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Anaemia’s
• Anaemia is present when there is a decrease in the level of haemoglobin in the
blood < 13.5 g/dL in adult males or < 12 g/dL in adult females.
Signs
a. Non-specific
• Paler skin, conjunctiva & mucous membrane.
• Tachycardia.
• High volume pulse.
• Ankle edema.
• Cardiac failure.
• Systolic flow murmur.
b. Specific
• Koilonoychia in iron deficiency.
• Jaundice (in haemolytic)
• Bone deformities (In thalassaemia major)
• Leg ulcers (in sickle cell anaemia)
Causes of Microcytic Anemia
1. Iron deficiency anemia
Iron deficiency anaemia develops when there is an inadequate amount of iron for
hemoglobin synthesis.
Causes
1. Deficient diet .
2. Decreased absorption Increased requirements.
3. Pregnancy.
4. Lactation Blood loss.
5. Gastrointestinal.
6. Menstrual.
7. Blood donation.
8. Hemoglobinuria.
9. Iron sequestration.
10. Pulmonary hemosiderosis.
Clinical features
1. Features of anemia.
2. Features due to iron deficiency in the tissues producing epithelial changes are:
o Brittle nails and nail cracking and koilonychias may be present.
o Atrophy of the papillae of the tongue.
o Angular stomatitis.
o brittle hair.
o Plummer-Vinson Syndrome (which is iron deficiency anemia with dysphagia due to
esophageal webs usually in middle aged women)
• Diagnosis
I. History
By asking the patient about dietary intake, regular self medication with aspirin,
presence of blood in faeces, and in women about the duration and flow of
menstruation.
II. Examination
By looking for features of iron def. anaemia, palpating the spleen to find out
chronic liver disease as a cause of chronic blood loss, PR examination and
proctoscopy.
III. Investigations
a. Blood picture: RBC’s are microcytic (MCV<80 fl), hypochromic (MCH<27 pg),
poikilocytosis, anicytosis.
b. Serum Ferritin: 30-300 microgram/L (which indicates nearly absent iron stores).
c. Serum iron &iron-binding capacity: Serum iron falls and the total iron-binding
capacity rises as compared to normal.
d. Plasma transferrin: raised.
e. Leucocyte count differential: normal.
f. Platelet count: normal or raised.
g. Bone marrow: Erythroid hyperplasia with ragged normoblast, and bone marrow
stain indicates iron depletion.
Management
Management
- Blood tranfusion in severe anaemia.
- The withdrawal of drugs or alchol if they are causative agents. In some cases folic
acid or pyridoxine may improve iron utilization.
3. Anaemia of chronic disease
This type of microcytic anaemia develops in patients with chronic infections such as
infective endocarditis, tuberculosis, osteomyelitis, RA, SLE, polymyalgia rheumatica
and malignancy.
Mechanism
• Theirs is decreased release of iron from bone marrow to developing erythroblasts.
• Decreased response to erythropiotein.
• Decreased red cell survival.
Investigations
• Serum iron and TIBC.
• Serum ferritin (normal or high due to inflammation)
• Iron is present in the marrow but not in developing erythroblasts.
Treatment
• Treatment of underlying cause
• No response to iron therapy
Causes of Macrocytic Anemia
1. Pernicious Anaemia
After being ingested, vitamin B12 is bound to intrinsic factor, a protein secreted by
gastric parietal cells. The vitamin B12–intrinsic factor complex travels through the
intestine and is absorbed in the terminal ileum by cells with specific receptors for
the complex. It is then transported through plasma and stored in the liver.
Since daily losses are 3–5 mcg/d, the body usually has sufficient stores of vitamin B12
so that vitamin B12 deficiency develops more than 3 years after vitamin B12
absorption ceases.
PA is megaloblastic anaemia due to vitamin B12 deficiency as a result of failure of
secretion of intrinsic factor by stomach due to atrophy of gastric mucosa.
It’s a hereditary disease.
Sings
1. Anaemia.
2. Skin with lemon yellow tint due to unconjugated hyperbilirubinaemia.
3. Spleen may be palpable
4. Purpura due to thrombocytopenia.
5. Low grade fever due to anaemia itself or infection.
6. Red sore tounge (glossitis) and angular stomatitis.
7. CNS examination shows signs of polyneuropathy or subactue combined degeneration
of the spinal cord
Investigations
1. Complete CBC
• Low Hb.
• MCV is raised (110-140 fl.)
• Peripheral film shows anisocytosis and poiklocytosis.
• WBC and platelet count may be low showing pancytopenia.
• Neutrophils are hypersegmented (6 lobes).
• Reticulocytes count is low.
2. Bone marrow
• Shows marked erythroid hyperplasia, abnormally large cell size, giant metamyelocytes.
3. Serum vit.. B12 is usually low below the normal level (150-350pg/ml)
4. LDH is elevated
5. Serum Unconjugated bilirubin is increased.
6. Vitamin b12 absorption test (schilling test)
Treatment
• Blood tranfusion (when Hb is very low)
• Treatment of infection.
• Packed platelets.
Inj vitamin b12 100 microgram daily for first week, weekly for first month, and then
monthly for life.
Iron : tab. Ferrous sulphate 200 mg.
2. Folic acid Deficiency anaemia
The most common cause of folic acid deficiency is inadequate dietary intake, malabsorpton
of folic acid is rare because it is absorbed from the entire GIT
Causes
1. Nutritional: poor intake (old age, starvation, and alcoholic excess, anorexia due to GIT
disease)
2. Antifolate drugs (Phenytoin, methotrexate, pyrimethamine, trimethoprim.
3. Excess utilization ( physiological like pregnancy, lactation, prematurity)
4. Pathological (haemolysis, malignat disease, inflammatory disease, haemocystinuria,
dialysis).
5. Malabsorption (small bowel disease)
• Clinical features
1. Features of anaemia and underlying cause.
2. Glossitis may occur.
3. Unlike B12 deficiency there is no neuropathy.
Investigations
1. Low serum folate level, fasting blood sample.
2. Red cells folate levels are low (but maybe normal if folate deficiency is of very recent
onset).
3. Macrocytic dysplastic blood picture, megaloblastic marrow.
Treatment
1. Tab. Folic acid 5mg orally/day.
2. Maintenance dose 5mg/day.
3. Prophylactically in pregnant women where there’s rapid cell turnover and in
patients taking methatrexate.
4. Folic acid should never be given before vit. B12 in B12 deficiency anaemia because
folic acid can aggrevate or precipitate neurological features of B12 depletion.
Causes of normocytic anaemia.
1. Aplastic Anaemia.
Defined as peripheral blood pancytopenia (low RBC’s. WBC’S, and platelets) with aplasia (inability to
produce blood cells) of the bone marrow.
It’s due to reduction in the number of pluripotential stem cells. Failure of one cell line may occur. A full
blood count demonstrates pancytopenia. Neutropenia is the most marked aspect of leukopenia;
anemia is normocytic normochromic and often marked; platelet production is often severely
affected and the last to recover.
Causes
1. Congenital: Fancol’s anemia.
2. Acquired:
• Idiopathic or primary aplastic anemia: cause unknown, may be due to autoimmune process.
• Secondary aplastic anemia due to
chemicals like benzene
drugs like sulfonamides, chloramphenicol, penicillamine, phenylbutazone, antithroid drug,
antiepileptic drugs, chemotherapy
Insecticides.
Ionizing radiation.
Infections (viral hep. , TB, EBV, HIV)
Pregnancy.
SLE.
Paroxysmal nocturnal hemoglobinuria.
Clinical features
a. Anemia due to low RBC count.
b. Infection due to low WBC count.
c. Bleeding due to low platelet count.
d. Fatigue, pallor , dyspnoea due to anaemia.
e. Persistant minor infection e.g fungal infection of mouth, sore throat and fever due to
low WBC count.
f. Petichiae and ecchymosis, bleeding disorders due to low platelet count.
Investigation
1. Blood complete picture
• Pancytopenia ( virtual absence of reticulocytes, anemia is normocytic normochromic type,
platelet count is very low, leucopenia)
2. Bone marrow biopsy
• Shows a hypocellurlar or aplastic bone marrow with increased fat spaces.
Management
I. Supportive masures:
Packed cell volume and platelet tranfusion for bleeding, vigorous antibiotics for infection, severe
aplastic anemia is defined by the presence of neutophils less than 500 /micro litres, platelets less
than 20000/ micro litres, reticulocytes count less than 1% and bone marrow cellularity less than
20%
II. Bone marrow transplantation.
III. Immunosuppressive therapy
IV. Treatment to stimulate hemopoiesis (androgenic steroids).
2. Haemolytic Anaemia
Haemolytic anaemias are caused by increased destruction of red cells. Shortening of reed
cell survival stimulates bone marrow to compensatory increase in red cell production
manifested as reticulocytosis and erythoid hyperplasia. If red cell loss is more than bone
marrow capacity, anaemia manifests.
Mechanisms of Haemolysis.
• Abnormalities of the red-cell membrane (in hereditary spherocytosis)
• Abnormal Hb. (Sickle cell anaemia and thalassemia).
• Abnormalities of vessel wall
• Sites of Haemolysis
1. Intravascular haemolysis: when red cells are rapidly destroyed within the destoyed
within the circulation.
Evidence of intravascular haemolysis.
• Raised level of plasma Hb..
• Haemoglobinuria or hemosiderenuria.
• Very low or absent heptoglobins.
• Presence of methamealbimin.
Causes of intravascular haemolysis.
• Falciparum malaria
• Transfusion reaction
• Microangiopathy.
2. Extravascular Haemolysis.
Here the red cells are removed from the circulation by macrophages in the reticuloendothelial system,
particularly the liver and the spleen.
Causes
A. Congenital
• Red cell membrane defect
Hereditary spherocytosis, hereditary elliptocytosis.
• Haemoglobin abnormalities
Thassemia, sickle cell disease.
• Metabolic defects
Glucose-6 phosphate dehydrogenase deficiency.
B. Acquired
• Immune
1. Alloimmune
Hemolytic transfusion reaction, hemolytic disease of new born, after transplantation.
2. Autoimmune
Warm antibody, cold antibody
3. Drug induced.
• Non-immune
1. Mechanical (burn, porsthetic valves)
2. Infections ( malaria, sepsis)
3. Hypersplenism
4. Drugs and chemicals
5. Systemic disease (renal or liver failure)
Inherited Haemolytic Anemias
• Hereditary spherocytosis.
• Hereditary elliptocytosis.
• Thalassemia.
• Sickle cell anaemia disease.
• Glucose-6-phosphate dehydrogenase deficiency.
Common investigations in blood disease.
Complete blood count (CBC) or complete picture (CP) is one of the most frequently
requested test by clinicians.