disorder of the skin ppt

Copyright © 2007 Lippincott Williams & Wilkins.

Chapter 45

Disorders of the Skin


Skin InfectionsSkin Infections

• Superficial fungal infections

– Ringworm, athletes foot

– Attack the keratinized (dead) cells

– Inflammatory reaction to toxins causes most signs and symptoms

• Deep fungal infections

– Candidiasis, sporotrichosis

– Attack living tissue

– May attack other organs


Bacterial Skin InfectionsBacterial Skin Infections

• Impetigo

– May lead to post-streptococcal hypersensitivity reactions

– These can cause glomerulonephritis


Viral Skin InfectionsViral Skin Infections

• Verrucae (warts)

– Benign neoplasms (papillomas)

• Herpes simplex (cold sores)

• Herpes zoster (shingles)

– Herpes invades dorsal root ganglia

– Caused when chickenpox herpesvirus is reactivated

– Travels out nerve to skin and causes a new inflammation


Mrs. K Is Worried About Her Complexion …Mrs. K Is Worried About Her Complexion …

• She says she always had good skin, but now her face itches and burns on the right side, and there are red lumps on one side of her forehead

What are the possible causes?What are the possible causes?


AcneAcne

• Disorder of sebaceous glands

• Related to:

– Hormonal stimulation of sebaceous glands

– Increased number of sebaceous cells

– Increased sebum production

– Inflammatory response to bacteria in sebum


Allergic and Hypersensitivity DermatosesAllergic and Hypersensitivity Dermatoses

• Type I allergies

– Atopic eczema

– Urticaria (hives)


Mechanism of Type I Hypersensitivity

Mechanism of Type I Hypersensitivity

Mast cell

Mast cell degranulates

Sensitized Mast cell

IgE attaches to mast cell

Allergen attaches to IgE


Type I Allergies Are Mediated by IgEType I Allergies Are Mediated by IgE

• What cells must be involved in this process?

– On the first exposure to the allergen?

– On repeated exposure?

– When the allergen binds to IgE?

• What inflammatory mediators are involved? How?


In Autoimmune Urticaria, the Client Creates Anti-IgE Antibodies

In Autoimmune Urticaria, the Client Creates Anti-IgE Antibodies

• How would this cause hives?

• How would a deficiency in complement inhibitor cause hives?

• Why would antihistamines help?

• Why would corticosteroids help?


Drug-Induced Skin EruptionsDrug-Induced Skin Eruptions

• Erythema multiforme

– Occurs after herpes simplex; self-limiting

• Stevens-Johnson syndrome

– Skin detaches from body surface; <10% of body affected

• Toxic epidermal necrolysis

– >30% of epidermis detaches

– 30%–35% mortality rate


Papulosquamous DermatosesPapulosquamous Dermatoses

• Psoriasis

• Pityriasis rosea

• Lichen planus


PsoriasisPsoriasisActivated

T cells

growth factors

keratinocytes and blood

vessels grow

create papules

attract neutrophils

and monocytes

enter the

papules

create inflammation


BurnsBurns

• First-degree: outer layers of epidermis

• Second-degree: epidermis and dermis

– Partial-thickness: only part of dermis

– Full-thickness: entire dermis

• Third-degree full-thickness

– Extends into subcutaneous tissue

– May damage muscle, bone, blood vessels


Mr. D Was Boiling Corn …Mr. D Was Boiling Corn …

• The pot tipped over on him

• He has painful, bright pink, blistering burns over most of his left arm and chest

How would you categorize this burn?How would you categorize this burn?


Mr. D's Burns Are Pink …Mr. D's Burns Are Pink …

• But the rest of his body looks pale, and he has a rapid heart rate

• His pulses are weak

• Bowel sounds are absent

• Respiration is rapid

What has caused these signs? What has caused these signs?


Complications of BurnsComplications of Burns

• Burn shock

• Respiratory system dysfunction

• Hypermetabolic response

• Renal insufficiency

• Gastric ulceration

• Sepsis

• Constriction of areas under circumferential burns

• Systemic infection


A Woman Was Severely Burned …A Woman Was Severely Burned …

• She has been in the hospital for 8 days

• Why would she be developing:

– Increased urine production?

– Weight loss?

– Increased temperature?

– GI bleeding?


Pressure SoresPressure Sores

External pressure

obstructs blood flow

ischemia to skin

tissue damage

Shear

bends blood vesselsFriction

damages dermis/

epidermis interface


Ultraviolet radiation

hits melanocytes

melanin oxidized - TAN

some UV reaches lower skin layers

immune cells

damagedinflammatory

mediators released

DNA damage

sunburn

more melanin produced - delayed

tanning


UV Damage to DNAUV Damage to DNA

Two thymines next to one another become linked: thymine dimers


Sun Exposure Increases the Risk of Skin Cancer

Sun Exposure Increases the Risk of Skin Cancer

• Cumulative sun exposure increases risk of:

– Basal cell carcinoma

– Squamous cell carcinoma

• Severe sun exposure with blistering increases risk of:

– Malignant melanoma


Malignant MelanomaMalignant Melanoma

• Cancers arising from melanocytes

• Asymmetry

• Border irregularity

• Color variegation

• Diameter > 0.6 cm

• Evolving change over time


Types of MelanomasTypes of Melanomas• 70% are superficial spreading

– Raised edges; grow horizontally and vertically

– Ulcerate and bleed

• 15%–30% are nodular

– Dome-shaped, blue-black

• 4%–10% are lentigo maligna

– Slow growing, flat

• 2%–4% acral lentiginous

– On palms, soles, nail beds, mucous membranes


Skin Conditions of InfancySkin Conditions of Infancy

• Birthmarks• Diaper dermatitis• Prickly heat• Cradle cap• Infectious disease rashes

– Roseola (herpesvirus)– Rubeola (measles)– Rubella (German measles)– Varicella (chickenpox)


Skin Disorders of the ElderlySkin Disorders of the Elderly

• Actinic (solar) damage

– Keratoses: premalignant lesions

– Lentigines: liver spots

• Vascular lesions

– Angiomas

– Telangiectases

– Venous lakes

disorder of the skin ppt

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