Other Skin Conditions Flashcards by Katie Keller

Occurs most frequently on the trunk and intriginous areas of the body

A hot environment is most frequently the cause

Also known as a heat rash

Burning and itching – most common symptoms

Lesions consist of small, superficial, red, thin-walled, discrete vesicles, papules, or vesicopustules or pustules

Miliaria

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What are some treatment options for miliaria?

Keep patient cool and wear light clothing

Medications:
Triamcinolone acetonide 0.1% in Sarna lotion
Mid-potency corticosteroid in a lotion or cream BID-QID

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IgE mediated reaction

Wheals, itching, erythema secondary to a stimulus

Typically last less than 24 hours - Often on 2-4 hours

Can be acute or chronic

Urticaria/Angioedema

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What is the pathophysiology of Urticaria/Angioedema?

IgE mediated reaction

IgE or complement-mediated (type 1) edema of the dermis and/or subcutaneous tissue caused by antigens from foods, drugs, insects, physical stimuli, or idiopathically

Some patients with chronic urticaria demonstrate autoantibodies directed against mast cell IgE receptors

Another MOA involves the activation of the compliment cascade

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What is the difference between angioedema and urticaria?

Angioedema is involved with deeper subcutaneous tissue with
swelling of lips, eyelids, palms, soles, and genitalia

Angioedema is more likely to associate with a systemic complication
such as laryngeal edema or hypotension than urticaria

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Transient pink/red wheals with central pallor in oval and confluent
patterns

Sharply defined wheals

Erythematous or white with erythematous rim

Round, acriform, annular

Usually if you palpate it, it will blanch

Pruritis, pain, flushing, burning, concomitant wheezing

Anywhere on the skin - May be localized or generalized (can be confined to site of trigger mechanism)

Urticaria

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Skin colored

Distributions:
Eyelids
Lips
Tongue
Hands
feet

Angioedema

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What are some treatment options for Urticaria/Angioedema?

Avoidance/remove the trigger
Antihistamines - H1 blockers, H2 blockers
Systemic steroids (Prednisone)
Danazol - For hereditary angioedema
Doxepin (tricyclic antidepressant)
Epinephrine - For angioedema/anaphylaxis
Airway support

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Single or multiple subcutaneous tumors

Can affect all ages

Composed of fat cells

Benign

Easily recognized

Soft, rounded or lobulated and movable against the overlying skin

Lipomas

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What are some treatment options for lipomas?

Excision - Typically due to cosmetic reasons, or in a difficult location

liposuction

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Traumatically grafted epidermis grown in the dermis, with accumulation of keratin within the cyst, enclosed in a stratified squamous epithelium with a well-formed granular layer

Cheesy texture of the cyst

The lesion appears as a dermal nodule and most commonly occurs on
the palms, soles, and fingers

Epidermal Inclusion Cysts

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What is the definitive treatment of epidermal inclusion cysts?

Definitive treatment is excision

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Abscess in the natal cleft (buttcrack)

Results from cyst, abscess or sinus tract in upper part of the natal cleft

Also called “Jeep Riders disease”

Intense pain and drainage

Peak incident ages 16-26

More common in males than females

Pilonidal Disease

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What are some causes/risk factors for developing pilonidal disease?

Congenital defect (Congenital natal dimple)
Ingrown hair
Excessive sweating
Sitting for long periods
Excessive body hair
Obesity/increased sacrococcygeal fold thickness

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What is the treatment of pilonidal disease?

Cefazolin/Metronidazole

I&D with or without packing

Surgical excision

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Inflammatory process that occurs in the fat of the subcutis

Tender, deep-seated in subcutaneous fat, red-brown nodules

Occur on anterior shins or extensor surface of ulna (Note: easier to feel than see)

Duration: few weeks to a few months

Young adults

More common in females (3:1)

Panniculitis: Erythema Nodosum

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What are the two types of erythema nodosum?

Septa – fibrous divisions between fat compartments and contain the neurovascular bundles

Lobules – conglomerations of adipocytes demarcated by septa

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What is the pathogenesis of erythema nodosum?

Septa – fibrous divisions between fat compartments and contain the neurovascular bundles

Lobules – conglomerations of adipocytes demarcated by septa

Inflammation occurs in the septal compartment and consists of lymphocytes, histiocytes and granulocytes

Histiocytes within septa = diagnostic value

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Tender red nodules on anterior lower leg

Evolve to more “bruise-like” patches or thin plaques

May have fever and arthralgias as well

erythema nodosum

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List some causes of erythema nodosum

Infection
Medications - OCPs, sulfa
Hormones (pregnancy)
Inflammatory disease - Ulcerative colitis, sarcoidosis

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What is the management of erythema nodosum?

Typically spontaneous resolution
Bed rest
Compression
NSAIDs
Potassium iodide

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Inflammatory disorder affecting the wall of small blood vessels

Eruption of reddish or violaceous papules

palpable purpura - hallmark!

Develop in crops

NO itching

Persist for a few days or weeks, but less than a month

Vasculitis

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What is the hallmark presentation of vasculitis?

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palpable purpura

What is the pathogenesis of vasculitis?

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Immune complexes - Antibody bound antigens from microbial proteins or medications, After being trapped in tissue, complement activated leads to inflammatory reaction

Lesions contain number neutrophils

Purpuric quality attributed to RBCs (Hgb converted to hemosiderin in macrophages)

What are some common precipitants to vasculitis?

Infections - Post strep, Post staph Medications - NSAIDs, Thiazides, antibiotics

Eruption of reddish or violaceous papules that develop in crops Can develop on any site, Usually on lower extremities Other patterns: Ulcers, Vesicopustules, Necrotic pustules Vascular eruption is accompanied by arthralgias, myalgias, and malaise

Vasculitis

Red-brown dermal papules or nodules May occur anywhere, like the face Ranges from mild, asymptomatic skin papule to life-threatening lung disease More common in young adults and black African descent

Sarcoidosis Skin Manifestations

What is the pathogenesis of sarcoidosis skin manifestations?

Collection of tissue macrophages/histiocytes (granulomas) within the dermis Noncaseating and does not show central coagulation necrosis “naked granulomas” - small number of lymphocytes around granulomas

The clinical presentation of what disease process is described below? Dependent on what tissues are involved Skin lesions - Red-brown dermal papules or nodules, alopecia, pigmentary alterations, ulcers “Nasal rim sarcoidosis” - Bead-like papules at the rim of the naries

Sarcoidosis

What does "nasal rim sarcoidosis" indicate?

Indicates lung involvement

Bilateral pulmonary hilar lymphadenopathy and acute erythema nodosum Includes fever, arthralgias, uveitis and lung parenchymal involvement

Lofgren’s syndrome

List the types of burns

Thermal Chemical Electrical Radiation frostbite

Which burn degree is described below? Minimal injury Appearance: Red Surface: Dry or very small blisters Sensation: Painful Tissue involvement: Epidermis

First degree

Which burn degree is described below? Appearance: Pink or mottled red Surface: Bullae or moist weeping surface, Blistering present Sensation: Very painful – nerve endings intact, damaged Tissue involvement: Extends into the dermis Will spare the hair follicles and sweat/sebaceous glands

Second Degree – Superficial Partial-Thickness

Which burn degree is described below? Presentation: Dermis pale white to yellow, Does not blanch, Pain is absent, Skin blistering Tissue involvement: Extends into the dermis Involves the hair follicles and sweat/sebaceous glands Difficult to distinguish from full thickness

Second Degree – Deep Partial-Thickness

Which burn degree is described below? Appearance: Pearly-white, charred, translucent, or parchment-like, Thrombosed vessels, Skin is charred, pale, leathery Surface: Dry and inelastic Sensation: Insensate/painless (Burned through the nerves), may feel pain toward the outside of the burn zone Tissue involvement: Tissue is destroyed below the hair follicle and sweat glands (entire skin thickness) All dermal elements are destroyed

Third Degree- Full Thickness

What is the treatment for a first degree burn?

Will heal in about 7 days without scarring Only symptomatic treatment is required

What is the treatment for a second degree superficial partial-thickness burn?

Silver sulfadiazine Will heal in about 14-21 days Minimal scarring Return of full function

What is the treatment for a second degree deep partial-thickness burn?

Silver sulfadiazine Will heal in 3 weeks to 2 months May need surgical debridement/skin grafting to obtain maximum function

What is the treatment for a third degree- full thickness burn?

Significant scarring Surgical repair and skin grafting is necessary

Which burn degree is described below? Presentation: Devastating and life-threatening Tissue involvement: Full thickness, plus it extends into the muscle, fat, and bone

Fourth Degree

What is the treatment for a fourth degree burn?

Amputation and/or extensive reconstruction is required (nothing to salvage)

What are the Rule of Nines percentages in an adult?

Each upper extremity: 9% Each lower extremity: 18% Anterior trunk: 18% Posterior trunk: 18% Head and neck: 9% Palm: 1*

Describe the burn resuscitation for major burns

Remove every item of clothing – first thing Cover wounds with DRY sterile dressing No goo on major burns 100% oxygen Rapid intubation for any evidence of airway compromise Prompt fluid resuscitation 🡪 volume depletion is biggest problem Monitor urinary output with a Foley catheter Assess adequacy of circulation

In burn fluid resuscitation, what is the most commonly used formula in North America?

Parkland Formula

What is the Parkland Formula?

(4mL) x (weight in kg) x (% TBSA burn)

What is a major complication of burns (after patient is stabilized)?

Complications of edema – the next major battle after fluid resuscitation/stabilization

Result of external compression of the skin, shear forces, and friction which produce ischemic tissue necrosis Takes about 2 weeks to develop Commonly on “bony prominences” Classified into four stages

Decubitus Ulcers

What are some risk factors for developing decubitus ulcers?

Elderly Immobilization Chronically bedridden patients Malnutrition Impairments in perfusion Neuropathy incontinence

What stage of a decubitus ulcer is described below? Sores are not open wounds Skin may be painful but it has no breaks or tears Skin is reddened and does not blanch Warmth and induration

Stage 1

What stage of a decubitus ulcer is described below? The skin breaks open, wears away, or forms an ulcer or blister which is usually tender and painful Expands into deeper layers of the skin – extension through epidermis It can look like a scrape (abrasion), blister, or a shallow crater Some skin may be damaged beyond repair or may die

Stage 2

What stage of a decubitus ulcer is described below? The sore gets worse and extends into the tissues beneath the skin forming a small crater Full thickness skin loss - Fat may show but no muscle, tendon, bone May be little to no pain due to significant tissue damage Necrotic Pigment changes

Stage 3

What stage of a decubitus ulcer is described below? The sore is very deep, reaching into fascia, muscle, and bone causing extensive damage Full thickness wounds with extension into muscle, bone, or supporting structure (damage to deeper tissues, tendons, and joints may occur) May be little to no pain due to significant tissue damage Osteomyelitis or sepsis may be present

Stage 4

What are some ways to prevent decubitus ulcers?

Reposition Early mobilization Keep skin clean and dry Use cushions Control blood sugar Provide adequate nutrition

How do you manage/treat decubitus ulcers?

Antibiotics Wound care management Vacuum-assisted closure Vascular surgery plastics

Other Skin Conditions Flashcards

(55 cards)