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Oral Medicine and Diagnosis > Pigmented Lesions > Flashcards

Pigmented Lesions Flashcards

1
Q

what are the benign melanocytic lesions

A
  • physiologic
  • smoker’s melanosis
  • traumatic melanosis
  • ephelis
  • lentigo
  • oral melanotic macule
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2
Q

what are the neoplastic pigmented lesion

A
  • nevi
  • melanoma
  • neuroectodermal tumor of infancy
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3
Q

what are the exogenous pigmented lesion

A
  • metal pigment
  • amalgam tattoo
  • drug induced pigment
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4
Q

what is the endocrine pigmented lesion

A

addison disease

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5
Q

what is the genetic pigmented lesion

A

peutz jehger syndrome

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6
Q

what is the etiology of physiologic pigmentation disorders

A

normal melanocyte activity

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7
Q

what is the clinical presentation of physiologic pigmentation disorders

A
  • seen in all ages
  • symmetric distribution over many sites gingiva most commonly
  • surface architecture, texture unchanged
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8
Q

what is the dx of physiologic pigmentation disorders

A
  • history
  • distribution
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9
Q

what is the DDX of physiologic pigmentation disorders

A
  • mucosal melanotic macule
  • smoking associated melanosis
  • superficial malignant melanoma
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10
Q

what is the tx of physiologic pigmentation disorders

A

none

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11
Q

what is the prognosis of physiologic pigmentation disorders

A

excellent

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12
Q

what is the etiology for traumatic melanosis

A
  • a reactive and reversible alteration of oral mucosal and melanocytes and keratinocytes
  • usually associated with local trauma
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13
Q

what is the clinical presentation of traumatic melanosis

A
  • unilateral dark plaque, rarely multiple, bilateral
  • most often noted among blocks and other non caucasians
  • occurs more often in women than men by a ratio of 3:1
  • history of trauma and local irritation
  • forms rapidly most often on buccal/labial mucosa
  • asymptomatic melanotic pigmentation
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14
Q

what is the dx for traumatic melanosis

A
  • clinical history of rapid onset
  • histologic evaluation
  • scattered dendritic melanocytes within spongiotic and acanthotic epithelium
  • increased number of melanocytes along basal layer as single units
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15
Q

what is the DDX for traumatic melanosis

A
  • melanoma
  • drug induced pigmentation
  • smokers melanosis
  • mucosal melanotic macule
  • mucosal nevus
  • amalgam tattoo
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16
Q

what is the tx for traumatic melanosis

A
  • none after establishing the dx
  • often resolves spontaneously
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17
Q

what is the prognosis for traumatic melanosis

A

excellent

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18
Q

what is the etiology of smokers melanosis

A
  • melanin pigmentation of oral mucosa in heavy smokers
  • may occur in up to 1 of 5 smokers, especially females taking birth control pills or hormone replacement
  • melanocytes stimulated by a component in tobacco smoke
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19
Q

what is the clinical presentation of smokers melanosis

A
  • brownish discoloration of alveolar and attached labial gingiva, buccal mucosa
  • pigmentation is diffuse and uniformly distributed; symmetric gingival pigmentation occurs most often
  • degree of pigmentation is positively influenced by female hormones (birth control pills, hormone replacement therapy)
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20
Q

what are the microscopic findings in smokers melanosis

A
  • increased melanin in basal cell layer
  • increased melanin production by normal numbers of melanocytes
  • melanin incontinence
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21
Q

what is the dx for smokers melanosis

A
  • history of chronic, heavy smoking
  • biopsy
  • clinical appearance
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22
Q

what is the DDX for smokers melanosis

A
  • physiologic pigmentation
  • addisons disease
  • medication related pigmentation
  • malignant melanoma
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23
Q

what medications would cause smokers melanosis

A
  • chloroquine
  • clofazimine
  • mepacrine
  • chlorpromazine
  • quinidine
  • zidovudine
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24
Q

what is the treatment for smokers melanosis

A
  • non
  • reversible if smoking is discontinued
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25
Q

what is the prognosis for smokers melanosis

A
  • good with smoking cessatoin
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26
Q

what is the etiology for mucosal melanotic macule and ephelides

A
  • most idiopathic, some post inflammatory some drug induced
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27
Q

what do multiple lesions of mucosal melanotic macule and ephelides suggest syndrome wise

A
  • peutz jeghers
  • laugier hunziker
  • carneys syndrome
  • leopard syndrome
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28
Q

what is the clinical presentation of mucosal melanotic macule and ephelides

A
  • most in adulthood - 4th decade and up
  • most are solitary and well circumscribed
  • lower lip vermillion border most common site mostly in young women ( labial melanotic macule)
  • brown mucosa, palate, and attached gingiva also involved- mucosal melanotic macule
  • usually brown, uniformly pigmented, round to ovoid shape with slightly irregular border
  • usually less than 5mm in diameter
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29
Q

what is the etiology of a nevus

A

unknown but are benign tumors of melanocytes

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30
Q

what is the clinical presentation of a nevus

A
  • usually elevated, symmetric papule
  • pigmentation usually uniformly distributed
  • common on skin; unusual intraorally
  • palate and gingiva most often involved
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31
Q

what is the dx for a nevus

A
  • clinical features
  • biopsy
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32
Q

what is the DDX for a nevus

A
  • melanoma
  • hemangioma
  • amalgam tattoo/foreign body
  • mucosal melanotic macule
  • Kaposi’s sarcoma
  • ecchymosis
  • melanocanthoma
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33
Q

what is the tx for a nevus

A
  • excision of all pigmented oral lesions to rule out malignant melanoma is advised
  • malignant transformation of oral nevi probably does not occur
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34
Q

what is the prognosis for a nevus

A

excellent

35
Q

what are the variants of a nevus

A
  • blue nevus
  • compound
  • amelanotic
  • junctional
36
Q

what is the etiology of a malignant melanoma

A
  • unknown
  • cutaneous malignant melanoma with relation to sun exposure or familial dysplastic melanocytic lesions
37
Q

what is the etiology of mucosal malignant melanoma

A
  • unknown and unlike the cutaneous malignant melanoma with relation to sun exposure or familial dysplastic melanocytic lesions
38
Q

what is the clinical presentation of mucosal malignant melanoma

A
  • rare in oral cavity (less than 1% of all melanomas) and sinonasal tract
  • generally greater than 30 years of age
  • usually arises on maxillary gingiva and hard palate
  • may exhibit early in situ phase: a macular, pigmented patch with irregular borders
  • progression to deeply pigmented, nodular quality with ulceration
  • may arise de novo as a pigmented or amelanotic nodule
  • rarely may be metastatic to the oral cavity as a nodular, usually pigmented mass
39
Q

describe the mucosal spread of mucosal malignant melanoma

A
  • early stage: atypical melanocytes at epithelial-connective tissue interface, occasionally with intraepithelial spread
  • later infiltration into lamina propria and muscle
  • strict correlation to cutaneous malignant melanoma is not well established, as in skin, a similar horizontal or in situ growth phase often precedes the vertical invasive phase
  • a horizontal or in situ growth phase often precedes the vertical invasive phase
  • initially a macular pigmented. patch with irregular borders
  • progresses to deeply pigmented, nodular quality with ulceration
40
Q

what stain is used for amelanotic forms of mucosal malignant melanoma

A

immunohistolchemical identifications such as S-100 protein, HMB-45, and Melan-A expression

41
Q

what is the tx for mucosal malignant melanoma

A
  • surgical excision
  • marginal parameters related to depth of invasion and presence of lateral growth
  • wide surgical margins; resection (including maxillectomy) for large, deeper lesions
  • neck dissection in cases of deep invasion (less than 1.25mm)
42
Q

what is the prognosis for mucosal malignant melanoma

A
  • generally poor for most oral malignant melanomas
  • less than 20% survival at 5 years in most studies
43
Q

what is the etiology of amalgam tattoo

A

implantation of passtive/frictional transfer of dental silver amalgam into mucosa

44
Q

what is the clinical presentation of an amalgam tattoo

A
  • gray to black focal macules, usually well defined but may be diffuse with no associated signs of inflammation
  • typically in attached gingiva, alveolar mucosa, buccal mucosa
  • occasionally may be visible radiographically
  • intact mucosa overlying black spot
  • benign or malignant melanin pigmentation is usually brownish and occurs within the epithelium on the surfacr
45
Q

what is the dx for amalgam tattoo

A
  • radiographs
  • biopsy may be necessary if clinical dx is in doubt or to rule out lesions of melanocytic origin
46
Q

what is the ddx for amalgam tattoo

A
  • vascular malformation
  • mucosal nevus
  • melanoma
  • mucosal melanotic macule
  • melanocanthoma
47
Q

what is the tx for amalgam tattoo

A

biopsy or observation

48
Q

what is the prognosis for amalgam tattoo

A

little clinical significance if untreated

49
Q

what is Niksat

A
  • a cultural tattoo
  • age-old practice of body art in Ethiopia
  • drawn on faces, necks, gums, and hands of young girls
  • popular in older population
  • darker gums is a criterion of beauty in rural areas of ethiopia
  • drink a local liquir called Areki for conscious sedation
50
Q

what is Niksat for

A
  • beautification
  • identity indicator
  • ward off evil eyes
  • curing enlarged thyroid glands on the neck
  • gingival tattoos give healing powers for dental problems
51
Q

Niksat on men’s gingiva is referred to as:

A

guramayle

52
Q

what is the etiology of extrinsic drug or metal induced mucosal pigmentation

A
  • occupational exposure- metal vapors ( lead, mercury)
  • therapeutic - metal salts deposits (bismuth, cis platinum, silver, gold) also nonmetal agents such as chloroquine, minocycline, zidovudine, chlorpromazine, phenolphthalein, clofazimine, and others
53
Q

what is the clinical presentation for extrinsic drug related or metal induced mucosal pigmentation

A
  • focal to diffuse areas of pigmentary change
  • if heavy metal are the cause, a typical gray to black color is seen along the gingival margin or areas of inflammation
  • palatal changes characteristic with antimalarial drugs and minocycline
  • most medications cause color alteration of buccal labial mucosa and attached gingiva
  • darkened alveolar bone with minocycline therapy (10% at 1 year, 20% at 4 years)
54
Q

what is the dx of extrinsic drug induced or metal induced mucosal pigmentation

A
  • history of exposure to or ingestion of heavy metals of drugs
  • differentiation from melanocyte-related pigmentation by biopsy if needed
55
Q

what is the ddx of extrinsic drug induced or metal induced mucosal pigmentation

A
  • when localized: amalgam tatoo, mucosal melanotic macule, melanocanthoma, mucosal nevus, ephelides, Kaposi’s sarcoma, purpura, malignant melanoma, ecchymosis
  • when generalized: ethnic pigmentation, Addison’s disease
  • if asymmetric: in situ melanoma must be ruled out by biopsy
56
Q

what is the tx of extrinsic drug induced or metal induced mucosal pigmentation

A

investigation of cause and elimination if posible

57
Q

what is the prognosis of extrinsic drug induced or metal induced mucosal pigmentation

A

excellent

58
Q

what is argyria

A

Ag salts have antibacterial and anti neoplastic benefits
- bluish discoloration from therapeutic ingestion or industrial accident

59
Q

what is the etiology of drug induced pigmentation disorders

A
  • therapeutic drug related tissue pigmentation
  • many drugs cause change
60
Q

what is the clinical presenation of drug induced pigmentation disorders

A
  • macular mucosal discoloration ( brown, gray,black)
  • palate and gingiva are most common sites affected
  • in addition to mucosal changes, teeth in adults and children may be bluish gray owing to minocycline/tetracycline use
61
Q

what are the drugs capable of producing tissue pigmentation

A
  • antimalarials: chloroquine, mepacrine, quinidine, old time antimalarials
  • antibiotics: tetracycline group, minocycline
  • antivirals: azidothymidine
  • phenothiazine: chlopromazine, clofazimine
  • heavy metals: gold, mercury salts, silver nitrate, bismuth, lead
  • hormones: ACTH, oral contraceptives
  • cancer/chemotherapy drugs: busulfan, cyclophosphamide, cis-platinum
  • other: methyldopa
62
Q

what is the etiology for tetracycline staining

A
  • prolonged ingestion of tetracycline or its congeners during tooth development
  • less commonly, tetracycline ingestion causes staining after tooth formation is complete: reparative (secondary) dentin cementum may be stained
63
Q

what is the clinical presentation of tetracycline staining

A
  • yellowish to gray (oxidized tetracycline) color of enamel and dentin
  • may be generalized or horizontally banded depending on duration of tetracycline exposure
  • alveolar bone may also be stained bluish red (particularly with minocycline use, 10% after 1 year and 20% after 4 years of therapy)
64
Q

what is the dx for tetracycline staining

A

clinical appearance and histroy
- fluorescence of teeth may be noted with ultraviolet illumination

65
Q

what is the ddx for tetracycline staining

A

dentinogenesis imperfecta

66
Q

what is the tx for tetracycline staining

A

restorative/cosmetic dental techniques

67
Q

what is the prognosis for tetracycline staining

A

good

68
Q

what is addisons disease

A

destruction of adrenal cortex
- lowered cortisol and increased ACTH
- cannot tolerate stress: adrenal crisis

69
Q

what is the etiology of addisons disease

A
  • most commonly autoimmune
  • chornic infectious disease and sepsis: HIV, CMV, fungal infection
  • drugs
70
Q

what does addisons disease require fot tx

A
  • cortisol replacement
  • surgery and stress may require supplemental corticosteroids
  • pain control is important
71
Q

what are the cutaneous findings in addison disease

A

-hyperpigmentation of skin and mucous membranes
- longitudinal pigmented bands in the nails
- vitiligo
- decreased axillary and pubic hair in women
- cailcification of auricular cartilage in men

72
Q

what are the related features of addison disease

A

-abdominal pain
- electrolyte abnormalities - hyponatremia and hyperkalemia
- postural hypotension
- anorexia and weight loss
- fatigue
- shock, coma and death if untreated

73
Q

how is addison disease dx

A
  • failure to respond adequately to corticotropin stimulation test
74
Q

what is the mangement for addison disease

A

lifelong replacement therapy of glucocorticoids and mineralocorticoids

75
Q

what is secondary adrenal insufficiency and how is it treated

A
  • impaired/destructive pituitary disease
  • low cortisol and low ACTH; aldosterone unchanged
  • lower dose replacement therapy
76
Q

what is tertiary adrenal insufficiency and what is the treatment

A
  • impaired function of hypothalamus
  • most commonly a result of chronic exogenous steroid use
  • lower dose replacement therapy
77
Q

what needs to be considered with hyperadrenalism

A
  • BP and glucose levels
  • avoid NSAIDs and aspirin -> peptic ulcers, GI bleed
  • if osteoporosis and osteopenia
  • more prone to periodontal bone loss
  • may have history of bisphosphonate use
  • impaired wound healing may be a result of both hyperadrenalism and adrenal insufficiency
78
Q

what does the neccesity for supplemental corticosteroids in adrenal insufficiency depend on

A
  • type
  • severity/stability/ medical status
  • dental proceudre being performed (long: more than 1 hour or invasive)/ type of stress/dental infection
79
Q

what are the signs of adrenal crisis

A
  • hypotension - monitor BP- vasopressors, patient position, fluid replacement
  • abdominal pain
  • myalgia
  • fever
  • supplement with 100mg of hydrocortisone and send to ED
80
Q

what needs to be considered with pain control with adrenal insufficiency

A
  • adequate anesthesia, long acting agent at end of procedure
  • good post op pain control
81
Q

what is peutz jeghers and when do symptoms appear

A
  • an autosomal dominant genetic condition affecting around 1 in 50,000 and 1 in 200.000 individuals
  • symptoms usually appear during the first decade of life
82
Q

what is seen in peutz jeghers

A
  • dark skin freckling (melanocytic macules) around the mouth, eyes, nostrils, fingers, oral mucosa and perianal
  • GI polyps (hamartomatous polyposis) causing nausea, vomiting, abdominal pain, intestinal obstruction and rectal bleeding
  • increased risk for intestinal and other GI cancers
83
Q

describe the mucocutaneous pigmentation seen in peutz jeghers

A
  • seen in 95% of patients
  • 1mm to 5mm in size
  • appears by 1 or 2 years of age. fades after puberty except buccal mucosa
84
Q
A

Oral Medicine and Diagnosis (5 decks)

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