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Pathology > 2nd Exam: Plasma Cell Disorders > Flashcards

2nd Exam: Plasma Cell Disorders Flashcards

1
Q

CD 3, 4, 5:

A

T lymphocytes

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2
Q

CD 13:

A

most granulocytees

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3
Q

CD15:

A

granulocyes

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4
Q

List the 5 heavy chains:

A

GAMED

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5
Q

Common Ig’s?

A

IgG: most common, A and M: next most common, D and E: fairly uncommon

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6
Q

1 plasma cell, 1:

A

Ig (one type of each chain)

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7
Q

3 classifications o plasma cell disorders:

A

MGUS, plasma cell myeloma Plasmsmacytoma

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8
Q

MGUS:

A

Monoclonal gammopathy of undertermined significance

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9
Q

Solitary lesion of neoplastic monoclonal plasma cells morphologically the same as myeloma, bone or soft tissue:

A

plasmacytoma

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10
Q

Related Ig producing disorders:

A

Ig depositiondisease, ie primary amyloidosis, Heavy chain disease, adn lymphoplasmacytoid Lymphoma

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11
Q

progressive, incurable, excess light chains bind, producing amyloidosis: abnormal protein deposition in one or more organs or body systems.

A

primary amyloidosis

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12
Q

Heavy chains produced in Heavy Chain Disease:

A

G, A, or M, no light chains

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13
Q

Lymphoplasmacytoid Lymphoma

A

Subset IgM producing: Waldenstrom’s Macroglobulinemia

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14
Q

Waldenstrom’s Macroglobulinemia is what type of disorder:

A

Lymphoplasmacytoid lymphoma

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15
Q

Disorder of malig neo of lympholyctes stuck at lympho and plasma cell differentiation border:

A

Lymphoplasmacytoid Lymphoma

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16
Q

Antigen binding-sites on Ig’s are made of:

A

amino ends (NH2)

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17
Q

kappa/lambda light chain ration in peripheral blood:

A

2:1

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18
Q

Digests IgG:

A

papain

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19
Q

IgG is broken into these via papain:

A

2 identical FAB, 1 Fc

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20
Q

FAB sf:

A

Fragment antigen binding

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21
Q

Fc sf:

A

fragment-crystallizable (constant end of Ig)

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22
Q

Major Ig in serum:

A

G

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23
Q

Major Ig of external secretions:

A

A

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24
Q

1st Ig presesnt after primary antigenic stimulus:

A

M

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25
Q

Ig that crosses placenta and Ig that does not.

A

G, M

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26
Q

Ig in trace amts in normal serum:

A

D

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27
Q

define reaginin:

A

allergic

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28
Q

This has reaginic antibody activity

A

IgE

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29
Q

IgE is involved in:

A

immediate hypersensititvity, eosinophilic response

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30
Q

IgG crosses placenta via:

A

active transport

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31
Q

When is IgG produced:?

A

response to 2nd exposure to an antigenic stimulus

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32
Q

Major Ig in GI secretions:

A

A

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33
Q

Ig considered large size “macrolobulin:

A

M, polymer/ pentamer

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34
Q

1st Ab produced in infectious mononucleosis:

A

M

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35
Q

infectious mononucleosis develops from:

A

EBV esp. college age

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36
Q

Test for these Ig’s if you suspect infectious mononucleosis:

A

M, G, and A

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37
Q

Ig levels that rise in response to EBV virus:

A

M and A

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38
Q

Ig’s levels increased with recent exposure to EBV, recent mono infection:

A

lots of M, no G

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39
Q

Test for mono, IgG is high and IgM is not:

A

had mono in past, not current infection

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40
Q

Order of Ig presentation in mono infection:

A

M then G, stays high for a while later

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41
Q

If Rafi were tested now for mono, which Ig would be present in higher conc’s?

A

G

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42
Q

Ig produced to fight issues in GI tract:

A

A

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43
Q

EBV is aka:

A

HHV-4

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44
Q

Swollen lymph nodes and suspected mono indicates:

A

G could be high or not, mono in past

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45
Q

Slide appearance of plasma cells when they are mounting a response:

A

making lots of Ig, bluish cytoplasm, eccentric nucleus

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46
Q

Polyclonal proliferation of plasma cells that are each different, many types of Ig, some kappa, some lambda:

A

polyclonal plasma cell proliferation

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47
Q

Plasma cells proliferate in response to:

A

antigen presentation by B lymphos, many lines searching for best Ig to produce

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48
Q

polyclonal plasma cell proliferation, neoplastic or malignant cell line?

A

either

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49
Q

neoplastic or malignant cell line, one or many cells of origin?

A

1, same products, 1 light chain, 1 Ig type, 1 marker

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50
Q

Leads to a monoclonal serum protein or “M” protein:

A

production of a monoclonal light chain by neoplastic plasma cells or B-lymphos

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51
Q

Stain this for monoclonal plasma cells:

A

either light chain

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52
Q

SPEP sf:

A

serum protein electrophoresis, agarose gel electrophoresis to id different proteins in serum via size and electrical charge

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53
Q

Clinical syms pointing toward monoclonal gammopathy:

A

abnormal SPEP, intermittent, “non-sp” joint pain, no swelling or redness

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54
Q

Test to use when a monoclonal serum protein is suspected:

A

SPEP

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55
Q

Normal SPEP has, abnormal has:

A

5 regions, goal post spikes at either end/ gamma region: albumin on L, Gamma globulin on R

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56
Q

List the 5 regions in normal SPEP:

A

serum albumin, alpha-1, alpha 2, beta, gamma globulins

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57
Q

Spike on normal SPEP with 2 hills:

A

beta

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58
Q

What spike would be down in SPEP w nutritional problems?

A

albumin region spike

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59
Q

What does a broad, increased band in gamma region indicate?

A

fighting infection, probably polyclonal

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60
Q

Test to measure kidney function:

A

BUN/ Creatinine

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61
Q

Normal % of plasma cells in bone marrow:

A

less than 5%

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62
Q

What test next with slight increase in monoclonal protein in blood, all else WNL, spike in y-region of SPEP:

A

IFE: Immunofixation electrophoreses

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63
Q

IFE sf:

A

Immunofixation electrophoreses

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64
Q

When to do IFE:

A

to further evaluate SPEP findings, id and characterize monoclonal proteins in serum or urine

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65
Q

In IFE, after proteins from urine or serum are separated they are incubated with:

A

antisera against Ig of interest, precipitates at sites of Ag-Ab reaction

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66
Q

Band intesity of IFE correlates with:

A

protein concentration

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67
Q

Tx for MGUS:

A

none, asymptomatic, simply follow

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68
Q

monoclonal serum protein is aka:

A

“M” protein

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69
Q

TF? Presence of an expanded clone of Ig-secreting cells is considered neoplastic.

A

F, does not always progress to overt malignancy

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70
Q

What is present in serum with MGUS?

A

small amt monoclonal serum protein (“M” protein”, <3gm/dl), bm plasma cells <10%

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71
Q

Most common cause of monoclonal gammopathy:

A

MGUS

72
Q

MGUS common in this pop:

A

elderly: 3% over 50yo, 5% over 70yo

73
Q

Symptoms of MGUS:

A

none

74
Q

MGUS may evolve to become:

A

well defined palsma cell or lymphoid neolpasm

75
Q

Risk of MGUS progression per year:

A

1.6%, increased likelihood of having it every year

76
Q

Clinical symps of plasmacytoma:

A

peristant pain in discreet region, osteolytic lesion on x-ray, elevated IgG, IgA and IgM: low normal, low % of plasma cells in bm, sheet of monoclonal plasma cell, high density (1 light chain type) in biopsy

77
Q

Tx of plasmacytoma:

A

focal radiation therapy

78
Q

Plasmacytoma has similar clinical presentation as:

A

myeloma, but no lytic bone lesions, normal bm biopsy

79
Q

Name of plasmacytoma found in bone:

A

“solitary plasmacytoma of bone”

80
Q

Name of plasmacytoma found in soft tissue:

A

extra-osseous plasmacytoma

81
Q

Most common site of solitary plasmacytoma of bone

A

Spine/vertebra

82
Q

Fraction of plasmacytomas that progress to myeloma or additional plasmacytomas:

A

up to 2/3

83
Q

Initial symptoms of plasmacytoma :

A

swelling or bone pain, lesion on xr

84
Q

Clinical sym of plasma cell myeloma:

A

dizziness, light headed, inc bone pain, IgG increased, decreased IgA and IgM, generalized osteoporosis, lytic lesions/ dec bone mass, impaired renal function (abnormal BUN/creatinine), bm packed with monoclonal plasma cells, many abnormally shaped

85
Q

TF? There is a finite level to the amt of Ig your body can produce.

A

T. One level goes up, another goes down

86
Q

Plasma cell myeloma is aka:

A

multiple myeloma

87
Q

Abnormal SPEP is found in:

A

monoclonal gammopathy and multiple/ plasma cell myeloma

88
Q

Difference bw SPEP of monoclonal gammopathy and multiple/ plasma cell myeloma:

A

monoclonal: posts about same height, multiple: y-region taller than albumin region

89
Q

Clinical dx of symptomatic multiple myeloma:

A

M-protein in serum or urine, bm clonal plasma cells or plasmacytoma, related organ tissue impairment: CRAB, suppression of normal Ig’s leading to infection, excessive IgG or IgA (kidney damage)

90
Q

CRAB sf:

A

Hypercalcemia, renal insufficiency, anemia, bone lesions

91
Q

Clinical problems pts with multiple myeloma may encounter:

A

CRAB

92
Q

Clinical dx of asymptomatic multiple myeloma:

A

M protein in serum/urine (<3% g/dl) AND/OR 10% or more clonal plasma cells in bm marrow BUT no related organ or tissue impairment (no CRAB) or myeloma related symptoms

93
Q

asymptomatic multiple myeloma is aka:

A

smoldering plasma cell myeloma

94
Q

If a young person got MM (rare) this procedure would probably be done:

A

bm transplant

95
Q

Median age for MM onset:

A

70yo, 1% US cancer deather

96
Q

Most common plasma cell dyscrasia:

A

MM

97
Q

Tx for MM:

A

chemo, radiation for sp lesions (palliation), bm transplant

98
Q

define palliate:

A

make less unpleasant wo removing cause:

99
Q

Hypercalcemia seen in MM is due to:

A

bone destruciton

100
Q

Inceased levels of these Ig’s can lead to kidney damage:

A

G, A

101
Q

Suppression of normal Ig’s leads to:

A

infection

102
Q

This presents as “punched out” bone:

A

MM

103
Q

What to suspect if a pt breaks a bone during normal life activities:

A

MM, underlying bone destruction

104
Q

Hypercalcemia leads to:

A

confusion, weaknesss, lethargy, deposits

105
Q

Why does anemia present as a symptom of MM?

A

bm infiltration

106
Q

Can MM involve organs besides bone and soft tissues?

A

ys

107
Q

Most common site of lytic bone lesions in MM:

A

vertebrae

108
Q

somnolent:

A

sleepy, drowsy

109
Q

Lab results with MM:

A

inc blood Ca2+ CPR, B2-microglobulin, anemia, monoclonal protein id’ed using SPEP and IFE

110
Q

B2-microglobulin

A

component of MHC class I mol’s, on all nucleated cells

111
Q

Why to take multiple xr’s with MM:

A

punched out appearance is not present throughout entire body

112
Q

Lesions of vertebrae with red marrow, juicy, cellular, many abnormal plasma cells, rounded lesions suspect this:

A

MM

113
Q

Disorder that can lead to collapsed vertebrae:

A

MM

114
Q

Do normal plasma cells have nucleoli?

A

no

115
Q

Ig inclusions are called:

A

Russell bodies

116
Q

Russel bodies are seen in:

A

normal plasma cells and myeloma cells, pts with M spike

117
Q

cells with many Ig inclusions:

A

Mott cells, pts with m spike

118
Q

TF? The presence of mott cells indicates malignancy.

A

F.

119
Q

Found in the vacuoles of mott cells and russell bodes:

A

Ig

120
Q

Tx to reverse spinal cord compression due to MM:

A

emergency bm biopsy, chemo

121
Q

BM findings with MM:

A

increase plasma cells, often abnormal, variable disease distribution in bm

122
Q

Peripheral blood findings with MM:

A

anemia w or wo dec wbcs, thrombocytopenia (dec platelets), maybe plasma cells, stacking of rbcs (rouleaux) due to inc serum protein, maybe plasmacytoid lymphos (increased calcium, right? CRAB?)

123
Q

Cause of roleaux:

A

inc serum protein

124
Q

What is roleaux?

A

rbc stacking due to inc protein in blood

125
Q

Why is the background bluish when staining of MM peripheral blood:

A

protein staining

126
Q

To test for amyloid

A

Congo red stain

127
Q

amyloid due to MM can cause

A

enlarged tongue

128
Q

leading causes of death with MM:

A

1: infections, #2: kidney failure

129
Q

Cause of kidney damage with MM:

A

monoclonal light chains form tubular casts, toxic to tubular epi cells, plasma infiltration, inc Ca2+ levels due to renal vasoc, leading to intra-tubular Ca+2 deposits, infection, amyloid deposition (how are IgG and A involved?)

130
Q

monoclonal light chains in urine:

A

Bence Jones proteins

131
Q

Kindey can be damaged by hypercalceremia due to:

A

renal vasoc, leads to intra-tubular calcium deposition

132
Q

use dipstick urine test to detect:

A

only albumin, not immunoglobulin

133
Q

to detect monoclonal light chains in urine:

A

urine protein electrophoresis

134
Q

Tests to order of pts with MM and kidney issues:

A

SPEP and immunohistochemistry

135
Q

How do light chains damage kidney tubules?

A

solidify to form light chain casts, cast nephropathy

136
Q

formation of plugs in renal tubules from free Ig light chains leading to renal failure in context of MM:

A

cast nephropathy

137
Q

Where does Ca2+ precipitate in body?

A

random spots, including kidney

138
Q

Myeloma staging is based on:

A

bone lesions, anemia, inc blood Ca2+, creatinine, Ig levels, Bence-Jones proteins in urine

139
Q

Creatinine measures are related to:

A

kidney function

140
Q

Hct sf:

A

hematocrit

141
Q

Tx for myeloma:

A

radiation, chemo, stem cell transplant, velcade, Interferon-y (anti-IL-6 agent), interferon-a, thalidomide, bisphosponates

142
Q

Velcade is aka:

A

bortezomib

143
Q

Anti-IL6-agent:

A

interferon-y

144
Q

Function of bisphosphonates:

A

inhibit bone resorption, reduce osteoclasts

145
Q

Drugs used for chemo tx of MM:

A

melphalan, cyclophosphamide, prednisone

146
Q

Side effect of chem tx for MM:

A

myelosuppression

147
Q

Velcade (bortezomib):

A

proteasome inhibitor, inc myeloma cell response to chemo, induce apoptosis of tumor cells, side effect: neuropathy

148
Q

Drugs used to tx MM besides chemo:

A

velcade (bortezomib), anti-Il-6 agents (iterferon-y), interferon-a,m thalidomide, bisphosphonates

149
Q

We want to decrease IL-6 in MM tx because:

A

IL-6 promotes myeloma cell proliferation

150
Q

Function of interferon-a:

A

turns off osteoclasts, aimed at bone lesions (how do we ensure only the lesion osteoclasts are turned off?)

151
Q

Functions of thalidomide:

A

anti-TNFa-immunomodulating, inhibits angiogensis

152
Q

Pink stained kidney indicates:

A

amyloid in kidney, light chain deposition, deproteinaseous material

153
Q

Test to detect amyloid in kidney:

A

Congo red staining, polarized light, apple green

154
Q

Plasma cell disorder with increased amyloid levels (amyloidosis):

A

any

155
Q

Fibrillary protein deposited in various tissues, may damage organs:

A

amyloid

156
Q

plasma cell neoplasm, amyloid derived from all or part of monoclonal Ig light chain secreted by plasma cells:

A

primary amyloidosis

157
Q

TF? Amyloidosis is always related to plasma cell disorders.

A

F, can be seen by itself

158
Q

These combine to form amyloid fibrils:

A

protofilaments

159
Q

Test to id amyloid fibers:

A

congo red, apple green birefringence under polarized light or EM

160
Q

Risk factors for primary amyloidosis:

A

60-70yo, male (2/3)

161
Q

How to dx primary amyloidosis:

A

demonstration of amyloid in biopsy specimen (Congo red stain)

162
Q

Test to id the type of amyloid in 1’ amyloidosis:

A

mass spec

163
Q

Oral manifestations of amyloidosis:

A

enlarged tongue, periorbital bleeding, should biopsy

164
Q

Waldenstrom’s macroglobulinemia:

A

IgM secretions, monoclonal protein (macroglobulin), diffuse infiltrate of neoplastic B-cells (small lymphos with plasmacytoid features) in bm, lymph nodes, liver and spleen

165
Q

Median survival of Waldenstrom’s macroglobulinemia:

A

4y

166
Q

Clinical presentation of Waldenstrom’s macroglobulinemia:

A

weaknes, fatigue, w8 loss, lymphadenopathy, large liver or spleen, hyperviscocity syndrome, typically 50-60yo

167
Q

hyperviscocity syndrome:

A

visual and nerve problems, bleeding (acquired factor deficiencies, cryoglobulinemia, proteins insoluble at temps below body)

168
Q

macroglobulin Ig:

A

IgM

169
Q

Ig precipitation at cold temperatures, in fingers is indicative of:

A

Waldenstrom’s macroglobulinemia

170
Q

Hyperviscocity in Waldenstrom’s macroglobulinemia is due to:

A

Inc IgM production, neoplastic production, can’t get through caps, think of eyes, bleeding, absorb clotting factors

171
Q

Tx for blood build up in eyes due to Waldenstrom’s macroglobulinemia:

A

plasmaphoresis to remove protein: blood run through machine, prevent retina destruction

172
Q

Gelling or precipitation of a monoclonal protein at low temp:

A

cryoglobulin

173
Q

Ig most often to become a cryglobulin:

A

IgM

174
Q

Clinical presentation of cryoglobulinemia:

A

sluggish blood flow, purpura, Reynaud’s phenomenon, gangrene

175
Q

artery spasm, dec blood, typically fingers, sometimes toes, rarely nose, ears, lips, turns white, then blue, numb, painful, red and burning when blood flow returns, Recurrent attacks - brittle nails w longitudinal ridges:

A

Reynaud’s phenom

Pathology (23 decks)

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