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Oral Path 2, Exam 3 > Malignant Mesenchymal Tumors > Flashcards

Malignant Mesenchymal Tumors Flashcards

1
Q

Malignant mesenchymal tumor of fibrous origin

A

Fibrosarcoma

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2
Q

Malignant mesenchymal tumor of nerve origin

A

Malignant peripheral nerve sheath tumor (MPNST)

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3
Q

Malignant mesenchymal tumor of endothelial cell origin

A

Kaposi cell

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4
Q

Malignant mesenchymal tumor of muscle origin

A

Rhabdomyosarcoma

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5
Q

Lymphoreticular tumors (4)

A

Langerhans Cell Histiocytosis
Leukemia
Lymphoma
Multiple Myeloma/Plasmocytoma

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6
Q

Malignancy of fibroblastic differentiation

A

Fibrosarcoma

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7
Q

Fibrosarcoma can be seen as a ___ ___ mass or as an ____ lesion

A

Soft tissue

Intrabony

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8
Q

When do patients report pain with a fibrosarcoma?

A

Late

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9
Q

Describe the histopathology of fibrosarcoma

A

Fascicles of spindle-shaped cells often forming a “herringbone” pattern. Variable number of mitoses

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10
Q

Treatment for fibrosarcoma

A

Wide to radical surgical excision

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11
Q

Does fibroscarcoma respond to radiation and chemotherapy?

A

No

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12
Q

Describe the prognosis of fibrosarcoma

A

Only about 1/2 live past 5 years

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13
Q

Routes of metastasis for fibrosarcoma via the blood

A

Lung, liver, bone

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14
Q

Also known as neurogenic sarcoma or neurofibrosarcoma

A

Malignant Peripheral Nerve Sheath Tumor (MPNST)

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15
Q

What are half of MPNSTs associated with?

A

NF1

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16
Q

Is the mean age of an MPNST patient higher or lower if the patient has NF1

A

Younger if the patient has NF1 (29 vs 46)

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17
Q

What are radiographic features associated with MPNST?

A

Widening of the canal and mental foramen, scooping of cortex. Obliteration of mandibular canal

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18
Q

What shape are the cells and nuclei of MPNST? Is there mitosis?

A

Spindle-shaped cells with wavy nuclei

Yes

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19
Q

What is the treatment for MPNST?

A

Surgical resection, radical excision, amputation +/- radiation

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20
Q

Is the prognosis better or worse for an MPNST patient with NF1

A

Prognosis is worse with NF1

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21
Q

First described as a disease affecting elderly white males of Mediterranean descent but was also seen in sub-Saharan Africans, transplant recipients, and HIV+ males

A

Kaposi Sarcoma

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22
Q

Kaposi Sarcoma is caused by an infection with ___-__

A

HHV-8

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23
Q

4 clinical presentations of Kaposi sarcoma

A
  1. Classic
  2. Endemic (African)
  3. Iatrogenic (Transplant-associated)
  4. Epidemic (AIDS-related)
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24
Q

Where does the classic form of Kaposi sarcoma usually appear? In what types of patients?

A

On the lower extremities of elderly patients, most often male

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25
Q

Kaposi Sarcoma is _____ (painful/painless), with a ____ color

A

Painless

Purple-red

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26
Q

Describe the transformative stages for Kaposi Sarcoma

A

Macule –> Plaque –> Tumor

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27
Q

Clinical feature suggesting Kaposi Sarcoma

A

Does not blanch on pressure

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28
Q

What age range is mainly affected by Endemic Kaposi Sarcoma?

A

Wide age range - esp. young adults and children

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29
Q

How can Endemic Kaposi Sarcoma present?

A

Anywhere from indolent skin lesions to aggressive tumors

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30
Q

Young children with Endemic Kaposi Sarcoma will often have tumors within their ___ ___

A

Lymph nodes (lymphadenopathic)

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31
Q

What type of transplants are mainly associated with Iatrogenic Kaposi Sarcoma?

A

Solid organ transplants (0.5% renal)

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32
Q

When will a patient develop Iatrogenic Kaposi Sarcoma?

A

Months to years after their transplant

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33
Q

What areas do Iatrogenic Kaposi Sarcomas affect?

A

Skin and oral mucosa

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34
Q

What may cause regression of Iatrogenic Kaposi Sarcoma?

A

Reducing degree of immune-suppression

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35
Q

Epidemic Kaposi Sarcoma mainly affects:

A

HIV-infected adult male homosexuals

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36
Q

Epidemic Kaposi Sarcoma skin lesions have a predilection for what areas?

A

Face and lower extremities

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37
Q

The oral cavity is the initial site of presentation for this lesion in ~22% of patients

A

Epidemic (AIDS-related) Kaposi Sarcoma

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38
Q

True/False: Oral involvement is rare in Epidemic (AIDs-related) Kaposi Sarcoma?

A

False - 70% will develop oral lesions

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39
Q

What areas in the oral cavity are affected by Epidemic Kaposi Sarcoma?

A

Hard palate, gingiva, tongue

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40
Q

How can Epidemic Kaposi Sarcoma cause tooth movement?

A

If it invades the bone

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41
Q

Histology of Kaposi Sarcoma: Cellular ____ cell tumor within _____ tissue and _____ blood

A

Spindle
Connective
Extravasated

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42
Q

Kaposi Sarcoma has many poorly defined ___ ___

A

Vascular slits

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43
Q

Kaposi Sarcoma has ____ positivity in endothelial cells

A

HHV-8

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44
Q

Treatment for Kaposi Sarcoma for small lesions? For larger lesions?

A

Excision for small cosmetically problematic lesions
Radiation
Injections of chemotherapeutic agents

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45
Q

Prognosis for Classic Kaposi Sarcoma

A

Fair - patients usually die of something else (MI, CVA, etc.)

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46
Q

Prognosis for Endemic Lymphadenopathic Kaposi Sarcoma

A

Poor

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47
Q

Prognosis for Iatrogenic Kaposi Sarcoma

A

Fair to poor

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48
Q

Prognosis for AIDs related Kaposi Sarcoma

A

Fair

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49
Q

3 types of Rhabdomyosarcoma

A
  1. Embryonal
  2. Alveolar
  3. Pleomorphic
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50
Q

How common is Rhabdomyosarcoma? Who does is affect?

A

Rare

Children or adolescents

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51
Q

Most common soft tissue sarcoma in children under 15 yo

A

Rhabdomyosarcoma

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52
Q

Most common intraoral site for Rhabdomyosarcoma

A

Palate

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53
Q

Radiographic feature of Rhabdomyosarcoma

A

Expansion

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54
Q

Term to describe Rhabdomyosarcoma that grows in a body cavity

A

Sarcoma Botryoides

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55
Q

What does Sarcoma Botryoides look like?

A

A bunch of grapes

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56
Q

What kind of cells does Rhabdomyosarcoma have? What type of nuclei?

A

Small cells with hyperchromatic nuclei

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57
Q

What might you see in the histology of Rhabdomyosarcoma

A

Strap-shaped rhabdomyoblasts with cross striations

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58
Q

Treatment for Rhabdomyosarcoma

A

Wide excision, multiagent chemotherapy, post-op radiation

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59
Q

What does prognosis for Rhabdomyosarcoma depend on?

A

Type, location, stage, age

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60
Q

Spectrum of disorders characterized by proliferation of histiocyte-like cells accompanied by varying numbers of eosinophils, lymphocytes, plasma cells and multinucleated giant cells

A

Langerhans Cell Histiocytosis

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61
Q

Langerhans Cell Histiocytosis was previously known as:

A

Histiocytosis X

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62
Q

What are Langerhans Cells?

A

Tissue-resident Macrophages (related to monocytes) that serve as antigen-presenting cells

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63
Q

Clonal proliferation confirms that Langerhans Cell Histiocytosis is a ____ process

A

Neoplastic

64
Q

What is significant about the age range for Langerhans Cell Histiocytosis?

A

More than half of cases are in patients younger than 15

65
Q

3 Clinical presentations of Langerhans Cell Histiocytosis

A
  1. Acute Disseminated
  2. Chronic Disseminated
  3. Eosinophilic Granuloma (monostotic or polyostotic)
66
Q

Acute Disseminated Histiocytosis is also called

A

Letterer-Siwe Disease

67
Q

Who is affected by Acute Disseminated Histiocytosis?

A

Infants

68
Q

What can occur due to Acute Disseminated Histiocytosis?

A

Skin rash, splenic, hepatic, and marrow involvement.

69
Q

Chronic Disseminated Histiocytosis is also called

A

Hand-Schuller-Christian Disease

70
Q

Who is affected by Chronic Disseminated Histiocytosis?

A

Older children

71
Q

Which is more aggressive: Acute or Chronic Disseminated Histiocytosis?

A

Acute

72
Q

What is the classic triad for Chronic Disseminated Histiocytosis?

A
  1. Exopthalmos
  2. Diabetes insipidus (kidneys unable to prevent water excretion)
  3. Bone lesions
73
Q

What is significant about Eosinophilic granulomas in Langerhans Cell Histiocytosis

A

They are intrabony only - no visceral involvement

74
Q

What patients are affected by eosinophilic granulomas?

A

Teenagers and young adults

75
Q

Which patients have polyostotic eosinophilic granulomas? Which have monostotic?

A

Poly - Teenagers

Mono - Adults

76
Q

What are the most frequent bones affected by Langerhans Cell Histiocytosis

A

Skull, Mandible, Ribs, Vertebrae

77
Q

Severe bone loss from Langerhans Cell Histiocytosis can resembly:

A

Periodontal disease

78
Q

Superficial bone has a ____ ____ radiographic appearance with Langerhans Cell Histiocytosis. Teeth appear to be _____ due to extensive _____ involvement.

A

Scooped out
Floating
Alveolar

79
Q

____ _____ in the cytoplasm of Langerhans cells can be seen by an electron microscope

A

Birbeck bodies

80
Q

Treatment for Acute Langerhans Cell Histiocytosis

A

Chemotherapy

81
Q

Treatment for Chronic Langerhans Cell Histiocytosis

A

Radiation and/or chemotherapy

82
Q

Treatment for Eosinophilic Granuloma

A

Curettage or radiation

83
Q

Prognosis for Acute Langerhans Cell Histiocytosis

A

Poor

84
Q

Prognosis for Chronic Langerhans Cell Histiocytosis

A

Guarded

85
Q

Prognosis for Eosinophilic Granuloma

A

Good

86
Q

Group of hematologic malignancies characterized by tumor cells circulating in the blood

A

Leukemia

87
Q

Where does leukemia begin?

A

In the bone marrow

88
Q

In leukemia, what type of cells go through malignant transformation and proliferation - eventually overflowing into the peripheral blood

A

Hematopoietic stem cells

89
Q

4 broadly divided types of leukemia

A
  1. Lymphocytic
  2. Myelomonocytic
  3. Acute
  4. Chronic
90
Q

2 groups of lymphocytic leukemia

A
  1. Acute Lymphocytic Leukemia (ALL)

2. Chronic Lymphocytic Leukemia (CLL)

91
Q

2 groups of myelomonocytic leukemia

A
  1. Acute Myeloid Leukemia (AML)

2. Chronic Myeloid Leukemia (CML)

92
Q

Patients with leukemia often present with ____ _____

A

Myelophthisic anemia

93
Q

Myelophthisic anemia

A

Normal bone marrow cells replaced by leukemic cells

94
Q

Symptoms of myelophthisic anemia and their causes

A
  1. Fatigue, shortness of breath, pallor (decreased RBCs)
  2. Easy bruising (decreased platelets)
  3. Infection (decreased WBCs)
95
Q

Oral involvement is most often in ______ forms of leukemia

A

Myelomonocytic

96
Q

Focal proliferation of leukemic cells at one soft tissue site

A

Granulocytic sarcoma

97
Q

Oral clinical feature of leukemia

A

Diffuse gingival enlargement

98
Q

How do you diagnose leukemia?

A
  1. Finding increased atypical WBCs

2. Type determined by immunohistochemical/cytogenetic studies

99
Q

General histology of leukemia

A

Diffuse infiltration and destruction of normal tissue by sheets of poorly differentiated cells with either myelomonocytic or lymphoid characteristics

100
Q

3 treatments for leukemia

A

Chemotherapy, bone marrow/stem cell transplant, targeted gene therapy

101
Q

Is the prognosis for ALL better for adults or children?

A

Children

102
Q

Is the prognosis for AML better or worse if the patient is under 60 yo

A

Better if the patient is under 60

103
Q

What is the prognosis for CLL

A

Incurable

104
Q

What is the prognosis for CML

A

Indolent period has a better survival. Quick death after blast transformation

105
Q

Where does Hodgkin Lymphoma develop?

A

Lymph nodes

106
Q

Where does Non-Hodgkin Lymphoma arise from/

A

Mostly lymph nodes, but also soft tissue or bone

107
Q

Hodgkin Lymphoma has a _____ predilection

A

Male

108
Q

_______ is a common site of initial involvement for Hodgkin Lymphoma; however, _____ involvement is rare

A

H&N

Oral

109
Q

Hodgkin Lymphoma has a ______ age distribution

A

Bimodal

110
Q

Clinical feature of Hodgkin Lymphoma

A

One or more non-tender, palpable, rubbery-firm, enlarging lymph nodes

111
Q

Most involved lymph nodes in Hodgkin Lymphoma

A

Supraclavicular and Cervical

112
Q

Describe Category A and B for Hodgkin Lymphoma

A

A - no systemic signs

B - “B signs” (fever, weight loss, night sweats, generalized itching (pruritus))

113
Q

What type of cells are seen in Hodgkin Lymphoma

A

Reed-Sternberg cells

114
Q

What do Reed-Sternberg cells look like?

A

Owl-eyes or Pennies on a plate

115
Q

What is a disadvantage of treatment for Hodgkin Lymphoma

A

Treatment can result in post-treatment complications

116
Q

Is the prognosis better for Hodgkin Lymphoma or Non-Hodgkin Lymphoma

A

Hodgkin Lymphoma

117
Q

Is the prognosis better or worse for patients who show “B signs”

A

Worse

118
Q

Most post-treatment mortality with Hodgkin Lymphoma is due to:

A

Secondary malignancy or cardiovascular disease

119
Q

Are patients with Non-Hodgkin Lymphoma typically older or younger than patients with Hodgkin Lymphoma?

A

Older

120
Q

Which is more common: Hodgkin or Non-Hodgkin Lymphoma

A

Non-Hodgkin Lymphoma

121
Q

Prevalence of Non-Hodgkin Lymphoma is increased in patients who have ____ ____

A

Immunologic problems (ex: HIV, organ transplant, congenital and autoimmune disease)

122
Q

Where do most Non-Hodgkin Lymphomas arise?

A

Lymph nodes but some can be extranodal

123
Q

What is often the primary site for extranodal Non-Hodgkin Lymphoma

A

Oral cavity

124
Q

Where is Non-Hodgkin Lymphoma often found within the oral cavity?

A

Soft palate or buccal mucosa

125
Q

Non-Hodgkin Lymphoma lesions of the PDL may be mistaken for:

A

Periapical or periodontal disease

126
Q

What sign may a patient with Non-Hodgkin Lymphoma express if there is mandibular canal involvement?

A

Numb chin (paresthesia)

127
Q

Non-Hodgkin Lymphoma has a ____ consistency

A

Boggy

128
Q

What may an edentulous patient with Non-Hodgkin Lymphoma complain of?

A

“Denture is too tight”

129
Q

What might a vague oral pain in a patient with Non-Hodgkin Lymphoma be mistaken for?

A

Toothache

130
Q

Radiographic feature of Non-Hodgkin Lymphoma

A

“Moth-eaten” or ill-defined radiolucency and expansion

131
Q

What do you need to ID Non-Hodgkin Lymphoma

A

Immunohistochemistry

132
Q

What is the treatment if a patient has localized Non-Hodgkin Lymphoma

A

Radiation and chemo

133
Q

What is the treatment if a patient has generalized Non-Hodgkin Lymphoma

A

Chemo

134
Q

What do plasma cells produce?

A

Protein immunoglobulins (Ig) (also known as antibodies)

135
Q

What does clonal proliferation of one specific immunoglobulin type indicate?

A

Disease

136
Q

Multiple Myeloma/Plasmacytoma has ___ ___ origin

A

Plasma cell

137
Q

What are immunoglobulins made of?

A

2 heavy chains and 2 light chains (2 light = kappa and lambda)

138
Q

What is wrong with the heavy and light chains in multiple myeloma?

A

The light chain (usually kappa) is not attached to the heavy chain

139
Q

What happens to circulating unattached light chains?

A

They are filtered in the kidney and secreted in the urine (Bence Jones proteins)

140
Q

What is smoldering multiple myeloma? How is it diagnosed?

A

Asymptomatic - often by a chance finding on a blood test

141
Q

What type of patients often get MM?

A

Older patients (rare < 40)

142
Q

MM has a ____ predilection and affects ___ ___ 2x more than ___ ___

A

Male
Black men
White men

143
Q

Most common hematologic malignancy in black persons in the US

A

MM

144
Q

Most characteristic symptom of MM

A

Bone pain, especially lumbar spine

145
Q

Why would patients with MM experience pathologic fractures and renal failure?

A

Fractures due to tumor destruction of bone. Renal failure due to circulating light chain proteins

146
Q

What are metastatic calcifications (soft tissue) caused by in MM

A

Hypercalcemia secondary to tumor-related osteolysis

147
Q

Why would a patient with MM have petechial hemorrhages of skin and oral mucosa?

A

If platelet production is affected

148
Q

What would cause fever in MM?

A

Neutropenia and increased susceptibility of infection

149
Q

What may be the initial manifestation in patients with MM?

A

Deposition of amyloid (accumulation of light chains) in soft tissue

150
Q

Sites classically affected by amyloid:

A

Periorbital skin and oral mucosa (especially tongue)

151
Q

Periorbital skin lesion in MM appears:

A

Waxy, firm, plaque-like

152
Q

Tongue lesion in MM appears:

A

Diffuse enlargement, firmness, nodular, sometimes ulcerated

153
Q

Radiographic feature of MM

A

Punched out non-corticated radiolucencies, especially skull

154
Q

What might MM appear as in a radiograph?

A

Osteomyelitis

155
Q

What is the purpose of treatment for MM?

A

To control disease and keep patient comfortable

156
Q

Is the prognosis better or worse for younger patients? What about patients with comorbidities?

A

Better for younger patients. Worse for comorbidities

Oral Path 2, Exam 3 (6 decks)

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