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Semestre 6: bloque 2 > Hemato Week 3/4 > Flashcards

Hemato Week 3/4 Flashcards

(74 cards)

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1
Q

Defect of follicular lymphoma

A

t(14:18) → overexpression BCL2

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2
Q

Defect of diffuse large cell lymphoma

A

Dysregulation BCL6

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3
Q

Defect in Burkitt lymphoma

A

Translocations MYC gene
Translocations IGH locus t(8:14)

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4
Q

Main characteristic of Hodgkin lymphoma

A

Reed-Sternberg cells

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5
Q

Classification of Hodgkin lymphoma

A

Nodular sclerosis: classic
Mixed cellularity: classic
Lymphocyte-rich: classic
Lymphocyte depletion: classic
Nodular lymphocyte predominance: No RS cells

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6
Q

Characteristic of Reed-Sternberg cells

A

Originate from germinal center
Fail to express most B cell specific genes (Ig genes)

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7
Q

Pathophysiology of classic Hodgkin lymphoma

A

Activate NF-kB

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8
Q

Defect of Hodgkin lymphoma

A

HLA class I expression lost
Mutation B2-microglobulin gene
EBV genome

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9
Q

Clinical features of Hodgkin lymphoma

A

Young males
Constitutional symptoms
Enlargement of lymph nodes: painless, asymmetrical, firm and discrete
Lymph nodes increase and decrease size

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10
Q

Late complication of Hodgkin lymphoma

A

Cutaneous HL

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11
Q

Labs of Hodgkin lymphoma

A

Normochromic normocytic anemia
Neutrophilia and eosinophilia
Advanced → lymphopenia
Platelets: normal/increased in early phase, reduced in later stage
ESR, C reactive protein, and LDH: raised

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12
Q

Markers of Reed-Sternberg cells

A

CD30+ and CD15+
CD10-, CD19-, CD20-

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13
Q

Marker of poor prognosis in Hodgkin lymphma

A

CD68

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14
Q

Which feature would be most concerning for a neoplastic process in Hodgkin lymphoma

A

Preponderance of lymphocytes with a single immunoglobulin variable domain allele

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15
Q

Paraneoplastic symptom in Hodgkin lymphoma

A

Hypercalcemia: increased extra renal consumption of vitamin D12
Causes secretion of y-interferon

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16
Q

Etiology of non Hodgkin lymphomas

A

Unknown etiology
Infectious agents important

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17
Q

Difference between low grade and high grade NHL

A

Low grade → indolent, responds to chemo, difficult to cure
High grade → aggressive and urgent tx but often curable

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18
Q

Clinical features of NHL

A

Superficial lymphadenopathy: asymmetric painless enlargement
Constitutional symptoms less frequent
Oropharyngeal involvement (Waldeyer ring) → sore throat

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19
Q

Most common extranodal site (after bone marrow) of NHL

A

Gastrointestinal

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20
Q

What do NHL B cell lymphomas express in biopsy

A

K or N light chains

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21
Q

Prognostic marker of NHL

A

LDH: raised more rapidly in proliferating and extensive disease

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22
Q

Cytogenetics of NHL

A

Follicular lymphoma → t(14:18)
Mantle cell lymphoma → t(11:14)
Burkitt lymphoma → t(8:14)
Anaplastic large cell → t(2:5)

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23
Q

Epidemiology of SLE

A

Women; fertile age (15-44 yo)

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24
Q

Etiology of SLE

A

Genetic: HLA-DR2 and DR3
Hormonal: Estrogens
Environmental: UV light or drugs

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25
Drugs that can influence in SLE
Procainamide or hydralazine
26
Pathophysiology of SLE (2 mechanisms)
Autoantibody development: due to deficiency of complement proteins Autoimmune reactions: type III hypersensitivity
27
What characterizes the clinical features of SLE
Systemic diseases characterized by phases of remission and relapse
28
Most common clinical features of SLE
Constitutional symptoms Joints → arthritis and arthralgia Skin → malar rash (butterfly rash); photosensitivity
29
Type of endocarditis in SLE
Libman-Sacks endocarditis
30
Labs in SLE
General → Antinuclear antibodies (ANAs) Specific → Anti-dsDNA and Anti-Sm antibodies Antiphospholipid antibodies
31
Pharmacotherapy of SLE
Hydroxychloroquine
32
Epidemiology of rheumatoid arthritis
Women 30-55 yo
33
Etiology of rheumatoid arthritis
Genetic → HLA-DR4 and DR1 Environmental → smoking Female sex hormones Obesity
34
Post-translational modification that initiates the autoimmune response in RA
Citrullination
35
Immune cells that recognize citrullinated proteins as foreign
APCs which present them to CD4+ T cells.
36
What does IL-4 produced by activated CD4+ T cells promote?
B-cell proliferation and production of anti-citrullinated peptide antibodies (ACPAs).
37
What cytokines are secreted by CD4+ T cells in synovial joints?
IFN-γ and IL-17
38
Which cytokines are released by recruited macrophages in RA?
TNF-α, IL-1, and IL-6
39
What is the synnovial pannus
Proliferative granulation tissue with mononuclear inflammatory cells leading to joint destruction
40
Role of rheumatoid factor
IgM antibody against the Fc portion of IgG Forms immune complexes and contributes to type III hypersensitivity
41
Typical symptoms of RA
Symmetrical polyarthralgia, morning stiffness improving with activity, joint deformities
42
Joint deformities in RA
Swan neck deformity: hyperextension of PIP and flexion of DIP joints Boutonnière deformity: flexion of PIP and hyperextension of DIP Hitchhiker thumb (Z thumb): hyperextension of the IP joint with fixed flexion at the MCP Piano key sign: dorsal subluxation of the ulna.
43
What does the Gaenslen squeeze test indicate?
Pain at the MCP joints due to inflammation.
44
Most common extra articular symptoms in RA
Fatigue, rheumatoid nodules, secondary Sjögren's, Raynaud phenomenon, carpal tunnel syndrome
45
Nocturnal paresthesias, thenar atrophy, difficulty making a fist
Carpal tunnel syndrome
46
Cause of tissue damage in RA joints
Synovial pannus with fibroblast-like mesenchymal cells and mononuclear infiltrates
47
Histology of rheumatoid nodules
Central fibrinoid necrosis surrounded by palisading histiocytes
48
Most specific test in RA
Anti-citrullinated peptide antibodies (ACPA)
49
Tx of RA
Glucocorticoids and NSAIDs
50
Group of conditions arising from transformed marrow stem cells or hematopoietic progenitors and characterized by clonal proliferation of 1+ hematopoietic components in bone marrow
Myeloproliferative neoplasms
51
Myeloproliferative neoplasms most likely to progress to acute myeloid leukemia
Primary myelofibrosis
52
Most common mutation of myeloproliferative neoplasms
JAK2
53
Second most common mutation of myeloproliferative neoplasms
CALR
54
Increase in hemoglobin concentration
Polycythemia
55
Hb and hematocrit levels in polycythemia
Hb >185 men and >165 women Hematocrit >0.52 men and >0.47 women
56
Classification of absolute polycythemia
Primary → rare congenital (genetic changes in O2 sensing) and polycythemia vera Secondary → increase erythropoietin factors (smoking, sleep apnea, altitude)
57
Increase RBC volume caused by clonal malignancy marrow stem cell
Polycythemia vera
58
Mutation in polycythemia vera
95%: JAK2 V617F mutation 5%: mutation in exon 12
59
Causes for the clinical features of polycythemia vera
Hyperviscosity, hypervolemia, hypermetabolism, thrombosis
60
Clinical features of polycythemia vera
Mucosal bleeding and visual changes Pruritus after hot bath Splenomegaly and thrombosis Plethroic appearane: cyanosis Gout
61
Tx for polycythemia vera
Therapeutic phlebotomy and aspirin
62
Characteristic defect of CML
Philadelphia chromosome → t(9:22)
63
How is the Philadelphia chromosome composed
Translocation between chromosome 9 (ABL1) and chromosome 22 (BCR)
64
How is the Ph chromosome detected
Karyotypic examination FISH or PCR
65
Main cause of death of CML
Transformation to blast phase
66
Clinical features of CML
Incidental dx Symptoms hypermetabolism Massive splenomegaly Bruising, epistaxis, menorrhagia Gout
67
Rare for clinical feature of CML
Priapism!!
68
Labs for CML
Leukocytosis: neutrophils and myelocyes Increased basophils, platelets, uric acid Normochromic normocytic anemia Hypercellular bone marrow
69
Mainstay tx for CML
TKIs (imatinib)
70
Tx for pregnant women with CML
a-interferon
71
Acute transformation of CML
>20% blasts May occur rapidly over days/weeks
72
Accelerated phase of CML
Anemia, thrombocytopenia, increase basophils >20% or 10-19% blast cells, splenomegaly; may take several months, disease less easy to control
73
Antibodies present in drug induced SLE
Anti-histone antibodies
74
Most likely myeloproliferative disorder to turn into acute myeloid leukemia
Primary myelofibrosis

Semestre 6: bloque 2 (10 decks)

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