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Oral Pathology- Hematology > Lecture > Flashcards

Lecture Flashcards

1
Q

Four oral cavity sites for normal accessory lymphoid tissues

A
  1. Floor of mouth
  2. Soft Palate
  3. Posterior lateral border of tongue
  4. Ventral tongue
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2
Q

Can lymphoid hyperplasia be acute or chronic?

A

Both

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3
Q

What areas can lymphoid hyperplasia affect?

A

Lymph nodes
Lymphoid tissue of Waldeyer ring
Aggregates of lymphoid tissue that are normally scattered throughout the oral cavity

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4
Q

Lymphoid Hyperplasia Intraoral Clinical Appearance

A

Discrete, non-tender, submucosal swelling, <1cm, multifocal

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5
Q

Should we biopsy lymphoid hyperplasia?

A

Does not require biopsy unless:

  • Progressive enlarging -> biopsy to rule out lymphoma
  • Overgrowth effects patient function
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6
Q

What should be done with progressive asymmetric enlargement of tonsillar tissue or cervical lymph nodes?

A

-Consider referral to ENT for evaluation/work-up to rule out lymphoma or other malignancy

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7
Q

Hemophilia A Inheritance Pattern

A

X-linked recessive

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8
Q

Hemophilia A Etiology

A

Mutation in gene responsible for clotting Factor 8

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9
Q

Hemophilia A:

The greater proportion of gene mutation=

A

Worse disease

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10
Q

Hemophilia A:

Patients with _____% or greater Factor 8 production live fairly normal lives

A

25%

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11
Q

Hemophilia A:

Patients with ___% bruise with minor trauma

A

5%

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12
Q

Hemophilia A: Lab Values

A
  • Abnormal PTT

- Usually normal PT and platelets

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13
Q

Hemophilia B:

Inheritance Pattern

A

X-linked recessive

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14
Q

Hemophilia B:

Alternative name

A

Christmas Disease

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15
Q

Hemophilia B:

Etiology

A

Factor 9 Deficiency

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16
Q

Hemophilia B:

Lab Values

A

Abnormal PTT

-Usually normal PT and platelets

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17
Q

What is the most common bleeding disorder?

A

Von Willebrand Disease

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18
Q

Von Willebrand Disease:

Inheritance Pattern

A

Usually autosomal dominant

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19
Q

Von Willebrand Disease:

Etiology

A

Abnromal von Willebrand factor and abnormal platelets

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20
Q

Define Von Willebrand Factor

A

Glycoprotein in plasma that aids in adhesion of platelets to a bleed site
Factor also binds to factor 8 and acts as a transport molecule

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21
Q

Von Willebrand Disease:

Lab values

A

Abnormal PTT and platelet function

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22
Q

What are two major oral path considerations with hemophilia and VWD?

A
  • Pseudo tumor of hemophilia

- Bleeding risk if biopsy is needed

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23
Q

Describe a pseudotumor of hemophilia

A

Hemorrhage within the bone or soft tissue that produces a tumor like clinical swelling

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24
Q

What may be needed in the med consult before a biopsy in a hemophilia or VWD patient?

A
  • Assess risk for bleeding
  • Replacement of clotting factor
  • Epsilon-aminocaproic acid
  • Desmopressin
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25
Q

If a biopsy is needed in hemophilia or VWD patient, what type of closure is needed?

A

Primary Closure

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26
Q

Plasminogen Deficiency:

Inheritance Pattern

A

Rare; autosomal recessive inheritance

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27
Q

Plasminogen Deficiency:

Mutation

A

Mutation in gene for plasminogen

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28
Q

Plasminogen Deficiency: Why is plasminogen important?

A

Necessary for breaking down cloths as part of normal healing.
Without this -> clot grows and persists

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29
Q

Plasminogen Deficiency:

Clinical Presentation

A

Irregular fibrin deposited in plaques and nodules primarily in the mucosal surface

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30
Q

Plasminogen Deficiency:

Treatment of oral lesions

A
  • Med consult & partnership
  • Topical plasminogen not commercially available
  • Topical heparin and prednisone combined
  • Surgical excision of large nodules + systemic doxyclycline, systemic warfarin, topical chlorhexidine
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31
Q

Plasminogen Deficiency:

Life expectancy; what does the patient not suffer from?

A

Normal; patient does not have intravascular thrombus formation

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32
Q

Aplastic Anemia:

Rare, _____-threatening hematologic disorder

A

Life

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33
Q

Aplastic Anemia:

Characterized by:

A

Failure of hematopoietic precursor cells in the bone marrow to produce adequate numbers of all types of blood cells

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34
Q

Aplastic Anemia:

Describe Pancytopenia

A

less than 500 granulocytes, 20,000 platelets and 20,000 reticulocytes

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35
Q

Aplastic Anemia:

Etiology

A

Immune-mediated destruction

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36
Q

Aplastic Anemia:

Triggers

A

Not fully understood

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37
Q

Aplastic Anemia:

Two associated inherited conditions

A
  • Fanconi anemia

- Dyskeratosis congenita

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38
Q

Aplastic Anemia:

Clinical characteristics

A

-Thrombocytopenia: Gingival hemorrhages - petechiae, purpura ecchymosis
Neutropenia: gingival ulcers

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39
Q

Aplastic Anemia:

Treatment/Prognosis

A

-Systemic therapy: initially palliative, eventually bone marrow transplant/peripheral blood stem cell transplant

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40
Q

What occurs in agranulocytosis?

A

Cells of the granylocyte lineage are absent

Particularly neutrophils

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41
Q

Agranulocytosis:

Etiology; when do symptoms appear?

A

Caused by a drug. Symptoms begin a few days after drug ingestion.

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42
Q

Agranulocytosis:

Clinical Features

A
  • Related to increase in infection risk
  • Fever, chills, malaise
  • Oral Lesions: Deep, nectrotizing ulcerations, gingiva prone to infection that resembles NUG
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43
Q

Agranulocytosis:

Treatment

A
  • Discontinuation of offending drug unless drug is a necessity
  • Oral hygeine, antibiotic therapy as necessary, consider chlorhexidine mouth wash
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44
Q

Cyclic Neutropenia:

What occurs?

A

Idiopathic reductions in the neutrophil count of affected patients that occur as uniformly spaced episodes

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45
Q

Cyclic Neutropenia is caused by what type of mutation?

A

A specific genetic mutation in neutrophil elastase gene

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46
Q

When is cyclic neutropenia noticed?

A

In childhood

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47
Q

General symtpoms of cyclic neutropenia

A

Fever, anorexia, cervical LAD, malaise, pharyngitis, lower GI ulcers

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48
Q

Oral Symptoms of Cyclic neutropenia

A
  • Oral ulcers that occur anywhere with minor trauma

- Severe periodontal bone loss and gingival recession

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49
Q

Cyclic Neutropenia Diagnosis

A

Sequential blood counts; neutrophil count falls to 500 for 3-5 days in at least 3 sucessive cycles for diagnosis

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50
Q

Cyclic Neutropenia Treatment

A
  • Optimal oral hygeine to reduce risk for infection
  • Can consider topical steroids for painful oral ulcers
  • Systemic therapies are used by medical colleagues
  • Severity of symptoms usually diminishes after the second decade of life (even though the cycling is still occurring)
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51
Q

Define Amyloidosis

A

Group of conditions characterized by deposition of an abnormal protein called amyloid

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52
Q

Where may amyloid deposit? What does it cause?

A

In multiple vital organs (heart, brain, kidneys, liver); significant dysfunction

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53
Q

What are two types of Amyloidosis?

A

Organ-limited/localized Amyloidosis

Systemic Amyloidosis

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54
Q

Amyloidosis:

Describe Organ-limited/localized Amyloidosis

A
  • Single focus of disease

- Limited or no complications

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55
Q

Amyloidosis:

Describe systemic Amyloidosis

A

-Multifocal/widespread disease

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56
Q

Primary & Myeloma Associated Amyloidosis:

Etiology

A

Primary: Idiopathic

Myeloma Associated: Caused by patient having the condition multiple myeloma

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57
Q

Primary & Myeloma Associated Amyloidosis:

What is the abnormal light chain associated with these conditions?

A

AL Amyloidosis

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58
Q

Primary & Myeloma Associated Amyloidosis:

Population affected

A

Older adult -> 65

Slight male predilection

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59
Q

Primary & Myeloma Associated Amyloidosis:

Initial Symptoms

A

Nonspecific; fatigue, weight loss, hoarseness

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60
Q

Primary & Myeloma Associated Amyloidosis:

Later signs

A

Carpal tunnel, mucocutaneous lesions, hepatomegaly, macroglossia, xerostomia and xerophthalmia

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61
Q

Head and Neck Involvement by Amyloid:

Skin Characteristics

A
  • Smooth-surfaced, firm, waxy papules and plaques +/- petechiae and or ecchymosis
  • Most commonly affect the eyelids, neck, lips
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62
Q

Head and Neck Involvement by Amyloid:

Describe amyloid lesions

A
  • Similar to the skin
  • Smooth surfaced, firm, waxy papules and plaques +/- petechiae and or ecchymosis
  • Nodules/plaques may ulcerate and show submucosal hemorrhage
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63
Q

Head and Neck Involvement by Amyloid:

Describe population and presentation of macroglossia

A

Reported in 10 to 40% of patients

Diffuse or nodular enlargement of the tongue

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64
Q

Describe Secondary Amyloidosis

A

Chronic inflammatory disease results in over production of serum amyloid A

65
Q

What amyloid protein creates hemodialysis associated amyloidosis

A

B2-microglobulin

66
Q

What occurs in hemodialysis associated amyloidosis?

A

Microglobulin normally occurs in the body and is not removed by dialysis -> accumulation and formation of deposits particularly in bone and joints

67
Q

Heredofamilial amyloidosis is an _____ disorder

A

Inherited

68
Q

Systemic Amyloidosis:

If caused by underlying inflammatory disease (secondary amyloidosis) treat ->

A

Systemic disease

69
Q

Systemic Amyloidosis:

If caused by need for hemodialysis ->

A

Kidney transplant

70
Q

Systemic Amyloidosis:

If idiopathic or myeloma associated ->

A

Systemic medications have shown efficacy

71
Q

Systemic Amyloidosis:

Long term prognosis

A

Poor

-Most patients die of cardiac failure, arrhythmia or renal disease within months to a few years after diagnosis

72
Q

Describe Thrombocytopenia

A

Marked decrease in circulating platelets

73
Q

Thrombocytopenia:

Three main etiologies

A
  • Decreased production
  • Increased destruction
  • Increased use of platelets
74
Q

Thrombocytopenia:

Described decreased production

A

Decreased production in the bone marrow from malignant infiltration or chemotoxicity

75
Q

Thrombocytopenia:

Describe increased destruction

A

Introduction of an offending agent (ex. viral infection) -> immunologic reaction -> autoantibodies to platelet surface glycoproteins

76
Q

Thrombocytopenia:

What two diseases can cause increased destruction of platelets?

A

SLE and HIV

77
Q

Thrombocytopenia:

Describe why there is an increased use of platelets

A
  • Disorders of abnormal blood clot formation

- Disorders than cause splenomegaly (increased platelet trapping in the spleen)

78
Q

Thrombocytopenia: When are symptoms usually noticeable?

A

When platelets are below 100,000

79
Q

Thrombocytopenia: What is the first sign?

A

Oral lesions

80
Q

Thrombocytopenia: How are oral lesions most commonly created?

A

Minor trauma from eating causes petechiae and they can have spontaneous gingival hemorrhage from minor trauma sites

81
Q

Thrombocytopenia:

Mucosa and skin may show what three signs?

A

Petechiae, ecchymosis and hematoma

82
Q

Thrombocytopenia:

Other signs and symptoms

A

Epistaxis, hemoptysis, GI bleeding, urinary bleeding, intracranial hemorrhage

83
Q

Thrombotic Thombocytopenic Purpura TTP:

Define

A

Increased use of platelets which results in thrombocytopenia

84
Q

Thrombotic Thombocytopenic Purpura TTP

Caused by:

A

Deficiency in von Willebrand factor cleaning metalloprotease (ADAMTS13)

85
Q

Thrombotic Thombocytopenic Purpura TTP Triggers formation of what?

A

Numerous thrombi within small vessels

86
Q

Thrombotic Thombocytopenic Purpura TTP:

Inheritance pattern/cause

A

Either from autoantibodies to ADAm or can be inherited -> autosomal recessive when ADAm is mutated

87
Q

Thrombotic Thombocytopenic Purpura TTP

Treatment

A

With adequate systemic therapy -> 70 percent survial rate

88
Q

Immune Thrombocytopenic Purpura (ITP):

Define

A

Increased destruction of platelets results in thrombocytopenia.

89
Q

Immune Thrombocytopenic Purpura (ITP):

Etiology

A

Autoantibodies directed against antigens on the platelet surface result in sequestration and destruction of the platelets in the spleen

90
Q

Immune Thrombocytopenic Purpura (ITP):

Acute or chronic?

A

Both

91
Q

Immune Thrombocytopenic Purpura (ITP):

Describe population affected by acute ITP

A

Children following non-specific infection

92
Q

Immune Thrombocytopenic Purpura (ITP): Describe how long acute ITP occurs

A

4-6 weeks

90% of patients recover in 3-6 months

93
Q

Immune Thrombocytopenic Purpura (ITP):

Describe population affected by chronic ITP

A

Older patients; women; 20-40 years old

94
Q

Immune Thrombocytopenic Purpura (ITP): Treatment

A

Frequently treated with splenectomy

95
Q

Define Lymphoproliferative disorder

A

Disease in which cells of the lymphatic system grow excessively

96
Q

Lymphoproliferative disorder: Name the types of cancers associated

A

Leukemia, lymphoma, multiple myeloma

97
Q

Monoclonal cell population arises from what?

A

A single progenitor cell

98
Q

Polyclonal cell population arises from what?

A

Two or more distinct progenitor cells

99
Q

Describe what occurs in B symptoms

A

Unexplained fever, night sweats, greater than 10 percent involuntary weight loss

100
Q

What are langerhans cells?

A

Dendritic mononuclear cells that process and present antigens to T cells

101
Q

Langerhans cell histiocytosis (LCH):

Describe

A

Monoclonal proliferation of langerhan cells

102
Q

Langerhans cell histiocytosis (LCH):

Cause

A

Gene mutation (BRAF in 40 to 60%)

103
Q

Langerhans cell histiocytosis (LCH):

Two types of classifications

A
  • Single organ involvement

- Multi organ involvement

104
Q

Langerhans cell histiocytosis (LCH):

Where does single organ involvement usually occur?

A

Bone or skin; can be unifocal or multifocal

105
Q

Langerhans cell histiocytosis (LCH):

Describe two types of multi-organ involvement

A

No organ dysfunction

Organ dysfunction

106
Q

Langerhans cell histiocytosis (LCH):

Describe what areas are affected in low risk organ involvement

A

Skin, bone, lymph nodes, pituitary gland

107
Q

Langerhans cell histiocytosis (LCH): Describe what areas are affected in high risk organ involvement

A

Lung, liver, spleen, bone marrow

108
Q

Langerhans cell histiocytosis (LCH):

Describe population affected

A

More than 50% of cases are patients younger than 15

109
Q

Langerhans cell histiocytosis (LCH):

Hard Tissue manifestations

A

Jaw is affected in 10-20 percent of cases

110
Q

Langerhans cell histiocytosis (LCH): Jaw presentation in radiographs

A

Radiolucent, sharp, punched-out or “scooped out” bony lesions
-Posterior mandible most often affected

111
Q

Langerhans cell histiocytosis (LCH): Can mimic what disease?

A

Periodontal disease

112
Q

Langerhans cell histiocytosis (LCH):

Describe soft tissue manifestations

A

Gingival mass lesion with ulceration

113
Q

Langerhans cell histiocytosis (LCH):

Treatment with localized disease

A
  • Accessible lesions are curretted (ensure there are no other organs involved)
  • Low dose radiation used for non-acessible bone lesions
  • Corticosteroid infections
  • Prognosis of local disease is good
114
Q

Langerhans cell histiocytosis (LCH):

Treatment with multiorgan involvement

A
  • Low risk pattern -> significant morbidity, but much lower mortality than high risk patterns
  • Treated with systemic chemotherapy and prednisone combination
  • Younger onset of disease -> worse prognosis
115
Q

Rosai-Dorfman Disease:

Alternative Name

A

Sinus Histiocytosis with Massive Lymphadenopathy

116
Q

Rosai-Dorfman Disease:

Describe

A

Rare proliferative disorder of histiocytes

117
Q

Rosai-Dorfman Disease:

Proliferation of histiocytes may involve?

A
  • Lymph nodes

- Extranodal sites: skin, oral cavity, nasal cavity, respiratory tract, eyelids, salivary glands, bone

118
Q

Rosai-Dorfman Disease:

Describe population affected

A

Children and young adults; males

119
Q

Rosai-Dorfman Disease: Presenting symptoms

A

-Massive, non-tender bilateral cervical lymph node enlargement, fever

120
Q

Rosai-Dorfman Disease: Oral manifestations

A

Ill-defined radiolucency of bone; bony destruction

  • Bone is infiltrated with abnormal histiocytes
  • May mimic periodontal disease or periapical pathology
  • Associated bone resorption may cause tooth mobility
121
Q

Rosai-Dorfman Disease: Treatment/Prognosis

A
  • Non-standardized: Excision of oral lesions without recurrence.
  • Systemic treatments: variable, include corticosteroids, chemotherapy agents, radiation
122
Q

Polycythemia Vera:

Define

A

Rare idiopathic myeloproliferative disorder

123
Q

Polycythemia Vera: Results in over production of what?

A

Blood cells in the bone marrow

124
Q

Polycythemia Vera: What population does this occur in?

A

Older adults; 60 years old

125
Q

Polycythemia Vera: Etiology

A

Acquired mutation in JAK2

126
Q

Polycythemia Vera: General symptoms

A

Headaches, weakness, dizziness, sweat, weight loss, epigastric pain

127
Q

Polycythemia Vera:

40% of patients have what symptom?

A

Generalized pruiritis w/o rash

128
Q

Polycythemia Vera: An increased viscosity of blood from excess blood cells puts patients at increased risk for what two conditions?

A

Cerebrovascular accident and MI

129
Q

Polycythemia Vera: Symptom causing painful burning sensation, erythema and warmth of hands and feet

A

Erythomelalgia

130
Q

Polycythemia Vera: Can cause loss of circulation causing ______

A

Gangrene

131
Q

Polycythemia Vera: Oral Symptom

A

Gingival hemorrhage

132
Q

Polycythemia Vera: Treatment

A

Phlebotomy, low dose aspirin, myelosupressive therapy

133
Q

Leukemia: Signs and symptoms

A

Myelophthisic anemia

134
Q

Leukemia: Diagnostic techniques

A

Peripheral blood smear, flow cytometry, bone marrow biopsy

135
Q

Leukemia: Intraoral symptoms

A
  • ulceration and infection more common
  • Leukemic cells can infiltrate the gingiva
  • Myeloid sarcoma
136
Q

Define myeloid sarcoma

A

Tumor-like growth of leukemia cells

137
Q

Define lymphoma

A

-Malignant transformation of cells of the B and T cell lineages.

138
Q

Where does lymphoma arise?

A

-Initially arise within lymph nodes and tend to grow as solid masses.

139
Q

Hodgkin Lymphoma:

Signs and symptoms

A
  • Persistent enlarging, nontender, massess in a lymph node region
  • Cervical and supraclavicular nodes
140
Q

Hodgkin Lymphoma: Diagnostic techniques

A

Lymph node biopsy

141
Q

Non-hodgkin Lymphoma:

Describe beginning stages

A

Proliferation in the lymph nodes but can expand to other body sites

142
Q

Non-hodgkin Lymphoma: What is the most frequent oral site being affected?

A

Palate

143
Q

Non-hodgkin Lymphoma: Describe oral lesions in the palate

A
  • Intraoral lesions most commonly present as red/purple/blueish “boggy” swellings
  • Telengiectasias overlying the affected site is note uncommon
144
Q

Non-hodgkin Lymphoma: Four subtypes

A
  • DLBCL
  • MALT definition
  • Burkitt lymphoma
  • Mycosis fungoides skin
145
Q

Diffuse Large B Cell Lymphoma: Describe

A
  • High grade Lymphoma

- Often represents transformation of another low-grade lymphoma

146
Q

What is the most common lymphoma affecting the oral cavity?

A

Diffuse large B cell lymphoma

147
Q

MALT Lymphoma: Describe

A

B Cell NHL that specifically occurs outside of the lymph nodes

148
Q

MALT Lymphoma affects what areas most commonly?

A

Stomach and in patients with chronic inflammation (Such as H. Pylori infection)

149
Q

MALT Lymphoma Can also occur in what places?

A

Small intestine, salivary glands, thyroid, eyes, lungs

150
Q

Patients with what syndrome have a 20x increased risk for developing lymphoma?

A

Sjogren Syndrome

151
Q

Mycosis Fungoides:

Describe

A

Cutaneous T cell lymphoma; most common cutaneous lymphoma

152
Q

Mycosis Fungoides:

Oral Cavity Complications

A

Rarely can affect the oral cavity

Erythametous, indurated plaques or nodules that frequently are ulcerated

153
Q

What is Sezary syndrome?

A

Aggressive form of mycosis fungoides

154
Q

Multiple Myeloma: Etiology

A

Hematologic malignancy of plasma cells

155
Q

Describe Plasmacytoma

A

If there are only 1 tumor-like mass of malignant plasma cells

156
Q

Multiple plasmacytomas=

A

Multiple myeloma

157
Q

Multiple Myeloma Diagnosis

A
  • Serum eletrophoresis
  • Biopsy of bony or soft tissue lesions
  • Urine test
158
Q

Multiple Myeloma Oral Findings

A

-Multiple punched out radiolucencies of the jaw bones

Oral Pathology- Hematology (1 decks)

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