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Haematology Flashcards

1
Q

Haemophilia A + B have which inheritance pattern?

A

X-linked recessive

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2
Q

Is haemophilia A or B more common?

A

A

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3
Q

Haemophilia A is a deficiency of which clotting factor?

A

Factor 8

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4
Q

Haemophilia B is a deficiency of which clotting factor?

A

Factor 9

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5
Q

How is mild haemophilia defined

A

Haematomas following severe trauma

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6
Q

How is moderate haemophilia defined

A

Haematomas following mild trauma

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7
Q

How is severe haemophilia defined

A

Spontaneous haematomas

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8
Q

Haemophilia causes ? PT and ? APTT

A

Normal PT

Prolonged APTT

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9
Q

What special test can you do with blood to confirm a diagnosis of haemophilia?

A

Mixing study

Mixing patients blood with external plasma will correct the APTT

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10
Q

Besides replacing factor 8, what else can be used to treat haemophilia A?

A

Desmopressin (vasopressin triggers the release of factor VIII from endothelial cells)

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11
Q

What is the most common inherited bleeding disorder?

A

Von Willebrand Disease

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12
Q

In VWD what happens to bleeding time, PT and APTT?

A

Bleeding time increased
PT normal
APTT sometimes normal, sometimes raised

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13
Q

VWD causes high/low factor 8 levels?

A

Low
Factor VIII levels are a good assessment for vWD because this factor is found bound to vWF in blood, in which state it is protected from rapid breakdown

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14
Q

How do you manage VWD?

A

Recombinant VWF
Desmopressin (stimulated VWF release from endothelial cells)
Factor 8 concentrate

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15
Q

Which type of VWD won’t respond to Desmopressin?

A

Type 3

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16
Q

What is the inheritance pattern for type 1 VDW?

A

Autosomal dominant

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17
Q

What is the inheritance pattern for type 2 VWD?

A

Autosomal dominant

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18
Q

What is the inheritance pattern for type 3 VWD?

A

Autosomal recessive

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19
Q

How is type 1 VWD described?

A

A quantitative deficiency of VWF

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20
Q

How is type 2 VWD described?

A

A qualitative defect in VWF

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21
Q

How is type 3 VWD described?

A

Complete absence of VWF

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22
Q

What are the two main types of acute leukaemia?

A

Acute lymphocytic leukaemia

Acute myeloid leukaemia

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23
Q

Does ALL more commonly affect children or adults?

A

Children

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24
Q

Does AML more commonly affect children or adults?

A

Adults

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25
Q

Which cells develop from the lymphocytic cell line?

A

Natural killer cells
B cells –> plasma cells
T cells

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26
Q

Which cells develop from the myeloid cell line?

A

Basophils
Eosinophils
Neutrophils

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27
Q

Describe the pathophysiology of acute leukaemia

A

Acquired gene mutations affect how bone marrow cells divide and mature
Either lymphoid/myeloid stem cells proliferate but differentiation/maturation stops in the early stages
This results in accumulation of abnormal and dysfunctional blasts
This disrupts normal haematopoiesis –> leukopenia, thrombocytopenia, anaemia
Abnormal cells also infiltrate organs such as liver, spleen, nodes, skin

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28
Q

Risk factors for ALL

A

Risk factors = often none, HTLV (Human T-cell lymphotropic virus), Down syndrome, neurofibromatosis type 1, ataxia telangiectasia

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29
Q

Risk factors for AML

A

Risk factors = pre-existing haematopoietic disorder (myelodysplastic syndromes, aplastic anaemia, myeloproliferative disorders), previous chemotherapy or radiation, smoking, benzene exposure, Down syndrome, Fanconi anaemia

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30
Q

Clinical features of acute leukaemia

A

Sudden onset, rapid progression over days/weeks
Fatigue, pallor, weakness
Bleeding, petechiae, purpura
Frequent infections, fever

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31
Q

Features that are more common/specific to AML rather than ALL

A

Leukaemia cutis/myeloid sarcoma (blue/puruple/grey nodular skin lesions)
Gingival hyperplasia
Extremely high WBC counts that can cause leukostasis

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32
Q

Features that are more common/specific to ALL rather than AML

A 
Fever and constitutional sx
Lymphadenopathy
Hepatosplenomegaly
Bone pain
Mediastinal involvement
CNS involvement
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33
Q

Are Auer rods seen in ALL or AML

A

AML

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34
Q

What is ‘leukaemic hiatus’ on blood film?

A

A way to differentiate AML from CML

In CML myeloid cells of all stages are present whereas in AML its mainly blasts and mature (no in-between).

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35
Q

What are the nuclei of lymphoblasts like in ALL

A

Large and irregular

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36
Q

What are the nuclei of myeloblasts like in AML

A

Round or kidney shape

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37
Q

Is myeloperoxidase positive or negative in ALL and AML

A

Negative in ALL

Positive in AML

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38
Q

What symptoms/problems can leukostasis cause?

A

Chest pain, headache, altered mental status, priapism, DIC

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39
Q

What is tumour lysis syndrome?

A

Rapid destruction of tumour cells causing a massive release of intracellular components –> renal damage

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40
Q

What happens to K, Ca, PO4 and urea in tumour lysis syndrome?

A

High K
High PO4
Low Ca
High urea

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41
Q

What are some clinical features of tumour lysis syndrome?

A

Nausea, vomiting, diarrhoea, lethargy, haematuria, seizures, arrhythmias, tetany, muscle cramps, paraesthesia

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42
Q

What is the basic pathological difference between acute and chronic leukaemia?

A

In acute leukaemia cells dont mature

In chronic leukaemia cells don’t work effectively (CLL cells dont die as they should, CML cells divide too quickly)

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43
Q

What are the two main types of chronic leukaemia?

A

Chronic lymphocytic leukaemia

Chronic myeloid leukaemia

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44
Q

Who tends to be affected by CLL?

A

Elderly men

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45
Q

What are some clinical features of CLL?

A 
Constitutional/B symptoms
Painless lymphadenopathy
Recurrent infections
Sx of anaemia
Sx of thrombocytopenia
Chronic pruritus/urticaria
Hepatomegaly/splenomegaly
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46
Q

What would an FBC show in CLL?

A

Persistent lymphocytosis with high percentage of small mature lymphocytes
Granulocytopenia
Anaemia
Thrombocytopenia

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47
Q

What does blood film show in CLL?

A

Smudge cells (Gumprecht shadows)

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48
Q

Is CLL a low or high grade malignancy?

A

Low grade

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49
Q

What is Richter’s transformation/syndrome?

A

Transformation of CLL into a high grade NHL

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50
Q

How can Richter’s transformation/syndrome present?

A

Rapidly progressive lymphadenopathy
New onset of B symptoms
High LDH

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51
Q

What are the three distinct clinical phases of CML?

A

Chronic
Accelerated
Terminal/Blast crisis

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52
Q

Describe the chronic phase of CML

A

The chronic phase is characterized by nonspecific symptoms (fever, weight loss, night sweats) and splenomegaly and can persist for up to 10 years

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53
Q

Describe the accelerated phase of CML

A

The accelerated phase is characterized by complications secondary to the suppression of the other cell lines (thrombocytopenia, anemia, neutropenia, recurrent infections, leukostasis). Develop extreme splenomegaly in accelerated phase and this is often a sign of transition to terminal phase.

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54
Q

Describe the terminal phase/blast crisis of CML

A

The clinical picture of the terminal phase, blast crisis, resembles that of acute leukemia. Rapid progression of bone marrow failure causes pancytopenia and bone pain Blast crisis (progression of CML to AML) occurs when increased division of myeloid cells in CML leads to increased mutations resulting in totally immature cells being produced (AML).

55
Q

Is hepatosplenomegaly more common in CML or CLL?

A

CML

56
Q

What drug is really good at treating CML?

A

Imatinib (tyrosine kinase inhibitor)

57
Q

What would FBC show in CML?

A

Extrememe leukocytosis
Basophilia
Thrombocytosis

58
Q

What is lymphoma

A

A type of blood cancer that causes tumours to form in lymph nodes

59
Q

What are the two broad types of Hodgkin lymphoma

A

Classical

Nodular lymphocyte predominant

60
Q

What are the four types of classical Hodgkin lymphoma?

A

Nodular sclerosing
Mixed cellularity
Lymphocyte rich
Lymphocyte depleted

61
Q

Where does nodular sclerosing classical hodgkin lymphoma most commonly localise?

A

Mediastinal and cervical lymph nodes

62
Q

Where does mixed cellularity classical hodgkin lymphoma most commonly localise?

A

Abdominal and splenic lymph nodes

63
Q

Where does lymphocyte rich classical hodgkin lymphoma most commonly localise?

A

Cervical and axillary nodes

64
Q

What are some risk factors for developing hodgkin lymphoma?

A

EBV mononucleosis
Immunodeficiency - HIV, meds, chemo
Autoimmune diseases

65
Q

Clinical features of hodgkin lymphoma

A 
Painless lymphadenopathy
Sx of mediastinal mass (chest pain, SOB)
B symptoms
Hepatosplenomegaly
Pel-Ebstein fever (temp for 1-2 weeks, normal for 1-2 weeks)
Alcohol induced pain
Pruritus
66
Q

Reed-Sternberg cells are pathognomic for X?

A

Hodgkin Lymphoma

67
Q

What is the name of the classification system for Hodgkin lymphoma?

A

Ann-Arbor classification

68
Q

Describe the Ann-Arbor classification for HL

A

I. 1 lymph node area
II. 2+ but confined to one side of the diaphragm
III. 2+ on both sides of the diaphragm
IV. Disseminated spread into an extralymphatic organ. IVA if asymptomatic, IVB if B symptoms, IVX if bulky disease

69
Q

Which chemo regimen is typically used for HL

A

ABVD - adriamycin (doxorubicin), bleomycin, vinblastine, dacarbazine)

70
Q

Is HL or NHL more common?

A

NHL

71
Q

How are non-hodgkin lymphomas categorised?

A

B cell or T cell

High grade or low grade

72
Q

Are B-cell or T-cell NHL more common?

A

B cell

73
Q

What are the low grade B-cell non-hodgkin lymphomas?

A 
Chronic lymphocytic leukaemia
Hairy cell leukaemia
Waldenstroms macroglobulinaemia
Follicular lymphoma
MALT lymphoma
74
Q

What is the most common low-grade non-hodgkin lymphoma?

A

Follicular lymphoma

75
Q

What are the high-grade non-hodgkin lymphomas?

A

Burkitt lymphoma
Diffuse large B cell lymphoma
Precursor B cell lymphoblastic lymphoma
Mantle cell lymphoma

76
Q

What is the most common NHL in adults?

A

Diffuse large B cell lymphoma

77
Q

What is the low grade T cell NHL?

A

Mycosis fungoides (cutaneous lymphoma)

78
Q

What are the high grade T cell NHLs?

A

Adult T cell lymphoma
Cutaneous T cell lymphoma
Precursor T cell lymphoblastic lymphoma

79
Q

What are the risk factors for developing NHL

A 
Chromosomal translocations
EBV
HIV
HTL
HCV
H.pylori (MALT)
Autoimmune disease
Immunodeficiency
Benzene exposure
Radiation
80
Q

Clinical features of NHL

A 
Painless lymphadenopathy (insidious onset in low grade, generalised in high grade)
Splenomegaly
Hepatomegaly
GI/skin/thyroid/CNS involvement
B symptoms
Fatigue/weakness
Anaemia
Bleeding
Infections
81
Q

FBC findings in NHL

A

Anaemia
High/low WBC
Thrombocytopenia
High LDH

82
Q

All NHL is treated with a curative approach apart from which category?

A

Advanced low-grade

83
Q

Multiple myeloma is a malignant disease causing uncontrolled proliferation of which type of cell?

A

Plasma cells

84
Q

Clinical findings of multiple myeloma

A 
Bone pain (back, spontaneous fractures)
Sx of hypercalcaemia
B symptoms
Weakness and anaemia
Recurrent infection
Petechial bleeding
Foamy urine (caused by Bence Jones proteinuria)
85
Q

Blood test findings in multiple myeloma

A 
Anaemia
Thrombocytopenia
Leukopenia
Low reticulocyte count
Raised ESR
High Ca
High creatinine
High total protein levels
Raised beta-2-microglobulin
86
Q

Diagnostic criteria for multiple myeloma

A 
Marrow biopsy showing >10% monoclonal plasma cells plus one of:
Hypercalcaemia
Renal insufficiency
Anaemia
Bone lesions
>60% monoclonal plasma cells in marrow
87
Q

What is TTP?

A

Thrombotic thrombocytopenic purpura

A thrombotic microangiopathy

88
Q

Who typically gets affected by TTP?

A

Previously healthy adults

89
Q

What caused TTP?

A

Acquired autoantibodies that result in accumulation of von Willebrand factor

90
Q

What are the 5 key clinical findings in TTP?

A
  1. Fever
  2. Neurological signs/symptoms
  3. Thrombocytopenia
  4. Haemolytic anaemia
  5. Impaired renal function
91
Q

How do you manage TTP

A

Treat without waiting to confirm diagnosis
Fluid status, electrolytes, acid base
Plasma exchange/FFP
Prednisolone

92
Q

Who is typically affected by HUS?

A

Children <5 after 5-10 days of diarrhoea (usually bloody)

93
Q

What is HUS?

A

Haemolytic uraemia syndrome

A thrombotic microangiopathy

94
Q

What causes HUS?

A

Usually secondary to E.coli 0157:H7 producing shiga-like toxin

95
Q

What are the 3 key clinical findings of HUS?

A
  1. Thrombocytopenia
  2. Haemolytic anaemia
  3. Renal insufficiency
96
Q

What is the management for HUS?

A

Treat without waiting to confirm diagnosis
Avoid antibiotics and anti-motility agents
Fluid status
Electrolytes
Acid-base balance
BP

97
Q

When should you suspect ITP?

A

Isolated thrombocytopenia

98
Q

Who gets affected by ITP?

A

Children after a viral illness (acute ITP)

Women of childbearing age (chronic, insidious onset)

99
Q

What is the management of ITP?

A

Usually just watch and wait - spontaneously resolves within 6 months for most children
In adults, if platelet count is <30,000 can give corticosteroids

100
Q

Causes of microcytic anaemia

A 
IDA (late phase)
Chronic disease (late phase)
Sideroblastic anaemia
Lead poisoning
Thalassaemia
101
Q

What does blood film show in sideroblastic anaemia?

A

Basophilic stippling

Ringed sideoblasts

102
Q

Causes of normocytic anaemia

A 
Sickle cell disease
Pyruvate kinase/G6PD deficiency
Hereditary spherocytosis
Autoimmune haemolytic anaemia
Microangiopathic haemolytic anaemia (TTP, HUS)
Blood loss
Aplastic anaemia
CKD 
IDA (early phase)
Chronic disease (early phase)
103
Q

Causes of megaloblastic macrocytic anaemia

A

Vitamin B12 deficiency
Folate deficiency
Medication - Phenytoin, trimethoprin, hydroxyurea, MTX
Fanconi anaemia

104
Q

Causes of non-megaloblastic macrocytic anaemia

A 
Liver disease
Myelodysplastic syndrome
Diamond Blackfan anaemia
Hypothyroidism
Multiple myeloma
105
Q

How can you differentiate megaloblastic and non-megaloblastic anaemia on blood film?

A

Megaloblastic has hypersegmented neutrophils, non-megaloblastic doesn’t

106
Q

What can be used to reverse the effects of unfractionated heparin?

A

Protamine sulphate

107
Q

How long does Warfarin take to reach therapeutic range?

A

48-72 hours

108
Q

What is Virchow’s triad?

A

Virchows triad = the three main pathophysiological components of thrombus formation

  1. Hypercoagulability – increased platelet adhesion, increased clotting tendency (thrombophilia)
  2. Endothelial damage – inflammatory, traumatic
  3. Venous stasis – varicose veins, immobilisation, local heat application
109
Q

Risk factors for DVT

A 
History of VTE
Immobilisation
Age >60
Malignancy
Hereditary thrombophilia (Factor V Leiden)
Pregnancy
Estrogen use
Obesity
Smoking
110
Q

Clinical features of DVT

A

Unilateral
Swelling
Heavy/tight feeling
Progressive tenderness/dull pain - worse when walking, better when leg elevated
Homan sign (pain on ankle dorsiflexion)
Superficial vein distention
Calf circumference >3cm difference (mark 10cm from tibial tuberosity)

111
Q

DVT differentials

A 
Post-traumatic swelling
Haematoma
Lymphoedema
Venous insufficiency
Ruptured popliteal cyst
Cellulitis
Compartment syndrome
112
Q

How id D-dimer used in the assessment of VTE?

A

Used to rule it out if Wells score is low probability

113
Q

What is the minimum length of anticoagulation prophylaxis after VTE?

A

3 months

114
Q

Clinical features of PE

A 
Acute onset 
Dyspnea
Tachypnea
Sudden onset pleuritic chest pain
Cough
Haemoptysis
Tachycardia +/- hypotension
JVP distention
Co-existing DVT
115
Q

What may an ABG show in PE?

A

Respiratory alkalosis with hypocapnia

116
Q

What is a massive PE?

A

A large clot which affects perfusion of the right side of the heart

117
Q

A Wells score of ? makes DVT likely

A

2 or more

118
Q

A Wells score of ? makes PE likely?

A

More than 4

119
Q

Which coagulation pathway does PT measure?

A

Extrinsic

120
Q

Which coagulation pathway does APTT measure?

A

Intrinsic

121
Q

What can we used to measure the common coagulation pathway?

A

Fibrinogen

TT, PT and APTT all affected

122
Q

What can cause a prolonged PT

A 
Warfarin
Factor 7 deficiency
Factor 2 deficiency
Factor 5 deficiency
Factor 10 deficiency
123
Q

What can cause a prolonged APTT

A 
Heparin
Factor 8 deficiency
Factor 9 deficiency
Von Willebrands Disease
Factor 11 deficiency
Factor 12 deficiency (but no bleeding)
124
Q

Mouth slits on RBCs on a blood film indicates what disease?

A

Hereditary stomatocytosis

125
Q

What kind of cells are seen on blood film in G6PD deficiency?

A

Bite cells

126
Q

What kind of cells are seen on blood film in pyruvate kinase deficiency?

A

Sputnik cells with protruding spikes

127
Q

What is the inheritance pattern for thalassaemia?

A

Autosomal recessive

128
Q

What is splenic sequestration crisis in sickle cell disease?

A

Occlusion of splenic artery causes blood to pool and get trapped in the spleen causing LUQ pain, anaemia, reticulocytosis and hypotension

129
Q

What causes aplastic crisis in sickle cell disease?

A

Parvovirus B19 infection

130
Q

Which medication can be used to try and prevent sickle cell crisis?

A

Hydroxyurea

131
Q

What can trigger sickle cell crisis?

A 
Reduced oxygen tension/hypoxia
Dehydration
Stress
Infection
Pregnancy
Acidosis
132
Q

How do you manage acute sickle cell crisis?

A 
Hydration
Analgesia
Nasal oxygen
VTE prophylaxis
Bed rest
Exchange transfusions if severe
133
Q

Difference in blood test results between Von Willebrands disease and Haemophilia A

A

Both with have prolonged APTT
VWD will have prolonged bleeding time
HA will have normal bleeding time

Finals (32 decks)

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