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Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

What are the causes of microcytic anaemia?

A

Thalassaemia, anaemia of chronic disease (CKD), iron deficiency anaemia, lead poisoning, sideroblastic anaemia

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2
Q

What are the causes of normocytic anaemia?

A

Acute blood loss, anaemia of chronic disease, aplastic anaemia, haemolytic anaemia, hypothyroidism

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3
Q

What are the causes of macrocytic anaemia?

A

Megaloblastic = B12 and folate deficiency
Normoblastic = alcohol, reticulocytosis, hypothyroidism, liver disease, azathioprine

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4
Q

What are the signs and symptoms of anaemia?

A

Tiredness, SOB, headcahes, dizziness, palpitations, pale skin, conjunctival pallor, tachycardia, raised respiratory rate

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5
Q

What investigations should you do in someone with suspected anaemia?

A

FBC, reticulocyte count, blood film, renal profile, LFTs, ferritin and haemtinics, intrinsic factor antibodies, TFTs, coeliac disease serology, myeloma screening, direct coombs test, bone marrow biopsy

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6
Q

What are the causes of iron deficiency anaemia?

A

Insufficient dietary iron, coeliac disease, pregnancy, bleeding, heavy periods

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7
Q

What signs are specifically associated with iron deficiency anaemia?

A

Pica, hair loss, koilonychia, angular cheilitis, atrophic glossitis, brittle hair and nails

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8
Q

What does the iron profile look like in someone with iron deficiency anaemia?

A

Low ferritin, total iron binding capacity is raised, transferrin low

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9
Q

What are the common side effects associated with oral iron replacement?

A

Constipation, black stools

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10
Q

What should be done in adults with new iron deficiency without a clear cause?

A

Colonoscopy and OGD

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11
Q

What are the causes of B12 deficiency anaemia?

A

Pernicious anaemia, insufficient B12 intake (veggies/vegans), PPI and metformin (reduce B12 absorption)

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12
Q

What is the pathophysiology of pernicious anaemia?

A

Parietal cells of the stomach produce intrinsic factor, intrinsic factor is essential for absorption of B12 in the distal ileum - autoantibodies target either parietal cells or intrinsic factor leading to lack of absorption of vitamin B12

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13
Q

What neurological symptoms are associated with B12 deficiency anaemia?

A

Peripheral neuropathy, loss of vibration sense, loss of proprioception, visual changes, mood and cognitive changes

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14
Q

How can you differentiate between megaloblastic and normoblastic macrocytic anaemia?

A

On blood film - megaloblastic anaemia will have hyper-segmented neutrophils

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15
Q

What is the management of B12 anaemia?

A

IM hydroxocobalamin

If no neuro symtpms - 3 times weekly for two weeks

If neuro symptoms - alternate days until there is no further improvement in symptoms

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16
Q

How do you manage pernicious anaemia?

A

2-3 monthly injections of B12 for life

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17
Q

Which do you have to treat first B12 deficiency or folate deficiency?

A

B12 before folate as it can cause subacute degeneration of the cord

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18
Q

What is haemolytic anaemia?

A

Destruction of RBC resulting in low haemoglobin concentration

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19
Q

What are the features of haemolytic anameia?

A

Anaemia, splenomegaly, jaundice

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20
Q

What are the investigations and results would you find in haemolytic anaemia?

A

FBC - normocytic anaemia
Blood film - schistocytes
Direct Coombs test - positive in autoimmune haemolytic anaemia

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21
Q

What is hereditary spherocytosis and what is the inheritance pattern?

A

Autosomal dominant

Most common inherited haemolytic anaemia

Sphere-shaped RBC that easily break down when passing through the spleen

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22
Q

What results would be found on FBC and blood film in someone with hereditary spherocytosis?

A

Raised reticulocyte count due to rapid turnover of RBC, spherocytes on blood film

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23
Q

Infection with what organism causes an aplastic crisis in spherocytosis?

A

Parvovirus

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24
Q

What is G6PD deficiency and what is the inheritance pattern?

A

X-linked recessive

Caused by a defect in the gene causing for G6PD an enzyme responsible for protecting the cells for oxidative damage

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25
Q

What triggers are there for haemolytic anaemia in those with G6PD deficiency?

A

Infections, drugs, fava beans, medications (ciprofloxacin, sulfonylurea, sulfasalazine)

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26
Q

What are the two types of autoimmune haemolytic anaemia and which is more common?

A

Warm and cold
Warm is more common

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27
Q

What is the management for autoimmune haemolytic anaemia?

A

Blood transfusions, prednisolone, rituximab, splenectomy

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28
Q

What is alloimmune haemolytic anaemia and what are some common causes?

A

Occurs due to foreign red blood cells or foreign antibodies

Transfusion reactions and haemolytic disease of the newborn

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29
Q

What is the inheritance pattern of sickle cell anaemia?

A

Autosomal recessive condition affecting the gene for beta globin on chromsome 11

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30
Q

What screening is done for sickle cell anaemia?

A

Tested on the newborn blood spot screening

Pregnant women at high risk are offered testing

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31
Q

What is a sickle cell crisis?

Including triggers and general management

A

Acute exacerbations that can occur in response to dehydration, infection, stress or cold weather

Management = keeping warm, good hydration and analgesia

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32
Q

What is a vaso-occlusive crisis?

A

Sickle shaped RBC clog capillaries causing distal ischaemia

Presents with pain and swelling in hands or feet

Can cause priapism in men which requires urgent aspiration

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33
Q

What is a splenic sequestration crisis?

A

Caused by RBC blocking blood flow within the spleen which leads to severe anaemia, splenomegaly and hypovolaemic shock

If recurrent - splenectomy can be done to prevent

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34
Q

What is an aplastic crisis?

A

Temporary absence of the creation of new RBC

Usually triggered by infection with parvovirus B19

Treated with blood transfusions

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35
Q

What is acute chest syndrome (in sickle cell disease)?

A

Vessels supplying the lungs become clogged with RBC

Presents with fever, SOB, chest pain, cough and hypoxia

CXR will show new pulmonary infiltrates

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36
Q

How is sickle cell anaemia definitively diagnosed?

A

Haemoglobin electrophoresis

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37
Q

What is the general management of sickle cell anaemia?

A

Antibiotic prophylaxis - usually penicillin V

Hydroxycarbamide - stimulates production of HbF

Crizanlizumab - prevents RBC from sticking to blood vessel wall and thereby reduced crises

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38
Q

What is the inheritance pattern of thalassemia?

A

All types of autosomal recessive

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39
Q

What is the pathophysiology of thalassaemia?

A

RBC are more fragile and break down easily causing a haemolytic anaemia due to defects in protein in haemoglobin

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40
Q

What type of anaemia is seen in thalassemia?

A

Microcytic anaemia that does not respond to iron (microytosis is disproportionate to the Hb drop)

Iron studies will often show iron overload

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41
Q

What investigations can be used to diagnose thalassaemia?

A

Haemoglobin electrophoresis, DNA testing, all women are offered thalassaemia testing during pregnancy

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42
Q

Which ethnicities are more commonly known to have thalassemia?

A

Asian, middle eastern or Mediterranean

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43
Q

Why does thalassemia result in iron overload and what is done to prevent this?

A

There is increased iron absorption in the GI tract or due to multiple blood transfusions

Limit blood transfusions where possible and iron chelation may be required

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44
Q

What is seen on a blood film of someone with alpha thalassaemia?

A

Heinz bodies in the RBCs

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45
Q

What is the difference between beta thalassaemia minor, intermedia and major?

A

Minor = carrier of abnormally functioning beta globin gene

Intermedia = two abnormal copies of beta globin gene or one defective and one deletion gene

Major = two deletion genes

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46
Q

What features are seen in thalassaemia major?

A

Bone marrow is under so much strain to produce extra RBC that is expands –> frontal bossing, enlarged maxilla, depressed nasal bridge and protruding upper teeth

47
Q

What management is used in thalassaemia?

A

Blood transfusions + iron chelation with desferrioxamine, splenectomy, bone marrow transplant

48
Q

What are the risk factors for lymphoma?

A

HIV, EBV, autoimmune conditions, family history, hepatitis

49
Q

What is the presentation of lymphoma?

A

Lymphadenopathy (may be in the neck, axilla or inguinal region) - non-tender, firm or rubbery

In Hodgkin’s may experience lymph node pain after drinking alcohol

B symptoms - fever, weight loss, night sweats

May also have itching, fatigue, cough, SOB

50
Q

What investigation is done in suspected lymphoma and what may you find?

A

Lymph node biopsy

In Hodgkin will find reed-sternberg cells

51
Q

What are the different stages of lymphoma?

A

1 = confined to one node or group of nodes

2 = in more than one group of nodes but on the same side of the diaphragm

3 = affects nodes both above and below the diaphragm

4 = widespread involvement including non-lymphatic organs such as lungs/liver

A = absence of systemic symptoms, B = has B symptoms

52
Q

What is the management of lymphoma?

A

Chemotherapy, radiotherapy, stem cell transplant

53
Q

What is tumour lysis syndrome?

A

Usually triggered by introduction of chemotherapy

Occurs from the breakdown of tumour cells and subsequent release of chemicals

Present with AKI, high phosphate and high uric acid

54
Q

What is used to treat tumour lysis syndrome?

A

IV fluids, allopurinol, rasburicase

55
Q

What is the pathophysiology of multiple myeloma?

A

Affects the plasma cells in the bone marrow which leads to production of large quantities of specific paraprotein, affects multiple bone marrow areas in the body

56
Q

What two conditions can progress to multiple myeloma?

A

MGUS, smouldering myeloma

57
Q

Which antibody is most commonly produced in multiple myeloma?

A

IgG

58
Q

What are the features of multiple myeloma?

A

Elevated calcium, renal failure, anaemia, bone lesions and bone pain

59
Q

Why does anaemia occur in myeloma?

A

Cancerous plasma cells invade the bone marrow resulting in suppression of other blood lines leading to anaemia, leukopenia and thrombocytopenia

60
Q

Why does myeloma result in bone disease?

A

Cytokines are released from the abnormal plasma cells –> increased osteoclast activity and suppressed osteoblast activity –> osteolytic lesions –> high calcium

61
Q

Why does myeloma result in kidney disease?

A

Paraproteins are deposited in the kidneys, hypercalcaemia affects kidney function, dehydration, glomerulonephritis and medications that are used to treat the condition

62
Q

Which investigations are done in myeloma?

A

Serum protein electrophoresis - detect paraproteinemia

Urine protein electrophoresis - detect Bence-Jones protein

Bone marrow biopsy - shows plasma cells

63
Q

What is used to treat myeloma?

A

Chemotherapy and stem cell transplant can be used

64
Q

Which type of leukaemia can result in transformation from a myeloproliferative disorder and is associated with Auer rods?

A

AML

65
Q

Which leukaemia is most common in children and is associated with Downs syndrome?

A

ALL

66
Q

Which type of leukaemia is associated with the Philadelphia chromosome?

A

CML

67
Q

Which type of leukaemia is associated with warm haemolytic anaemia, Richter’s transformation and smudge cells?

A

CLL

68
Q

What is seen on a FBC in those with leukaemia?

A

Can result in a pancytopenia due to excessive production of a single type of white blood cells which suppresses all other cells lines - often will be isolated rise in WBC

69
Q

What symptoms are associated with leukaemias?

A

Fatigue, fever, pallor, petechiae, bruising, abnormal bleeding, lymphadenopathy, hepatosplenomegaly

70
Q

In those with suspected leukaemia what investigations should be done?

A

FBC within 48 hours
Blood film
Bone marrow biopsy

71
Q

What is the philadelphia chromosome translocation?

A

t(9:22) - translocation between chromosome 9 and chromosome 22

72
Q

How is leukaemia managed?

A

Chemotherapy and targeted therapies such as rituximab and tyrosine kinase inhibitors

73
Q

Are blast cells seen in acute or chronic leukaemias?

A

Acute

74
Q

What are the risks factors for VTE?

A

Immobility, recent surgery, long haul travel, pregnancy, oestrogen therapy, malignancy, polycythaemia, SLE, thrombophilia

75
Q

What are some examples of thrombophilias?

A

Antiphospholipid syndrome, factor V leiden

76
Q

What are the contraindications of LMWH?

A

Active bleeding or existing anticoagulation

77
Q

What are the contraindications to anti-embolic stockings ?

A

Peripheral arterial disease

78
Q

What is done if the well score indicates DVT is unlikely?

A

D-dimer is performed and if D-dimer is raised a USS of leg vein is done

79
Q

What is done if well score demonstrates that DVT is likely?

A

Leg vein USS is performed immediately

80
Q

What is the first line anticoagulant in VTE normally, in pregnancy and those with antiphospholipid syndrome?

A

Normally = DOAC
Antiphospholipid syndrome = warfarin
Pregnancy = LMWH

81
Q

How long is anticoagulation continued for those with provoked and unprovoked DVT?

A

Provoked = 3 months
Cancer = 6 months
Unprovoked = long-term

82
Q

What are the causes of thrombocytopenia?

A

B12/folate deficiency, liver failure, leukaemia, chemotherapy, medications (sodium valproate, methotrexate), ITP, TTP

83
Q

What symptoms can occur when platelets drop below 50 and then below 10?

A

Nosebleeds, bleeding gums, heavy periods, easy bruising, haematuria, rectal bleeding

Platelets below 10 –> GI bleeding and intracranial haemorrhage

84
Q

What is ITP, how does it present and how is it managed?

A

Antibodies are created against platelets leading to isolated low platelet count

Presents with bleeding and purpura

Managed with prednisolone or IV immunoglobulins

85
Q

What is TTP, how does it present and how is it managed?

A

Condition where tiny thrombi develop throughout the small vessels using up platelets

Causes low platelets, purpura, tissue ischaemia and end organ damage

Managed with plasma exchange, steroids and rituximab

86
Q

What is heparin induced thrombocytopenia, how does it present and how is it managed?

A

Development of antibodies against platelets in response to heparin

Presents 5-10 days after starting heparin with DVT and low platelets

Stop heparin and use alternative anticoagulant

87
Q

What are some complications associated with multiple myeloma?

A

Infection, VTE, stroke, bone pain/fractures, peripheral neuropathy, spinal cord compression

88
Q

What is the most common inherited cause of prolonged bleeding?

A

Von Willebrand disease

89
Q

How is Von Willebrand disease managed?

A

Does not require daily treatment but needed in response to severe bleeding or in preparation for surgery

Includes desmopressin, tranexamic acid, von willebrand factor infusion

90
Q

Which factors are deficient in Haemophilia A and B?

A

A = VIII
B = IX

91
Q

What is the inheritance pattern of von willebrand disease?

A

Most commonly autosomal dominant

92
Q

What is the inheritance pattern of haemophilia?

A

X-linked recessive

93
Q

How does haemophilia present?

A

Spontaneous bleeding or severe bleeding in response to minor trauma

Spontaneous haemarthrosis in ankle, knee or elbow

94
Q

How is haemophilia managed?

A

Affected clotting factor can be given by IV infusion given regularly or in response to bleeding

95
Q

What are relative causes of polycythaemia?

A

Dehydration or stress

96
Q

What are the secondary causes of polycythaemia?

A

COPD, altitude, OSA, excessive EPO e.g. uterine fibroids

97
Q

Which gene is associated with myeloprolifertaive disorders?

A

JAK2

98
Q

What are the FBC findings in someone with myelofibrosis?

A

Low Hb, high or low WBC, high or low platelet count

99
Q

What are the FBC findings in someone with polycythaemia Vera?

A

High Hb, often associated with high WBC and platelets

100
Q

What are the FBC findings associated with essential thrombocythaemia?

A

High platelet count

101
Q

How are myeloprolifertaive disorders diagnosed?

A

Bone marrow biopsy

102
Q

What clinical signs are seen in someone with polycythaemia?

A

Ruddy complexion, conjunctival plethora, splenomegaly, hypertension

103
Q

What is the treatment for primary myelofibrosis?

A

No active treatment if mild
Manage any complications
Hydroxycarbamide chemotherapy
JAK2 inhibitors
Allogenic stem cell transplantation

104
Q

What is the treatment for polycythaemia vera?

A

Venesection to keep Hb in normal range
Aspirin to reduce thrombus formation
Hydroxycarbamide chemotherapy

105
Q

What is the treatment for essential thrombocythaemia?

A

Aspirin to reduce risk of thrombus formation
Hydroxycarbamide chemotherapy

106
Q

What can myeloproliferative disorders develop into?

A

They can develop into acute myeloid leukaemia

107
Q

What is myelodysplastic syndrome?

A

Form of cancer that results in inadequate production of blood cells –> anaemia, neutropenia and thrombocytopenia

108
Q

What is the treatment for myelodysplastic syndrome?

A

Watchful waiting, supportive treatment with blood transfusions and platelet transfusions, EPO, allogenic stem cell transplant

109
Q

What clotting abnormality will be present in von willebrand disease?

A

Prolonged APTT

normal INR

110
Q

What features are seen in the bloods of someone with DIC?

A

Low platelets, prolonged clotting times and raised fibrin degradation products

111
Q

What features indicate poor prognosis in lymphoma?

A

B symptoms, increasing age, advanced disease, male, lymphocyte depleted subtype

112
Q

What is the classic symptom of polycythaemia rubra vera?

A

Itching following exposure to hot water/hot weather

113
Q

What is the 1st line treatment for CML?

A

Tyrosine kinase inhibitors such as imatinib (87% effective)

114
Q

How is superficial thrombophlebitis managed?

A

Oral NSAIDs and compression stockings

Finals (21 decks)

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