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D2: 622 Oral Pathology > Chapter 16: Dermatologic > Flashcards

Chapter 16: Dermatologic Flashcards

1
Q

Autosomal Dominant
Thick white buccal mucosa bilaterally
Benign hyperparakeratotic
No treatment

A

White sponge nevus

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2
Q 
Autosomal dominant
NC Lumbi Indians
Thick white plaques on buccal mucosa
Dyskeratosis
Benign, no Tx
A

Hereditary Benign Intrepithelial Dyskeratosis

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3
Q

Autosomal dominant

Red, itchy papules with foul ododr

Trunk and scalp
Ridges and split nails

Oral white papules
Keratolytic agents

A

Darier’s Disease

Keratosis Follicularis

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4
Q

Identical histology to Darier’s disease

Orally: Single white papule on hard palate or alveolar ridge

Tx: excision

A

Warty Dykeratoma

Isolated Darier’s Disesase

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5
Q

Autosomal dominant
Freckle like lesions in and around oral cavity and hands

Oral oncogenes

Intestinal polyposis that can change to adenocarcinoma

A

Peutz-jeghers syndrome

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6
Q 
Autosomal dominant
Vascular hamartomas 
Frequent epistaxis
Telangiectasias: intraoral, hands, feet, GI, GU, eye
Iron deficiency including anemia
A

Hereditary Hemorrhagic Telangiectasia

Osler-Weber-Rendu Syndrome

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7
Q

Abnormal collagen production due to genetic abnormalities

Hypermobility of joints and elasticity of skin

A

Ehlers-danlos syndrome

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8
Q

Number of closely related lichenoid reactions that reflect immunologic recognition of a variety of stimuli

A

Lichen planus

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9
Q

Purple
Polygonal
Papular
Pruritic

A

Skin Lichen Planus

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10
Q 
Educate patients
Photograph
Erosive form see four times a year
Biopsy
Reassure
A

How to monitor Lichen Planus in patients

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11
Q

First used in 1895 to diagnose pemphigus
Dislodgement of skin by lateral pressure
Multiple Diseases

A

Nikolsky sign

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12
Q

Average age 60
Women 2:1
Oral Lesions: Conjunctival, nasal, esophageal, laryngeal, vaginal
Clinical vesicles and bullae

A

Benign mucus membrane pemphigoid

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13
Q

Vesicles, bullae, ulcers occur anywhere in oral cavity
Blood filled characteristics
Complaints of oral bleeding, sore gums, difficulty swallowing

A

Clinical signs of Benign Mucus Membrane Pemphigoid

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14
Q

Dapsone (CI: G6PD deficiency)
Steroids
Tetracycline & Niacinamide
Immunosuppresive agents

A

BMMP Tx

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15
Q

Mucocutaneous AI disease characterized by acantholysis due to immune complex deposition at cellular attachment bridges
Intraepithelial clefting

A

Pemphigus Vulgaris

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16
Q

Adults age 50
Rare in kids
Males = Females
Almost all cases have oral involvement

A

Clinical signs of Pemphigus Vulgaris

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17
Q

Intra-epithelial separation

Immunofluorescence testing shows autoantibodies to the spinous layer of skin

A

Pemphigus Vulgaris

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18
Q

Jewish predilection
Ragged erosions and ulcers of ANY oral mucosa
Bullae rupture early and are rarely seen by DDS
(+) Nikolsky sign

A

Pemphigus vulgaris

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19
Q

Oral lesions precede skin lesions
Large, ragged ulcerations
Marginal gingiva erosions early
1-5 Million /year

A

Pemphigus vulgaris

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20
Q

Oral lesions may be the first to present in the potentially fatal disease

Blistering due to autoimmune attack of desmosomes

A

Pemphigus vulgaris

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21
Q

The oral lesions are the first to show and the last to go!

A

Pemphigus vulgaris

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22
Q

Incisional biopsy ASAP
Steroids from dentist and dermatologis
60-80% die w/o steroids
5-10% dies with steroids

A

Pemphigus vulgaris

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23
Q

Intraepithelial separation just above the basal cell layer leaving “row of tombstones”
Acantholsysis with floating Tzanck cells
Positive indirect IF for intercullular IgG, IgM, C3

A

Pemphigus Vulgaris Histology

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24
Q

Cross-reacting antibodies in lymphoma or leukemia attack desmosomal complex
May precede the discovery of the underlying malignancy

Often fatal.

A

Paraneoplastic pemphigus

Neoplasia-Induced Pemphigus

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25
Q

Prioons to steroids, 60-80% cases fatal from infections and electrolyte imbalance

Today 5-10% mortality from complications of medications to manage

A

PV Treatment

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26
Q

Occurs in recipients of allogenic bone marrow transplants

A

Graft vs. Host Disease (GVHD)

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27
Q

HLA matched donor
Hematopoietic stem cells from either bone marrow, peripheral blood or umbilical cord blood

Engrafted cells recognize body as foreign

A

Graft versus host disease

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28
Q 
Conical teeth
Hypohydrosis
Hypodontia
Missing sweat glands
Missing hair
A

Ectodermal dysplasia

29
Q

Milder disease seen:

Patients with better histocompatibility match

Younger patients

Cord blood

Females

A

Graft versus host diesease

30
Q

Occurs a few weeks after transplant

Affects 50% of patients

Mild rash to TEN

Diarrhea, nausea, vomiting, abdominal pain and liver dysfunction

A

Acute Graft versus Host Disease

31
Q

Continuation of acute disease

100 days to years and develops in 33-64%

Mimics autoimmune disease

Skin lesions resemble LP or systemic sclerosis

A

Chronic GVHD

32
Q

33-75% of AGVHD and 80% of CGVHD

Resembles lichen planus

Some complain of burning sensation (R/O candidiasis)

A

Oral Graft vs. Host Disease

33
Q

Ulcerations that are related to chemotherapeutic conditioning and neutropenic state develop first two weeks after BMT

Ulcers that last longer then two weeks AGVHD

A

Oral GVHD

34
Q

Xerostomia is a common complaint

Immunologic response destroying salivary glands

Mucoceles of soft palate

A

Oral GVHD

35
Q

Oral lesion highly predictive index of this disease

Goal of therapy is to prevent occurrence

Careful tissue histocompatibility matching is key

A

Graft versus host disease

36
Q

Prophylactic therapy with immunomodulatory and immunosuppressive agents such as cyclosporine & prednisone

Methotrexate has been added and reduced disease further

A

Treatment of Graft vs Host Disease

37
Q

Thalidomine has shown some promise

Topical CS oral lesions

Psoralen and Ultraviolet A (PUVA) improve lichenoid form

Treat xerostomia

A

Treatment of Graft v. Host Disease

38
Q

Increased proliferative activity of cutaneous keratinocytes

Immunologic with activated T-lymphocytes

A

Psoriasis

39
Q

Well demarcated silvery plaque with silvery scale of surface

Non-symptomatic to itching

Psoriatic arthritis

A

Signs of Psoriasis

40
Q

2nd-3rd decade, persists for years

Improves during the summer/UV light

Symmetrical/scalp, elbows, knees

Oral uncommon?

A

Psoriasis

41
Q

Mild disease has no treatment

Moderate: coal tar, keratolytic agents & UV light, Vit. D analogs, retinoids, trazarotine and calcipotriene

Severe cases: PUVA, methotrexate and cyclosporine

A

Treatment of psoriasis

42
Q

Parakeratosis with elongated rete ridges

CT papillae dilated capillaries close to epithelial surface

Perivacular chronic inflammation

Munroe abscesses

A

Histology of Psoriasis

43
Q

Immunologically mediated condition

Most common of the collagen vascular disorders

1.5 million affected

A

Lupus Erythematous

44
Q

Increased activity of the humoral limb of the immune system (B lymphocytes)

Abnormal function of T lymphocytes

Genetic factors (identical twins 32%/fraternal twins 6%)

A

Systemic lupus erythematous

45
Q

Woman 8x

Average age at diagnosis is 31

Weight loss, arthritis, fatigue, malaise

40-50% butterfly rash

Sunlight makes lesions worse

A

Systemic lupus erythematous

46
Q

40-50% kidney problems, may lead to renal failure (most significant aspect of disease)

Cardiac: Pericarditis, 50% at autopsy have warty vegitations of heart valves (Libman-Sacks endocarditis), sterile overgrowth of fibrinoid material and CT celles (may lead to BE)

A

Systemic lupus erythematous

47
Q

5-40% of cases
P, BM, and G, appears lichenoid

Lupus cheilitis

Varying degrees of ulceration, pain, erythema and hyperkeratosis

A

Systemic lupus erythematous Oral

48
Q

Ulcerated or atrophic with erythematous central zone surrounded by white radiating striae and may show fine stippling of white dots

Lichenoid and may be painful

A

Oral lesions of Lupues erythematous

49
Q

Scaly erythematous patches of sun exposed skin, head and neck common, sun makes it worse

Heal in one area only to appear in another

Oral lesions not without skin

Lichenoid appearance

A

Chronic Cutaneous Lupus Erythematous

50
Q

Patch deposits of PAS and material in BM zone

Subepithelial edema

Direct IF show deposition of one or more, IgM, IgG or C3 in a shaggy granular band at BM zone

Normal skin shows and lupus band test

A

Histology of Lupus erythematous

51
Q

95% of patients + ANA

Antibodies against double stranded DNA in 70% patients with SLE more specific for the disease

A

Lupus erythematous

52
Q

With treatment 5 year survival = 95%, 15 year = 75%

Depends of organs affected and remissions, renal failure most common cause of death

Worse for men

A

Prognosis of systemic lupus erythematous

53
Q

Avoid sun exposure

NSAID with antimalarial drugs (hydroxycloroquine) for mild disease

Severe disease: heart, renal, thrombocytopenia, arthritis (CS + other immunosuppressive agents)

A

Treatment of Lupus erythematous

54
Q

Known as scleroderma and immunologically mediated

Dense collagen deposited in tissues

Adults: Women 3x

First sign is Raynaud’s phenomenon (vasoconstrictive event triggered by emotional distress or exposure to cold)`

A

Systemic sclerosis

55
Q

Organ involvement is subtle at first

Fibrosis of lung, heart, kidney, and GI tract

Pulmonary fibrosis significant leading to pulmonary hypertension and heart failure are primary cause of death

A

Systemic sclerosis

56
Q

Acro-osteolysis: resorption of terminal phalanges and flexure contractures produce shortened club-like fingers

Vascular events and abnormal collagen deposition produces ulceration of the fingertips

A

Systemic sclerosis

57
Q

Collagen deposition results in smooth, taut, mask-like face

Nasal alae atrophied in a pinched nose (mouse facies)

A

Systemic sclerosis

58
Q

Microstomia 70%, pulse string furrows radiating from mouth

Loss of attached gingiva

Dysphasia: deposition of collagen results in hypomobile tongue and inelastic esophagus hindering swallowing

A

Oral systemic sclerosis

59
Q

Widened PDL space

Resorption of posterior ramus, coronoid process and condyle in 10-15% of patients (resorbed due to increased pressure associated with abnormal collagen production)

A

Oral systemic sclerosis

60
Q

D-penicillamine inhibits collagen production

Esophageal dilation

Calcium channel blockers help peripheral blood flow

Angiotension-converting enzyme for HTN if kidney is involved

A

Treatment of systemic sclerosis

61
Q

Hard to wear dentures with microstomia and inelasticity of mouth

80% survival = 2 years

30-50% = 8 years

15-3-% = 15 years

A

Systemic Sclerosis

62
Q

Calcinosis cutis

Raynaud’s phenomenon

Esophageal dysfunction

Sclerodactly

Telangiectasias

A

CREST Syndrome

63
Q

Movable, non-tender subcutaneous nodules

.5 cm to 2 cm in size

Deposition of calcium salts

A

Calcinosis Cutis

64
Q

Dramatic blanching of digits (dead white) when exposed to cold, turns bluish few minutes later (venous stasis)

After warming dusky-red hue (return of hyperemic blood flow)

May have throbbing pain

A

Raynaud’s Phenomenon

65
Q

Cause is abnormal collagen deposition in esophageal submucosa

not noticeable early in CREST but may cause difficulty in swallowing later

Barium swallow x-ray studies to diagnose

A

Esophageal Dysfunction

66
Q

A result from fibrosis and atrophy of smooth muscle in the GI tract

Decreased function may cause: hyper-mobility, dysphasia, reflex esophagitis and fibrotid strictures

Symptoms are not progressive, but are not reversible

A

Esophageal dyfunction

67
Q

Fingers become stiff and skin takes a smooth, shiny appearance

May undergo permanent flexure and “claw” deformity

Abnormal deposition of collagen in the dermis is the cause

A

Sclerodactyly

68
Q

Similar to those seen in HHT

Bleeding form fuperficial dilated capillaries may occur

Facial skin and vermillion zone of lips commonly affected

A

Telangiectasias

69
Q

Anticentromere antibodies

HHT in differential if other signs of CREST not there

Histopathologic findings similar to scleroderma but milder

Prognosis better then scleroderma with 80T

A

CREST Syndrome

D2: 622 Oral Pathology (36 decks)

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