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Pathology > Haematology > Flashcards

Haematology Flashcards

1
Q

Pathological increase of myeloid cells?

A

myeloproliferative neoplasms

leukaemia (acute and chronic)

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2
Q

Physiological increase of myeloid cells?

A

neutrophilia
eosinophilia
monocytosis

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3
Q

Examples of myeloproliferative neoplasms?

A 
Polycythaemia Rubra Vera
Essential thrombocytosis
Chronic Myeloid Leukaemia
Primary myelofibrosis
Systemic mastocytosis
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4
Q

Causes of neutropenia?

A 
inadequate production (bone marrow infiltration, cytotoxic chemo)
accelerated destruction (fever, autoimmune, drugs, splenic sequestration)
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5
Q

Causes of lymphopenia?

A 
Retrovirus (HIV)
Drugs (steroids, chemo)
Autoimmune
Malnutrition
Immunodeficiency
Some acute viral infections (CMV, EBV)
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6
Q

What is caused by the Epstein-Barr Virus?

A

Infectious mononucleosis

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7
Q

What virus causes infectious mononucleosis?

A

Epstein-Barr Virus

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8
Q

What is infectious mononucleosis and what symptoms does it cause?

A

benign, self-limiting lymphoproliferative disorder
fever, lymphadenopathy, splenomegaly, sore throat
symptoms last 4-6 weeks
(sometimes hepatitis, meningoencephalitis, pneumonitis)

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9
Q

When do symptoms of infectious mononucleosis begin to appear?

A

When the host response is initiated- cellular immunity mediated by CD8 cytotoxic T cells and NK cells

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10
Q

What is leukaemia?

A

neoplasms of white blood cells, which present with involvement of bone marrow, usually with large numbers of cells in peripheral blood

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11
Q

What is lymphoma?

A

neoplasms of lymphocytes, which present as discrete tissue masses
start in LNs and sometimes spread to bone marrow

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12
Q

Types of acute leukaemia?

A

Acute myeloid leukaemia

Acute lymphoblastic leukaemia

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13
Q

Types of chronic leukaemia?

A

Chronic myeloid leukaemia

Chronic lymphoid leukaemia

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14
Q

What is the Philadelphia Chromosome and what does it occur in?

A

t (9,22) translocation

Chronic Myeloid Leukaemia

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15
Q

Blast cells in blood film indicates?

A

AML or ALL

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16
Q

What is myelodysplasia?

A

pre-leukemic condition that presents with infection of anaemia

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17
Q

Who is early myelodysplasia common in?

A

The elderly

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18
Q

What occurs in myelodysplasia?

A

Macrocytosis very likely
Mild neutropenia is common
Thrombocytopenia is less common

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19
Q

3 types of anaemia?

A

Microcytic
Macrocytic
Normocytic

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20
Q

What is the commonest cause of anaemia worldwide?

A

Iron deficiency anaemia

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21
Q

Symptoms and signs of iron deficiency anaemia?

A 
fatigue, shortness of breath
Pica- coal, ice
sore mouth
nail changes- koilonychia
pallor
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22
Q

Causes of iron deficiency?

A

inadequate intake
failure of absorption (coeliac)
inc. blood loss (blood loss from bowel, menorrhagia)
inc. requirements (pregnancy)

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23
Q

What type of anaemia is iron deficiency anaemia?

A

Microcytic

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24
Q

Causes of microcytic anaemia?

A 
TAILS
Thalassemia
Anaemia of chronic disease
Iron deficiency
Lead poisoning
Sickle Cell/ Sideroblastic
(also myelodysplasia)
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25
Q

Causes for raised ferritin levels?

A 
acute inflammation
acute liver disease
lymphomas
solid tumours 
haemochromatosis
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26
Q

Diagnosis of anaemia of chronic disease?

A

MCV normal or reduced slightly
MCH normal
ESR raised
CRP raised

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27
Q

Mechanisms behind anaemia of chronic disease?

A

shortened red cell survival
impaired marrow response to anaemia
impaired erythropoietin production
defective iron transport

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28
Q

Causes of macrocytic anaemia?

A 
Megaloblastic anaemia
Vit B12 deficiency
Folate deficiency
Myelodysplasia
Liver disease
Alcohol
Hypothyroidism
Aplastic anaemia
Cytotoxic drugs
Smoking
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29
Q

What is Vitamin B12 important for?

A

pyrimidine synthesis in the production of DNA

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30
Q

What does Vitamin B12 attach to to facilitate its absorption?

A

Intrinsic Factor (IF)

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31
Q

Causes of Vitamin B12 deficiency?

A

strict vegetarianism

malabsorption (pernicious anaemia, gastrectomy, coeliac, disease involving terminal ileum)

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32
Q

What is pernicious anaemia?

A

autoimmune disorder that results in gastric atrophy

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33
Q

What antibodies are present in pernicious anaemia?

A

anti parietal antibodies (90%)

anti intrinsic factor antibodies (70%)

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34
Q

Clinical features of B12 deficiency?

A

anaemia
peripheral neuropathy
loss of vibration and position sense
demyelination of spinal cord

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35
Q

Diagnosis of pernicious anaemia?

A

B12 levels
IF/Parietal cells antibodies
Bone marrow

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36
Q

Treatment of pernicious anaemia?

A

Lifelong B12 replacement

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37
Q

Causes of folate deficiency?

A

Diet (infancy and old age)
Malabsorption (coeliac)
Inc. utilisation (pregnancy, breastfeeding, haemolytic anaemia)
Antifolate drugs (methotrexate, anticonvulsants)

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37
Q

Causes of folate deficiency?

A

Diet (infancy and old age)
Malabsorption (coeliac)
Inc. utilisation (pregnancy, breastfeeding, haemolytic anaemia)
Antifolate drugs (methotrexate, anticonvulsants)

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38
Q

2 types of haemolytic anaemia?

A

Congenital

Acquired

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39
Q

2 types of acquired haemolytic anaemia?

A

Immune-related

Non-immune

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40
Q

3 types of immune-related haemolytic anaemia?

A

autoimmune
alloimmune
drug-induced

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41
Q

2 types of autoimmune haemolytic anaemia?

A

Warm antibody

Cold antibody

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42
Q

Causes of warm antibody autoimmune haemolytic anaemia?

A

Idiopathic

Secondary to CLL, CT disorders, lymphomas, drugs (methyldopa)

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43
Q

Causes of cold antibody autoimmune haemolytic anaemia?

A

Idiopathic

Secondary to mycoplasma, mono, lymphoma, paroxysmal cold haemoglobinuria

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44
Q

Features of warm antibody autoimmune haemolytic anaemia?

A

usually IgG
max activity @ 37 degrees
any age, either sex
splenomegaly

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45
Q

Diagnosis of warm antibody autoimmune haemolytic anaemia?

A

micro-spherocytes and polychromasia on blood film

Direct Coombes Test positive

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46
Q

Features of cold antibody autoimmune haemolytic anaemia?

A

usually IgM

max activity @ 4 degrees

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47
Q

Diagnosis of cold antibody autoimmune haemolytic anaemia?

A

Cold agglutination on blood film

Positive DCT

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48
Q

Causes of alloimmune haemolytic anaemia?

A

haemolytic transfusion reactions (ABO mismatch)

Rhesus disease of the new-born

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49
Q

Non-immune causes of haemolytic anaemia?

A

Red cell fragmentation
Infections
Chemical/Physical

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50
Q

Clinical features of haemolytic anaemias?

A 
anaemia symptoms
jaundice
pigmented gallstones
splenomegaly
leg ulcers (sickle cell, hereditary spherocytosis)
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51
Q

3 groups of congenital haemolytic anaemias?

A

Red cell membrane defects
Red cell metabolism disorders
Abnormal haemoglobins

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52
Q

What causes hereditary spherocytosis?

A

defect in a red cell membrane protein

cells destroyed prematurely in the spleen (splenomegaly common)

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53
Q

Inheritance pattern of hereditary spherocytosis?

A

Autosomal Dominant

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54
Q

Abnormalities of Red Cell Metabolism include?

A

Glucose-6-phosphate dehydrogenase deficiency

Pyruvate Kinase deficiency

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55
Q

2 types of abnormal haemoglobins causing haemolytic anaemia?

A

Disorders of globin chain synthesis (thalassemia)

Structural defects of haemoglobin (sickle cell)

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56
Q

What causes sickle cell anaemia?

A

point mutation in the beta globin gene

causes insolubility of Haemoglobin in the deoxygenated state

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57
Q

What occurs as a consequence of sickle cell anaemia?

A

Vascular occlusion

Severely -> bone pain, stroke, visceral infarction, dactylitis (children), acute chest syndrome

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58
Q

Inheritance pattern of the Thalassemias?

A

Autosomal recessive

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59
Q

Laboratory findings in the Thalassemias?

A

variable anaemia
hypochromic microcytic cells
BM erythroid hyperplasia
DNA analysis

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60
Q

What is monoclonal gammopathy of undetermined significance?

A

presence of a monoclonal protein in the serum or urine without evidence of myeloma or other plasma cell disorders

61
Q

What percentage of the population have monoclonal gammopathy of undetermined significance?

A

1%

increases with age (14%>90yrs)

62
Q

What is multiple myeloma?

A

abnormal plasma cells that build up in the bone marrow and form tumours in multiple bones of the body

63
Q

Median age at diagnosis of multiple myeloma?

A

70 years

64
Q

Clinical presentation of multiple myeloma?

A 
bone pain
pathological fracture
recurrent infections
renal impairment
anaemia
hypercalcemia
hyperviscosity
65
Q

Prognosis for multiple myeloma?

A

Can treat but can not cure

66
Q

Main functions of platelets?

A

form a mechanical plug during the normal haemostatic response to vascular injury

67
Q

What is the major regulator of platelet production and where is it produced?

A

Thrombopoietin

liver and kidneys

68
Q

Normal lifespan of platelets?

A

7-10 days

69
Q

What is the normal amount of platelets in the spleen?

A

1/3

if more- splenomegaly

70
Q

What is von Willebrand factor involved in?

A

platelet adhesion and aggregation

acts as a carrier protein for Factor VIII

71
Q

Primary vs secondary haemostasis?

A

Primary haemostasis involves platelet adhesion and aggregation
Secondary haemostasis involves activation of the coagulation cascade

72
Q

Stages of coagulation cascade?

A

Initiation- endothelial cells activated -> express tissue factor (TF) -> forms TF-FVIIa complex
Amplification- generates small amounts of thrombin
Propagation- positive feedback results in much larger amounts of thrombin
Thrombin results in fibrinogen being converted to fibrin

73
Q

Inhibitors of coagulation?

A

Antithrombin
Protein C
Protein S

74
Q

Which types of bleeding suggest primary vs secondary haemostasis defects?

A

Primary- mucosal superficial bleeding

Secondary- deep tissue bleeding

75
Q

What is the purpose of 50/50 mixing studies when investigating PT/APTT?

A

factor deficiencies- normal

inhibitors- won’t be normal

76
Q

What is von Willebrand disease?

A

bleeding disorder due to defects involved with platelets

chromosome 12

77
Q

Types of von Willebrand disease?

A

Qualitative (type 1, 3) (Type 3 = near absence)

Quantitative (type 2)

78
Q

What type of bleeding predominates in von Willebrand disease?

A

Mucosal bleeding

79
Q

Which type of von Willebrand disease is most common?

A

Type 1 (60-80%)

80
Q

What population is Factor XI deficiency common in?

A

Ashkenazi Jews

consanguinity

81
Q

What factor is deficient in Haemophilia A?

A

Factor VIII

X-linked

82
Q

What factor is deficient in Haemophilia B?

A

Factor IX

X-linked

83
Q

Causes of quantitative platelet disorders?

A 
consumptive
premature destruction
decreased production
drug reaction
congenital
84
Q

Causes of qualitative platelet disorders?

A

drugs, uraemia, inherited

85
Q

Risk factors for VTE?

A 
major surgery
active cancer
neurological disease with leg paralysis
hospitalisation for acute illness
nursing home confinement
trauma/fracture
pregnancy/postpartum
oral contraception
86
Q

When should combined oral contraception be avoided?

A

In patients who have a first degree relative with a history of thrombosis

87
Q

What increases the risk of thrombus posed by the combined OCP?

A

smoking and obesity

super additive is hereditary thrombophilia

88
Q

What is the leading cause of death in pregnancy in UK and Ireland?

A

Thrombosis

89
Q

Factors that further increase risk of thrombosis in pregnancy?

A 
maternal age > 35
high BMI
immobility
operative delivery
thrombophilia
90
Q

What is the second most common cause of death in cancer patients (after cancer itself)?

A

Thrombosis

91
Q

What is Hospital Acquired Thrombosis (HAT)?

A

development of a thrombosis within 90 days of hospital admission
leading cause of preventable hospital morbidity

92
Q

What does Lupus Anticoagulant in APS prolong and increase risk of?

A

Lupus Anticoagulant prolongs Activated Partial Thromboplastin Time
But increases risk of thrombosis, not bleeding

93
Q

When can a Lupus Anticoagulant test give a false positive?

A

When the patient is on anticoagulants

94
Q

What is Thrombotic Thrombocytopenic Purpura (TTP)?

A

unexplained thrombocytopenia and non-immune haemolysis
thrombocytopenic but pro-thrombotic
medical emergency- 90% fatality if untreated

95
Q

What causes Thrombotic Thrombocytopenic Purpura (TTP)?

A

Deficiency of ADAMST13 (regulator of von Willebrand factor)

96
Q

What percentage of patients acquire Heparin Induced Thrombocytopenia?

A

3% in Unfractionated Heparin

<1% in LMWH (tinzaparin, enoxaparin, dalteparin)

97
Q

Consequences of VTE?

A

post-thrombotic syndrome

Chronic Thromboembolic Pulmonary hypertension

98
Q

Investigations of thrombophilia?

A

Antithrombin
Protein C
Protein S

99
Q

When may Protein C and Protein S be spuriously low?

A

if the patient is on warfarin (as they are Vitamin K dependent factors)

100
Q

When will antithrombin, Protein C and Protein S all be spuriously low?

A

At the time of clot diagnosis

Used in the acute phase

101
Q

Which anti-phospholipid syndromes can be tested for when the patient is on anticoagulants?

A

Anticardiolipin and anti-B2GPl antibodies

NOT Lupus Anticoagulant

102
Q

How long is documentation regarding blood transfusions kept in the EU?

A

30 years

103
Q

2 major categories of Lymphoma?

A

Hodgkin Lymphoma

Non-Hodgkin Lymphoma

104
Q

Clinical presentation of Hodgkin Lymphoma?

A

painless lymphadenopathy (v small percent of patients experience pain after consuming alcohol)
itchy skin
+ systemic symptoms

105
Q

Clinical presentation of Non-Hodgkin Lymphoma?

A

painless lymphadenopathy (low grade)
rapidly enlarging mass (high grade)
if extra nodal- symptoms relate to site

106
Q

Characteristic features of Hodgkin lymphoma?

A

arises in a single node or chain of nodes and spreads anatomically

107
Q

Most common site for Hodgkin lymphoma to arise?

A

cervical nodes

108
Q

What distinctive cells are found in Hodgkin lymphoma?

A

Reed Sternberg Cells (giant cells)

109
Q

Average age at diagnosis for Hodgkin Lymphoma?

A

32 years

110
Q

Average age at diagnosis for Hodgkin Lymphoma?

A

32 years

111
Q

2 major types of Hodgkin Lymphoma?

A

Nodular lymphocyte predominant Hodgkin Lymphoma

Classical Hodgkin Lymphoma

112
Q

What differentiates between NLPHL and CHL?

A

immunophenotype

Reed-Sternberg cells express the protein CD30 in CHL but not in NLPHL

113
Q

What percentage of Hodgkin Lymphomas are NLPHL?

A

5%

114
Q

Cellular Features of Nodular Lymphocyte Predominant Hodgkin Lymphoma?

A

Popcorn cells/ L + H cells

background of small B lymphocytes

115
Q

Clinical features of Nodular Lymphocyte Predominant Hodgkin Lymphoma?

A

no bimodal age pattern
tend to be restricted to cervical nodes
v good prognosis

116
Q

4 types of Classical Hodgkin Lymphoma?

A 
Lymphocyte Rich (5%)
Nodular Sclerosis (66%)
Mixed Cellularity (25%)
Lymphocyte Depleted (>5%)
117
Q

Who gets each of the 4 types of Classical Hodgkin Lymphoma?

A

Lymphocyte rich- M>F, older patients
Nodular sclerosis- M=F, young adults
Mixed Cellularity- M>F, true bimodal pattern
Lymphocyte depleted- M>F, older patients, HIV

118
Q

Prognosis of Hodgkin Lymphoma?

A

generally better than NHL
depends more on stage than histological subtype
Stage I and II- 90-100% curable
Stage IV- 5yr survival 60-70%

119
Q

Clinical divisions of Non-Hodgkin Lymphomas?

A 
Low grade (slow-growing but resistant to therapy and rarely curable, painless generalised lymphadenopathy)
High grade (rapid-growing but sensitive to therapy and potentially curable, rapidly enlarging mass)
120
Q

3 types of Non-Hodgkin Lymphoma?

A

Mature B Cell
Mature T/NK Cell
Precursor B and T Cell

121
Q

4 types of mature B cell neoplasms?

A

Follicular lymphoma
Diffuse large B Cell lymphoma
MALT lymphoma
Burkitt lymphoma

122
Q

How does follicular lymphoma present?

A

painless, generalised lymphadenopathy
usually in middle age
low grade

123
Q

Prognosis of follicular lymphoma?

A

incurable but low grade and slow growing (median survival 7-9 years)
can transform to a high grade (usually DLBCL)

124
Q

Cause of follicular lymphoma?

A

t(14;18)(q32;q21) translocation most frequent

leads to excess bcl2 (anti-apoptosis -> slow collection of neoplastic cells)

125
Q

Diffuse Large B Cell Lymphomas defining factors?

A

Large Cell size
Diffuse growth pattern
Express B-cell markers (CD20, CD79a)

126
Q

2 groups of DLBCLs?

A

Germinal centre type (CD10)

Activated B cell type (MUM1)

127
Q

Presentation and Prognosis of Diffuse Large B Cell Lymphoma?

A

rapidly enlarging mass at a single nodal or extra nodal site
if untreated- rapidly fatal
if treated- 60-80% achieve remission, 50% cure

128
Q

Causes of MALT lymphoma?

A

Gastric- H pylori
Salivary- Sjogren’s Syndrome
Cutaneous- Borrelia Burgdorferi (Lyme)
Conjunctival- Chlamydia

129
Q

What is Burkitt Lymphoma usually?

A

an extranodal lymphoma

130
Q

Features of endemic Burkitt Lymphoma?

A

sub-Saharan Africa
M:F 2:1
age 4-7
tumours of jaw and facial bones

131
Q

Features of sporadic Burkitt Lymphoma?

A

worldwide in children and young adults

ileocecal, breasts, kidneys, ovaries

132
Q

3 types of Burkitt Lymphoma?

A

Endemic
Sporadic
HIV- related

133
Q

What is present in 100% of Endemic Burkitt Lymphoma and 20% of others?

A

latent EBV infection

134
Q

Genetic factor of Burkitt Lymphoma?

A

translocations of c-MYC gene on chromosome 8

t(8;14)

135
Q

Prognosis of Burkitt Lymphoma?

A 
v aggressive but usually responds well to high-dose, short-course chemotherapy
frequently curable (especially in children)
136
Q

What percentage of Non Hodgkin Lymphomas are mature T/NK cell lymphomas?

A

15%

137
Q

4 types of mature T/NK cell lymphomas?

A

mycosis fungoides/ Sezary syndrome
anaplastic large cell lymphoma
extra nodal NK/T cell lymphoma
peripheral T cell lymphoma

138
Q

What cells are involved in mycosis fungoides/sezary syndrome?

A

CD4+ helper T cells

139
Q

What is Sezary syndrome associated with?

A

a leukaemia of ‘Sezary’ cells in the blood

140
Q

Prognosis of mycosis fungoides/Sezary syndrome?

A

low grade, median survival 8-9yrs

may transform to high grade T cell lymphoma as terminal event

141
Q

Types of cells involved in anaplastic large cell lymphoma?

A

‘Hallmark cells’ with horse-shaped nuclei

142
Q

What gene is associated with anaplastic large cell lymphoma?

A

ALK gene

143
Q

Prognosis of anaplastic large cell lymphoma?

A

Cases with ALK rearrangement- usually in children, v good prognosis
Cases without ALK rearrangement- usually in older adult, bad prognosis

144
Q

Prognosis of extra-nodal NK/T cell lymphoma?

A

bad- aggressive and respond poorly to therapy

145
Q

What are peripheral T cell lymphomas, NOS?

A

T cell lymphomas which can not be fitted into any of the other diagnostic categories
25%
v bad prognosis, rarely curable

146
Q

Precursor B and T cell neoplasm?

A

Acute lymphoblastic lymphoma/leukaemia

147
Q

What percentage of ALL are B cell and T cell?

A

85% B cell- childhood acute leukaemias

15% T cell- adolescent male lymphomas

148
Q

Clinical features of ALL?

A

more common in males
abrupt stormy onset
depression of normal bone marrow (anaemia, infections)
bone pain and tenderness
lymphadenopathy, splenomegaly, hepatomegaly
CNS manifestations (tumour cells can cross the BBB)

149
Q

Prognosis of ALL?

A

generally good with treatment

90% children achieve remission, 70% cure

150
Q

Poor prognostic factors for ALL?

A

age < 2
adulthood
certain genetic abnormalities

151
Q

What are Auer rods a typical finding in?

A

Acute myeloid leukaemia

Pathology (13 decks)

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