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Haematology > Haematology Conditions > Flashcards

Haematology Conditions Flashcards

1
Q

Which drugs can commonly cause platelet dysfunction?

A

NSAIDs
Aspirin
Clopidogrel

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2
Q

How can you differentiate between platelet disorders caused by destruction of platelets and those caused by deficiencies of platelets?

A

Look at megakaryocytes (platelet precursors) on bone marrow examination - they will be high in destruction and low in deficiency

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3
Q

What are the causes of platelet dysfunction?

A

Drugs - NSAIDs, aspirin
Uraemia e.g. in end stage renal failure
Myeloproliferative disorders

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4
Q

What is immune thrombocytopenia purpura?

A

Destruction of platelets caused by autoantibody to antigen on the platelet surface.

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5
Q

What are the differences in clinical presentation of immune thrombocytopenic purport (ITP) in adults and in children?

A

Adults: Slow onset, no identified infective cause, requires treatment, chronic / relapsing

Children: Acute onset usually of bruising, usually follows viral infection, usually self-limiting and not requiring treatment

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6
Q

What treatment is used for ITP (immune thrombocytopenic purpura)?

A
  • Oral corticosteroids e.g. prednisolone (produces response in 60-80% of patients)
  • Immunoglobulin infusion e.g. IV IgG
  • Splenectomy (because platelets are destroyed in the spleen)
  • Thrombopoeitin agonist
  • Rituximab
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7
Q

What are the 5 key features of thrombotic thrombocytopenic purpura?

A
  • Thrombocytopenia
  • Microangiopathic haemolytic anaemia
  • Neurological disturbance
  • Fever
  • Renal failure
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8
Q

What is the pathophysiology of thrombotic thrombocytopenic purpura?

A

Deficiency in ADAMTS 13 - a protease which is normally responsible for degredation of vWF. Results in thrombus formation in the smallest vessels, profound thrombocytopenia and end-organ ischaemia.

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9
Q

What causes thrombotic thrombocytopenic purpura?

A

Congenital
Sporadic e.g. pregnancy
Autoimmune e.g. SLE
Drug induced e.g. clopidogrel

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10
Q

What is the treatment of thrombotic thrombocytopenic purpura?

A

Plasma exchange - removes the ADAMTS 13 autoantibody
Steroids e.g. methylprednisolone
Rituximab

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11
Q

What is disseminated intravascular coagulation (DIC) and what causes it?

A

Massive activation of the clotting cascade usually due to traumatic processes to the vascular endothelium. Causes include sepsis, burns, advanced cancer, obstetric complication, major trauma, acute promyelocytic leukaemia

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12
Q

When would you suspect a patient is suffering from post-transfusion purpura?

A

Thrombocytopenia occuring 10 days after transfusion.

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13
Q

What is the pathophysiology which causes post-transfusion purpura?

A

Affects patients who lack the HPA-1a antigen on their platelet surface (about 98% of the population DO have this antigen). When transfused with HPA-1a positive platelets, the recipient develops an antibody to them and their own platelets will cross react with the new ones, causing thrombocytopenia.

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14
Q

What is the treatment of post-transfusion purpura?

A

Intravenous immunoglobulin

Avoid HPA-1a positive platelet transfusion

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15
Q

How do aspirin and NSAIDs affect platelet function?

A

Inhibit cyclo-oxygenase 1 enzyme and thus prevent thromboxane synthesis which consequently decreases platelet aggregation (because thromboxane causes platelet aggregation)

Aspirin does this irreversibly, while the mechanism in NSAIDs is reversible.

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16
Q

Why is recombinant Factor VIII preferable in patients with Haemophilia A than plasma-derived Factor VIII?

A

Hep C and HIV infections have historically been associated with plasma-derived Factor VIII so recombinant is much safer

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17
Q

What might cause Vitamin K deficiency?

A

Malnutrition
Malabsorption e.g. in obstructive jaundice
Warfarin treatment

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18
Q

What is a thrombus?

A

A mass in the lumen of a vessel, made up of fibrin and blood components

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19
Q

True or false - Thrombus formation can only occur in the venous system

A

False. Thrombus formation can occur in either venous or arterial vessels.

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20
Q

What is Virchow’s Triad?

A

Describes 3 prerequisites for thrombus formation:

1) Stasis e.g. in venous obstruction due to tumour, bed rest, long plane/car journey, plaster cast
2) Damage to vessel wall e.g. atheroma, trauma, invasion by malignancy
3) Hypercoagulability e.g. pregnancy, oestrogen therapies, thrombophilia

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21
Q

List some rick factors for venous thromboembolism

A

Age >60, obesity (BMI > 30), immobility, high oestrogen (e.g. pregnancy, postpartum, contraceptive pill, HRT), trauma and surgery, ITU admission, history of VTE, FHx of VTE, thrombophilic disorders, varicose veins with phlebitis, dehydration, medical comorbidities (e.g. heart disease)

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22
Q

Define the term ‘thrombophilia’

A

Patients with an increased tendency towards thrombus formation (usually venous), due to an inherited or acquired cause.

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23
Q

Give 4 inherited disorders of thrombophilia

A

Factor V Leiden
Prothrombin 20210A Mutation
Protein C and Protein S Deficiency
Antithrombin Deficiency

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24
Q

List some clinical features of DVT

A 
Pain and swelling of affected limb
Calf tenderness
Local increase in temperature
Unilateral oedema
Accentuation of venous pattern
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25
Q

What is the use of the Well’s Score?

A

Assesses a patient’s pre-test probability of having a DVT and directs further investigation and management. If score 1 or less, DVT is unlikely (Perform D-dimer: If -ve exclude DVT, if +ve perform ultrasound)…If score 2 or more, DVT is likely (Perform D-dimer and ultrasound and only exclude DVT if both negative)

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26
Q

What is the treatment for DVT?

A

LMWH e.g. enoxaparin 1.5mg/kg/24hrs or fondaparinux. Continue this for at least 5 days, until INR stable at 2-3 for 2 days

Start warfarin simultaneously…most treated for 3 months (longer if unprovoked DVT or high risk of recurrence)

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27
Q

List the 4 types of leukaemia

A

Acute myeloid leukaemia
Acute lymphoblastic leukaemia
Chronic myeloid leukaemia
Chronic lymphocytic leukaemia

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28
Q

What is the commonest malignancy in childhood?

A

Acute lymphoblastic leukaemia

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29
Q

What is occurring in acute lymphoblastic leukaemia?

A

Malignancy involving the lymphoid tissue, responsible for production of T and B lymphocytes. There is arrested maturation and rapid proliferation of immature blast cells, with bone marrow failure and tissue infiltration.

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30
Q

List 5 clinical features of tissue infiltration in acute leukaemia

A 
Lymphadenopathy
Gum hypertrophy
Hepatosplenomegaly
Rash
CNS involvement
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31
Q

List some clinical features of acute lymphoblastic leukaemia

A

Signs of bone marrow failure: anaemia, infection, bleeding
Signs of tissue infiltration: hepatosplenomegaly, lymphadenopathy, orchidomegaly, CNS involvement (meningism, cranial nerve palsies)

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32
Q

CNS involvement is more common in which type of acute leukaemia?

A

Acute lymphoblastic leukaemia. It is rare in acute myeloid leukaemia.

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33
Q

What is the key treatment for chronic myeloid leukaemia…and why?

A

Imatinib

It’s a BCR/ABL tyrosine kinase inhibitor which targets the specific Philadelphia mutation involved in CML

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34
Q

Which is the most common leukaemia?

A

CLL

35
Q

Which cell is characteristic of Hodgkin’s lymphoma?

A

Reed-Sternberg cell. It has a mirror-image nuclei.

36
Q

What is the peak incidence of Hodgkin’s lymphoma?

A

2 peaks - one in young adults and one in elderly people

37
Q

How is lymphoma diagnosed?

A

Tissue biopsy of lymph nodes

38
Q

How is Hodgkin’s lymphoma classified?

A 
I = One nodal region affected
II = Involvement of 2 or more nodal regions on the same side of the diaphragm
III = Nodal involvement on both sides of the diaphragm
IV = Spread beyond the lymph nodes e.g. to liver, bone marrow

Each stage is either ‘A’ or ‘B’ defined by the absence or presence of B symptoms.

39
Q

What are ‘B’ symptoms?

A

> 10% weight loss in 6 months
Night sweats
Unexplained fever >38 degrees

40
Q

What are the 4 drugs involved with the treatment of Hodgkin’s lymphoma?

A

ABVD

Adriamycin
Bleomycin
Vanblastine
Dacarbazine

41
Q

Give 2 low-grade and 2 high-grade Non-Hodgkin’s Lymphomas

A

Low grade: Follicular NHL, marginal zone lymphoma

High grade: Diffuse large B-cell lymphoma, Burkitt’s lymphoma

42
Q

What is polycythaemia?

A

Increase in red cell mass - this may be relative (due to normal red cell mass but decreased plasma volume e.g. in dehydration) or absolute (i.e. actual rise in red cell mass)

43
Q

List some causes of absolute polycythaemia

A

Primary - polycythaemia rubra vera
Secondary - due to hypoxia (high altitude, chronic lung disease, cyanotic congenital heart disease etc.), or inappropriate EPO production

44
Q

What mutation is present in >90% of patients with polycythaemia rubra vera?

A

Mutation in JAK2

45
Q

How might a patient with polycythaemia rubra vera present?

A
  • May be asymptomatic and only picked up via FBC
  • Non specific signs of hyper viscosity: headache, dizziness, tinnitus, visual disturbance
  • Itching after a hot bath
  • Erythromelalgia (burning in hands and feet)
  • Facial plethora
  • Signs of arterial or venous thrombosis
46
Q

What might you see on the blood count of someone with polycythaemia rubra vera?

A

Raised RCC, Hb, HCT, PCV, WCC and platelets

Raised B12

47
Q

What is essential thrombocythaemia?

A

Malignant proliferation of megakaryocytes causing persistently raised platelets

48
Q

What is the treatment for essential thrombocythaemia?

A

Aspirin 75mg daily
Or
Hydroxycarbamide if over 60 years old or previous thrombosis

49
Q

Give some causes of neutropenia

A

Drugs: Carbimazole, colchicine, chemotherapy, clonazepine, carbamazepine
Radiotherapy
Bone marrow failure
Sequestration in spleen e.g. Felty’s Syndrome
Viral infections
Benign Ethnic Neutropenia
Autoimmune conditions

50
Q

What is thalassaemia?

A

A haemoglobinopathy - Abnormal production of one or more types of haemoglobin ‘globin’ chains. There is precipitation of globin chains within red cells, resulting in cell damage, ineffective erythropoiesis, and haemolysis.

51
Q

List some clinical features of beta thalassaemia major

A 
Presents in 1st year of life
Severe anaemia
Failure to thrive
Recurrent infections
Skull bossing
Hepatosplenomegaly
52
Q

List some clinical features of beta thalassaemia trait

A

Asymptomatic carrier state

Anaemia is mild and usually well tolerated (reduced Hb, MCV and MCH)

53
Q

How would you treat beta thalassaemia?

A

Regular blood transfusions (every 2-4 weeks)
Iron chelators
Ascorbic acid to increase urinary excretion of iron

54
Q

Give 2 causes of relative polycythaemia

A

Dehydration

Diuretics

55
Q

What is the treatment for absolute polycythaemia?

A

Regular venesections to keep haematocrit

56
Q

What is the inheritance pattern of sickle cell anaemia?

A

Autosomal recessive

57
Q

What is the pathophysiology of sickle cell anaemia?

A

Deoxygenated HbS polymerises, causing abnormal ‘sickle’ red blood cells. These sickle cells are fragile and can undergo haemolysis. They also cause occlusion in small vessels.

58
Q

What is the character of the anaemia in sickle cell anaemia?

A

Hb 60-90g/L

Raised reticulocytes

59
Q

What does the blood film show in sickle cell anaemia?

A

Sickle cells

Target cells

60
Q

How long can erythrocytes for transfusion be kept?

A

Up to about 35 days

They are stored at 4 degrees

61
Q

True / False: Platelets are stored at 4 degrees

A

False

Platelets are stored at room temperature.

Red blood cells are stored at 4 degrees.

62
Q

When might someone be given fresh frozen plasma (FFP)?

A

When a patient is actively bleeding and has abnormalities in their clotting tests.

Also warfarin reversal e.g. in urgent surgery

63
Q

What type of antibodies are the A, B and O antibodies?

A

IgM

64
Q

What is the mechanism of action of [unfractionated] heparin?

A

Binds to and activates antithrombin. This inhibits thrombin and other proteases (especially Factor Xa) which are involved in clotting.

65
Q

Give 3 example of low molecular weight heparins

A

Dalteparin
Enoxaparin
Tinzaparin

66
Q

What is the difference in mechanism between unfractioned heparin and LMWH?

A

Unfractionated heparin binds to antithrombin to increase it’s ability to inactivate thrombin. LMWH just inactivates Factor Xa

67
Q

What is the method of administration of LMWH?

A

subcutaneous injection

68
Q

What might be some advantages of using unfractionated heparin?

A

In patients with high bleeding risk - can be stopped quickly as has a very short half life
Also consider in renal failure patients where LMWH might be inappropriate due to accumulation

69
Q

List some side effects of using heparin

A

Bleeding
Thrombocytopenia (heparin-induced thrombocytopenia)
Hyperkalaemia
Osteoporosis (with long-term use)

70
Q

What is the mechanism of action of warfarin?

A

Inhibits a reductase enzyme responsible for regenerating active Vitamin K, thus leaving Vitamin K ‘deficient’

71
Q

What is the target INR for a patient with DVT or PE on warfarin?

A

2-3
or
3.5 if recurrent

72
Q

What is the target INR for a patient with a prosthetic heart valve?

A

3-4

73
Q

What is the target INR for a patient with AF who is on warfarin?

A

2-3

74
Q

What is the treatment durations for a patient on warfarin with DVT / PE?

A

If provoked below knee DVT = 6 weeks
If provoked above knee DVT or PE = 3 months
If unprovoked = 6 months

75
Q

How would you measure the effect of unfractionated heparin?

A

Measure the APTT

76
Q

Give 2 examples of Factor Xa inhibitors

A

Rivaroxaban

Apixaban

77
Q

Give an example of a direct thrombin inhibitor

A

Dabigatran

78
Q

What is Bence-Jones protein and when is it relevant?

A

Free immunoglobulin light chains (kappa and lambda type) which are filtered by the kidney into the urine in 2/3 of cases of myeloma.

79
Q

List some clinical features of myeloma

A 
Bone pain/pathological fractures
Anaemia, neutropenia, thrombocytopenia
Renal failure
Recurrent infections (due to increased levels of IgG and/or IgA but low levels of all other immunoglobulins)
Hypercalcaemia
80
Q

What might you see on blood film of a patient with myeloma?

A

Rouleaux

81
Q

What is the diagnostic criteria for myeloma?

A

Monoclonal band on urine or serum electrophoresis
Raised plasma cells on bone marrow biopsy
Signs of end-organ damage from myeloma e.g. hypercalcaemia, anaemia, renal impairment
Bone lesions

82
Q

What investigations would you carry out for suspected myeloma and what would they show?

A

FBC - Normochromic, normocytic anaemia
ESR raised due to hyperviscosity
Blood film - Rouleaux formation
Urine test - Bence Jones protein
Serum immunoglobulins - Certain types will be raised
U+Es - Raised urea, creatinine (due to renal failure) and calcium (due to increased osteoclast activity)
Bone marrow sample - Raised plasma cells
X-ray - Lytic bone lesions, collapse fractures

83
Q

What is the treatment for myeloma?

A 
Required if there are symptoms:
Bisphosphonates
Analgesia
Blood transfusion or EPO for anaemia
Chemotherapy: Steroids, cytotoxic
IVIg for infections if necessary

Haematology (4 decks)

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