Unit III Flashcards
1
Q
Congenital AML translocations (5)
A
- t(8,21)
- inv(16) or t(16;16)
- t(15;17)
- t91;22)
- 11q23
2
Q
t-AML (2)
A
- alkylating reagent or radiation (whole/partial loss of 5/7)
- Topo II inhib (rearrangement of MLL) 11q23
3
Q
NOS-AML (3)
A
- FLT3 (ITD)
- NPM1
- CEBPA
4
Q
Markers for B-ALL (4)
A
- CD19
- 22
- 79a
- Lack CD20
5
Q
3 B-ALL
A
- t(9;22)- p190
- MLL, 11q23
- t(12,21)
6
Q
Markers for T-ALL (7)
A
- cd2
- 3
- 7
- 4/8 + or -
- 99
- 1a
7
Q
CML
A
- t(9,22), p210
8
Q
PV
A
JAK2 mutation (V617F), nearly all have this mutation
9
Q
MPNs (4)
A
- CML- neutrophilia
- polycythemia vera-erythrocytosis
- Primary myelofibrosis- granu/megakaryocytic lineages
- Essential thrombocytopenia- thrombocytosis
10
Q
Burkett’s positive (5)
A
GC B cell
- cd19
- 20
- 10
- BCL6
- c-myc
11
Q
Burkett’s neg (4)
A
- BCL2
- CD5
- CD23
- TdT
12
Q
Follicular lymphoma + (5)
A
- 19
- 20
- BCL-2
- 10
- BCL-6
13
Q
Mantle cell lymphoma + (6)
A
- 19
- 20
- 5 ***
- BCL-1 **
- 10
- BCL-6
14
Q
SLL/CLL + (3)
A
5
23
19
15
Q
Signs/sympt of anemia (4)
A
fatigue, malaise, pallor, dyspnea
16
Q
Signs/symptoms of thrombocytopenia (3)
A
bruising, petechial, hemorrhage
17
Q
Signs/symptoms of neutropenia
A
fever, infections
18
Q
The genetic perturbations that cause AML appear to occur at the level of the
A
pluripotential stem cell
one of committed progenitors
19
Q
The genetic perturbations that cause ALL appear to occur at the level of the
A
lymphoid stem cell
20
Q
WBC in ALL
A
increased, normal, or decreased
21
Q
CML philias
A
neutrophils
sometime baso and platelets
22
Q
OV philias
A
RBC
neutrophils and platelets
23
Q
Thinking PV but no JAK2 mutation->
A
secondary erythrocytosis
24
Q
Splenomegaly in ET
A
NOT COMMON
25
CD20
mantle cell B-cells and germinal center B-cells
26
CD3
T cells in paracortex
27
Smudge cell
CLL
28
CD38-, ZAP-70-, germline IGH@ V, pre-germinal center
| in CLL
Favorable
29
Neg mantle cell lymphoma
CD23
30
T cell deficiencies infection (2)
candida albicans
| pneumocystis jirovecci
31
(2) complement mediated damage Type II diseases
1. myasthenia gravis
| 2. goodpasture
32
Many drugs, such as
| ___ ____ _____ ____ can induce AIHA,
penicillin, methyldopa, chlorpromazine and quinidine,
33
Two steps of Type IV hypersensitivity
1. Initiation
| 2. Elicitation
34
mantoux skin test is injected
intradermally (necessary to see bubble)
35
+ PPD test, you will see which cell predominantly if biopsied
macrophages
| Th1 can attract 1000
36
Anergy
lack of reaction by the body's defense mechanisms to foreign substances, and consists of a direct induction of peripheral lymphocyte tolerance.
37
2 ways to get a false positive TB test
1. exposure to other species of mycobacteria
| 2. BCG vaccine
38
Monoclonal antibody to CD20 on B cells in treatment of rheumatoid arthritis
rituximab
39
TH2 cells in immunopathology
asthma and chronic worm infestation
40
Mycobacterium leprae
- leprosy
| some people have TH1 responses and others have Th2 responses
41
TH1 response to mycobacterium leprae
tuberculoid leprosy but control infection
42
TH2 response to mycobacterium leprae
lepromatous leprosy
| uncontrolled with small granulomas
43
PRR present in the gut that detects foreign bacterium
NOD2
44
NOD2
- detects muramyl dipeptide (component of bacterial cells walls)
- Activates NFKB
45
Diagnosing celiacs
1/ small intestine biopsy
| 2. antibody to transglutaminase 2
46
Autoantibody to transglutaminase 3->
dermatitis herpetiformis
47
HLA chronis beryllium disease
HLA-Dp
48
HLA Psoriasis
HLA-Cw*06:02
49
Psoriasis common in
African American
| - not Africans though-> environmental factors
50
anti-IL-23 antibody for psoriasis treatment
tildrakizumab
51
Pseudo-pelger-Huet cells
neutrophils with bi-lobed nuclei
*** dysgranulopoiesis
52
Dysmegakaryopoiesis
megakaryocytes w/ hypolobated or non-lobated nuclei. hyperchromatic nuclei. small
53
Signs/ symptoms of ET
- 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
Common genetic findings of CLL
1. deletion of 13q14- most common
2. trisomy 12
3. deletion of 11q22-23
4 deletion 17p13
55
M protein
monoclonal protein
56
Extraosseous plasmacytomas are present where?
upper respiratory tract
57
Binucleated plasma cells in marrow->
Plasma cell myeloma
58
NLPHL
type of hodgkins lymphoma
- indolent malignancy
- popcorn or lymphocyte predominant cells
59
Hodgkin cell
Mononuclear variant of reed-Sternberg cells
60
Sudden onset of TB->
think HIV OR targeted immunity to IFN gamma
61
Neutralization example
In SE asia-> neutralizing antibodies to IFN gamma-> makes T cells worthless
62
Poison ivy toxic compound
urushirol
63
CVID-> increased risk of
lymphoma, enteropathy, autoimmunity
64
Memory T cells have a lower
activation threshold (takes less antigen)
65
Shogren syndrome involves what type of t cells
CTL
66
Symptoms of acute GvHD
- maculopapular skin rash
- diarrhea
- hepatic inflammation w/ jaundice
- infections
67
TGF beta favors differentiation of ___ to ___
Tho into Treg
68
Peyers path composition
- Lots of TGFbeta
- dendritic cells make Il-10-> Treg
- Lots of Treg cells
- Tfh cells that drive B cells to IgA
69
Symptoms of Type III hypersens
1. arthralgia/arthritis
2. pleurisy/pleural effusion
3. sterile peritonitis
4. skin rash- esp on shins
5. CNS- confusion
6. glomerulonephritis
70
In plasma cell myeloma, M proteins are typically:
IgG, and sometimes IgA
71
Chronic spontaneous urticaria
- 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
Nucala (mepolizumab)
interleukin 5 agonist
| reduces sever asthma attacks by reducing levels of eosinophils
73
Size of immune complexes that activate complement but are too small to be removed by the RE system
about a million daltons
74
Serum sickness like symptoms can be seen with
patients with viral infections-> especially hepatitis
75
In hypersensitivity pneumonitis (farmer's lung) Type III progresses to ->
Type IV
76
Distinct features of IgA1
- long hinge region
| - terminal sugars of the carbohydrate chain in the hinge are missing
77
Carbohydrate epitope in IgA1
N-acetyl-galactosamine (frequent in bacteria and viruses)
78
Low levels of complement C1 and C4
Lupus
