ANEMIA

By

Mohamed M. Abdo Internal Medicine

Faculty of Medicine Suez Canal University

Anemia?

Production? Survival/Destruction?

General Principles

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.

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.

IRON METABOLISM ABSORPTION IN DUODENUM TRANSFERRIN TRANSPORTS IRON TO THE CELLS FERRITIN AND HEMOSYDERIN STORE IRON

10% of daily iron is absorbed

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)

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.

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”.

CAUSES OF IRON DEFICIENCY ANEMIA

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.

IRON DEFICIENCY ANEMIA

GENERAL ANEMIA’S SYMPTOMS: FATIGABILITY DIZZENES HEADACHE SCOTOMAS IRRITABILITY PALPITATION CHD, CHF

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.

  

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…

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.

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).

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.

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.

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).

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.

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.

GUM HYPERTROPHY AND HEMORRHAGE IN ACUTE MONOCYTIC LEUKEMIA

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.

IRON DEFICIENCY ANEMIACURE

PARENTERAL IRON SUBSTITUTION Bad oral iron tolerance (nausea, diarrhoea) Negative oral iron absorption test Necessity of quick management (CHD, CHF) 50 - 100 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

HEREDITARY HEMORRHAGIC TELANGIECTASIA

ANGULAR CHEILITIS

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.

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

The most likely diagnosis of this patient’s disorder is:

(A) Acute leukemia(B) Bacterial endocarditis(C) Thromboci thrombocytopenic purpura(D) Hemolytic uremic syndrome(E) Systemic Lupus erythematosus

SPLEEN INFILTRATED BY HODGKIN'S DISEASE