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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Infectious Dermatoses

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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…
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Acute Inflammatory Dermatoses

A

Urticaria
Acute Eczematous dermatitis
Erythema Multiforme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Acute Eczematous dermatitis-classification

A
Allergic Contact Dermatitis
Atopic Dermatitis.
Drug-related Dermatitis.
Photoeczematous Dermatitis.
Primary Irritant Dermatitis.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Chronic Inflammatory Dermatoses

A

Psoriasis

Lichen Planus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
Epidermal Tumors
Seborrheic Keratosis(benign) Actinic Keratosis(benign) Basal Cell Carcinoma(malignant) Squamous Cell Carcinoma(malignant)
26
Seborrheic Keratosis.
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
Actinic Keratosis
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
Basal Cell Carcinoma
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
Basal Cell Carcinoma-Pathogenesis
Immunosuppression PTCH gene mutation (patched) gene on 9q22.3 involved involved in signalling pathway P53 mutation
30
Basal Cell Carcinoma-Picture
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
Squamous Cell Carcinoma
Commmon tumor but less common than BCC Develops in sun-exposed skin of fair patients Mucosa may be affected (oral)
32
Squamous Cell Carcinoma-etiology
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
Squamous Cell Carcinoma-picture
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
Melanocytic Tumors of the Skin
``` Melanocytic Nevus(benign) Dysplastic Nevus(benign) Malignant Melanoma ```
35
Melanocytic Nevus
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
Melanocytic Nevus-Picture
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
Dysplastic Nevus
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
Malignant Melanoma
``` 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
Malignant Melanoma-Predisposing factor
``` Pre-existing lesions : Dysplastic nevus Exposure to carcinogens Hereditary conditions : -Xeroderma Pigmentosum -Retinoblastoma -Familial melanoma Many gene mutations (CDKN2A,BRAF,RAS) Stepwise accumulation ```
40
Malignant Melanoma-type of growth
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
Malignant Melanoma-Microscopic features
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
Malignant Melanoma-Clinical Diagnosis
``` 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 ```