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Theme III > Haem/Onc > Flashcards

Haem/Onc Flashcards

1
Q

Protein C is a natural antagonist to which factor?

A

Factor V

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2
Q

What is the role of activated Factor V?

A

Activated Factor V converts Prothrombin (Factor II) into Thrombin

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3
Q

What is the role of Thrombin?

A

Thrombin activates Fibrinogen into Fibrin which forms a cross-linked clott

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4
Q

What factors are involved with the intrinsic pathway?

A

Factor 12, 11, 9, 8, 10, 5, 2,1

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5
Q

What factors are involved in the extrinsic pathway?

A

Factor 7, 10, 5, 2, 1, ?12?

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6
Q

Difference between Leukaemia and Lymphoma?

A

In Leukaemia, malignant cells rise in the bone marrow and spread elsewhere.
In Lymphoma, the malignant cells arise in the lymph nodes and lymphoid tissue and spread everywhere.

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7
Q

What is Acute Myeloid Leukaemia?

A

It is a rapidly progressive malignancy characterized by failure of myeloid (blast) cells to differentiate beyond blast stage and hence accumulation in bone marrow

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8
Q

What are myeloid cells?

A

Erythrocytes, Thrombocytes, Mast cells, Eosinophils, Basophils, Neutrophils, Macrophages (Monocytes)

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9
Q

Auer Rods on the Blood film – ??

A

AMLeukaemia

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10
Q

What are some secondary causes for AML?

A

Haemotological malignancies (Myelodysplastic syndromes) or previous chemotherapy agents (benzena, Alkylating agents)

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11
Q

Basic Clinical features seen in AML?

A

Anaemia, Thrombocytopenia, Neutropenia (even with Normal WBC - since that is separate lineage)
- Skeletal pain and bone tenderness from accumulation of blast cells in bone marrow

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12
Q

Signs of Organ-filtration in AML?

A
  • Gingival hypertropy (particularly in myelomonocytic leukaemia)
  • hepatosplenomegaly
    Lymphadenopathy (not marked)
  • Gonads?
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13
Q

What is leukocytosis/Hyperleukosis syndrome?

A

It is a syndrome that can happen in AML.
There is a large number of blasts that interfere with circulation and leads to hypoxia and haemorrhage - can cause pulmonary infiltrates, CNS bleeding, respiratory distress, altered mental status, priapism

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14
Q

What would a Bone marrow aspirate in AML show?

A
  • A blast count of more than 20% (normally less than 5%)

- may show other morphological, cytochemical and immunotypic features

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15
Q

What other investigations for Complications would you do in AML?

A

CXR to r/o pneumonia, MUGA prior to chemotherapy (cardiotoxic)

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16
Q

Treatment for AML?

A

Chemotherapy - Rapidly fatal without treatment

All AML subtypes treated similarly except pro-myelotic variant

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17
Q

What is the role of tran-retinoic acid in therapy?

A

To induce differentiation

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18
Q

What are the two stages of treatment in AML?

A
  1. Chemotherapy to induce complete remission (must also ensure reversal of DIC)
  2. Consolidation: to prevent recurrence (intensive chemo + possible stem cell transplantation?)
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19
Q

What is CLL? (Chronic Lymphocytic leukaemia)?

A

Indolent disease characterised by clonal malignancy of mature B-cells

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20
Q

What is the most common leukaemia in the western world?

A

CLL - affects older patients and M>F

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21
Q

Clinical features of CLL?

A

25% Asymptomatic, 5-10% B symptoms, 50-90% sLymphadenopathy, Splenomegaly in 25-55%, hepatomegaly in 15-25%

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22
Q

What does peripheral blood film show in CLL?

A

Lymphocytes are small and mature

There are smudge cells - these are artifacts of damaged lymphocytes from slide preparation

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23
Q

What does flow Cytometry in CLL look for?

A

CD5, CD20, CD23

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24
Q

What does a Bone marrow Aspirate in CLL show?

A

Lymphocytes more than 30% of all nucleated cells!

o Infiltration of marrow by lymphocytes in 4 patterns:
Nodular (10%), Interstital (30%), diffuse (35%, worse prognosis), MIXED (25%)

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25
Q

Lineage of a Common Lymphoid progenitor?

A

Common Lymphoid progenitor –> Natural Killer cell + small lymphocytes

Small Lymphocytes –> T Lymphocyte + B lymphocytes (which becomes plasma cell)

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26
Q

Natural history and treatment of CLL?

A
  • Observe if early, stable and asymptomatic
  • Intermittent cholarmbucil or fludarabine chemotherapy combined wih rituximab,
  • Corticosteroids, IVIG; especially for autoimmune phenomenon
  • Radiotherapy
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27
Q

What is multiple Myeloma?

A

A type of cancer that develops from cells in the bone marrow called plasma cells. It can be in bone marrow anywhere - pelvis, spine, ribcage and since it occurs over several places it is called Multiple Myeloma

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28
Q

What is the role of Plasma cells?

A

Plasma cells are WBC that secrete large volumes of antibodies. B cells differentiate into plasma cells that produce antibody molecules that closely model the receptors of the precursor B cell. Once released into the blood and lymph, these antibody molecules bind to the target antigen (foreign substance) and initiate its neutralization or destruction

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29
Q

What is the most common antibody produced in Multiple myeloma?

A

95% produce M protein/

Classified by antibody they produce.
50% produce IgG, 20% IgA

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30
Q

Clinical features of Multiple Myeloma?

A

CRAB

Increase Calcium (Increased bone resorption secondary to osteoclast activating factors such as PTHrP)

Renal Failure (cast nephropathy)
Anaemia
Bony lesions (Lytic lesions on skull, spine, long bones or osteoporosis)

Also get increased infections, Hyperviscosity of blood (stroke, PVD, CVD), Bleeding, immune Thrombocytopenia purpura, Amyloidosis

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31
Q

What are some symptoms of hypercalcaemia?

A

Stones: kidney stones.
Bones: bone pain and fractures.
Groans: N/V, anorexia, constipation
Moans: fatigue, myalgia, proximal muscle weakness, joint pain.
Psychic Overtones: depression, memory loss, confusion, lethargy, coma

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32
Q

What would a blood film show in MM?

A

Roleux formation, Normocytic anaemia, thrombocytopenia?

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33
Q

What would biochemistry show in MM?

A

Increased Ca2+, Inccreased ESR, decreased anion ap, increased Cr, albumin, proteinura

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34
Q

How would you detect monoclonal proteins in MM?

A

Serum Protein Electropheresis, urine protein electropheresis, Immunofixation

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35
Q

Diagnosis Criteria for Myeloma?

A
  1. Serum or urinary monoclonal protein
  2. Presence of cloncal plasma cells in bone marrow or plasmacytoma
  3. Presence of end-organ damage related to plasma dyscrasia such as increased serum Ca, Lytic bone lesions, anaemia, Renal Failure
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36
Q

What are the treatment goals in MM?

A

• Treatment is non curative
• Treatment goals:
o Improvement in quality of life (improve anaemia, reverse renal failure, bony pain)
o Prevention of progression and complications
o Increased overall survival

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37
Q

What is treatment in MM?

A

if 65yo then Chemo

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38
Q

What does supportive management of MM include?

A
  • Bisphosphonates for those with Osteopenia or Lytic Bone Lesions
  • local XRT for bone pain, spinal cord compression
    Treat complications
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39
Q

What is Hodgkin’s lymphoma?

A

This is a malignant proliferation of Lymphoid cells thought to arise from germinal centre in b cells

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40
Q

What are Reed-Sternberg cells associated with?

A

Hodgkin’s Lymphoma

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41
Q

What are the bimodal peaks of hodgkin’s Lymphoma?

A

Peaks at 20yr and just above 50yr

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42
Q

What are B Symptoms?

A

Unintentional weight loss (10% body weight in 6 mo), Temperature more than 38 degrees, Night sweats for more than 2 weeks without evidence of infection, extreme Fatigue

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43
Q

Clinical features of Hodgkin’s Lymphoma?

A

Asymptomatic Lymphadenopathy (non-tender, rubbery), Splenomegaly, Mediastinal mass

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44
Q

What are some things associated with Hodgkin’s?

A

EBV in 50% of cases and Alcohol makes the lymphadenopathy worse?

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45
Q

Treatment of Hodgkin’s?

A

Treatment:
• Stage I-II: Chemotherapy (ABD) followed by involved field radiotherapy (XRT)
• Stage III=IV: chemotherapy with XRT for bulky disease
• Relapse, resistant to therapy: high dose chemo, bone marrow transplant
o New imaging modalities increasingly used including PET scans used to follow response to treatment

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46
Q

Treatment of Hodgkin’s?

A

Treatment:
• Stage I-II: Chemotherapy (ABD) followed by involved field radiotherapy (XRT)
• Stage III=IV: chemotherapy with XRT for bulky disease
• Relapse, resistant to therapy: high dose chemo, bone marrow transplant
o New imaging modalities increasingly used including PET scans used to follow response to treatment

47
Q

Complications of Hodgkin’s?

A

2% risk of MDS, Cardiotoxicity (adriamycin), Pulmonary disease (Secondary to bleomycin), Solid tumour, non-hodgkins?

48
Q

Prognostic factors for Hodgkin’s?

A
  1. Serum Albumin (below 40)
  2. haemoglobin (Below 105)
  3. Male
  4. Stage IV disease
  5. Age more then 45
  6. Leukocytosis
  7. Lymphocytopenia (less than 0.06 or 8% of WBC count)

LESS THE BETTER

49
Q

What is non-Hodgkin’s lymphoma?

A

Malignant proliferation of lymphoid cells of progenitor or Mature B or T cells

50
Q

What are the types of B- cell NHL?

A

Diffuse B cell lymphoma, Follicular Lymphoma, Burkitt’s Lymphoma, mantle cell lymphoma

51
Q

What are the types of T cell NHL?

A

Mycosis fungoides, anaplastic large cell lymphoma

52
Q

What are the WHO/REAL classification of NHL?

A

INDOLENT - follicular lymphoma, Small Lymphotic cell lymphoma/CLL, mantle cell lymphoma

Aggressive - Diffuse B cell lymphoma

Highly aggressive - Burkitt’s Lymphoma

53
Q

What is the most common NHL?

A

Diffuse Large B cell lymphoma - 33%. Aggressive

54
Q

What genetic mutations is Diffuse Large B cell Lymphoma associated with?

A

Bcl-2, Bcl-6 and MYC ra-arrangement

55
Q

What is Richter’s transformation?

A

5% of CLL patients progress to DLBCL

56
Q

Are indolent lymphomas harder or easier to treat?

57
Q

What is the second most common NHL?

A

Follicular Lymphoma - Indolent

58
Q

What is the C-myc chromosome mutation linked to?

A

Burkitt’s Lymphoma

59
Q

RF for Burkitt’s Lymphoma?

A

EBV, C-MYC mutation, Africa

60
Q

Pruritus after a hot shower?

A

PRV (Polycythaemia Rubra Vera)

61
Q

What mutation is PRV related to?

A

JAK-2 Mutation

62
Q

What are some interesting manifestations of Mantle Cell Lymphoma?

A

Lymphomatosis in GIT, and Waldeyer’s ring

63
Q

What is mantle Cell lymphoma associated with?

A

Over expression of Cyclin D1 (BCL-1 activation)

64
Q

Howell Jolly Bodies occur in which illness?

A

Hyposplenism - Maybe due to Hereditary spherocytosis

65
Q

What is the chromosomal dislocation in CML?

A

9:22 dislocation.

66
Q

What is the treatment for CML?

A

Tyrosine Kinase Inhibitor- Imatanib

67
Q

3 causes of a massive spleen?

A

Malaria, CML, Myelofibrosis

68
Q

What is Myelofibrosis?

A

Bone marrow is fibrosed

69
Q

Where do you see Tear drop cells?

A

In myelofibrosis - unable to aspirate - dry tap

70
Q

CLL is a B disease -associated with four B’s:

A

B Lymphocytes
Bone marrow failure
Bleeding
Broken cells (smear cells)

71
Q

What are the five investigative markings seen in Haemolytic anaemia?

A 
Increased LDH, 
Decreased Haptoglobin, 
Increased Urobilogen, 
Increased Reticulocytes
Positive Direct Coomb's test
72
Q

What is the management of thalassemia?

A

Blood transfusion and iron Chelation

73
Q

Thrombotic crises is precipitated by …. (3)

A

Infection, dehydration and deoxygenation

74
Q

Burkitt’s lymphoma involves which chromosomes?

What is the pathophysiology?

A

Chromosome 8 and 14

Myco oncogene is translocated to an immunoglobulin gene

75
Q

Most common leukaemia?

76
Q

Heparins generally act by activating _______

A

Anti-thrombin III

77
Q

Unfractionated heparin forms a complex which inhibits ______ and Factors ___ ___ __ _____

A

Thrombin, Factor 10, 9, 10i, 12

78
Q

Pruritius with History of alcohol excess, spider naevi, bruising, palmar erythema
Jaundice

A

Liver disease

79
Q

Pruritus with Pallor, kolynychia, atrophic glossitis, post-cricoid webs, angular stomatitis

A

Iron deficiency anaemia

80
Q

Pruritus with Warm baths, ruddy complexion, hx of Gout and PUD

A

Polycythaemia

81
Q

Pruritus with lethargy, pallor, oedema, weight gain and HTn

A

Chronic Kidney disease

82
Q

Pruritus with Night sweats, Lymphadenopathy, splenomegaly

83
Q

Prior to an elective splenectomy a patient should receive the following vaccinations:

A

HiB, Meningitis A & C, Annual influenzae and pneumococcal vaccine very 5 years.
Consider Abx prolophylaxis

84
Q

The only blood product that doesn’t have to be ABO compatible and can just be given is ____

85
Q

Usually administered to patients that thrombocytopaenic and are bleeding or require surgery

A

Platelet rich plasma

86
Q

Fresh Frozen plasma contains _______ (3)

A
  1. Clotting factors
  2. Albumin and
  3. Immunoglobulin
87
Q

FFP is used in _____ and for patients with ______ failure who are undergoing surgery.

A

DIC or Clotting deficiency or in people with liver failure

88
Q

FFP should or should not be first line for hypovolaemia?

A

Should not

89
Q

Rich source of Factor VIII and fibrinogen. Allows large concentration of Factor VII to be administered in small volume. First line in DIC

A

Cryoprecipitate

90
Q

aplastic anaemia, cafe au lait spots, short stature, acute myeloid leukaemia

A

Fanconi Anaemia

91
Q

Cold Agglutin disease or cold Autoimmune haemolytic anaemia is associated with cold/purple peripheries, anaemia, direct coombs test +ve and involved which type of antibody?

92
Q

Smudge/smear cells –>

93
Q

Auer rods –>

94
Q

Tear drop Polikocytes –>

A

Myelofibrosis

95
Q

Target cells are associated with –> (5)

A 
Sickle cell anaemia
Thalassaemia
Fe def anaemia
Hyposplenism
Liver disease
96
Q

Spherocytes are associated with

A

Hereditary spherocytosis and

Autoimmune haemolytic anaemia

97
Q

Basophilic stippling is associated with –> (4)

A

Lead poisoning
thalassaemia
Sideroblastic anaemia
Myelodysplasia

98
Q

Howell-Jolly bodies –>

A

Hyposplenism

99
Q

Heinz bodies –>

A

G6PD deficiency

sometimes Alpha-thalassaemia

100
Q

Schistocytes (helmet cells) –> (3)

A

Intravascular haemolysis
Mechanical heart valve
Disseminated intravascular coagulation

101
Q

Pencil Poikilocytes –>

A

Iron def. anaemia

102
Q

Burr cells (echinocytes) –> (2)

A

Uraemia,

Pyruvate kinase def

103
Q

Acanthocytes –>

A

Abetalipoproteinaemia

104
Q

Hypersegmented neutrophils –>

A

Megaloblastic anaemia

105
Q

Treatment of choice for CML?

106
Q

Polycythaemia Rubra vera is related to _____ mutation

107
Q

Treatment of choice for essential thrombocytopenia?

A

Hydroxyurea

108
Q

Activated Protein C resistance leads to ____

A

Factor V Leiden

109
Q

Liver disease leads to _______ anaemia

A

Liver disease leads to macrocytic (normoblastic) anaemia

110
Q

Man immigrated from Haiti, Lymphadenopathy, hepatosplenomegaly and skin lesions. With elevated calcium levels and bone scan shows numerous lytic lesions

A

Adult T cell Lymphoma

111
Q

Person from africa with lymphadenopathy. Jaw or facial bone tumour in 4-10 year old

A

Burkitt Lymphoma

112
Q

Atypical CD4+ T cells in the periphery cause skin patches or plaques seen below. This condiiton can progress to Sezary syndrome which is a T cell leukaemia

A

Mycosis Fugoides

113
Q 
Fever
Neurological change
Renal failure
thromboctyopenia
and haemolytic anaemia

Is the classic pentad for ____

A

Thrombotic thrombocytopenia purpura

114
Q

50 year old man, with splenomegaly, pancytopenia , peculiar mycobacterial infections and lymphoid infiltration of the hepatic portal triad.

A

Hairy cell Leukaemia (disease of B cells)

Theme III (15 decks)

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