week 5 powerpoint chapter 46
TRANSCRIPT
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Chapter 46
Disorders of Skin Integrity and Function
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Skin Infections• Superficial fungal infections
– Examples: Ringworm, athlete’s foot
– Attack the keratinized (dead) cells
– Inflammatory reaction to toxins causes most signs and symptoms
• Deep fungal infections
– Examples: Candidiasis, sporotrichosis
– Attack living tissue
– May attack other organs
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Bacterial Skin Infections
• Impetigo
– May lead to post-streptococcal hypersensitivity reactions
– These can cause glomerulonephritis
• Remember “acute post infectious glomerulonephritis”?
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Viral 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
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Question
Which of the following microbes cause warts?
a. Fungus
b. Virus
c. Bacteria
d. Any of the above may cause warts.
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Answer
b. Virus
Warts are caused by viruses; they’re benign neoplasms (abnormal tissue growths).
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Acne
• 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
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Allergic and Hypersensitivity Dermatoses
• Type I allergies
– Atopic eczema
• Chronic inflammatory
• Pruritic
– Urticaria (hives)
• Edematous wheals
• Can be acute or chronic
• Many causes, known and unknown
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Type I AllergiesType I allergies are mediated by IgE
Consider these questions:
• 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?
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Question
Which chemical mediator is released by mast cells as part of the inflammatory response?
a. Histamine
b. Leukotriene
c. Cytokine
d. All of the above
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Answer
a. Histamine
Histamine (stored in mast cells) is one of the first substances to be released during the inflammatory response. Histamine release results in bronchoconstriction, mucosal edema, and increased mucus production.
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Drug-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
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Papulosquamous Dermatoses
• Psoriasis
• Pityriasis rosea
• Lichen planus
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PsoriasisActivated
T cells
growth factors
keratinocytes and blood
vessels grow
create papules
attract neutrophils
and monocytes
enter the
papules
create inflammation
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Burns
• 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
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Scenario
Mr. D was boiling water and the pot tipped over on him…
• He has painful, bright pink, blistering burns over most of his left arm and chest
Question
• How would you categorize this burn?
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Complications of Burns
• Burn shock
• Respiratory system dysfunction
• Hypermetabolic response
• Renal insufficiency
• Gastric ulceration
• Sepsis
• Constriction of areas under circumferential burns
• Systemic infection
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Question
Treatment for third-degree burn patients includes all but which of the following?
a. Fluid replacement
b. Removal of dead tissue/eschar
c. Antibiotics
d. Aloe
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Answer
d. Aloe
Patients suffering from third-degree (full thickness) burns lose fluid through the skin and are prone to infection. They must receive fluid replacement and antibiotics to fight or prevent infection. Dead tissue (eschar) must be removed daily (debridement) in order to prevent infection. Because third-degree burns destroy the epidermis, the application of topical aloe would serve no purpose.
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Pressure Sores
External pressure
obstructs blood flow
ischemia to skin
tissue damage
Shear
bends blood vesselsFriction
damages dermis/
epidermis interface
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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
Sunburn – everything you didn’t want to
knonw
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Sun Exposure
• 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
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Malignant Melanoma
• Cancers arising from melanocytes
• Asymmetry
• Border irregularity
• Color variegation
• Diameter >0.6 cm
• Evolving change over time
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Types 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
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Question
Which type of skin cancer is associated with the worst prognosis?
a. Basal cell
b. Squamous cell
c. Malignant melanoma
d. Ependymal cell
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Answer
c. Malignant melanoma
Malignant melanoma begins in the melanocytes, and possesses all of the characteristic features associated with cancer (asymmetry, irregular border, many colors, and a diameter >0.6 cm) as defined by the American Cancer Society.
Basal cell cancer has the best prognosis, and squamous cell cancer has a good prognosis as long as it is detected early.
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Skin Disorders of the Elderly
• Actinic (solar) damage
– Keratoses: premalignant lesions
– Lentigines: liver spots
• Vascular lesions
– Angiomas
– Telangiectases
– Venous lakes
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Can you believe it?
• This is the final slide from the final chapter in the book.
• It’s been an interesting journey through the body and the disease and injury processes that can occur.
• Thank you for joining us as we explored Human Pathophysiology