a reduced haemoglobin level Chronic anaemia is associated with ill health, loss of productivity, poorer mental activity, an increased susceptibility to disease & an increased risk of maternal and neonatal death Threshold for defining anaemia: gender Non-pregnant women pregnant women Children (yrs)  0.5-4.9  5-11.9  12-14.9 Men (>15yrs) amount (g/L) <120 <110 <110 <115 <120 <130

main causes 1. Nutritional - lack of iron, folic acid, vitamin B12, protein and vitamin A 2. Infection - helminths (worms). Malaria, schistosomiasis, AIDS, TB 3. Genetic disorders of haemoglobin - sickle cell diseases, thalassaemia, G6PD. The pathophysiological reasons for anaemia a) Decreased production b) Increased destruction (shorter RBC life span - haemolysis) or loss (bleeding) c) A combination of decreased production and shortened RBC life span d) Redistribution of RBCs in splenomegaly - "pooling" of RBCs in the spleen. A haematinic deficiency is due to one of three causes: 1. Decreased dietary intake 2. Impaired absorption 3. Increased loss or utilization

Anaemias are considered in three groups: Microcytic, hypochromic (MCV ˂78 fL) Normocytic, normochromic Macrocytic (MCV ˃100 fL) Microcytic, hypochromic anaemia (low MCV & MCH), A number of chemical tests may be used to differentiate between these disorders, which are listed in the table below summarized in the figure:

hypochromic red cells (Dimorphic .a genetic disorder of globin chain synthesis.Iron deficiency anaemia is due to:  An inadequate dietary iron intake  Increased loss of iron from: o gastrointestinal bleeding o increased menstrual blood loss o impaired iron absorption as in coelic disease (gluten sensitivity) o competition from gut parasites (plus increased blood loss) Anaemia of chronic disease is common in:  Chronic infection  Inflammation  Connective tissue diseases (e. The causes of microcytic hypochromic anaemia . rheumatoid arthritis)  neoplasia Severity of the anaemia depends on the time it has been present Thalassaemia trait .two populations of red cells)  Due to ineffective erythropoiesis. most commonly affecting the α or β globin chain. it may be severe and is generally refractory to treatment.g. Sideroblastic anaemia  seen in the elderly  usually a mild macrocytic anaemia with a variable population of small. iron deficiency may need to be excluded and frequently complicates the condition in pregnancy.

liberating about 20 mg of iron. each molecule can carry up to 2 atoms of iron. to reduce iron absorption and it reduces the level of iron in the plasma. o it is raised. as: i. In effect.Nutrition and the blood . iron loss is balanced by iron absorption Iron absorption and balance      takes place through the epithelial cells of the duodenum From a normal diet is just sufficient to compensate for the loss of 1-2 mg/day from desquamation of gut cells and menstruation. The rest is recycled. The overall controller of iron metabolism is HEPCIDIN. which is synthesised in the liver. Sources of iron There are 2 sources of iron: . with daily external losses of 1 mg or 2 mg. inflammation and neoplasia to limit the supply of iron to developing red cells. b) Iron is stored in tissue macrophages in the liver. largely back to the bone marrow for new RBC production."Haematinics" IRON . transferrin receptor 1 (TfR1) and ferritin a) Transferrin. about 20 mL of red cells are destroyed by bone marrow and splenic macrophages. the main carrier of iron in serum.a very common element. in infection. The amount of Iron absorbed is controlled by the iron level The rate of red cell production and the control of iron balance is at the level of absorption as there is no physiological mechanism for iron excretion. in response to cytokines. in men and women respectively. a water-soluble complex  Ferritin is present in the plasma and can be measured. o The level is low in persons with a normal haemoglobin level and in irondeficiency anaemia. Ferritin. but iron deficiency is the most common cause of anaemia Body iron distribution Free iron is toxic and must always be transported and stored bound to a protein: transferrin (Tf). Haemosiderin The iron in both ferritin and haemosiderin is in the ferric (Fe3+) form and must be reduced to the ferrous (Fe2+) form before it can be mobilized. The daily kinetics of iron      Plasma iron in a dynamic state continuosly circulates bound to transferrin with iron balance being finely maintained Each day. ii.  the amount bears an approximate relationship to the total body iron stores. Delivers iron to tissues that have transferrin receptors. bone marrow and spleen.

pregnancy/lactation. fortified bread and cereals. The development of IDA goes through well-recognized stages:    depletion of tissue iron stores iron-deficient erythropoiesis frank iron deficiency with a low haemoglobin level Reduced by Organic iron Ferric form Alkalis Phosphates & pyrates Tea. hypochromic anaemia (low MCV and MCH) Reduced serum iron. nuts. TfR is not an acute phase protein.coeliac disease. liver and fish non-haem iron: oatmeal. growth Excessive loss (chronic blood loss) . gastrectomy Intravascular haemolysis . inflammation or o malignancy is present. bran Decreased erythropoiesis Iron overload Inflammation (Hepcidin) Causes:      Inadequate dietary iron increased physiological requirement . hookworm Malabsorption . raised total-iron binding capacity.    haem iron: Meat (best source).renal excretion of iron Assessment of iron status      Microcytic. chocolate Foods rich in vitamin C enhance iron absorption Factors affecting Iron Absorption Increased by Inorganic iron Ferrous form Gastric acidity Vitamin C Iron deficiency anaemia Increased erythropoiesis Pregnancy Hypoxia Iron deficiency ( IDA ) The commonest cause of anaemia throughout the world. Ferritin is an acute phase protein) Raised transferrin receptor concentration (can differentiate IDA from anaemia of o chronic disease.GI bleeding. menorrhagia. unlike ferritin) . dried fruit.ferritin may be raised if infection. and a reduced transferrin saturation Low serum ferritin (caution. vegetables. red wine.

eggs and dairy produce. prematurity. spinach. mad Malabsorption: coeliac disease. Diet: animal products liver. food fads. ill. myelofibrosis. It is biochemically active when reduced to dihydrofolic acid (by hydrolysis) and then to tetrahydrofolic acid.100-200 pg/day Stores . alcoholics. jejunum resection. greens & nuts(cooking destroys) Requirements .5 mg (3-5 years) .MACROCYTIC ANAEMIA FOLIC ACID In nature. tropical sprue Increased requirement: pregnancy.nucleotide at right angles to the planar group iii) A cobalt atom linked to the corrin nucleus. the elderly. malignancy. An elevated level of homocysteine in folic acid deficiency (& B12) is a risk factor for coronary artery disease and other vascular disorders. contaminated vegetables Requirements . Bread/flour is now a fortified product. haemolytic anaemia. heart failure. ii) A ribo.1 pg/day Stores . folate antagonists.liver. folates are present as polyglutamates. chronic inflammation Increased urinary loss: long term dialysis. alcohol Folic acid is an important factor in the causation of neural tube defects (spina bifida and anencephaly) and folate therapy is recommended in pregnancy.       Folate deficiency causes a megaloblastic anaemia due to defective DNA synthesis Humans cannot synthesise folates Diet: present in most foods . Monoglutamate is very quickly absorbed Causes of deficiency:      Diet: the poor. yeast.10-25 mg (3-4 months supply) Absorption . Vitamin B12 Family of cobalamins (cobalt-containing) The B12 molecule is composed of: i) A planar corrin nucleus of 4 pyrrole rings. which humans cannot absorb.jejunum. fish. acute liver disease Drugs -anticonvulsants. MW 1355      Synthesised by bacteria An external source is required for humans.

peripheral neuropathy. nuclear abnormalities in all cell lines megaloblasts.Absorption: a) b) c) d) e) Food B12 released from protein by pepsin in stomach and binds to R-binder B12 released from R-binding protein in jejunum by pancreatic trypsin Intrinsic factor produced by gastric parietal cells B12/IF complex allows B12 absorption in terminal ileum (site of IF receptor) Transport: transcobalamin Function: A Coenzyme for 2 biochemical reactions   methyl B12 is a cofactor for methionine synthase for the methylation of homocysteine to methionine.hypercellular. Essential for DNA synthesis conversion of methylmalonyl CoA to succinyl CoA Clinical effects of vitamin B12 and folate deficiency:       Macrocytic. megaloblastic anaemia macrocytic anaemia neutropenia and hypersegmented neutrophils thrombocytopenia bone marrow . sub-acute combined degeneration of the spinal cord (not folate deficiency) . giant metamyelocytes) Vitamin B12 neuropathy .

tropical sprue. congenital selective B12 malabsorption . gastrectomy. fish tapeworm. Crohn's disease. congenital deficiency of IF (rare) Intestinal causes: Blind loop syndrome.Mechanisms and causes of vitamin B12 deficiency     Nutritional (Inadequate intake) . ileal resection. jejunal diverticula.Pernicious anaemia.vegans Inadequate secretion of Intrinsic factor .

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