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Metabolism, Endocrinology, Haematology > Haematology Session 4 > Flashcards

Haematology Session 4 Flashcards

1
Q

Why can changes to the blood occur in systemic disease?

A
  • Underlying physiological causes (eg. abnormal cytokines)
  • Complications of the disease
  • Adverse treatment effects
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2
Q

Why might anaemia develop in chronic kidney disease?*

A
  • Damaged kidney stops making erythropoietin

- No response in haemostatic loop

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3
Q

Why can anaemia happen in cancer patients/patients with infections?*

A

Bone marrow not able to respond to erythropoietin and therefore can’t produce RBCs

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4
Q

What is a functional anaemia?

A
  • Anaemia of chronic disease

- Iron is sufficient but is not made available to the bone marrow for RBC production.

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5
Q

What are the 3 contributors to anaemia of chronic disease, and what are they caused by?

A
  • Available iron not released
  • Lack of response to erythropoietin
  • Reduced red cell lifespan

All caused by inflammatory cytokines.

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6
Q

What is meant by a functional iron deficiency?

A

There is sufficient iron available in the body, but it is not available to the developing erythroid cells.

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7
Q

What transporter is needed to recycle iron from old/broken down erythrocytes?

A

Ferroportin.

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8
Q

What is hepcidin regulated by?

A
  • HFE
  • Transferrin receptor
  • Inflammatory cytokines
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9
Q

What is inhibited when ferroportin is degraded?

A
  • Iron release from macrophage

- Iron absorption from gut

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10
Q

How is iron dysregulated in anaemia of chronic disease?*

A

Production of hepcidin by the liver acts on ferroportin, preventing the release of ferric iron out of the cell.

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11
Q

What is the process through which anaemia develops in chronic inflammation?*

A
  • Inflammation causes cytokines to be released by immune cells
  • Cytokines stimulate hepcidin production in liver
  • Ferroportin inhibited
  • Iron not released from reticuloendothelial system
  • Iron not absorbed in gut
  • Inhibition of erythropoiesis
    = ANAEMIA
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12
Q

What are the factors contributing to anaemia of chronic kidney disease?

A
  • Damaged kidneys produce less erythropoietin
  • Reduced hepcidin clearance
  • Increased cytokines = more hepcidin produced
  • Dialysis damages red blood cells
  • Uraemia reduces RBC lifespan and inhibits megakaryocytes
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13
Q

How to treat anaemia of chronic disease when it’s associated with renal failure?

A
  • Recombinant human erythropoietin (intramuscular injection)
  • Ensure that Vit B12, folate and iron are adequate
  • Transfusion if other doesn’t work and symptoms present
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14
Q

How to assess for functioning iron deficiency?

A

Use reticulocyte haemoglobin content (CHr)

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15
Q

Why should iron be given in IV form in anaemia of chronic renal failure?

A

Absorption is impaired

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16
Q

When should iron be given?

A
  • Ferritin below <200micrograms/L or low CHr
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17
Q

What are the haematological abnormalities of red cells in kidney disease?

A
  • Anaemia: blood loss, etc

- Secondary polycythaemia: renal transplant/tumour

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18
Q

What are haematological abnormalities of neutrophils in kidney disease?

A

Neutropenia: immunosuppression (post transplant), autoimmune kidney disease

Neutrophilia: inflammation, infection, steroids

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19
Q

What are possible haematological abnormalities of platelets in kidney disease?

A

Thrombocytopenia: uraemia, drugs, haemolytic uraemic syndrome (acute kidney injury)

Thrombocythaemia: Inflammation, bleeding, iron deficiency

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20
Q

What is rheumatoid arthritis?

A

A chronic immune mediated inflammatory condition.

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21
Q

What are the now rarely seen changes to hands in rheumatoid arthritis?*

A
  • Boutonniere thumb deformity
  • Ulnar deviation of metacarpopharyngeal joint
  • Swan neck finger deformity
22
Q

What is rheumatoid arthritis treated with?

A
  • NSAIDs (pain relief)
  • Corticosteroids and chemotherapy (disease modifying, slow progression)
  • Monoclonal antibodies against cytokines for patients with very active rheumatoid arthritis
23
Q

Why can NSAIDs cause blood loss?

A

Prolonged use can cause GI bleeding.

24
Q

Why can high platelets, neutrophils and CRP occur in rheumatoid arthritis but also low platelets and neutrophils?

A
  • High platelets, CRP and neutrophils when the disease is active due to inflammation
  • Low platelets and neutrophils due to treatment and autoimmune reaction to hypersplenism
25
Q

What is Felty’s syndrome?*

A
  • Triad of arthritis, splenomegaly and neutropenia
  • Splenomegaly may destroy neutrophils
  • Insensitivity of myeloid cells to GCSF (granulocyte colony stimulating factor)
26
Q

Why does chronic liver disease cause portal hypertension and therefore splenomegaly?

A
  • Vessels in liver are damaged/blocked off
  • Blood redirected through the portal system, therefore hypertension
  • Causes splenomegaly and trapping of red cells, platelets and white cells in spleen = pancytopenia
27
Q

Why can alcohol abuse cause megaloblastic anaemia?

A

It’s a common cause of folic acid deficiency.

28
Q

What can portal hypertension lead to?

A
  • Higher pressure = distended vessels
  • Oesophageal and gastric varices
  • More prone to bleeding and are a leading death cause
29
Q

Why are patients in liver disease deficient in clotting factors?

A
  • Most made by the liver

- Synthesis of some dependent in vitamin K (also deficient in patients with liver damage

30
Q

Why is thrombocytopenia present in most patients with liver disease?

A
  • Impaired production (made in liver)
  • Splenic pooling
  • Increased destruction
  • Reduced function
31
Q

Why are target cells seen often in liver disease?*

A

Increased cholesterol:phospholipid ratio.

32
Q

What are haematological features of liver disease due to alcohol excess?

A
  • Pancytopenia (directly toxic to BM)

- Secondary malnutrition - folic acid deficiency

33
Q

What are haematological features of liver disease due to viral hepatitis?

A

Bone marrow failure

34
Q

What are haematological features of autoimmune liver disease?

A
  • Neutropenia
  • Thrombocytopenia
  • Immune mediated anaemia
35
Q

Why can anaemia be present post-operatively?

A
  • Blood loss pre and post operation
36
Q

Why can neutropenia and neutrophilia be present post operatively?

A
  • Neutropenia: severe sepsis

- Neutrophilia: bleeding, infection

37
Q

Why can thrombocytosis and thrombocytopenia occur postoperatively?

A

Thrombocytosis: infection, bleeding

Thrombocytopenia: drugs, sepsis, DIC

38
Q

What is bacterial infection usually associated with?

A

Neutrophilia

39
Q

What is severe bacterial infection usually associated with?

A

Neutropenia

40
Q

What are parasitic infections associated with?

A

Eosinophilia

41
Q

What are viral infections associated with?

A

Lymphocytosis and neutropenia

42
Q

What is disseminated intravascular coagulation (DIC)?*

A
  • Pathological activation of coagulation (continued when not needed)
  • In severe sepsis
  • Microthrombi formed in circulation
  • Consumption of clotting factors and platelets
  • Microangiopathic haemolytic anaemia (MAHA)
  • Long clotting, low fibrinogen and higher fibrin degradation products
  • Risk of bleeding (low platelet) and thrombosis (cut off circulation)
43
Q

What types of cells are usually present in DIC?*

A
  • Schistocytes

- Low platelets

44
Q

What cells are seen in patients post-splenectomy?

A
  • Howell-Jolly bodies

- Thrombocytosis and lymphocytosis

45
Q

What are the causes of anaemia and polycythaemia in cancer?

A

Anaemia:

  • Bleeding
  • Iron deficiency
  • Chemotherapy
  • Infiltration of bone marrow by cancer cells
  • Anaemia of chronic disease

Polycythaemia:
- Tumours that produce erythropoietin (eg. adrenal tumour)

46
Q

Why can cancer cause neutropenia and neutrophilia?

A

Neutropenia:

  • Chemotherapy
  • Marrow infiltration by cancer
  • HIGH VULNERABILITY TO SEPSIS

Neutrophilia:

  • Inflammation
  • Infection
47
Q

What are causes of thrombocytopenia and thrombocytosis in cancer?

A

Thrombocytopenia:

  • Sepsis
  • DIC
  • Marrow infiltration

Thrombocytosis:

  • Inflammation
  • Bleeding
  • Iron deficiency
48
Q

Why are people with cancer at a higher risk of deep vein thrombosis and pulmonary emboli?

A
  • Increased clotting

- Inflammation

49
Q

What is often seen when the marrow is infiltrated by cancer cells?*

A

Leucoerythroblastic film - immature red and white cells due to spilling out from the marrow when under stress.

50
Q

When else are leucoerythroblastic films seen?

A
  • Sepsis
  • Megaloblastic anaemia
  • Primary myelofibrosis
  • Leukaemia

Metabolism, Endocrinology, Haematology (16 decks)

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