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Oral Pathology, Stephen > Chpt 16- dermatology > Flashcards

Chpt 16- dermatology Flashcards

1
Q

group of inherited conditions in which two or more ectodermally derived anatomic structures fail to develop

A

ectodermal dysplasia

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2
Q

Ectodermal dysplasia can affect what

A 
skin
Hair
Nails
Teeth
Sweat glands
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3
Q

Skin and hair problems associated with Ectodermal dysplasia

A

sparse hair, eyebrows (blond)
Periocular hyperpigmentation (dark circles around eyes)
Dystrophic nails

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4
Q

Why would an ectodermal dysplasia patient have xerostomia

A

decreased salivary gland development

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5
Q

Tooth problems with ectodermal dysplasia

A

hypodontia

Cone shaped teeth

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6
Q

3 treatments for Ectodermal dysplasia

A

genetic counseling (w/ Dr. Elsea)
Prosthetic teeth
Do a pedigree and a microarray

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7
Q

Autosomal dominant inherited skin disorder manifesting as thick white buccal mucosa bilaterally, may be corrugated or velvety

A

White sponge nevus

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8
Q

Is White Sponge nevus malignant and is there treatment

A

benign, no treatment

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9
Q

Autosomal dominant condition seen in descendants of North Carolina Indians, with thick white plaques on the buccal mucosa(like white sponge nevus) and the conjunctiva

A

Hereditary Benign Intraepithelial Dyskeratosis

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10
Q

Histology Dr Siversky said to know for Hereditary Benign Intraepithelial Dyskeratosis

A

Epithelial clefting

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11
Q

Autosomal dominant skin problem with erythematous puritic papules on the trunk and scalp with foul odor, dystrophic nails (ridged and split)

A

Keratosis follicularis (Darier’s disease)

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12
Q

What is the oral manifestations of Keratosis Follicularis/ Darier’s Disease

A

multiple white papules

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13
Q

How treat Keratosis Follicularis/ Darier’s Disease

A

Keratolytic agents or emollients

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14
Q

Histopathologically identical to Darier’s Disease, but manifests orally as a single white papule

A

Warty dyskeratosis

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15
Q

Where does the single white papule of Warty dsykeratoma appear

A

on hard palate or alveolar ridge

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16
Q

Autosomal dominant with freckle like lesions in and around oral cavity, on the hands, and having intestinal polyps with a predisposition to go to adenocarcinoma

A

Peutz-Jeghers

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17
Q

What is the difference, as far as the intestinal polyps, between Peutz-Jeghers and Gardners Syndrome

A

Peutz-Jeghers has benign intestinal polyps while Garderns are going to go malignant

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18
Q

Treatment for Peutz-Jeghers

A

Genetic counseling
Monitor for intussusceptions(one part of intestine invaginates into another section, like a telescope [Wikipedia] or malignant transformation

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19
Q

Autosomal dominant conditions of multiple vascular hamartomas due to decreased blood vessel wall intregrity. Pt can have frequent epistaxis (nose bleeds) . Telangiectasias can be intraoral, hands, feet, GI tract, GU tract and eye

A

Hereditary Hemorrhagic telangiectasia

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20
Q

With any bleeding disorder, even Hereditary Hemoorhagic Telangiectasia, what should always be considered as another problem that might follow

A

Iron deficiency anemia

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21
Q

Genetic abnormalities that lead to abnormal collagen manifesting as hypermobile joints, elasticity of skin (carnival person)

A

Ehlers-Danlos

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22
Q

Oral concerns with Ehlers-Danlos

A

subluxation of TMJ

Don’t respond well to surgery due to defective collagen Bruise and bleed easily

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23
Q

Chronic inflammatory disease causing white striations, papules or plaques on buccal mucosa, tongue and gingival, thought to be autoimmune related by CD8 T cells causing oral epithelial cells apoptosis

A

Lichen Planus

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24
Q

Demographics for Lichen planus

A

45-60 y.o (rare in children) Women 2x more than men

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25
Q

Is Lichen planus only caused by autoimmune response

A

No, there can be drugs whose side effects cause a Lichenoid drug reaction, however, that goes away when drugs are stopped. True Lichen planus is chronic

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26
Q

If you see this phrase, you should think of Lichen Planus

A

Striae of Wickham

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27
Q

What are the skin manifestations of Lichen planus

A

purple puritic polygonal papules

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28
Q

When biopsying Lichen planus, do you biopsy the red or the white area

A

White area, red will just show ulceration (basement membrane with no epithelial covering)

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29
Q

Histology for Lichen Planus

A

saw tooth rete pegs and loose basal cell layer

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30
Q

Which phase of Lichen planus is treated: Reticular or erosive, and with what

A

Erosive. Corticosteroids because it is autoimmune mediated

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31
Q

What can superimpose on top of Lichen planus especially during corticosteroid treatment of the Erosive form

A

candidiasis

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32
Q

Dislodgement of skin by lateral pressure, can be a symptom in multiple diseases

A

Nikolsky sign

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33
Q

2 disease we have been taught that have a positive Nikolsky sign

A

Pemphigus

Pemphigoid

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34
Q

Histologically, which has a change in the basement membrane: Pemphigoid or pemphigous

A

Pemphigoid (goid goes down to the basement)

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35
Q

Histologically, which has intraepithelial separation: Pemphigoid or pemphigous

A

Pemphigus

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36
Q

Which has larger lesions Pemphigoid or pemphigous and why

A

pemphigoid, because they are thicker (all the way to the basement)

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37
Q

Pemphigoid type that affects women over the age of 60 manifesting orally as vesicles or bullae

A

benign mucous membrane pemphigoid

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38
Q

What are the clinical sizes of the benign mucous membrane pemphigoid vesicles and bullae

A

vesicles are less than 5mm

Bullae are greater than 5 mm

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39
Q

What is the histology for benign mucous membrane pemphigoid (Siversky says to be able to ID this for the final

A

subepithelial clefting

Immunofluorescence at basement membrane

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40
Q

Most commonly used antibiotics for treating benign mucous membrane pemphigoid

A

Tetracycline
Niacinamide
Nicotinamide

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41
Q

If going to treat someone with benign mucous membrane pemphigoid with Dapsone, what must you check first

A

that they are not Glucose-6-Phosphate dehydrogenase deficient. Can cause aplastic anemia

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42
Q

Most common of the autoimmune blistering conditions

A

bullous pemphigoid

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43
Q

mucocutaneous autoimmune disease that has intrapepithelial acantholysis resulting in intraepithelial clefting . If untreated is fatal

A

pemphigus vulgaris

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44
Q

What is usually the first sign of Pemphigus Vulgaris, but also the hardest to treat

A

oral lesion, “first to show, last to go”

45
Q

Pemphigus Vulgaris intraepithelial clefting has what in the middle

A

Tzank cells (floating cells in the intraepithelial cleft)

46
Q

Where does the Immunofluorescence show up in Pemphigus vulgaris versus pemphigoid

A

Pemphigus vulgaris at immunofluoresces at the spinous layer while pemphigoid does so at the basement membrane

47
Q

What is a major distinction demographically between pemphigus and pemphigoid

A

pemphigous affects M=F
Pemphigoid prefers males
Pemphigous has Jewish predilection

48
Q

Pemphigus should be managed by what medical specialty

A

rheumatologist

49
Q

How is pemphigus diagnosed

A

incisional biopsy

50
Q

How is pemphigus treated

A

jointly with dermatologist with Steroids

51
Q

What is patient outcome if not treated with steroids for pemphigus

A

60-80% die without steroid treatment

52
Q

The intraepithelial separation just above the basement membrane in Pemphigus casues what look histologically

A

row of tombstones (the basal layer sticking up into the intraepithelial cleft)

53
Q

pemphigus type caused by cross-reacting antibodies in lymphoma or leukemia attacking desmosomal complexes that may precede the discovery of an underlying malignancy

A

paraneoplastic pemphigus/ neoplasia-induced pemphigus

54
Q

Occurs in recipients of allogenic bone marrow transplantation. The HLA matched donor hematopoietic stem cells recognize their new host as foreign and begin to attack

A

Graft Versus Host Disease

55
Q

only transplant that does not require immunosuppressive drugs for life

A

successful bone marrow transplant

56
Q

What factors can make Graft versus host disease milder

A

young pt
Good histocompatability match
Cord blood
Female

57
Q

Graft versus host disease seen within a few weeks of transplant and can manifest as a mild rash to severe sloughing that resembles Toxic epidermal necrolysis

A

Acute Graft Versus Host Disease

58
Q

can be seen 100 days to years after transplant. Considered a continuation of acute graft versus host disease. Will mimic an autoimmune disease

A

Chronic Graft Versus Host Disease

59
Q

Chronic Graft Versus Host disease will resemble what clinically

A

Lichen planus or systemic sclerosis

60
Q

Which manifests more orally, Chronic or Acute Graft versus host disease

A

Chronic (80%)

61
Q

Oral graft versus host disease will show ulcerations within the first two weeks post bone marrow transplant why

A

caused by chemotherapeutic conditioning and the neutropenic state

62
Q

If the ulcers last longer than 2 weeks beyond the 2 week post bone marrow transplant buffer zone have what

A

Acute Graft Versus Host Disease

63
Q

beyond ulcers, what are 2 other oral manifestations of oral Graft Versus Host Disease

A

Xerostomia due to immunologica destruction of salivary glands
Mucocelles on soft palate

64
Q

Mucoceles, which are seen commonly on lips and buccal mucosa of young males, if seen on the soft palat, one should think what

A

Graft Versus Host Disease

65
Q

Primary strategy for dealing with Graft versus host disease

A

reduce or prevent occurrence with good histocompatability match

66
Q

What is the prophylaxis for Graft Versus host disease

A

immunomodulatory + immunosuppressive: prednisone + cyclosporine or tacrolimus. Give corticosteroids for oral lesions and treat xerostomia

67
Q

Common chronic skin disease characterized by an increased proliferative activity of the cutaneous keratinocytes. Mild disease that can be treated with keratolytic agents, sunlight, Vit D analogues

A

Psoriasis

68
Q

Classic example of an immunologically mediated condition (794)

A

Lupus Erythematosus

69
Q

Most common of the collagen vascular and connective tissue disease in the US

A

Lupus Erythematosus

70
Q

Most immunologic diseases, including Lupus Erythematous, affect which gender predominantly

A

females

71
Q

Common findings of systemic lupus erythematosus (794)

A 
fever
Weight loss
Arthritis
Fatigue
Malaise
Characteristic butterfly pattern rash over malar area and nose that spares the nasolabial folds and is exacerbated by sun exposure
72
Q

Most significant aspect of systemic lupus erythematosus (794)

A

kidney failure

73
Q

Systemic lupus is caused by increased activity of what part of the immune system

A

humoral limb (B lymphocytes [stimulated by abnormally functioning T lymphocytes ?])

74
Q

What is another systemic mortality risk in systemic lupus erythematosus

A

bacterial endocarditis

75
Q

How can systemic lupus erythematous manifest orally

A

look lichenoid on palatal, buccal mucosa, and gingival. Ulcers, pain, erythema, hyperkeratosis

76
Q

if Lupus manifests on the vermillion zone of the lower lip it is called

A

Lupus cheilitis

77
Q

Lupus type with no systemic symptoms, and only lesions on the skin and mucosal surfaces, called discoid lupus erythematous and present on sun-exposed areas of skin.

A

Chronic cutaneous Lupus erythematosus

78
Q

What is the character of the oral lesions in Chronic Cutaneous Lupus erythematosus versus erosive lichen planus, since they both look alike orally

A

Chronic cutaneous Lupus erythematosus oral lesions will not manifest without skin lesions

79
Q

What is a lab test that is high in Lupus erythematous patients

A

high in ANA = autonucleic antibody

80
Q

Most common cause of death in systemic lupus erythematosus

A

renal failure

81
Q

Treatments for Lupus if mild

A

avoid sun
NSAIDs
Antimalarials (hydroxychloroquine)

82
Q

Treatment for Lupus if severe

A

corticosteroids and other immunosuppressives

83
Q

If see lichen planus, what else can be put on the differential

A

Lupus erythematous

84
Q

immunologically mediated deposition of dense collagen in tissues. Also known as Scleroderma

A

Systemic sclerosis

85
Q

First sign of Systemic sclerosis, but is not diagnostic for the disease

A

Raynaud’s phenomenon

86
Q

Systemic sclerosis higher in which gender

A

females

87
Q

What is the cause of death in systemic sclerosis

A

pulmonary fibrosis, leading to pulmonary hypertension and heart failure

88
Q

What does pulmonary fibrosis do

A

reduces lung surface area for oxygen exchange

89
Q

resorption of terminal phalnages and flexure contractures producing club like fingers in systemic sclerosis and some other diseases

A

acro-osteolysis

90
Q

What is the clinical appearance of a person with systemic sclerosis

A

smooth, taut, mask-like face, nasal alae atrophy = mouse facies

91
Q

Character of the mouth of pt with systemic sclerosis

A

microstomia with purse-string furrows radiating from the mouth

92
Q

Character of the gingival in pt with systemic sclerosis

A

lose attached ginigva

93
Q

Why dysphagia in systemic sclerosis

A

collagen deposits cause hypomobile tongue coupled with inelastic esophagus

94
Q

Radiographic appearance of person with systemic sclerosis

A

widened PDL (isn’t that a sign in Paget’s Disease also?)

95
Q

Does systemic sclerosis with its widened PDL and loss of attached gingival respond to periodontal therapy

A

NO

96
Q

Siversky loves this disease and brought up the fact that this disease, radiographically, shows a loss of the lamina dura

A

hyperparathyroidism

97
Q

Systemic sclerosis that is localized usually leaving a scar called en coup de sabre, Dr, Siversky mentioned it as Morpha

A

localized scleraderma

98
Q

What can the pressure of collagen deposition cause orally and skeletally

A

resorption of posterior ramus, coronoid process and condyle

99
Q

What systemic medication is prescribed to try and inhibit collagen production in systemic sclerosis

A

D-penicillamine

100
Q

Prescribing calcium channel blockers to increase peripheral blood flow or Angiotensin-converting enzyme inhibitors if the kidney is involved, all have the goal of doing what for systemic sclerosis

A

slow the disease process

101
Q

would it be smart to fabricate dentures for a systemic sclerosis patient

A

No, due to microstoma and inelasticity of mouth

102
Q

What does CREST stand for

A 
Calcinosis cutis 
Raynaud’s phenomenon 
Esophageal dysfunction 
Sclerodactyly 
Telangiectasias
103
Q

Part of CREST syndrome characterized by movable, non-tender, subcutaneous nodules, .5cm to 2cm in size caused by the deposition of calcium salts

A

Calcinosis cutis

104
Q

Part of CREST as well as other syndromes characterized by dramatic blanching of digits (dead white) when exposed to cold or even stress. Digit will turn blue a few minutes later with venous stasis, then a final dusky red hue as hyperemic blood flow returns. May be accompanied by throbbing pain

A

Raynaud’s phenomenon

105
Q

Is Raynaud’s phenomenon indicative of scleraderma or CREST

A

No

106
Q

Diagnosed with a barium swallow, this part of CREST is due to abnormal collagen deposition in esophageal submucosa. It is not noticed early in CREST, but will affect swallowing later

A

Esophageal dysfunction

107
Q

Part of CREST caused by abnormal deposition of collagen in the dermis leading to fingers becoming stiff, skin becoming shiny, and digits can undergo permanent flexture to a claw-like deformity

A

Sclerodactyly

108
Q

Part of CREST due to fragile vessels, and is similar to Hereditary Hemorrhagic Telangiectasia

A

Telangiectasias

109
Q

Which has better prognosis, CREST or systemic sclerosis/scleraderma

A

CREST

Oral Pathology, Stephen (13 decks)

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