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Finals Revision > Haematology > Flashcards

Haematology Flashcards

1
Q

What is pernicious anaemia?

A

B12 deficiency

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2
Q

What cells in the stomach produce intrinsic factor?

A

Parietal cells

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3
Q

Where is B12 absorbed?

A

Ileum

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4
Q

What is the pathophysiology of pernicious anaemia?

A

Autoimmune - antibodies against the parietal cells or intrinsic factor

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5
Q

What are the symptoms of B12 deficiency?

A

Peripheral neuropathy
Loss of vibration sense or proprioception
Visual changes
Mood or cognitive changes

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6
Q

What is the management for pernicious anaemia?

A

Oral cyanocobalamin
If severe: IM hydroxycobalamin

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7
Q

If you have folate and B12 deficiency, which one should you treat first?

A

B12 first: otherwise it can cause subacute combined degeneration of the cord.

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8
Q

What does the Direct Coombs test test for?

A

Autoimmune haemolytic anaemia

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9
Q

What is the inheritance pattern in hereditary spherocytosis?

A

Autosomal dominant

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10
Q

What virus can cause an aplastic crisis in hereditary spherocytosis?

A

Parvovirus

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11
Q

What is the management of hereditary spherocytosis?

A

Folate supplementation
Splenectomy
Cholecystectomy if gallstones are a problem

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12
Q

What is the inheritance pattern of hereditary elliptocytosis?

A

Autosomal dominant

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13
Q

What is the inheritance pattern of G6PD deficiency?

A

X linked recessive. More common in mediterranean and African patients

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14
Q

What can trigger a crisis in G6PD?

A

Fava beans, antimalarial primaquine, ciprofloxacin, sulfonylureas, sulfasalazine and other sulphonamide drugs, infections.

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15
Q

What are the two types of autoimmune haemolytic anaemia?

A

Warm type and cold type (what temperature the antibodies attach themselves - agglutination)

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16
Q

What conditions is cold type autoimmune haemolytic anaemia secondary to?

A

Lymphoma
Leukaemia
SLE
Infections such as: mycoplasma, EBV, CMV, HIV

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17
Q

What is the management of autoimmune haemolytic anaemia?

A

Blood transfusion
Prednisolone
Rituximab (monoclonal antibody against B cells)
Splenectomy

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18
Q

What is alloimmune haemolytic anaemia?

A

Foreign red blood cells causing an immune reaction (transfusion or newborn)

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19
Q

What is paroxysmal nocturnal haemoglobinuria?

A

Genetic mutation in the stem cells
Realists in loss of proteins on the surface of red blood cells that inhibit the complement cascade -> complement cascade is activated and RBCs are destroyed

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20
Q

What is the characteristic presentation of paroxysmal nocturnal haemoglobinuria?

A

Red urine in the morning
Also:
Anaemia
Predisposed to thrombosis and smooth muscle dystonia (e.g. oesophageal spasm and erectile dysfunction)

21
Q

What is microangiopathic haemolytic anaemia secondary to?

A

Haemolytic uraemia syndrome
DIC
Thrombotic thrombocytopenia purpura
SLE
Cancer

22
Q

Myeloma is a cancer of which cells?

A

Plasma cells (the B lymphocytes that produce antibodies)

23
Q

What are Bence Jones proteins

A

Light chains of antibodies found in the urine of patients with myeloma

24
Q

What causes renal impairment in patients with myeloma?

A

High levels of immunoglobulins can block flow
Hypercalcaemia
Dehydration
Bisphosphonates

25
Q

Raised plasma viscosity in myeloma can cause what?

A

Easy bruising
Easy bleeding
Reduced or loss of sight due to vascular disease in the eye
Purple discolouration to the extremities
heart failure

26
Q

What does CRAB stand for in myeloma?

A

Calcium (elevated
Renal failure
Anaemia
Bone lesions/pain

27
Q

What are the risk factors for myeloma?

A

Older age
Male
Black African ethnicity
Family history
Obesity

28
Q

What investigations do you do for myeloma? (BLIP)

A

Bence Jones protein (request urine electrophoresis)
L - Serum free light chain assay
I - Serum Immunoglobulins
P- Serum Protein electrophoresis

Bone marrow biopsy

29
Q

What are the x-ray signs in myeloma?

A

Punched out lesions
Lytic lesions
‘Raindrop skull’

30
Q

What is the first line management for myeloma?

A

Chemo: Bortezomid, Thalidomide, Dexamethasone
VTE prophylaxis if on thalidomide

31
Q

What is the management for myeloma bone disease?

A

Bisphosphonates (suppress osteoclasts activity)
Radiotherapy
Orthopaedic surgery
Cement augmentation (injecting cement into vertebral fractures)

32
Q

What is myelofibrosis?

A

Fibrosis of the bone marrow, due to cytokines released from he proliferating cells

33
Q

Why does myelofibrosis cause organomegaly?

A

Extramedullary haematopoiesis has to happen in the liver and spleen. Can cause portal hypertension or spinal cord compression

34
Q

What are the signs of polycythaemia vera?

A

Conjunctival plethora (redness
A ruddy complexion
Splenomegaly

35
Q

What can a blood film look like in myelofibrosis?

A

Teardrop-shaped RBCs, varying sizes of RBCs (poikilocytosis) and immature red and white cells.

36
Q

How do you diagnose myelofibrosis

A

Bone marrow biopsy: dry bone marrow on aspiration

37
Q

What is the difference between myeloproliferative disorders and myelodysplastic syndrome?

A

Myeloproliferative: one stem cell is proliferating much more than it should
Myelodysplastic: myeloid bone marrow cells not maturing properly and so low levels of the cells that should be being produced

38
Q

What can myelodysplastic and myeloproliferative syndromes transform into?

A

Acute myeloid leukaemia

39
Q

What does myelodysplastic syndrome present with?

A

Anaemia/neutropenia/thrombocytopenia.
Often have a history of chemo or radiotherapy and are over 60.
Confirmed on bone marrow aspiration and biopsy

40
Q

What is the most common inherited cause of abnormal bleeding?

A

Von Willebrand disease

41
Q

What is the inheritance pattern of VWD?

A

Autosomal dominant

42
Q

What is VWF?

A

A glycoprotein

43
Q

What is the management of VWD?

A

Desmopressin - can stimulate the release of VWF
Infused VWF +/- factor VIII
Women with heavy periods: tranexamic or mefanamic acid, norethisterone, COCP, Mirena,

44
Q

What can affect the production of platelets?

A

Sepsis
B12 or folate def.
Liver failure causing reduced thrombopoietin production
Leukaemia
Myelodysplastic syndrome

45
Q

What can cause the destruction of platelets?

A

Medications (sodium valproate, methotrexate, isotretinoin, antihistamines, proton pump inhibitors)
Alcohol
ITP
Thrombotic thrombocytopenia purpura
Heparin-induced thrombocytopenia
HUS

46
Q

What platelet count is at high risk for spontaneous bleeding?

A

Below 10 x 10tothe9

47
Q

What is the pathophysiology of thrombotic thrombocytopaenic purpura?

A

Tiny blood clots form in the small vessels, using up platelets. A microangiopathy.
These develop due to a shortage in the protein ADAMTS13 (either due to genetic mutation or autoimmune disease).
This protein normally inactivates vWF and reduced platelet adhesion and clot formation.

48
Q

What is the management for thrombotic thrombocytopaenic purpura?

A

Plasma exchange
Steroids
Rituximab

49
Q

What is the pathophysiology of heparin induced thrombocytopenia?

A

Antibodies are formed against platelets in response to exposure to heparin.
These antibodies activate clotting mechanisms and lead to thrombosis, as well as breaking down platelets.
A surprising picture of a patient on heparin with low platelets forming unexpected blood clots.

Finals Revision (20 decks)

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