics:
Absorption: iron (Fe++; more readily absorbed) absorb
from duodenum and upper jejenum Fe+++ (ferric) in→
the intestinal mucosal cell.
Ferric iron binds with transferrin in plasma and
transported in other tissues and stored as ferritin and
hemosiderin form.
About 10 -20% of dietary iron is absorbed, for e.g. a
standard diet if contain 10-15mg of iron, only 1mg is
absorbed.
Absorption when iron requirement is as in↑ ↑
pregnancy, menstruation, growing children

11. Abs is increased by: glucose, amino acids & ascorbic
acid.
& decreased by : phosphate bicarbonate bile
acids, antacids & tetracycline.
Heme iron in meat Hg & myoglobin can be absorbed
intact.
Iron in vegetables & grains, tightly bound to organic cpds;
< available for abs.

13. Anti anaemic Drugs
Distribution:
 ferric from iron store sites through transferrin goes in the
RBCS.
200- 400 mg oral elemental iron daily should be given to
correct anemia (27% absorbed ,so 50-100mg iron can be
incorporated in Hb).
Treatment should be continued for 3-6 months, this not only
to correct the anemia but will replenish iron stores.
(Hb should reach normal level in 1-3 months).
Failure to respond to oral iron therapy may be due to
incorrect diagnosis.

14. Storage:
When free iron levels are H, apoferritin is produced to
sequester iron & protect organs from toxic effect of excess
free iron.
Iron is stored in intestinal mucosal cells & as ferritin, in
macrophages in liver, spleen, & bone.
Elimination:
No mechanism for excretion
Small amounts in feces & bile.

15. Anti anaemic Drugs
Adverse effects:
- Due to oral iron therapy;
Nausea, epigastric discomfort, abdominal cramps,
constipation, diarrhea, black stool.
They may be minimized by lowering the daily dose or by
taking iron tablets immediately after or with meals.

16. Anti anaemic Drugs
Parenteral iron therapy:
1. It should be reserved for patients with documented iron
deficiency unable to tolerate or absorb iron ( patients With
post gastrectomy, previous small bowel resection,
malabsorption syndrome, inflammatory bowel D,
noncompliance of patient, advanced chronic renal Disease .
2. Patients. With extensive chronic blood loss who can not
be maintained with oral iron alone.

17. Anti anaemic Drugs
Iron dextran (ferric hydroxide + dextran), 50mg elemental
iron/ml
Route of administration: I/M, or by I/V infusion in 1-2
hours.
Advantage of IV: eliminates local pain & tissue staining (SE:
IM). + allow delivery of entire iron dose.
Also Iron sorbitol (IM
Most adults needs about 1-2 G (20-40 ml) iron dextran for
iron deficiency anemia.

18. Anti anaemic Drugs
Adverse effects:
Local pain, tissue staining (brown discoloration of tissues
overlying the inj. site), headache, fever, arthralgia, nausea,
vomiting, bronchospasm, urticaria, anaphylaxis, and death.
Rare: anaphylactic & death.
Also dextran can cause hypersensitivity rxs.
Alternative preparations:
Iron-sucrose complex & iron Na+
gluconate complex. ONLY (IV)
less hypersensitivity than dextran.

19. Anti anaemic Drugs
Chronic toxicity:
 known as hemochromatosis, when excess iron is
deposited in heart, liver, pancreas and other organs cause
organ failure and death.
It occurs in patients with inherited hemochromatosis
(excessive iron absorption), in patients who receive many
red cell transfusions for long period

20. Anti anaemic Drugs
2- coblamine
 a cobalt containing molecule is along with folic acid, a
cofactor in the transfer of 1- carbon units, a step necessary
for the synthesis of DNA.
Impairment of DNA synthesis affects all cells, but
because red blood cells must be produced continuously,
deficiency of either coblamine or folic acid usually
manifests first as anemia (megaloblastic anemia)
Deficiency;; anemia, GI symptoms, & neurologic
abnormalities.

21. Anti anaemic Drugs
Pharmacokinetics:
Source: Meat (liver), eggs, & dairy products.
coblamine is absorbed from the GIT in the presence of intrinsic
factor, a product of the parietal cells of the stomach.
Plasma transport is accomplished by binding to transcobalamin II.
Coblamine is stored in the liver in large amounts; a normal
individual has enough to last 5 years.
It is available in 2 forms
1. cyanocobalamine
2. hydroxy cobalamine has a longer circulating half life.

23. Anti anaemic Drugs
Clinical uses and toxicity:
Both agents have equivalent effects.
1. Treatment of naturally pernicious anemia
2. anemia caused by gastric resection
Because coblamine deficiency anemia is almost always caused
by inadequate absorption, therapy should be by replacement of
coblamine, using parenteral therapy.
No significant toxicity of coblamine occurred

25. 25

26. 26
Uses:
1- Pernicious anemia
2- Neurologic abnormalities
3- Gastrectomy
4- Cyanide poisoning.

27. 27
• Initial therapy: 100-1000 mcg of vit B12 IM
daily or every other day for 1-2 wks
• Maintenance: 100-1000 mcg IM once a month
for life.
• .

28. Anti anaemic Drugs
 administration of folic acid to patients with coblamine
deficiency helps refill the tetrahydrofolate pool and partially
or fully corrects anemia
However exogenous folic acid does not correct the
neurologic defects of coblamine deficiency
[Note: Folic acid administration alone reverses the
hematologic abnormality and, thus, masks the coblamine
deficiency, which can then proceed to severe neurologic
dysfunction and disease. Therefore, megaloblastic anemia
should not be treated with folic acid alone.

29. Anti anaemic Drugs
Folic acid:
Like coblamine folic acid is required for normal DNA
synthesis, and its deficiency usually presents as megaloblastic
anemia.
In addition deficiency of folic acid during pregnancy increase
the risk of neural tube defects in the fetus

30. Anti anaemic Drugs
Pharmacokinetics:
Source: yeast, liver, kidney, & green vegetables.
Folic acid is readily absorbed from GIT.
Only modest amount are stored in the body, so a decrease in
dietary intake is followed by anemia within few months
Pharmacodynamics:
Folic acid is converted to tetrahydrofolate by the action of
dihydrofolate reductase

31. Anti anaemic Drugs
One important set of reactions involving tetrahydrofolate
and dihydrofolate constitutes the dTMP cycle, which
supplies the dTMP required for DNA synthesis.
Rapidly dividing cells are highly sensitive to folic acid
deficiency.
For this reason, antifolate drugs are useful in the treatment
of various infections and cancers

32. Anti anaemic Drugs
Clinical use and toxicity:
Folic acid deficiency is most often caused by dietary
insufficiency and malabsorption.
Anemia resulting from folic acid deficiency is readily treated
by oral folic acid.
Maternal folic acid deficiency is associated with increased
risk of neural tube defects in the fetus, folic acid
supplementation is recommended prior to and during
pregnancy

33. Anti anaemic Drugs
Folic acid supplements will correct the anemia but not the
neurologic deficits of coblamine deficiency.
Folic acid has no recognized toxicity

34. Anti anaemic Drugs
Erythropoietin:
ERYTHROPOIETN is produced by the kidney
Reduction in its synthesis is responsible for anemia of renal
failure
Activation of receptors on erythroid progenitors in the bone
marrow, it stimulates the production of red cells and increases
their release from Bone Marrow.

35. Anti anaemic Drugs
Erythropoietin is used for anemia associated with renal
failure and some time effective for patients with other forms
of anemia e.g. primary bone marrow disorder or anemia
secondary to cancer chemotherapy or HIV treatment, bone
marrow transplantation, AIDS or cancer
Toxicity: thrombosis ,cardiovascular events when used
along with some other erythropoietic agents

36. Darbepoetin [dar-be-POE-e-tin] is a long-acting version of
erythropoietin
Therefore, darbepoetin has decreased clearance and has a half
life about three times that of erythropoietin.
Supplementation with iron may be required to assure an
adequate response.
The protein is usually administered intravenously in renal
dialysis patients, but the subcutaneous route is preferred.

37. When erythropoietin is used to target hemoglobin
concentration 11.5g/dl, serious and life-threatening
cardiovascular events, increased risk of death, shortened
time to tumor progression and/or decreased survival have
been observed.
The recommendations for all patients receiving erythropoietin
include a minimum effective dose that does not exceed a
hemoglobin level of 11.5 g/dl and this should not rise more
than 1 g/dL over a 2-week period.

38. Agents Used to Treat Sickle-Cell Disease
Clinical trials have shown that hydroxyurea can relieve the painful
clinical course of sickle-cell disease.
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 the treated patients so that
painful crises are not caused by sickled cells blocking capillaries and
causing tissue anoxia.

39. Important side effects of hydroxyurea include bone marrow
suppression and cutaneous vasculitis.
It is important that hydroxyurea is administered under the
supervision of a physician experienced in the treatment of
sickle-cell disease.

40. A 22-year-old woman who experienced pain and swelling in her
right leg presented at the emergency room. An ultrasound study
showed thrombosis in the popliteal vein. The patient, who was in
her second trimester of pregnancy, was treated for 7 days with
intravenous unfractionated heparin. The pain resolved during the
course of therapy, and the patient was discharged on Day 8. Which
one of the following drugs would be most appropriate out-patient
follow-up therapy for this patient, who lives 100 miles from the
nearest hospital?
A. Warfarin.
B. Aspirin.
C. Alteplase.
D. Unfractionated heparin.
E. Low-molecular-weight heparin (LMWH).

41. A 60-year-old man is diagnosed with deep-vein thrombosis. The
patient was treated with a bolus of heparin, and a heparin drip
was started. One hour later, he was bleeding profusely from the
intravenous site.The heparin therapy was suspended, but the
bleeding continued. Protamine was administered intravenously,
and the bleeding resolved. The protamine:
A. Degraded the heparin.
B. Inactivates antithrombin.
C. Activates the coagulation cascade.
D. Activates tissue-plasminogen activator.
E. Ionically combines with heparin.