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Phase 2a - Systems > Haematology > Flashcards

Haematology Flashcards

1
Q

give 3 causes of microcytic anaemia

A

iron-deficiency anaemia.
thalassaemia.
sideroblastic anaemia.

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2
Q

give 3 causes of normocytic anaemia

A

acute blood loss; anaemia of chronic disease; bone marrow failure; renal failure; hypothyroidism; haemolysis; pregnancy

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3
Q

give 3 general symptoms of anaemia

A

fatigue, dyspnoea, faintness, palpitations, headache, tinnitus, anorexia

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4
Q

give 3 general signs of anaemia

A

pallor, tachycardia, systolic flow murmurs, enlarged heart

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5
Q

give a physiological cause of anaemia

A

pregnancy (normocytic)

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6
Q

give 3 causes of iron-deficiency anaemia

A

blood loss, poor diet, malabsorption, hookworm

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7
Q

describe what is seen on a peripheral blood film in iron-deficiency anaemia

A

microcytic hypochromic RBCs, varying in size and shape (anisocytosis and poikilocytosis)

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8
Q

give 3 specific features of iron deficiency anaemia

A

koilonychias, angular chelitis and glossitis

spoon nails, inflammation in corner of mouth, inflammation of tongue

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9
Q

In iron deficiency anaemia, what will happen to the iron, ferritin and total iron binding capacity (TIBC)?

A

iron and ferritin are decreased.

TIBC is increased.

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10
Q

how would you treat iron deficiency anaemia? how long would this treatment be given?

A

oral ferrous sulphate - given until anaemia resolved + further 3/12

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11
Q

what are some side effects of ferrous sulphate?

A

nausea, abdominal discomfort, diarrhoea/constipation, black stools

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12
Q

what diagnostic tests would you perform if you suspected anaemia?

A

blood count and film.

ferritin, B12 etc.

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13
Q

how would you treat anaemia of chronic disease?

A

treat underlying disease.

give Epo.

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14
Q

what is sideroblastic anaemia?

A

microcytic hypochromic.

inherited or acquired disorder - body has enough iron but can’t incorporate it into Hb.

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15
Q

how would you diagnose sideroblastic anaemia?

A

bone marrow sample - presence of sideroblasts - RBCs being produced with a ring of excess iron around the nucleus.

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16
Q

how would you treat sideroblastic anaemia?

A

Pyridoxine (vit B6).

repeated RBC transfusion (+iron chelation!)

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17
Q

give 3 causes of sideroblastic anaemia.

A

inherited; myeloid leukaemia; drugs (isoniazid); alcohol misuse; lead toxicity.

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18
Q

what causes pernicious anaemia?

A

autoimmune disease - antibodies against parietal cells and intrinsic factor, so these are destroyed leading to achlorydia and B12 malabsorption

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19
Q

how does B12/folate deficiency lead to anaemia?

A

B12 and folate needed for DNA synthesis - developing red cells can’t divide, they are stuck as large immature cells (megaloblastic) which then become macrocytic RBCs

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20
Q

what specific sign characterises pernicious anaemia?

A

mild jaundice due to haemolysis - pallor + jaundice = lemon tinge to skin

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21
Q

what specific tests would you perform if you suspected pernicious anaemia?

A

FBC, blood film and:

parietal cell antibodies, intrinsic factor antibodies

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22
Q

how would you treat pernicious anaemia?

A

IM injection of hydroxycobalamin

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23
Q

give some causes of folate deficiency

A

poor diet.
increased demand - pregnancy or increased cell turnover.
malabsorption.
drugs, alcohol.

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24
Q

how would you treat folate-deficiency anaemia?

A

oral folic acid + B12

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25
Q

give some acquired causes of haemolytic anaemia

A

Drug-induced, autoimmune haemolytic anaemia (AIHA), hep B and C, haemolytic-uraemic syndrome (HUS), TTP, DIC, malaria

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26
Q

give some hereditary causes of haemolytic anaemia

A

G6PD deficiency, pyruvate kinase deficiency, hereditary spherocytosis, sickle cell disease, thalassaemia

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27
Q

what is aplastic anaemia?

A

anaemia due to bone marrow failure - pancytopenia with hypoplastic marrow - marrow stops making all cells

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28
Q

give some causes of aplastic anaemia

A

autoimmune, drugs, irradiation, inherited

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29
Q

give 2 specific features of aplastic anaemia

A

bruising with minimal trauma.

blood blisters in mouth.

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30
Q

what test would you perform in aplastic anaemia? what would it show?

A

bone marrow biopsy - hypocellular aplastic bone marrow with increased fatty spaces

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31
Q

how would you treat aplastic anaemia?

A

allogenic marrow transplant.

or immunosuppression - ciclosporin.

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32
Q

what is sickle cell anaemia?

A

autosomal recessive disorder causing production of abnormal beta globin chains.
HbSS/HbAS instead of HbA (HbAS is carrier state)

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33
Q

being a carrier of sickle cell protects you against what disease?

A

falciparum malaria

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34
Q

what is the pathogenesis of sickle cell anaemia?

A

HbS polymerizes when deoxygenated causing RBCs to sickle - rigid, fragile cells that occlude small vessels and have short lifespan (haemolyse).

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35
Q

describe the clinical features of vaso-occlusive crises seen in sickle-cell anaemia

A

severe pain due to effect on marrow of microvascular occlusion. acutely painful hands and feet.

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36
Q

what is splenic sequestration?

A

a type of sickle-cell crisis:
vaso-occlusion produces acute painful enlargement of spleen.
pooling of RBCs in spleen = hypovolaemia = circulatory collapse and death.
immediate transfusion needed.

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37
Q

give 3 long-term complications of sickle-cell disease

A

poor growth, bone problems, infections, leg ulcers, neurological complication, gallstones, retinal disease, lung fibrosis, pulmonary hypertension

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38
Q

what tests would you perform in a case of sickle cell disease? what would you see?

A

FBC.
blood film - sickle cells and target cells (pale centre).
sickle solubility test - HbSS/HbAS instead of HbA
Hb electrophoresis - distinguishes HbSS and HbAS.

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39
Q

how would you treat sickle cell disease?

A

hydroxycarbamide.
prophylactic abx/immunisations.
bone marrow transplant.

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40
Q

describe the genetics of beta thalassaemia

A

mutations in beta-globin genes (chromosome 11) leading to decreased/no beta chain production

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41
Q

how does beta thalassaemia cause anaemia?

A

unmatched globins and excessive alpha chains precipitate - increased haemolysis and ineffective erythropoiesis.

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42
Q

what are the features of minor beta thalassaemia?

A

symptomless carrier state. mild anaemia. hypochromic and microcytic.

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43
Q

what are the features of medium beta thalassaemia?

A

moderate anaemia with splenomegaly, gallstones, leg ulcers etc. doesn’t require transfusions.

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44
Q

what are the features of major beta thalassaemia?

A

severe anaemia - needs regular transfusions.
presents in 1st year - abnormalities in both beta globin genes.
characteristic head shape and hepatosplenomegaly.

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45
Q

how would you treat beta thalassaemia?

A

folate supplements.
regular blood transfusions - desferrioxamine (iron-chelator) to prevent iron overload.
bone marrow transplant = cure.

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46
Q

what are the genetics of alpha thalassaemia?

A

gene deletions (not point mutations as in beta) in alpha globin chain genes on chromosome 16

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47
Q

describe the features of a 4+ gene deletion alpha thalassaemia

A

no alpha chains synthesised.

infants = stillborn, or die very quickly.

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48
Q

describe the features of a 3 gene deletion alpha thalassaemia

A

moderate anaemia and splenomegaly, jaundice, leg ulcers

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49
Q

describe the features of a 2 gene deletion alpha thalassaemia

A

microcytosis ± mild anaemia

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50
Q

how many alpha globin gene deletions may a patient have and still appear clinically normal?

A

1

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51
Q

what is glucose-6-phosphate dehydrogenase (G6PD) deficiency?

A

X linked haemolytic condition caused by mutation in the G6PD gene

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52
Q

what does G6PD do?

A

enzyme of the hexose monophosphate pathway - needed for generating reduce glutathione which protects RBC membrane from damage

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53
Q

does G6PD deficiency affect mainly men or women?

A

men

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54
Q

give some precipitants of G6PD deficiency crises

A

henna.
favism (ingesting fava beans).
drugs, infections.

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55
Q

what are the features of an acute G6PD deficiency haemolytic episode?

A

anaemia, fever, jaundice, dark urine.

bite and blister cells on blood film.

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56
Q

what is polycythaemia?

A

an increase in Hb, PCV - packed cell volume (haematocrit) - or RCC (red cell count)
PCV = % by volume of RBCs in blood

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57
Q

what is the difference between relative and absolute polycythaemia?

A 
relative = low plasma volume, but no change in cell numbers.
absolute = increase in RBC mass.
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58
Q

who gets relative polycythaemia?

A

middle aged obese males, smokers, high alcohol intake, hypertension

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59
Q

what causes primary polycythaemia?

A

polycythaemia rubra vera - malignant proliferation of a clone from one pluripotent marrow stem cell

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60
Q

what causes secondary polycythaemia?

A

due to hypoxia - high altitudes, chronic lung disease, heavy smoking

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61
Q

what gene mutation causes polycythaemia rubra vera?

A

JAK2

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62
Q

In polycythaemia rubra vera, what is there an excess proliferation of?

A

red cells, white cells and platelets - hyperviscosity/hypervolaemia.

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63
Q

give 3 symptoms of polycythaemia

A

headache, dizziness, tinnitus, visual disturbance, itching after warm bath, burning in fingers and toes.

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64
Q

give 3 things you might find on examination in polycythaemia

A

facial plethora (red, turgid face), splenomegaly (only in PRV), gout, arterial/venous thrombosis

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65
Q

why do polycythaemia patients get gout?

A

increased urate from RBC turnover

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66
Q

what will the marrow of a patient with polycythaemia rubra vera show?

A

hypercellularity with erythroid hyperplasia

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67
Q

how would you treat polycythaemia rubra vera?

A

venesection, hydroxycarbamide, low dose aspirin

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68
Q

how would you treat secondary polycythaemia?

A

treat primary cause.

oxygen therapy + smoking cessation.

69
Q

list 4 risk factors of DVT

A

increasing age, pregnancy, synthetic oestrogens (pill, HRT), trauma, surgery, past DVT, cancer, obesity, immobility, thrombophilia

70
Q

what other disease may a DVT present as?

A

pulmonary embolism

71
Q

describe the clinical features of a DVT

A

warm, tender calf, with erythema. fever. pitting oedema.

72
Q

what investigations would you do on a patient with a suspected DVT?

A

D-dimer - -ve result excludes DVT, +ve doesn’t mean it is DVT.
doppler US.

73
Q

give 4 features included in the Wells score

A

active cancer, immobility, major surgery in last 4 weeks, local tenderness, swollen leg, pitting oedema, collateral superficial veins

74
Q

how would you manage a patient with a DVT?

A

LMWH or fondaparinux - short term anticoagulation.
warfarin or NOAC - long term anticoagulation.
compression stockings.
mobilise, stop the pill.

75
Q

what steps can be taken to prevent DVT?

A

stop the pill.
early mobilisation.
compression stockings/leg elevation.
LMWH/fondaparinux.

76
Q

how does fondaparinux work as an anticoagulant?

A

factor Xa inhibitor - prevents the final coagulation pathway from continuing, preventing formation of fibrin clot.

77
Q

how do heparins work as anticoagulants?

A

activate antithrombin, which inactivates factor Xa.

LMWHs also act to inhibit factor Xa directly.

78
Q

how would you stop bleeding in an over-anticoagulated patient?

A

IV vitamin K - warfarin ‘antidote’

protamine = heparin antidote

79
Q

what is disseminated intravascular coagulation?

A

massive activation of clotting cascade leads to lots of fibrin deposition within vessels.
using up all your platelets and coagulation factors forming these intravascular clots - so get bleeding elsewhere.

80
Q

give 2 causes of DIC?

A 
sepsis.
major trauma/burns.
advanced cancer.
obstetric complications.
acute promyelocytic leukaemia.
81
Q

what are the clinical features of DIC?

A

profuse bleeding where there shouldn’t be any - from venepuncture sites, from nose/mouth

82
Q

what results would you find on investigation of a patient with DIC?

A

low platelets, prolonged prothrombin time, very low fibrinogen, increased D dimer

83
Q

other than treating the underlying cause, how would you manage a patient with DIC?

A

maintain blood volume and tissue perfusion - replacement platelets FFP (fresh frozen plasma) and cryoprecipitates

84
Q

what is immune/idiopathic thrombocytopenia purpura (ITP)?

A

antiplatelet autoantibodies lead to immune destruction of platelets - low platelet count

85
Q

what are the main features of ITP?

A

easy bruising + purpura - rash of purple spots on skin due to internal bleeding.

isolated thrombocytopenia - low platelets, but everything else is normal.

86
Q

how would you treat ITP?

A

prednisolone.

splenectomy or chemo

87
Q

what is thrombotic thrombycytopenia purpura (TTP)?

A

deficiency of protease that breaks down vWF - widespread platelet adhesion/aggregation leading to microvascular thrombosis + thrombocytopenia.

88
Q

what is thrombocytopenia?

A

lack of platelets

89
Q

give some causes of TTP

A

congenital
sporadic
autoantibody mediated - pregnancy, SLE, infection

90
Q

how might a patient with TTP present?

A

purpura, fever, fluctuating cerebral dysfunction, haemolytic anaemia

91
Q

how would you treat a patient with TTP?

A

plasma exchange.

steroids/monoclonal antibodies.

92
Q

what is haemophilia A?

A

X-linked recessive inherited factor VIII deficiency

93
Q

how would a patient with haemophilia A present?

A

early in life/after surgery or trauma.

bleeds into joints and muscles - arthropathy and haematomas.

94
Q

how would you diagnose and treat haemophilia A?

A

factor VIII assay

IV recombinant factor VIII

95
Q

what is haemophilia B? how is it treated?

A

factor IX deficiency - same clinical behaviour as haemophilia A.
treat with factor IX.

96
Q

what is von Willebrand’s disease?

A

deficiency of vWF - leads to platelet dysfunction

97
Q

what clinical signs indicate a platelet disorder (e.g. von Willebrand’s disease)?

A

bruising, epistaxis, menorrhagia, excessive bleeding after tooth extraction

98
Q

how would you treat von Willebrand’s disease?

A

desmopressin for mild bleeds.

vWF-containing factor VIII concentrate.

99
Q

what cell lines are affected in acute lymphoblastic leukaemia (ALL)?

A

lymphoblasts - B/T cell precursors

100
Q

which leukaemia most commonly affects children?

A

ALL - acute lymphoblastic leukaemia

101
Q

name a trigger of ALL

A

ionising radiation during pregnancy

102
Q

which of the leukaemias is associated with Downs syndrome?

A

ALL - acute lymphoblastic leukaemia

103
Q

give some clinical features of ALL

A

marrow failure - anaemia, infections, bleeding.

hepatosplenomegaly, lymphadenopathy, CNS involvement, bone pain.

104
Q

what infections are commonly seen in ALL patients?

A

CMV, measles, candidiasis, Pneumocystis pneumonia (PCP)

105
Q

what investigations would you carry out on an ALL patient? what would the results show?

A

peripheral blood film and bone marrow aspirate - blast cells.
CXR/CT scan for lymphadenopathy.
LP for CNS involvement.

106
Q

how would you treat ALL?

A

allopurinol. prophylactic abx, antifungals, antivirals.
Chemo - vincristine, prednisolone + daunorubicin.
bone marrow transplant.

107
Q

what cell lines are affected in acute myeloid leukaemia (AML)?

A

blast cells

108
Q

what may trigger AML?

A

long-term chemotherapy

radiation

109
Q

what is the typical age of onset of AML?

A

around 65

110
Q

give some clinical features of AML

A

DIC, hepatosplenomegaly, gum hypertrophy, bleeding, infections, skin involvement

111
Q

how would you diagnose AML?

A

bone marrow biopsy - Auer rods are characteristic

112
Q

how would you treat AML?

A

chemo - daunorubicin and cytarabine.
bone marrow transplant.
ciclosporin ± methotrexate after transplant.

113
Q

what cell lines are affected in chronic myeloid leukaemia (CML)?

A

myeloid

114
Q

what are the genetics behind CML?

A

Philadelphia chromosome - translocation between chromosomes 9 and 22 - t(9;22).
affects tyrosine kinase activity.

115
Q

describe the clinical features of CML

A

chronic and insidious.
weight loss, fatigue, fever, sweats.
gout, bleeding, splenomegaly, bruising, abdo discomfort.

116
Q

which of the leukaemias doesn’t cause recurrent infections?

A

CML - chronic myeloid leukaemia

117
Q

what investigations would you do in CML? what results would you expect?

A

FBC - WCC raised. Hb low.
bone marrow aspiration - hypercellular.
cytogenetic analysis - Ph chromosome.

118
Q

how would you treat CML?

A

Chemo: IMATINIB - tyrosine kinase inhibitor.

stem cell transplant.

119
Q

what cell lines are affected in chronic lymphocytic leukaemia?

A

mature B cells - they have escaped programmed cell death.

120
Q

who does CLL affect? what is the prognosis like?

A

it’s an incurable disease of older people - but some show no/slow progression - have a near normal life expectancy.
(others show active progression so have a worse prognosis).

121
Q

what can trigger CLL?

A

pneumonia

122
Q

give some clinical features of CLL

A

fever, painless lymphadenopathy (rubbery nodes), weight loss, anorexia, hepatospenomegaly, LUQ pain.

123
Q

what would a FBC show in CLL?

A

raised WCC, especially lymphocytes.

low Hb/neutrophils/platelets.

124
Q

how would you treat CLL?

A

chemo: fludarabine + cyclophosphamide + rituximab.
radiotherapy.
stem cell transplants.

125
Q

what histological feature differentiates Hodgkin’s lymphoma from NHL?

A

presence of Reed-Sternberg cells (mirror-image nuclei)

126
Q

what are lymphomas?

A

neoplastic transformations of B and T cells which accumulate in lymph nodes - lymphadenopathy

127
Q

give 3 risk factors for Hodgkin’s lymphoma

A

affected sibling; EBV; SLE; post-transplant; obesity; Westernization

128
Q

at what ages are the 2 peaks of incidence of Hodgkin’s lymphoma?

A

young adults and the elderly

129
Q

describe the lymphadenopathy seen in Hodgkin’s lymphoma. give 2 possible sites.

A

enlarged, painless, rubbery superficial lymphadenopathy.

cervical, axillary, inguinal.

130
Q

give 3 systemic features of Hodgkin’s lymphoma

A

fever; drenching night sweats; weight loss; pruritus; fatigue; anorexia

131
Q

list some differential diagnoses of Hodgkin’s lymphoma

A

any cause of lymphadenopathy - infections, secondary carcinoma, leukaemia, systemic diseases (e.g. SLE, rheumatoid arthritis, sarcoidosis)

132
Q

what investigations would you carry out in Hodgkin’s lymphoma? what results would you expect?

A

lymph node biopsy - histology for Reed Sternberg cells.

FBC - low Hb, raised ESR.

133
Q

describe the staging of Hodgkin’s lymphoma

A

Ann Arbor system:
I = single region
II = 2+ nodal areas involved on one side of diaphragm
III = involvement on both sides of diaphragm
IV = spread beyond nodes
then divided into A and B - B if systemic symptoms are present.

134
Q

how would you treat Hodgkin’s lymphoma?

A

ABVD chemo + radiotherapy - curative.

135
Q

give 3 causes of Non-Hodgkin’s lymphoma (NHL)

A

immunodeficiency - drugs, HIV.

HLTV-1; H pylori; toxins; congenital.

136
Q

what AIDS defining illness is associated with NHL?

A

Burkitt’s lymphoma - jaw lymphadenopathy

137
Q

give some clinical features of NHL

A

painless peripheral lymph node enlargement. systemic symptoms the same as for Hodkin’s - weight loss, fever, sweats.
bone marrow failure, bleeding.

138
Q

what investigations would you do in NHL? what would you expect to see?

A

bloods - normocytic anaemia, raised WCC, neutropenia, thrombocytopenia.
raised ESR/LDH. raised urate.
Lymph node biopsy + bone marrow aspirate.

139
Q

what staging system is used for non-Hodgkin’s lymphoma?

A

Ann Arbor system

140
Q

how would you treat low grade NHL?

A

radiotherapy.

chlorambucil, interferon or rituximab.

141
Q

how would you treat high grade NHL?

A

RCHOP - rituximab, cyclophosphamide, hydroxydaunorubicin, oncovin prednisolone.

142
Q

what cell line is affected by myeloma?

A

plasma cells - malignant clonal expansion - produce excessive amounts of one type of Ig

143
Q

what are the diagnostic criteria for myeloma?

A

1) monoclonal protein band on serum/urine electrophoresis
2) increased plasma cells on bone marrow biopsy
3) evidence of end organ damage (hypercalcaemia, renal failure, anaemia)

144
Q

describe the clinical features of myeloma

A

bone pain, osteolytic lesions, pathological fractures, anaemia, bleeding, recurrent bacterial infection. renal impairment.

145
Q

what investigations would be carried out in myeloma? what would you see?

A

blood film - Rouleaux formation (RBCs stack on top of each other).
urine - Bence Jones protein.
X ray - punched out lesions e.g. pepper pot skull.

146
Q

how would you treat myeloma?

A

bone pain - bisphosphonates and analgesia - avoid NSAIDs (kidneys).
fluids, abx, correct anaemia.
Chemo - melphalan + prenisolone ± thalidomide.

147
Q

give 3 complications of myeloma

A

hypercalcaemia of malignancy.
spinal cord compression.
hyperviscosity.
acute renal failure.

148
Q

how is malaria transmitted?

A

protozoa that is transmitted by bite of infected female Anopheles mosquito

149
Q

what are the 4 species of plasmodium that cause malaria?

A

P vivax, P ovale, P malariae, P falciparum

150
Q

give 3 general clinical features of malaria

A

fever, malaise, headache, vomiting, diarrhoea, rigors, sweats

151
Q

give 3 features of Vivax/ovale malaria

A

anaemia, tender hepatosplenomegaly, mild illness

152
Q

give 3 features of Malariae malaria

A

relatively mild, more chronic, glomeulonephritis/nephrotic syndrome

153
Q

give 3 features of Falciparum malaria

A

anaemia, jaundice, hepatosplenomegaly, cerebral malaria (fits, confusion, coma), metabolic acidosis, pulmonary oedema, hypoglycaemia, diarrhoea, DIC

154
Q

what investigation would you perform to diagnose malaria? what does this tell you?

A

thick and thin blood smears
thick - diagnoses malaria
thin - quantifies % of infected RBCs, identifies species

155
Q

what must you take into account, before treating a malaria patient?

A

whether they’ve taken any prophylaxis - which type? likely their malaria is resistant, so don’t treat them with this!

156
Q

how would you treat falciparum malaria?

A

uncomplicated - oral riamet or quinine ± doxycycline.

complicated - IV artesunate or quinine.

157
Q

how would you treat non-falciparum malaria?

A

oral chloroquine

158
Q

what drugs can be used as prophylaxis for malaria?

A

mefloquine, atovaquant, proguanil, chloroquine, doxycycline.

159
Q

list 3 causes of macrocytic anaemia

A

B12/folate deficiency.
haemolytic anaemias.
alcoholism, liver disease, hypothyroidism.

160
Q

what must you assess before giving anticoagulation therapy? how would you assess this?

A 
bleeding risk.
HAS-BLED.
Hypertension.
Abnormal liver/renal function.
Stroke.
Bleeding.
Labile INR.
Elderly.
Drugs/alcohol.
161
Q

give a main advantage and disadvantage of NOACs

A

adv - no need for regular INR monitoring - easier for patient.
dis - don’t have an antidote, so patient at risk of massive haemorrhage if injured etc.

162
Q

which leukaemia commonly affects the elderly?

A

CML

163
Q

if you see blast cells on a blood film, what does this suggest?

A

an acute leukaemia

164
Q

if Auer rods are seen on a blood film, which leukaemia is this?

A

AML

165
Q

if smudge cells are seen on a blood film, which leukaemia is this?

A

CLL

166
Q

what are the signs of end-organ damage seen in myeloma?

A 
CRAB.
Calcium - hypercalcaemia (bones).
Renal failure
Anaemia
Bone lytic lesions e.g. pepperpot skull.
167
Q

give an example of an iron chelator.

how do these drugs work?

A

desferrioxamine.

binds free iron in bloodstream and enhance its elimination in urine.

168
Q

list some triggers of sickle cell crisis

A

cold, dehydration, infection, hypoxia.

Phase 2a - Systems (18 decks)

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