Unit III Flashcards

1
Q

Congenital AML translocations (5)

A
  1. t(8,21)
  2. inv(16) or t(16;16)
  3. t(15;17)
  4. t91;22)
  5. 11q23
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2
Q

t-AML (2)

A
  1. alkylating reagent or radiation (whole/partial loss of 5/7)
  2. Topo II inhib (rearrangement of MLL) 11q23
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3
Q

NOS-AML (3)

A
  1. FLT3 (ITD)
  2. NPM1
  3. CEBPA
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4
Q

Markers for B-ALL (4)

A
  1. CD19
  2. 22
  3. 79a
  4. Lack CD20
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5
Q

3 B-ALL

A
  1. t(9;22)- p190
  2. MLL, 11q23
  3. t(12,21)
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6
Q

Markers for T-ALL (7)

A
  1. cd2
  2. 3
  3. 7
  4. 4/8 + or -
  5. 99
  6. 1a
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7
Q

CML

A
  1. t(9,22), p210
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8
Q

PV

A

JAK2 mutation (V617F), nearly all have this mutation

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9
Q

MPNs (4)

A
  1. CML- neutrophilia
  2. polycythemia vera-erythrocytosis
  3. Primary myelofibrosis- granu/megakaryocytic lineages
  4. Essential thrombocytopenia- thrombocytosis
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10
Q

Burkett’s positive (5)

A

GC B cell

  1. cd19
  2. 20
  3. 10
  4. BCL6
  5. c-myc
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11
Q

Burkett’s neg (4)

A
  1. BCL2
  2. CD5
  3. CD23
  4. TdT
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12
Q

Follicular lymphoma + (5)

A
  1. 19
  2. 20
  3. BCL-2
  4. 10
  5. BCL-6
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13
Q

Mantle cell lymphoma + (6)

A
  1. 19
  2. 20
  3. 5 ***
  4. BCL-1 **
  5. 10
  6. BCL-6
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14
Q

SLL/CLL + (3)

A

5
23
19

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15
Q

Signs/sympt of anemia (4)

A

fatigue, malaise, pallor, dyspnea

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16
Q

Signs/symptoms of thrombocytopenia (3)

A

bruising, petechial, hemorrhage

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17
Q

Signs/symptoms of neutropenia

A

fever, infections

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18
Q

The genetic perturbations that cause AML appear to occur at the level of the

A

pluripotential stem cell

one of committed progenitors

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19
Q

The genetic perturbations that cause ALL appear to occur at the level of the

A

lymphoid stem cell

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20
Q

WBC in ALL

A

increased, normal, or decreased

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21
Q

CML philias

A

neutrophils

sometime baso and platelets

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22
Q

OV philias

A

RBC

neutrophils and platelets

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23
Q

Thinking PV but no JAK2 mutation->

A

secondary erythrocytosis

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24
Q

Splenomegaly in ET

A

NOT COMMON

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25
Q

CD20

A

mantle cell B-cells and germinal center B-cells

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26
Q

CD3

A

T cells in paracortex

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27
Q

Smudge cell

A

CLL

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28
Q

CD38-, ZAP-70-, germline IGH@ V, pre-germinal center

in CLL

A

Favorable

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29
Q

Neg mantle cell lymphoma

A

CD23

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30
Q

T cell deficiencies infection (2)

A

candida albicans

pneumocystis jirovecci

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31
Q

(2) complement mediated damage Type II diseases

A
  1. myasthenia gravis

2. goodpasture

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32
Q

Many drugs, such as

___ ____ _____ ____ can induce AIHA,

A

penicillin, methyldopa, chlorpromazine and quinidine,

33
Q

Two steps of Type IV hypersensitivity

A
  1. Initiation

2. Elicitation

34
Q

mantoux skin test is injected

A

intradermally (necessary to see bubble)

35
Q

+ PPD test, you will see which cell predominantly if biopsied

A

macrophages

Th1 can attract 1000

36
Q

Anergy

A

lack of reaction by the body’s defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance.

37
Q

2 ways to get a false positive TB test

A
  1. exposure to other species of mycobacteria

2. BCG vaccine

38
Q

Monoclonal antibody to CD20 on B cells in treatment of rheumatoid arthritis

A

rituximab

39
Q

TH2 cells in immunopathology

A

asthma and chronic worm infestation

40
Q

Mycobacterium leprae

A
  • leprosy

some people have TH1 responses and others have Th2 responses

41
Q

TH1 response to mycobacterium leprae

A

tuberculoid leprosy but control infection

42
Q

TH2 response to mycobacterium leprae

A

lepromatous leprosy

uncontrolled with small granulomas

43
Q

PRR present in the gut that detects foreign bacterium

A

NOD2

44
Q

NOD2

A
  • detects muramyl dipeptide (component of bacterial cells walls)
  • Activates NFKB
45
Q

Diagnosing celiacs

A

1/ small intestine biopsy

2. antibody to transglutaminase 2

46
Q

Autoantibody to transglutaminase 3->

A

dermatitis herpetiformis

47
Q

HLA chronis beryllium disease

A

HLA-Dp

48
Q

HLA Psoriasis

A

HLA-Cw*06:02

49
Q

Psoriasis common in

A

African American

- not Africans though-> environmental factors

50
Q

anti-IL-23 antibody for psoriasis treatment

A

tildrakizumab

51
Q

Pseudo-pelger-Huet cells

A

neutrophils with bi-lobed nuclei

*** dysgranulopoiesis

52
Q

Dysmegakaryopoiesis

A

megakaryocytes w/ hypolobated or non-lobated nuclei. hyperchromatic nuclei. small

53
Q

Signs/ symptoms of ET

A
  • transient ischemic attacks (TIAs) (these are essentially small strokes causing no
    permanent damage)
  • digital ischemia with paresthesias
  • thrombosis of major arteries or veins (less common than in PV)
  • splenomegaly is not common in PV, and is more suggestive of another MPN
54
Q

Common genetic findings of CLL

A
  1. deletion of 13q14- most common
  2. trisomy 12
  3. deletion of 11q22-23
    4 deletion 17p13
55
Q

M protein

A

monoclonal protein

56
Q

Extraosseous plasmacytomas are present where?

A

upper respiratory tract

57
Q

Binucleated plasma cells in marrow->

A

Plasma cell myeloma

58
Q

NLPHL

A

type of hodgkins lymphoma

  • indolent malignancy
  • popcorn or lymphocyte predominant cells
59
Q

Hodgkin cell

A

Mononuclear variant of reed-Sternberg cells

60
Q

Sudden onset of TB->

A

think HIV OR targeted immunity to IFN gamma

61
Q

Neutralization example

A

In SE asia-> neutralizing antibodies to IFN gamma-> makes T cells worthless

62
Q

Poison ivy toxic compound

A

urushirol

63
Q

CVID-> increased risk of

A

lymphoma, enteropathy, autoimmunity

64
Q

Memory T cells have a lower

A

activation threshold (takes less antigen)

65
Q

Shogren syndrome involves what type of t cells

A

CTL

66
Q

Symptoms of acute GvHD

A
  • maculopapular skin rash
  • diarrhea
  • hepatic inflammation w/ jaundice
  • infections
67
Q

TGF beta favors differentiation of ___ to ___

A

Tho into Treg

68
Q

Peyers path composition

A
  • Lots of TGFbeta
  • dendritic cells make Il-10-> Treg
  • Lots of Treg cells
  • Tfh cells that drive B cells to IgA
69
Q

Symptoms of Type III hypersens

A
  1. arthralgia/arthritis
  2. pleurisy/pleural effusion
  3. sterile peritonitis
  4. skin rash- esp on shins
  5. CNS- confusion
  6. glomerulonephritis
70
Q

In plasma cell myeloma, M proteins are typically:

A

IgG, and sometimes IgA

71
Q

Chronic spontaneous urticaria

A
  • IgG to FcR1 receptor on mast cells-> chronic release of histamine

Test: inject their own serum intradermally
Treat: omalizumab- binds to Fc of IgE

72
Q

Nucala (mepolizumab)

A

interleukin 5 agonist

reduces sever asthma attacks by reducing levels of eosinophils

73
Q

Size of immune complexes that activate complement but are too small to be removed by the RE system

A

about a million daltons

74
Q

Serum sickness like symptoms can be seen with

A

patients with viral infections-> especially hepatitis

75
Q

In hypersensitivity pneumonitis (farmer’s lung) Type III progresses to ->

A

Type IV

76
Q

Distinct features of IgA1

A
  • long hinge region

- terminal sugars of the carbohydrate chain in the hinge are missing

77
Q

Carbohydrate epitope in IgA1

A

N-acetyl-galactosamine (frequent in bacteria and viruses)

78
Q

Low levels of complement C1 and C4

A

Lupus