PTH-04-Disease of Skin Flashcards

1
Q

Macroscopic Terms

A
  • Papule-Elevated dome-shaped or flat-topped lesion 5 mm or less across.
  • Plaque-Elevated flat-topped lesion usually greater than 5 mm across (coalescent papules).
  • NODULE-elevated lesion with spherical contour greater than 5 mm across
  • Vesicle-Fluid-filled raised lesion 5 mm or less across.
  • Bulla-Fluid-filled lesion greater than 5 mm across.
  • Blister-Common term used for vesicle or bulla.
  • PUSTULE(Infected)-Discrete, pus-filled, raised lesion.
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2
Q

Microscopical Terms

A
  • HYPERKERATOSIS: Thickening of the stratum corneum
  • PARAKERATOSIS: Retention of the nuclei in the stratum corneum.
  • ACANTHOSIS: Diffuse epidermal hyperplasia
  • PAPILLOMATOSIS: Surface elevation caused by hyperplasia and enlargement of contiguous dermal papillae.
  • DYSKERATOSIS: Abnormal keratinization occurring prematurely within individual cells or groups of cells below the stratum granulosum.
  • ACANTHOLYSIS: Loss of intercellular connections resulting in loss of cohesion between keratinocytes.
  • SPONGIOSIS:-Intercellular edema of the epidermis.
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3
Q

Infectious Dermatoses

A

A- Bacterial Infections(Impetigo)
B- Viral Infections(verrucae)
C- Fungal Infections(Tinea, Onchomycosis,Candida)
D- Arthropod bites & stings

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4
Q

A- Bacterial Infections(Impetigo)

A

Common superficial bacterial infection of the skin.
Pathogenesis:
-Staphylococcus aureus**
-Beta-hemolytic streptococci
Spongiotic epidermis with heavy neutrophil infiltrate

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5
Q

B- Viral Infections- Verrucae (warts)

A

Common lesions of children, adolescents, any age.
Cause : human papillomaviruses types 6 &11
Generally self-limited, spontaneous regression
-Verruca vulgaris
-Verruca plana
-Verruca plantaris
-Verruca palmaris
-Condyloma acuminatum (venereal wart)

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6
Q

C- Fungal Infections(Tinea, Onchomycosis,Candida)

A
Superficial Skin Infection :
-Caused primarily by dermatophytes. 
--Tinea capitis ( hair shaft)
--Tinea corporis (arms & legs)
--Tinea pedis (athlete’s foot)
-Spread to or primary infection of the nails is referred to as onychomycosis.
Mucosal & systemic : Candida
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7
Q

D- Arthropod bites & stings

A

Arthropods can produce lesions:

  • By direct irritant effects of insect parts or secretions.
  • By immediate or delayed hypersensitivity responses (including an anaphylactic reaction)
  • By specific effects of venoms
  • By serving as vectors for secondary invaders e.g. virus,bacteria,parasite…
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8
Q

Acute Inflammatory Dermatoses

A

Urticaria
Acute Eczematous dermatitis
Erythema Multiforme

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9
Q

Urticaria

A

Localized mast cell degranulation resulting in dermal microvascular hyperpermeability
Tranzient pruritic ‘ Wheels’ (few hours)
Results from AG induced release of mediators from mast cells following specific sensitization to food, pollen, drugs ….etc
Morphology : Almost normal, edema, minimal mononuclear cells ± eosinophils.

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10
Q

Acute Eczematous dermatitis

A

Eczema is a clinical term of pathogenetically different conditions.
All are characterized by papulovesicular, oozing, crusted lesions, may later develop into raised, scaly plaques.

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11
Q

Acute Eczematous dermatitis-classification

A
Allergic Contact Dermatitis
Atopic Dermatitis.
Drug-related Dermatitis.
Photoeczematous Dermatitis.
Primary Irritant Dermatitis.
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12
Q

Acute Eczematous dermatitis-Morphology

A

The main feature is spongiosis which is the accumulation of edema within the epidermis
Superficial perivascular infiltrate
In some cases, eosinophils may be present
Lesions are pruritic, edematous containing vesicles and bullae.

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13
Q

Erythema Multiforme

A

Self limiting hypersensitivity reaction to some infections & drugs
Variable erythematous lesions, sometimes with vesicles
Perivascular inflammation, dermal edema
Degeneration of keratinocytes ± epidermal necrosis in severe cases.

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14
Q

Chronic Inflammatory Dermatoses

A

Psoriasis

Lichen Planus

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15
Q

Psoriasis

A

Common scaly dermatosis, sometimes associated with arthritis , myopathy & enteropathy. Immunologically mediated.
Most frequently affects the skin of elbows, knees, scalp and glans penis.
Typical lesion is a well demarcated pink plaque covered by loosely adherent scales.

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16
Q

Psoriasis-Main Feature

A

Parakeratosis , mild hyperkeratosis
Loss of granular layer
Epidermal hyperplasia (Acanthosis )
Munro microabscess (neutrophils in parakeratotic scale)
Prominent dermal capillaries → Auspitz sign

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17
Q

Lichen Planus

A

Result from CD8+ T cell mediated immune response against AG in dermo-epidermal junction→ separation → Interface Dermatitis
? Viral ? drugs
Pruritic purple papules & plaques distributed mainly on extremities , often wrists & elbows.
Self limited and generally resolves within 1-2 years leaving zones of hyperpigmentation
Oral lesions may persist for years.

18
Q

Lichen Planus-Morphology

A

Dense continuous lymphocytic infiltrate ‘hugging’ dermoepidermal junction
Vacuolar degeneration of basal layer, necrotic basal cells in the papillary dermis (Civatte bodies)
The dermoepidermal junction assume zigzag pattern (Saw tooth appearance).
Acanthosis, hyperkeratosis & hypergranulosis

19
Q

Bullovesicular Diseases

A

Pemphigus Vulgaris (Suprabasal)
Bullous Pemphigoid
Dermatitis Herpetiformis

20
Q

Pemphigus Vulgaris (Suprabasal)

A
  • IgG AB→ Intercellular attachments in epidermis & mucosal epithelium →destruction & loosening
  • Superficial blisters that easily rupture
  • Different types, some associated with internal malignancy
21
Q

PV-Morphology

A

The main feature is Acantholysis (dissolution of intercellular adhesion sites)
Suprabasal acantholytic blister.
Infiltration by lymphocytes, histiocytes and eosinophils.
By immunoflurorescence :
-Netlike pattern of intercellular IgG deposits localized to sites of acantholysis

22
Q

Bullous Pemphigoid(subepi)

A

IgG AB to BM → Subepidermal bullous disease
Tense bullae filled with clear fluid on erythematous base.
Lesions up to 5 cm and do not rupture easily.
Oral involvement is seen in 10-15 %

23
Q

Dermatitis Herpetiformis(subepi)

A

Grouped vescicles
More in males
Sometimes associated with celiac disease
IgA antibodies to dermal epidermal junction→ Subepidermal bulla
Neutrophilic microabscesses at tips of dermal papillae

24
Q

Skin Tumors

A
Epidermis**
Dermis
Skin appendages
Melanocytic tumors**
Vascular tumors
25
Q

Epidermal Tumors

A

Seborrheic Keratosis(benign)
Actinic Keratosis(benign)
Basal Cell Carcinoma(malignant)
Squamous Cell Carcinoma(malignant)

26
Q

Seborrheic Keratosis.

A

Benign neoplasm most in elderly,
Raised, flat, soft, well demarcated brown lesion.
Located mostly on the trunk, limbs & head.
Micro: proliferation of squamous epithelium + cysts filled with keratin

27
Q

Actinic Keratosis

A

Due to excessive, chronic exposure to sunlight → Face & hands of middle aged & elderly
Considered as “premalignant”
Typically seen as hyperkeratotic, scaly plaques
Micro : Parakeratosis & atypical keratinocytes , may evolve to CA
In situ →Invasive Squamous Cell CA

28
Q

Basal Cell Carcinoma

A

Most common malignant tumor due to sun exposure in patients over 40´s with pale skin
Sun exposed skin (face ) never mucosal
Sporadic or familial(GORLIN’S Syndrome)
Infiltrative but Rare METASTASES !

29
Q

Basal Cell Carcinoma-Pathogenesis

A

Immunosuppression
PTCH gene mutation (patched) gene on 9q22.3 involved involved in signalling pathway
P53 mutation

30
Q

Basal Cell Carcinoma-Picture

A

Superficial ,or Nodular growth, ulcerative, erythematous or sclerosing
May be pigmented
Gross: Papule, rodent ulcer, pigmented lesion
Micro: nests of epithelial cells that resemble basal cells forming palisades separated from surrounding fibroblasts by a cleft like space.
Basosquamous histology has worse prognosis
↑P53 expression → poor prognosis

31
Q

Squamous Cell Carcinoma

A

Commmon tumor but less common than BCC
Develops in sun-exposed skin of fair patients
Mucosa may be affected (oral)

32
Q

Squamous Cell Carcinoma-etiology

A

Exposure to UVB light & ionizing radiation
Arsenicals & industrial carcinogens
Actinic keratosis
Chronic scarring ulcers, burns…etc
Immunosuppression (HPV 16 & 18)
Xeroderma pigmentosum, P53 & RAS mutations

33
Q

Squamous Cell Carcinoma-picture

A

Sites : dorsal surface of hands, face ,ears, mucosal surfaces
Gross features : Small scaly lesion → ulceration later
Microscopic :Full thickness epidermal dysplasia (CA in situ)
-Invasive carcinoma
-Variable degrees of keratinization
It has an increased tendency to infiltrate and metastasize locally to regional lymph nodes

34
Q

Melanocytic Tumors of the Skin

A
Melanocytic Nevus(benign)
Dysplastic Nevus(benign)
Malignant Melanoma
35
Q

Melanocytic Nevus

A

Commonest benign tumor in the body
Derived from dendritic melanocytes present in basal layer of the epidermis
Immature at junction, but mature as cells migrate down into dermis.
Activating BRAF or RAS mutation identified
There are several locations: junctional, compound & intradermal.

36
Q

Melanocytic Nevus-Picture

A

Gross: Uniform tan/brown color with sharp delineation & tendency to be stable in size & shape.
Microscopic picture :Nests or cords of uniform nevus cells ± pigment
Malignant transformation is uncommon

37
Q

Dysplastic Nevus

A

Sporadic low risk of transformation
Familial autosomal dominant with melanoma risk up to 100%
Considered a marker for future melanoma
Usually large, multiple & on nonexposed skin
Activating BRAF or RAS mutations
Features : Compound nevus with increased melanocytes , cytological atypia, dermal fibrosis around proliferating cells

38
Q

Malignant Melanoma

A
Sunlight on exposed white skin
More in New Zealand & Australia
Intense intermittent exposure at early age
Sporadic OR Familial  (>5%-10%)
Sites : Skin, mucosa, eye …..etc
39
Q

Malignant Melanoma-Predisposing factor

A
Pre-existing lesions : Dysplastic nevus
Exposure to carcinogens
Hereditary conditions :
-Xeroderma Pigmentosum
-Retinoblastoma
-Familial melanoma
Many gene mutations (CDKN2A,BRAF,RAS)
Stepwise accumulation
40
Q

Malignant Melanoma-type of growth

A

First Radial ( Superficial)
Later downgrowth ( Nodular)
Staging & prognosis depends on DEPTH OF INVASION
-Breslow Staging: Depth of invasion in mm.
-Clark’s Staging: Depth of invasion by location
Spread is by lymphatics & blood to any site (liver,lung , brain…etc)

41
Q

Malignant Melanoma-Microscopic features

A

Neoplastic melanocytes are much larger
Large nucleii with prominent nucleoli
Tumor cells grow horizontally & vertically
Loss of nesting pattern ( sheets)
Loss of maturation
Prognosis is better in radial growth but bad in deeper vertical growth

42
Q

Malignant Melanoma-Clinical Diagnosis

A
Change in color or size of an existing lesion,itching, ulceration
New pigmented lesion in an adult
Main  signs summarized -
A. Asymmetry of shape 
B. Border is irregular
C. Color is uneven 
D. Diameter is enlarged
E. Evolution