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Pathophys > Neoplastic DO > Flashcards

Neoplastic DO Flashcards

1
Q

what are four main types of WBC neoplasms?

A

1) . malignant lymphomas
2) . leukemias
3) . polycythemia vera
4) . plasma cell disorders

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2
Q

what type of tumors are found with non-Hodgkin’s lymphoma? where do these tumors arise? distribution at diagnosis?

A

monoclonal solid tumors of B or T cells; arise in lymphoid tissues (usually nodes); usually widely distributed at diagnosis

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3
Q

what is the usual way of acquiring mutations in non-Hodgkin’s?

A

chromosomal translocations

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4
Q

the main types of non-Hodgkin’s lymphoma (5)

A

1) . diffuse large B cell lymphoma
2) . follicular lymphoma
3) . small lymphocytic lymphoma
4) . MALT lymphoma
5) . Burkitt’s lymphoma

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5
Q

three treatment options for non-hodgkin’s

A

chemo, radiation and immunotherapy

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6
Q

non Hodgkin’s: _________ type is more important than ______ in prognosis

A

histologic type > stage

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7
Q

NHL more common in what gender? two specific risk factors for it?

A

men

H. pylori (MALT lymphoma of stomach) and immunocompromise (several NHL)

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8
Q

what type of symptoms in non-hodgkins?

A

B symptoms: fatigue, malaise, night sweats, fever, weight loss

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9
Q

where do the majority of non-Hodgkin’s originate? how do most present?

A

in the nodes and present as non tender lymphadenopathy

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10
Q

where do NHL’s metastasize?

A

other lymphoid tissues and bone marrow (follow cell of origin, B or T)

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11
Q

B cell NHL goes to where in lymph node?

A

goes to germinal centers and mantles, outer white pulp

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12
Q

T cell NHL goes to where in lymph node?

A

superior mediastinum, paracortical zones, inner white pulp

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13
Q

follicular lymphomas form follicles where? what’s their origin? what’s their prognosis?

A

in nodes; B cell; better prognosis

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14
Q

what are the two translocations for follicular lymphomas?

A

11:14 or 14:18

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15
Q

follicular lymphoma: ___ heavy chain becomes contiguous with oncogene product

A

Ig

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16
Q

most NHL look ______ and lack __________ __________

A

bland and lack normal variability

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17
Q

most NHL and HL produce __________- _____ dysfunction with propensity towards infection

A

generalized-cell

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18
Q

most common NHL?

A

diffuse large B cell

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19
Q

Diffuse Large B cell: patient type? some related to what two infections? often _______ at presentation

A

older adults
related to EBV or HIV infection
often multifocal (nodal and extranodal)

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20
Q

progression and treatment of diffuse Large B cell

A

rapidly fatal if untreated

R-CHOP protocol (rituximab and chemo)

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21
Q

what does diffuse large B cell histology look like?

A

no follicles being formed, very bland and uniform

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22
Q

follicular NHL: / of adult NHL in US. patient type? where is it found? symptomatic?

A

1/3 of US adults
older adults
usually only nodal involvement and asymptomatic

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23
Q

prognosis of follicular NHL? treatment?

A

slow growing, prolonged survival; if healthy then offered chemo, if going to die from something else first then just clinically follow

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24
Q

50% of follicular NHL may transform into which type of NHL?

A

diffuse large B cell

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25
Q

small lymphocytic NHL: ___-_________ B cell form. lacks formation of what? patient type? where is it found at diagnosis?

A

well-differentiated; lacks follicle formation; older adults, often systemic involvement at diagnosis

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26
Q

follicular NHL histology looks like?

A

large purple circles (space between)

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27
Q

progression of small lymphocytic?

A

slow, seldom fatal

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28
Q

small lymphocytic: “______ ____ of chronic lymphocytic leukemia”

A

solid phase

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29
Q

histology of small lymphocytic

A

small bluish purple dots very close together

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30
Q

Burkitt’s Lymphoma is a ___ cell lymphoma. endemic where? common arises from what body part?

A

B cell lymphoma (B cell proliferation); endemic in Africa; commonly arises in jaw (from cervical lymph nodes) and involves abdomen

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31
Q

which type of NHL is the fastest growing solid tumor in humans?

A

Burkitt’s lymphoma

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32
Q

burkitts: patient type? endemic cases strongly linked to what infection?

A

children and young adults; EBV infection

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33
Q

burkitts treatment?

A

curable with chemo

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34
Q

what is the translocation for burkitts?

A

8: 14 (myc oncogene moved next to Ig heavy chain gene)

* *cell multiplies explosively when told to make antibodies

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35
Q

histology for burkitts

A

“starry sky”
lipid droplets inside macrophages
(macrophages engulf lipid from dead tumor cells)

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36
Q

hodgkins: curable? patient type? usually presents as what two types of mass?

A

common, usually curable; affects young adults (15-140) and less commonly older adults (>55); neck or mediastinal mass

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37
Q

Hodgkin’s: origin of malignant cell? name of malignant cell?

A

unknown, likely B cell

Reed- Sternberg (R-S) cell

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38
Q

what is required for diagnosis of HL?

A

R-S cell

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39
Q

HL: tumor masses comprised largely of what?

A

inflammatory reaction to CA

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40
Q

R-S cells: account for what minority of tumor cells? what do nuclei look like? what do Nucleoli look like? surrounded by what color cytoplasm?

A

<1%
bi-lobed (mirror image) nuclei
owl’s eye nucleoli
pink/lavender cytoplasm

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41
Q

R-S cells: CD15 is _________ (except one type called nodular lymphocyte predominant)

A

positive

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42
Q

R-S cells are typically surrounded by what?

A

reactive lymphocytes

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43
Q

HL: ________ is more important in diagnosis

A

staging

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44
Q

HL: __________ lymphadenopathy. mass usually limited to _____ _______

A

painless; above diaphragm

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45
Q

HL: “___-____” fevers…what type of symptoms?

A

Pel-Ebstein

B symptoms: intermittent spiking fevers, night sweats, weight loss

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46
Q

how is the prognosis for people with HL B symptoms?

A

worse prognosis than asymptomatic people

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47
Q

5 different types of HL

A

1) . nodular/follicular lymphocyte predominant
2) . lymphocyte predominant (classical)
3) . mixed cellularity
4) . lymphocyte depleted
5) . nodular sclerosis

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48
Q

nodular lymphocyte predominant: negative for what? noted for late _________

A

CD15 negative

late recurrence is common (these patients are followed more closely)

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49
Q

lymphocyte predominant: mostly ____, __________ lymphocytes. RS cells may be very ________

A

small, monotonous

rare

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50
Q

Mixed cellularity: many ____ cells and variants

A

RS

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51
Q

lymphocyte depleted: mostly ________ cells, often _________ stage at presentation

A

cancer cells; advanced stage

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52
Q

which type of HL is the most common?

A

nodular sclerosis

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53
Q

nodular sclerosis: presence of _______ _______ bands

A

dense collagen

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54
Q

what is the main reason for typing HL?

A

to rule in/out nodular lymphocyte predominant type

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55
Q

Stage I of HL

A

one node group or organ

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56
Q

Stage II of HL

A

one side of the diaphragm involving 2 or more lymph node groups

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57
Q

Stage III of HL

A

two or more lymph node groups on both sides of the diaphragm

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58
Q

Stage IV of HL

A

extra nodal involvement- marrow or two extra lymphatic organs (skin, liver, lung)

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59
Q

Stage IV can be further classified into what two types?

A

A- no systemic symptoms

B- means fever, weight loss (>10%), or night sweats

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60
Q

staging of HL involves what 3 tests?

A

node biopsy, CT chest/abd, PET

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61
Q

treatment of stage 1 and 2A

A

radiation

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62
Q

HL: get biopsy of _________ _____ _______ in suspected advanced disease

A

bilateral bone marrow

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63
Q

HL Stages IIB and higher treatment

A

combination chemo (50% cure rate at stage IV)

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64
Q

what is a leukemia?

A

replacement of bone marrow by cancerous blood cells (usually originates in packed marrow), which then spills over into bloodstream

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65
Q

leukemias can be what two types of cells?

A

lymphocytes OR myeloids (lymphoma is always lymphocytes)

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66
Q

leukemias can infiltrate which tissues?

A

liver, spleen, nodes, brain

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67
Q

what s the most common CA of children?

A

leukemia

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68
Q

is there a staging system for leukemia?

A

no due to infiltrative nature of WBC

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69
Q

acute leukemia: cells that fail to ______, differentiation is ______

A

mature (blast stage); poorly-differentiated

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70
Q

is acute or chronic leukemia more dangerous?

A

acute is more aggressive and deadly (death within weeks-months)

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71
Q

acute leukemia presents with what two things?

A

acute cytopenia (marrow replaced by cancer cells) and bone pain/aches from marrow expansion

72
Q

acute leukemias: _________ bleeding present

A

spontaneous

73
Q

chronic leukemia: cells that _______, differentiation is _____

A

mature; well-differentiation

74
Q

chronic leukemia patients present with one of two things on lab tests?

A

present with cytopenia OR leukocytosis

75
Q

chronic leukemia: what can happen to organs? (2)

A

organomegaly or lymphadenopathy

76
Q

how is chronic leukemia usually found?

A

secondarily by testing of a mass or cytopenia on labs

77
Q

lymphoid leukemias are precursors of? infiltrate what two things?

A

precursors of lymphocytes; spleen and nodes

78
Q

myeloid leukemias are usually precursors of ___________. Interfere with maturation of?

A

granulocytes (can be erythrocyte or platelet precursors tho)
maturation of all blood cells

79
Q

4 leukemias

A

1) . acute lymphoblastic leukemia (ALL)
2) . acute myeloid leukemia (AML)
3) . Chronic lymphocytic leukemia (CLL)
4) . chronic myeloid leukemia (CML)
* **ALL can be seen in adults but AML, CLL, CML more adult

80
Q

what is the classic childhood leukemia?

A

ALL

81
Q

leukemias can be caused by what three chromosomal probs?

A

translocations, inversions, and deletions (unknown how these chromosomes changes occur)

82
Q

leukemia disrupts genes that do what?

A

regulate blood cell development

83
Q

what is the Philadelphia chromosome?

A

characteristic of CML (some acute leukemias) where part of chromosome 9 is switched (translocated) with a part of chromosome 22 = new chromosome 22 has new BCR-ABL gene

84
Q

what does the new BCR-ABL gene code for?

A

a tyrosine kinase = potent oncogene

85
Q

ALL: peak incidence age? prognosis for adult ALL? risk factors for ALL?

A

4 y/o
worse prognosis for adult ALL
few risk factors known but radiation exposure and Down’s

86
Q

signs and symptoms of ALL (6)

A

fatigue/SOB, fever, night sweats, bruising/bleeding (bleeding gums), bone pain, increased infectious risk

87
Q

ALL is what type of mutation?

A

spontaneous

88
Q

ALL: ______ involvement more common; what two organs can be enlarged? two other things seen in ALL

A

CNS; spleen and liver; petechiae and lymphadenopathy

89
Q

ALL: CBC results

A

> 30% lymphoblasts (anemia, thrombocytopenia)

90
Q

ALL: bone marrow biopsy results

A

packed marrow, >20% lymphoblasts

91
Q

besides CBC and biopsy, what two other tests might you do for ALL?

A

LP (to assess CNS involvement) or CT chest/abd

92
Q

what are the three phases of chemo for ALL?

A

1) . induction therapy- kills tumor cells (initial phase)
2) . consolidation therapy- knock off surviving cells (maintains remission)
3) . maintenance therapy- prolongs symptom free survival

93
Q

ALL: cancerous and normal marrow cells die by the _______ and what pours into the blood?

A

pound; K, uric acid, get metabolic acidosis

94
Q

ALL: if chemo fails what is next tx?

A

bone marrow transplant (kill off marrow again before transplant)

95
Q

___% of children with ALL get apparent cure

A

90%

96
Q

AML: leukemia of __________. potential risk factors? (6)

A

adulthood; downs, radiation exposure, benzene, previous CA chemo, CML, smoking

97
Q

signs/symptoms of AML

A

SAME AS ALL: fatigue/SOB, night sweats, bruising/bleeding, bone pain, increased infectious risk (same lymph swelling, organ enlargement, etc as ALL)

98
Q

one staging classification of AML M0-M7

A 
M0- minimal differentiated
M1- AML with granulocyte maturation
M2/M3- slightly more mature, heading down granulocyte pathway (MOST COMMON ONES)
M4/M5- going down monocyte pathway
M6- trying to become erythrocytes
M7- trying to become platelets
99
Q

which stage of AML are auer rods present?

A

a lot in M3, little in M2 (red stained rods)

100
Q

what do auer rods mean?

A

tells you that cells are immature granulocytes (no lobed nucleus yet)

101
Q

AML: biopsy results

A

packed marrow, myeloid line precursors with varying maturation

102
Q

AML: CBC results

A

> 30% myeloblasts, anemia, thrmbocytopenia

103
Q

untreated AML is fatal within ______. treatment?

A

weeks

tx: chemo (3 stages), M3 stage responds best; bone marrow transplant less common in adults

104
Q

what spills into blood when a person has AML?

A

SAME AS ALL type

hyperkalemia, hyperuricemia, and metabolic acidosis

105
Q

CLL: usually cancer of ?

A

immature, nonfunctional B cells

106
Q

what is CLL’s “liquid phase of small lymphocytic lymphoma?”

A

when the cancer cells spill into the blood stream and invades other tissues to form small masses

107
Q

what is the only known risk factor for CLL?

A

ataxia-telangiectasia

108
Q

what is the most common cause of adult leukemia?

A

CLL (peak incidence >60yr)

109
Q

what is the most common mutation for CLL?

A

deletion of chromosome 14 long arm (good prognosis)

110
Q

CLL: CBC results

A

lymphocytes (>5000/ul, often much higher)

111
Q

CLL: bone marrow biopsy results

A

infiltration with mature lymphocytes

112
Q

CLL histology results

A

“smudge cells”

CA cells deficient in cytoskeletal vimentin, fragile and crush on smear (higher smudges have better prognosis)

113
Q

CLL: cancer cells can infiltrate ______ ______. (can get what three things from this?)

A

lymphoid tissues: lymphadenopathy, splenomegaly, and small lymphocytic lymphoma

114
Q

CLL: if infiltrates the marrow, what two things can it cause?

A

anemia and thrombocytopenia

115
Q

CLL: are cancer cells functional?

A

NO, defects in complement fixation and antibody production

116
Q

what is the problem with bacteria/infection in people with CLL?

A

When there’s a defect in antibody production, you get a decrease in optimization of the immune system. If the body can’t optimize (place antigen and complement protein on bacteria) appropriately, it cant identify bacteria and macrophage wont destroy it. Encapsulated bacteria flourish

117
Q

what three bacteria can flourish with CLL?

A

S pneumo, S aureus, H flu

118
Q

small percentage of CLL turn into?

A

diffuse large-cell lymphoma (rapidly fatal Richter’s syndrome)

119
Q

CLL: symptomatic? survival risk?

A

often asymptomatic; untreated survival measured in years

120
Q

high risk/troublesome CLL treated with?

A

ibrutinib (tyrosine kinase inhibitor)- stops abnormal B cells from dividing

121
Q

typical presentation for CLL?

A

adult with unexplained lymphocytosis with leukocytosis

122
Q

CML results in overgrowth of? which type of precursors dominate?

A

normally maturing and functional myeloid cells; granulocyte precursors dominate

123
Q

CML: patient type? two known risk factors for it? cancer cells contain what special chromosome?

A

middle-age adults
radiation and benzene
Philadelphia chromosome

124
Q

survival for CML?

A

people can live months to years with this

125
Q

CML: CBC results

A 
ridiculously high WBC (>100K)
high basophil count
marked left shift (immature leukocyte)
low leukocyte alkaline phosphatase
anemia and thrombocytopenia
126
Q

why do you get anemia and thrombocytopenia in CML?

A

CA cells crowd out the bone cells

127
Q

what test is not normally required for CML?

A

bone marrow biopsy

128
Q

how do granulocytes show up on histology for CML?

A

they are black because they are negative for alkaline phosphatase

129
Q

what is the chronic phase of CML?

A

non specific symptoms, where patient has anemia and thrombocytopenia (variable length)

130
Q

what is thrombocytopenia?

A

low platelet count

131
Q

what is the accelerated phase of CML?

A 
*if the pt lives long enough*
lasts 6-12 months
massive splenomegaly
basophilia
typical leukemia symptoms (fever, night sweats, weight loss, bone pain)
132
Q

what is a blast crisis? how long does it last? what forms in the blood? what do cancer cells infiltrate? tx?

A
  • terminal event of someone with CML where cancer turns from mature chronic to acute immature leukemia
  • lasts 3 months or less
  • increased immature WBC forms in blood (>30% blasts)
  • infiltrate CNS and lymphoid organs
  • responds poorly to tx
133
Q

what is leukostasis? what can it cause? what leukemia is it found in?

A
  • plugging of small vessels due to massive numbers of WBC (BLOOD SLUDGING)
  • can cause brain ischemia and infarcts of other organs
  • found in CML blast crisis
134
Q

CML treatment: what controls symptoms? what suppresses cancer cells? curative?

A

symptoms: busulphan and hydroxyurea
suppresses cancer cells: alpha-interferon +/- cytarabine
newer drug: Imatinib & dasatinib
allogenic bone marrow transplant may be curative

135
Q

what is polycythemia? what two things is it due to?

A

abnormally high hemoglobin

  • relative rise due to loss of plasma volume (dehydration)
  • absolute rise due to increased red cell mass
136
Q

absolute rise in hemoglobin can be what two types?

A

primary: problem with red blood cells (red cell mass)

secondary- problem elsewhere

137
Q

what are five secondary causes of absolute rise in hemoglobin?

A

1) . renal artery insufficiency/stenosis
2) . emphysema/sleep apnea
3) . anabolic steroid use
4) . post-kidney transplant
5) . altitude (>10,000 ft)- hypoxia induces it

138
Q

what is polycythemia vera (PV)?

A

proliferation of myeloid stem cells

139
Q

PV: sensitive to what cell type? what do most cells mature into? are these cells functional?

A

erythropoietin-sensitive; mostly mature into red cells (high WBC and platelets as well); all are fully functional

140
Q

PV: affects what patient type? what is the problem with PV?

A

older middle age individuals

problems mainly due to increased blood viscosity (blood sludges up)

141
Q

what are five results of increased blood viscosity due to PV?

A

organ congestion (plethoric face), venous thrombosis (DVTs common), venous rupture (thinning of walls) and hemorrhage, decreased cardiac output, platelet dysfunction later

142
Q

what type of mutation occurs in PV?

A

JAK2 (janus, tyrosine, kinase)

143
Q

what does JAK2 mutation do?

A

its a cytokine receptor (that stays turned on) that stimulates RBC, platelet, and neutrophil development

144
Q

besides cytokine activation, what two things also result from a JAK2 mutation?

A

essential thrombocytosis and primary myelofibrosis

145
Q

PV: normal stem cells eventually replaced by what? survival rates? death occurs due to?

A

normal cells replaced by mutated cells; generally normal survival rates; death due to transformation into AML

146
Q

how do you diagnose someone with PV?

A

A1 + A2 + A3

OR A1 + A2 + any B

147
Q

A1-B4 values for PV

A 
A1-Hct > 52% male, 46% female
A2-normal pO2
A3-splenomegaly
B1-platelet > 400K
B2-WBC > 12K
B3-leukocyte alk phos > 100
B4-elevated vit B12
148
Q

what is the minor mystery of PV?

A

itchiness after hot shower

149
Q

two treatments for PV

A

therapeutic phlebotomy to control RBC mass or JAK2 inhibitors (ruxolitinib)

150
Q

what does treatment with chemo do to PV?

A

increased transformation to AML

151
Q

what are five types of plasma cell dyscrasias?

A

1) . multiple myeloma
2) . MGUS
3) . Waldenstrom’s macroglobulinemia
4) . amyloidosis B
5) . lymphoplasmacytic lymphoma

152
Q

what happens to bone marrow in multiple myeloma (aka plasma cell myeloma)? present in what % of people

A

there are multiple punched out lytic lesions in the marrow and cortex BUT only present in 50% of affected patients

153
Q

plasma cell myeloma patient type? what type of CA?

A

older black men (over 70); differentiated B cell cancer

154
Q

PCM: cells secrete what? what can detect them?

A

a complete immunoglobulin (M protein) and/or at least a light chain (kappa or lambda, never both)
**basically activated B cells are creating antibodies
detectable on serum or urine protein electrophoresis

155
Q

PCM: always involves what?

A

bone (only 50% of cases will you see lytic lesions)

156
Q

PCM: disruption of bone and marrow leads to ________

A

anemia (neutropenia and thrombocytopenia less common)

157
Q

bone lysis in PCM causes?

A

hypercalcemia

158
Q

PCM: light chain secretion plugs what and therefore leads to?

A

renal tubules, leading to renal insufficiency (“myeloma kidney”)

159
Q

most PCM tumors secrete what M protein type? what % only secrete light chains?

A

IgG- 55%

light chain only- 18% (bence jones protein)

160
Q

most myelomas produce what two things?

A

both complete and BJ proteins

161
Q

what is a common finding on serum electrophoresis for PCM? urine electrophoresis?

A

serum: complete immunoglobulin seen “M spike”
urine: Bence-jones proteins, since they are filtered at glomerulus

162
Q

what are two main differences seen on normal serum protein electrophoresis vs PCM electrophoresis?

A

smaller albumin level and way elevated antibody level (“Y”) on PCM

163
Q

what is the usual method of diagnosis for PCM?

A

serum M protein and/or urine bence-jones protein (serum level >3g/dl)

164
Q

what is seen on bone marrow biopsy for PCM?

A

> 10% plasma cells (normal is about 3%)

**don’t really need this test tho

165
Q

what are signs of end organ damage in PCM?

A

1) . lytic bone lesions/osteoporosis
2) . anemia
3) . hypercalcemia: STONES, BONES, GROANS
4) . myeloma kidney- decreased GFR*

166
Q

what are some paraneoplastic problems associated with PCM? (7)

A

1) . Osteoporosis
2) . Pathologic fractures
3) . Hypercalcemia
4) . Infections (suppression of normal plasma cells)
5) . Anemia & neutropenia (crowding out of normal cells)
6) . Kidney failure (BJ precipitates in renal tubules)
7) . Plasma cell leukemia (terminal stage)

167
Q

treatment for PCM

A

high dose chemo to kill existing marrow
maybe allogenic bone marrow transplant
high mortality*

168
Q

asymptomatic “smoldering” PCM patients man only require what to manage disease?

A

prophylactic bisphosphonates

169
Q

what is MGUS?

A

benign monoclonal proliferation of plasma cells, which then produce a lot of antibodies

170
Q

__% of MGUS go on to develop plasma cell myeloma

A

25%

171
Q

MGUS: tumor cells produce what?

A

single complete immunoglobulin (usually IgG)

172
Q

MGUS:

A

<10%, <3g

NO end organ damage

173
Q

tx for MGUS?

A

precursor to PCM so follow these patients for the rest of their lives

174
Q

difference between PCM and MGUS?

A

don’t get hypercalcemia or spitting out of light chains (no renal insufficiency) in MGUS

175
Q

MGUS vs PCM electrophoresis

A

PCM: smaller albumin spike but higher antibody (Y) spike

Pathophys (13 decks)

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