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MEH > Anemia > Flashcards

Anemia Flashcards

1
Q

Anaemia

A

A haemoglobin concentration lower than normal range.

Anaemia is a manifestation of an underlying disease, not a diagnosis in itself.

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2
Q

Koilonychia

A

Spoon shaped nails, caused by iron deficiency.

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3
Q

Angular stomatitis

A

Inflammation of corners of the mouth, caused by iron deficiency.

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4
Q

Glossitis

A

Inflammation and depapillation of tongue, caused by vitamin B12 deficiency.

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5
Q

Abnormal facial bone development

A

Associated with thalassemia, due to expansion of haematopoietic tissues into skull and facial bones - extramedullary haemopoiesis.

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6
Q

Erythropoiesis

A

Red blood cell production.

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7
Q

Erythropoietin (EPO)

A

Hormone produced by interstitial cells in kidney. It stimulates RBC production in the bone marrow.

In negative feedback loop ie low blood oxygen = more EPO produced by kidney and released into bloodstream = stimulates RBC production.

Therefore anaemia can result from chronic kidney disease or bone marrow’s inability to respond to EPO.

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8
Q

Myelofibrosis

A

Bone marrow infiltrated by cancer cells or fibrous tissue = number of normal haemopoietic cells is reduced.

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9
Q

Myelodysplastic syndromes

A

Rare form of blood cancer where abnormal clones of marrow stem cells limit the capacity to make red and white blood cells.

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10
Q

Sideroblastic anaemia

A

Body produces enough iron but is unable to put it into haemoglobin. Defects in haem pathway can lead to this.

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11
Q

Haemolytic anaemia - causes and symptoms

A

RBC’s are destroyed faster than they are made. Caused by either inherited factors or acquired damage.

Inherited factors eg glycolysis defect, G6PDH deficiency, Hb defect (sickle cell)

Acquired damage eg mechanical damage, heat damage (severe burns), oxidant damage

Symptoms: splenomegaly (overwork of red pulp), accu. of bilirubin = jaundice, and pigment gallstones.

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12
Q

Causes of haemolytic anemia

A

Inherited - mutations in genes coding for proteins involved in interaction between plasma membrane and cytoskeleton - cells are less flexible, more easily damaged.
They break up in the circulation or are removed more quickly by RES (spleen).
—Eg hereditary spherocytosis

Acquired damage - mechanical damage eg shear stress as cells pass through defective heart valve; cells snagging on fibrin strands in small blood vessels where increased activation of clotting cascade.
—Eg microangiopathic haemolytic anaemias
- heat damage from severe burns (dehydration)
- osmotic damage (drowning in freshwater)

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13
Q

Hereditary spherocytosis
Causes?
Treatment?

A

Inherited blood disorder where RBC’s have a spherical shape rather than a biconcave shape. They are more fragile and get stuck in capillaries as they are less flexible.

Proteins involved: ankyrin, band 3, protein 4.2, beta-spectrin, alpha-spectrin - defects in these cause disease.

Caused by mutation in a gene coding for one of these proteins, which are involved in interactions between the plasma membrane and cytoskeleton.

Splenectomy to limit the effects of the disease.

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14
Q

Microangiopathic haemolytic anemias

A

Anaemia that results from mechanical damage.
eg Shear stress as cells pass through defective heart valve; cells snagging on fibrin strands in small vessels with increased activation of clotting cascade (DIC).

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15
Q

Schistocytes

A

Fragments of RBC’s resulting from mechanical damage.

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16
Q

Pyruvate kinase

A

Catalyses intermediate of glycolysis into pyruvate; the final enzyme in glycolysis.

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17
Q

Pyruvate kinase deficiency

A

As RBC lack mito, they rely on glycolysis for energy production. Defective glycolytic pathway causes RBC to become deficient in ATP and they undergo haemolysis.

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18
Q

G6PDH deficiency

A

Catalyses glucose 6P into 6-phosphogluconate, generating NADPH. Occurs in PPP.
NADPH needed to protect against oxidative stress as NADPH is used to reduce GSSG back to 2GSH, which donates H+ and e- to ROS.

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19
Q

Haemolysis

A

Break down of RBC.

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20
Q

Heinz bodies

A

Aggregates of cross-linked haemoglobin - due to protein damage eg due to ROS.

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21
Q

Reticuloendothelial system (RES)

A

Part of immune system that consists of phagocytic cells located in reticular connective tissue - the cervical lymph nodes, diaphragm, liver, thymus, axillary lymph nodes, spleen and inguinal lymph nodes.

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22
Q

Intravascular/ extravascular haemolysis

A

Damage occurring within the blood vessels/ within the RES.

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23
Q

Autoimmune haemolytic anaemia

A

Autoantibodies bind to red cell membrane proteins, causing them to be recognised by macrophages in the spleen and are destroyed.

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24
Q

Thalassemia

A

Inherited disorders resulting from decreased or absent alpha or beta globin chain production.

Imbalance in composition of Hb alpha2 beta2 tetramer results in defective microcytic hypochromic red cells.

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25
Q

Microcytic

A

Smaller than average RBC’s due to insufficient Hb.

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26
Q

Hypochromic

A

RBC’s are less pigmented than normal, usually due to decreased Hb.

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27
Q

Extramedullary haemopoiesis

A

Formation and activation of blood cells outside bone marrow, eg in spleen and liver.

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28
Q

Reticulocytosis

A

Increase of reticulocytes in blood.

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29
Q

Reticulocytes

A

Immature RBC’s.
They have no nucleus and need to eliminate remaining mitochondria, but do have some residual RNA.

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30
Q

Macrocytic

A

RBC’s that are larger than normal.

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31
Q

Normocytic

A

RBC’s contain a lower than normal amount of Hb.

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32
Q

Macrocytic anaemia

A

Anaemias where RBC’s are larger than normal.

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33
Q

Megaloblastic anaemia

A

Interference with DNA synthesis during erythropoiesis causes development of nucleus to be retarded in relation to maturation of cytoplasm.

Cell division delayed and erythroblasts continue to grow and form megaloblasts which give rise to larger red cells.

Thymidine deficiency - in its absence, uracil is incorporated. DNA repair enzymes detect errors and constantly repair by excision
= asynchronous maturation between nucleus and cytoplasm where the nucleus does not fully mature.

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34
Q

Macronormoblastic erythropoiesis

A

Normal development of nucleus and cytoplasm but erythroblasts are larger than normal and give rise to larger RBC.

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35
Q

‘Stress’ erythropoiesis

A

High reticulocyte count, and high level of erythropoietin, which leads to expanded and accelerated erythropoiesis.

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36
Q

Folate

A

Synthetic form is folic acid.

Absorbed mainly by duodenum and jejunum. Converted to FH4 by intestinal cells. Taken up by liver which acts as a store.

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37
Q

Folate deficiency - causes

A

Caused by: poor diet; increased requirements eg pregnancy; disease of duodenum and jej; drugs eg methotrexate; alcoholism; urinary loss of folate in liver disease and heart damage.

! Folic acid taken before conception/during1st 12 weeks of pregnancy prevents most neural tube defects.

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38
Q

What prevents most neural tube defects in babies and why?

A

Folic acid

Vit B12 deficiency is associated with focal demyelination, as it is needed for myelin sheath production.

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39
Q

What is vitamin B12 needed for?

A

Required for normal erythropoiesis.
Essential for normal function and development of CNS.

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40
Q

Haptocorrin
*

A

Produced by salivary glands; protects vit B12 from acid degradation in stomach.

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41
Q

Receptor-mediated endocytosis

A

Protein on transport vesicle binds to receptor on cell

In vit B12 absorption and cholesterol absorption via LDLs.

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42
Q

Transcobalamin
*

A

Vit B12 binds to transcobalamin in blood and is transported around bloodstream.

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43
Q

Pernicious anaemia

A

A cause of vit B12 deficiency:
Decreased or absent intrinsic factor (IF) which causes progressive exhaustion of vit B12 reserves.

An autoimmune disease; 2 types of antibody - blocking Ab that blocks binding to B12 and IF; binding Ab prevents receptor mediated endocytosis.

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44
Q

3 most common causes of vit B12 deficiency

A

-Dietary deficiency
-Pernicious anaemia (lack of intrinsic factor)
-Diseases of the ileum eg Crohn’s disease

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45
Q

Intrinsic factor (IF)

A

Binds to vit B12 which is then taken up by the cell.

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46
Q

How do B12 and folate link?
*

A

Lack of B12 will ‘trap’ folate in the stable methyltetrahydrofolate form, prevents its use in other reaction eg synthesis of thymidine for DNA synthesis.

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47
Q

Why do B12 and folate deficiency cause megaloblastic anaemia?

A

Both deficiencies lead to thymidine deficiency. In its absence, uracil is incorporated. DNA repair enzymes detect errors and constantly repair by excision
= asynchronous maturation between nucleus and cytoplasm where the nucleus does not fully mature.

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48
Q

Anisopoikilocytosis

A

Variance in size and shape of RBC.

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49
Q

Ovalocytes

A

Oval shaped RBC.

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50
Q

Hypersegmented neutrophils

A

6 or more lobes in nuclei rather than normal 2-5.

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51
Q

Pancytopenia

A

Low levels of all cell lines in blood - low platelets, low RBC, low WBC.

52
Q

Lactate dehydrogenase

A

Converts lactate to pyruvate, generating NADH.

Raised levels in blood can be raised due to increased cell destruction and production.

53
Q

How to test for megaloblastic anaemias?

A

Vit B12 levels in blood - this can be unreliable as other factors affect it.

Check for anti-intrinsic factor antibodies.

54
Q

Microcytic anaemias

A

RBCs smaller than normal - reduced rate of Hb synthesis. Cells often paler than normal - hypochromic.

55
Q

Causes of microcytic anaemias

A

TAILS - thalassaemia, anaemia of chronic disease, iron deficiency, lead poisoning, sideroblastic anaemia

Reduced globin chain synthesis - alpha and beta thalassaemia

Reduced haem synthesis - AILS

56
Q

Ferrous iron

A

Fe2+ - reduced form

Body uses this form, it is absorbed from diet.

57
Q

Ferric iron

A

Fe3+ - ferric form

Ferric form is icky - body doesn’t use this form. Must be reduced to ferrous form before being absorbed from diet.

58
Q

Reductase

A

Involved in dietary absorption of iron. (step 1)

Protein in plasma membrane of apical surface of enterocyte that reduces Fe3+ to Fe2+ within chyme (acidic fluid from stomach containing partially digested food).

Vit C needed for this to donate e-.

59
Q

DMT1

A

Involved in dietary absorption of iron. (step 2)

Protein in plasma membrane of enterocyte that transports Fe2+ into the cell.

60
Q

Ferritin

A

Involved in dietary absorption of iron. (step 2b)

For iron storage.

It is a blood protein that contains Fe3+. Fe2+ is converted into Fe3+ and bound to protein.

61
Q

Ferroportin

A

Involved in dietary absorption of iron. (step 3)

Transmembrane protein that transports Fe2+ into the blood across the basolateral surface of enterocytes.

62
Q

Hepcidin

A

Involved in dietary absorption of iron. (step 3b)

Inhibits ferroportin so as to trap iron in the cell. Excreted by the liver.

In functional iron deficiency, iron is present but trapped in enterocytes - overexpression of hepcidin. Causes microcytic hypochromic RBCs.

Increased production can be caused by release of cytokines by immune cells.

63
Q

Hephaestin

A

Involved in dietary absorption of iron. (step 4)

Protein in membrane of enterocyte in basolateral surface that oxidises Fe2+ to Fe3+.

64
Q

Transferrin

A

Involved in dietary absorption of iron. (step 5)

Transport protein that transports iron in blood around body by binding to 2 Fe3+ ions.

Fe3= bound to transferrin called plasma iron pool.

65
Q

How does vit C affect iron absorption?

A

Increases iron absorption, as it helps to reduce ferric to ferrous iron.
Also prevents the formation of insoluble iron compounds.

66
Q

Haemosiderin

A

A form of stored iron - aggregates of clumped ferritin particles.
Insoluble
Accumulate in macrophages, esp. in liver, spleen and marrow.

Excess iron is deposited in organs as haemosiderin.

67
Q

Kupffer cell

A

Liver macrophages

68
Q

Enterocyte

A

A cell of the intestinal lining.

69
Q

Describe how anaemia of chronic disease occurs

A

Inflammatory condition eg rheumatoid arthritis
= Cytokines released by immune cells.

= 1 Increased production of hepcidin by liver
(2 inhibition of erythropoietin production in kidneys)
= Inhibition of ferroportin by interleukin 6
= Decreased iron released from RES + decreased iron absorbed from gut
= Plasma iron reduced
= Inhibition of erythropoiesis in bone marrow
= Anaemia

70
Q

Test for iron deficiency

A

Plasma ferritin
- reduced = iron deficiency
- normal or increased = does not exclude iron deficiency but doesn’t indicate for definite

CHr (reticulocyte haemoglobin content) used to test for functional iron deficiency.

71
Q

Treatment for iron deficiency

A

1st - diet
2nd - oral iron supplements
3rd - IM iron injections, IV iron
4th - blood transfusion (only in severe cases)

Response that it’s working = 20g/L rise in Hb in 3 weeks

72
Q

Transfusion associated haemosideris

A

Disease that results in excess iron, caused by repeated blood transfusions which give a gradual accumulation of iron.

Treat with iron chelating agents eg desferrioxamine.

73
Q

Hereditary haemochromatosis

A

Disease that results in excess iron; an autosomal recessive disease caused by mutation in HFE gene.

Mutated HFE results in loss of negative influences on iron uptake and absorption. It normally reduces affinity of transferrin receptor, and promotes hepcidin expression.

Treat with venesection.

74
Q

Methotrexate

A

Inhibits folate; can lead to pancytopenia

75
Q

Haemoglobinopathies

A

Inherited disorders, typically autosomal recessive, where either globin gene mutation alters the structure, function or stability of the Hb tetramer, or there is reduced expression of normal globin chains.

Abnormal globin chain variants = sickle cell disease

Reduced or absent expression of normal globin chains = thalassaemias

76
Q

Fetal Hb

A

HbF - the main form just before birth.

2 alpha chains, 2 gamma chains.

Has a higher affinity for oxygen that HbA.

77
Q

Thalassaemias

A

Reduced expression of normal globin chains.
A heterogenous group of genetic disorders.

Alpha thalassaemia - alpha chain gene expression affected
Beta thalassaemia - beta chain gene expression affected

78
Q

Alpha thalassaemia

A

Caused by deletion of alpha-globin genes.

1 deleted - silent carrier
2 deleted - alpha-thalassaemia trait (minimal or no anaemia)
3 deleted - Hb H disease (moderately severe)
4 deleted - hydrops fetalis (severe, usually intrauterine death)

79
Q

Beta thalassaemia

A

Caused by mutation on beta globin gene, rather than deletion.

Beta thalassaemia trait - usually asymptomatic (heterozygous)
Beta thalassaemia intermedia - severe anaemia (heterozygous, some mild variants of homozygous)
Beta thalassaemia major - severe transfusion-dependent anaemia (homozygous)

80
Q

Thalassaemia - what do the RBC look like? Why?

A

Hypochromic and microcytic - low Hb.
Anispoikilocytosis with target cells, nucleated RBC and Heinz bodies.

Excess of unaffected globin chain => defective nature of RBC - Hb aggregates get oxidised and result in:

  • premature death of erythroid precursors in bone marrow —> ineffective erythropoiesis
  • excessive destruction of mature RBC in spleen

Therefore thalassaemia is a form of haemolytic anaemia.

81
Q

Iron overload; why?

A

Major cause of premature death.

Iron overload occurs due to:
- excessive absorption of dietary iron due to ineffective haemopoiesis
- repeated blood transfusions required to treat anaemia

82
Q

Iron overload; treatment?

A

Iron chelation (delays iron overload).

83
Q

Sickle cell - 3 types of crises

A
  1. Vase-occlusive
    Painful bone crises; organ - chest, spleen
  2. Aplastic - failure of organ to function normally (often triggered by parvovirus)
  3. Haemolytic
84
Q

The spleen in sickle cell vs thalassaemia

A

In sickle cell: spleen infarction resulting in hyposplenism as spleen necrotises

In thalassaemia: splenomegaly due to splenic pooling

85
Q

Key lab findings in haemolytic anaemia

A

Raised reticulocytes (marrow tries to compensate)
Raised bilirubin (haem breakdown)
Raised LDH (red cells contain a lot of this)

86
Q

Hereditary eliptocytosis

A

RBC are elliptical rather than biconcave.

Caused by spectrum defect most commonly.
(Can also be defects in band 4.1, band 3 and glycophorin C proteins)

87
Q

Hereditary pyropoikilcytosis

A

Severe form of hereditary elliptocytosis.

Caused by spectre defect.

Abnormal sensitivity of RBC to heat.

88
Q

How can haemopoiesis go wrong? (Overview)

A

Overproduction:
- myeloproliferative disorders/ neoplasms

Underproduction:
- aplastic anaemia
- thrombocytopenia

89
Q

Myeloproliferative disorders

A

Aka myeloproliferative neoplasms.

These disorders involve the dysregulation at the multipotent haemopoietic stem cells.

  • essential thrombocytopenia
  • polycythaemia vera
  • myelofibrosis
  • chronic myeloid leukaemia
90
Q

Features of myeloproliferative disorders

A

Overproduction of one or more blood elements.
Hyper cellular marrow/ marrow fibrosis - fewer fat spaces/ laying down fibrous tissue
Cytogenetic abnormalities
Extramedullary haemopoiesis
Increased tendency to bleed or bruise

91
Q

Polycythaemia vera

A

Too many RBC.

High haematocrit
Causes arterial thrombosis (strokes clots, angina)
Venous thrombosis
Haemorrhage into skin or GI tract due to high pressure
Pruritis (itchy)
Splenomegaly

Treat with venesection and aspirin, manage CVS risk factors

92
Q

Polycythaemia

A

An increase in circulating RBC concentration typified by a persistently raised haematocrit.

93
Q

Causes of polycythaemia

A
  • Relative = normal RBC mass with less plasma volume (dehydration)
  • Absolute = increased RBC mass
    — Primary = polycythaemia vera
    — Secondary = driven by erythropoietin production
    — Physiologically appropriate - in response to tissue hypoxia
    — Physiologically inappropriate
94
Q

Causes of secondary polycythaemia

A

Physiologically appropriate - EPO drive increased
- central hypoxia (smoking, training at altitude eg) - less O2 reaching tissues
- renal hypoxia (renal artery stenosis, polycystic disease) - kidney has decreased blood supply so produces more EPO to counteract this

Physiologically inappropriate - cancers secrete EPO, eg hepatic Elul are carcinoma, renal cell cancer, uterine tumours, phaeochromocytoma
- all produce ectopic EPO

95
Q

Essential thrombocythaemia

A

= High platelet count that is not caused by another health condition

A genetic condition (mutations in Jak2 and CALR)

Large and excess megakaryocytes in bone marrow

Treat with aspirin, any CVS risk factors should be managed, reduce platelet count with hydroxycarbomide.

96
Q

Megakaryocytes

A

They are hematopoietic cells, which are responsible for the production of blood platelets.

97
Q

Causes of high platelet count

A

Infection - cytokines increase thrombopoietin production, which increases megakaryocyte production, so more platelets are made.
Inflammation
Tissue injury
Haemorrhage
Cancer
Redistribution of platelets - post-splenectomy and hyposplenism

98
Q

Thrombocythaemia vs thrombocytosis

A

Thrombocythemia refers to a high platelet count that is not caused by another health condition. This condition is sometimes called primary or essential thrombocythemia.

Thrombocytosis refers to a high platelet count caused by another disease or condition.

99
Q

Myelofibrosis

A

Heavily fibrotic tissue - little space for haemopoiesis so fewer haemopoietic cells - fewer RBC.

Blood film shows tear drop RBC - get deformed as they squeeze out of bone marrow

Deformed RBC -> removed by spleen -> anaemia and splenomegaly

Also splenomegaly/ hepatomegaly caused by extramedullary haemopoiesis.

Also causes progressively hardening bone marrow.

100
Q

Features of myelofibrosis

A

Advanced disease - fatigue, sweats, weight loss.

Massive splenomegaly - pain in LUQ, early satiety, splenic infarction

Can transform into leukaemia

101
Q

Chronic myeloid leukaemia

A

Usually very high WCC
Symptomatic splenomegaly, hyperviscosity, bone pain
Hyperviscosity -> lots of granular precursors

Most often in adults

102
Q

Causes of pancytopenia

A

Reduced production of cells

Increased removal of cells
- immune destruction (autoantibody)
- splenic pooling (hypersplenism)
- haemophagocytosis (chewing up of cells in bone marrow - very very rare!)

103
Q

Aplastic anaemia

A

Pancytopenia with hypocellular bone marrow in the absence of an abnormal infiltrate with no increase in fibrosis.
—> progressive pancytopenia and empty bone marrow

104
Q

Thrombocytopenia

A

Low platelet count.

105
Q

Types of thrombocytopenia

A

Acquired (common)
— decreased platelet production
— increased platelet consumption
— increased platelet destruction

Inherited (rare)

106
Q

Immune platelet destruction

A

Immune thrombocytopenia purpura most common cause.

Treated with immunosuppression (corticosteroids)
Platelet transfusions do not work as transfused platelets also get destroyed.

107
Q

Pericytes

A

Cells comprising capillaries eg in the kidney.

108
Q

What happens to EPO in chronic kidney disease?

A

The kidney stops making EPO.

109
Q

Anaemia of chronic disease

A

Anaemia caused by chronic inflammation.

There are 3 contributors all caused by inflammatory cytokines:
1. Iron dysregulation - available iron not released for use in bone marrow
2. Marrow shows a lack of response to EPO
3. Reduced lifespan of RBC

110
Q

Functional iron deficiency

A

This means that there is sufficient iron in the body but not available to developing RBC.

Ferroportin is main exporter out of macrophage so is needed to recycle iron.

This is the iron deficiency in ACD.

111
Q

Hepcidin

A

Degrades ferroportin - the protein involved in moving iron out of cells.
- prevents iron release from macrophages
- prevents iron absorption in gut

Regulated by HFE, transferrin receptor and inflammatory cytokines.

112
Q

Anaemia of chronic kidney disease - 6 factors

A

Factors involved:
- less EPO made due to kidney damage
- the underlying cause of CKD often associated with raised cytokines
- dialysis causes damage to RBC -> haemolytic anaemia (schistocytes due to mechanical damage)
- uraemia causes reduced lifespan of RBC
- uraemia also inhibits megakaryocytes -> low platelets
- reduced clearance of hepcidin + increased production due to inflam. cytokines

113
Q

Treatment for ACD

A

Recombinant human EPO - if associated renal failiure

Ensure vit B12 and folate and iron stores are adequate

Transfuse RBC if all else fails

114
Q

How to test for functional iron deficiency

A

CHr test - reticulocyte haemoglobin content

(Give iron if low)

115
Q

Rheumatoid arthritis - treatment

A

Analgesics, often NSAIDs
Disease Modifying Agents (DMARDs)
- corticosteroids
- chemo
- biological agents (eg monoclonal antibodies)

116
Q

Felty’s syndrome

A

Triad of rheumatoid arthritis, neutropenia and splenomegaly.

117
Q

Varices

A

Dilated veins more prone to bleeding.

Eg oesophageal and gastric varices are caused by portal hypertension - higher than normal pressure.

118
Q

Clotting factors in the liver - what are they dependent on for their synthesis?

A

Vitamin K - so in patients with liver disease, they become deficient, so cannot synthesise clotting factors.

Therefore patients with liver disease can slowly become haemorrhagic.

119
Q

Where is thrombopoietin made?

What does this mean for patients with disease of that body part?

A

In the liver - so patients with liver disease can develop thrombocytopenia.
- also leads to splenic pooling and increased destruction of RBC, as target cells are present.

The platelets that are made often have reduced function.

=> patients more likely to bleed

120
Q

Why can target cells be seen in the blood of a patient with liver disease?

A

Target cells are present due to increased cholesterol to phospholipid ratio.

121
Q

Bacterial infection is often associated with ___?
Severe bacterial infection/sepsis can cause ___?
Parasitic infections are associated with ___?
Viral infections can cause ___ and ___?

A

Bacterial infection is often associated with neutrophilia.
Severe bacterial infection/sepsis can cause neutropenia.
Parasitic infections are associated with eosinophilia.
Viral infections can cause lymphocytosis and neutropenia.

122
Q

Disseminated intravascular coagulation (DIC)

A

The pathological activation of coagulation.

Numerous microthrombi are formed in the circulation, which leads to consumption of clotting factors and platelets, and then microangiopathic haemolytic anaemia.
- platelets are consumed quicker than can be made

There is a risk of both bleeding and thrombosis.

123
Q

DIC - clotting tests

A

Long clotting times, low fibrinogen, raised D-diners or fibrin degradation products.

124
Q

Leucoerythroblastic film
Cause?

A

Granulocyte precursors and nucleated RBC seen on blood film.

Caused by spilling out from bone marrow into the blood when the marrow is under stress.

125
Q

Causes of bone marrow being under stress

A

Sepsis/shock
Bone marrow infiltration - eg by cancer
Severe megaloblastic anaemia
Primary myelofibrosis (with tear drop RBCs)
Leukaemia
Storage disorders

126
Q

How does sickle cell result in jaundice?

A

Increased unconjugated bilirubin due to increased chronic haemolysis.

MEH (14 decks)

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