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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
Lineage of a Common Lymphoid progenitor?
Common Lymphoid progenitor --> Natural Killer cell + small lymphocytes Small Lymphocytes --> T Lymphocyte + B lymphocytes (which becomes plasma cell)
26
Natural history and treatment of CLL?
- Observe if early, stable and asymptomatic - Intermittent cholarmbucil or fludarabine chemotherapy combined wih rituximab, - Corticosteroids, IVIG; especially for autoimmune phenomenon - Radiotherapy
27
What is multiple Myeloma?
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
28
What is the role of Plasma cells?
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
29
What is the most common antibody produced in Multiple myeloma?
95% produce M protein/ Classified by antibody they produce. 50% produce IgG, 20% IgA
30
Clinical features of Multiple Myeloma?
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
31
What are some symptoms of hypercalcaemia?
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
32
What would a blood film show in MM?
Roleux formation, Normocytic anaemia, thrombocytopenia?
33
What would biochemistry show in MM?
Increased Ca2+, Inccreased ESR, decreased anion ap, increased Cr, albumin, proteinura
34
How would you detect monoclonal proteins in MM?
Serum Protein Electropheresis, urine protein electropheresis, Immunofixation
35
Diagnosis Criteria for Myeloma?
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
36
What are the treatment goals in MM?
• 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
37
What is treatment in MM?
if 65yo then Chemo
38
What does supportive management of MM include?
- Bisphosphonates for those with Osteopenia or Lytic Bone Lesions - local XRT for bone pain, spinal cord compression Treat complications
39
What is Hodgkin's lymphoma?
This is a malignant proliferation of Lymphoid cells thought to arise from germinal centre in b cells
40
What are Reed-Sternberg cells associated with?
Hodgkin's Lymphoma
41
What are the bimodal peaks of hodgkin's Lymphoma?
Peaks at 20yr and just above 50yr
42
What are B Symptoms?
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
43
Clinical features of Hodgkin's Lymphoma?
Asymptomatic Lymphadenopathy (non-tender, rubbery), Splenomegaly, Mediastinal mass
44
What are some things associated with Hodgkin's?
EBV in 50% of cases and Alcohol makes the lymphadenopathy worse?
45
Treatment of Hodgkin's?
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
46
Treatment of Hodgkin's?
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
Complications of Hodgkin's?
2% risk of MDS, Cardiotoxicity (adriamycin), Pulmonary disease (Secondary to bleomycin), Solid tumour, non-hodgkins?
48
Prognostic factors for Hodgkin's?
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
What is non-Hodgkin's lymphoma?
Malignant proliferation of lymphoid cells of progenitor or Mature B or T cells
50
What are the types of B- cell NHL?
Diffuse B cell lymphoma, Follicular Lymphoma, Burkitt's Lymphoma, mantle cell lymphoma
51
What are the types of T cell NHL?
Mycosis fungoides, anaplastic large cell lymphoma
52
What are the WHO/REAL classification of NHL?
INDOLENT - follicular lymphoma, Small Lymphotic cell lymphoma/CLL, mantle cell lymphoma Aggressive - Diffuse B cell lymphoma Highly aggressive - Burkitt's Lymphoma
53
What is the most common NHL?
Diffuse Large B cell lymphoma - 33%. Aggressive
54
What genetic mutations is Diffuse Large B cell Lymphoma associated with?
Bcl-2, Bcl-6 and MYC ra-arrangement
55
What is Richter's transformation?
5% of CLL patients progress to DLBCL
56
Are indolent lymphomas harder or easier to treat?
Easier
57
What is the second most common NHL?
Follicular Lymphoma - Indolent
58
What is the C-myc chromosome mutation linked to?
Burkitt's Lymphoma
59
RF for Burkitt's Lymphoma?
EBV, C-MYC mutation, Africa
60
Pruritus after a hot shower?
PRV (Polycythaemia Rubra Vera)
61
What mutation is PRV related to?
JAK-2 Mutation
62
What are some interesting manifestations of Mantle Cell Lymphoma?
Lymphomatosis in GIT, and Waldeyer's ring
63
What is mantle Cell lymphoma associated with?
Over expression of Cyclin D1 (BCL-1 activation)
64
Howell Jolly Bodies occur in which illness?
Hyposplenism - Maybe due to Hereditary spherocytosis
65
What is the chromosomal dislocation in CML?
9:22 dislocation.
66
What is the treatment for CML?
Tyrosine Kinase Inhibitor- Imatanib
67
3 causes of a massive spleen?
Malaria, CML, Myelofibrosis
68
What is Myelofibrosis?
Bone marrow is fibrosed
69
Where do you see Tear drop cells?
In myelofibrosis - unable to aspirate - dry tap
70
CLL is a B disease -associated with four B's:
B Lymphocytes Bone marrow failure Bleeding Broken cells (smear cells)
71
What are the five investigative markings seen in Haemolytic anaemia?
``` Increased LDH, Decreased Haptoglobin, Increased Urobilogen, Increased Reticulocytes Positive Direct Coomb's test ```
72
What is the management of thalassemia?
Blood transfusion and iron Chelation
73
Thrombotic crises is precipitated by .... (3)
Infection, dehydration and deoxygenation
74
Burkitt's lymphoma involves which chromosomes? What is the pathophysiology?
Chromosome 8 and 14 Myco oncogene is translocated to an immunoglobulin gene
75
Most common leukaemia?
CLL
76
Heparins generally act by activating _______
Anti-thrombin III
77
Unfractionated heparin forms a complex which inhibits ______ and Factors ___ ___ __ _____
Thrombin, Factor 10, 9, 10i, 12
78
Pruritius with History of alcohol excess, spider naevi, bruising, palmar erythema Jaundice
Liver disease
79
Pruritus with Pallor, kolynychia, atrophic glossitis, post-cricoid webs, angular stomatitis
Iron deficiency anaemia
80
Pruritus with Warm baths, ruddy complexion, hx of Gout and PUD
Polycythaemia
81
Pruritus with lethargy, pallor, oedema, weight gain and HTn
Chronic Kidney disease
82
Pruritus with Night sweats, Lymphadenopathy, splenomegaly
Lymphoma
83
Prior to an elective splenectomy a patient should receive the following vaccinations:
HiB, Meningitis A & C, Annual influenzae and pneumococcal vaccine very 5 years. Consider Abx prolophylaxis
84
The only blood product that doesn't have to be ABO compatible and can just be given is ____
Platelets
85
Usually administered to patients that thrombocytopaenic and are bleeding or require surgery
Platelet rich plasma
86
Fresh Frozen plasma contains _______ (3)
1. Clotting factors 2. Albumin and 3. Immunoglobulin
87
FFP is used in _____ and for patients with ______ failure who are undergoing surgery.
DIC or Clotting deficiency or in people with liver failure
88
FFP should or should not be first line for hypovolaemia?
Should not
89
Rich source of Factor VIII and fibrinogen. Allows large concentration of Factor VII to be administered in small volume. First line in DIC
Cryoprecipitate
90
aplastic anaemia, cafe au lait spots, short stature, acute myeloid leukaemia
Fanconi Anaemia
91
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?
IgM
92
Smudge/smear cells -->
CLL
93
Auer rods -->
AML
94
Tear drop Polikocytes -->
Myelofibrosis
95
Target cells are associated with --> (5)
``` Sickle cell anaemia Thalassaemia Fe def anaemia Hyposplenism Liver disease ```
96
Spherocytes are associated with
Hereditary spherocytosis and | Autoimmune haemolytic anaemia
97
Basophilic stippling is associated with --> (4)
Lead poisoning thalassaemia Sideroblastic anaemia Myelodysplasia
98
Howell-Jolly bodies -->
Hyposplenism
99
Heinz bodies -->
G6PD deficiency sometimes Alpha-thalassaemia
100
Schistocytes (helmet cells) --> (3)
Intravascular haemolysis Mechanical heart valve Disseminated intravascular coagulation
101
Pencil Poikilocytes -->
Iron def. anaemia
102
Burr cells (echinocytes) --> (2)
Uraemia, | Pyruvate kinase def
103
Acanthocytes -->
Abetalipoproteinaemia
104
Hypersegmented neutrophils -->
Megaloblastic anaemia
105
Treatment of choice for CML?
Imantinib
106
Polycythaemia Rubra vera is related to _____ mutation
JAK 2
107
Treatment of choice for essential thrombocytopenia?
Hydroxyurea
108
Activated Protein C resistance leads to ____
Factor V Leiden
109
Liver disease leads to _______ anaemia
Liver disease leads to macrocytic (normoblastic) anaemia
110
Man immigrated from Haiti, Lymphadenopathy, hepatosplenomegaly and skin lesions. With elevated calcium levels and bone scan shows numerous lytic lesions
Adult T cell Lymphoma
111
Person from africa with lymphadenopathy. Jaw or facial bone tumour in 4-10 year old
Burkitt Lymphoma
112
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
Mycosis Fugoides
113
``` Fever Neurological change Renal failure thromboctyopenia and haemolytic anaemia ``` Is the classic pentad for ____
Thrombotic thrombocytopenia purpura
114
50 year old man, with splenomegaly, pancytopenia , peculiar mycobacterial infections and lymphoid infiltration of the hepatic portal triad.
Hairy cell Leukaemia (disease of B cells)

Theme III (15 decks)

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