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Medicine Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

When will you see target cells on a blood film?

A

Iron deficiency anaemia

Hyposplenism

Sickle cell anaemia

Liver disease

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2
Q

What do Heinz bodies on a blood film indicate?

A

G6PD deficiency

Alpha thalassaemia

May also be a feature of splenectomy/hyposplenism

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3
Q

What do Howell-Joly Bodies on a blood film indicate?

A

Post-splenectomy (hyposplenism)

Megaloblastic anaemia (bone marrow produces unusually large and structurally abnormal red blood cells - megaloblasts) - B12/folate deficiency

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4
Q

When do you see schistocytes on a blood film?

A

All types of haemolytic anaemia - sickle cell, G6PD, hereditary spherocytosis, hereditary elliptocytosis, autoimmune haemolytic anaemia

Also DIC/TTP

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5
Q

When do you see sideroblasts on blood film?

A

Myelodysplastic syndrome

Sideroblastic anaemia

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6
Q

What does smudge cells on a blood film indicate?

A

Chronic lymphocytic leukaemia

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7
Q

What does tear drop poikilocytes on blood film indicate?

A

Myelofibrosis and Myelodysplastic syndromes

Also possibly iron deficiency anaemia

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8
Q

What are causes of microcyctic anaemia?

A

Iron-deficiency anaemia

Thalassaemia

Sideroblastic anaemia

Lead poisoning

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9
Q

What are causes of normocytic anaemia?

A

Anaemia of chronic disease (CKD, Myeloma, sickle cell)

Acute blood loss

Haemolytic anaemia (G6PD, spherocytosis)

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10
Q

What are causes of macrocytic amaemia?

A

Megaloblastic:

B12 or folate deficiency

Normoblastic:

Alcohol

Liver disease

Pregnancy

Reticulocytosis

Myelodysplasia

Hypothyroidism

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11
Q

What are causes of iron-deficiency anaemia?

A

Insufficient dietary iron

Increased iron requirements (eg pregnancy)

Iron being lost (eg slow bleeding from heavy periods or a colon cancer)

Inadequate iron absorption (eg IBD/coeliac)

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12
Q

What is seen on iron studies in iron deficiency anaemia?

A

Low ferritin

Low transferrin saturation

High total iron binding capacity

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13
Q

What is seen on blood film in iron deficiency anaemia?

A

Target cells

Pencil poikilocytes

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14
Q

What is the management of iron deficiency anaemia?

A

Iron supplementation e.g. ferrous sulphate / ferrous fumarate

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15
Q

What is the main side effect of iron supplementation?

A

Constipation

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16
Q

What are causes of vitamin b12 deficiency?

A

Pernicious anaemia

Inflammatory bowel disease/coeliac disease

Vegan diet

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17
Q

What type of anaemia does a vitamin b12 deficiency cause?

A

Megaloblastic macrocytic anaemia

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18
Q

How does vitamin B12 deficiency present?

A

Symptoms of anaemia (fatigue, pallor, postural hypotension)

Neurological symptoms - distal parasthaesia, mood changes, peripheral neuropathy, vision changes

Glossitis (swollen tongue)

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19
Q

What is pernicious anaemia?

A

A cause of b12 deficiency

Intrinsic factor autoantibodies

Intrinsic factor is needed for b12 deficiency

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20
Q

How is pernicious anaemia diagnosed?

A

Intrinsic factor antibody testing

Also maybe gastric parietal cell antibodies

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21
Q

How is vitamin b12 deficiency managed?

A

If due to diet - oral cyanocobalamin

If not due to diet - IV Hydroxycobalamin

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22
Q

How is pernicious anaemia treated?

A

IV Hydroxycobalamin

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23
Q

What condition does pernicious anaemia predispose to?

A

Gastric carcinoma

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24
Q

What type of hereditary pattern does hereditary spherocytosis have?

A

Autosomal dominant

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25
Q

How does hereditary spherocytosis present?

A

At birth with neonatal jaundice

Splenomegaly

Aplastic crisis if Parvovirus B19 infection

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26
Q

What GI condition is associated with hereditary spherocytosis?

A

Gallstones

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27
Q

How is hereditary spherocytosis diagnosed?

A

EMA binding tests

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28
Q

How is hereditary spherocytosis managed?

A

Folate supplementation

Splenectomy

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29
Q

What inheritance pattern does G6PD deficiency have?

A

X-linked recessive

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30
Q

What type of anaemia does G6PD deficiency cause?

A

Normocytic haemolytic anaemia

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31
Q

How does G6PD deficiency present?

A

Neonatal jaundice (due to blood cell breakdown)

Splenomegaly (due to haemolysis)

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32
Q

Which medications cause crises in G6PD deficiency?

A

Sulf- drugs

Ciprofloxacin

Anti-malarials

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33
Q

Which food causes a crises in G6PD deficiency?

A

Broad beans (fava beans)

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34
Q

What type of inheritance pattern does thalassaemia have?

A

Autosomal recessive

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35
Q

Which features can be seen in beta thalassaemia major?

A

Severe symptomatic anaemia

Frontal bossing

Maxillary overgrowth

Extramedullary haematopoiesis

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36
Q

What type of anaemia does thalassaemia cause?

A

Microcytic anaemia

MCV may be disproportionately low to Hb –> Sign of thalassaemia rather than other causes of microcytic anaemia

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37
Q

How is thalassaemia diagnosed?

A

FBC - haemolytic anaemia

Haemoglobin electrophoresis

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38
Q

How is thalassasmia managed?

A

If severe microcytic anaemia=

Regular transfusions

Iron chelation (in case of iron overload)

Splenectomy

In beta thalassaemia trait = no management required

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39
Q

How can iron overload in thalassaemia present?

A

Similar to haemochromatosis

Liver cirrhosis

Infertility/impotence

Arthritis

DM

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40
Q

What inheritance pattern does sickle cell anaemia have?

A

Autosomal recessive

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41
Q

What type of anaemia does sickle cell disease cause?

A

A haemolytic normocytic anaemia

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42
Q

How is sickle cell disease diagnosed?

A

Usually picked up on newborn screening

Haemoglobin electrophoresis

Schistocytes on blood film

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43
Q

How is sickle cell disease managed?

A

Hydroxycarbamide - stimulates production of fetal haemoglobin

Pneumococcal vaccine every 5 years

Avoid dehydration

If severe anaemia - blood transfusion

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44
Q

How does an aplastic crisis present?

A

Usually due to Parvovirus B19 infection

Low Hb

Low platelets

Low WCC

Low reticulocytes

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45
Q

How does a vaso-occlusive crisis in sickle cell present?

A

Pain in extremities

Can cause priapism

Usually triggered by dehydration

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46
Q

How does a splenic sequestration crisis in sickle cell present?

A

Acute drop in haemoglobin

Splenomegaly

High reticulocytes

Can cause hypovolaemic shock

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47
Q

How does acute chest syndrome in sickle cell present?

A

Hypoxia

Chest pain

Dyspnoea

New infiltrates on CXR

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48
Q

What kind of inheritance pattern does fanconi anaemia have?

A

Autosomal recessive

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49
Q

What are features of fanconi anaemia?

A

Haematological - aplastic anaemia, increased risk of AML

Skeletal abnormalities -short stature, thumb abnormalities

Cafe au lait spots

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50
Q

What type of anaemia does Sideroblastic anaemia cause?

A

Microcytic anaemia

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51
Q

What is seen on iron studies in sideroblastic anaemia?

A

Raised ferritin

Raised transferrin saturation

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52
Q

What is seen on blood film in sideroblastic anaemia?

A

Basophilic stippling of RBCs

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53
Q

What is seen on bone marrow biopsy in sideroblastic anaemia?

A

Ringed sideroblasts

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54
Q

How is sideroblastic anaemia treated?

A

Supportive - transfusions may be needed (+Iron chelation with Desferrioxamine)

Pyirodixine

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55
Q

What is the most common type of Hodgkin’s Lymphoma?

A

Nodular sclerosing

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56
Q

How does Hodgkin’s Lymphoma present?

A

Non-tender lymphadenopathy associated with alcohol induced pain

B symptoms: fever, weight loss, night sweats

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57
Q

What is seen on lymph node biopsy in Hodgkin’s Lymphoma?

A

Reed-Sternberg cells

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58
Q

How is Hodgkin’s Lymphoma diagnosed?

A

Reed-Sternberg cells on lymph node biopsy

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59
Q

Which marker may be raised in lymphoma?

A

Lactate dehydrogenase

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60
Q

How is Lymphoma staged?

A

Ann Arbor staging

I: single lymph node

II: 2 or more lymph nodes on the same side of the diaphragm

III: Lymph nodes on both sides of the diaphragm

IV: spread beyond the lymph nodes

All stages can be A or B
B = Presence of B symptoms

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61
Q

How does Non-Hodgkin’s Lymphoma present?

A

Painless lymphadenopathy

B symptoms (these present later than in Hodgkin’s)

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62
Q

What conditions are associated with Non-Hodgkin’s Lymphoma?

A

Gastric MALT

HIV

EBV

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63
Q

How is Non-Hodgkin’s Lymphoma treated?

A

R-CHOP

Rituximab
Cyclophosphamide
Doxorubicin
Vincristine
Prednisolone
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64
Q

What is seen on microscopy in Burkitt’s lymphoma?

A

Starry sky appearance

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65
Q

What is the differential diagnosis for petechiae?

A

Leukaemia

Meningococcal septicaemia

Vasculitis

HSP

ITP

Non-accidental injury

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66
Q

Which leukaemia is most common in children?

A

Acute Lymphoblastic Leukaemia

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67
Q

What genetic condition is associated with ALL?

A

Down Syndrome

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68
Q

What is seen on blood film in ALL?

A

Blast cells

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69
Q

Which leukaemia is most common in adults overall?

A

Chronic Lymphocytic Leukaemia

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70
Q

What is seen on blood film in chronic lymphocytic leukaemia?

A

Smudge cells

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71
Q

What is Richter’s transformation?

A

Chronic lymphocytic leukaemia transforms into high grade lymphoma

72
Q

What is seen on blood film in acute myeloid leukaemia?

A

Blast cells with Auer rods

73
Q

Which conditions puts someone at risk of developing acute myeloid leukaemia?

A

Myeloproliferative disorders - essential thrombocytosis, myelofibrosis, polycythaemia vera

74
Q

Which chromosome is associated with chronic myeloid leukaemia?

A

Philadelphia chromosome (9;22 translocation)

75
Q

Which leukaemia is associated with Philadelphia chromosome?

A

Chronic myeloid leukameia

76
Q

Which marker may be decreased in chronic myeloid leukaemia?

A

Leukocyte alkaline phosphatase

77
Q

How is chronic myeloid leukaemia treated?

A

Imatinib

78
Q

Which type of leukaemia has raised lymphocytes?

A

ALL and CLL

79
Q

What is seen on blood film in chronic myeloid leukaemia?

A

Band cells

80
Q

What type of leukaemia has all stages of granulocyte maturation?

A

Chronic leukaemia

81
Q

What is tumour lysis syndrome?

A

Life threatening condition related to treatment of leukaemia and lymphoma (usually triggered by chemo)

Due to release of uric acid from cells

82
Q

What is tumour lysis syndrome and how does it present?

A

Life threatening complication of chemotherapy to lymphomas/leukaemias

Due to release of uric acid from cells being destroyed by chemo

AKI (raised creatinine)

Abdominal pain

May be arrhythmia/seizure

High uric acid

Hyperkalaemia

Hyperphosphataemia

Hypocalcaemia

83
Q

What are the 4 main features of multiple myeloma?

A

CRAB

Raised calcium

Renal failure

Anaemia

Bone pain

84
Q

How does multiple myeloma present?

A

Often presents with persistent lower back pain

85
Q

What is seen in urine protein electrophoresis in multiple myeloma?

A

Bence-Jones protein

86
Q

What is seen in serum protein electrophoresis in multiple myeloma?

A

Increased monoclonal IgG

87
Q

Which 4 tests do you need to do to investigate multiple myeloma?

A

BLIP

Bence Jones protein (urine electrophoresis)

Serum-free light assay

Serum immunoglobulins

Serum protein electrophoresis

88
Q

How is multiple myeloma definitively diagnosed?

A

Bone marrow biopsy

89
Q

What blood lab results are seen in multiple myeloma?

A

FBC - anaemia, low WCC

Raised calcium

Raised ESR

Raised plasma viscosity

90
Q

Why is plasma viscosity increased in multiple myeloma?

A

Due to the presence of proteins in the blood (immunoglobulins and fibrinogen)

91
Q

Why does renal failure occur in multiple myeloma?

A

Immunoglobulins blocking flow through the renal tubules

Hypercalcaemia

92
Q

Why does raised calcium and bone pain occur in multiple myeloma?

A

Increased osteoclast activity

Decreased osteoblast activity

93
Q

What X-ray signs are seen in multiple myeloma?

A

Punched out lesions

Lytic lesions

Raindrop skull

94
Q

How is multiple myeloma managed?

A

Chemotherapy

Bisphosphonates

Analgesia

IV fluids for hypercalcaemia

95
Q

What is neutropenic sepsis?

A

A common complication of chemotherapy - raised temperature and other signs of sepsis

96
Q

How is neutropenic sepsis managed?

A

IV Tazocin

97
Q

What is myelodysplastic syndrome?

A

Myeloid bone marrow cells don’t mature properly - lead to anaemia, neutropaenia and thrombocytopaenia

98
Q

What is a complication of myelodysplastic syndrome?

A

Development of AML

99
Q

Which haematological conditions are associated with a JAK2 mutation?

A

Primary myelofibrosis

Polycythaemia Vera

Essential thrombocytosis

100
Q

What is seen on blood film in primary myelofibrosis?

A

Tear drop poikilocytes

Blasts

101
Q

How is primary myelofibrosis diagnosed?

A

Bone marrow biopsy

Will get a dry tap

102
Q

What are causes of thrombocyosis?

A

Reactive - in response to severe infection/surgery, iron-deficiency anaemia

Malignancy

Essential thrombocytosis or another myeloproliferative disorder

Hyposplenism

103
Q

How does thrombocytosis present?

A

Thrombosis

Bleeding

Headache

Dizziness

Burning/tingling sensation in hands and feet

Splenomegaly

Livedo reticularis

104
Q

How is essential thrombocytosis managed?

A

Hydroxycarbamide / Hydroxyurea (same thing)

Low dose aspirin (to reduce thrombus risk)

105
Q

What is polycythaemia?

A

Increased red blood cells

Raised Hb and raised haematocrit

106
Q

What are causes of polycythaemia?

A

Primary polycythaemia (polycythaemia Vera)

Secondary polycythaemia - increased EPO production, COPD, altitude, obstructive sleep apnoea ((body increases red blood cell production to compensate for low oxygen levels)

Reactive polycythaemia (due to low blood plasma)

107
Q

What is polycythaemia rubra vera / polycythaemia vera?

A

Primary cause of polycythaemia

Myeloproliferative disorder - JAK2 mutation

108
Q

How does polycythaemia present?

A

Headache

Visual disturbances

Pruritus especially after a hot bath

Splenomegaly

Ruddy complexion

Conjunctival plethora (excessively red conjunctiva)

109
Q

What lab results are seen in polycythaemia vera?

A

Raised haemoglobin

Raised haematocrit/red cell mass

Raised neutrophils, basophils and platelets

Low ESR

Raised leukocyte alkaline phosphatase

110
Q

How is polycythaemia vera managed?

A

Venesection to reduce Hb

Aspirin to reduce risk of thrombotic events

111
Q

What is immune thrombocytopenic purpura?

A

Idiopathic autoimmune mediated thrombocytopenia leading to purpura

112
Q

What type of hypersensitivity reaction is ITP?

A

Type II

113
Q

How does ITP present?

A

Bleeding (from gums, epistaxis or menorrhagia)

Bruising

Petechiae/purpura

Can sometimes be triggered by a viral infection

114
Q

How is ITP managed?

A

Oral prednisolone

IV Immunoglobulins

If unstable - blood transfusions

115
Q

What is thrombotic thrombocytopenic purpura?

A

Blood clots develop throughout the small vessels of the body - using up platelets

116
Q

Which protein is deficient in thrombotic thrombocytopenic purpura?

A

ADAMTS13

117
Q

How is TTP managed?

A

Plasma exchange

Oral steroids

118
Q

What are causes of TTP?

A

Post infection

Tumours

SLE

HIV

Medication

119
Q

What is the most common inherited bleeding disorder?

A

von Willebrand’s disease

120
Q

What is the inheritance pattern of von willebrand’s?

A

Autosomal dominant

121
Q

How does von Willebrand’s disease present?

A

Epistaxis and menorrhagia

Bleeding into joint and muscle is rare

122
Q

What clotting results are seen in vWD?

A

Prolonged bleeding time

Prolonged APTT

Normal prothrombin time

123
Q

How is Von Willebrand’s disease managed?

A

Desmopressin - stimulates release of vWF

Tranexamic acid for menorrhagia

VWF infusion

124
Q

What is the inheritance pattern of haemophilia?

A

X-linked recessive

125
Q

What is haemophilia A?

A

Lack of factor VIII

126
Q

What is haemophilia B?

A

Lack of factor IX

127
Q

What clotting test results are seen in haemophilia?

A

Raised APTT

Normal bleeding time

Normal prothrombin time

128
Q

How does haemophilia present?

A

Bleeding into joints (haemarthroses) and muscle haematomas

129
Q

How is haemophilia managed?

A

Desmopressin/tranexamic acid for bleeding

IV infusion of factor VIII/IX

130
Q

What is factor V Leiden?

A

The most common inherited cause of thrombocytosis

Activated protein C resistance - activated factor V is inactivated 10 times more slowly than normal

Increased risk of VTE

131
Q

What clotting results are seen in vitamin K deficiency?

A

Raised APTT

Raised prothrombin time

Normal bleeding time

132
Q

What is disseminated intravascular coagulation?

A

Inappropriate activation of the clotting cascade - thrombus formation and depletion of platelets

133
Q

How does DIC present?

A

Excess bleeding - epistaxis, gingival bleeding, haematuria, bruising, petechiae, bleeding from cannula site

134
Q

What are causes of DIC?

A

Sepsis

Trauma

Obstetric complications e.g HELLP syndrome

Malignancy

135
Q

What clotting results are seen in DIC?

A

Low platelets

Low fibrinogen

Prolonged prothrombin time

Prolonged APTT

Prolonged bleeding time

Raised D-dimer

136
Q

What test is used to diagnose autoimmune haemolytic anaemia?

A

Direct coombs test will be positive

137
Q

Where does haemolysis usually occur in warm AIHA?

A

At the spleen

138
Q

Which antibody is responsible in warm AIHA?

A

IgG

139
Q

Which antibody is responsible in cold AIHA?

A

IgM

140
Q

How does cold AIHA present?

A

Symptoms of Raynaud’s

141
Q

Which type of AIHA is SLE associated with?

A

Warm

142
Q

What is Graft versus Host disease?

A

Multi system complication of bone marrow transplantation

Can also occur after organ transplant or blood transfusion in immunocompromised patients

143
Q

How does Graft versus Host disease present?

A

Painful maculopapular rash

Jaundice

Watery/bloody diarrhoea

Nausea and vomiting

144
Q

Transfusion reactions: Fever and chills following a transfusion?

A

Non-haemolytic febrile reaction

Slow or stop the transfusion and give paracetamol

145
Q

Transfusion reaction: Pruritus and urticaria following a blood transfusion?

A

Minor allergic reaction

Temporarily stop the transfusion and give anti-histamines

146
Q

Transfusion reaction: hypotension, angioedema and wheezing following blood transfusion?

A

Anaphylactic reaction

Stop transfusion

IM Adrenaline, oxygen, IV fluids

147
Q

Transfusion reaction: fever, abdominal pain and hypotension following a transfusion?

A

Acute haemolytic reaction

Stop transfusion

IV fluid resus

148
Q

Transfusion reactions: pulmonary oedema and hypertension following a blood transfusion?

A

Transfusion-associated circulatory overload (usually in pre-existing heart failure)

Slow or stop transfusion

Consider a loop diuretic

149
Q

Transfusion reactions: hypoxia, hypotension, fever, infiltrates on CXR following transfusion reaction?

A

Transfusion related acute lung injury

Stop transfusion, give oxygen

150
Q

What is post-thrombotic syndrome? How is it managed?

A

A complication which can follow a DVT

Painful, heavy calves

Pruritus

Swelling

Varicose veins

Venous ulceration

Managed with compression stockings and keeping leg elevated

151
Q

What is the transfusion threshold for packed red cells?

A

Hb of 70

Unless in ACS - then Hb threshold of 80

1 unit Packed red cells over 90-120 mins (if non urgent)

152
Q

Which blood product can be used for emergency reversal of anticoagulation?

A

Prothrombin complex concentrate

E.g. Beriplex

153
Q

When should platelet transfusion be offered?

A

In active bleeding - if platelets less than 30

If no active bleeding - if platelets less than 10

Pre-invasive procedure - if platelets less than 50 (or 100 of surgery at critical site)

Bleeding at critical site - less than 100

154
Q

Patient on Warfarin: major bleeding

A

Stop warfarin

Give IV vitamin K 5mg

Prothrombin complex concentrate

155
Q

Patient on warfarin: INR >8 and minor bleeding

A

Stop warfarin

IV Vitamin K 1-3mg

Repeat vitamin K if INR is still high after 24 hours

Restart warfarin when INR is less than 5

156
Q

Patient on warfarin: INR >8 and no bleeding

A

Stop warfarin

Oral vitamin K

Restart warfarin when INR less than 5

157
Q

Patient on warfarin: INR 5-8 and minor bleeding

A

Stop warfarin

IV vitamin K

Restart warfarin when INR less than 5

158
Q

Patient on warfarin: INR 5-8 and no bleeding

A

Withhold one or two doses

Reduce subsequent doses

159
Q

What are adverse effects of methotrexate?

A

Bone marrow suppression

Hepatotoxicity

Renal impairment

160
Q

What are complications of chronic lymphocytic leukaemia?

A

Richters transformation

Bone marrow failure

Warm AIHA

Recurrent infection

161
Q

What is seen on blood film in hyposplenism?

A

Target cells

Howell-Joly bodies

Siderotic granules

Acanthocytes

Pappenheimer bodies

162
Q

What is seen on blood film in thalassaemia?

A

Heinz bodies

Target cells

Basophilic stippling

163
Q

What is seen on blood film in lead poisoning?

A

Basophilic stippling

Clover leaf morphology

164
Q

Which leukaemia is associated with massive splenomegaly?

A

Chronic myeloid leukaemia

165
Q

How is autoimmune haemolytic anaemia diagnosed?

A

Direct Coombs Test

166
Q

When are spherocytes seen on blood film?

A

Hereditary Spherocytosis

Autoimmune haemolytic anaemia

167
Q

What is the reversal agent for Apixaban and Rivaroxaban?

A

Andexanet alfa

168
Q

What is the target INR for AF?

A

2-3

169
Q

What is the target INR for recurrent VTE e.g. antiphospholipid syndrome

A

3-4

170
Q

Microcytosis which is disproportionate to the anaemia?

A

Consider beta thalassaemia trait

171
Q

What chromosome is affected in thalassaemia?

A

Alpha thalassaemia = chromosome 16

Beta thalassaemia = chromosome 11

172
Q

Which haematological conditions cause pathological neonatal jaundice? (<24 hours)

A 
G6PD
Hereditary spherocytosis/elliptocytosis
Alpha thalassaemia
Sickle cell disease
(Also ABO haemolytic diseae and rhesus haemolytic disease)
173
Q

Aplastic crisis vs. Splenic sequestration crisis

A

Aplastic crisis = Low reticulocytes

Splenic sequestration crisis = High reticulocytes, splenomegalyy

174
Q

Why does haemolytic anaemia lead to gallstones?

A

Haemolysis –> Increased bilirubin –> Excreted into the bile

175
Q

Which lymphoma is associated with alcohol induced pain?

A

Hodgkin’s

176
Q

How is autoimmune haemolytic anaemia managed?

A

Corticosteroids

Medicine Finals (32 decks)

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