Haematology Flashcards

1
Q

What are the three types of anameia? (and explain)

A

Microcytic = small RBCs, Noromocytic = normal RBCs, Macrocytic = large RBCs

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2
Q

What causes anaemia with small RBCs?

A

THIS IS MICROCYTIC ANAEMIA - iron deficiency, chronic disease (e.g. renal failure) or thalassaemia

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3
Q

What causes anaemia with normal RBCs?

A

THIS IS NORMOCYTIC ANAEMIA - Acute blood loss, chronic disease (e.g. renal failure) or combined haematinic deficiency (e.g. iron and B12)

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4
Q

What causes anaemia with large RBCs?

A

THIS IS MACROCYTIC ANAEMIA - B12 deficiency, alcohol excess/liver damage, hypothyroidism, bone marrow failure/infiltration or haemolysis

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5
Q

Define anaemia

A

A reduced red cell mass with or without reduced haemoglobin concentration

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6
Q

What is a sickle cell crisis?

A

The RBCs stick together and block the capillaries. In bones = sharp severe stabbing pains, in brain = stroke, in lungs = pneumonia like disease

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7
Q

S&S of sickle cell disease?

A

Sickle cell crisis, infections, anaemia, renal impairment, pulmonary hypertension and joint damage

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8
Q

Treatment of sickle cell disease?

A

Transfusions, gene editing, stem cell transplant and hydroxycarabamide

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9
Q

What is the difference between alpha and beta thalassaemia?

A

Alpha = globin chain altered due to a deletion, beta = globin chain altered due to a mutation

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10
Q

What are the three types of Beta Thalassaemia? (and give symptoms)

A
Minor = carrier - asymptomatic
Intermedia = moderate anaemia, splenomegaly, bone deformities and increased infections
Major = failure to feed, severe anaemia, hepatosplenomegaly, bone abnormalities and increased infection
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11
Q

What treatment is required in the most severe cases of Beta Thalassaemia?

A

THIS IS MAJOR THALASSAEMIA - usually diagnosed in the first year, requires frequent transfusions with iron chelation to prevent iron over load. May require bone marrow transplant

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12
Q

What are the four types of Alpha Thalassaemia? (and give symptoms)

A

4 gene deletion = still born
3 gene deletion = moderate anaemia and splenomegaly
2 gene deletion = microcytosis with/without anaemia
1 gene deletion = asymptomatic

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13
Q

What is lymphoma?

A

A cancerous growth of the lymphocytes - may be caused by immunodeficiency, reccurent infection, autoimmune disorders etc.

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14
Q

What are B symptoms?

A

Systemic symptoms of lymphoma: fever, night sweats, rapid weight loss, appetite loss

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15
Q

How can you tell between Hodgkin’s and Non-Hodgkin’s lymphoma?

A

Reed-Sternberg cells present = Hodgkin’s and absent = Non Hodgkin’s

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16
Q

What are the risk factors and symptoms for Hodgkin’s lymphoma?

A

Epstein-Barr Virus, SLE, obesity, affected sibling.
Painless lymphadenopathy, B symptoms
Mainly seen in young people

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17
Q

What is the treatment for Hodgkin’s lymphoma?

A

ABVD combination chemotherapy (A - ADRIAMYCIN, B - BLEOMYCIN, V - VINBLASTINE, D - DACARBAZINE) // just learn the acronym for now

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18
Q

What are the symptoms of Non-Hodgkin’s lymphoma?

A

Painless lymphadenopathy, Gastric MALT, pancytopenia and B symptoms

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19
Q

What are the two types of Non-Hodgkin’s lymphoma?

A

Indolent/low grade - slow growing, usually advanced at presentation and incurable
Aggressive/high grade - usually nodal presentation, patient is unwell with a short history

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20
Q

What is the treatment for Non-Hodgkin’s lymphoma?

A

R-CHOP regimen (R - RITUXIMAB, C - CYCLOPHOSPHAMIDE, H - HYDROXY-DAUNORUBICIN, O - VINCRISTINE (Oncovin brand name), P - PREDNISOLONE)

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21
Q

What are the side effects of chemotherapy?

A

Nausea & vomiting, reduced fertility, fatigue, hair loss, loss of appetite, loss of gut squamous lining = diarrhoea and loss of taste

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22
Q

What is leukaemia?

A

Malignant proliferation of immature blast cells

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23
Q

Name the types of leukaemia

A

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

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24
Q

What is the epidemiology of ALL?

A

LYMPHOBLASTIC
Most common in cildren aged 2-4 it is the immature proliferation of lymphoid cells. This affects the B/T cells, if all B cells = children, if all T cells = adult.
Ionising radiation during pregnancy and Downs Syndrome are risk factors

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25
Q

S&S of ALL?

A

Anaemia, reccurent infections, easy bruising, hepatosplenomegaly, lympadenopathies, bone pain, cranial nerve palsies

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26
Q

What is the epidemiology of AML?

A

Mostly affects adults. The neopalstic proliferation of blast cells from marrow myeloid (will affect the basophils, neutrophils and eosinophils). Radiation and Down’s increase risk

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27
Q

S&S of AML?

A

Anaemia, increased infections, easing bruising, hepatosplenomegaly, gum hypertrophy.

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28
Q

Treatment drug for AML/ALL?

A

Allopurinol

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29
Q

What is the epidemiology of CML?

A

Almost exclusivley affects adults. It is the uncontrolled clonal proliferation of myeloid cells - the Philadelphia chromosome is nearly always present.

30
Q

S&S of CML?

A

Anaemia, splenomegaly, fever/night sweats, gout, bleeding, weight loss

31
Q

Treatment of CML?

A

Oral inatinib

32
Q

What is the epidemiology of CLL?

A

This is the most common leukaemia. It is the accumulation of mature B cells which have escaped cell death and undergone cell cycle arrest. Pneumonia may be a triggering event

33
Q

S&S of CLL?

A

Often asymptomatic but in severe cases there may be lymphadenopathy, hepatosplenomegaly, weight loss, sweats and anaemia

34
Q

What is MRD?

A

Minimal Residual Disease monitoring - carried out to monitor patietns in remission and detect the disease if it reoccurs

35
Q

What is the epidemiology of myeloma?

A

Cancer of immature malignant proliferation of the bone marrow plasma cells

36
Q

S&S of myeloma?

A

CRAB - Calcium raised, Renal failure, Anaemia, Bone lytic lesions leading to back pain

37
Q

What is the treatment of myeloma

A

Bisphosphonates plus CTD chemotherapy (Cyclophosphamide, Thalidomide and Dexamethosone) or MPT (Melphalan, Prednisolone and Thalidomide)

38
Q

What is polycythaemia?

A

Abnormally increased concentration of haemoglobin in the blood, either through reduction of plasma volume or increase in red cell numbers

39
Q

What causes polycythaemia?

A
Primary = Polycythaemia Ruba Vera
Secondary = High EPO (e.g. in renal carcinoma), hypoxia (e.g. smoking, altitude)
40
Q

What is Neutrophillia?

A

Too many neutrophils

41
Q

What causes Neutrophillia?

A
Proliferative = CML
Reactive = infection, inflammation, malignancy
42
Q

What is neutropenia?

A

Too few neutrophils

43
Q

What causes neutropenia?

A

Underproduction (due to bone marrow failure/infiltration) or over removal due to autoimmune disease

44
Q

What is lymphocytosis?

A

Too many lympocytes

45
Q

What causes lymphocytosis?

A
Proliferative = CLL
Reactive = infection, inflammation and malignancy
46
Q

What is thrombocytosis?

A

Too many platelets

47
Q

What causes thrombocytosis?

A
Proliferative = essential thrombocytopoenia (abnormal function)
Reactive = infection, inflammation and malignancy
48
Q

What is thrombocytopenia?

A

Too few platelets

49
Q

What causes thrombocytopenia?

A

Underproduction (congenital or due to drugs/BM infiltration/low TPO), overremoval (splenomegaly/autoimmune diseases), decreased function (myelodysplasia) or over consumption (DIC)

50
Q

What are the types of immune thrombocytopenia?

A
Primary = after viral infection
Secondary = in some malignancies (CLL) and infection (HIV)
51
Q

What is the difference between an arterial and a venous clot?

A
Arterial = platelet rich - white
Venous = fibrin rich - red
52
Q

What are the causes and S&S of an arterial clot?

A

Caused by atheroma formation.

Critical limb ischaemia = painful, perishingly cold, pallour, paraesthesia and paralysis of limb.

53
Q

What may an arterial clot cause in the coronary and cerebral criculation?

A
Coronary = MI (STEMI)
Cerebral = CVA
54
Q

What may cause a venous clot?

A

Immobility, surgery, genetics (factor V Leiden/PT20210A), lupus or anti-phospholipid syndrome

55
Q

S&S of venous clot?

A

Painful calf, hot, swelling/redness, odemea

56
Q

S&S of PE?

A

Cyanosis, chest pain, dysponea, hypotension, tachycardia, tachyponea, pleural rub

57
Q

What drug can be given for sickle cell disease?

A

Oral Hydroxycarbamide

58
Q

What three drugs can be used to prevent arterial thrombosis?

A

Aspirin, Clopidogrel, Dipyramidole

59
Q

What drugs can be used to treat DVT?

A

LMW Heparin (e.g. SC Enoxaparin)m oral warfarin and Direct-acting Oral Anti-Coagulants (DOACs) - do NOT use in pregnancy

60
Q

What drug can be used to treat CML?

A

Oral Imatinib

61
Q

What drug can be used to treat CLL?

A

Human IV immunoglobulins

62
Q

Name a bisphosphonate?

A

Zolendronate or alendronate

63
Q

What are the risk factors for chronic/acute polycythaemia?

A
Chronic = obesity/smoking/alcohol/hypertension
Acute = dehydration
64
Q

Name some chronic diseases/infections

A

TB, Chron’s, Rheumatoid arthritis, SLE, Malignant disease

65
Q

Describe how folate deficiency can cause anaemia

A

Megaloblastic anameia. Folate is essential for DNA synthesis so impairment will affect the bone marrow and lead to large RBCs and decreased production.

66
Q

Who is affected by folate deficiency?

A

People who don’t eat enough green vegetables, pregnant women, Chron’s/Coeliac sufferers and methotrexate users (it is antifolate)

67
Q

What is haemolytic anaemia?

A

The premature breakdown of RBCs (before 120 days)

68
Q

What is hereditary spherocytosis?

A

An autosomal dominant cause of haemolytic anaemia where RBCs become sphere shaed and rigid

69
Q

S&S of hereditary spherocytosis?

A

Jaundice at birth, splenomegaly, ulcers on the leg, gall stones

70
Q

What is G6PD deficiency?

A

An X-linked cause of haemolytic anaemia where G6PD isn’t produced so RBCs are not protected from oxidation

71
Q

S&S of G6PD deficiency?

A

Asymptomatic.

Oxidative crisis = rapid anaemia, jaundice and haemolysis. THIS IS ACUTE