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Exam 2 Skin block > Dermatophatology part 5 > Flashcards

Dermatophatology part 5 Flashcards

1
Q

Pempphigus vulgaris

A

most common and most severe type of pemphigus, 80% of cases

30-50 y.o., men and women

involves scalp, face, axillae, groin, trunk, points of pressure, oral ulcers

5-15% mortality

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2
Q

Pemphigus vulgaris path

A

IgG against desmogleins 1 and 3 in desmosomes in the suprabasal deep epidermis and mucosal epithelium

suprabasal split; acantholytic blisters

80-90% with oral lesions

general involvement with flaccid blisters which rupture leaving erosion with crust

psoitive nikolsky sign (pressure on blister caues later spread of lesion.)

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3
Q

pEMPHIGUS VULGARIS histo

A

acatholysis (lysis of intracellular adhesions connecting squamous epithelial cells)

single layer of intact basal cells forms the blister base (row of tombstones)

superficial lymphocytic inflammatory infiltrate in dermis

eosinophils may be seen within the dermal infiltrate

DIF: net like patter of intercellular IgG deposits

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4
Q

pemphigus vegetans

A

rare form

large moist verrucous, vegetating plaques rather than blisters

oral lesions common

assocaited with ulcerative colitis

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5
Q

pemphigus foliaceus

A

brazil and other geographic regions

taret Ag is Dsg1

subcorneal blister

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6
Q

Pempphigus tx

A

immunosuppressives and supportive

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7
Q

Bullous pemphigoid

A

elderly individuals

inner aspects of thigs, flexor surfaces of forearms, axillae, groin and lower abdomen

oral lesions in 10-15%, usually after cutaneous lesions

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8
Q

Bullous pemphigoid pathology etiology

A

targets BPAg1 and 2 in the hemidesmosomes (only BPAg2 is known to cause blisters)

subepidermal, nonacantholytic blisters

sturdy blisters (roof is full thickness of epidermis), usually 2 cm but up to 4-8 cm, do not ruputres as easily as pemphigus, without infection will heal without scarring

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9
Q

bullous pemphigoid histo

A

subepidermal, nonacantholytic blisters

early perivascular infiltrate of lymphocytes

eosinophils typically present in blister cavity

peripheral eosinophilia and elevated serum IgE often present

direct immuno fluorecence shows linear deposition of c3 and igG along dermoepidermal junction.

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10
Q

Dermatitis herpetiformis

A

Incidience is 39/100000

onset is 20-60 years with 2:1 M:F ration

etiology: IgA autoantibodies to transglutaminases bind to TG in gut and cross react with reticulin in fibrils in skin

associated with HLA B8, DR, DQ

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11
Q

Dermatitis herpetiforms Pathology etiology

A

IgA autoantibodies to transglutaminases which cross react with reticulin in the fibrils that anchor hemidesmosomes to the dermis

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12
Q

dermatitis herpetiformis gross

A

symmetrically grouped lesions

papules and plaques progressing to vesicles and bullae

buttocks, elbows, knees, scapular areas

very pruritic

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13
Q

Dermatitis herpetiforms associations

A

gluten sensitive enteropathy occurs in nearly all patients and must be demonstrated by small bowel biopsy

there may be no GI symptoms

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14
Q

Dermatitis herpetiformis histo

A

microabscesses at dermal papillae

Subepidermal blsiter

neutrophil microabscesses and fibrin depsotion in tips of dermal papillae

basal cells overlying tips show dermoepidermal separation eventually coalescing to form blister

direct immunofluorescence demosntrates discontinous granular deposition if IgA in tips of dermal papillae.

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15
Q

Dermatitis herpetiformis diagnosis

A

skin biopsy

antiendomysial antibodies (specific for TG)

endoscopy blunting of villi in small bowel

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16
Q

Dermatitis herpetiformis tx

A

gluten free diet: response is very slow\

dapsone: response within hours, check G6PD level, monitor methemoglobin and CBC levels

a chronic disease, 1/3 pts may have spontaneous remission

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17
Q

Epidermylysis bullosa

A

group of disorders caused by inherited defects in proteins that lend stability to the skin

at least ten genes have been implicated

common to all is tendency to form blisters at points of pressure, rubbing, trauma

sx at or soon after brith

18
Q

Epidermolysis bullosa simplex type

A

mutations in either gene encoding keratin 14 or 5 which form a functional keratin fiber resulting in a basal cell layer defects

19
Q

Epidermolysis bullosa: Jucntional type

A

blisters formed from separation of lamina lucida

20
Q

Epidermolysis bullosa: Dystrophic types

A

blister below lamina densa, from defect in collagen VII, scar formation on healing

21
Q

Epidermolysis bullosa: Non herlitz junctional

A

defect in laminin VB3

22
Q

Epidermylysis bullosa: Histo

A

fibrin deposition in the floor of the blister cavity

some cases may show neutrophils within the papillary dermis, while other cases are histologically indistibguishable from bullous pemphigoid

dermal fibrosis (scar) may be present in the dermis

23
Q

Prophyria cutanea tarda assocations

A

30-50 years, females on OCP, alcohol use, associated Hep C

24
Q

Prophyria cutanea tarda etiology

A

uroporphyrinogen decarboyxlase (UROD deficiency > excessive accumulation of porphyrins

25
Q

Prophyria cutanea tarda Type 1

A

acquired by exposure to drugs/chemicals, hepatic UROD is inhibited

26
Q

Prophyria cutanea tarda Type 2

A

Autosomal dominant, deficient in RBCs and fibroblasts

27
Q

Porphyria cutanea Tarda gross and sx

A

porphyrins make skin photosensitive

tense subepidermal bulla on normal appearing skin in sun expsoed areas

may also get hypertrichosis on face

exacerbated by iron; alcohol; smoking; estrogens; hepatitis C; HIV; halogenated hydrocarbons

28
Q

Prophyria cutanea tarda: Diagnosis

A

test for increased uroporphyrin in urine, will fluoresce orange under wood’s lamp

29
Q

Porphyria cutanea tarda: TX

A

avoid alcohol, estrogens, fungicides

phlebotomy to reduce iron stores

low dose of chloroquine if low Hgb

30
Q

Prophyria cutanea tarda histology

A

subepidermal vesiculation

acral skin with compact orthokeratosis

solar elastosis (due to patient age and characteristics acral location)

minimal inflammatory infiltrate

protuberance of rigid dermal papillae into blister cavity (festooning)

thickening of walls of superficial dermal vessels

31
Q

Acne vulgaris

A

may begin as early as 9-11 years old

may continue into 3rd and 4th decade of life

Most patients have both obstructive and inflammatory lesions

distribution is on face, chest, and upper back

32
Q

Acne vulgaris: pathogenesis

A

obstruction of sebaceous follicles by sebum promotes proliferation of propionibacterium acnes (anaerobe)

33
Q

Obstructive acne: Closed comedones

A

whiteheads. flesh colored dome shaped papules

34
Q

Obstructive acne: Open comedones

A

blackheads. Dilated pore filled with keratinous material (not dirt)

35
Q

Inflammatory acne

A

lesions progress from papules/pustules to nodules to cysts

36
Q

Acne vulgaris risk factors

A

male sex

puberty

cushing’s syndrome

oily complexion

androgen excess

eating chocolate and fatty foods does not worsen acne

37
Q

ACne vulagaris histology

A

keratinization of lower portion of the follicular infundibul;um with development of keratin plug blocking outflow of sebum to skin surface

hyperatrophy of sebaceous glands with puberty (or increased hormonal stimulation)

lipase synthesizing bacter (propiuonibacterium acnes) colonizing the upper and midportion of the hair follicle converting lipids within sebum to proinflammatory fatty acids

inflammation of the folice associated with release of cytotoxic and chemotactic factors

38
Q

Acne vulgaris tx

A

start with 1 drug and then add to regimen if no improvement within 6 weeks

  1. topical bezoyl peroxide- destroys bacteria and dries skin
  2. topical retinoids: causes peeling of skin which prevents pore clogging, good for comedonal acne (tretinoin, adapalene, tazarotene)
  3. topical erythromycin or clindamycin: suppress P. acnes.
  4. systemic antibiotics: tetracyclines, erythromycin, clindamycin, bactrim
  5. Oral retinoids: for severe cystic acne unresponsive to the above treatments. (teratogen)

Some oral contraceptive may improve patient’s acne

39
Q

ACne rosacea

A

4 stages

  1. flushign episodes (pre rosacea)
  2. Persisten erythema and telangeictasias
  3. Pustules and papules
  4. Rhinophyma: skin on nose becomes thick and greasy, hyperplasia of sebaceous glands, connective tissue and vasculature. (Nose)

comedoens are not found

affect nose and cheeks including nasolabial folds

40
Q

Acne rosacea tx

A

diagnosis si made clinically

avoid alcoholic and hot bevarages, extremes of temperature and emotional stressors

treat long term with topical metronidazole gel and oral doxycycline

41
Q

Rosacea histo

A

perfollicular infiltrate of lymphocytes

surrounded by ermal edema and telangiectasia

rhinophyma: hypertrophy of sebaceous glands

and follicular plugging by keratotic debris

Exam 2 Skin block (22 decks)

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