Thermal and Radiation Injury Flashcards

1
Q

What are the three types of thermal burns?

A
  1. Superficial burns - limited to epidermis (i.e. sunburn)
  2. Partial thickness burns - extend into the dermis
  3. Full thickness burns - destruction through dermis, can involve subcutaneous tissue, tends, skeletal muscle, and bone
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2
Q

How does the skin regenerate in a partial thickness burn? What structure will exist on an acute lesion?

A

Via the remaining stem cells in the adnexal structures (i.e. matrix cells of the epidermis)

Lesion typically features a prominent blister

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3
Q

How does pathology of superficial / partial thickness burns differ from full thickness burns with respect to inflammaton / appearance?

A

Superficial / partial thickness -> acute inflammation with coagulative necrosis. Pain will be present.

Fullthickness -> extensive damage to blood vessels, nerve endings, and adnexal structures (i.e. sweat glands)
-> no pain at site of lesion, which will be black and leathery. Periphery may have pain due to partial thickness components.

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4
Q

What type of shock do burns cause initially and why?

A

Hypovolemic

  • > increased vascular permeability due to inflammation and vessel damage (subsequent hypercoagulability)
  • > evaporation of interstitial fluid due to loss of skin
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5
Q

What electrolyte imbalance happens in burns and why?

A

Hyperkalemia, due to cellular lysis from heat (high K+ in cells is released into interstitium)

Also hyponatremia due to loss of plasma into the interstitium and evaporation

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6
Q

What other type of shock can burns cause and how? What will this result in?

A

Septic shock, due to bacteremia which results from loss of skin barrier.

Septic shock can lead to multisystem organ failure and diffuse alveolar damage -> adult respiratory distress syndrome (ARDS) = respiratory failure

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7
Q

What GI side effect is a result of the acute, extreme physiological distress of burns?

A

Curling ulcers (think “Curling irons can burn”) -> gastric ulcers in the setting of a burn

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8
Q

What are the chronic results of burns in some people, and especially in children?

A

Children - contractures

Adults - Hypertrophic scars and keloids (extensive form of scar overgrowth)

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9
Q

What are the three responses to hyperthermia, from mildest to most severe?

A
  1. Heat cramps
  2. Heat exhaustion
  3. Heat stroke
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10
Q

What are the signs and symptoms of heat cramps, and what causes them?

A

Involuntary, painful muscle spasms during or after strenuous exercise

Caused by electrolyte abnormalities like hyponatremia (due to only replenishing water but not electrolytes)

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11
Q

What are the signs and symptoms of heat exhaustion? How will the skin feel?

A

Sudden dizziness, nausea, headache, profuse sweating, fatigue associated with hypotension, tachycardia, and a low-grade fever

Skin feels pale, cool, and moist -> vasoconstriction due to hypovolemia with sweating

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12
Q

What is the pathogenesis of heat exhaustion?

A

Extreme sweating leads to inadequately compensated hypovolemia, with slightly elevated body temperature and peripheral vasoconstriction to maintain blood pressure

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13
Q

What is the pathogenesis of heat stroke?

A

Inability to dissipate heat quickly enough and dehydration leads to loss of sweat.

  • > highly elevated body temperature
  • > denaturation of proteins / cell membranes with expression of heat shock proteins and amplified acute phase response
  • > hsp’s will create septic shock-like response
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14
Q

What are the signs and symptoms of heat stroke?

A

High core body temp (>104F/40C)
Hot, dry, flushed skin (peripheral vasodilation for convection)
Tachycardia, neurologic symptoms, difficulty breathing

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15
Q

What are the most severe manifestations of heat stroke?

A

Multiorgan failure and rhabdomyolysis (skeletal muscle lysis)

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16
Q

Does alcohol use affect hyperthermia or hypothermia and why?

A

Hyperthermia - makes worse -> diuresis contributes to hypovolemia and makes you less likely to notice

Hypothermia - makes worse -> peripheral vasodilation (flushing) will make you lose more heat

17
Q

Where does focal tissue injury tend to occur in hypothermia, and what is its mechanism?

A

Peripheral areas with poor collateral circulation, which become ischemic due to peripheral vasoconstriction
(toes, fingers, nose, ears)
-> interstitial fluid crystallizes, proteins denature, and vascular permeability increases due to endothelial cell injury by these crystals.
-> hypercoagulant prothrombotic state results

18
Q

What is the first manifestation of focal tissue injury in hypothermia, what does this look like, and what can it progress to?

A

Frostbite -> appears like blisters due to edema in the injured area, which becomes discolored and eventually turns black / loses sensation.

Progresses to gangrene

19
Q

What is immersion foot and what causes it? What is it most similar to?

A

Trench foot

  • > due to constrictive footwear in damp, unsanitary conditions
  • > Vascular, soft tissue, and nerve injury with secondary infections

Most similar to wet gangrene

20
Q

What is perniosis?

A

Chilblains - abnormal vascular reactions to cold

21
Q

How do childblains appear? Why does thishappen?

A

Appear as small, itchy, swollen, painful lesions which go from red to blue upon rewarming
-> seen in temperate, humid climates due to overdilation / hyperactivity of blood vessels on rewarming (like Reynaud’s phenomenon in reverse)

22
Q

Why is radiation often given in fractionated doses now?

A

Allows time for repair of normal cells, but hopefully not cancer cells

23
Q

What types of tissues are most susceptible to radiation, with respect to cellular proliferation rate, availability of oxygen, and vascularization?

A
  1. Rapidly proliferating cells are most vulnerable (GI tract, bone marrow)
  2. Well-oxygenated tissues are more vulnerable due to oxygen-derived free radicals
  3. Vascularization predisposes to damage due to acute / chronic effects of radiation on blood vessels
24
Q

What is the primary effect of radiation on cells?

A

Results in double-stranded breaks in DNA, which may be recovered in slower growing cells, or lead to apoptosis or carcinogenesis

25
Q

What are the early complications of radiation exposure?

A
  1. Parenchymal cell injury (Reversible or irreversible in susceptible tissues)
  2. Endothelial damage -> leads to hyperemia, increased vascular permeability, hemorrhage, and thrombosis (blood vessels very susceptible)
26
Q

How might radiation-induced proctitis occur?

A

Hitting the rectum on accident when trying to irradiate prostate cancer (radiation travels through tissues)

27
Q

What are the late vascular and interstitial manifestations of radiation exposure?

A

Vascular and interstitial fibrosis, with associated tissue atrophy

-> telangectasia and pallor are very common

28
Q

How can radiation cause dental caries?

A

Fibrosis of salivary gland -> dry mouth (no saliva production) -> dental caries

29
Q

What is radiation dermatitis?

A

Induction of skin ulceration due to tissue atrophy and necrosis, often associated with pallor and telangectasia

30
Q

What organ is particularly susceptible to fibrosis via radiation?

A

Lungs

31
Q

What is the most common ocular manifestation of long-term radiation?

A

Cataracts

32
Q

What is the most common malignancy overall as a result of radiation? In exposed children, specifically?

A

Overall: Leukemias

In exposed children: Thyroid carcinoma

33
Q

What are the cardiovascular effects of radiation, longterm?

A

Atherosclerosis and MI due to endothelial damage initiating this process

34
Q

What are the in utero effects of radiation?

A

Impaired physical and mental development (teratogenic)

35
Q

What are radiation-induced cytologic atypia and why is this an issue?

A

Enlarged, hyperchromatic, pleomorphic, wild-looking nuclei with abnormal mitotic figures and bizarre giant cells

-> after you’ve treated a cancer with radiation, it’s difficult to tell if the neoplasia has returned because all the remaining cells will look crazy