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MEH > 6.1 Haematology in systemic disease > Flashcards

6.1 Haematology in systemic disease Flashcards

1
Q

why are changes to the blood in systemic disease often multi-factorial?

A
  1. Underlying physiological or external cause
  2. complications of the disease
  3. treatment (adverse effects)
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2
Q

where is erythropoietin produced?

A

kidneys

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3
Q

which cells sense hypoxia in the kidney?

A

pericytes in the kidney. Detection of hypoxia stimulate the kidney to produce erythropoietin.

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4
Q

How can chronic kidney disease cause anaemia?

A

As it causes a lack of response in the haemostatic loop that causes the kidney to stop making erythropoietin.

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5
Q

how does erythropoietin function?

A

stimulates production of erythrocytes by binding to receptors on erythroblasts in bone marrow.

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6
Q

what causes anaemia in anaemia of chronic disease?

A
  1. Iron dysregulation (iron is not made available to marrow for RBC production)
  2. The marrow shows lack of response to erythropoietin
  3. There is a reduced lifespan of red cells
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7
Q

give examples of diseases that cause anaemia of chronic disease

A

rheumatoid arthritis
inflammatory bowel disease (ulcerative colitis or crohns disease)
Chronic infections e.g. bronchiectasis and TB)

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8
Q

what is a functional iron deficiency?

A

Sufficient iron in the body but not available to the developing erythroid cells

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9
Q

what is ferroportin?

A

ferroportin is the main exporter of iron out of the macrophage (and out of the gut cell)

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10
Q

what is hepcidin?

A

A protein hormone that prevents iron release from macrophages and iron absorption from gut by degrading ferroportin the protein involved in moving iron out of cells

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11
Q

how is hepcidin regulated?

A

HFE gene
Transferrin receptor
Inflammatory cytokines

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12
Q

how do cytokines such as interleukin6 (IL6) cause anaemia?

A
  • anaemia of chronic disease
  • more cytokines released by immune cells due to inflammation
  • stimulates increased production of hepcidin by liver
  • hepcidin inhibits ferroportin
  • decreased iron release from RES and decreased absorption in gut
  • plasma iron reduced
  • inhibition of erythropoiesis in the bone marrow
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13
Q

how does the kidney appear in chronic kidney disease?

A

shrivelled small and dark.

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14
Q

what proteins may appear raised in chronic kidney disease?

A

cytokines ( including interleukins)

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15
Q

what 5 factors of chronic kidney disease cause anaemia?

A
  1. Reduced erythropoietin production due to damage to kidneys
  2. Reduced clearance of hepcidin
  3. Increased hepcidin production due to inflammatory cytokines
  4. Dialysis damage (sheer stress) to RBCs
  5. Reduced lifespan of RBCs as a direct effect or uraemia (high levels of urea)
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16
Q

what is the treatment for anaemia of chronic disease?

A
  1. Treat the underlying condition. If associated with renal failure, recombinant human erythropoietin injection.
  2. vitamin B12, folate and iron stores should all be adequate (supplement if not)
  3. Only transfuse RBCs in a symptomatic patient if all else fails
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17
Q

what abnormalities of RBCs may be seen in kidney disease?

A
  1. anaemia

2. secondary polycythaemia (elevated RBCs)

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18
Q

what abnormalities of neutrophils may be seen in kidney disease?

A

neutropenia (immunosuppression and autoimmune kidney disease)

neutrophilia ( inflammation, infection )

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19
Q

what abnormalities of platelets may be seen in kidney disease?

A

thrombocytopenia (uraemia)

thrombocytosis (inflammation, bleeding, iron deficiency)

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20
Q

what deformities of the hand can be seen in late stage rheumatoid arthritis?

A

Boutonniere deformity of the thumb
Ulnar deviation of metacarpophalangeal joints
Swan neck deformity of the fingers

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21
Q

How is rheumatoid arthritis treated?

A
  1. Pain relief, often NSAIDs
  2. Disease Modifying Agents (DMARDs) (Corticosteroids, Chemotherapy eg methotrexate, Biological agents – monoclonal antibodies against the cytokines)
22
Q

what is the function of disease modifying agents?

A

to slow the inflammatory process. Used to treat rheumatoid arthritis

23
Q

why is anaemia secondary to rheumatoid arthritis multifactorial?

A
  1. anaemia of chronic disease ( functional iron deficiency)
  2. GI blood loss due to NSAIDS and steroids
  3. risk of autoimmune haemolytic anaemia
24
Q

What is Felty’s syndrome?

A

An autoimmune disorder in which neutropenia is associated with rheumatoid arthritis and an enlarged spleen.

25
Q

what traid of symptoms are associated with Felty’s syndrome?

A

Splenomegaly
Rheumatoid arthritis
Neutropenia

26
Q

Why is neutropenia an associated factor of Felty’s syndrome?

A
  1. as splenomegaly contributes to peripheral destruction of neutrophils
  2. Failure of bone marrow to produce neutrophils as there is insensitivity of the myeloid cells to the stimulator GCSF (Granulocyte colony stimulating factor)
27
Q

How does a liver with Cirrhosis look?

A

lots of yellow nodules on the surface

28
Q

why does chronic liver disease cause low blood counts?

A
  1. Chronic liver disease will cause portal hypertension
  2. portal hypertension causes splenomegaly due to back pressure
  3. splenomegaly leads to splenic sequestration of cells and overactive removal of cells resulting in low blood counts
29
Q

what is portal hypertension?

A

high blood pressure in the system that connects the liver and the spleen

30
Q

what are the haematological features of liver disease?

A
  1. oesophageal and gastric varices due to portal hypertension causing huge back pressure.
  2. low blood counts due to splenomegaly
  3. blood loss
31
Q

how does liver disease result in blood loss?

A
  1. Liver disease leads to oesophageal and gastric varies. These very dilated varices can burst causing acute blood loss and death.
  2. deficiencies of coagulation factors
  3. endothelial dysfunction
  4. thrombocytopenia
  5. defective platelet function
32
Q

where are clotting factors produced?

A

made predominantly in the liver. Synthesis is dependent on Vitamin K. Patients with liver disease quickly become deficient in these clotting factors.

33
Q

where is erythropoietin produced?

A

kidney

34
Q

where is thrombopoietin produced?

A

liver

35
Q

why do the majority of patients with liver disease suffer from thrombocytopenia?

A

impaired production of thrombopoietin
splenic pooling due to splenomegaly
increased destruction
platelets have a reduced function

36
Q

what are target cells?

A

Red blood cells with the haemoglobin disposed as an outer ring and a small circular central mass. Target cells are seen in liver disease and in the HAEMOGLOBINOPATHIES.

37
Q

what abnormal RBCs are often seen in liver disease?

A

Target cells - due to increased cholesterol to phospholipid ratio

38
Q

Describe the haematological features of liver disease caused by alcohol excess

A
  1. pancytopenia as alcohol is directly toxic to bone marrow cells
  2. secondary malnutrition common
39
Q

describe the haematological features of liver disease caused by viral hepatitis

A

Bone marrow failure (hypoplastic/ aplastic marrow) can develop after an episode of hepatitis

40
Q

describe the haematological features of liver disease caused by autoimmune liver disease

A

Immune mediated anaemia, thrombocytopenia or neutropenia

41
Q

what haematological changes can be seen post operatively?

A
  1. anaemia (blood loss pre and during op)
  2. temporary relative polycythaemia (dehydration)
  3. neutropenia (sepsis)
  4. Neutrophilia (post op reactive, infection, severe bleeding)
  5. thrombocytopenia (drugs, sepsis, D.I.C)
  6. Thrombocytosis (post op reactive, infection, bleeding)
42
Q

what changes can be seen in erythrocytes due to infection?

A
  1. chronic infection can lead to anaemia of chronic disease

2. Malaria can cause haemolytic anaemia

43
Q

what changes can be seen in granulocytes in response to infection?

A

Bacterial infection = neutrophilia
Severe bacterial infection = neutropenia
Parasitic infections = eosinophilia
Viral infections = lymphocytosis and neutropenia

44
Q

what changes in platelets can be seen in platelets in response to infection?

A

infection = reactive thrombocytosis
severe infection = thrombocytopenia
DIC and severe sepsis = thrombocytopenia

45
Q

what is disseminated intravascular coagulation?

A
  • Pathological activation of coagulation
  • Numerous microthrombi are formed in the circulation
  • This leads to consumption of clotting factors and platelets, and a consequent microangiopathic haemolytic anaemia (MAHA)
    Clotting tests are affected - usually long clotting times, low fibrinogen and raised D-dimers or fibrin degradation products
  • Risk of both bleeding and thrombosis
46
Q

what is microangiopathic haemolytic anaemia?

A

Haemolysis attributed to narrowing or obstruction of small blood vessels usually due to inflammation; causes fragmentation and distortion in the shape of red blood cells.

47
Q

what changes can be seen in erythrocytes in response to cancer?

A 
Anaemia
• Bleeding eg bowel, stomach, bladder, endometrium
• Iron deficiency
• ACD
• Treatments – chemotherapy

Polycythaemia
• EPO producing tumours

48
Q

what changes can be seen in granulocytes in response to cancer?

A

Neutropenia
• Chemotherapy
• Marrow infiltrated by cancer cells

Neutrophilia
• Inflammation
• Infection

49
Q

what changes can be seen in platelets in response to cancer?

A 
Thrombocytopenia
• Chemotherapy
• Sepsis
• D.I.C
• Marrow infiltrated
Thrombocytosis
• Inflammation
• Infection
• Bleeding
• Iron deficiency
50
Q

what is a leucoerythroblastic film?

A

blood film showing white and red immature precursor cells spilling out of bone marrow into the circulating peripheral blood when the marrow is under stress.

51
Q

what abnormalities can be seen on a blood film of a patient with a leucoerythroblastic film?

A

granulocyte precursors

nucleated RBCs

52
Q

what conditions can cause a leucoerythroblastic film?

A
  • Sepsis/shock
  • Bone marrow infiltration by carcinoma or haematological malignancy
  • Severe megaloblastic anaemia
  • Primary Myelofibrosis (with tear drop RBCs)
  • Leukaemia
  • Storage disorders

MEH (23 decks)

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