For medical students

1. ANEMIA
ANEMIA

2. CONTENTS:
 Definition.
 Pathophysiology.
 Etiology.
 Clinical manifestation.
 Complications.
 Diagnosis/ Investigations.
 Management.

3. DEFINITION
 Anemia is a reduction in hemoglobin and oxygen
capacity in relation to age and sex.
 Anemia is classified according to the cause:
1. Microcytic.
2. Macrocytic.
3. Nomocytic.

4. CLASSIFICATION

5. PATHOPHYSIOLOGY
 Anemia is characterized by a decrease in red blood
cell (RBC) mass. The function of RBC is to deliver
oxygen from the lungs to the tissues and Carbon
dioxide from the tissues to the lungs.
 This is accomplished by using hemoglobin (Hb), a
tetramer protein composed of heme and globin.
 In anemia, a decrease in the number of RBCs
transporting oxygen and carbon dioxide impairs the
body’s ability for gas exchange as a result of blood
loss, increased destruction of RBCs (hemolysis) or
decreased production of RBCs.

6. TYPES OF ANEMIA
 There so many types of anemia but our focus is on
the following types include:
1. Iron deficiency anemia.
2. Hemolytic anemia.
3. Aplastic anemia.

7. IRON DEFICIENCY ANEMIA
 Iron deficiency anemia developes when the body
stores of iron drop too low to support normal red
blood cell production.
 Normal intake is usually 10-20mg/day
 10% is usually absorbed which is about 1-2mg
 1mg is lost through sweat, shedded cells in skin
and faeces.
 Meat (heme iron i.e Fe2+ or ferrous state)
 Vegetables (non-heme iron Fe3+ in spinach/beans)
 Recycled iron from RBC.

8. ETIOLOGY
 Reduced intake
 Infants
 vegetarians
 Reduced absorption
 Gastrectomy
 Inflammatory bowel disease
 Increased demand
 Children/adolescents
 Pregnancy
 Increased loss
 Chronic slow bleeding e.g PUD
 Heavy menstruation
 Colon cancer

9. CLINICAL MANIFESTATIONS
 Cold intolerace.
 Reduced resistence to infections.
 Dysphagia with solid foods ( from esophageal
webbing).
 Fatigue and dimished capability to perform hard
labour.
 Leg cramps on climbing stairs.
 Hypoxia.

10. CLINICAL MANIFESTATIONS CONTINUA…
Findings on physical examinations may include the
following:
 Spoon shaped nails (koilonychia)
 Fissures at the corners of the mouth (angular
stomatitis)
 Splenomegaly (in severe, persistent, untreated
cases).
 Pallor of the mucous membranes.
 A glossy tongue, with atrophy of the lingual papillae.

11. DIAGNOSIS/INVESTIGATIONS
 Complete blood count (CBC);
Low mean corpuscular volume (MCV)
Low mean corpuscular hemoglobin
concentration (MCHC).
Elevated platelet count.
 Peripheral blood smear;
RBCs are microcytic and hypochromic
Platelets usually are increased etc.
 Serum iron, total iron binding capacity (TIBC) and
serum ferritin.

12. MANAGEMENT
Treatment of iron deficiency anemia consist of
correcting the underlying etiology and replenishing
iron stores. Iron therapy is as follows:
 Oral ferrous iron salts e.g ferrous sulfate.
 Parenteral iron for patients who are unable to
absorb oral iron.
 Transfusion of Packed RBCs for patients who are
experiencing significant acute bleeding or in danger
of hypoxia.

13. HEMOLYTIC ANEMIA
 Hemolytic anemia is a disorder in which there is a
premature destruction of erythrocytes.
 It develops when the bone marrow activity can not
compesate for the erythrocyte loss.
 The severity of anemia depends on whether the
onset of hemolysis is gradual or abrupt and on the
extent of erythrocyte destruction.
 Mild hemolysis can be asymptomatic while the
anemia in severe hemolysis can be life threatening
and cause angina and cadiopulmonary
decompensation.

14. ETIOLOGY
Hereditary causes includes:
 Sickle cell anemia;
sickled RBCs are fragile, the mechanical trauma of
circulation causes hemolysis.
 Hereditary spherocytosis;
RBCs in this condition called spherocytes are more
fragile than disk-shaped RBCs therefore they break
down faster and more easily than normal RBCs.
 Deficiency of Glucose-6-phosphate dehydrogenase;
This enzyme is important in the metabolism of RBC in
the pentose pathway, deficiency results in increased
oxidative stress thereby RBCs break down prematurely.

15. ETIOLOGY CONTINUA….
Aquired causes includes:
 Infections e.g Malaria.
 Toxic chemicals and drugs.
 Blood transfusion reaction.
 Autoimmunity.
 Physical damage.
 Thallassemia.

16. CLINICAL MANIFESTATION
 Tachycardia.
 Dyspnea.
 Angina.
 Hemoglobinuria (dark urine).
 Jaundice.
 Leg ulcers.

17. DIAGNOSIS/INVESTIGATION
 Peripheral smear and reticulocyte count are the
most important tests to diagnose hemolysis.
 CBC (complete blood count).
 Urine tests.
 Bone marrow biopsy.
 Liver Function Test.

18. MANAGEMENT
Treatment may differ depending on the type of
hemolysis and may include:
 Corticosteroids (e.g in AIHA).
 Blood Transfusion.
 Erythropoietin Therapy.
 IVIG.
 Surgery (e.g Splenectomy).

19. APLASTIC ANEMIA
 Aplastic anemia is a syndrome of bone marrow
failure characterized by peripheral pancytopenia
and marrow hypoplasia.
 Pancytopenia comprises of reduction in WBCs,
RBCs and plateletes.

20. ETIOLOGY
 Autoimmune destruction.
 Radiation.
 Toxins.
 Drugs (e.g anti-seizures).
 Infections (e.g HIV).
 Genetic disorders.

21. CLINICAL MANIFESTATION
 Pallor.
 Headache.
 Palpitation, dyspnea.
 Fatigue.
 Foot swelling.
 Gingival bleeding, petechial rashes.
 Oropharyngeal ulcerations.

22. DIAGNOSIS/INVESTIGATION
Laboratory testing for suspected aplastic anemia
includes the following:
 Complete blood count.
 Peripheral blood smears.
 Biochemical profile.
 Serology for hepatitis and other viral entities.
 Bone marrow aspiration.
 Bone marrow biopsy.

23. MANAGEMENT
Management is according to the etiology and may
include:
 Immunosuppressive agents (e.g
methylprednisolone, equine antithymocyte globulin,
cyclophosphamide).
 Hematopoietic growth factors (filgrastim).
 Bone marrow transplant.

24. COMPLICATIONS OF ANEMIA IN GENERAL
 Shock.
 Hypotension.
 Motor or cognitive development delays in children.
 Coronary and pulmonary insufficiency.
 Pregnancy complication such as premature birth.

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