Case 3

Large blood loss

Water shift from interstitial → plasma

Haemodilution,

↓ Haematocrit

↓ Oxygenation

Haemorrhagic Anaemia

Billirubin accumulation, jaundice

Juxtoglomerular apparatus in kidney

↑ Erythropoietin

↑ Proliferation and premature release of reticulocytes

Remnants of nucleus and organelles in blood film

Abnormal GI tract bleeding

Heavy menstrual bleeding

↓ Ferritin

↓ Haemosiderin

↓ Iron stores, serum iron, ferritin, transferrin saturation

↑ Erythroid activity in bone marrow

Hypochromic and microcytic RBCs

↓ Hb, MCV, MCHC;

↑ RBCWD

↓ Haemoglobin content in RBC

↓ α-globin production

Deletion mutation of α-globin alleles

Consistent RBCWD

Thalassemia

(α and β variants)

Iron deficiency anaemia

Pallor, fatigue

Haemolytic

Anaemia

Activation of monocytes, T-cells

Inflammatory stimulus

↑ Hepcidin synthesis, consequent

↓ Ferroportin

Normal serum ferritin levels;

↓ Serum iron

↓ Iron availability, despite high storage supply

↓ Normal Hb values until inflammation is resolved

↓ Erythropoietin

↓ Erythropoiesis

Inflammatory mediators

Anaemia of chronic inflammation/

disease

Normocytic, immature cells

Vegetarian diet, insufficient dietary iron

Chronic conditions

Malaena

Haemorrhoid

Fatigue, pallor

Darker urine

Oral iron replacement therapy

Intravenous iron replacement therapy

Iron chelation therapy to avoid haemochromatosis

↓ β-globin production

Deletion mutation of β-globin alleles

Folic acid

supplementation

Treatment of underlying disease

Corticosteroids

Correction of avenue of bleeding

Correction of abnormal RBC breakdown

Abnormal breakdown of RBCs

Microcytic RBCs with chronic bleeding

Inherited conditions causing RBC membrane defects

Autoimmune diseases

Peptic ulcer

Epithelial injury

Diffusion of H+ across gastric mucosa

H. pylori infection attacks gastric mucous

Bloody stool

Tenderness of epigastrum

H. pylori produces urea, detected in urease test

Triple therapy

Diet and lifestyle