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Oral Pathology Exam 2 > 2. WBC Neoplasms > Flashcards

2. WBC Neoplasms Flashcards

1
Q

What are the 3 Etiologies of Leukemia?

A
  1. Genetic Factors
    • Some Syndromes
    • Gene translocation (philadelphia translocation)
    • Genetic alterations of stem cells
      • Myelodysplasia
  2. Environmental
    • Pesticides, Benzene
    • Ionizing Radiation (WWII)
  3. Viruses
    • HTLV-1
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2
Q

What is the Pathophysiology of Leukemia?

A
  • Replacement of normal hematopoietic cells in bone marrow
  • Derived from a single transformed cell exhibiting clonal growth
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3
Q

What are the General Symptoms of Leukemia? (3)

A
  • Fatigue, SOB, Pallor
    • Decreased RBCs
  • Easy Bruising
    • Decreased Platelets
  • Infection
    • Decreased WBCs
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4
Q

What does Leukemia cause? (3)

A
  • Neutropenia
    • _​_Bacterial, viral and fungal infections
    • Oral ulcers, herpes, candida
  • Thrombocytopenia
    • Gingival bleeding
    • Palatal petechiae
  • Myelophthisic Anemia
    • Lack RBCs - hypoxia
    • Causes Extramedullary Hematopoiesis
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5
Q

What are the Oral Presentations and in what type of Leukemia are they normally seen?

A

Myelomonocytic forms of leukemia

  • Focal Soft Tissue Tumor Mass
    • Myeloid Sarcoma or Granulocytic Sarcoma
    • Firm, redish/purple mass
      • ~ Kaposi sarcoma
  • Diffuse Gingival Enlargement
    • ​Not just gm, but down in the vestibule
  • Mimic Periapical Ds
    • ​RL in bone
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6
Q

How is Leukemia usually diagnosed?

A
  • Increased #s of atypical WBCs in blood and bone marrow
  • Type is determined by:
    • Immunohistochemical and Cytogenetic studies
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7
Q

What are the Clinical Features of Hodgkin Lymphoma? (4)

A
  • Teenagers/young adults OR >50yrs
  • EBV linked to a significant number of lesions
  • 1 or more rubbery-firm, enlarging, non-tender lymph nodes
  • Rare intraorally
    • NHL is in the oral cavity
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8
Q

What are the Constitutional Symptoms of Hodgkin Lymphoma? (4)

A
  • Progressive Fever OR Pel-Ebstein Fever
  • Night sweats
  • Weight loss
  • Generalized Pruritis (itchiness all over body)
    • UNIQUE SYMPTOM
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9
Q

What does the Diagnosis of Hodgkin Lymphoma depend on?

A
  • Reed-Sternberg cells
    • ​Large, either multinucleated, or have a bilobed nucleus “owl eye”
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10
Q

What is the Treatment of Hodgkin Lymphoma?

A
  • ABVD
    • Adriamycin
    • Bleomycin
    • Vinblastine
    • Dacarbazine
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11
Q

What is the prognosis of Hodgkin Lymphoma

A

Stage - most important prognostic indicator

  • 10 yr survival
    • Stage I/II = 80-90%
    • Stage III/IV = 55-75%
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12
Q

What are the Clinical Features of Non-Hodgkin Lymphoma (NHL)? (4)

A
  • Most are B-cell in origin (85%)
  • Middle-aged to Older Adults
    • Not in kids, like HL can be
  • May develop in nodes (~75%) or extranodal sites:
    • spleen, mucosal lymphoid tissue (MALT), skin, CNS, bone, viscera
  • Some may involve bone marrow and spill over into blood becoming a leukemia
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13
Q

What is the nodal disease progression of NHL?

A
  • Nontender mass or lymph node enlarging over months, may be freely moveable –>
  • Expands to involve a set of local lymph nodes (cervical, axillary, inguinal) –>
  • Nodes become fixed/matted –>
  • Invasion into normal tissue
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14
Q

What are the Clinical Features of NHL in the Oral Cavity?

A
  • Usually extranodal ds
  • In Soft Tissue
    • _​_non-tender, diffuse swelling
    • Buccal vestibule, posterior hard palate, or gingiva
    • Normal to red/purple
    • Possibly ulcerated, often with a boogy consistency
  • In the Jaws
    • ​Vague pain, paresthesia, “numb chin” sign
    • Ill-defined/ragged RL
    • With time, expansion and perforation into soft tissue
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15
Q

What is the Histopathology of NHL?

A
  • Variably differentiated lymphocytic cells
  • Grow as infiltrative, diffuse sheets of relatively uniform cells
    • Diffuse Large B Cell Lymphoma
      • Wall to wall cells, with lots of apoptic cells
    • Follicular B Cell Lymphoma
      • Expansion of follicle germinal center
  • IHC always needed to ID which type of NHL
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16
Q

What is the Treatment for Low Grade (indolent type) NHL?

A
  • “Incurable”
  • Chemotherapy: Anti-CD20 monocolonal antibodies +/- CHOP (Cytoxan, Hydroxyrubicin (adriamycin), Oncovin (vincristine), Prednisone
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17
Q

What is the Treatment for Intermediate/High Grade (aggressive types) Localized Disease?

A
  • radiation therapy + chemotherapy
18
Q

What is the Treatment for Intermediate/High Grade (aggressive types) Generalized Disease?

A

Chemotherapy

19
Q

What constituets 98% of NHL Oral Lesions?

A
  • B Cell Lymphomas
    • Diffuse Large B cell lymphomas (~60%)
    • Follicular Lymphoma (~15%)
    • Marginal Zone Lymphoma (~12%)
20
Q

What are the Clinical Features of Diffuse Large B Cell Lymphoma?

A
  • Older adults
  • Localized
  • Rapidly growing mass in:
    • lymph nodes, waldeyer’s ring or extranodal sites (oral cavity)
  • Also can occur:
    • Transformation from a previous low grade lymphoma
    • Associated with HIV and other immunodeficiencies
21
Q

What is the pathogenesis of Burkitt Lymphoma?

A

8:14 translocation causes rapid growth

22
Q

What is the histologic pattern of Burkitt Lymphoma?

A
  • “starry sky”
    • macs gobbling up all of the dead cells leaving holes in the tissues
23
Q

What are the 2 types of Burkitt Lymphoma?

A
  • African Type (endemic)
    • _​_EBV almost always present
    • Usually a jaw lesion (50-70%) in young pt
  • American Type (sporadic)
    • ​Usually abdominal mass
      • May spread to jaw
24
Q

What is the Treatment and Prognosis for Burkitt Lymphoma?

A
  • Death within 6 months without tx
  • Tx: intensive chemotherapy
25
Q

What are the Clinical Features of Mycosis Fungoides? (4)

A
  • Cutaneous T cell Lymphoma
  • Stages:
    • Erythematous patch (eczematous) –> plaque –> tumor
  • Rare intraorally - usually appear late in ds course, after skin lesions
  • Sezary Syndrome
    • ​Aggressive systemic involvement leading to death in 2-3 yrs
26
Q

What are the Clinical Features of Angiocentric T Cell Lymphoma? (4)

A
  • Destructive tumor of midline of palate and nasal cavity may cause palatal perforation
  • Nasal stuffiness, epitaxis and pain may proceed
  • Significant number linked to EBV
  • Treatment
    • Radiation –> localized lesions
    • Chemotx –> disseminated ds
27
Q

What are the Clinical Features, Treatment, and Prognosis of Plasmacytoma?

A
  • Lymphoma of plasma cells, usually within bone but can be in soft tissue (extramedullary)
  • Solitary, well-defined or ragged unilocular radiolucency
  • ~25% of soft tissue lesions affect the H/N
  • Least aggressive end of the spectrum of Multiple Myeloma
  • Treated with Radiation
  • ~50% develop multiple myeloma within 2-3 yrs
28
Q

What are the Clinical Features of Multiple Myeloma? (5)

A
  • Lymphoma of plasma cells forming tumor masses within bone, sometimes extramedullary sites
  • Mostly in male, older adults
  • 1/2 of all bone malignancies
  • Begins in marrow with slow, asymptomatic growth over yrs –> elevation in its Ig (M protein), light chains (Bence-Jones protein) or heavy chains
  • Diagnosed when bone lesions finally cause pain, fractures
29
Q

What are the Secondary Effects of Multiple Myeloma? (4)

A
  • Hypercalcemia from bone destruction
  • Myelophthisic anemia, thrombocytopenia, neutropenia with attendant infections and coagulopathy
  • Light chain proteins that filter into renal tubules are toxic
  • Amyloid from light chains collects in organs (heart, tongue, GI tract, skin, and kidney)
30
Q

What is the pathology of Multiple Myeloma?

A

Affected bones (vertebrae, ribs, skull, mandible) develop multiple punched-out radiolucencies containing sheets of plasma cells

31
Q

How do you Diagnose Multiple Myeloma?

A
  • Biopsy of radiographic lesions
  • Bence-Jence Protein in urine
  • Detection of M protein in blood (monoclonal gammopathy)
32
Q

What is the Treatment and Prognosis for Multiple Myeloma?

A
  • Steroid + alkylating agents
    • 60% initial response
    • Frequent recurrence
  • Bisphosphonates
    • Inhibit bone resorption
      • Reducing fractures, pain, and hypercalcemia
    • Medication-related osteonecrosis of the jaws
  • 3-4 yr survival
33
Q

What are the Clinical Features of Langerhans Cell Histiocytosis? (6)

A
  • A group of related disorders caused by proliferation of Langerhans cells
    • ​Langerhans cels are related to monocytes and present antigen to T cells
  • Monoclonal proliferation (true neoplasm)
  • BRAF mutation noted in 40-60% of lesions
  • Lesions form where Langerhans and dendritic cells live
    • skin, lymph nodes, marrow, mucosa
  • Favored bones include:
    • skull, ribs, vertebrae, mandible
      • ~ locations to Multiple Myeloma
  • Wide age range (50% over 15yrs)
34
Q
  • Infants with bone marrow, skin and visceral involvement
  • Usually follows a very aggressive course
A

Acute Disseminated Histiocytosis

(Letterer-Siwe Ds)

35
Q
  • Bone, skin and viscera in older children
A

Chronic Disseminated Histiocytosis

(Hand-Schuler Christian Ds)

36
Q
  • Localized form in bone
  • Adults (monostotic) and teenagers (polyostotic)
  • Well-defined, but non-corticated radiolucency “scooped out”
A

Eosinophilic Granuloma of Bone

37
Q

What is the most common Clinical Presentation of Langerhans Cell Histiocytosis? (5)

A
  • Bone lesions are the most common clinical presentation
    • Dull pain and tenderness often present
    • Punched-out or ill-defined RL
    • Posterior mandible involvement “scooped out”
    • May mimic severe periodontitis with teeth “floating in air”
    • May mimic periapical disease
  • Soft tissue mass may occur in isolation or from a lesion breaking out of bone
38
Q

What are the Histopathologic Features of Langerhans Cell Histiocytosis?

A
  • Sheets of large, histiocytic-appearing cells (neoplastic Langerhans cells)
  • Variable numbers of eosinophils (eosinophilic granuloma), lymphocytes, plasma cells, multinucleated giant cells
39
Q

What is the Treatment for Langerhans Cell Histiocytosis accessible bone lesions (Md/Mx)?

A

Curettage or intralesional steroid injection

40
Q

What is the Treatment for Langerhans Cell Histiocytosis disseminated disease?

A

Single or multiagent chemotx depending on how widespread the disease is

41
Q

When does a poorer prognosis occur in Langerhans Cell Histiocytosis?

A
  • The earlier the onset of symptoms, the more widespread (more organs involved) the presentation
  • and lack of response to induction chemotx
42
Q

What is the biological behavior of lymph node group in Hodgkin Lymphom?

A
  • Cerivcal or Supraclavicular (70-75%)
    • mediastinal node –> spleen, liver, bm, lung
  • If enlarged nodes are absent it could present with a, mediastinal mass = massive nelargement on midline of lungs
    • ​CLASSIC for HL

Oral Pathology Exam 2 (7 decks)

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