Dermatopathology Flashcards
(48 cards)
1
Q
Macule
A
A flat, non-elevated, circumscribed lesion < 1cm
2
Q
Patch
A
A flat, non-elevated, circumscribed lesion > 1cm
3
Q
Papule
A
An elevated lesion < 5 mm in diameter
4
Q
Nodule
A
An elevated lesion > 5 mm in diameter, but less than 2 cm
5
Q
Tumor
A
An elevated lesion > than 2 cm in size (any lump)
6
Q
Plaque
A
An elevated, flat-topped lesion, usually > 5 mm across
7
Q
Vesicle
A
A fluid-filled cavity < 5mm in diameter
8
Q
Bullae
A
A fluid-filled cavity > 5mm in diameter
9
Q
Blister
A
An informal, lay term for a vesicle or bulla
10
Q
Pustule
A
A purulent (pus-filled) vesicle or bulla
11
Q
Crust
A
A dried collection of blood, serum, or pus
12
Q
Lichenification
A
Thickening of the skin with increases markings due to repetitive trauma (scratching)
13
Q
Atrophy
A
An area of skin that has become very thin and wrinkled
14
Q
Wheal
A
A skin elevation caused by swelling (dermal edema) that can be itchy and usually disappears soon after erupting
15
Q
Onycholysis
A
Separation of the nail from the nail bed.
16
Q
Koebner phenomenon
A
Refers to skin lesions that appearing in lines of trauma
17
Q
Telangiectasia
A
Small, dilated blood vessels that appear close to the surface of the skin
18
Q
Ulcer
A
Lesion that involves loss of the upper portion of the skin (epidermis) and part of the lower portion (dermis)
19
Q
Excoriation
A
A scratch which causes epithelial disruption with bleeding and ulceration
20
Q
Hyperkeratosis
A
Increased thickness of the stratum corneum
21
Q
Parakeratosis
A
Retention of keratinocyte nuclei in hyperkeratosis
In mucous membranes parakeratosis is normal
Usually associated with thinning of granular layer and see with diseases associated with increased turnover: psoriasis or dandruff.
22
Q
Orthokeratosis
A
No retention of keratinocyte nuclei in hyperkeratosis
23
Q
Acanthosis
A
Increased thickness of the squamous epithelium (hyperplasia)
24
Q
Acantholysis
A
Loss of intercellular desmosomes leads to discohesion and separarion of the keratinocytes (chronic problem)
25
Dyskeratosis
Abnormal (premature) keratinization of the keratinocytes below the stratum granulosum.
Dyskeratosis congenita is congenital disease associated with reticular skin pigmentation, nail degeneration, leukoplakia on mucous membranes associated with short telomeres
26
Spongiosis
Intercellular edema in epidermis with fluid between the squamous epithelial cells and easily identified desmosomes
Easily characterized by intraepidermal vesicles (fluid containing spaces in the epidermis), juicy papules, and/ or lichenification
27
Lentiginous
A linear pattern of melanocytic proliferation at the dermal-epidermal junction
28
Albinism
that there are normal numbers of melanocytes, but these cells lack of or have a defective tyrosinase enzyme and cannot produce melanin pigment
29
Vitiligo
Non-inflammatory
Disorders of Pigmentation
Loss of pigment producing melanocytes - can be complete or partial. May display koebner phenomenon.
Segmental form associated with autoimmune disease, non-segmental forms often display symmetry.
Patients treated with UV light and psoralen.
Immunostain reveals no reaction with tyrosinase, Melan-A or S100 stains.
30
Epheliis
Non-inflammatory
Disorders of Pigmentation
Freckle - typically small red-brown macules.
Increase in melanin with basal keratinocytes.
31
Melanotic Macules
Non-inflammatory
Disorders of Pigmentation
benign, localized dark brown pigmentation of the mucosa. Most commonly on the lip, oral mucosa and the genitalia.
Increased melanin pigmentation in the basal layer
32
Melasma
Non-inflammatory
Disorders of Pigmentation
Mask of pregnancy
mask-like tan-brown macules and patches on the face. Hormone related (estrogen and progesterone) may spontaneous regression after delivery.
May also be seen Native Americans - (forearms) as well as Russians, Germans, and Jews (face)
Due to increase in melanin pigment in basal layer of epidermis or within dermal macrophages.
33
Lentigo
Due to increase in number of melanocytes at dermal junction. Not related to sun exposure.
34
Urticaria
Inflammatory - Acute processes
Hives - raised erythematous plaques or papules which arise quickly and disappear within 24 hours.
Skin exposed to foreign material taken up by langerhan cells and causes allergic reaction (IgE mediated). Can also occur independent of IgE with opiates and and some antibiotics
Minimal increase in inflammatory cells around the superficial vascular plexus, including lymphocytes, eosinophils, neutrophils
Increased dermal edema, NO epidermal changes
35
Acute eczematous (spongiotic) dermatitis
Inflammatory - Acute processes
eczema - All are characterized by erythematous, oozing, scaly vesicles and bullae that develop into scaly plaques over time
Spongiotic dermatitis - Intraepidermal edema; mild, superficial perivascular lymphocyte infiltrate, eosinophils present in some subtypes.
36
Erythema Multiform
Inflammatory - Acute processes
See macules, papules, vesicles and bullae. The characteristic lesion is a targetoid lesion or “iris-like” lesion. Most common on the acral (limb or other extremity) surfaces.
Minor form associated with herpes, major form associated with anaphylactic shock associated with drug ingestion.
Superficial perivascular lymphocyte infiltrate. Can become confluent epidermal necrosis, particularly in major forms.
37
Psoriasis
Inflammatory - Chronic inflammatory dermatoses
Affects 1%-2% of the population
Erythematous, well demarcated, silvery-white scaly plaques. Most common on the elbows, knees, lumbosacral regions and intergluteal folds
30% of patients see nail changes - oil spots, pits and onycholysis (nail detachment).
Pustular variant much less common (very rare) - characterized by raised bumps filled with noninfectious pus.
Confluent parakeratosis with hypogranulosis, regular acanthosis, suprapapillary thinning with Auspitz's sign.
Munro microabscesses
38
Lichen planus
Inflammatory - Chronic inflammatory dermatoses
Pruritic, purple, polygonal, papules and plaques
Wickham’s stria - Scaly lace-like lines on the surface the papules and plaques
Most common on the flexor surfaces of extremities, but can be anywhere. 70% will also have oral lesions – first presentation usually in the mouth. If this affects the scalp- Lichen Planopilaris (allopecia).
Hyperkeratosis with hypergranulosis, acanthuses with saw tooth appearance.
39
Lupus erythematosus
Inflammatory - Chronic inflammatory dermatoses
Systemic and localize (discoid) forms
Malar (butterfly) erythema or rash, Sun exposure worsens the symptoms (photosensitivity), Disc-like, shiny, epidermis, Telangiectasia, hypo/hyperpigmentation, keratotic follicular plaques and loss of hair
Epidermal atrophy
Interface lymphocytic infiltrate
Superficial and deep chronic inflammation
Peri-adnexal/perifollicular/perivascular
Keratotic follicular (hair follicle) plugging
Vacuolar change with thickened basement membranes.
Direct immunofluorescence - granular deposit at the dermal-epidermal junciton - IgG and Complement (band test)
System lupus - Both normal and lesional skin are positive
Discoid lupus - Only lesional skin is positive
40
seborrheic dermatitis
Inflammatory - Chronic inflammatory dermatoses
More prevalent in high density sebceous glands
Presents as macules and papules on erythmatous, yellow, greasy base. Plaques and crust is greasy due to overproduction of sebum.
Dandruff - SD of scalp; infants cradle cap.
Parkinson disease, HIV infections and stroke are also associated with this cutaneous disorder.
Epidermal edema with spongiosis early on then progresses to acanthosis and mounds of parakeratosis with neutrophils and serum (crust).
Parakeratosis at margins of hair follicle ostea
Perivascular inflammatory infiltrates containing lymphocytes and neutrophils - plasma cells seen with HIV infections.
41
Pemphigus
Bullous (Blistering) Disorders - Inflammatory forms
Flaccid blisters, most commonly on mouth, also on scalp, face, axilla and groin. Shallow erosions with overlying crusts.
Pemphigus vulgaris is the most common (80%) - Suprabasilar split; antibodies against desmoglein III
Pemphigus vegetans
Pemphigus foliaceus - more of a tissue paper scale, no real blisters; Acantholysis in the granular layer; antibodies against desmoglein I
Pemphigus erythematosus - Acantholysis in the granular layer
Acantholysis due to dissolution of intercellular bridges. Mild lymphocytic and eosinophilic infiltrates
Direct immunofluorescence
“Chicken wire” pattern of intercellular deposits of IgG and C3 around each keratinocytes.
42
Bullous Pemphigoid
Bullous (Blistering) Disorders - Inflammatory forms
Abundant tense bullae occurring on erythematous base. Bullae are filled with clear fluid. Common on flexors surfaces, the groin, the axillae and the trunk.
Subepidermal bullous formation - abundant eosinophils in bullous cavity.
Superficial perivascular inflammatory infiltrate of lymphocytes and eosinophils.
No necrosis of keratinocytes or acantholysis
Direct immunofluorescence - linear staining with IgG and C3 along the dermal epidermal junction
Antibodies are directed against the “bullous pemphigoid” antigen located in hemidesmosomes and the lamina lucida
Hemidesmosomes lose function, leading to split at the dermal-epidermal junction
43
Dermatitis Herpetiformis
Bullous (Blistering) Disorders - Inflammatory forms
Intensely pruritic vesicles on the extensor surfaces of the extremities symmetrically, also seen on the buttocks and upper back.
Excoriations due to the intense pruritis are the usual clinical appearance.
Associated with gluten-sensitive enteropathy (Celiac Disease). IgA antibodies to dietary gluten (from wheat) cross react with reticulin within the anchoring fibrils (hold epidermis attached to dermis).
Subepidermal vesicle formation (Smaller blisters than other diseases discussed so far (vesicles))
Neutrophils present within the papillary dermis about the superficial capillary loops. No overlying epidermal necrosis or acantholysis.
Direct immunofluorescence - Granular deposits of IgA and C3 in papillary dermal tips
No epidermal staining
44
Epidermolysis Bullosa
Bullous (Blistering) Disorders - Non-inflammatory forms
Acquired and inherited forms. Blisters form at sites of pressure, trauma or rubbing. Some inherited forms manifest soon after birth can lead to squamous carcinoma. Simplex form - Keratin 14 & 5 genes mutations.
Blisters develop beneath the lamina densa due to defective anchoring filaments. Defective Type VII collagen gene.
Salt split-skin test is used to differentiate this disorder from Bullous Pemphigoid
45
Porphyria
Bullous (Blistering) Disorders - Non-inflammatory forms
Hereditary and acquired forms - due to abnormalities in porphyrin metabolism (five major forms). Cutaneous manifestions include urticaria and vesicles. A scaring disorder that is aggravated by sunlight.
Subepidermal, non-inflammatory vesicles. Marked dermal vessels thickening. Caterpillar bodies in the epidermis.
46
Diabetes Mellitus induced dermatosis
Bullous (Blistering) Disorders - Non-inflammatory forms
47
Dialysis-induced dermatosis
Bullous (Blistering) Disorders - Non-inflammatory forms
48
Nikolsky Sign
Dermatological sign present when slight rubbing of the skin results in exfoliation of the outermost layer forming a blister in minutes.
Useful in differentiating between pemphigus vulagris from bullous pemphigoid
