1. ANEMIA Mohamed M. Abdo By Internal Medicine Faculty of Medicine
Suez Canal University

2. Anemia?
Production?
Survival/Destruction?

3. General Principles Anemias are a dynamic process.
Anemia is a sign, not a disease.
Anemias are a dynamic process.
Its never normal to be anemic.
The diagnosis of iron deficiency anemia mandates further work-up.

4. Introduction:
Anemia is a very common medical problem and affects different age groups including children, adults and older age groups.
Anemia is not a specific diagnosis, it is rather a manifestation of an underlying disorder.
In one study anemia affects 20-40% of hospitalized patients.

5. 10% of daily iron is absorbed
IRON METABOLISM
ABSORPTION IN DUODENUM
TRANSFERRIN TRANSPORTS IRON TO THE CELLS
FERRITIN AND HEMOSYDERIN STORE IRON
10% of daily iron is absorbed

6. Most body iron is present in hemoglobin in circulating red cells
The macrophages of the reticuloendotelial system store iron released from hemoglobin as ferritin and hemosiderin
Small loss of iron each day in urine, faeces, skin and nails and in menstruating females as blood (1-2 mg daily)

7. Pathogenesis:
A circulating erythrocyte has an average life span of 120 days.
RBCs are non-nucleated, non-dividing cell.
Erythropoiesis is controlled by a negative feed-back mechanism.
Tissue hypoxia increases the production of erythropoietin.
90% of erythropoietin is of renal origin where as 10% are of hepatic origin.

8. Pathogenesis:
Erythropoietin acts by preventing apoptosis “programmed cell death” of erythoid precursors and stimulates their proliferation.
Under normal conditions, the rate of RBCs production and destruction is nearly constant.
It’s apparent that the main mechanisms of anemia are;
Decreased RBCs production “aplastic anemia”.
Increased RBCs destruction “hemolytic anemia”.
RBCs loss “anemia of blood loss, deficiency anemias”.

9. CAUSES OF IRON DEFICIENCY ANEMIA

10. Presentation: Anemia usually presents in different ways.
Asymptomatic, accidentally discovered “most common”.
General weakness, easy fatigue, poor concentration.
Behavioral changes in children.
Pica, a perverted appetite towards dirt.
Severe cases are associated with palpitation, dyspnea and anemic heart failure.

11. IRON DEFICIENCY ANEMIA
GENERAL ANEMIA’S SYMPTOMS:
FATIGABILITY
DIZZENES
HEADACHE
SCOTOMAS
IRRITABILITY
PALPITATION
CHD, CHF

14. Clinical examination:
Clinical signs varies according to the cause, but usually there pallor.
Koilonychia with iron deficiency.
Jaundice with hemolytic anemia.
Splenomagly with hypersplenism.
Leg ulcer with sickle cell anemia “vaso-occlusion”.
Box shape skull and bronze discoloration with thalassemia.
Gum discoloration “blue lines” in anemia of lead poisoning.

17. Approach to diagnosis:
Good history taking will reveal the cause of anemia in most cases.
Menorrhagia is a common cause in females.
History of NSAIDs ttt and occult blood loss.
Family history of hemolytic anemia.
History of chronic systemic disease as renal failure, CLD…

18. Approach to diagnosis:
After history and examination, you should have performed an idea about the nature of anemia.
Then ask the patient to do CBC.
You will have either;
(A) Microcytosis: mean corpuscular volume less than 80 f.c.
Most common causes are:
Iron deficiency anemia.
Thalassemia.
Lead poisoning.

19. The reticulocyte count
Increased reticulocytes (greater than 2-3% or 100,000/mm3 total) are seen in blood loss and hemolytic processes, although up to 25% of hemolytic anemias will present with a normal reticulocyte count due to immune destruction of red cell precursors.
Retic counts are most helpful if extremely low (<0.1%) or greater than 3% (100,000/mm3 total).

20. The reticulocyte count
To be useful the reticulocyte count must be adjusted for the patient's hematocrit. Also when the hematocrit is lower reticulocytes are released earlier from the marrow so one can adjust for this phenomenon. Thus:
Corrected retic. = Patients retic. x (Patients Hct/45)
Reticulocyte index (RPI) = corrected retic. count/Maturation time
(Maturation time = 1 for Hct=45%, 1.5 for 35%, 2 for 25%, and 2.5 for 15%.)
Absolute reticulocyte count = retic x RBC number.

21. Approach to diagnosis:
(B) Normocytosis:
Acute blood loss.
Hemolytic anemia.
Aplastic anemia.
Anemia of chronic disease.
(C) Macrocytosis:
B12 and folate deficiency.
Liver disease.
Myelodysplasia.
Myxoedemia.
Alcohol methotrexate toxicity.

22. Approach to diagnosis:
(D) Dimorphic picture:
When 2 causes act together e.g. parasitic infestation causing iron and folate deficiency.
Here the red cell distribution width (RDW) increases which measures the variation of RBCs size.
The next step is to look at the reticulocytic count.
Increased reticulocytic count points to hemolytic anemia or anemia of blood loss.
Low reticulocytic count points to bone marrow disorder e.g. bone marrow failure, aplastic anemia or secondary to drugs (e.g. cholera mephinicol).

23. Approach to diagnosis:
Increased serum ferritin and bilirubin points to hemolytic anemia.
Decreased s. iron and increased TIBC in iron deficiency anemia. There is also decreased transferrin saturation.
When the above measures fail to establish diagnosis, bone marrow aspiration is mandatory.
Bone marrow aspiration will reveal the uncommon causes of anemia such as myelodysplasia, myelosclerosis and lymphoproliferative disorders.

24. Pseudo-anemia: Certain conditions leads to expansion of plasma volume.
These includes pregnancy, volume over-load and certain drugs as interleukins and colony stimulating factors.
This type usually resolves after delivery and diuresis respectively.

25. GUM HYPERTROPHY AND HEMORRHAGE IN ACUTE MONOCYTIC LEUKEMIA

26. Management: Treatment of anemia is essentially ttt of the cause.
Oral or parenteral iron in iron deficiency anemia.
Recombinant erythropoietin for anemia of renal failure.
Colony stimulating factors for aplastic anemia, cyclosporine may be also used.
Bone marrow transplantation for cases not responding to cyclosporine therapy and it is the ttt of choice in lymphoproliferative disorders.
Anti-parasitic ttt for helminthic infestation.

27. IRON DEFICIENCY ANEMIA CURE
PARENTERAL IRON SUBSTITUTION
Bad oral iron tolerance (nausea, diarrhoea)
Negative oral iron absorption test
Necessity of quick management (CHD, CHF)
mg daily
I.v only in hospital (risk of anaphilactic shock)
I.m in outpatient department
iron to be injected (mg) = (15 - Hb/g%/) x body weight (kg) x 3

29. HEREDITARY HEMORRHAGIC TELANGIECTASIA

30. ANGULAR CHEILITIS

31. Case #1
A 34- year old woman presents to your office with a 1-week history of generalized weakness, easy fatiguability and shortness of breath. One hour ago, she developed a headache and left hemiparesis. Two days ago, she noted easy bruisability and bleeding gums. Three days ago, she developed a fever. A history reveals that she had no previous serious illnesses and review of systems is normal.

32. Case 1 Physical Exam: Temp: 40°, 120/70, 70, 16, 96% on RA
Gen: Alert oriented, but appears weak
petechiae on soft palate with some fresh blood on gingiva
high-pitched holosystolic murmur
Neuro: mild left hemiparesis with hyperactive reflexes and positive babinkski on the left
Skin: scattered pupuric lesions on lower extremities

33. The most likely diagnosis of this patient’s disorder is:
Acute leukemia
Bacterial endocarditis
Thromboci thrombocytopenic purpura
Hemolytic uremic syndrome
Systemic Lupus erythematosus

34. SPLEEN INFILTRATED BY HODGKIN'S DISEASE

35. Thank You