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General Medicine > Hematology > Flashcards

Hematology Flashcards

1
Q

Risk factors for VTE

A 
Age >60
Surgery >30 mins
Immobilisation 
Trauma
Obesity
COCP
previous VTE
Congenital / acquired hypercoagulable states
Pregnancy
HF
Malignancy
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2
Q

Management of urticarial reaction to a blood transfusion

A

Slow / temporarily stop blood transfusion

IV / oral chlorphenamine

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3
Q

Symptoms of haemolytic transfusion reaction

A 
Burning at infusion site
Headache
Nausea
Chills
Fever
Chest tightness
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4
Q

In what condition howel jolly-bodies occur?

A

Hyposplenism

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5
Q

When do Burr cells occur?

A

Uraemia

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6
Q

When do Heinz bodies occur?

A

Glucose-6-phosphate dehydrogenase deficiency

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7
Q

When may reticulocytosis occur?

A

Bleeding, haemolysis

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8
Q

When may target cells occur?

A

Liver disease,

Iron deficiency anaemia

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9
Q

What causes macrocytic anaemia with glossitis and peripheral neuropathy?

A

B12 deficiency

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10
Q

What drugs may cause folate deficiency?

A 
Phenytoin
Trimethoprim
Methotrexate
Sulfasalazine
Oral contraceptive pill
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11
Q

Causes of a macrocytic anaemia?

A 
B12deficiency, 
folate deficiency, 
hypothyroidism
Alcohol excess
Reticulocytosis
Multiple myeloma
Myeloproliferative disorders
Aplastic anaemia
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12
Q

Causes of a Microcytic anaemia?

A

Iron deficiency
Thalassaemia
Sideroblastic anaemia

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13
Q

Causes of a Normocytic anaemia?

A

Chronic disease (E.g. malignancy, rheumatoid arthritis)
Haemolytic anaemia
Acute blood loss
Marrow infiltration

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14
Q

Signs and symptoms of sickle-cell anaemia?

A 
Anaemia
Shortness of breath
Dizziness
Headaches
Cold hands and feet
Pain
Splenic crisis
Infections
Priapism 
Stroke
Gallstones
Leg ulcers
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15
Q

What causes dark urine in the morning and a positive hams test?

A

Paroxysmal nocturnal haemalobinuria

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16
Q

Weightloss plus anaemia and dysphagia suggests what ?

A

Oesophageal carcinoma

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17
Q

Weightloss plus anaemia and painless obstructive jaundice suggests what ?

A

Carcinoma of the head of the pancreas

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18
Q

In what condition do reed Sternberg cells occur?

A

Hodgkin’s lymphoma

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19
Q

In what condition do auer Rods occur?

A

Acute myeloid leukaemia

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20
Q

In what condition does the Philadelphia chromosome occur?

A

Chronic myeloid leukaemia

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21
Q

Features of myeloma?

A 
Bone pain
Fractures
Nerve compression
Hypercalcaemia
Bone marrow failure --> Anaemia, Clotting problem, Infection
Hyperviscosity --> retinal haemorrhage 
Renal failure
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22
Q

What is myeloma?

A

malignant proliferation of plasma cells

Leading to bone marrow infiltration and bone destruction and bone marrow failure

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23
Q

Causes of pancytopenia

A

Aplastic anaemia,
Bone tumours,
hypersplenism,
sepsis,

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24
Q

Causes of excess erythropoietin?

A 
Polycystic kidney disease
Renal cell carcinoma,
adrenal tumour,  
hepatocellular carcinoma
Cerebellar haemangioblastoma
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25
Q

Common symptoms of antiphospholipid syndrome

A 
DVT
Stroke
Multiple miscarriage
Placental infarction
Migraine
Livedo reticularis
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26
Q

Syx of anaemia

A 
Fatigue
Dizziness
Palpitations
Pallor
Cold skin
SOB
Muscle weakness
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27
Q

Signs of anaemia

A

Low BP
Tachycardia
Splenomegally
Pallor

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28
Q

What is thrombopoiesis

A

Platelet formation in the bone marrow

Formed from megakaryocytes

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29
Q

When are basophils raised

A

Allergy

Parasitic infection

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30
Q

When are eosinophils raised

A

Allergy

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31
Q

When are neutrophils raised

A

Acute inflammation

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32
Q

What are the primary lymphoid tissues?

A

Bone marrow

Thymus

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33
Q

What are the secondary lymphoid tissues

A

Lymph nodes
Spleen
Mucosal associated lymphoid tissue

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34
Q

What is phlebitis

A

Inflammation of a vein

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35
Q

What is thrombophlebitis

A

Inflammation of a vein associated with a clot

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36
Q

Risk factors for peripheral vascular disease

A 
Male
History CVD
Increased age
Family history
DM
Hypercholesterolaemia
Hypertension
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37
Q

Symptoms of idiopathic thrombocytopenia purpura

A

Easy bruising
Mucosal bleeding
Menorrhagia
Epistaxis

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38
Q

Features of thrombotic thrombocytopenic purpura (TTP)

A 
Thrombocytopenia
Microangiopathic haemolytic anaemia
Neurological signs
Renal impairment
Fever
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39
Q

Features of hereditary haemorrhagic telangiectasia (HHT)

A

Telangiectasias On skin, lips and mucosal surfaces
Small aneurysms on fingertips, face, nasal passage, tongue, lung, GIT.
AV malformations
Recurrent bleeding (E.g. Epistaxis)

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40
Q

Causes of thrombocytopenia

A 
Leukaemia 
myeloma 
bone marrow cancer 
myelofibrosis 
B12 deficiency 
folate deficiency 
Marrow hypoplasia
DIC
ITP
TTP
EBV
Gram negative septicaemia
Hypersplenism
Liver disease
 SLE
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41
Q

What is the most common congenital bleeding disorder?

A

Haemophilia A

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42
Q

What is the inheritance of haemophilia A?

A

X linked recessive

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43
Q

Features of haemophilia A?

A

Bruising
Excess bleeding
Spontaneous haemarthrosis
Muscle haematoma

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44
Q

What is Christmas disease?

A

Haemophilia B

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45
Q

What is von Willebrand disease.

A 
Common
Mild
Bleeding disorder
Autosomal dominant
Onset in adolescence
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46
Q

Features of von Willebrand disease

A 
Bruising 
epistaxis 
menorrhagia 
GI haemorrhage 
gum bleeding
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47
Q

What may initiate DIC?

A

Infections
Cancers
Obstetric complications

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48
Q

Signs of DIC

A

Acutely ill patient
Shock
Bruising, purpura
Initial thrombosis then bleeding e.g From mouth,nose, vene puncture sites
Prolonged PT, APTT, TT
Low fibrinogen
End organ ischaemia –> Multiorgan failure

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49
Q

Causes of secondary polycythaemia

A 
Chronic hypoxia (incl COPD)
Renal cancer 
renal cyst  
hydronephrosis
Hepatocellular carcinoma 
Cerebellar haemangioma
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50
Q

What is Fanconi anaemia

A

Inherited aplastic anaemia

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51
Q

Causes of haemolytic anaemia

A 
Membrane defects
Sepsis
Sickle cell
Thalassaemia
Autoimmune
Transfusion reaction
Haemolytic disease of the newborn
HUS
DIC
Malignant hypertension
Mechanical valves
Penicillin
Malaria
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52
Q

What may precipitate sickling in sickle cell anaemia

A

Infection
DeHydration
Acidosis
Hypoxia

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53
Q

What type of thalassaemia is most common?

A

Beta thalassaemia

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54
Q

What is wergener’s granulomatosis

A

Necrotising small vessel vasculitis
Multi system disorder
Commonly involves lungs and kidneys
Associated with cANCA

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55
Q

What is polycythaemia rubra vera

A

High Hb due to myelo-proliferation

Potential to transform into acute myeloid leukaemia

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56
Q

What does the prothrombin time best represent?

A

The intrinsic pathway

The effect of heparins

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57
Q

Causes of iron deficiency anaemia

A

Menorhagia
Blood loss. E.g. GI
Hookworm
Malabsorption (coeliac)

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58
Q

Signs of iron deficiency anaemia

A

Koilonychia
Atrophic glossitis
Angular cheilosis
Post-cricoid webs

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59
Q

Where is folate absorbed

A

Duodenum and proximal jejunum

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60
Q

Causes of folate deficiency

A 
Poor diet
Pregnancy
Coeliac
Alcohol
Phenytoin
Sodium valproate
Methotrexate
Trimethoprim
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61
Q

Causes of b12 deficiency

A

Decreased dietary intake (vegan)

Decreased absorption - pernicious anaemia, gastrectomy, crohn’s, tropical sprue, ileal resection

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62
Q

Where is b12 absorbed

A 
Terminal ileum 
(Bound to intrinsic factor)
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63
Q

Features of b12 deficiency

A 
Pallor
Mild jaundice 
Glossitis 
Red beefy tongue
Subacute combined degeneration of the cord
Paraesthesia 
Peripheral neuropathy 
Depression 
Psychosis
Dementia
64
Q

Management of a low-grade fever (No other symptoms) when giving a blood transfusion

A

Slow transfusion and prescribe paracetamol

Close monitoring

65
Q

Presentation of an acute Haemolytic transfusion reaction

A 
Starts within minutes
Fever
Chest pain
Abdominal pain 
loin pain
DIC
Acute renal failure
66
Q

Management of an acute Haemolytic transfusion reaction

A 
Immediately stop transfusion
Return blood and giving set Blood Bank
Take blood for FBC, clotting screen and Coombs test
ABC
Fluid resuscitation
Cryoprecipitate or FFP for DIC
Transfer to HDU/ITU
67
Q

Complications of massive blood transfusion

A 
Hypothermia 
thrombocytopenia 
hyperkalaemia
Hypocalcaemia
Deranged clotting
68
Q

What is DIC?

A

Acquired consumptive coagulopathy
Widespread inappropriate activation of the clotting cascade.
Conversion of fibrinogen To fibrin
Multiple thrombi –> End organ ischaemia
Intravascular haemolysis
Platelet destruction
Rapid consumption of clotting factors platelets and fibrinogen

69
Q

Clotting studies in DIC

A

Prolonged PT

Prolonged APTT

70
Q

Treatment of DIC

A

Correct cause

Platelets, FFP, cryoprecipitate

71
Q

What is haemophilia A

A

X-linked recessive disorder of congelation
Cannot synthesise factor VIII due to gene mutation
Prolonged APTT (Extrinsic clotting Cascade)
Normal PT (Intrinsic clotting Cascade)

72
Q

What is haemophilia B

A

Christmas disease
Inability to synthesise factor IX
Prolonged to APTT
Normal PT

73
Q

Presentation of congenital haemophilia

A

Presents when child begins to crawl or walk
Recurrent painful bleeds into joint and soft tissue
Arthropathy and neuropathy

74
Q

Treatment of haemophilia A

A

Factor VIII concentrate -Regular infusion or when actively bleeding
Mild disease can be treated with desmopressin to release factor VIII from internal stores.

75
Q

Treatment of haemophilia B

A

Factor IX concentrate

76
Q

What causes a global reduction in clotting factor synthesis?

A

Chronic liver cirrhosis and hepatitis

77
Q

Why is vitamin K essential in clotting factors synthesis

A

Carboxylation of clotting factors II, VII, IX, X

78
Q

What does vitamin K deficiency do

A

Causes a hypocoagulable state

79
Q

Common causes of inappropriately high INR While on warfarin

A

Dosing error,
Accidental overdose,
Drug interaction - Antibiotics, thyroxine, alcohol, antidepressants, aspirin, amiodarone, quinine

80
Q

What is pernicious anaemia

A

Autoimmune loss of parietal cells
And / or intrinsic factor

Prevents absorption of b12

81
Q

What does the schilling test do

A

Distinguishes pernicious anaemia from intestinal causes of b12 deficiency

82
Q

What causes a macrocytic, megaloblastic anaemia with hypersegmented neutrophils

A

B12 deficiency

83
Q

Management of b12 deficiency

A

IM hydroxocobalamin (preparation of b12)
1mg every other day until blood film normal
Then 1mg every 3m

84
Q

Management of anaemia secondary to chronic renal failure

A

Exogenous erythropoietin administration

85
Q

Which haemoglobin chain is not produced in a beta-thalassaemia

A

The beta-globin chain

86
Q

Presentation of beta-thalassaemia major

A 
Presents in 1st year of life
Failure to thrive
Lethargy 
Pallor
Jaundice
Hepatosplenomegaly 
Frontal bossing
Long bone deformity
87
Q

Treatment of beta-thalassaemia major

A

Regular blood transfusions
Regular iron chelation therapy - desferrioxamine

Or allergenic bone marrow transplant

88
Q

Presentation of beta-thalassaemia minor

A

Mild anaemia

Usually asymptomatic

89
Q

What are the four variants of alpha-thalassaemia

A

Asymptomatic - 1 gene corruption
Mild hypochromic anaemia - 2 gene corruptions
HbH disease - 3 gene corruptions
Death in uterine - all 4 genes corrupted

90
Q

What drugs may trigger an autoimmune haemolytic anaemia

A

Methyldopa
Penicillin
Cephalosporins
Quinine

91
Q

What is the direct Coombs test

A

Used to test for autoimmune hemolytic anaemia.
It detects RBC that are coated with autoantibodies
Coombs agent = antibodies which are added to the RBC and adhere to any antibodies on the RBC causing RBC agglutination

92
Q

What is the indirect Coombs test

A

indirect Coombs’ test is done on the plasma.
It detects antibodies that are present in the bloodstream and could bind to certain red blood cells and destroy them.

Used in prenatal testing of pregnant women and testing blood prior to transfusion.

93
Q

What is multiple myeloma

A

Multisystem disease

malignant proliferation of plasma cells

94
Q

Investigation findings in multiple myeloma

A

Monoclonal band on serum Electrophoresis

Free immunoglobulin light chains in urine

95
Q

Presentation of multiple myeloma

A 
Lethargy
Bone pain
Pathological fracture
Renal failure
Amyloidosis
Pancytopenia -due to marrow infiltration
96
Q

Diagnosis of multiple myeloma

A

Two or more of:

  • Marrow plasmacytosis
  • serum/urinary immunoglobulin light chains (Bence-Jones protein)
  • skeletal lesions (osteolytic lesion, pepperpot skull pathological fracture)
97
Q

Management of multiple myeloma

A

Bone pain control with analgesia, bisphosphonate, orthopaedic intervention
Renal failure managed by increased fluid intake
Broad-spectrum antibiotics for infection
Erythropoietin for anaemia
Blood transfusion for pancytopenia

98
Q

Prognosis of multiple myeloma

A

Death Within 4 years

Stem cell transplant offers hope of cure - but 30% mortality from treatment

99
Q

Typical age of presentation of Hodgkin’s lymphoma

A

Bimodal age distribution

Peak onset in third and sixth decades

100
Q

Presentation of Hodgkin’s lymphoma

A

Asymmetrical painless lymphadenopathy
Usually as single rubbery lymph-node - cervical or inguinal or axillary
Node may be painful after alcohol

101
Q

B symptoms of Hodgkin’s lymphoma

A

Weight loss
sweating
pruritis
general lethargy

102
Q

Diagnosis of Hodgkin’s lymphoma

A

Lymph node biopsy showing Reed-Sternberg cells

CT for spread and staging (Ann Arbor staging system)

103
Q

Management of Hodgkin’s lymphoma

A

Early stage radiotherapy alone

Advanced/bulky disease radiotherapy and chemotherapy

104
Q

What infection is Hodgkin’s lymphoma associated with

A

History of glandular fever

105
Q

What virus is non-Hodgkin’s lymphoma associated with

A

Epstein Barr virus
HIV
Helicobacter pylori

106
Q

Presentation of non-Hodgkin’s lymphoma

A

Painless lymphadenopathy

+/- Systemic symptoms

107
Q

Diagnosis of non-Hodgkin’s lymphoma

A

Lymph node biopsy

108
Q

Management of non-Hodgkin’s lymphoma

A

CHOP chemotherapy

109
Q

What is Burkitt’s lymphoma

A

Type of non-Hodgkin’s lymphoma which frequently involves the jaw
Most often seen an African children with EBV

110
Q

What is mycosis fyngoides

A

A cutaneous T-cell lymphoma

111
Q

What is polycythaemia rubra Vera

A

Myeloproliferative disorder
Mutation of a single pluripotent stem cell
Causes excessive erythrocyte production

112
Q

Features of polycythaemia rubra vera

A

Raised haemoglobin
raised red-cell account
raised Packed cell volume (Haematocrit)
Viscous blood –> Increased risk of thrombosis and paradoxical bleeding

113
Q

Symptoms of polycythaemia rubra Vera

A

Headache
Lethargy
Pruritus
Pruritus is worse after bathing in warm water

114
Q

Treatment of polycythaemia Rubra Vera

A

Venesection

Chemotherapy with hydroxyurea

115
Q

Prognosis of polycythaemia rubra Vera

A

30% develop myelofibrosis

5% develop acute myeloid leukaemia

116
Q

What is myelofibrosis

A

A myeloproliferative disorder characterised by replacement of erythropoietic bone marrow with inert fibrotic material.

117
Q

Presentation of myelofibrosis

A

Bone marrow failure - Pancytopenia

Extramedullary erythropoiesis in the liver and spleen produces massive hepatosplenomegaly

118
Q

Diagnosis of myelofibrosis

A

Pancytopenia blood film - tear drop poikilocytes
Dry bone marrow aspirate
Trephine biopsy showed densify fibrosis of bone marrow

119
Q

Management of myelofibrosis

A

Blood transfusion
Chemotherapy
Splenectomy

120
Q

A bone marrow biopsy with excess plasma cells occurs in what condition

A

Multiple myeloma

121
Q

Most common leukaemia in children

A

Acute lymphoblastic leukaemia (ALL)

primarily affects 2-8 yo.
equal risk between males and females

122
Q

Are leukaemias more common in males or females

A

ALL is equally common in both genders

all other leukaemias occur more frequently in males

123
Q

Presentation of acute leukaemias

A

bone marrow failure:
Anaemia – tired, SOB on exercise, weakness
Bleeding and bruising – due to thrombocytopaenia
Infection – result of leukopaenia
Bone pain – result of bone marrow infiltration

124
Q

auer rods are pathognomonic For what condition

A

AML

125
Q

Is the presence of lymphoblasts in the blood more common in ALL or AML

A

ALL
Always present

(May or may not be present in AML)

126
Q

Is the presence of bone and joint pain and hepatosplenomegaly more common in ALL or AML

A

ALL

127
Q

Prognosis of ALL in childhood

A

Complete remission obtained in almost all patients.
80% alive without recurrence at 5 years.

Failure of treatment occurs most commonly occurs in those with:
a high blast count
a T(9:22) translocation

128
Q

What age group does chronic myeloid leukaemia commonly affect

A

Almost exclusively an adult disease

peak age of incidence is 40-60 years.

129
Q

What disease is characterised by the presence of the Philadelphia chromosome

A

CML

130
Q

What cells does CML affect

A

CML affects the myeloid cells

i.e. basophils, neutrophils and eosinophils.

131
Q

What is the natural progression of CML

A

The natural progression of CML is as follows: chronic phase → aggressive/accelerated phase → blast phase/crisis.

132
Q

What is the most common leukaemia in adults

A

Chronic lymphocytic leukaemia (CLL)

mainly in later life

Median survival is 10 years

133
Q

What cell abnormality is responsible for CLL

A

CLL results from a progressive accumulation of functionally incompetent B lymphocytes.

134
Q

Presentation of CML and CLL

A

Many Asymptomatic,

or 
SOB due to anaemia, marrow failure immunosuppression, 
splenic pain, 
weight loss, 
fever and sweats, 
lymphadenopathy
hepatosplenomegaly.

CML usually presents in the chronic phase
CLL is often asymptomatic and discovered incidently.

135
Q

Management of CML

A

Imatinib ( tyrosine kinase inhibitor)

prevents the action of the BCR-ABL fusion protein = the abnormal protein produced by the Ph mutation

Continue indefinitely

136
Q

Management of CLL

A

Chlorambucil first-line therapy

combined with prednisone

137
Q

What is a Myelodysplastic syndromes (MDS)

A

generally considered to benprecursors to leukaemia.
30% with MDS will develop acute myoblastic leukaemia (AML).

generally occur in the elderly.
Usually associated pancytopaenia.

138
Q

What is Acute promyelocyte leukaemia (APML)

A

an uncommon variant of AML
involves a specific translocation mutation, t(15:17).

almost always coagulopathy - this is often the cause of death.

139
Q

What is a blast crisis

A

The acute terminal phase of CML.
Mortality is very high.
blast crisis = > 20-30% blast cells in the blood or bone marrow.
Symptoms include:
- rapid increase in proportion of blast cells
- fever
- bone pain
- fatigue
- increased severity of anaemia, e.g. fatigue
- increased severity of thrombocytopaenia, e.g. bleeding and/or bruising
- splenomegaly
- large clusters of blasts on bone marrow film

140
Q

What is Richter syndrome

A

where CLL is transformed into an aggressive, large B-cell lymphoma.
Epstein-Barr virus may play a role in transformation.
Lymph node biopsy is necessary for diagnosis

141
Q

H pylori increases the incidence of what lymphoma

A

gastric MALT lymphoma

142
Q

What is MALT lymphoma

A

Mucos associated lymphoid tissue.

Most commonly occurs in the stomach.
Abnormallly large collection of lymphocytes and macrophages

143
Q

Differentials of cervical lymph node enlargement

A

Infection - Acute

  • Infective mononucleosis
  • Toxoplasmosis
  • Infected eczema
  • Cat scratch fever – bartonella. .
  • Acute childhood exanthema –Includes Measles, rubella and scarlet fever

Infection -Chronic
- TB. - HIV. - Syphilis. - Sarcoidosis

Malignancies - Primary

  • Hodgkin’s / Non-Hodgkin’s lymphoma
  • Chronic lymphocytic leukaemia / Acute lymphoblastic leukaemia

Malignancies - Secondary

  • Naropharyngeal / Pharyngeal. - Thyroid
  • Lung. - Breast. - Stomach

Others

  • Rheumatoid arthirits
  • Reaction to phenytoin
  • Kawasaki’s syndrome
144
Q

Post splenectomy prophylaxis rules

A

Cary a splenectomy card
Vaccination against pneumonia, HIB, Neisseria meningitides
Prophylactic amoxicillin (erythromycin) until age 15

145
Q

What is the upper age limit for bone marrow transplant

A

55

146
Q

Complications of bone marrow transplant

A

Graft vs host disease
Pneumonitis
Infection
Secondary malignancy

147
Q

In CML do patients with or without the Philadelphia chromosome have a worse prognosis

A

Without Philadelphia = worse prognosis

148
Q

What is tumour lysis syndrome

A

Seen I. Patients with a lymphoproloferative malignancy following chemotherapy.
Massive cell death releases k+, phosphate, uric acid.
Phosphate binds Ca2+
Hyperkalaemia, hyperphosphataemia, hyperuricaemia
Hypocalcaemia

149
Q

Management of tumour lysis syndrome

A

IV fluids
Allopurinol (lower uric acid level)
Renal support
Correct electrolyte imbalance

150
Q

What is the most effective way of preventing neutropenic sepsis in post-chemotherapy patients

A

Hand hygiene

Reverse barrier nursing

151
Q

When do tear drop shaped cells appear on blood film

A

Myelofibrosis

152
Q

Cause of idopathic thrombocytopenic purpura

A

Autoantibodies form against platelets

Usually seen after a viral illness e.g. Chicken pox

153
Q

Causes of pancytopenia

A

Marrow infiltration in multiple myeloma
Severe megaloblastic anaemia
Aplastic anaemia
Hypersplenism

154
Q

What is essential thrombocytopenia

A

Myeloproliferative disorder

Excess production of defective platelets derived from abnormal megakaryocytes in the bone marrow

155
Q

Symptoms of essential thrombocytopenia

A

Headache
Digital ischaemia
Abdominal pain secondary to splenic infarction

156
Q

Causes of warm autoimmune haemolytic anaemia

IgG

A 
Idiopathic 
Leukaemia - CLL
Lymphomas - non-Hodgkin's lymphoma
Other autoimmune diseases - SLE
Drug
HIV infection
157
Q

Causes of cold autoimmune haemolytic anaemia

IgM

A 
Idiopathic
Epstein-Barr virus and infectious mononucleosis
Mycoplasma pneumoniae,
non-Hodgkin's lymphoma 
CLL
Mycoplasma pneumoniae

General Medicine (25 decks)

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