Successfully reported this slideshow.
We use your LinkedIn profile and activity data to personalize ads and to show you more relevant ads. You can change your ad preferences anytime.

of

Integumentary system Slide 1 Integumentary system Slide 2 Integumentary system Slide 3 Integumentary system Slide 4 Integumentary system Slide 5 Integumentary system Slide 6 Integumentary system Slide 7 Integumentary system Slide 8 Integumentary system Slide 9 Integumentary system Slide 10 Integumentary system Slide 11 Integumentary system Slide 12 Integumentary system Slide 13 Integumentary system Slide 14 Integumentary system Slide 15 Integumentary system Slide 16 Integumentary system Slide 17 Integumentary system Slide 18 Integumentary system Slide 19 Integumentary system Slide 20 Integumentary system Slide 21 Integumentary system Slide 22 Integumentary system Slide 23 Integumentary system Slide 24 Integumentary system Slide 25 Integumentary system Slide 26 Integumentary system Slide 27 Integumentary system Slide 28 Integumentary system Slide 29 Integumentary system Slide 30 Integumentary system Slide 31 Integumentary system Slide 32 Integumentary system Slide 33 Integumentary system Slide 34 Integumentary system Slide 35 Integumentary system Slide 36 Integumentary system Slide 37 Integumentary system Slide 38 Integumentary system Slide 39 Integumentary system Slide 40 Integumentary system Slide 41 Integumentary system Slide 42 Integumentary system Slide 43 Integumentary system Slide 44 Integumentary system Slide 45 Integumentary system Slide 46 Integumentary system Slide 47 Integumentary system Slide 48 Integumentary system Slide 49 Integumentary system Slide 50 Integumentary system Slide 51 Integumentary system Slide 52 Integumentary system Slide 53 Integumentary system Slide 54
Upcoming SlideShare
What to Upload to SlideShare
Next
Download to read offline and view in fullscreen.

3 Likes

Share

Download to read offline

Integumentary system

Download to read offline

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

Related Books

Free with a 30 day trial from Scribd

See all

Related Audiobooks

Free with a 30 day trial from Scribd

See all

Integumentary system

  1. 1. INTEGUMENTARY SYSTEM Dr. Saugat Chapagain
  2. 2. COURSE OF CONTENT • Squamous cell Carcinoma • Basal cell Carcinoma • Dermatitis • Dermatophytes • Warts • Leprosy
  3. 3. 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
  4. 4. 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.
  5. 5. 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
  6. 6. DERMATOSES (CNTD….)
  7. 7. 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
  8. 8. 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
  9. 9. DERMATITIS (ECZEMA)
  10. 10. 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.
  11. 11. 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
  12. 12. 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
  13. 13. 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
  14. 14. DERMATOPHYTOSIS (SUPERFICIAL MYCOSIS)
  15. 15. 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.
  16. 16. 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.
  17. 17. 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
  18. 18. 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
  19. 19. 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
  20. 20. SQUAMOUS CELL CARCINOMA
  21. 21. 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
  22. 22. 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.
  23. 23. MANAGEMENT Investigations: • Excisional biopsy Treatment • Surgical excision • Curettage and electrodessication • Radiation therapy • Chemotherapy
  24. 24. WARTS (VERRUCAE)
  25. 25. 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.
  26. 26. 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)
  27. 27. 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).
  28. 28. 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
  29. 29. BASAL CELL CARCINOMA (RODENT ULCER)
  30. 30. 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.
  31. 31. 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
  32. 32. 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
  33. 33. 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.
  34. 34. LEPROSY (HANSEN’S DISEASE)
  35. 35. 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
  36. 36. 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.
  37. 37. 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)
  38. 38. 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
  39. 39. 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
  40. 40. 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
  41. 41. 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.
  42. 42. 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
  43. 43. 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
  44. 44. 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
  45. 45. THE END THANK YOU
  • ShweetaBhati2

    Dec. 9, 2020
  • VIPULJADVANI1

    Feb. 21, 2018
  • SuSmaThapa6

    Jan. 11, 2018

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

Views

Total views

1,034

On Slideshare

0

From embeds

0

Number of embeds

14

Actions

Downloads

30

Shares

0

Comments

0

Likes

3

×