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Med School Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

Components of blood?

A

Plasma (clotting factors, albumin and Igs)
Cells (RBCs, WBCs and platelets)

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2
Q

Granulocytes vs agranulocytes?

A

Granulocytes = neutrophils, eosinophils, basophils
Agranulocytes = monocytes, lymphocytes

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3
Q

Main types of lymphocyte?

A

B cell
T cell
NK cell

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4
Q

Main types of differentiated T cell, CD expressed and MHC they present to?

A

T helper (CD4+) cell
→ presents to MHC class II
Cytotoxic (CD8+) cell
→ presents to MHC class I

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5
Q

What does CD stand for and represent?

A

Cluster of differentiation
Specific set of antigens on a cell’s surface

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6
Q

CD used to calculate total T cell count and why?

A

CD3
Present on all mature T cells

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7
Q

Average lifespan of RBCs, platelets and neutrophils?

A

RBCs = 90-120 days
Platelets = 10 days
Neutrophils = 4 days

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8
Q

Cell morphology associated with IDA, thalassaemia, hyposplenism, G6PD deficiency, myelofibrosis, haemolysis?

A

IDA = target cells, “pencil” pokilocytes
Thalassaemia = target cells, basophilic stippling
Hyposplenism = target cells, howell-jolly bodies
G6PD deficiency = heinz bodies, bite cells
Myelofibrosis = leukoerythroblastosis, “tear drop” poikilocytes
Haemolysis = schistocytes

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9
Q

Adult haemoglobin composition and globin chain structures?

A

96% HbA = 2 α and 2 β chains
2% HbA2 = 2 α and 2 δ chains
2% HbF = 2 α and 2 γ chains

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10
Q

Clinical relevance of Hb, Hct, MCV, MCH, MCHC, retic count, haptoglobin, ferritin, transferrin, TIBC, transferrin saturation?

A

Hb = amount of Hb in blood
Hct = % of blood that is RBCs
MCV = average RBC size
MCH = amount of Hb per RBC
MCHC = conc. of Hb in a given volume
Retic count = number of immature RBCs, indicator of bone marrow activity
Haptoglobin = decreased if free Hb
Ferritin = amount of iron stores
Transferrin = amount of iron transporters
TIBC = amount of transferrin available to bind iron
Transferrin saturation = % of transferrin bound to iron

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11
Q

Features of anaemia?

A

Fatigue
SOB
Pallor
Angina
Palpitations
Koilonychia
Atrophic glossitis
Angular stomatitis

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12
Q

Causes of microcytic anaemia (MCV < 80fL)?

A

Iron deficiency anaemia (IDA)
Thalassaemia
Sideroblastic anaemia

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13
Q

Where is iron absorbed vs stored?

A

Absorbed = duodenum and proximal jejunum
Stored = RBC (2/3rds), ferritin and haemosiderin (1/3rd)

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14
Q

Blood test features of IDA?

A

Low iron
Low ferritin
High TIBC
High transferrin
Low transferrin saturation

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15
Q

New iron deficiency in an adult without a clear cause?

A

Refer for OGD and colonoscopy

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16
Q

Management options for IDA?

A

Increase dietary iron
Oral ferrous sulfate
IV iron infusion
Blood transfusion

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17
Q

How much should iron rise during treatment?

A

10 grams/litre/week

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18
Q

Genetic inheritance of thalassaemias?

A

Autosomal recessive

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19
Q

Features of thalassaemia?

A

Anaemia symptoms
Haemolysis e.g. jaundice
Hepatosplenomegaly
Bone deformities
Failure to thrive (kids)

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20
Q

Outline the genetics of α-globin chains?

A
  • 2 genes on chromosome 16 code for α-globin
  • 2 copies of chromosome 16 in each diploid cell means 4 α-globin alleles (e.g. αα/αα)
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21
Q

α thalassaemia mutations and their clinical name?

A

1 deleted allele = silent carrier
2 deleted alleles = α thalassaemia trait
3 deleted alleles = HbH disease
4 deleted alleles = Hb Barts

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22
Q

What is HbH disease?

A

Lack of α-globin production causes excessive amounts of β-globin
β-globins bind together to form HbH

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23
Q

Outline the genetics of β-globin chains?

A
  • 1 gene on chromosome 11 codes for β-globin
  • 2 copies of chromosome 11 in each diploid cell means 2 β-globin alleles (e.g. ββ)
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24
Q

Types of β-globin mutation?

A

β+ = reduced chain synthesis
β0 = no chain synthesis

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25
Q

β thalassaemia mutations and their clinical name?

A

β0β or β+β = thalassamia minor
β+β+ or β+β0 = thalassaemia intermedia
β0β0 = thalassaemia major

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26
Q

Investigation for thalassaemia and feature of β?

A

Hb electrophoresis
β thalassaemia = increased HbA2

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27
Q

Management of thalassaemia?

A

Blood transfusions (if symptomatic)
Iron chelation e.g. desferrioxamine (if iron overload)
Splenectomy (if severe haemolysis)
Bone marrow transplantation

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28
Q

Outline the pathophysiology of sideroblastic anemia?

A
  • Defect in heme synthesis within RBC mitochondria
  • Iron unable to be incorporated so low Hb
  • Iron accumulates within mitochondria
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29
Q

Sub-types and causes of macrocytic anaemia (MCV > 100fL)?

A

Megaloblastic
→ B12 deficiency, folate deficiency
Normoblastic (non-megaloblastic)
→ alcohol, liver disease, hypothyroidism, pregnancy, myelodysplasia, reticulocytosis

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30
Q

Where is B12 vs folate absorbed?

A

B12 = terminal ileum
Folate = duodenum and jejunum

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31
Q

Most common cause of B12 deficiency?

A

Pernicious anaemia

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32
Q

Features of B12 deficiency?

A

Anaemia symptoms
Atrophic glossitis
Angular stomatitis
Mood changes
Peripheral neuropathy
Loss of vibration or proprioception

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33
Q

Management of B12 deficiency?

A

IM hydroxocobalamin
→ 3 times a week for 2 weeks
→ then once every 3 months

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34
Q

Management of folate deficiency?

A

PO folate
→ once every day for 3 months

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35
Q

Advice for treating mixed B12 and folate deficiency?

A

Treat B12 deficiency first!
Starting with folic acid can cause subacute combined degeneration of the spinal cord

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36
Q

Causes of normocytic anaemia (MCV 80-100 fL)?

A

Anaemia of chronic disease
Chronic kidney disease
Aplastic anaemia
Haemolytic anaemia
Acute blood loss

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37
Q

Spurious (false) normocytic anaemia cause?

A

Fluid overload e.g. heart failure, CKD
(Increased plasma volume dilutes RBCs)

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38
Q

Outline the pathophysiology of anaemia of chronic disease?

A
  • High levels of inflammatory cytokines
  • IL-6 causes hepcidin release from the liver
  • Hepcidin decreases ferroportin activity
  • Less iron is absorbed so less Hb produced
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39
Q

Outline the pathophysiology of aplastic anaemia?

A
  • Immune destruction of bone marrow or premature death of haematopoietic stem cells
  • Causes pancytopaenia and hypocellular marrow
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40
Q

Triggers of aplastic anaemia?

A

Infection e.g. parvovirus
Drugs e.g. carbamazepine
Autoimmune disease
Radiation/chemical exposure

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41
Q

Features of haemolysis?

A

Anaemia symptoms
Jaundice
Gallstones
Hepatosplenomegaly

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42
Q

Pathophysiology of intravascular haemolysis and causes?

A

RBCs destroyed within vessels
→ ABO mismatched blood transfusion
→ cold-agglutinin disease (IgM)
→ red cell fragmentation e.g. DIC, TTP, HUS, prosthetic heart valve
→ paroxysmal nocturnal haemoglobinruria
→ G6PD deficiency

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43
Q

Blood test feature of intravascular haemolysis?

A

Low haptoglobin

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44
Q

Pathophysiology of extravascular haemolysis and causes?

A

RBCs destroyed in the spleen
→ haemoglobinopathies e.g. sickle cell
→ warm-agglutinin disease (IgG)
→ hereditary spherocytosis
→ haemolytic disease of the newborn

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45
Q

Outline the pathophysiology of Disseminated Intravascular Coagulation (DIC)?

A
  • Trigger e.g. infection causes mass release of procoagulants
  • Widespread formation of thrombi
  • Thrombi damage RBCs causing haemolysis
  • Clotting factors diminish causing bleeding
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46
Q

Blood test features of Disseminated Intravascular Coagulation (DIC)?

A

Prolonged PT/APTT
Thrombocytopenia
Low fibrinogen
Fibrinolysis products (e.g. D-dimer)

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47
Q

Outline the pathophysiology of Thrombotic Thrombocytopenic Purpura (TTP)?

A
  • Deficiency of metalloprotease (ADAMTS13) which cleaves vWF multimers
  • Large vWF multimers cause platelets to clump within vessels and form thrombi
  • Thrombi damage circulating RBCs causing haemolysis
  • Platelets diminish causing thrombocytopenia
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48
Q

AIHA vs non-AIHA examples and test to differentiate?

A

AIHI = warm-agglutinin and cold-agglutinin disease
Non-AIHI = all other haemolytic anaemias
Investigation = direct Coomb’s test

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49
Q

Management options for warm (IgG) AIHI?

A

1st line = steroids
2nd line = rituximab
3rd line = splenectomy

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50
Q

Management options for cold (IgM) AIHI?

A

1st line = supportive e.g. avoid cold
2nd line = rituximab

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51
Q

Patient with VTE and dark urine in the morning? Investigation of choice?

A

Paroxysmal nocturnal haemoglobinuria
Investigation = flow cytometry

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52
Q

Male baby with jaundice and anaemia? Investigation of choice?

A

G6PD deficiency
Investigation = G6PD enzyme assay

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53
Q

Triggers of G6PD crisis?

A

Infection
Fava beans
Anti-malarials
Ciprofloxacin
Sulph-group drugs

54
Q

Patient with haemolysis and raised MHCH? Investigation of choice?

A

Hereditary spherocytosis
Investigation = mostly clinical if family history + blood film evidence, EMA binding test if unsure

55
Q

Genetic inheritance of sickle cell?

A

Autosomal recessive

56
Q

Sickle cell mutations and their clinical name?

A

HbAS = sickle cell trait
HbSS = sickle cell disease

57
Q

Outline the pathophysiology of sickle cell anaemia?

A
  • Glutamate (polar) is substituted for valine (non-polar) in the β chains
  • Deoxy-Hb becomes less water soluble
  • HbS molecules polymerise to form sickle shape
  • Sickle cells are fragile and haemolyse easily
58
Q

Sickle cell investigation and management?

A

Investigation = Hb electrophoresis
Management = hydroxyurea/hydroxycarbamide

59
Q

Types of sickle cell crises and cause?

A

Vaso-occlusive = infarct
Acute chest syndrome = infarct +/- infection
Aplastic crisis = parvovirus infection
Sequestration crisis = pooling of blood in spleen
Severe infection = encapsulated bacteria

60
Q

Sickle cell crisis management?

A

Analgesia
IV fluids +/- antibiotics
High-flow oxygen
Exchange transfusion

61
Q

Threshold and target for blood transfusion in non-ACS vs ACS?

A

Patient without ACS:
→ Hb < 70g/L threshold
→ 70-90g/L target
Patient with ACS:
→ Hb < 80g/L
→ 80-100g/L target

62
Q

Threshold for platelet transfusion in active vs non-active bleeding?

A

Active = < 30 (moderate bleed) or < 100 (severe bleed)
Non-active = ≤ 10

63
Q

Universal RBC donor vs plasma donor?

A

RBC = O-
Plasma = AB+

64
Q

When to use FFP vs cryoprecipitate vs prothrombin complex?

A

FFP = patients with prolonged PT/APTT
Cryoprecipitate = patients with low fibrinogen
Prothrombin complex = major haemorrhage

65
Q

What is cryoprecipitate and components?

A

Concentrated FFP:
→ factor VIII
→ factor XIII
→ fibrinogen
→ vWF

66
Q

Features of non-haemolytic transfusion reaction and management?

A

Fever, chills
Management = slow/stop transfusion, paracetamol

67
Q

Features of transfusion-associated allergic reaction and management?

A

Pruritis, urticaria
Mangement = stop transfusion, antihistamine

68
Q

Features of transfusion-associated anaphylaxis and management?

A

Hypotension, angioedema, wheezing
Management = stop transfusion, IM adrenaline, ABCDE

69
Q

Features of acute haemolytic reaction and management?

A

Hypotension, abdominal pain, fever
Management = stop transfusion, IV fluids

70
Q

Features of TACO and management?

A

Hypertension, pulmonary oedema
Management = stop transfusion, IV loop diuretic, oxygen

71
Q

Features of TRALI and management?

A

Hypotension, hypoxia, pulmonary infiltrate on CXR
Management = stop transfusion, oxygen

72
Q

Primary vs secondary haemostasis?

A

Primary = formation of the platelet plug
Secondary = intrinsic or extrinsic pathway leading to conversion of fibrinogen to fibrin

73
Q

Outline primary haemostasis?

A
  • Damaged endothelium exposes collagen
  • Endothelial cells release vWF which binds to collagen
  • Platelets bind to vWF and release platelet activating factors (e.g. TXA2, vWF)
  • More platelets arrive at injury site and clump together
74
Q

Factors involved in the extrinsic vs intrinsic vs common pathway?

A

Extrinsic = XII, XI, IX, XIII (12, 11, 9, 8)
Intrinsic = III, VIII (3, 7)
Common = X, V, II, I (10, 5, 2, 1)

75
Q

Factor names for tissue factor, prothrombin, thrombin, fibrinogen and fibrin?

A

Tissue factor = III
Prothrombin = II
Thrombin = IIa
Fibrinogen = I
Fibrin = Ia

76
Q

Factor with the shortest half life?

A

VII

77
Q

Vitamin K dependent clotting factors?

A

II, VII, IX, X (2, 7, 9, 10)

78
Q

Laboratory measurements of the intrinsic vs extrinsic pathway?

A

Intrinsic = PTT
→ play table tennis (inside)
Extrinsic = PT
→ play tennis (outside)

79
Q

Outline the pathophysiology of ITP?

A
  • Antibodies against glycoprotein IIa/IIIb or Ib-V-IX
  • Platelet destruction causes isolated thrombocytopenia
80
Q

Management options for ITP?

A

Prednisolone
Splenectomy
IV immunoglobulins
Immunosuppressants

81
Q

Most common cause of thrombophilia?

A

Factor V Leiden (activated protein C resistance)

82
Q

Outline the pathophysiology of Factor V Leiden?

A
  • Normal factor V broken down by protein C
  • Factor V Leiden is a mutated form of factor V
  • Degraded 10 x more slowly by protein C leading to increased VTE risk
83
Q

Features of VWD?

A

Easy bruising
Menorrhagia
Epistaxis
GI bleeds
Prolonged bleeding

84
Q

Types of VWD and cause?

A

Type 1 = reduction in vWF quantity
Type 2 = reduction in vWF quality
Type 3 = absence of vWF

85
Q

Coagulation screen features of VWD?

A

Prolonged APTT
Normal PT
Prolonged bleeding time

86
Q

Management options for VWD?

A

Tranexamic acid
DDAVP (desmopressin)
Factor VIII concentrate

87
Q

Tranexamic acid mechanism of action?

A

Bind to lysine receptors on plasminogen and plasmin to prevent plasmin breaking down fibrin

88
Q

Inheritance of haemophilia?

A

X-linked recessive

89
Q

Factor affected in haemophilia A vs B?

A

A = factor VIII
B = factor IX

90
Q

Features of haemophilia?

A

Severe bleeds
Haemarthroses
Haematomas

91
Q

Coagulation screen features of haemophilia?

A

Prolonged APTT
Normal PT
Normal bleeding time

92
Q

Management options for haemophilia A vs B?

A

A = DDAVP (acute) and recombinant factor VIII (long-term)
B = recombinant factor IX

93
Q

Cells produced from myeloid vs lymphoid progenitors?

A

Myeloid = neutrophils, eosinophils, basophils, monocytes, RBCs, platelets and mast cells
Lymphoid = B cells, T cells, NK cells

94
Q

What is myeloproliferative disease and give examples?

A

Bone marrow makes too much of a myeloid cell
→ polycythaemia vera (RBCs)
→ essential thrombocytosis (platelets)
→ myelofibrosis (myeloid cells)

95
Q

Blood test features of high cell turnover?

A

High LDH
High urate
High retic count

96
Q

Features and management of polycythaemia vera?

A

Pruritis (after hot bath)
Thrombosis
Erythromelalgia
Red complexion
Splenomegaly
Management = aspirin + venesection

97
Q

Blood test features of polycythaemia vera?

A

JAK2 mutation
High Hb
High Hct

98
Q

Complication of polycythaemia vera?

A

Progression to myelodysplastic syndrome
Progression to acute myeloid leukemia

99
Q

Feature of myelodysplastic syndrome?

A

Complete bone marrow failure (pancytopaenia)

100
Q

Features and management of essential thrombocytosis?

A

Thrombosis
Erythromelalgia
Splenomegaly
Livedo reticularis
Management = aspirin + hydroxurea

101
Q

Blood test features of essential thrombocytosis?

A

JAK2 mutation
High platelet count (> 600)

102
Q

Features of myelofibrosis?

A

Anaemia symptoms
Massive splenomegaly
Weight loss, night sweats, fever

103
Q

Bone marrow biopsy features of myelofibrosis?

A

Unsuccessful “dry” tap (due to bone marrow fibrosis)
Trephine biopsy required

104
Q

Leukemia vs lymphoma?

A

Both are malignancies of haematopoetic stem cells
Leukemia = originates in the bone marrow, can affect myeloid OR lymphoid cells, classified as acute or chronic
Lymphoma = originates in the lymph nodes, only affects lymphoid cells, classified as Hodgkin or non-Hodkin

105
Q

Main types of leukemia?

A

Classified by how fast they develop and whether they affect myeloid or lymphoid cells
→ acute myeloid leukemia (AML)
→ chronic myeloid leukemia (CML)
→ acute lymphoblastic leukemia (ALL)
→ chronic lymphocytic leukemia (CLL)

106
Q

Outline the pathophysiology of leukemia?

A
  • Proliferation of a single type of abnormal WBC (usually B cells)
  • Excess of one cell type suppresses all others leading to pancytopaenia
107
Q

Features of leukemia?

A

Anaemia symptoms
Petechiae
Easy bruising
Frequent infection
Lymphadenopathy
Hepatosplenomegaly

108
Q

Most common cancer in children?

A

ALL

109
Q

Key blood film feature of AML?

A

Auer rods

110
Q

Key blood film feature of CLL?

A

Smear/smudge cells

111
Q

Leukemia linked to the ABL mutation?

A

CML

112
Q

Leukemias linked to the Philadelphia chromosome t(9;22)?

A

ALL and CML

113
Q

Stages of CML?

A

Chronic phase
Accelerated phase
Blast phase (20% of bone marrow is blasts)

114
Q

Management of leukemia?

A

Chemotherapy regime
Imatinib if philadelphia +ve

115
Q

Features of lymphoma?

A

Lymphadenopathy
Hepatosplenomegaly
B symptoms (weight loss, fever, night sweats)

116
Q

Types of Hodgkin lymphoma?

A

Nodular sclerosing (most common)
Mixed-cellularity
Lymphocyte-predominant
Lymphocyte-depleted

117
Q

Blood film feature of Hodgkin lymphoma?

A

Reed-Sternberg cells

118
Q

Main CD markers for Hodgkin lymphoma?

A

CD15 and CD30

119
Q

Ann Arbour staging of lymphoma?

A

Stage I = single node
Stage II = ≥ 2 nodes on same side of diaphragm
Stage III = nodes on both sides of diaphragm
Stage IV = spread beyond nodes
A or B depending on presence of B symptoms

120
Q

Management of Hodgkin lymphoma?

A

Chemotherapy regime
Usually ABVD (doxorubicin, bleomycin, vincristine, dacarbazine)

121
Q

Examples of non-Hodgkin lymphoma?

A

Burkitt’s lymphoma
Diffuse large B cell lymphoma
MALT lymphoma
Mantle cell lymphoma
Follicular lymphoma
Waldenstrom’s macroglobinaemia

122
Q

Lymphoma linked to BCL-2?

A

Follicular lymphoma

123
Q

Lymphoma linked to c-MYC translocation t(8;14)?

A

Burkitt’s lymphoma

124
Q

Blood film feature of Burkitt’s lymphoma?

A

“Starry sky” appearance

125
Q

Which cell is affected in multiple myeloma?

A

Plasma cells

126
Q

Features of multiple myeloma?

A

CRABBI:
Calcium (hypercalcaemia)
Renal impairment
Anaemia
Bleeding
Bone lesions
Infection

127
Q

Imaging for multiple myeloma?

A

Whole body MRI

128
Q

Blood film feature of multiple myeloma?

A

Rouleux formation

129
Q

Bence Jones proteins?

A

Monoclonal immunoglobulin light chains
Classified as kappa or lambda

130
Q

Asymptomatic paraproteinaemia?

A

MGUS

Med School Finals (18 decks)

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