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22 Cards in this Set

  • Front
  • Back
Hemangiomas:

1) What are they?
2) Most common ___
3) 4 types?
4) Primarily tumors of what age?
5) What % of newborns?
6) Most common location?
1) Benign proliferation of blood vessels - probably a hamartoma or malformation
2) Tumor of infancy and childhood
3) Capillary, juvenile, cavernous, AV hemangioma (malformation)
4) Childhood
5) 1.1-2.6% of newborns
6) H&N
Capillary hemangioma:

1) T or F: this is the most common type of hemangioma
2) What size? What color?
3) 3-5x more common in males/females
4) How does it look?
5) What size does it reach?
6) Treatment and prognosis?
1) T
2) Capillary size of blood vessels. Bright color, "strawberry hemangiomas.
3) Females
4) Skin as flat area of red pigmentation very early in life, rapidly proliferates, produces an elevated and lobulated mass - red to purple
5) Stabilizes in size and eventually regresses over several years, by 7, most involute
6) "Watchful neglect" until the involute - systemic steroids may reduce size of lesion
Juvenile Hemangioma:

1) Also known as?
2) How does it start and progress?
1) Cellular hemangioma
2) Immature and highly cellular stage of a capillary hemangioma, as tumor ages, it becomes less cellular and is indstinguishable from typical capillary hemangioma
Cavernous hemangioma:

1) What size? How does it look compared to other hemangiomas?
2) When does it occur? Predilection for?
3) T or F: it does not undergo regression
4) Tx?
1) Larger diameter of proliferating blood vessels. Larger and less circumscribed and more involve deeper structure
2) In childhood, females and H&N
3) T
4) Surgery may be necessary
Arteriovenous hemangioma:

1) What is it?
2) What are the symptoms?
3) Tx?
1) Abnormal communication between arterial and venous circulation, bypassing the capillary bed
2) Thrill or bruit, overlying skin feels warm
3) Surgery may be necessary
1) Alternative options for tx hemangiomas?
1) Laser ablation, embolization for large, inaccessible lesions, or injection of sclereosing agents, Na morrhuate
Sturge-Weber Syndrome:

1) What kind of condition is it?
2) What is it characterized by? What organs are involved?
3) What is it caused by?
4) Clinical features?
5) What is associated with the cerebral cortex?
6) What other conditions are associated with Sturge-Weber?
7) What does it look like on a x-ray?
8) T or F: intraoral involvement is common
9) What does the gingiva look like?
10) Treatment and prognosis depends on?
1) Rare, nonhereditary developmental condition
2) Hamartomatous vascular proliferation, involves brain and face
3) Persistence of vascular plexus around the cephalic portion of the neural tube which normally regresses
4) Vascular malformation of the face - port-wine stain or nevus flammeus - deep purple color. Usually unilateral along trigeminal nerve.
5) Leptomeningeal angiomas
6) Convulsions and mental retardation
7) Gyriform "tram-line" calcifications
8) T
9) Vascular hyperplasia or massive hemangiomatous proliferation - like pyogenic granuloma
10) Nature + severity
Reactive lesion - Varicosity

1) What is it?
2) What is an important factor?
3) Most commonly seen in who?
4) What does it look like?
5) Less often, solitary varices can occur where else?
6) When are they usually first noticed?
1) Abnormally dilated and tortuous vein
2) Age
3) 2/3rds older in 60 years
4) Multiple bluish-purple, elevated or papular blebs on ventral-lateral border of tongue (or lips and buccal mucosa) - firm, nontender, bluish-purple nodule, looks like a BB shot beneath mucosal surface
5) Lips + buccal mucosa
6) After they thrombose
Pyogenic granuloma

1) What is it?
2) This represents an exuberant response to...
3) Clinical features?
4) Does it grow?
5) Where does it normall happen?
6) What are the precipitating factors?
7) Who is it most common in?
8) Tx in pregnancy
9) Other d/d?
10) Treatment and prognosis?
1) Reactive, common tumor-like growth
2) Local irritation or trauma - not a true granuloma
3) Smooth or lobulated mass usually pedunculated, surface usually ulcerated, pink to red to purple dpeneding on age of lesion, small to large size, painless and bleeds easily
4) May exhibit rapid growth
5) Gingiva (75%), lips, tongue, buccal mucosa - more common in maxillary anterior region
6) Gingival irritation and inflammation
7) Children and young adults, especially females
8) Resolves on its own without tmt or fibrous maturation
9) Peripheral giant cell granuloma, peripheral ossifying fibroma
10) Conservative surgical excision down to periosteum, teeth shoudl be thoroughly scaled to remove source of irritation
Peripheral giant cell granuloma:

1) What is it?
2) Microscopically, what does it closely resemble?
3) Where is it found?
4) What does it look like?
5) Peak prevalence at what age?
6) Radiographically, what do you see?
7) Treatment and prognosis?
1) Common tumor-liek growth, not a true neoplasm but reactive (local irritation or trauma)
2) Central giant cell granuloma - may representa soft tissue counterpart of the central bony lesion
3) Exclusively on gingiva/edentulous alveolar ridge
4) Red or reddish-blue nodular mass, <2 cm in diameter
5) 50-60 y/o
6) Cupping resorption of alveolar bone
7) Local surgical excision down to the underlying bone, 10% recur, re-excision must be performed
Erythroplakia:

1) What is it?
2) True erythroplakias demonstrate what?
3) What is more common, leukoplakia or erythroplakia?
4) T or F: erythroplakia has significant potential for dysplasia or malignancy
5) What is it most related to?
6) Who does it mostly affect?
7) Sites?
8) How does it look?
9) Clinical d/d?
10) Histopathologically, 90% have what?
11) % of benign keratosis found within? Mild dysplasia? Severe dysplasia? Invasive carcinoma?
12) T or F: red lesions should be viewed with suspicion
13) What is mandatory?
14) Do these recur?
15) What is suggested for "treated" patients?
1) Red patch that can't be clinically or pathologically diagnosed as any other condition
2) Significant dysplasia, carcinoma-in-situ, or invasive SCC
3) Leukoplakia 77x more common than erythroplakia
4) T
5) Alcohol and tobacco use
6) Men 65-74 years old
7) FOM, tongue, soft palate (high risk locations)
8) Well-demarcated, erythematous macule or plaque with a soft, velvety texture
9) Inflammation, candidiasis, vascular lesions
10) Severe epithelial dysplasia, carcinoma-in-situ, SCC
11) 0%, 10%, 40%, 50%
12) T
13) Biopsy
14) Yes, recurrence and multifocal involvement common
150 Long-term-follow-up
Kaposi's Sarcoma:

1) What is it?
2) What is implicated?
3) What are the 4 clinical presentations?
4) Typically evolves through what 3 stages?
5) Histologically, what do you see?
6) Treatment and prognosis depends on?
7) How to tx the classic form?
8) How quickly does the classic form progress?
1) Vascular neoplasm that most likely arises from endothelial cells
2) CMV - HHV 8?
3) Classic, endemic (African), iatrogenic, AIDS-related
4) Patch (macular), plaque, nodular
5) Proliferation of spindle-shaped endothelial cells with extravasated RBCs
6) Clinical subtype and stage
7) Radiation therapy, surgical excision on individual skin or mucosal lesions, systemic or intralesional chemo with vinblastine
8) Slowly - only 10-20% die of disease after 8-10 years (25% die of a lymphoma)
Iron deficiency anemia:

1) This is the most common cause of?
2) Why does this happen?
3) Happens to 20% of women who? 2% of men who?
4) Clinical features?
5) Oral manifestations?
6) What does the glossitis look like?
1) Anemia in the world
2) Iron can't keep pace w/ the need (excessive blood loss, increased demand for RBC, decreased intake of iron, decreased absorption of iron)
3) Are of childbearing age (period). Men w/ GI disease e.g. peptic ulcers, hiatal hernia, or malignancy
4) Fatigue, easy tiring, palpitations, lightheadedness, lack of energy
5) Angular cheilitis, atrophic glossitis, generalized oral mucosal atrophy
6) Diffuse or patchy atrophy, often accompanied by tenderness, burning, candidiasis
Pernicious anemia:

1) Uncommon condition found among who?
2) What is it caused by?
3) Most patients lack intrinsic factor which results in?
4) Clinical features?
5) Oral features?
1) Elderly patients of northern European heritage
2) Megaloblastic anemia caused by poor absorption of cobalmin (vitamin B12, extrinsic factor)
3) Decreased absorption of cobalamin/vitamin B12/extrinsic factor
4) Fatigue, weakness, shortness of breath, headache, and feeling faint, paresthesia, tingling, or numbness of the extremities
5) Burning sensation of tongue, lips, buccal mucosa, focal patchy areas of erythema and atrophy
Immunologic abnormalities - plasma cell gingivitis

1) Most related to?
2) What happens when it occurs?
3) Where can the erythematous areas extend?
4) What do you need to do?
1) Hypersensitivity to component of cinnamon chewing gum
2) Rapid onset of sore mouth - worse with spicy or hot foods, entire gingiva becomes diffuse enlargement with bright erythema and loss of normal stippling
3) To palate or edentulous areas
4) Complete dietary history, extensive allergy testing, elimination diet, topical corticosteroids
Pigmented lesions - Smoking associated melanosis:

1) What is it caused by?
2) What modifies it? Who is more affected?
3) Where does it occur most often?
4) T or F: smokeless tobacco is linked to melanosis
5) Intensity of pigmentation is related to?
6) D/D with melanosis?
1) Abnormal melanin pigmentation, related to component in tobacco smoke that stimulates melanocytes
2) Female sex hormones (women on birth control are more commonly affected than men)
3) Anterior labial gingiva - palate and buccal mucosa w/ pipe smoking
4) F - not linked
5) Time and dose
6) Physiologic pigmentation, Peutz-Jeghers syndrome, Addison's disease, melanoma
Oral melanotic macule

1) Etiology?
2) T or F: related to sun exposure
3) Females or males more affected?
4) What part of the mouth is most affected?
1) Unknown - just a focal increase in melanin
2) F
3) Females, 2:1
4) Vermillion border > buccal mucosa > gingiva > palate
Acquired melanocytic nevus:

1) Also known as?
2) What is a nevus?
3) What is the most common?
4) What kind of cells do they arise from?
1) "Mole"
2) Congenital or developmental malformations of skin & mucosa
3) Acquired melanocytic nevus (common mole)
4) Neural crest cells "nevus cells"
Melanocytic Nevus (mole)

1) Most common?
2) Who is most often affected? How many nevi do they normally have?
3) T or F: they are common intraorally. What are the sites you'll find them at?
4) Most are present before what age? Males or females?
5) What is a common site?
6) What does it look like?
7) How does it progress?
8) How are they classified? Describe
9) T or F: melanomas can arise from acquired nevi (skin)
10) The risk of transformation to carcinoma is?
11) What should be done with all oral melanotic lesions?
1) Tumor
2) White adults, 10-40 cutaneous nevi
3) F. Palate or gingiva
4) 35. Females
5) Skin of head and neck
6) Slightly elevated, smooth surfaced brown tan papule (compound)
7) Gradually loses pigmentation, becomes papillomatous, hairs grow from center (intradermal), remains <6 mm. Many involute and disappear (few detected in elderly)
8) Histopathologically according to stage of development (Junctional - cells nest within epithelium. Compound - within epithelium and connective tissue. Intramucosal - only within CT - most common)
9) T
10) 1/1 million
11) Biopsied to rule out melanoma
Blue nevus:

1) What is it?
2) Second most frequent...
3) Predilection for what parts of the body?
4) Intraorally, where are they most common?
5) What does it mimic?
1) Benign proliferation of dermal melanocytes deep in CT (which is why the'yre dark, sometimes blue)
2) Melanocytic nevus in mouth
3) Dorsum of hands + feet, scalp, face
4) Palate
5) Early melanoma - biopsy all intraoral pigmented lesions
Melanoma:

1) What is it? How does it arise?
2) What causes it? What is the most important cause?
3) The risk of melanoma is 2-8x greater with?
4) Additional risk factors?
5) ___ (#) most common skin cancer
6) __% of cutaneous malignancies
7) How many new cases each year? How many die?
8) Lifetime risk of melanoma?
9) Average age?
10) 4 clinicopathologic types?
11) ABCD's?
1) Malignant neoplasm, melanocytic origin, arises from benign melanocytic lesion or de novo from melanocytes
2) UV radiation - chronic sun exposure NOT significant - ACUTE sun damage is more important
3) Familial history
4) Fair complexion/light hair, sunburn easily, hx painful or blistering sunburns in childhood, personal hx of melanoma or dysplastic/congenital nevus
5) Third
6) 5%
7) 32k, 6800 persons die
8) 1/100
9) 50-55
10) Lentigo maligna melanoma, superficial spreading melanoma, nodular melanoma, acral lentiginous melanoma
11) Asymmetry, Border, Color variation, Diameter
Oral melanoma:

1) Rare of requent?
2) 4/5ths found where in the mouth?
3) Prognosis? What correlates with prognosis?
4) What is the only curative tx?
5) What is the recommended extent of excision?
6) Removal of regional lymph nodes for lesions with depth of invasion?
7) Stage 1 survival rate?
8) Stage 2?
9) Stage 3?
10) Overall 10 year survival rate?
11) High risk sites?
1) Rare
2) Hard palate and maxillary gingiva or alveolar mucosa
3) Extremely poor - 4-20% survive 5 years. Depth of invasion correlates w/ prognosis
4) Surgical excision
5) Controversial - 1 cm for small tumors
6) >1.24 mm
7) Before metastasis - 89% 5-year survival 81% 10 year.
8) Local lymph nodes, 61%/47
9) Disseminated disease, always fatal
10) 79%
11) BANS