Microcytic Hypochromic Anemia

Iron deficiency anaemia Anaemia of chronic disease Sideroblastic

anaemia

Causes: 1- Inadequate iron: 1- Arthritis. Sideroblastic

a- Dietary deficiency. 2- Inflammatory bowel diseases. anemias (SA) are
b- Malabsorption: Gastrectomy and Coeliac disease. 3- Malignancies. a group of rare
2- Increased physiological demands e.g. multiple pregnancies. 4- CKD. bone marrow
3- Loss of blood: disorders,
a- Excess menstruation. characterized by
b- GIT bleeding. decreased
c- Parasitic infestation e.g. hookworm (Ankylostoma): GIT blood loss hemoglobin
synthesis,
Patho- Defective synthesis of haem part of Hb leading to decreased proliferation and 1- Infection, inflammation and malignancy because of
physiology: differentiation of precursors. increase iterlukin-6 (IL-6). defective
2- IL-6 stimulate the hepatocytes to secret a use of iron
peptide called hepcidin. (although
3- Hepcidin: plasmatic iron
a- Reduces intestinal absorption of iron. levels may be
b- Locks iron within hepatocytes and normal or
macrophages. elevated)
4-Decrease circulating iron despite normal iron and the
stores = Functional iron deficiency. presence of
ringed
Signs and 1- General manifestations of anemia. 2- Other features: a- Brittle hair. b- Painless 1- General manifestations of anemia. sideroblasts in
Symptoms glossitis and angular stomatitis. c- Unusual cravings e.g. Pica. d- Atrophic gastritis. 2- Manifestations of the chronic disease. the bone
e- Brittle nails and Koilonychia (Spoon shaped). marrow due to
the
Investigatio 1- Hb: Low = Anemia. 1- Microcytic hypochromic anemia. pathologic iron
ns 2- Haemtocrit: Low 2- Low plasma iron. overload in
3- MCV: Low = Microcytic 3- Normal or raised plasma ferritin. mitochondria
4- MCH and MCHC: Low = Hypochromic 4- Normal or low total iron binding capacity
5- Plasma ferritin : Low = Iron deficiency (TIBC).

Treatment 1- Treatment of the underlying cause. 1- Treatment of the underlying cause.

2- Eradication of H. pylori aids recovery from anemia. 2- Erythropoietin may be tried.
(H. pylori infection is associated with anemia by impairing iron absorption as a 3- Drugs under trial:
result of a- Decrease IL-6.
chronic gastritis). b- Decrease Hepcidin.
3- Prophylaxis, Iron supplementation for:
a- Poor nutrition in children in some cities and communities: Milk and cereals
fortified with iron.
b- Pregnancy: Iron + Folic acid.
c- Menorrhagia.
d- Premature and low-birth weight infants especially twins.
e- After gastrectomy.
4- Blood transfusion in cases of acute blood loss.
5- Iron supplementation:
a- It takes 1 – 2 weeks for Hb to rise 1 g / dl.
b- About 6 months are needed to both correct the anemia and replenish body
stores.
c- The rate of response is the same whether iron was given orally or parenterally.
d- Oral iron is better absorbed if given before meals on an empty stomach. If GIT
discomfort occurs, give iron after meals.
e- Parenteral iron is reserved for especial situations:
- Poor compliance. - Patients who can not tolerate oral iron.
- Start by small test dose to detect anaphlactoid reaction.
Facilities for cardiopulmonary resuscitation must be available -
6- Preparations:
a- Oral:
- Ferrous fumarate
- Ferrous gluconate
b- Parenteral iron: Slow I.V. injection of infusion
- Iron dextran: Also Deep I.M. (Use Z-line technique).
- Iron sucrose.

Patient 1- Relation of intake of oral iron to meals. Explain to the patient why to avoid purchasing
Education In most cases, the best time to take iron supplement is about one hour before or over-the-counter iron or
and two hours after meals. Iron supplements are best taken with water on an empty other supplements.
Counseling: stomach.
2- What meals and drugs that:
- Aids to oral iron absorption (e.g. Vit. C)
- Hinder oral iron absorption (e.g. Coffee, tea and milk)
3- Stool may become darker, and not to be misdiagnosed with melena.
4- Length of treatment.
5- Importance of compliance.
 Megaloblastic Anemias (Macrocytic anemia)
Folate deficiency. Vitamin B-12 deficiency. Pernicious:
Autoimmune
disease.

Causes: 1- Decreased dietary folate intake. Especially alcoholics 1- Nutritional deficiency e.g. strict vegans. 1- Autoimmune
and elderly. 2- Decreased absorption: disease.
Diet rich in folate includes fruit, green vegetables and a- Gastrectomy. Formation of
yeast. b- Achlorhydria. antibodies against
2- Decreased absorption: Gut disease and gastrectomy. c- Pernicious anemia. the
3- Increased demands: Pregnancy and haemolytic d- Diseases of the ileum. parietal cells or
anaemias. e- Fish tapeworm infection. the intrinsic
4- Drugs: f- Drugs: Metformin. factor.
a- Dihydrofolate reductase enzyme inhibitors: 2- Management
- Cytotoxic: Methotrexate. similar to Vitamin
- Anti-malarial: Pyrimethamine. B-12 deficiency
- Anti-bacterial: Trimethoprim and Co-trimoxazole. anemia.
- Diuretics: Triamterene
b- Inhibit folate absorption: Phenytoin, babiturates,
sulfasalazine, cholestyramine and
oral contraceptives.

Patho- Defective DNA synthesis that will affect cells with rapid 1- Defect in demethylation of methyl tetrahydrofolate monoglutamate
physiolog turnover: (MTHFM),
y: 1- Haemopoietic system especially RBCs. which is an important step in the activation pathway of folate → Defect in
2- G.I.T. DNA and
3- Gonads. RNA synthesis → Affect rapidly dividing cells such as RBCs, GIT and gonads.
2- Defect in myelination of neurons → Peripheral neuritis and subacute
combined
degeneration of the spinal cord.

Signs and 1- General manifestations of anemia. Similar to folate deficiency anaemia +

Symptom 2- Insidious onset. 1- Fever.
s 3- Glossitis: Sore, pale and smooth tongue. 2- Neuropathy:
4- Angular stomatitis. a- Bilateral peripheral neuropathy affecting the legs rather than the arms
5- Anorexia. → Tingling
6- Altered bowel habits: Diarrhea or constipation. and loss of vibration sense.
7- Sterility. b- Muscle weakness → Difficulty in walking and frequent falls.
8- Mild jaundice.

Investigat 1- Hb: Low = Anemia 1- Hb: Low = Anemia.

ions 2- Haematocrit: Low 2- RBCs count: Low = Anemia
3- MCV: High = Megaloplastic = Macrocytic. 3- Haematocrit: Low
4- Decreased RBCs and plasma folate level. 4- MCV: High = Megaloplastic = Macrocytic
5- Thrombocytopenia. 5- Plasma Vitamin B-12 level: Low
6- Serum folate: Normal or high.
7- Schilling test to measure oral vit B-12 absorption.

Treatmen 1- Exclude Vitamin B-12 deficiency. Folate alone will
t correct the blood
picture but will worsen the neurological manifestations.
2-Treatment of the underlying cause.
3- Change dietary habits.
4- Daily requirements about 100 ug.
5- Folate replacement therapy 5 – 15 mg / days.
6- Prophylaxis in pregnancy to prevent neural tube
defect. Daily folate
350 – 500 ug + Iron.
1- Treatment of the underlying cause e.g. Fish tapeworm.
2- Vitamin B-12 (Hydroxocobalamin or Cyanocobalamin):
a- Treatment is life-long.
b- I.M.
- 1 mg 3 times/week x 2 weeks, then 1 mg/3 months.
- If neurological involvement: 1 mg every other day till no further
improvement, then 1 mg/2 months.
c- Oral and Sublingual 1 – 2 mg daily in vegan patients or who are unable
to
have injections.
3- Monitor improvement: Subjective before objective
a- Patients feels better within 1 – 2 days.
c- Rise in reticulocyte count within 3 – 4 days and peaking after 7 – 8 days.
d- RBCs and platelet counts return to normal after 7 – 10 days.
e- Hb rises 2 – 3 g/dL every 2 weeks.
f- Sore tongue starts to improve within 2 days and returns to normal after
2- 4 weeks.
g- Recent peripheral neuropathy improves partially.
h- Spinal cord damage is irreversible.
4- Monitor plasma levels of Potassium and iron. Correct their deficiency.
In the early stage of treatment, careful attention to blood potassium
levels is necessary in severe cases, as the B12 pushes potassium into the
blood cells, making the blood level very low.
5- Blood transfusion if necessary.

Patient 1- Nutritional advice (Fruits, green vegetables, no 1- Subjective improvement does not mean objective improvement.
Education alcohol). 2- Importance of the life long treatment.
and 2- Patient will feel better within few days = Subjective
Counselin improvement.
g: 3- Correction of blood pictures needs treatment for 4 –
6 months = Objective improvement.
 Hemolytic Anemia
General Clinical 1- During acute hemolytic attack:
Manifestations
a- Symptoms: Malaise, fever, abdominal pain, jaundice and dark urine.
b- Investigations: Haemoglibinaemia, hyperbilirubinaemia, reticulocytosis
and increased urobilinogen in urine.
2- Chronic haemolytic anemia:
a- Normocytic normochromic anemia
b- Splenomegaly.
General 1- Folate supplement to satisfy the needs of expanded and hyperactive
Treatment
bone marrow.
2- Infusion of Desferrioxamine and oral Deferiprone and Deferasirox to
treat iron overload in patients who require frequent transfusions.
Causes A) Genetic Disorders:
1- Abnormal Hb: Sickle cell anaemia and Thalassemias.
2- Energy pathway: Glucose-6-phospahte dehydrogenase deficiency.
3- Membrane: Hereditary Spherocytosis and Ovalcytosis.
B) Acquired Disorders:
1- Immune: Autoimmune, and Rh or ABO incompatibility.
2- None-immune: Infections, Drugs and chemicals and Hypersplenism
Autoimmune Sickle Cell Anaemia Thalassaemias G6PD-D = Favism
Haemolytic
Anaemia

Causes: - Presence of 1- Globin of normal 1- Globin of normal 1- G6PD is essential for the production of NADPH.
autoantibodies haemoglobin (Hb A) is haemoglobin (Hb A) is 2- NADPH is needed to keep glutathione in the
that agglutinate composed of 2 α and 2 composed of 2 α and 2 β reduced form.
or lyse the β polypeptides. 3- Reduced glutathione (G-SH) protects RBCs from
patient’s polypeptides. 2- In thalassaimia there is oxidative stress.
own RBCs. 2- Sickle cell disease reduced or absent 4- In G6PD-D: Oxidizing agents damage cell
has abnormal Hb S, production of α or β membrane and Hb, to be
detected by polypeptides of globin → removed by the spleen.
electrophoresis. Formation of abnormal Hb
3- Formation of (Hb Bart’s or Hb
crescent-shaped cells. H), which is unstable and
4- Sickle cells are less physiological useless.
flexible than normal 3- Short life span of the
RBCs → Impaired abnormal cells and trapping
blood by the spleen.
flow through
microcirculation.
5- Increased
destruction of sickle
cells in spleen.

Investigations Positive direct

Coomb’s test
indicating the
presence
of antibodies to
RBCs

Treatment Immuno- a- Sickle cell patients No specific treatment:

suppressants have high incidence of a- Frequent transfusions.
a- Large doses pneumococcal Manage iron load.
of infections: b- Splenectomy.
corticosteroids. - Prophylaxis by
b- Cytotoxic Penicillin V or
drugs such as Eryhtromycin.
Cyclophosphami - Vaccination against
de. pneumococcal and H.
c- Monoclonal influenza.
antibodies such b- Folic acid
as Rituximab. supplements.
c- Vit B-12 and
erythropoietin.
c- Blood infusion or
exchange. Manage iron
overload.