A NAEMIA ’ S Shannon and Rick

A NAEMIA A Hb deficit of whole-body circulating blood volume Dependant on age and gender Creates the risk of tissue hypoxia

C LASSIFYING A NAEMIA Cause Failure of RBC production Loss/destruction of RBC’s Morphology Cell Size Microcytic Normocytic Macrocytic Cell Shape Poikilocytes Sickle cell Cell Colour Normochromic Hypochromic

A NAEMIA OF B LOOD L OSS Acute Blood loss + IV therapy  anaemia of dilution ↓PCV Normochromic, normocytic  macrocytic, hypochromic (reticulocytes from ↑ EPO) Chronic Rate of blood loss > erythropoeisis or iron stores depleted

H AEMOLYTIC A NAEMIA Intravascular (vessels) vs. Extravascular (spleen) Premature RBC destruction ↑EPO  ↑erythropoeisis  marrow erythroid hyperplasia + Reticulocytosis ↑ Hb degradation products  mild jaundice Splenomegaly

H EREDITARY S PHEROCYTOSIS Protein defect  lipid destabilization and membrane fragility  membrane loss  altered shape to accommodate volume  Spleen food Spherical, normochromic ↑MCHC due to dehydration Tx.: Splenectomy, folate, genetic counselling, transfusinon (w. iron-chelator), bone marrow transplant

G6PD D EFICIENCY Oxidant damage Recessive X-linked trait + infection (stress) Intra/extravascular Normochromic, normocytic Tx. : stop offending drugs, treat infection, transfusion as required.

T HALASSEMIA Varying types, symptoms dependent. Reduced or absent α/β globin chains due to recessive inherited genetic traits. Unimpaired chain gets put into overdrive. Ineffective erythropoesis (apoptosis in marrow), haemolysis, decreased O2 carrying capability Hypochromia, microcytic

S ICKLE C ELL ANAEMIA Abnormal Hb that crystallizes once offloaded the oxygen: point mutation in β globin Changed shape leads to removal in spleen or impairment of circulation Reversible. Normochromic, sickle-shaped cells due to fibres.

I MMUNOHEMOLYTIC A NAEMIA Type II hypersensitivity (Ab and complement attach on  lysis/phagocytosis) Normochromic, normocytic Tx. : remove offending source (drug, chemical, environment), splenectomy, corticosteroids.

P AROXYSMAL N OCTURNAL H EMOGLOBINURIA Mutation in gene for an enzyme essential for cell membrane synthesis. Complement (more active at night) says “whats up with this cracker?” and takes him out Tx. : Immunosuppressive drugs, bone marrow transplant.

A NAEMIA ’ S OF D IMINISHED E RYTHROPOIESIS Megaloblastic (Pernicious) Anaemia Megaloblastic (folate Deficiency) Anaemia Iron Deficiency Anaemia Anaemia of Chronic Disease Aplastic Anaemia

P ERNICIOUS A NAEMIA AND F OLATE D EFICIENCY A NAEMIA Vit B12 deficiency (potentially due to lack of parietal cells. Vit B9 deficiency. Megaloblastic (normochromic, macrocytic – due to disabling of mitosis) Tx. B12/B9

I RON D EFICIENCY A NAEMIA Hypochromic, microcytic anaemia. Hb is not made, hence no O2 transport. Lots of common signs and symptoms Check iron tests Tx: iron! Beware haemochromotosis.

A NAEMIA OF C HRONIC D ISEASE Cytokines  ↑hepatic hepcidin  inhibit ferriportin.  no iron delivered to developing RBC’s Normochromic/normocytic or hypochromic/microcytic Ferritin should be normal/ high (diff. to iron deficiency), TIBC low or normal

A PLASTIC A NAEMIA Bone marrow not having enough RBC progenitors to replenish aged RBC’s. Autoimmune destruction, drugs, cancer. Pancyopenia symptoms Tx. : immune suppression + marrow transplant and supportive therapy

S YMPTOMS Glossitis papillae atrophy due to high turn over of mucosal cells, is very sensitive to nutritional deficiencies. Reveals vasculature below, and can lead to inflammation. Easily fatigued/Tiredness Lack of O2 carrying ability of the blood due to lack of circulating Hb means not enough O2 available for aerobic metabolism to occur. Tachypnea due to above, therefore resp rate is increased in an effort to accommodate for this and ‘get more O2 in” Tachycardia as above again, in an effort to ‘deliver’ more O2 to O2 starved sites. Koilonychia no idea why we get this, we just do.