Term
Burns are #2 cause of death in children _______ y/0 (MVA #1)
and #3 cause of injury/death _____ y/o (after MVA, drowning) |
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Definition
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Term
| Describe epidemiology of burns. |
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Definition
House fires (smoking, heating/electrical equipment) are responsible for 84% deaths
Preschool-aged children: most burn injuries are by hot liquids (intentional abuse, accidents)
School children & young adolescents: most injuries are from motor vehicles, fireworks & flammables
Older adolescents & adults: most injuries caused by some type of flammable liquid
Risk factors: very young age, male, elderly, inebriation with alcohol, mental handicap, and history of previous burn
Development of multidisciplinary burn centers and better understanding of pathophysiology has increased the survival of 2nd/3rd degree burn patients by about 6-fold over the last 30 years. |
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Term
| Recall functions of skin. |
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Definition
Protection from external trauma
Resists temperature variation (insulation / cooling)
Blocks entry of microorganisms
Prevents moisture loss from underlying tissues
Immune surveillance functions
Decreases penetration of some types of radiation
Aids metabolism (e.g. Vitamin D, chemicals, drugs)
Produces lubricants and moisturizers for hair & surface
Provides the organism with a sense of “touch” |
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Term
| What are the 3 zones of injury due to a burn? |
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Definition
Zone of Hyperemia
Zone of Stasis
Zone of Coagulation |
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Term
| Describe Zone of Hyperemia. |
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Definition
Zone of Hyperemia -
Outermost or most peripheral area to the site of wound or injury
Tissue is characterized by inflammatory changes and minimal damage |
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Term
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Definition
Zone of Stasis -
Extends inward toward the central site of injury
Tissue is ischemic, typically with blood vessel endothelium damaged and with vessels partially thrombosed
Vessel endothelial damage may trigger further thrombosis, resulting in further ischemia, cell death and deepening of the wound
Drying and/or infection can also cause deepening of injury by preventing re-establishment of circulation to the injured tissues
Initial 24 to 48 hours post-injury can show progressive degeneration if situation is not quickly stabilized |
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Term
| Describe zone of coagulation |
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Definition
Zone of Coagulation -
Central-most area, where most energy causing the burn was absorbed
Characterized by thrombotic vessels and necrotic tissue
Minor burns will lack this “zone” entirely, while major burns will have all three described zones of injury |
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Term
| Estimate extent of injury by "the rule of Nines" in order to estimate BSA |
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Definition
Severity is proportional to the percent of body surface area (BSA) involved and the depth of the burn
For adult BSA: each arm is 9%, the head 9%, each leg 18%, the front or back of the torso 18% and the area of the genitalia 1%
For children (<10 yrs), an adjustment is made for the head, which is more, and for the legs, which are less than the values for adults |
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Term
| Classification by depth of tissue damage produced. Basic principles. |
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Definition
Determination of depth is difficult in the first 24 to 48 hours due to edema, ischemia and infection, which cause deepening of the wound
Depth can vary considerably, even within the same burn, and skin surface characteristics may not coincide with underlying tissue damage, making accurate assessment difficult
Burn depth is classified by assignment of categories as First, Second, Third or Fourth degree burns
Should you be asked by a patient for advice regarding a burn injury they have sustained, you will need some basic knowledge about how to distinguish the above categories of wound produced. |
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Term
| Describe first-degree burn. |
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Definition
Result from injury to the superficial cells of the skin, i.e. only the epidermis
Common example is a mild sunburn
Blisters are not seen, but there is erythema and some mild pain
Described as a “partial thickness” burn, that heals within 3-4 days with no scarring evident |
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Term
| Describe second-degree, superficial burn. |
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Definition
Involve tissue damage to both epidermis and dermis
Considered “superficial” if the extent of involvement of the dermis is minimal
Burn surface is erythematous, blistered, weeping and painful – sensitive to various stimuli
Erythema will blanch with pressure
Generally the hair follicles, sweat glands and sebaceous glands are spared
If truly superficial and uncomplicated, healing will be spontaneous within 3 weeks with little or no scarring |
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Term
| Describe second-degree, deep burn. |
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Definition
Involve deeper elements of the dermis
May be difficult to distinguish from 3rd degree burns
Burn surface is pale, and may feel either indurated (hardened) or “boggy”
The surface does not blanch with pressure
The wound is less painful than more superficial burns with some areas insensitive to stimuli
Healing occurs slowly over 4-6 weeks with eschar (border between healthy and damaged tissue) formation and possible severe scarring
There may be permanent loss of hair follicles, sweat glands and sebaceous glands in the area of the burn |
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Term
| Describe third-degree burn. |
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Definition
Characterized by complete destruction of the full thickness of the skin and all associated skin elements and systems
Wound may appear pearly white, gray or brown and is dry and inelastic
Pain is sensed only when deep pressure is applied
If area of the wound is small, healing can occur over several months by migration of intact epithelial cells from the margins of skin surrounding the wound
Scarring and contracture formation may be evident
Most often, repair of 3rd degree burns is done by excision and grafting of the wound to prevent contractures |
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Term
| Describe fourth-degree burn. |
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Definition
Tissue damage extends well below the dermis and into the subcutaneous tissue, fascia and bone
The wounds are blackened and charred in appearance
They are dry and generally painless due to extensive destruction of nerve endings
Great risk of infection and other complications |
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Term
| Describe the complication of fluid loss due to burns. |
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Definition
In severe burn, capillary damage is widespread and vasoactive mediators are released
Large amounts of fluid, plasma and electrolytes move to extravascular compartments of the body
Fluid redistribution is compounded by the loss of fluid, protein and electrolytes into the open wound
Cumulative effect is a marked fall in blood volume, cardiac output and tissue/organ perfusion
Fluid & electrolytes must be given to balance the losses; otherwise shock, organ failure and death may result
Timeline: critical in first 24 hours |
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Term
| Where do infections of second-degree, deep burns thrive? |
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Definition
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Term
| Describe the complication of infection due to burns. |
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Definition
Infection is the most important threat to survival of a burned patient with stable BP/HR/RESP
Sepsis and pneumonia are the leading causes of death (a sepsis-like state is observed in burn patients even in absence of an infection focus)
Loss of mechanical protection of skin permits entry of microorganisms, and poor blood flow to the area reduces infiltration of immune systems in response
GPOS colonization usually begins immediately, with GNEG organisms often predominating by Day 5
Systemic antibiotics are of limited usefulness with poor circulation, but may be used when wound biopsy demonstrates >10,000 bacteria per gram tissue
Topical antibiotics, local wound care and strict infection control practices are the mainstays of control |
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Term
| Describe complication of inhalation injury due to burns. |
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Definition
If there is an accompanying inhalation injury, mortality rates of burn injury are greatly increased
Bronchospasm, ulceration of membranes, edema and impairment of ciliary clearance of bacteria may result
Even patients with minor burns may have inhalation injury and require hospitalization (Facial burn? Closed space?)
Early symptoms may not develop for 24-48 hours, and include hoarseness, dyspnea, tachypnea and wheezing
Proper recognition and diagnosis of suspected inhalation injury must not be lost in the rush to address the burn wound itself; singed nasal hair, soot-coated tongue/mouth and upper airway edema are indications of interest |
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Term
| Describe diagnosis and therapy for inhalation injury. |
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Definition
Diagnosis established by bronchoscopy
Management may include endotracheal intubation and mechanical ventilation
Maintenance of fluid status is critical
Corticosteroids do not influence survival rates and should not be recommended; they also increase the risk of infection and subsequent morbidity/mortality |
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Term
| American Burn Assoc. Treatment Category of Major burn injury |
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Definition
Major burn injury
Second-degree burns with >25% BSA in adults, >20% in children
All third-degree burns with at least 10% BSA
All burns of hands, face, eyes, ears, feet and perineum with possible functional or cosmetic impairment
High-voltage electrical injury
Burns complicated by inhalation injury, major trauma or poor-risk patients (very young, elderly, debilitated) |
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Term
| American Burn Assoc. Treatment Category of moderate, uncomplicated burn injury |
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Definition
Moderate, Uncomplicated Burns
Second-degree burns with 15-25% BSA in adults and 10-20% in children
Third-degree burns 2-10% BSA
Burn must not have risk to key areas of specialized function (e.g. eyes, ears, face, hands, feet or perineum) |
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Term
| American Burn Assoc. Treatment Category of minor burn injury |
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Definition
Minor Burn Injury
Second-degree burns with <15% BSA in adults and <10% in children
Third-degree burns with <2% BSA
Burn must not involve risk to specialized functional or cosmetic areas of the body (e.g. eyes, ears, face, hands, feet or perineum) |
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Term
| When is outpatient therapy for burns appropriate? |
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Definition
Patients with minor burn injuries generally may be treated as outpatient if:
No other trauma is present
No circumferential burns are present
Patient or caregiver is able to comply with therapy
Many will require initial evaluation by a health care provider, with follow-up self-care as outpatients |
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Term
| When should a person have hospital admission for a burn? |
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Definition
Major Burns or Moderate, Uncomplicated Burns necessitate hospital admission
Surgical referral is usually made for all patients with deep second or third-degree burns covering 3% BSA
Transfer to a burn center is recommended for all acutely burned patients meeting any of a long list of special criteria [e.g. high-voltage electrical, lightning, caustic chemical, additional medical disorders, multiple trauma, etc |
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Term
| How does age change a burn recommendation? |
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Definition
Age –related recommendations
All children less than 2 years old and the frail & elderly should be referred to a physician for evaluation; they may not tolerate any trauma associated with the burn
Some burns in children will be due to child abuse and legal, protective and psychological issues will surface
Burns on children in varying stages of healing or with demarcated patterns of injury (e.g. “stocking” or “glove” distribution), or more than two burn sites may be clues to a suspected abuse situation |
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Term
| Patients with burns that also have other medical conditions may also change your recommendation. How? |
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Definition
Burn patients with other medical conditions will obviously be more susceptible to complications and may be less likely to heal quickly
What are the candidates to be alert for?
Diabetes mellitus
Cardiovascular disease
Immune deficiency disorders
Therapy with immune suppressants (cancer, steroids)
Renal disease, alcoholism, obesity |
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Term
| Etiology of burn may change a burn recommendation. |
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Definition
Electrical burns can appear to be superficial
Such burns can cause extensive damage to underlying tissues and organs that is not initially evident
Except for the most minor electrical burns, all should be referred to a professional for further evaluation |
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Term
| What are the goals of treatment for burns? |
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Definition
Relieve pain associated with the burn using drug agents
Prevent desiccation and deepening of the wound (cool, wet compresses)
Prevent infection by use of aseptic or sterile techniques
Provide a protective environment for healing and restoration of circulation
Begin an evaluation to determine if more extensive measures are required, such as surgery / skin grafts; a number of such products are available to mimic the functions of the lost dermis and epidermis |
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Term
| Describe the skin substitutes for burns. |
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Definition
Human cadaver skin (allograft) – considered the ultimate for temporary closure of burn wounds; cost, rejection and possible transmission of disease are disadvantages
Epidermal substitutes: Cultured Epithelial Allograft – epithelial cells derived from skin biopsy and grown in culture into sheets ; they lack mechanical stability and create an imperfect cover
Animal substitute: Pig Skin (xenograft) – adheres well, lower cost than human skin, covers nerve endings and diminishes fluid, protein and electrolyte loss; stored frozen with a shelf life of up to 18 months
Dermal substitutes: Allodermal Grafts – cadaver dermis can be rendered acellular, freeze-dried and shelf-stored until used underneath a mesh of autograft epidermis from the burned patient; other techniques use a preparation of collagen fibers from bovine sources as the lower layer underneath a thin film of polysiloxane polymer as the outer layer |
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Term
| Describe human cadavar skin substitute. |
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Definition
| Human cadaver skin (allograft) – considered the ultimate for temporary closure of burn wounds; cost, rejection and possible transmission of disease are disadvantages |
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Term
| Describe epidermal skin substitutes. |
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Definition
| Epidermal substitutes: Cultured Epithelial Allograft – epithelial cells derived from skin biopsy and grown in culture into sheets ; they lack mechanical stability and create an imperfect cover |
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Term
| Describe animal skin substitutes. |
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Definition
| Animal substitute: Pig Skin (xenograft) – adheres well, lower cost than human skin, covers nerve endings and diminishes fluid, protein and electrolyte loss; stored frozen with a shelf life of up to 18 months |
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Term
| Describe dermal skin substitutes. |
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Definition
| Dermal substitutes: Allodermal Grafts – cadaver dermis can be rendered acellular, freeze-dried and shelf-stored until used underneath a mesh of autograft epidermis from the burned patient; other techniques use a preparation of collagen fibers from bovine sources as the lower layer underneath a thin film of polysiloxane polymer as the outer layer |
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Term
| Describe Synthetic Dressings and Bioengineered Products for skin substitutes. |
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Definition
Biobrane (Bertek) is a sheet of silicone bonded to a nylon mesh, with collagen peptides protruding downward from the nylon underlayer to promote adherence to underlying tissue; others are available containing carboxymethylcellulose or elastomeric polyurethanes to provide a barrier to microorganisms and fluid loss
Tissue-engineered biological dressings are recent developments, but hold much promise; these involve repeated applications to the injury site of a special mesh/preparation of skin cells, e.g. keratinocytes and fibroblasts (from the patient or pooled donors); some brands are Dermagraft, Apligraf or Epicel |
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Term
| Describe silver sulfadiazine as topical antimicrobial agent for burn patient. |
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Definition
Silver Sulfadiazine (Silvadene)
Often the agent of choice; 1% suspension in a cream
Has broad spectrum G+ and G- activity
Some penetration of eschar tissue (necrotic tissue adhering to healthy, viable tissue), but agent lacks good water solubility
Painless, easily applied & washed off
Most effective when applied immediately after injury; not very useful for an established infection
Free of acid-base & electrolyte disturbances
Adverse effects seen (systemic absorption): neutropenia (reversible with d/c agent) and rare hypersensitivity
Evidence of greater efficacy for wound healing or reduced infection versus other topical agents is not strong
Avoid skin areas near the eyes and mouth, patient with known hypersensitivity (e.g. sulfa) or with pregnancy/nursing |
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Term
| Describe mafenide acetate as topical antimicrobial agent for burn patients. |
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Definition
Mafenide Acetate (Sulfamylon)
Formulated as 11.1% cream or 5% powder
Water soluble, diffuses easily and penetrates eschar areas (the non-viable/viable skin interface is often a key site of bacterial proliferation prior to further invasion)
Probably the best agent for use when the patient has contaminated burn wounds, if treatment has been delayed several days, or if dense bacterial growth is evident
Adverse effects include hypersensitivity reactions (7%), pain upon application (20-30 minutes) and inhibition of carbonic anhydrase (↑HCO3- excretion & hyperventilation).
Note: The latter action causes a reduced serum bicarbonate level and renders the patient susceptible to development of metabolic acidosis. If pH begins to fall, reduce dosing interval to once daily or suspend use for 24-48 hours, with buffering therapy as necessary. Maintain good pulmonary function. |
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Term
| Describe silver nitrate as a topical antimicrobial agent for burn patients. |
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Definition
Silver Nitrate
If true topical antimicrobial agents are not available, silver nitrate may be used as a 0.5% solution applied to multilayered occlusive gauze dressings
Its use is actually as a “wet dressing” (see later slide)
Dressings are moistened every 2 hours and changed 2-3 times per day; avoid evaporation of water (↑ AgNO3)
Anticipate loss of Na, K, Cl & Ca across the eschar interface and be prepared to replace these electrolytes
This agent should be applied immediately after injury if possible, since AgNO3 precipitates immediately upon contact with proteins. Thus it does not penetrate far into the eschar and so is not useful for established infections
May be painful for some patients |
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Term
| HOw are topical antimicrobials applied for use on burn patients? |
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Definition
For Silver Sulfadiazine or Mafenide Acetate, a one-eighth inch thick layer is applied to the entire burn wound with a sterile gloved hand immediately after initial debridement and emergency wound care
Depending on size and severity of the wound, and other treatment goals, it may be covered with absorbent gauze and wrapped
Twelve hours later another application is made, especially for small wounds and ambulatory patients, e.g. if the agent is removed by clothing or otherwise abraded
Cleanse and inspect the wound at least once daily
In-patients with more serious burns may require daily debridement; in some cases to the point of bleeding or pain, as tolerated without anesthesia
Wound is then recovered with the topical preparation |
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Term
| Summarize wet dressings for burns. |
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Definition
Aluminum Acetate (Burow’s Solution)
Actions - Mild germicidal and astringent activity
Easy dilution of tablet or packet in water to prepare
Potassium Permanganate
Actions – Moderate germicidal activity; not astringent
Stains skin and clothing
Silver Nitrate
Actions – Good germicidal and astringent activity
Stains skin and clothing; sometimes painful
Acetic Acid
Actions – Good germicidal and astringent activity
Unpleasant, strong odor; can be irritating |
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Term
| Describe aluminum acetate (burow's solution) as wet dressing for burn. |
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Definition
Aluminum Acetate (Burow’s Solution)
Actions - Mild germicidal and astringent activity
Easy dilution of tablet or packet in water to prepare |
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Term
| Describe potassium permanganate as a wet dressing for a burn. |
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Definition
Potassium Permanganate
Actions – Moderate germicidal activity; not astringent
Stains skin and clothing |
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Term
| Describe silver nitrate as a wet dressing for burn. |
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Definition
Silver Nitrate
Actions – Good germicidal and astringent activity
Stains skin and clothing; sometimes painful
Acetic Acid
Actions – Good germicidal and astringent activity
Unpleasant, strong odor; can be irritating |
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Term
| Describe acetic acid as wet dressing for burns. |
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Definition
Acetic Acid
Actions – Good germicidal and astringent activity
Unpleasant, strong odor; can be irritating |
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Term
| Describe traditional antibiotics as for use in burns. |
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Definition
Traditional Antibiotics
Use of traditional antibiotics, whether topical or systemic, would be by judgment of the physician
Dependent on the nature of the organism, presence of blood circulation to the burn locale, whether the infection has spread beyond the location of the burn, etc |
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Term
| Describe analgesics for use of burns. |
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Definition
Analgesics
Oral OTC products usually appropriate for many patients with less severe pain
Severity of pain may require upgrade to opiates depending on the patient and status |
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Term
| Describe topical protectants for use in burns. |
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Definition
Topical protectants
Palliative preparations such as allantoin, calamine, white petrolatum or zinc oxide are safe and effective in helping with first-degree and minor second-degree burns.
These agents not only sooth the injury and prevent excessive drying, but also help to protect it from mechanical friction and rubbing if not occluded. |
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Term
| Describe post-wound, follow-up care of burns. |
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Definition
Essential component of total burn management
Ensures adequate wound healing as well as psychological support with regard to cosmetics and presence of scarring
Principles:
Healed wounds should be moisturized regularly
Pruritis can be a problem after injury; antihistamines may be required to alleviate this; moisturizers will help
Protection from sun important; this will prevent further thermal damage or pigmentation changes to the healed area
Patient and care-givers should be alert to surface changes, e.g. hypertrophy of skin or new blisters and wounds
Advise patient to return to their health care provider if these signs appear |
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Term
| Classification of steroids is based on what? |
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Definition
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Term
| How is steroid potency determined? |
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Definition
| Determined experimentally by forearm blanching test (↓NO-related vasoconstriction) using serial dilutions of the product, and by clinical experience |
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Term
| Which is most potent steroids? I or VII? |
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Definition
| Group I is most potent, ranging down to Group VII as the least potent – some in Group VII are OTC |
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Term
Describe Group I steroids.
Potency? Used for? Duration? |
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Definition
*Super-potent types reserved for use in severe and non-responding dermatoses
*Not for face, axillae, groin or under breasts (facial and “intertriginous” areas (latter term means skin-to-skin contact zones)
*Typical use in psoriasis and hand eczema
*Duration of therapy typically not > 14 days or so, followed by a “rest” for most all members of this group
*Occlusive dressings not recommended for most members of this group except diflorasone |
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Term
| Describe the Steroid, Salt, strength, brand name, dosage form for Group I Clobetasol. |
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Definition
| Clobetasol proprionate 0.05% (Cormax® cream, ointment, scalp solution) |
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Term
| Describe the Steroid, Salt, strength, brand name, dosage form for Group I Betamethasone. |
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Definition
| Betamethasone diproprionate 0.05% (Diprolene® lotion, ointment, gel) |
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Term
| Describe the Steroid, Salt, strength, brand name, dosage form for Group I Halobetasol . |
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Definition
| Halobetasol proprionate 0.05% (Ultravate® cream, ointment) |
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Term
| Describe the Steroid, Salt, strength, brand name, dosage form for Group I Diflorasone. |
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Definition
| Diflorasone diacetate 0.05% (Psorcon® ointment) |
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Term
| Ointment/gels (more/less) potent and thus push drug into lower tissues |
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Definition
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Term
| What body regions can Group II & III be used for? What is the limit time? |
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Definition
| Group II & III not for face, axillae, groin; limit use to about 21 days followed by a rest from therapy |
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Term
| What body regions can Group IV & V be used for? What is the limit time? |
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Definition
| Groups IV – V often used in children for atopic dermatitis but for 7-21 days only; limited use in intertriginous areas |
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Term
| What body regions can Group VI & VII be used for? What is the limit time? |
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Definition
| Groups VI – VII used in intertriginous areas and delicate skin such as eyelids and other facial areas, or with occluded conditions such as under diapers |
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Term
| Cortisol is active at how many nuclear receptors? |
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Definition
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Term
| What are the 2 nuclear receptor types of cortisol? What do they alter? |
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Definition
Glucocorticoid Receptor
Mineralocorticoid Receptor
*alter gene expression |
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Term
| Where are the GR and MR located and how do they work? |
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Definition
*These receptors are found in the cytoplasm of many cell types in an inactive form
*When cortisol binds, the complex is translocated to the nucleus where it may up-regulate genes, or in some cases down-regulate the expression of genes controlling various systems and the synthesis of proteins |
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Term
| Describe cortisol <--> cortisone reaction. |
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Definition
**Recall 20% of cortisol is converted to cortisone (by the enzyme 11-Beta-Hydroxysteroid dh Type 2); cortisone does not bind to either GR or MR
*In some tissues, the conversion of cortisol to cortisone is quickly reversible by a Type 1 enzyme, and so cortisol may be regenerated
*Kidney has high activity of the Type 2 enzyme only, and so cortisol levels are maintained at very low levels in that tissue; cortisone predominates and the 11-Keto function of cortisone makes it receptor-inactive
*This permits the MR activity of aldosterone to be revealed – otherwise the huge relative concentration of cortisol would swamp the latter hormone’s action in kidney |
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Term
| What characterizes psoriasis? |
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Definition
Psoriasis
*Chronic papulosquamous skin disease, most commonly with scaly papules and plaques
*Autoimmune in nature
*Develops to sharply defined red patches & silvery flaky surface
*Primarily an epidermal disease, but inflammation is dermal |
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Term
| What measures severity of psoriasis? |
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Definition
Standard techniques exist for
scoring the severity and the
response to treatment – the
Psoriasis Area Severity Index (PASI) |
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Term
| Describe occurence and transmission of psoriasis. |
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Definition
*Occurs is 1-3% of population
*Transmitted genetically, most likely in dominant mode of unknown origin
*Disease is lifelong and characterized by chronic, recurrent exacerbations and remissions that are emotionally and physically debilitating
*Many people may have the potential for psoriasis, lacking only the correct combination of factors such as stress or other disease, which then act to precipitate the initial episode |
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Term
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Definition
*Genetic abnormalities of the immune system are now considered to be the driving force for the skin changes; thus an autoimmune disorder
*There is a role of memory T-cells in driving or propagating the disease
*Dysregulation of feedback mechanisms for control of keratinocyte proliferation
*Triggered by stress and other environmental factors, e.g. such as streptococcal pharyngitis |
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Term
| In psoriasis, Keratinocytes (increase/decrease), capillaries (constrict/dilate) which increases blood supply. Langerhans cells (increase/decrease). |
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Definition
**Increase
Keratinocytes accumulate in thick, dry patches of excessive amounts of stratum corneum (silvery, flaky areas)
**Capillaries dilated: increased blood supply to abnormally multiplying keratinocytes (produce inflammation and characteristic redness or erythema – extends to dermis)
Infiltration of epidermis and papillary dermis with lymphocytes and later neutrophils appear in greater numbers
**Decreased number of Langerhans cells (immature Dendritic cells) |
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Term
| Where do psoriasis plaques most commonly occur? adults vs children? |
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Definition
*Plaques most often occur on the elbows, knees, scalp, lower back and gluteal cleft; less commonly on palms, soles, genital areas, thighs, calves, fingers and toes
*May occur on other intertriginous areas of skin (i.e. where opposing skin surfaces meet and touch; axillae, groin, etc)
*50% of adult patients develop psoriasis of the scalp, but only rarely on face
- In children, scalp is a common site, and may also occur on face and ear |
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Term
| Describe what psoriasis looks like. |
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Definition
| Well-defined oval reddish plaques, with inflammatory infiltrate progressing to drive output of Stratum Corneum to produce silver-white scaly surface |
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Term
| Which drugs are contraindicated with psoriasis? |
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Definition
*Lithium – not a general contraindication, but be alert; may require Li dosage reduction and more aggressive psoriasis therapy
*Beta-Blockers – may well exacerbate the condition; need for such meds should be evaluated critically
*Antimalarial Agents – incidence of problems is low, but well documented; not contraindicated if appropriate
*Systemic Steroids – rapidly clears psoriasis, but when withdrawn, the disease flares up and often evolves and worsens; for this reason, routine use of systemic steroids has been abandoned in most all cases |
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Term
| What is guttate psoriasis? |
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Definition
Represents a minority of cases of Psoriasis (about 2%)
* >30% patients have first episode by age 20
May be first indication of problem, often preceded (2 weeks) by viral upper resp infection or strep pharyngitis
*Small papules appear (guttate = drop shaped) on the trunk and extremities and soon develop a scale
*May resolve spontaneously, but if treated are much more responsive to therapy than chronic forms |
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Term
| What is chronic plaque psoriasis? |
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Definition
*Chronic and well-defined plaques are the most common presentation
*Flaky, silvery-white crust is characteristic feature, with well-defined border of erythema visible at the periphery of the crust
*Lesions can appear anywhere on the skin surface, but there are characteristic sites that are more common
*They enlarge to a certain size and then remain stable for months or years
*Even if the plaque subsides, a red, brown or white macule typically remains for some time in that same area of the skin |
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Term
| What is Generalized Pustular Psoriasis? |
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Definition
| Generalized Pustular Psoriasis – serious to fatal disease with erythema and pustules. Patient is toxic, febrile and has leukocytosis. |
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Term
| What is Erythrodermic Psoriasis? |
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Definition
| Erythrodermic Psoriasis – usually occurs in patients with other serious chronic diseases, stress or infection. Severe, unstable & labile. |
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Term
| What is Keratoderma blennorrhagicum? |
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Definition
| Keratoderma blennorrhagicum (Reiter’s Syndrome) - an immune response triggered in a genetically susceptible individual following certain Yersinia infections |
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Term
| What is Psoriasis inversus? |
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Definition
| Psoriasis inversus – limited to involvement of the flexural and intertriginous areas, with cracking and fissuring prominent features |
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Term
| What is HIV-induced psoriasis? |
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Definition
| HIV-induced Psoriasis – may be a first sign of HIV infection, often atypical and unusually severe (or not). If explosive in onset, with rapidly developing and confluent pustular lesions, one should suspect AIDS. |
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Term
| What is psoriatic arthritis? |
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Definition
| Psoriatic arthritis – a distinct form of arthritis that may precede, accompany or more often, follow the skin manisfestations of 5-8% patients. May be progressive and deforming as time passes. |
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Term
| What is eczema and how does it differ from dermatitis? |
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Definition
Eczema is the most common inflammatory skin disease
The term dermatitis is often used to refer to an eczematous eruption, but strictly speaking, dermatitis means only an “inflammation of the skin” and is not exactly synonymous with the term eczema
Eczema refers to a skin disorder with erythema, scale and vesicles, often accompanied by pruritus, and almost inevitably seen with secondary changes due to scratching, irritation, infection and/or topical treatment
Often, the two terms are used interchangeably, with irritant and allergic contact forms usually called “dermatitis” and the endogenous or constitutional forms termed as “eczema” |
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Term
| List examples of dermatitis. |
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Definition
Contact Dermatitis – two forms
Irritant form – e.g. soaps, detergents, chemicals
Allergic form – e.g. latex, metals, perfumes, adhesives, poison ivy
Seborrheic Dermatitis
Oily skin and the yeast Pityrosporum ovale are offered as contributing factors
Atopic Dermatitis
Chronic itchy eczematous disease beginning in early life and flaring off & on throughout life
Stasis Dermatitis
↓ Blood flow, typically lower limbs |
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Term
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Definition
Hand Eczema
Palmar peeling, fingers and fingertips
Body sites
Numerous sites of inflammation, scale and vesicles
Sometimes self-inflicted or psychogenic (“skin-pickers”) |
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Term
| What is Atopic dermatitis? |
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Definition
Atopic Dermatitis is a chronic, pruritic eczematous disease, nearly always beginning in childhood and following a remitting/flaring course throughout life of the patient
*Develops as a complex interplay of environmental, genetic, immune and pharmacologic factors in the body
*Exacerbated by infection, stress, seasonal/climatic change, irritants and allergens
*Typically moderates with age, but patients carry a life-long sensitivity to irritants and this “atopy” predisposes them to skin disease (Atopy is an old term used to designate a group of patients with family history of one or more of hay fever, asthma, dry skin or eczema; aspirin allergy is also common) |
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Term
| Describe features and diagnosis of Atopic Dermatitis. |
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Definition
No specific cutaneous signs, no known distinctive histologic features and no characteristic laboratory findings for atopic dermatitis (AD)
There are diagnostic criteria that allow a diagnosis to be made (when the patient has ≥3 major features and ≥3 minor features; next slide)
Not an emotional disorder – although many patients are emotional due to a very frustrating disease course
Not precipitated by an allergic reaction – although many have increased levels of IgE and respiratory allergies; if skin tested, will most likely be told that they are “allergic to everything”
In fact, atopic patients may react with a wheal, when challenged only with a needle during skin testing
All evidence to date shows that most all cases of AD are precipitated by environmental stress on genetically compromised skin and not by interaction with an allergen |
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Term
| What are the major features of atopic dermatitis? |
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Definition
Pruritus
Typical morphology & distribution
Flexural lichenification in adults
Facial & extensor surface involvement in infants & children
Chronic or chronic-relapsing dermatitis
Personal or family history of atopy |
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Term
| What are the minor features of atopic dermatitis? |
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Definition
Cataracts or Conjuctivitis
Facial pallor or erythema
Food intolerance
Hand eczema – irritant
Ichthyosis (skin resembles fish scales)
Elevated IgE (role unknown)
Immediate (Type I) skin test positive
Pityriasis alba (asymptomatic, hypopigmented, round areas, slightly elevated scaling plaque in dry winter months; common on face in children)
Itching upon sweating
Palmar hyperlinearity (excessive number of palm creses)
White dermographism (blanching of skin with pressure point)
Xerosis (dry, scaly, compromised skin following inflammation)
Keratosis pilaris (small rough follicular papules most often on posterolateral upper arms and anterior thighs; if on face may be confused with acne) |
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Term
| A person must have ___ of the features on each minor and major features of atopic dermatitis. |
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Definition
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Term
| What is the prevalence of Atopic dermatitis? |
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Definition
Prevalence in children is 7-17%, trending up greatly since the early 1960s
This is not due to genetic changes, but suggests a connection to the environment or increased diagnosis
*More than 50% kids with AD develop asthma and allergic rhinitis by age 13, even with improving dermatitis
*Extensive disease involvement (>50% body) will retard growth of the child
*About 70% patients have family or personal history of “atopy” |
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Term
| Describe what atopic dermatitis looks like. |
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Definition
| May be seen in any age group, and vary from oozing & crusting conditions, to diffuse rashes with hypopigmentation and/or lichenification – should be distinguished from other conditions such as contact/irritant/allergic dermatitis or psoriasis, etc. |
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Term
| What are the stages of eczematous inflammation? |
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Definition
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Term
| Therapy for acute atopic dermatitis. |
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Definition
Topical steroids are of little use in acute stages, because they do not penetrate well through the often dense accumulation of vesicles or blisters – oral dosing may be necessary
Wet dressings used to dry the acute inflammatory stages of these diseases should be discontinued when the disease evolves into the subacute stage – too much drying creates cracking and fissuring, which predisposes to infections
Presence of secondary bacterial infection may may dictate need for antibiotics, e.g. SMZ/TMP (Bactrim) or Clindamycin for MRSA, Cephalexin or Dicloxacillin commonly used for other bugs |
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Term
| Acne is a disease of what? |
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Definition
| A disease of the pilosebaceous unit of skin (oil ducts leading to skin surface) |
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Term
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Definition
Typically the condition becomes less active as adolescence ends
Highly variable intensity and duration of activity; varies from minor comedones and pustules to highly inflammatory and diffusly scarring forms
Most severe forms of the disease occur in males, but the more persistent forms occur in females |
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Term
| Differentiate between acne and perioral dermatitis. |
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Definition
| Important to differentiate from perioral dermatitis, a condition of female childhood (i.e.<14 yr) related to skin treatments with moisturizing creams and cosmetics |
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Term
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Definition
*Change in keratinization pattern of the hair follicle, with blockage of the *Seborrheic Duct is the basic cause of acne
*Skin oils (lipids), keratin and debris accumulate and may protrude to surface if an exit point along the follicle can be reached; if not, the process initially remains under the surface
*Anaerobic bacteria produce proteases, chemotactic factors and lipases (exacerbate e.g. by metabolism of lipids to fatty acids)
*Sebum and fatty acids initiate a sterile inflammatory process
*Hormones, genetics and resulting
infection may produce an enlarged
area of involvement that ruptures into the dermis, with pustules, nodules, and immune reactions |
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Term
| What is pyoderma faciale? |
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Definition
| Pyoderma faciale – distinctive variant of cystic acne affecting only the face of adult females (teens to 40 yr); rapid onset of large, tender erythematous-to-purple cysts, predominantly on the central cheeks; erythema may be intense with purulent drainage of the cysts. |
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Term
| Neonatal vs infantile acne? |
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Definition
Neonatal acne – lesions confined to nose and cheeks at birth or developing in early infancy; stimulated by maternal androgens; lesions clear spontaneously without treatment as the sebaceous glands become smaller and less active
Infantile Acne - a male predominant form of acne that may appear at 6 - 16 months of life, that should be distinguished from neonatal forms; lesions may be mild, moderate or severe, and is predominantly of the inflammatory type. It is treated by conventional adult means (no tetracycline type meds however!!) |
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Term
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Definition
A chronic inflammatory disorder, typically appearing after age 30 yr.
Involves the nose, cheeks and forehead, with congestion, flushing, telangiectasia and nodular swelling (esp. nose).
Ocular involvement may be seen in 60% or more of patients with Rosacea
Accentuated or precipitated by such factors as skin follicle mites, alcohol, sun exposure and hot drinks |
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