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Medicine and Surgery Mushkies > Passmed Haematology Mushkies > Flashcards

Passmed Haematology Mushkies Flashcards

1
Q

Unprovoked DVT investigations?

A

1, Underlying malignancy (CXR, bloods, urine, CT abdo pelvis if >40y/o)
2. Anti-phospholipid Abs
3.

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2
Q

Smear/smudge cells?

A

CLL

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3
Q

Why recurrent infections in CLL?

A

Due to hypogammaglobulinaemia

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4
Q

What AIHA is a complication of CLL?

A

Warm

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5
Q

4 complications of CLL?

A
  1. Anaemia
  2. Hypogammaglobulinaemia –> recurrent infections
  3. Warm AIHA
  4. Richter’s transformation
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6
Q

What is Richter’s transformation?

A

When CLL cells enter the lymph node and changer into a high grade, fast-growing NHL (DLBCNHL)

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7
Q

Howell-Jolly bodies?

A

Hyposplenism

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8
Q

Basophilic stippling?

A
  1. Lead poisoning
  2. Thalassaemia
  3. Sideroblastic anaemia
  4. Myelodysplasia
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9
Q

Cabot rings?

A

Lead poisoning

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10
Q

Rouleaux?

A

Chronic inflammation and myeloma

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11
Q

Schistocytes?

A
  1. Intravascular haemolysis
  2. Mechanical heart valve
  3. DIC
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12
Q

Dohle bodies?

A

Neurtrophil response to infection

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13
Q

Hyposplenism on blood film?

A
  1. Howell-Jolly bodies

2. Siderocytes

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14
Q

Causes of hyposplenism?

A
  1. Splenectomy
  2. SCD
  3. Coeliac
  4. Graves
  5. SLE
  6. Amyloid
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15
Q

Most common hereditary haemolytic anaemia in people of northern European descent?

A

Hereditary spherocytosis

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16
Q

Hereditary spherocytosis inheritance?

A

AD

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17
Q

Osmotic fragility test?

A

Hereditary spherocytosis

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18
Q

Current main test for hereditary spherocytosis?

A
  1. Cryohaemolysis testing

2. EMA binding test

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19
Q

Mx of hereditary spherocytosis?

A
  1. Folate replacement

2. Splenectomy

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20
Q

What kind of haemolysis is found in hereditary spherocytosis?

A

Extravascular haemolysis

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21
Q

G6PDD inheritance?

A

X-linked recessive

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22
Q

G6PDD ethinicity?

A

African and Mediterranean

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23
Q

Hereditary spherocytosis ethnicity?

A

North European

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24
Q

Heinz bodies?

A
  1. G6PDD

2. Alpha thalassaemia

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25
Q

G6PDD test?

A

Enzyme activity of G6PD

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26
Q

Presentation of G6PDD/HS?

A
  1. Neonatal jaundice
  2. Gallstones
  3. Infection/drugs precipitate haemolysis
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27
Q

Thymoma condition association?

A
  1. Myasthenia Gravis (30-40% pts with thymoma)
  2. Red cell aplasia
  3. Dermatomyositis
  4. SLE, SIADH
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28
Q

Lambert Eaton syndrome association?

A

Small cell lung cancer

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29
Q

What is a thymoma?

A

Most common tumour of the anterior mediastinum and is usually detected between the 6th and 7th decades of life

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30
Q

How do thymomas cause death?

A
  1. Airway compression

2. Cardiac tamponade

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31
Q

Transfusion threshold for pts with ACS?

A

80g/L

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32
Q

Transfusion threshold for pts without ACS?

A

70g/L

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33
Q

RBC storage temperature?

A

4 degrees

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34
Q

RBC transfusion time in non-emergency?

A

90-120 mins

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35
Q

Spherocytes causes?

A
  1. Congenital = HS

2. Acquired = AIHA

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36
Q

AIHA Ix?

A

Direct Coombs Test

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37
Q

Decrease in serum haptoglobins?

A

Intravascular haemolysis

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38
Q

Target cells causes?

A
  1. SCD/Thalassaemia
  2. IDA
  3. Hyposplenism
  4. Liver disease
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39
Q

Tear drop poikilocytes?

A

Myelofibrosis

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40
Q

Pencil poikilocytes?

A

IDA

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41
Q

Burr cells aka?

A

Echinocytes

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42
Q

Burr cells?

A
  1. Uraemia

2. Pyruvate kinase deficiency

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43
Q

Acanthocytes?

A

Abetalipoproteinaemia

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44
Q

Hypersegmented neutrophils?

A

Megaloblastic anaemia

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45
Q

Thrombophilia cause classification?

A
  1. Congenital

2. Acquire

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46
Q

Acquired thrombophilia causes?

A
  1. Antiphospholipid syndrome

2. Drugs, most commonly COCP

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47
Q

Congenital thrombophilia causes?

A
  1. Gain of function polymorphisms

2. Natural anticoagulant deficiencies

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48
Q

Gain of function polymorphisms causing thrombophilia?

A
  1. Factor V Leiden (Activated Protein C resistance)

2. Prothrombin gene mutaiton

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49
Q

Natural anticoagulant deficiencies causing thrombophilia?

A
  1. Antithrombin III deficiency
  2. Protein C deficiency
  3. Protein S deficiency
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50
Q

Macrocytic anaemia with hypersegmented neutrophils?

A

Megaloblastic anaemia

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51
Q

Macrocytic anaemia causes?

A
  1. Megablastic

2. Non-megaloblastic

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52
Q

Megaloblastic anaemia causes?

A
  1. Vit B12 deficiency

2. Folate deficiency

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53
Q

Non-megaloblastic anaemia causes?

A
  1. Alcohol
  2. Liver disease
  3. Hypothyroidism
  4. Pregnancy
  5. Reticulocytosis
  6. Myelodysplasia
  7. Drugs = cytotoxics
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54
Q

HL/NHL features?

A
  1. Lymphadenopathy
  2. Constitutional B symptoms (fever, weight loss, night sweats, lethargy)
  3. Extranodal disease = gastric, BM, lungs, skin, CNS
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55
Q

What are the B symptoms?

A
  1. Weight loss >10% in 6m
  2. Fever > 38C
  3. Night sweats
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56
Q

Staging for HL?

A

Ann Arbor

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57
Q

What is the Ann Arbor Staging?

A

CT CAP for HL

  1. Single lymph node region
  2. Two or more regions on same side of diaphragm
  3. Lymph node involvement on both sides of the diaphragm
  4. Extranodal site involvement
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58
Q

HL on histology?

A

Reed Sternberg cells

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59
Q

Hodgkins lymphoma classification?

A
  1. Classical (4 types)

2. Nodular lymphocyte-predominant HL

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60
Q

Classical HL types?

A
  1. Nodular sclerosing HL
  2. Mixed cellularity HL
  3. Lymphocyte rich HL
  4. Lymphocyte deplete HL
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61
Q

Tx of HL?

A

Chemo and radiotherapy

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62
Q

Dx of HL?

A

Histology of lymph node

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63
Q

Viral assocation of HL?

A

EBV

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64
Q

Prognosis of HL?

A

Stage I = 85% survival at 5 years

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65
Q

Best HL prognosis subtype?

A

Lymphocyte rich HL

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66
Q

Worst HL prognosis subtype?

A

Lymphocyte deplete HL

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67
Q

Should compression stocking be offered routinely to all pts with DVT?

A

No

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68
Q

What is post-thrombotic syndrome?

A

Clinical syndrome occurring after thrombosis due to venous outflow obstruction and venous insufficiency, leading to chronic venous hypertension

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69
Q

Features of post-thrombotic syndrome?

A
  1. Painful, heavy calves
  2. Pruritis
  3. Swelling
  4. Varicose veins
  5. Venous ulceration
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70
Q

Mx of post-thrombotic syndrome?

A
  1. Keep leg elevated

2. Graduated Compression stockings

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71
Q

AML blood film?

A

Auer rod

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72
Q

Pseudo Pelger-Huet cells?

A

CML

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73
Q

What is CLL?

A

A monoclonal proliferation of well differentiated lymphocytes, usually B cells (99%)

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74
Q

Most common leukaemia in adults?

A

CLL

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75
Q

CLL presentation?

A
  1. Usually none
  2. Constitutional = anorexia, weight loss
  3. Bleeding, infection
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76
Q

Ix of CLL?

A
  1. Blood film –> smudge/smear cells

2. Immunophenotyping

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77
Q

EMA binding test?

A

Hereditary spherocytosis

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78
Q

Platelet transfusion threshold if actively bleeding?

A

<30

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79
Q

Platelet transfusion threshold if severe bleeding at critical site e.g. CNS?

A

<100

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80
Q

Presurgical prophylactic platelet level targets?

A
  1. > 50 for most pts
  2. 50-75 if high risk of bleeding
  3. > 100 if at critical site
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81
Q

Platelet transfusion threshold if no active bleeding?

A

> 10

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82
Q

4 C/Is for platelet transfusions?

A
  1. TTP
  2. Heparin induced thrombocytopenia
  3. AI thrombocytopenia
  4. Chronic BM failure
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83
Q

Causes of aplastic anaemia?

A
  1. Idiopathic
  2. Congenital = Fanconi’s anaemia, dyskeratosis congenita
  3. Drugs
  4. Toxins e.g. benzene
  5. Infections
  6. Radiation
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84
Q

2 infections that cause aplastic anaemia?

A
  1. Parvovirus

2. Hepatitis

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85
Q

5 drugs that cause aplastic anaemia?

A
  1. Cytotoxics
  2. Phenytoin
  3. Chloramphenicol
  4. Suphonamides
  5. Gold
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86
Q

Blood finding of aplastic anaemia?

A

Pancytopenia

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87
Q

Acute haemolytic transfusion reaction management?

A
  1. Stop transfusion
  2. Generous fluid resuscitation
  3. Inform lab
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88
Q

Blood product transfusion complications?

A
  1. Immunological
  2. TRALI
  3. TACO
  4. Infective
  5. Other
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89
Q

Immunological complications of blood product transfusion?

A
  1. Acute haemolytic
  2. Non-haemolytic febrile (<1.5 increase)
  3. Allergic/anaphylaxis
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90
Q

What is TRALI?

A

Transfusion associated acute lung injury

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91
Q

What is TACO?

A

Transfusion associated circulatory overload

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92
Q

What are ‘other’ complications of blood transfusion?

A
  1. Hyperkalaemia
  2. Iron overload
  3. Clotting
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93
Q

What causes an acute haemolytic transfusion reaction (AHTR)?

A

Mismatch of ABO blood group that causes massive intravascular haemolysis

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94
Q

Acute haemolytic transfusion reaction features?

A
  1. Abdo and chest pain
  2. Agitation
  3. Hypotension
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95
Q

2 complications of acute haemolytic transfusion reaction?

A
  1. DIC

2. Renal failure

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96
Q

What causes a non-haemolytic febrile transfusion reaction?

A

Due to WBC HLA antibodies, often the result of sensitisation by previous pregnancies or transfusions

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97
Q

Mx of non-haemolytic febrile transfusion reaction?

A

Paracetamol

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98
Q

Dx of TRALI?

A

Development of hypoxaemia/ARDS within 6 hours of transfusion (hypoxia, fever, hypotension, pulmonary infiltrates on CXR)

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99
Q

Raised ESR and osteoporosis?

A

Multiple myeloma until proven otherwise

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100
Q

MM features?

A

CRAB + OTHER

  1. Hypercalcaemia
  2. Renal failure
  3. Anaemia
  4. Bone disease = pain, osteoporosis, pathological fractures, osteolytic lesions
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101
Q

What are the non-CRAB features of myeloma?

A
  1. Lethargy
  2. Infection
  3. Amyloidosis –> macroglossia, carpal tunnel syndrome, neuropathy, hyperviscosity
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102
Q

MM Ix?

A
  1. Monoclonal proteins (IgG or IgA) in the serum and urine (Bence Jones Proteins)
  2. Increased plasma cells in bone marrow
  3. Whole body MRI/skeletal survey for bone lesions (rain-drop skull)
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103
Q

MM Dx?

A

1 major + 1 minor OR 3 minor –> in a pt with s&s of myeloma

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104
Q

Major MM criteria?

A
  1. Plasmacytoma on biopsy
  2. 30% plasma cells in a BM sample
  3. Elevated M protein levels in blood or urine
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105
Q

Minor MM criteria?

A
  1. 10-30% plasma cells in a BM sample
  2. Minor elevated blood/urine M protein levels
  3. Osteolytic lesions
  4. Low levels of Abs
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106
Q

Hypercalcaemia in MM mechanism?

A
  1. Main = increased osteoclastic bone resorption caused by local cytokines e.g. IL1, TNF, released by the myeloma cells
  2. Impaired renal function
  3. Increased renal tubular calcium reabsorption
  4. PTHrp release
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107
Q

Decreased MCHC?

A

Microcytic anaemia

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108
Q

Increased MCHC?

A
  1. HS

2. AIHA

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109
Q

Normocytic anaemia with low iron, low TIBC, raised ferritin?

A

ACD

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110
Q

Microcytic anaemia, low ferritin, raised TIBC?

A

IDA

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111
Q

5 causes of normocytic anaemia?

A
  1. ACD
  2. CKD
  3. Aplastic anaemia
  4. Haemolytic anaemia
  5. Acute blood loss
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112
Q

Epidemiological distribution of Reed-Sternberg cells?

A

Bimodal, peaks in 3rd and 7th decades

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113
Q

Lacunar cells?

A

Nodular sclerosing HL

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114
Q

HL with a large number of Reed Sternberg cells?

A

Mixed cellularity HL

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115
Q

What is myelofibrosis?

A

A myeloproliferative disorder due to hyperplasia of abnormal megakaryocytes. The resultant release of PDGF stimulates fibroblasts

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116
Q

Dry tap?

A

Myelofibrosis –> trephine biopsy is required

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117
Q

vWD bleeding time, plt levels, and APTT?

A
  1. Increased bleeding time
  2. Normal plt levels
  3. APTT prolonged
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118
Q

Most common genetic bleeding disorder?

A

vWD

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119
Q

vWD inheritance?

A

AD

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120
Q

Why does vWD lead to prolonged APTT?

A

It is a carrier molecule for FVIII which is measured by APTT

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121
Q

What is the role of vWF?

A

A large glycoprotein which forms massive multimers, that promotes platelet adhesion to damaged endothelium. Also acts as a carrier for FVIII

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122
Q

3 types of vWD?

A
  1. Type I = partial reduction in vWF (80%)
  2. Abnormal form of vWF
  3. total lack of vWF (AR)
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123
Q

Mx of vWD?

A
  1. Tranexamic acid for mild bleeding
  2. DDAVP
  3. FVIII concentrate
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124
Q

Mechanism of DDAVP tx for vWD?

A

Raises levels of vWF by inducing release of vWF from Weibel-Palade bodies in endothelial cells

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125
Q

How does vWD present?

A

Mucocutaneous bleeding after mild injury e.g. nose-bleeds, bruising

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126
Q

MOA behind myeloma causing a stroke?

A

Paraproteinaemia –> hyperviscosity –> stroke

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127
Q

5 SCA crises?

A
  1. Thrombotis ‘painful’ crises
  2. Sequestration
  3. Acute chest syndrome
  4. Aplastic
  5. Haemolytic
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128
Q

SCA thrombotic crises aka?

A

Painful or vaso-occlusive crises

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129
Q

Precipitants of SCA thrombotic crises?

A
  1. Infection
    2, Dehydration
  2. Deoxygenation
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130
Q

Sites of SCA thrombotic crises?

A
  1. AVN of hip
  2. Hand-foot syndrome in children
  3. Lungs
  4. Spleen
  5. brain
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131
Q

What is SCA sequestration crisis?

A

Sickling of blood within organs e.g. spleen or lungs causes pooling of blood with worsening of the anaemia

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132
Q

Most common cause of SCA death after childhood?

A

Acute chest syndrome

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133
Q

SCA acute chest syndrome features?

A
  1. Dyspnoea
  2. Chest pain
  3. Pulmonary infiltrates
  4. Low pO2
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134
Q

Suspicious of myeloma initial investigation?

A

Urgent protein electrophoresis and Bence Jones Protein urine test (within 48 hours)

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135
Q

Mirror image nuclei?

A

Reed Sternberg cell

136
Q

Lymphadenopathy in HL features?

A

Painless, non-tender, asymmetrical

137
Q

How long taken for 1 unit RBC transfusion in pt with HF?

A

3 hours, to reduce chances of pt developing circulatory overload

138
Q

ITP stands for?

A

Immune/idiopathic thrombocytopenic purpura

139
Q

ITP pathophysiology?

A

Abs are directed against the glycoprotein IIb/IIIA or Ib-V-IX complex

140
Q

Classification of ITP?

A

Acute and Chronic

141
Q

Acute ITP features?

A
  1. More common in children, equal sex incidence
  2. May follow infection or vaccination
  3. Usually self limiting course over 1-2 weeks
142
Q

Chronic ITP features?

A
  1. More common in young/middle-aged women

2. Tends to run a relapsing-remitting course

143
Q

What is Evans syndrome?

A

ITP in association with AIHA

144
Q

How long before an operation should the COCP be stopped?

A

4 weeks to reduce risk of PE/DVT

145
Q

Drugs that are RFs for VTE?

A
  1. COCP
  2. HRT
  3. Raloxifene/Tamoxifen
  4. Antipsychotics (esp. olanzapine)
146
Q

What percentage of pts with a diagnosed PE have no major RFs?

A

40%

147
Q

Mx of urticarial blood transfusion reaction without anaphylaxis?

A

Antihistamine and transfusion temporarily stopped

148
Q

When is FFP needed?

A

Low levels of coagulation factors with a low INR

149
Q

Most common NHL in UK?

A

Diffuse Large B cell lymphoma (40%)

150
Q

What is more common, NHL or HL?

A

NHL

151
Q

RFs for lymphoma?

A
  1. Elderly
  2. Caucasian
  3. Hx of viral infection, esp EBV
  4. FHx
  5. Certain chemical agents e.g. pesticides, solvents
  6. Hx of chemo or radio
  7. Immunodeficiency e.g. transplant, HIV, DM
  8. AI disease e.g. SLE, Sjogrens, Coeliac
152
Q

HL characteristic SBA lymphadenopathy feature?

A

Alcohol-induced pain (only in 10%)

153
Q

B symptoms typically earlier in HL or NHL?

A

HL

154
Q

Extranodal disease more common in HL or NHL?

A

NHL

155
Q

Starry sky?

A

Burkitt’s lymphoma

156
Q

Haemophilia inheritance?

A

X linked recessive

157
Q

What percentage of haemophilia pts have no FHx of the condition?

A

Up to 30%

158
Q

What is christmas disease?

A

Haemophilia B

159
Q

Features of haemophilia?

A
  1. Haemarthroses, haemophilia

2. Prolonged bleeding after surgery or trauma

160
Q

Coag features of haemophilia?

A
  1. Prolonged APTT

2. Bleeding time, thrombin time, prothrombin time all normal

161
Q

What percentage of pts with Haemophilia A develop Abs to FVIII treatment?

A

10-15%

162
Q

Myelofibrosis, WBC and platelet count early in the disease?

A

Both high

163
Q

Urate and LDH levels in myelofibrosis?

A

Both high, reflect increased cell turnover

164
Q

2 characteristic HL FBC features?

A

Normocytic anaemia, eosinophilia

165
Q

2 major forms of Burkitt’s lymphoma?

A
  1. Endemic (African) form = typically involves maxilla or mandible
  2. Sporadic form = typically HIV associated, abdominal ileo-caecal tumours most common
166
Q

Burkitt’s lymphoma gene translocation?

A

c-Myc translocation, usually t(8:14)

167
Q

Explain starry sky appearance of Burkitt’s lymphoma?

A

Lymphocyte sheets interspersed with macrophages containing dead apoptotic tumour cells

168
Q

Which Burkitt’s lymphoma form is more associated with EBV?

A

Endemic

169
Q

Management of Burkitt’s lymphoma ?

A

Chemotherapy

170
Q

Common complication of Burkitt’s lymphoma tx?

A

Tumour lysis syndrome

171
Q

What is given before chemo to reduce chance of tumour lysis syndrome occuring?

A
  1. Allopurinol OR

2. Rasburicase

172
Q

Rasburicase MOA?

A
  1. A recombinant version of urate oxidase, an enzyme which catalyses the conversion of uric acid to allantoin
  2. Allantoin is 5-10 times more soluble than uric acid, so renal excretion is more effective
173
Q

5 complications of tumour lysis syndrome?

A
  1. Hyperkalaemia
  2. Hyperphosphataemia
  3. Hyperuricaemia
  4. Hypocalcaemia
  5. AKI
174
Q

Classification of generalised lymphadenopathy?

A
  1. Infection
  2. Inflammation
  3. Malignancy
175
Q

Infective causes of generalised lymphadenopathy?

A
  1. Viral = IM, HIV, Rubella, CMV, PVB19

2. TB, toxoplasmosis

176
Q

Neoplastic causes of generalised lymphadenopathy?

A
  1. Leukaemia

2. Lymphoma

177
Q

Inflammatory causes of generalised lymphadenopathy?

A
  1. AI = SLE, RhA
  2. Sarcoidosis
  3. Drugs
178
Q

3 drugs that cause generalised lympahdenopathy?

A
  1. Phenytoin
  2. Allopurinol
  3. Isoniazid
179
Q

Warfarin duration in pts with a provoked VTE?

A

3 months, then ‘assess the risks and benefits of extending treatment’

180
Q

Warfarin duration in pts with unprovoked VTE?

A

6 months

181
Q

LMWH duration for pts with active cancer?

A

6 months

182
Q

Pappenheimer bodies?

A

Hyposplenism

183
Q

4 cell types with hyposplenism?

A
  1. Target cells
  2. Howell Jolly bodies
  3. Pappenheimer bodies
  4. Acanthocytes
184
Q

What is cryoprecipitate?

A
  1. Blood product made from plasma

2. Usually transfused as a 6 unit pool

185
Q

Indications for cryoprecipitate?

A
  1. Massive haemorrhage

2. Uncontrolled bleeding due to haemophilia

186
Q

Components of cryoprecipitate?

A
  1. Factor VIII
  2. Factor XIII
  3. Fibrinogen
  4. vWF
187
Q

SCA crisis management?

A
  1. Analgesia e.g. opiates
  2. Rehydrate
  3. Oxygen
  4. Abx if infection
  5. Blood transfusion
  6. Exchange transfusion e.g. if neuro complications
188
Q

SCA long term management?

A
  1. Hydroxyurea

2. Pneumococcal vaccine every 5 yeras

189
Q

Hydroxyurea for SCA MOA?

A

Increases HbF levels and is used in the prophylactic management of SCA to prevent painful episodes

190
Q

Transmission of which type of infection is most likely to occur following a platelet transfusion and why?

A

Bacterial, as platelet concentrates are stored at room temperature

191
Q

DIC platelets, PT, APTT, and bleeding time?

A

Platelets low, all times prolonged

192
Q

4 causes of DIC?

A
  1. Sepsis
  2. Trauma
  3. Malignancy
  4. Obstetric complications e.g. amniotic fluid embolism, HELLP
193
Q

What is the critical mediator of DIC?

A

Tissue factor

194
Q

Warfarin effect on PT/APTT/bleeding time/plt count?

A

Prolonged PT

195
Q

Aspirin effect on PT/APTT/bleeding time/plt count?

A

Prolonged bleeding time

196
Q

Heparin effect on PT/APTT/bleeding time/plt count?

A

PT may be prolonged, APTT prolonged

197
Q

What does FFP contain?

A
  1. Clotting factors
  2. Albumin
  3. Immunoglobulin
198
Q

Warfarin reversal strategies?

A
  1. Stop warfarin
  2. Vitamin K (IV takes 4-6h to work, oral takes 24hrs to work)
  3. Human prothrombin complex (reversal within 1 hour, short half life therefore give with Vit K)
  4. FFP (only use if human prothrombin complex is not available)
199
Q

AKI with high phosphate and high uric acid?

A

Tumour lysis syndrome

200
Q

Grading system for tumour lysis syndrome?

A

Cairo-Bishop scoring system

201
Q

3 drugs to be avoided whilst pt is on methotrexate?

A
  1. Co-trimoxazole
  2. Trimethoprim
  3. Chloramphenicol eye drops
202
Q

Causes of a relative polycythaemia (pseudopolycythaemia)?

A
  1. Dehydration
  2. Diuretics
  3. Gaisbock syndrome
203
Q

Mutation in 95% of pts with Polycythaemia Rubra Vera?

A

JAK2

204
Q

Features of Polycythaemia Rubra Vera?

A
  1. Hyperviscosity
  2. Pruritis
  3. Splenomegaly
  4. Haemorrhage (secondary to abnormal plt function)
  5. Plethoric appearance
  6. HTN in 1/3rd of pts
  7. Low ESR
205
Q

Waldenstrom’s macroglobulinaemia demographic?

A

Older men

206
Q

Waldenstrom’s macroglobulinaemia aka?

A

Lymphoplasmacytic Lymphoma

207
Q

Waldenstrom’s macroglobulinaemia key feature?

A

Monoclonal IgM paraproteinaemia

208
Q

Presentation of Waldenstrom’s macroglobulinaemia?

A
  1. Constitutional symptoms
  2. Hyperviscoscity e.g. stroke, visual disturbance
  3. Hepatosplenomegaly
  4. Lymphadenopathy
  5. Cryoglobulinaemia e.g. Raynauds
209
Q

Why does hyperviscosity occur in Waldenstrom’s macroglobulinaemia?

A

Pentameric configuration of IgM increases serum viscosity

210
Q

Haemarthrosis without fracture?

A

Haemophilia A or B

211
Q

Factors affected by Heparin?

A

2, 9, 10, 11

212
Q

Factors affected by Warfarin?

A

2, 7, 9, 10

213
Q

Factors affected by DIC?

A

1, 2, 5, 8, 11

214
Q

Factors affected by liver disease?

A

1, 2, 5, 7, 9, 10, 11

215
Q

Bleeding with: increased APTT, normal PT, normal BT?

A

Haemophilia

216
Q

Bleeding with: increased APTT, normal PT, increased BT?

A

vWD

217
Q

Bleeding with increased APTT, increased PT, normal BT?

A

Vit K deficiency

218
Q

Causes of IDA?

A
  1. Inadequate intake
  2. Blood loss
  3. Poor intestinal absorption
  4. Increased requirement
219
Q

Mx of IDA?

A

Oral ferrous sulfate, pts should continue taking iron for 3m after the iron deficiency has been corrected in order to replenish iron stores

220
Q

2 sources of iron rich food?

A
  1. Dark-green leafy vegetables

2. Meat

221
Q

Most common cause of an isolated thrombocytopenia?

A

ITP

222
Q

Blue line along gum margin?

A

Lead poisoning (20% pts)

223
Q

Abdo pain and neurological signs ddx?

A
  1. Lead poisoning

2. Acute intermittent porphyria

224
Q

Mx of lead poisoning?

A
  1. Dimercaptosuccinic acid (DMSA)
  2. D-penicillamine
  3. EDTA
  4. Dimercaprol
225
Q

Mx of combined Vit B12 and folate deficiency?

A

IM Vitamin B12 and start folic acid when Vitamin B12 levels are normal

226
Q

Why do you manage B12 before folate?

A
  1. To avoid precipitating SCDSC

2. B12 is needed as part of folate metabolism and by increasing folate, you will further deplete B12 levels

227
Q

What is Gaisbock syndrome?

A

A symptom complex associated with polycythemia that cannot be attributed to a diagnosis of polycythemia rubra vera or to a secondary erythrocytosis that has occurred in response to hypoxemia.In order of decreasing importance, risk factors for the development of Gaisbock’s syndrome include male sex, hypertension, smoking, diuretic therapy, obesity, and emotional or physical stress. The polycythemia has been attributed to decreases in plasma volume, and may be associated with increases in blood viscosity and peripheral vascular resistance and a propensity to develop arterial and/or venous thromboses

228
Q

What is a primary cause of polycythaemia?

A

PRV

229
Q

What are some secondary causes of polycythaemia?

A
  1. COPD
  2. Altitude
  3. OSA
230
Q

Most common leukaemia in adults in the western world?

A

B-CLL

231
Q

Which has more marked lymphadenopathy, CLL or CML?

A

CLL

232
Q

CML translocation?

A

t(9:22) –> Philadelphia chromosome

233
Q

What happens if CML undergoes blast transformation?

A

Turns into AML (80%) or ALL (20%)

234
Q

Management of CML?

A
  1. 1st line = imatinib
  2. Hydroxyurea
  3. IFN-a
  4. Allogeneic BM transplant
235
Q

Imatinib MOA?

A

Tyrosine kinase inhibitor

236
Q

Classification of primary immunodeficiencies?

A
  1. Neutrophil disorders
  2. B cell disorders
  3. T cell disorders
  4. Combined B and T cell disorders
237
Q

Neutrophil disorder immunodeficiencies?

A
  1. Chronic granulomatous disease (CGD)
  2. Leukocyte adhesion deficiency (LAD)
  3. Chediak-Hidashi syndrome
238
Q

CGD defect?

A

Lack of NADPH oxidase

239
Q

LAD defect?

A

Defect of LFA1 integrin (CD18) protein on neutrophils

240
Q

B cell immunodeficiencies?

A
  1. CVID
  2. Bruton’s X-linked agammaglobulinaemia
  3. Selective IgA deficiency
241
Q

Bruton’s x-linked agammaglobulinaemia defect?

A

Bruton’s tyrosine kinase (BTK) gene defect

242
Q

Selective IgA defeciency?

A

Maturation defect in B cells

243
Q

Most common primary Ab deficiency?

A

Selective IgA deficiency

244
Q

T cell immunodeficiencies?

A

DiGeorge syndrome

245
Q

DiGeorge syndrome defect?

A

22q11.2 deletion, failure to develop 3rd and 4th pharyngeal arches

246
Q

Combined T and B cell immunodeficiencies?

A
  1. SCID
  2. Ataxia telangiectasia
  3. Wiskott-Aldrich syndrome
  4. Hyper IgM syndrome
247
Q

SCID inheritance?

A

Most commonly X-linked recessive

248
Q

SCID defect?

A

Most commonly IL-2R defect

249
Q

Wiskott-Aldrich syndrome defect?

A

WASP gener mutation

250
Q

Hyper IgM syndrome defect?

A

Mutation in CD40 gene

251
Q

Negative Nitroblue-tetrazolium test?

A

CGD

252
Q

Abnormal dihydrorhodamine test?

A

CGD

253
Q

Partial albinism, peripheral neuropathy, and recurrent bacterial infections?

A

Chediak-Higashi syndrome

254
Q

Chediak-Higashi syndrome defect?

A

Microtubule polymerisation defect

255
Q

Delay in umbilical cord sloughing, absence of pus at sites of infection?

A

LAD

256
Q

Low IgM, IgA and IgG?

A

CVID

257
Q

B cell immunodeficiency associated with Coeliac disease?

A

Selective IgA deficiency

258
Q

Ataxia telangiectasia defect?

A

DNA repair enzyme defect

259
Q

Ataxia telangiectasia inheritance?

A

AR

260
Q

Ataxia telangiectasia features?

A
  1. Cerebellar ataxia
  2. Telangiectasia
  3. Recurrent chest infections
  4. 10% chance of malignancy, lymphoma or leukaemia
261
Q

Suspected DVT Ix?

A

Two-level DVT Wells Score

262
Q

4 causes of severe thrombocytopenia?

A
  1. ITP
  2. DIC
  3. TTP
  4. Haem malignancy
263
Q

Neutropenic sepsis defn?

A

Neutrophil count <0.5 x0^9 in a pt having anticancer tx and has one of the following:

  1. Temp >38
  2. Other s&s consistent with clinically significant sepsis
264
Q

If it is anticipated that patients are likely to have a neutrophil count of < 0.5 * 10^9 as a consequence of their chemo treatment, what is the mx?

A

Offered a fluoroquinolone

265
Q

Abx tx of ?neutropenic epsis?

A

Tazocin (piperacillin with tazobactam) immediately

266
Q

Pt febrile and unwell after 48 hours of tx of neutropenic sepsis?

A

Meropenem +/- vancomycin

267
Q

Pt not responding after 4-6 hrs of tx for neutropenic sepsis?

A

Ix for fungal infections e.g. HR-CT

268
Q

Chronic H.pylori infection leads to what infection?

A

Gastric MALToma

269
Q

Where does gastric lymphoma typically arise?

A

Antrum of the stomach

270
Q

HTLV1 malignancy?

A

Adult T cell leukaemia/lymphoma

271
Q

Malaria associated malignancy?

A

Burkitt’s lymphoma

272
Q

Beta thalassaemia chromosome?

A

11

273
Q

Features of beta thalassaemia?

A
  1. Presents in st year of life with failure to thrive and hepatosplenomegaly
  2. Microcytic anaemia
  3. HbA2 and HbF raied
  4. HbA absent
274
Q

Management of beta thalassaemia?

A

Lifelong blood transfusions (maintain Hb and simultaneously uppress enhanced erythropoiesis)

275
Q

MOA of acute haemolytic transfusion rection?

A

RBC destruction by IgM type Abs

276
Q

All stages of granulocyte maturation seen?

A

CML

277
Q

When are irradiated blood products used?

A

If pt is depleted in T lymphocytes, to avoid GvHD caused by engraftment of viable donor T lympchytes

278
Q

G6PDD inheritance?

A

X linked recessive

279
Q

Pathophysiology of G6PDD?

A

Reduced G6PD –> reduced glutathione –> increased RBC susceptibility to oxidative stress

280
Q

Bite cells?

A

G6PDD

281
Q

Drugs that trigger haemolysis in G6PDD?

A
  1. Antimalarials
  2. Ciprofloxacin
  3. Sulfonamides, sulfasalazine, sulfonylureas
282
Q

Heinz bodies?

A

G6PDD

283
Q

Pts >60 y/o w/ IDA Ix?

A

Colonoscopy

284
Q

Philadelphia chromosome is seen in what other cancer in addition to CML?

A

ALL

285
Q

t(15;17)?

A
  1. Acute promyelocytic leukaemia (APML)

2. PML-RARA fusion gene

286
Q

t(8;14)?

A
  1. Burkitt’s lymphoma

2. c-MYC translocation

287
Q

t(11;14)?

A
  1. Mantle cell lymphoma

2. Deregulation of Cyclin D1 (BCL-1) gene

288
Q

t(14;18)?

A
  1. Follicular lymphoma

2. Increased BCL2 transcription

289
Q

Preferred NOAC for renal impairment and why?

A

Apixaban, due to minimal renal drug clearance

290
Q

3 NOACs?

A
  1. Dabigatran
  2. Rivaroxaban
  3. Apixaban
291
Q

Dabigatran MOA?

A

Direct thrombin inhibitor

292
Q

Rivaroxaban MOA?

A

Direct Xa inhibitor

293
Q

Apixaban MOA?

A

Direct Xa inhibitor

294
Q

Dabigatran excretion?

A

Majority renal

295
Q

Rivaroxaban excretion?

A

Majority liver

296
Q

Apixaban excretion?

A

Majority faecal

297
Q

Indications of NOACs?

A
  1. Prevention of VTE following hip/knee surgery
  2. Treatment of DVT and PE
  3. Prevention of stroke in non-valvular AF
298
Q

What is a reversal agent for dabigatran?

A

Idarucizumab

299
Q

Heparin reversal?

A

Protamine

300
Q

Warfarin reversal?

A

Vitamin K and FFP

301
Q

Microcytic anaemia causes?

A

TAILS

  1. Thalassaemia
  2. ACD
  3. IDA
  4. Lead poisoning
  5. Sideroblastic anaemia
302
Q

IV iron indication?

A

Pts with IDA prior to surgery where oral iron either cant be tolerated or the time interval is too short

303
Q

Shortest time interval for oral iron to work?

A

2-4 weeks

304
Q

What can be used to stimulated neutrophil growth in neutropenia secondary to chemo?

A

Filgrastim, a G-CSF

305
Q

Causes of acquired haemophilia?

A
  1. Elderly
  2. Pregnancy
  3. Malignancy
  4. AI conditions
306
Q

What may myelodysplasia progress to?

A

AML

307
Q

What proportion of myelodysplasia becomes AML?

A

A third

308
Q

What is myelodysplasia?

A

An acquired neoplastic disorder of haematopoietic stem cells

309
Q

FFP universal donor?

A

AB RhD -ive

310
Q

Why is AB RhD -ive the universal FFP donor?

A

Produce neither Anti-A or Anti-B and is therefore compatible with all ABO groups

311
Q

MOA of heparin?

A

Activates antithrombin III

312
Q

A common mode of presentation of SCA in late infancy?

A

Hand-foot syndrome

313
Q

Microcytosis disproportionate to anaemia?

A

Beta thalassaemia

314
Q

Most common cause of B12 deficiency?

A

Pernicious anaemia

315
Q

Causes of B12 deficiency?

A
  1. Pernicious anaemia
  2. Post gastrectomy
  3. Vegan/poor diet
  4. Terminal ileum disease e.g. Crohns
316
Q

Mx of B12 deficiency?

A

1mg IM hydroxycobalamin 3x week for 2 weeks, then once every 3m

317
Q

Causes of thrombocytosis?

A
  1. Reactive (acute phase reaction)
  2. Malignancy
  3. Essential
  4. Hyposplenism
  5. CML/PRV
318
Q

What is essential thrombocytosis?

A

One of the myeloproliferative disorders which overlaps with CML, PRV and myelofibrosis

319
Q

Mutation found in 50% pts with essential thrombocytosis?

A

JAK2

320
Q

Burning sensation in the hands and JAK2 mutation?

A

Essential thrombocytosis

321
Q

Mx of essential thrombocytosis?

A
  1. Hydroxyurea (hydroxycarbamide)
  2. IFNa
  3. Low dose aspirin to reduce thrombotic risk
322
Q

Haemolytic anaemia classification?

A
  1. Congenital

2. Acquired

323
Q

Congenital haemolytic anaemias?

A
  1. Membrane = hereditary spherocytosis/elliptocytosis
  2. Metabolism = G6PDD
  3. Haemoglobinopathies = SCD, thalassaemia
324
Q

Acquired haemolytic anaemia classification?

A
  1. Immune

2. Non-immune

325
Q

Immune acquired haemolytic anaemias?

A
  1. Autoimmune = warm/cold
  2. Alloimmune = transfusion reaction, HDN
  3. Drugs = methyldopa, penicillin
326
Q

Non-immune acquired haemolytic anaemias?

A
  1. MAHA = TTP/HUS, DIC, malignancy, pre-eclampsia
  2. Prosthetic cardiac valves
  3. PNH
  4. Infection = malaria
  5. Drug = dapsone
327
Q

What is SCA?

A

An AR condition that results from the synthesis of an abnormal Hb called HbS

328
Q

What percentage of UK Afro-carribeans are carriers of HbS?

A

10%

329
Q

Pathophysiology of SCA?

A

Polar aa glutamate is replaced by non-polar valine, decreasing water solubility of deoxy-Hb. In the deoxygenated state, the HbS molecules polymerise and cause RBCs to sickle

330
Q

At what pO2 do HbAS pts sickle?

A

2.5-4 kPa

331
Q

At what pO2 do HBSS pts sickle?

A

5-6 kPa

332
Q

When should furosemide be given alongside red cell transfusions?

A

Between every other unit in pts with HF

333
Q

How is tranexamic acid given in a major haemorrhage?

A

IV bolus followed by an infusion

334
Q

Tranexamic acid MOA?

A

Antifibrinolytic

335
Q

SCA Hb, MCV and reticulocytes?

A

Normocytic anaemia with raised reticulocyte count

336
Q

Myeloma Ca, P and ALP?

A

High Ca, Normal P, Normal ALP

Medicine and Surgery Mushkies (52 decks)

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