Week 1 Flashcards

1
Q

acute physical signs and symptoms of a severe thermal burn

-parts of body affected (4)

A
  • Skin
  • Cardiovascular
  • Respiratory
  • Mental status
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2
Q

Acute physcial sign: skin

-types of burns: how they will look

A
  • Superficial burns are erythematous and dry; blanch with pressure
  • Superficial partial-thickness burns are wet with clear bullae on erythematous skin; blanch with pressure
  • Deep partial-thickness burns are wet or waxy dry with variable color (whitish or red with white/yellow patches); no blanching with pressure5
  • Full-thickness burns range from waxy and white to leathery and gray to charred, black, and dry; do not blanch with pressure
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3
Q

Acute physical sign: cardio

A

• Hypotension and tachycardia in case of extensive burns

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4
Q

Acute physical sign: respiratory

A
- Facial burns
○ Singed facial/nasal hair
○ Carbonaceous sputum
○ Soot in or around the mouth
○ Inability to tolerate secretions
○ Hoarse voice
○ Stridor
○ Tachypnea
○ Wheezing
○ Decreased oxygen saturation
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5
Q

Acute physical sign: mental status

A

• Decreased level of consciousness may suggest carbon monoxide poisoning if associated with exposure to fire in enclosed space, hypoxia, substance use, or head injury

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6
Q

Types of burns

A
  • 1st degree: Superficial
  • 2nd degree: Superficial-partial thickness
  • 3rd degree: Deep-partial thickness
  • 4th degree: Full thickness
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7
Q

Second degree: Superficial Partial-thickness

A

○ Extends into superficial (papillary) layer of dermis
○ Red, possibly moist, and very painful
○ Blanches with pressure
○ Blisters are present (may take 12-24 hours to appear)
○ Generally heals within 7 to 20 days, usually without scarring

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8
Q

Third degree: Deep partial-thickness burn

A

○ Extends into deep (reticular) layer of dermis
○ Wet or waxy and dry with variable color (whitish or red with white/yellow patches)
○ No blanching with pressure
○ Sensitive to pressure only
-Blisters present
○ Healing takes longer than 21 days; results in significant hypertrophic scarring and risk of contracture3

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9
Q

• Fourth degree: Full-thickness (third-degree) burn

A

• Loss of all skin elements; thrombosis and coagulation of vessels
• Burns extending below subcutaneous tissue into fascia, muscle, or bone
• Waxy to leathery
• Stiff and dry
• White, gray, or charred
• No blanching with pressure
• Sensitive to deep pressure only
-Does not heal and requires grafting; results in severe scarring and contractures

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10
Q

Criteria used to determine burn severity

A
  • Depth of burns
  • Percentage of body surface involved
  • Internal injuries caused by the inhalation of hot and toxic fumes
  • Promptness and efficacy of therapy, especially fluid and electrolyte management and prevention or control of wound infections
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11
Q

Physiological mechanisms responsible for hypovolemic shock

A

Hypovolemiais due to massive fluid losses from the circulating blood volume. The losses are caused by an increase in capillary endothelial permeability, third spacing (fluid moves from the intravascular space into the interstitial or “third” space), exudation, and evaporation that persists for 24 hours after the burn injury. Fluid resuscitation: administration of intravenous fluids (lactated ringer) to restore circulating blood volume (due to hypovolemic shock).

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12
Q

Mechanisms underlying the risk of protein-energy malnutrition in thermal burn

A

-Burn injury causes a persistent and prolonged hypermetabolic state and increased catabolism that results in increased muscle wasting and cachexia. Metabolic rates of burn patients can surpass twice normal, and failure to fulfill these energy requirements causes impaired wound healing, organ dysfunction, and susceptibility to infection. Adequate assessment and provision of nutritional needs is imperative to care for these patients. Most clinicians advocate for early enteral nutrition with high-carbohydrate formulas.

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13
Q

Outline the protocols for wound care in 1st degree

A
  • Dressing:None required (except to protect from injury); topical antibacterial agents NOT recommended
  • Other:Emollients, cool compresses (avoid ice), if pruritic, trial of antihistamines
  • Prognosis:Heals within 1 week without scarring. May heal with pigmentary changes (limit by sunscreen and sun avoidance of area for 1 year).
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14
Q

Outline the protocols for wound care in 1st degree

A
  • Dressing:None required (except to protect from injury); topical antibacterial agents NOT recommended
  • Other:Emollients, cool compresses (avoid ice), if pruritic- trial of antihistamines
  • Prognosis:Heals within 1 week without scarring. May heal with pigmentary changes (limit by sunscreen and sun avoidance of area for 1 year).
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15
Q

Outline the protocols for wound care in 2nd degree

A
  • Blisters:Sharp debridement of ruptured blisters; leave intact blisters bc quicker healing and reduced infections. Consider unroofing blisters that show no sign of resorption over several weeks or contain cloudy fluid.
  • Dressing:Topical antimicrobial ointment (e.g., bactroban) or A&D ointment with nonadherent dressing twice a day. Alternate: biosynthetic dressing (alginates, hydrofibers, or foam dressings)—many with silver as antimicrobial (absorb exudates, maintain moist environment, require fewer dressing changes, which reduces pain/anxiety)
  • Prognosis:Heals with minimal scarring in 10 to 14 days. May heal with pigmentary changes (reduced with sunscreen and sun avoidance of area × 1 year)
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16
Q

Outline the protocols for wound care in 3rd degree

A

• Dressing:Silver sulfadiazine 1%: broader spectrum, better penetration of necrotic tissue than bactroban, but inhibits epithelialization and promotes hypertrophic scarring in studies. Must stop use once exudates and eschar have separated from wound. Alternative: enzymatic debrider (e.g., Santyl or Accuzyme)—chemically debrides devitalized tissue without harming healthy tissue.
• Referral:Burn specialist for consultation regarding need for excision and grafting.
-Prognosis:Deep partial thickness burns heal with significant scarring, often take 3 to 4 weeks to heal.

17
Q

Discuss the indications for and types of skin grafts.

A
  • Split-thickness skin grafts are harvested with a knife or dermatome, and only the superficial layer of the skin is taken. The donor site of a split-thickness graft will heal on its own from propagation of epithelial cells from the deeper skin appendages (hair follicles and sweat glands).
  • Full-thickness grafts are harvested with an incision of a knife and involve taking the entire layer of skin down to the subcutaneous fat. These donor sites must be closed as with an incision; otherwise the patient is left with a scar.
18
Q

Processes of grafting, healing and rejection with an autologous skin graft.

A
  • large sheets of the patient’s epidermal cells in tissue cultures which are transferred to the prepared burn wound
  • used on wounds that are too extensive to heal by primary closure
  • Since the cells are taken from the person, that person’s immune system will not reject them. However because these sheets are very thin (only a few cell layers thick) they do not stand up to trauma, and the “take” is often less than 100%.
19
Q

physiologic action of morphine that produces analgesia

A

-acts on the mu-opioid receptors which contributes to analgesic effect

20
Q

Identify common side effects associated with the acute administration of morphine

A

• Sedation
• Dizziness
-GI effects (nausea, vomiting, constipation)

21
Q

Clinical presentation of psoriasis

A

erythematous scaly plaques, round or oval, variable in size, frequently located in scalp, lower back, umbilical region, intergluteal cleft, knees, and elbows

22
Q

mechanism underlying the disease process of psoriasis

A

inflammatory skin condition with reactive abnormal epidermal differentiation and hyperproliferation. Current research suggests that the inflammatory mechanisms are immune based and most likely initiated and maintained primarily by T cells in the dermis. Reactivation of T cells in the dermis and epidermis and the local effects of cytokines such as tumor necrosis factor lead to the inflammation, cell-mediated immune responses, and epidermal hyperproliferation observed in persons with psoriasis.

23
Q

natural history of progression of psoriasis

A

caused by inappropriate activation of T-helper cells (may be triggered by drug aggravation, disease, lifestyle, or environment) which preferentially differentiate into Th17 cells leading to over production of Th17 related pro-inflammatory cytokines (IL-23, etc.). This causes over-activated pro-inflammatory immune response resulting in psoriasis.

24
Q

histopathologic features of plaque psoriasis

A
  • epidermis acanthotic in appearance and the rete ridges increase in size.
  • loss of the granular layer
  • corneum is also thickened, and the retention of cell nuclei in this layer is referred to as parakeratosis.
  • Neutrophils and lymphocytes can be observed migrating upwards from the dermis into the acanthotic epidermis.