anaemia Flashcards

1
Q

define anaemia, what values are raised

A

reduction in haemoglobin concentration compared to healthy person of same age and gender

thus, Hb reduced, but also RBC and HCT usually-

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2
Q

temporary cause of anaemia

A

usually due to lower absolute haemoglobin, but can be due to increase in plasma volume- in healthy person this is temporary as excess fluid excreted

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3
Q

mechanisms of anaemia, NOT causes

A

lower production of RBC/haemoglobin in bone marrow

loss of blood

reduced lifespan of RBC

large spleen may cause pooling of RBC rather than in blood

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4
Q

cause of lower haemoglobin production in bone marrow

A

either reduced synthesis of haem (due to lack of iron) or globin ( due to thalassemia

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5
Q

classifying anaemia

A

based on cell size

microcytic, normocytic or macrocytic

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6
Q

causes of microcytic anaemia

A

lower haem synthesis (due to iron deficiency, or anaemia of chronic disease, where chronic inflammation occurs)

defect in globin synthesis (thalassemia), either alpha (lower alpha chain) or beta (lower beta chain) thalassemia

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7
Q

macrocytic anaemia

A

abnormal erythropoeisis where precursors of RBC produce haemoglobin but they don’t divide, so become large

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8
Q

macrocytic vs megaloblastic

A

macrocytic= increased cell size

one cause is megaloblastic erythropoeisis, where nucleus maturation delayed (DNA synthesis impaired), but cytoplasm keeps growing, so cell becomes large- thus megaloblast is an abnormal erythroblast (red blood cell precursor with nucleus)

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9
Q

another MECHANISM of macrocytic anaemia

A

premature release of cells from bone marrow- reticulocytes are larger than RBC, so if there are more of them, average cell size increases

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10
Q

causes of macrocytic anaemia

A

megoblastic anaemia due to B12/folic acid deficiency

drugs affecting DNA synthesis

liver disease/alcohol toxicity

recent major blood loss (loads of reticulocytes produced to combat blood loss)

haemolytic anaemia (increases reticulocytes)

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11
Q

mechanisms of normocytic anaemia

A

recent blood loss (body hasn’t responded yet)

failure of stem cells to produce red cells

pooling of red cells in spleen

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12
Q

causes of normocytic anaemia/ normochromic (ie normal synthesis of haem)

A

blood loss- peptic ulcer, esophageal varices and trauma due to accident

failure of production- renal failure (less erythropoetin), bone marrow failure or early stages of iron deficiency/anaemia of chronic disease

pooling- hypersplenism eg in cirrhosis where spleen enlarges

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13
Q

what is haemolytic anaemia and 2 causes

A

anaemia due to shorter lifespan of RBC (greater haemolysis= more RBC broken down), either due to intrinsic abnormality (issue with RBC itself) or extrinsic abnormality (something acting on normal RBC)

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14
Q

inherited vs acquired haemolytic anaemia and causes of each

A

inherited anaemia due to abnormalities in cell membrane (eg hereditary spherocytosis), haemoglobin (sickle cell) or enzymes (defect in glycolysis due to pyruvate kinase deficiency, G6P dehydrogenase deficiency)

acquired due to extrinsic factors- can be autoimmune (macrophages damage membrane), drugs can cause oxidant damage, and malaria can damage whole cell as well

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15
Q

intravascular vs extravascular haemolytic anaemia

A

intravascular occurs in circulation- acute damage to RBC

extravascular occurs when RBC removed by spleen

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16
Q

when to suspect haemolytic anaemia

A

abnormal red cells (eg more fragments, spherocytes)

more RBC breakdown (high bilrubin- can lead to gallstones/yellow eyes)

more bone marrow activity (more reticulocytes)

anaemia can’t be explained otherwise and is normochormic and normocytic/macrocytic

17
Q

hereditary spherocytosis and effect

A

inherited intrinsic defect of membrane- cells lose membrane in spleen so become like a sphere

these RBC are more rigid so are removed by spleen (extravascular haemolysis)- bone marrow responds by reticulocytosis: leads to haemolytic anaemia and bilrubin production= jaundice

18
Q

treatment of hereditary spherocytosis

A

splenectomy- only done in severe cases

because bone marrow very active, folic acid deficiency can occur, so diet is important, and folic acid supplementation given as well

19
Q

G6P dehydrogenase importance

A

needed for pentose phosphate shunt- protects RBC from oxidant damage (oxidants either intrinsic from blood or extrinsic due to broad beans, chemicals and drugs)

20
Q

effect of G6P dehydrogenase deficiency and who usually vulnerable

A

gene for G6PD is on X chromosome, so usually occurs in males

causes intravascular haemolysis due to oxidants- forms irregularly contracted cells, and also denatured haemoglobin called heinz bodies

21
Q

treatment of someone with G6PD deficiency

A

blood transfusion may be needed- then diet restriciton, awareness of harmful drugs/chemicals important

22
Q

autoimmune haemolytic anaemia

A

autoantibodies bind to red cell antigens, which is recognised by splenic macrophages (complement often present as well), which remove bits of cell membrane= spherocytosis

combination of rigidity of spherocytes and recognition by macrophages leads to removal by spleen

23
Q

diagnosing autoimmune haemolytic anaemia

A

spherocytes and increased reticulocytes

detection of autoanitbodies to red cell antigens

24
Q

treatment of autoimmune haemolytic anaemia

A

immunosuppressive drugs like corticosteroids

splenectomy for severe cases

25
Q

microangiopathic haemolytic anaemia causes and treatment

A

hypertension- treat this

antibody in plasma that causes fibrin deposition in small blood vessels- treat by plasma exchange