a short clinical introduction regarding the integumentary system for medical and paramedical students.

1. INTEGUMENTARY
SYSTEM
Dr. Saugat Chapagain

2. COURSE OF CONTENT
• Squamous cell Carcinoma
• Basal cell Carcinoma
• Dermatitis
• Dermatophytes
• Warts
• Leprosy

4. NORMAL STRUCTURE• Epidermis –
• Basal cell layer (stratum germinatum)
• Prickle cell layer (stratum Spinosum, Stratum Malpighi)
• Granular cell layer (Stratum granulosum)
• Stratum Lucidum
• Horny layer (stratum Corneum)
• Dermis –
• Pars papillaris/ Papillary dermis
• Pars retucularis/ reticular dermis
Has nerve endings –
• Pacinian corpuscles – pressure (deep layer of skin)
• Meissner corpuscles – touch (skin of palms, soles, tips of fingers and toes)
• Ruffini corpuscles – cold receptors (external genitalia)
• End bulbs of Krause – cold receptors (external genitalia)
Cutaneous appendages –
• Sweat glands
• Sebaceous glands
• Hair
• Arrectores pilori
• Nails

5. HISTOPATHOLOGICAL TERMS
• Acanthosis – thickening of epidermis d/t hyperplasia of stratum Malpighi.
• Acantholysis – loss of cohesion between epidermal cells with formation of epithelial
cells
• Dyskeratosis – abnormal development of epidermal cells  pyknotic nuclei (f/s/o
malignant and premalignant lesion)
• Hyperkeratosis – thickening of horny layer.
• Parakeratosis – abnormal keratinization  horny layers have nucleated keratinocytes
instead of non-nucleated keratin layer.
• Spongiosis – intercellular oedema of epidermis  vesicle formation in the epidermis.
• Pigment incontinence – loss of melanin pigment from damaged basal cell layer 
pigment accumulates in the melanophages in the dermis.

6. DERMATOSES1. Genetic dermatoses:
• Ichthyosis –
• Ichthyosis vulgaris (autosomal dominant)
• Sex linked ichthyosis (x-linked recessive)
• Keratosis palmaris et plantaris (autosomal dominant/ recessive)
• Xeroderma pigmentosum (autosomal recessive)
• Darier’s disease (keratosis follicularis) (autosomal dominant)
• Utricaria pigmentosa
• Ataxia telangiectasia (autosomal recessive)
2. Non infectious inflammatory dermatoses
• Dermatitis (eczema)
• Utricaria
• Miliaria
• Panniculitis
• Acne vulgaris

7. DERMATOSES (CNTD….)

8. DERMATOSES (CNTD….)
5. Connective tissue diseases
• Lupus Erythematosus
• Systemic sclerosis (scleroderma)
• Lichen sclerosus et atrophicus
6. Non infectious bullous dermatoses
• Pemphigus
• Vulgaris
• Vegetans
• Foliaceous
• Erythematosus
• Pemphigoid
• Dermatitis herpeteformis
• Erythema multiforme

9. DERMATOSES (CNTD….)
7. Scaling dermatoses
• Psoriasis
• Lichen planus
8. Metabolic diseases of the skin
• Amyloidosis
• Lipoid proteinosis
• Porphyria
• Calcinosis cutis
• Gout d/t urate deposits or tophi
• Ochronosis d/t alkaptonuria
• Mucinosis in myxedema
• Idiopathic haemochromatosis with skin pigmentation

10. DERMATITIS (ECZEMA)

11. DERMATITIS (ECZEMA)
• Dermatitis (pathological term) & eczema (clinical term)
• Inflammatory response to a variety of agents acting on the skin form outside
or within the body (chemicals & drugs, Hypersensitivity reactions, etc)
• Histamines and cytokines induce acute inflammation.
• ‘rich-scratch-itch’ cycle causes lesions
• Clinical types (contact dermatitis, atopic dermatitis, drug induced dermatitis,
photo-eczematous dermatitis and primary ICD)
INVESTIGATIONS:
• BLOOD TESTS  reveal elevated IgE or eosinophilia.

12. MICROSCOPIC APPEARANCE
• Acute –
• spongiosis  formation of intraepithelial vesicles or bullae.
• Permeated by acute inflammatory cells
• Upper dermis  congested blood vessels and mononuclear infiltrate
• Subacute –
• Follows acute dermatitis
• Smaller spongiosis and vesicles
• Moderate acanthosis and varying degree of parakeratosis in horny layer
• Surface crust seen (with containing degenerated leucocytes, bacteria and fibrin)
• Dermis contains perivascular mononuclear infiltrate
• Chronic –
• Hyperkeratosis, parakeratosis and acanthosis
• Elongation of rete ridges & broadened dermal papillae
• Vesicles (-) slight spongiosis (+)
• Upper dermis  pervascular chronic inflammatory infiltrates and fibrosis

13. CLINICAL FEATURES
• Erythematous area of excessively dry skin
• Oedema, crusting, scaling by pruritus and scratching
• Pinkish, swollen upper eyelid and double fold under lower lid.
• Multiple areas of dry, scaly, blanching and lichenification
TREATMENT
• Eliminating allergens and avoiding irritants
• Prevent dry skin (hydration and moisturisation)
• Topical corticosteroid
• Systemic antihistamine
• Systemic corticosteroid
• In severe cases  cyclosporine A
• In case of positive culture  antibiotics/ anti fungal

14. Utricaria
• A.k.a. hives
• Presence of transient,
recurrent, pruritic wheals
(raised erythematous areas
of oedema)
Miliaria
• Cutaneous retention of sweat d/t obstruction
• Miliaria crystalline
• Obstruction of sweat duck within the stratum
corneum.
• In areas of sun exposed skin or during febrile illness.
• Miliaria rubra
• Obstruction within the deeper layers of epidermis
• In areas of skin covered by clothes following prosure
sweating
• Lesions are itchy

15. DERMATOPHYTOSIS
(SUPERFICIAL MYCOSIS)

16. DERMATOPHYTOSIS (SUPERFICIAL
MYCOSIS)
• Fungal infections of the skin, hairs and nails.
• Localised to stratum corneum in skin.
Common dermatophytes:
• Trichophyton rubrum,
• Pityrosporum
• Microsporum, epidermophyton
• Candida spp. (candidiasis = moniliasis)
• Tineasis  d/t contact with contaminated objects or surfaces
• Candidiasis causes neutropenia and bone marrow suppression in
immunocompromised patients.

17. PATHOPHYSIOLOGY
• Dermatophytes only grow on keratinized structures, make keratinase that digest
keratin and maintain the existence of fungi in the keratinized tissue.
• Presentation depends on species, site and susceptibility as well as immunity
• Candidiasis  organism penetrates the epidermis after binding to integrin receptors
and adhesion molecules  secrets proteolytic enzymes  tissue invasion.
• Inflammatory response (acute)  activates complement system.

18. CLINICAL FEATURES1. Tinea infection
• Erythema, scaling, pustules and vesicles
• Itching, stinging and burning
Types:
1. T. capitis – scalp (esp. in children)
2. T. barbae – beard region (esp. adult males)
3. T. corporis – body surface (all ages)
4. T. cruris – groin of obese men (esp. in warm climate)
5. T. pedis (athelete’s foot) – web spaces between the toes.
6. Onychomycosis – disintegration of nail substance
7. T. versicolor – caused by Malassezia furfur (usu. Upper trunk)
Microscopically –
• Fungal hyphae (mycellia) and arthrospores in stratum corneum
• Spores (round to oval) budding yeast cells
• Stains –
• periodic acid-schiff (PAS)  deeppink/red
• methamine silver nitrate  black

19. CLINICAL FEATURES….
2. Candidiasis
• Superficial papules and pustules, later erosions
• Erythema and oedema of epidermis or mucus membrane.
• White yellow curd like material over infected area
• Severe pruritus and pain at the lesion sites
INVESTIGATIONS
• Microscopy – KOH mount of skin scrapings or swabs
• Fungal culture

21. TREATMENT
1. Tinea :
• Topical fungicide (imidazone, KTZ, terbinafine)
• Oral agents (azoles or allylamines)
2. Candidiasis:
• Balantis, vulvitis, diaper dermatitis, paronychia  nystatin or imidazoles
• Oral candidiasis  azoles, imidazoles
• Systemic infections  Amp-B or oral KTZ

22. SQUAMOUS CELL CARCINOMA

23. SQUAMOUS CELL CARCINOMA
Invasive tumor with metastatic potential
Arises from any part of skin or mucosa lined by squamous epithelium
More likely to occur in sun exposed parts in older people
Causes & predisposing conditions
• Overexposure to sun’s UV rays
• Premalignant lesions (solar keratosis, chronic inflammation)
• X ray therapy
• Ingested herbicides, medications
• Chronic skin irritation or inflammation
• Hereditary diseases (xeroderma pigmentosum)
old burn scars (marjolin’s ulcer)
• Chemical burns
• Psoriasis, HIV infection
• Cheweing of betel nuts, tobacco

24. CLINICAL FEATURES
• Induration and inflammation of preexisting lesions
• Slowly growing nodule on a firm indurated base, eventual ulceration invasion of underlying
tissues
• Mets to LN  s/s of pain, malaise, fatigue, weakness, anorexia.
GROSS
• May be ulcerated or raised fungating/polypoid verrucous lesion without ulceration.
Microscopy
• Downward proliferation of epidermal cells to the dermis
• Cellular atypia seen
• Horn pearls (whorled arrangement of epithelium in better differentiated lesions)
• Higher grades have lesser or no horns
• Inflammatory infiltrates seen.

25. MANAGEMENT
Investigations:
• Excisional biopsy
Treatment
• Surgical excision
• Curettage and electrodessication
• Radiation therapy
• Chemotherapy

27. WARTS (VERRUCAE)

28. CAUSE AND PATHOPHYSIOLOGY
• Cause  HPV (a DNA oncogenic virus) of papovavirus group
• Infection acquired by direct contact or by autoinoculation
• Replicate in epidermal cells  irregular thickening of stratum corneum
• Higher incidence in those with impaired immunity.

29. TYPES
• Verruca vulgaris –
• Most common, caused by HPV 1 and 2
• Lesions – multiple <1cm in size, circumscribed, firm elevated papules
• Commonly on dorsal surface of hands and palms.
• Verruca plana –
• Flat/ slightly elevated
• Common on face and dorsal suface of hands
• a/w HPV – 10
• Verruca plantaris
• On sole of foot by HPV 1
• Covered with thick callus
• Epidermodysplasia verruciformis –
• Resembles verruca plana but has autosomal recessive inheritance
• Malignant change  bowen’s disease/ sq. cell Ca.
• Condyloma acuminata / genital warts –
• On penis, vulva or around anus by HPV – 6
• Soft, papillary, cauliflower like mass that may grow massive (giant c. acuminata)

30. CLINICAL FEATURES
• Rough, elevated, rounded surfaces
• Most frequently on extremities (esp hands and fingers)
• Mostly seen in children and young adults
MICROSCOPY
• Papillomatosis (papillary folds)
• Acanthosis
• Hyperkeratosis with parakeratosis
• Clumped keratohyaline granules in granular cells in papillary valleys
• Elongation of the rete ridges with lower tips bent inwards
• Virus infected epidermal cells contain prominent vacoulation (koilocytosis) & kerato hyaline
granules of intracytoplasmic keratin aggregates (d/t viral effect).

31. MANAGEMENT
Investigation
• Cytological study
• Application of 5% acetic acid turns warts whitish if they are papillomas
Treatment
• Electrodessication and curettage
• Cryotherapy – liq nitrogen
• Acid therapy – plaster patches impregnated with salicylic acid
• Genital warts – cryotherapy, podophyllin in tincture of benzoin, 25-50 % TCA acid
applied to wart and neutralized with baking soda or water
• CO2 laser therapy
• Antiviral drugs (under investigations)
• Possible resolution without treatment

32. BASAL CELL CARCINOMA
(RODENT ULCER)

33. BASAL CELL CARCCINOMA
• Locally invasive (rodent), slow growing tumor of middle aged
• Rare metastasis
• Exclusively on hairy skin (>90% on face)
• Common in Caucasians (fair skinned) and in those with prolonged exposure to strong
sunlight (Aus and NZ)
• Radiation exposure (important risk factor)
• Arsenic poisoning, burns or immunosuppresions (moderate risk factors)
• Pathogenesis is uncertain
• Hypothesis  undifferentiated cells become carcinomatous instead of differentiating into
sweat gland, sebum and hair.

34. CLINICAL FEATURES
GROSS
• Common pattern – nodulo ulcerative BCC (slow growing small nodule undergoing central
ulceration with pearly, rolled margins.
• Tumor grows by burrowing and local tissue destruction (rodent behavior)
• Less frequently, non-ulcerated nodular pattern, pigmented BCC and fibrosing variants
encountered.
Types:
1. Noduloulcerative BCC
• Usu. On face (forehead, eyelid margins, nasolabial folds)
• Small smooth, pinkish and translucent
• Large lesions – centers depressed and borders firmly elevated.
2. Superficial BCC
• Usu. Multiple on chest and back
• oval,/ irregular shape with elevated thready borders
3. Sclerosing BCC
• Waxy, sclerotic, yellow to white plaques with no distinct borders
• On head and neck

36. CLINICAL FEATURES
MICROSCOPIC
• Profileration of basaloid cells (resembling basal layer of epidermis)
Variety of pattern may be seen :
• Solid masses of pigmented cells,
• Strands and nests of tumor cells
• Keratotic masses
• Cystic changes with sebacious differentiation
• Most commonly  solid BCC with irregular masses of cells

38. MANAGEMENT
• Investigation – incisional/ excisional biopsy
Treatment :
• Surgical excision
• Curettage and electrodessication
• Topical 5-fluouracil
• Microscopic controlled surgical excision
• Irradiation
• Cryotherapy with liq. N2
• Chemotherapy for persistent or recurrent lesions.

41. LEPROSY
(HANSEN’S DISEASE)

42. HANSEN’S DISEASE
• Discovery of causitive organism by Hansen in 1874
• Mycobacterium leprae
• Chronic, non fatal , infectious granulomatous disease mainly affecting the cooler
parts of the body (skin, mouth, respiratory tracts, eyes, peripheral nerves, superficial
lymph nodes and testes)
Primarily damages body in 3 ways :
1. peripheral neuritis
2. Bacillary infiltration
3. Acute reactions

43. MODE OF TRANSMISSION
• Communicable disease (incubation period – 2-20 years)
• Direct contact with untreated person (damaged skin, nasal secretions, mucous
membrane of mouth and hair follicles)
• Materno –foetal transmission across the placenta
• Transmission via milk.

44. CLASSIFICATION
Conventionally: (2 polar forms)
• Lepromatous – low resistance
• Tuberculoid – high resistance
Clinico-pathological groups (Ridely & Jopling’s classification)
• TT – tuberculoid polar (high resistance)
• BT – Borderline tuberculoid
• BB – mid borderline (dimorphic)
• BL – borderline lepromatous
• LL – lepromatous polar (low resistance)

45. IMMUNOLOGY
T cell mediated delayed hypersensitivity (type IV)
No toxins produced,  tissue destruction is d/t immune mechanism.
Peculiar features:
• Antigents of bacilli and its actions on peripheral nerves
• Genotype of the host
• T- cell response
• Activation of CD4+ T cell & CD8+ T cells
• CD4+ T cells  helper, promoter + cytotoxic activity (high in TL)
• CD8+ T cells  suppressor T cell (high in LL)
• In LL, due to CD8+ cell defect, macrophages and suppressor T cells fails to destroy cells.
• Humoral response – Ig has minimal role

46. LEPROMIN TEST
• Not diagonistic
• Used for classification on basis of immune response
• Intradermal injection of lepromin (antigenic extract of M. leprae) reveals delayed
hypersensitivity reaction in TL
• Early positive reaction – an indurated area in 24-48 hrs (Fernandez reaction)
• Delayed granulomatous lesion after 3-4 weeks (Mitsuda reaction)
• LL – negative lepromin test

47. REACTIONSType I – reversal reactions
• Polar forms are stable but borderline forms may move across spectrum
in either direction
1. Upgrading reaction –
• Increased cell mediated immunity
• BL  BT /TT
2. Downgrading reaction –
• Lowering of cell mediated immunity
• BT  BL/ LL
Type II – ENL (erythema nodusum leprosum
• In Lepromatous cases after treatment
• Tender cutaneous nodules, fever, iridocyclitis, synovitis and LN
involvement
• M/E –
• PMN and eosinophilic infiltration with prominent vasculitis
• Inflammation reaches upto sc fat (causing panniculitis)
• Bacillary load increased

48. CLINICAL FEATURES
Lepromatous leprosy
• Skin lesions – symmetrical, multiple ,slightly hypopigmented and erythematous
macules, papules, nodules or diffuse infiltrates
• Leonine facies appearance (lesions on ears and face)
• Hypoasthetic or anaesthetic (sensory disturbance less than in TT)
Tuberculoid leprosy
• Single or few asymmetric, hypopigmented and erythematous macules.
• Distinct sensory impairment
• Lesion of any size occurring anywhere.

49. CLINICAL FEATURES (CNTD……)
• Nerve involvement –
• Anaesthesia first seen in distal aspect of forearms and legs
• Later, ‘glove and stocking’ anaesthesia progressing to entire trunk and face
• Ulnar nerve  claw hand
• Median nerve above elbow or wrist
• Radial nerve at wrist  wrist drop
• Great auricular, common peroneal (in popliteal fossa), posterior tibia (around medial malleolus)
• Wasting of muscles
• Testes  atrophy, impotence, gynaecomastia
• Mucosal involvement  rhinitis, hoarseness, perforation of nasal septum & palate, laryngeal
obstruction
• Bones of hands, feet and face  cystic lesions of phalanges, loss of upper incisor teeth, etc.
• Eye  keratitis, iridocyclitis & corneal anaesthesia  blindness

50. INVESTIGATIONS
1. Microbiology –
Sample  tissue sections, split skin smears, scraping from cut edges of dermis and nasal
smears
Culture media unavailable  9-banded armadillo (natural experimental animal model)
2. Lepromin test
3. Biopsy from skin/ nerve for cytology
Techniques:
• AFB (Ziehl-Neelsen) staining
• Modified ZN staining
• Gram staining
• PCR (molecular method)
• IgM antibodies

51. MANAGEMENT
• Personal and public awareness
• Specific chemotherapy –
• Management of nerve damage –
• Physiotherapy
• Daily inspection for trauma/ infection
• Tarsorrhapy if exposed to anaesthetic cornea
• Damage limitation prophylaxis and treatment
• Rehabilitation

54. THE END
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