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Finals > Haematology > Flashcards

Haematology Flashcards

1
Q

What is the lifespan of a RBC ?

A

4 months (120 days)

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2
Q

What is the lifespan of a platelet ?

A

10 days

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3
Q

What is a cause of target cells on a blood film ?

A
  • Iron deficiency anaemia
  • Sickle cell/thalassaemia
  • Post-splenectomy
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4
Q

What are heinz bodies on a blood film and what is it

A
  • G6PD deficiency
  • Alpha-thalassaemia
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5
Q

What causes Howell-Jolly bodies to be seen on a blood film ?

A
  • Post splenectomy
  • Non functioning spleen (sickle cell anaemia)
  • Coeliac disease (hyposplenism)
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6
Q

When would reticulocytes be seen on a blood film ?

A

Haemolytic anaemia

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7
Q

When are smudge cells seen on a blood film ?

A
  • CLL : they are ruptured white blood cells
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8
Q

When are spherocytes seen on a blood film ?

A
  • Autoimmune haemolytic anaemia or hereditary spherocytosis
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9
Q

When are ‘Tear-drop’ poikilocytes seen on a blood film ?

A

Myelofibrosis

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10
Q

What is associated with Schistocytes on a blood film ?

A
  • Intravascular haemolysis
  • Mechanical heart valve
  • DIC
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11
Q

What is associated with ‘pencil’ poikilocytes on blood film ?

A

IDA

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12
Q

What is associated with Burr cells on blood film

A

Uraemia
Pyruvate kinase deficiency

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13
Q

What is associated with hypersegmented neutrophils on blood films ?

A

Megaloblastic anaemia

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14
Q

Give the 5 causes of microcytic anaemia (low MCV)

A
  • T : thalassaemia
  • A : anaemia of chronic disease
  • I : IDA
  • L : lead poisoning
  • S : sideroblastic
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15
Q

Give the 5 causes of normocytic anaemia

A
  • A : anaemia of chronic disease
  • A : acute blood loss
  • A : aplastic anaemia
  • H : haemolytic anaemia
  • H : hypothyroid
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16
Q

What is anaemia of chronic disease

A

Anaemia caused by CKD -> reduced production of erythropoietin

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17
Q

Give the 2 causes of megaloblastic macrocytic anaemia

A

B12 deficiency
Folate deficiency

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18
Q

Give 5 causes of normoblastic macrocytic anaemia

A
  • Alcohol
  • Reticulocytosis
  • Hypothyroid
  • Liver diease
  • Drugs (e.g. azathioprine)
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19
Q

What can cause reticulocytosis ?

A
  • Haemolytic anaemia of blood loss
  • It is due to rapid RBC cell turnover
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20
Q

Give 5 generic Sx of anaemia

A

Tiredness
Shortness of breath
Headaches
Dizziness
Palpitations

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21
Q

Give 4 generic signs of anaemia

A

Pale skin
Conjunctival pallor
Tachycardia
Raised respiratory rate

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22
Q

What is the most common cause of IDA in adults

A

Blood loss

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23
Q

What is the most common cause of IDA in children ?

A

Dietary insufficiency -> Pica (eating soil) is a common presentation in children

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24
Q

Give 2 symptoms specific to IDA

A

Pica
Hair loss

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25
Q

Give 4 signs specific to IDA

A

Koilonychia
Angular cheilitis
Atrophic glossitis
Brittle hair and nails

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26
Q

Explain the blood profile of someone with IDA

A
  • FBC : hypochromic microcytic anaemia
  • Ferritin : low (correlates with iron stores)
  • TIBC : increased
  • Transferrin : increased
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27
Q

What is the transferrin saturation ?

A
  • Amount of iron bound to transferrin
  • Low iron = low saturation

Transferrin saturation = serum iron/TIBC

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28
Q

What should be done in new IDA without a clear underlying cause ?

A
  • Colonoscopy and OGD
  • Any pt >60 with new IDA = 2 week wait for colorectal cancer
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29
Q

Give the stepwise management of IDA

A
  • Oral iron (ferrous sulfate for 3 mnths)
  • Iron Infusion
  • Blood transfusion
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30
Q

Give 4 SE of ferrous sulfate

A

Nausea
Abdo pain
Constipation
Diarrhoea

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31
Q

When should iron infusions be avoided ?

A

During infection -> ‘feeds’ the bacteria’

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32
Q

What is the genetic inheritance of thalassaemia

A

Autosomal recessive

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33
Q

Give 4 signs of anaemia more specific to thalassaemia

A

Jaundice
Gallstones
Splenomegaly
Poor growth and development

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34
Q

Why does thalassaemia lead to splenomegaly ?

A
  • The RBCs are more fragile -> broken down more easily -> destroyed RBCs are collected by the spleen -> splenomegaly
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35
Q

What chromosome is involved in alpha thalassaemia

A

Chromosome 16 -> 2 separate alpha-globulin genes are located on each chromosome

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36
Q

Explain the 3 clinical severities on thalassaemia

A
  • Hypochromic and microcytic blood picture but normal Hb : 1 or 2 affected alleles
  • Hb H disease : 3 alleles affected = hypochromic microcytic anaemia
  • Hydrops fetalis : 4 alleles -> death in utero
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37
Q

What chromosome is involved in Beta-Thalassaemia ?

A
  • 11
  • Involves abnormal copies or deleted genes
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38
Q

What is Beta-thalassaemia trait ?

A
  • One abnormal and one normal gene
  • Mild-hypochromic microcytic anaemia
  • Usually asymptomatic
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39
Q

What is thalassaemia intermedia ?

A
  • Two abnormal copes (either 2 defective or one defective and 1 deleted)
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40
Q

What is Beta-thalassaemia major ?

A
  • Absence of beta globulin chains
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41
Q

How does beta-thalassaemia major present

A
  • First year of life with failure to thrive and and hepatosplenomegaly
  • Microcytic anaemia
  • HbA2 & HbF raised
  • HbA absent
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42
Q

How is Beta-thalassaemia major managed ?

A

repeated transfusion
this leads to iron overload → organ failure
iron chelation therapy is therefore important (e.g. desferrioxamine)

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43
Q

What is the blood profile of someone with anaemia of chronic disease

A
  • Low serum iron
  • Low TIBC
  • Low transferrin saturation
  • High ferritin
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44
Q

If not congenital, give 4 acquired causes of sideroblastic anaemia

A

Myelodysplasia
Alcohol
Lead
Anti-TB medications

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45
Q

What is seen on Ix in sideroblastic anaemia

A
  • FBC : hypochromic microcytic anaemia
  • Iron studies : high ferritin, iron and transferrin saturation
  • Blood film : basophilic stipling of RBCs
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46
Q

What staining is used in the bone marrow for diagnosing sideroblastic anaemia ?

A

Perussian blue and it will show ringed sideroblasts

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47
Q

What are 3 signs of haemolytic anaemia

A
  • Anaemia (fatigue, palpitations, SOB)
  • Splenomegaly
  • Jaundice : bilirubin is released when RBCs are destroyed

These are the signs of RBC destruction

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48
Q

What is seen on FBC and blood film in haemolytic anaemia ?

A
  • FBC : normocytic anaemia
  • Blood film : shistocytes (RBC fragments)
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49
Q

Give 5 hereditary causes of haemolytic anaemia

A
  • Hereditary elliptocytosis
  • Hereditary spherocytosis
  • Thalassaemia
  • Sickle cell anaemia
  • G6PD deficiency
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50
Q

Give 5 acquired conditions that can cause haemolytic anaemia

A
  • Autoimmune
  • Alloimmune
  • Paroxysmal nocturnal haemoglobinuria
  • Microangiopathic haemolytic anaemia
  • Prosthetic valve-related haemolysis
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51
Q

What is the inheritance of hereditary spherocytosis and Elliptocytosis ?

A

Autosomal dominant

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52
Q

Give 3 key blood findings in hereditary spherocytosis

A
  • Raised MCHC
  • Raised reticulocyte count
  • Spherocytes on blood film
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53
Q

What will the parvovirus cause in someone with hereditary spherocytosis ?

A
  • Aplastic crisis
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54
Q

How is hereditary spherocysis managed ?

A
  • Folate and blood transfusions when needed
  • Splenectomy
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55
Q

Explain the genetic inheritance of G6PD deficiency

A
  • X linked recessive
  • Defect in the gene coding for glucose-6 phosphate dehydrogenase
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56
Q

What is a characteristic feature of G6PD deficiency ?

A
  • Episodes of haemolytic anaemic triggered by :
  • Infection
  • Fava beans
  • Drugs : ciprofloxacin, sulfonylureas, sulfasalazine
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57
Q

What is seen on a blood film in G6PD deficiency and how is it diagnosed

A
  • Heinz bodies
  • G6PD enzyme assay
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58
Q

What is warm AIHA

A
  • Antibodies are created against RBCs
  • Usually IgG
  • Haemolysis occurs at normal or above-normal temperatures
  • Most common
  • Usually idiopathic
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59
Q

What is cold, reactive AIHA

A
  • Antibodies are created against RBCs
  • Usually IgM
  • Haemolysis occurs at low temps
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60
Q

What is cold AIHA secondary too ?

A
  • Lymphoma
  • Leukaemia
  • SLE
  • Infections (e.g., mycoplasma, EBV, CMV and HIV).
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61
Q

What is usued first line to treat warm AIHA?

A

Steroids (+/- rituximab)

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62
Q

Other than showing normocytic anaemia with shistocytes, what is a specific finding in AIHA ?

A

Positive Direct Coombs test

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63
Q

A patient presents with haemolytic anaemia, haemoglobinuria (RED URINE), thrombosis (DVT) and smooth muscle dystonia (erectile dysfunction).

What is the likely cause ?

A
  • Paroxysmal noctunal haemoglobinuria
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64
Q

How is paroxysmal noctunal haemoglobinuria managed ?

A
  • Eculizumab
  • Bone marrow transplant
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65
Q

What is microangiopathic haemolytic anaemia dna give 5 causes

A
  • Destruction of RBCs as they pass through circulation due to abnorm al clotting obstruction the blood vesels
  • HUS
  • DIC
  • TTP
  • SLE
  • Cancer
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66
Q

Explain the genetic inheritance of sickle cell anaemia

A
  • Autosomal recessive
  • Affects the beta-globin chain on chromosome 11
  • Results in the prodction of HbS = sickle shaped RBCs
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67
Q

How is sickle cell anaemia diagnosed

A

Haemoglobin electrophoresis

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68
Q

What is the general management of sickle cell anaemia ?

A
  • Antibiotic prophylaxis with Penicillin V (phenoxymethylpenicillin)
  • Long term Hydroxycarbamide
  • Crizanlizumab
  • Blood transfusions for severe anaemia
  • Bone marrow transplant can be curative
  • Pneumococcal polysaccharide vaccine every 5 yrs.
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69
Q

What can be given to increase the amount of HbF production in sickle cell anaemia

A

Hydroxyurea

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70
Q

Why is Crizanlizumab given in sickle cell anaemia ?

A
  • Monoclonal antibody targetting P-selectin, an adhesion molecule on endothelial cells inside of blood vessel and platelets.
  • Reduces frequency of vaso-occlusive crises by preventing RBCs sticking to the wall.
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71
Q

What is a vaso-occlusive crisis ?

A
  • The RBCs clog the capillaries causing distal ischaemia
  • Precipitated by infection, dehydration, deoxygenation
  • Presents with pain in hands or feet and associated fever
  • Urological emergency = priapism
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72
Q

What is a splenic sequestration crisis ?

A
  • RBCs block blood flow to spleen
  • Causing painful splenomegaly
  • Causes increased reticulocyte count
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73
Q

What triggers an aplastic crisis in sickle cell anaemia

A
  • Parvovirus B19
  • Causes a sudden fall in haemoglobin and bone marrow supression leading to reduced reticulocyte count
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74
Q

What is acute chest syndrome and how does it present?

A
  • Vessels supplying lungs become blocked by RBCs
  • Fever, SOB , Chest pain, cough and hypoxia
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75
Q

What will be seen on a chest X-ray in acute chest syndrome ?

A

Bilateral pulmonary infiltrates

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76
Q

Define leukaemia

A

Cancer of a particular line of stem cells in the bone marrow

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77
Q

what are the 4 types of leukaemia ?

A
  • Acute myeloid leukaemia
  • Acute lymphoblastic leukaemia
  • Chronic myeloid leukaemia
  • Chronic lymphocytic leukaemia
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78
Q

Give a characteristic feature for each of the 4 types of leukaemia

A
  • ALL : children and is associated with Down syndrome
  • CLL is associated with warm haemolytic anaemia, Richter’s transformation and smudge cells
  • CML has three phases, including a long chronic phase, and is associated with the Philadelphia chromosome
  • AML may result in a transformation from a myeloproliferative disorder and is associated with Auer rods
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79
Q

How can the features of ALL be divided ?

A

-Anaemia : lethargy and pallor
- Neutropaenia: frequent or severe infections
- Thrombocytopenia: easy bruising, petechiae

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80
Q

Give 5 poor prognostic factors for ALL

A
  • Age < 2 years or > 10 years
  • WBC > 20 * 109/l at diagnosis
  • T or B cell surface markers
  • Non-Caucasian
  • Male sex
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81
Q

What is the most common form of leukaemia in adults

A
  • CLL
  • Usually seen in adults >60
  • Proliferation of well-differentiated lymphocytes
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82
Q

What is seen on a blood film in CLL?

A

Smudge cells (smear cells)

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83
Q

Give 4 complications of CLL

A
  • Anaemia
  • Hypogammaglobulinaemia leading to recurrent infections
  • Warm autoimmune haemolytic anaemia in 10-15% of patients
  • Transformation to high-grade lymphoma (Richter’s transformation)
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84
Q

How would Richter’s transformation present in an exam question ?

A
  • Patient with leukaemia becomes unwell very suddenly.
  • Lymph node swelling, fever without infection, weight loss etc
85
Q

What are the 3 phases of CML ?

A
  • Chronic phase
  • Accelerated phase
  • Blast phase
86
Q

Explain the chronic phase of CML

A
  • Often asymptomatic, diagnosed after an incidental finding of a raised white cell count.
  • This phase can last several years before progressing.
87
Q

Explain the accelerated phase of CML

A
  • Occurs when the abnormal blast cells take up a high proportion (10-20%) of the bone marrow and blood cells.
  • Patients are more symptomatic and develop anaemia, thrombocytopenia and immunodeficiency.
88
Q

Explain the blast phase of CML

A
  • Involves an even higher proportion (over 20%) of blast cells in the blood.
  • Severe symptoms and pancytopenia and is often fatal.
89
Q

What is CML particularly associated with ?

A
  • Philadelphia chromosome
  • Abnormal chromosome 22
  • Caused by reciprocal translocation of a section of chromosome 9 and 22.
  • BCR-ABL1 = abnormal tyrosine kinase enzyme
90
Q

what is now considered first line treatment of CML

A

Imatinib -> inhibits tyrosine kinase

91
Q

What are the characteristic findings on blood film and bone marrow biopsy in AML ?

A
  • High proportion of blast cells
  • Aure rods
92
Q

What are the 4 U&E findings characteristic of tumour lysis syndrome

A
  • High uric acid
  • Hyperkalaemia
  • High phosphate
  • Low calcium
93
Q

What can the high uric acid and hyperkalaemia seen in tumiur lysis syndrome cause ?

A
  • Uric acid -> AKI
  • Hyperkalaemia -> cardiac arrhythmias
94
Q

What is the usual presentation of acute promyelocytic leukaemia

A
  • Younger patient (around 25) presenting with DIC
95
Q

what is lymphoma ?

A
  • A type of cancer affecting the lymphocytes inside the lymphatic system.
  • They proliferate inside the lymph nodes causing lymphadenopathy
96
Q

What age group is affected by Hodgkin’s lymphoma ?

A
  • Bimodal age distribution (20-25 and 80 yrs)
97
Q

Give 4 RF for Hodgkin’s lymphoma

A
  • HIV
  • Epstein-Barr virus
  • Autoimmune conditions, such as rheumatoid arthritis and sarcoidosis
  • Family history
98
Q

what is the main feature of Hodgkin’s lymphoma ?

A
  • Lymphadenopathy, most commonly cervical
  • Painless, non tender and asymmetrical
  • Alcohol-induced lymph node pain
99
Q

What B symptoms are seen in Hodgkin’s lymphoma

A

weight loss
pruritus
night sweats
fever

100
Q

what is the diagnostic investigation for lymphoma and what is seen in Hodgkin’s lymphoma ?

A

Lymph node biopsy
Reed-Sternberg cells
Large multinucleated cells with prominent eosinophilic nucleoli

101
Q

What is the treatment of Hodgkin’s lymphoma ?

A
  • Chemo and radiotherapy
102
Q

What is the new staging system used for lymphoma ?

A

Lugano classification

  • Stage 1: Confined to one node or group of nodes
  • Stage 2: In more than one group of nodes but on the same side of the diaphragm (either above or below)
  • Stage 3: Affects lymph nodes both above and below the diaphragm
  • Stage 4: Widespread involvement, including non-lymphatic organs, such as the lungs or liver
103
Q

Give 7 RF for Non-Hodgkin Lymphoma

A
  • HIV
  • EBV
  • H. pylori -> MALT lymphoma
  • Hep B or C
  • Exposure to pesticides
  • Exposure to trichloroethylene
  • FHx
104
Q

What is associated with Burkitt’s lymphoma and what is seen on microscopy

A
  • EBV
  • ‘Starry sky’ appearance on lymph node biopsy
105
Q

what is associated with gastric MALT lymphoma and what is a common feature ?

A
  • H. pylori
  • Paraproteinaemia
106
Q

What is often seen on routine bloods in lymphoma ?

A
  • Normocytic anaemia
  • Eosinophilia
  • Raised LDH
107
Q

What is essential for the absoprtion of B12 ?

A
  • Intrinsic factor produced by the parietal cells of the stomach
108
Q

What is pernicious anaemia ?

A
  • Autoimmune condition where antibodies are produced against parietal cells or intrisic factor (1st line Ix).
  • lack of B12 = macrocytic anaemia
109
Q

What 5 specific signs can be seen in pernicious anaemia ?

A
  • Peripheral neuropathy
  • Loss of vibration sense
  • Loss of proprioception
  • Visual changes
  • Mood and cognitive changes
110
Q

What is given initially for the management of B12 deficiency

A
  • IM hydroxycobalamin
  • No neurological Sx : 3x weekly for 2 wks
  • Neurological Sx : alternate days until no further improvement in Sx
111
Q

How is control of B12 deficiency maintained ?

A
  • Pernicious anaemia : 2-3 mnthly injections for life
  • Diet related : oral cyanocobalamin or twice-yearly injections
112
Q

What can happen if folate is given before treating B12 deficiency if a deficiency in both is present ?

A

Subacute combined degeneration of the cord

113
Q

What is myeloma ?

A

Malignancy of the plasma cells in the bone marrow

114
Q

Define multiple myeloma, MGUS and smouldering myeloma

A
  • Multiple myeloma : multiple bone marrow areas affected.
  • Monoclonal gammopathy of undetermined significance : production of paraprotein without other features of myeloma or cancer.
  • Smouldering : abnormal plasma cells & paraproteins but no Sx.
115
Q

What are the 5 feaures of myeloma ?

A

CRABBI

  • C : Calcium (elevated)
  • R : Renal damage
  • A : Anaemia
  • B : Bleeding (thrombocytopenia )
  • B : Bones : lytic bone lesions
  • I : Infection
116
Q

What is seen on bloods in myeloma ?

A
  • FBC : anaemia
  • Blood film : rouleaux formation
  • U&Es : renal failure
  • Bone profile : hypercalcaemia
117
Q

What would be seen on protein electrophoresis in myeloma ?

A
  • Serum : paraproteinaemia
  • Urine : Bence Jones in the urine
118
Q

what is used to confirm the diagnosis of myeloma ?

A

Bone marrow biopsy -> shows raised plasma cells

119
Q

What imaging is preferred for assessing bone lesions in myeloma ?

A
  • Whole-body MRI
  • Will show ‘punched out’ lesions, diffuse osteopenia and abnormal fracures
  • In the skull : ‘raindrop/pepper pot skull’
120
Q

What is the diagnostic criteria of myeloma

A
  • One major and one minor or 3 minor
  • Major : Plasmacytoma,
    30% plasma cells in a bone marrow sample, Elevated levels of M protein in the blood or urine.
  • Minor : 10% to 30% plasma cells in a bone marrow sample,
    Minor elevations in the level of M protein in the blood or urine, Osteolytic lesions,
    Low levels of antibodies (not produced by the cancer cells) in the blood.
121
Q

what is a myeloproliferative disorder and give 3 examples

A

Uncontrolled proliferation. of a single line of stem cells.

  • Primary myelofibrosis
  • Polycythaemia vera
  • Essential thrombocythaemia
122
Q

what mutation is thought to be associated with myeloproliferative disorders

A

JAK2

123
Q

what is myelofibrosis ?

A
  • When proliferation of a single line of stem cells leads to bone marrow fibrosis.
  • Can be : primary myelofibrosis, polycythaemia vera or essential thrombocytopenia
124
Q

What would be seen on bloods in myelofibrosis ?

A

Anaemia
Leukopenia
Thrombocytopenia

125
Q

What happens to the liver and spleen in myelofibrosis

A
  • They start producing RBC’s = hepatomegaly and splenomegaly
  • If it occurs in the spine = spinal cord compression
126
Q

What is seen on a blood film in myelofibrosis ?

A
  • Tear drop RBCs
  • Anisocytosis
  • Blasts
127
Q

What is seen on bloods in essential thrombocythaemia

A

Isolated raised plts

128
Q

What is seen in polycythaemia vera ?

A

High haemoglobin

129
Q

what is used to diagnose a myeloproliferative disorder and what would be seen in myelofibrosis ?

A
  • Bone marrow biopsy
  • Bone marrow aspiration might be ‘dry’ with myelofibrosis
130
Q

what clinical signs are seen in polycythaemia ?

A
  • Ruddy complexion (red face)
  • Conjunctival plethora
  • Splenomegaly
  • Hypertension
  • Pruitus
131
Q

What is a common complication of polycythaemia vera and essential thromboythaemia

A
  • Thrombosis
    = MI, stroke or DVT/PE
132
Q

How is polycythaemia vera managed ?

A
  • Venesection t
  • Aspirin to reduce the risk of thrombus formation
  • Chemotherapy (typically hydroxycarbamide) to help control the disease
133
Q

How is essential thrombocythaemia managed ?

A
  • Aspirin to reduce the risk of thrombus formation
    Chemotherapy (typically hydroxycarbamide) t
  • Anagrelide is a specialist platelet-lowering agent
134
Q

Myelodysplastic syndrome involves a mutation in which cells in the bone marrow ?

A

Myeloid cells

135
Q

What does myelodysplastic syndrome result in and what can it transform in to?

A
  • Ineffective haematopoiesis = lack of RBCs
  • Can transform to AML
136
Q

As it effects the myeloid cell line what is seen on bloods in myelodysplastic syndrome ?

A

Pancytopenia (low RBCs, neutrophils and platelets).

137
Q

How does moderate thrombocytopenia present ?

A

Nosebleeds
Bleeding gums
Heavy periods
Easy bruising
Haematuria (blood in the urine)
Rectal bleeding

138
Q

How does severe thrombocytopenia present ?

A
  • Intracranial haemorrhage
  • Gastrointestinal bleeding
139
Q

Give 4 top differentials for prolonged and abnormal bleeding

A
  • Thrombocytopenia (TTP, ITP, heparin induced)
  • Von Willebrand disease
  • Haemophilia A and B
  • DIC
140
Q

What is thrombotic thrombocytopenia purpura and what does it cause ?

A
  • Thrombi develop in the small vessels using up the plts
  • Thrombocytopenia
  • Purpura
  • Tissue ischaemia and end-organ damage
141
Q

What monoclonal antibody can be used in the management of ITP and TTP ?

A
  • Rituximab : it targets B cells which produce antbodies
142
Q

How long after starting treatment with heparin can heparin-induced thrombocytopenia develop ?

A
  • 5 to 10 days
  • They develop both. alow plt count and abnormal blood clots
143
Q

what is the most common inherited bleeding disorder and in what fashion is it inherited ?

A
  • Von Willebrand disease
  • Autosomal dominant
144
Q

what are the 3 types of VWD ?

A
  • Type 1 : partial deficiency of VWF and is the most common and mildest type
    Type 2 : reduced function of VWF
    Type 3 : complete deficiency of VWF and is the most rare and severe type
145
Q

How does VWD present ?

A
  • Bleeding gums with brushing
  • Epistaxis
  • Easy bruising
  • Menorrhagia
  • Heavy bleeding during and after surgical operations

Often a family history !

146
Q

when necessary what can be used to manage VWD

A
  • Desmopressin (stimulates the release of vWF from endothelial cells)
  • Tranexamic acid
  • Von Willebrand factor infusion
  • Factor VIII plus von Willebrand factor infusion
147
Q

What are the causes of haemophilia A and B and their pattern of inheritance ?

A
  • A = factor VIII deficiency
  • B = factor IX deficienct
  • X linked recessive
148
Q

what is seen on coagulation studies in haemophilia ?

A

Isolated prolonged APTT

149
Q

How does a DVT present ?

A
  • Calf or leg swelling (>3cm is significant)
  • Dilated superficial veins
  • Tenderness to the calf (particularly over the site of the deep veins)
  • Oedema
  • Colour changes to the leg
150
Q

what determines the investigations done into a DVT?

A
  • 2 level DVT Well’s score
  • Likely (2+) : proximal leg vein USS within 4 hrs.
  • Unlikely (1) : d-dimer, followed by USS if +ve.
151
Q

Is D-dimer sensitive or specific ?

A
  • Sensitive.
  • Almost always raised if DVT/PE present
  • But can ve raised due to other conditions
152
Q

what should be done if a patient likely to have a DVT but an USS cannot be done within 4 hrs ?

A
  • Interim therapeutic anticoagulation
  • Dalterparin : check weight and eGFR
  • 200 units/kg daily by sub cut injection
153
Q

how is a DVT managed ?

A
  • Doac (apixaban / rivaroxaban)
154
Q

when is LMWH given instead of a DOAC for a DVT?

A
  • Renal impairment (creatinine clearance of <15ml/min)
  • Antiphospholipid syndrome
  • Pregnancy
155
Q

How long is anticoagulation continued following a DVT?

A
  • 3 months with a reversible cause (then review)
  • 3-6 months in active cancer (then review)
  • Long-term for unprovoked VTE, recurrent VTE or an irreversible underlying cause (e.g., thrombophilia)
156
Q

what is the first line management of a DVT in someone with ant-phospholipid syndrome and a pregnant woman

A
  • Anti-phospholipid syndrome : warfarin
  • Pregnancy : LMWH
157
Q

What is Budd-Chiari syndrome and the triad of features ?

A
  • Hepatic vein thrombosis
  • Abdo pain : sudden and severe
  • Ascites
  • Tender hepatomegaly
158
Q

Give 4 causes of Budd-Chiari syndrome

A
  • Polycythaemia rubra vera
  • Thrombophilia: activated protein C resistance, antithrombin III deficiency, protein C & S deficiencies
  • Pregnancy
  • Combined oral contraceptive pill
159
Q

What clotting factors does heparin prevent the action of ?

A

2,9,10,11

160
Q

What factors does warfarin affect synthesis of due to action on vit K

A

10,9,7,2

161
Q

what would be seen on blood clotting tests results in VWD?

A

Increased APTT and bleeding time but normal PT

162
Q

What would be seen on blood clotting test results in vitamin K deficiency ?

A

Increased APTT and PT but normal bleeding time

163
Q

How is anti-phospholipid syndrome managed in pregnancy ?

A
  • Low-dose aspirin should once the pregnancy is confirmed on urine testing
  • Low molecular weight heparin once a fetal heart is seen on ultrasound. This is usually discontinued at 34 weeks gestation
164
Q

What does cryoprecipitate contain ?

A
  • Factor VIII
  • Fibrinogen
  • Von Willebrand factor
  • Factor XIII
165
Q

What is a typical blood picture seen in DIC ?

A

↓ platelets
↓ fibrinogen
↑ PT & APTT
↑ fibrinogen degradation products
schistocytes due to microangiopathic haemolytic anaemia

166
Q

What is the inheritance of fanconi anaemia ?

A

Autosomal recessive

167
Q

What are the features of fanconi anaemia ?

A
  • Haematological: aplastic anaemia,
    increased risk of AML
    neurological
  • Skeletal abnormalities: short stature, thumb/radius abnormalities
  • Cafe au lait spot
168
Q

Pt has a likely DVT based on well’s but leg scan is negative - what do you do >

A
  • If D dimer is +ve, re scan in 6-8v days
  • If D dimer is -ve, consder alt diagnosis
169
Q

Most common inherited thrombophilia creating PE/DVT risk

A

Factor V leiden = activated protein C resistance

170
Q

Manufactured version of B12, used to treat B!2 deficiency

A

Hydroxyocobalamin

171
Q

Transfusion threshold in pts without ACS

A

70g/l

172
Q

Transfusion threshold in pts with ACS

A

80g/l

173
Q

Management of neutropenic sepsis

A

Piperacillin with tazobactam (Tazocin)

174
Q

What are sickle cell patients started on long term to reduce incidence of complications and acute crises

A

Hydroxycarbamide

175
Q

What medications should ppl receiving transfusions for beta thalassaemia also be taking

A

Desforrioxamine = prevent iron overload due to repeat transfusions

176
Q

what are the laboratory requirements for blood in a pt with previous transplant

A

Irradiated blood products are used to avoid transfusion-associated graft versus host disease

177
Q

Clotting in antiphospholipid syndrome

A
  • Raised APTT
  • Normal PT
  • Possible thrombocytopenia
178
Q

Presentation of transfusion associated circulatory overload

A

Hypertension
Raised jugular venous pulse
Afebrile
S3 present.

179
Q

Management of TACO

A

Furosemide

180
Q

Presentation of transfusion related acute lung injury

A

Hypotension
Pyrexia
Normal/unchanged JVP

181
Q

Management of what chronic condition can lead to B12 deficiency and why

A
  • LLeocaecal resection in crohns disease
  • B12 is absorbed in the terminal ileum
182
Q

Most concerning sign when assessing possible blood transfusion reaction

A

Hypotension

183
Q

Management of co existing B12 and folate deficiency

A

1mg cyanocobalamin IM injections 3x weekly

Treat B12 deficiency first to avoid subacute combined degeneration of spinal cord

184
Q

Cause of macrocytic anaemia with hyper-segmented neutrophil polymorphs on blood film

A
  • B12 deficiency (vegan = RF)
  • Folate deficiency (methotrexate = possible cause).
185
Q

When should neutropenic sepsis be suspected whilst awaiting blood results and what should be done

A
  • In a person with a known cause for neutropenia
  • Presumed or confirmed infection
  • Temperature >38ºC
  • Respiratory rate >20 breaths per minute

(Begin immediate empirical antibiotic therapy before receiving blood results).

186
Q

what can be seen on a blood film in coeliac disease and why

A

Howell-jolly bodies : coeliac disease is associated with hyposplenism.

187
Q

Common presentation of CML in a question

A

Splenomegaly
Anaemia
Thrombocytosis
Raised neutrophils

188
Q

how can alpha and beta thalassaemia be distinguished ?

A
  • Beat thalassamiea : raised HbaA2 on electrophoresis

AND

Disproportionate microcytic anaemia (I.e - low Hb but MUCH lower MCV).

189
Q

Most common causative agents opf neutropenic sepsis

A
  • Coagulase-negative, Gram-positive bacteria
  • Particularly staphylococcus epidermidis = probably due to the use of indwelling lines in patients with cancer
190
Q

Bloods and blood film seen in CML

A
  • Blood film = myeloblasts and granulocytosis
  • Bloods : anaemia, thrombocytosis, raised neutrophils
191
Q

What can lead to gastric lymphoma (MALT)

A

H.pylori

192
Q

How can you distinguish an aplastic crisis from an haemolytic crisis / acute splenic sequestration in a sickle cell crisis

A
  • Aplastic crisis = there will be. drop in Hb but ALSO a drop in reticulocytes as the issue is with the bone marrow
  • Haemolytic / splenic sequestration = rise in reticulocyte count as the issue is RBC survival NOT production
193
Q

Management of ACS

A
  1. Analgesia
  2. Oxygen
  3. Antibiotics
  4. Transfusion (if indicated by Hb)
194
Q

common presentation of cold AIHA

A
  • In hospital with mycoplasma pneumonia (common cause)
  • Develops palpitations, pale skin, dark urine (haemolysis)
  • Bloods : drop in Hb, raised ESR and reticulocytes)
195
Q

Mechanism of action of rivaroxaban

A

Direct factor Xa inhibitor

196
Q

Mechanism of action of dabigatran

A

Direct thrombin inhibitor

197
Q

Action of heparin

A

Activates anti-thrombin III

198
Q

Action of warfarin

A

Inhibitors clotting factors 10, 9, 7, 2

199
Q

How should a vaso-occlusive crisis be diagnosed ?

A

CLINICALLY
No additional testing is needed

200
Q

what can cause secondary polycythaemia ?

A
  • OSA
  • COPD
201
Q

How can you distinguish secondary from primary polycythaemia ?

A
  • In secondary polycythaemia the SpO2 / EPO won’t be normal as it is reactive
202
Q

How to distinguish cold and warm AIHA in an exam question

A

Warm autoimmune haemolytic anaemia is associated with CLL

203
Q

Blood film suggestive of hyposplenism

A

Howell-Jolly bodies and siderocytes

204
Q

Reversal of dabigatran

A

Idarucizumab

205
Q

5 features of post thrombotic syndrome

A
  • painful, heavy calves
  • pruritus
  • swelling
  • varicose veins
  • venous ulceration
206
Q

what are irradiated blood products ?

A

Depleted in T lymphocytes to reduce risk of graft versus host disease

207
Q

what is given prior to surgery in a pt with VWD to reduce bleeding whilst awaiting theatre ?

A

Desmopressin

208
Q

treatment of acute attacks of intermittent porphyria

A

Haem arginate

209
Q
A

Finals (92 decks)

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