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
What are the early complications of radiation exposure?
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
How might radiation-induced proctitis occur?
Hitting the rectum on accident when trying to irradiate prostate cancer (radiation travels through tissues)
27
What are the late vascular and interstitial manifestations of radiation exposure?
Vascular and interstitial fibrosis, with associated tissue atrophy -> telangectasia and pallor are very common
28
How can radiation cause dental caries?
Fibrosis of salivary gland -> dry mouth (no saliva production) -> dental caries
29
What is radiation dermatitis?
Induction of skin ulceration due to tissue atrophy and necrosis, often associated with pallor and telangectasia
30
What organ is particularly susceptible to fibrosis via radiation?
Lungs
31
What is the most common ocular manifestation of long-term radiation?
Cataracts
32
What is the most common malignancy overall as a result of radiation? In exposed children, specifically?
Overall: Leukemias In exposed children: Thyroid carcinoma
33
What are the cardiovascular effects of radiation, longterm?
Atherosclerosis and MI due to endothelial damage initiating this process
34
What are the in utero effects of radiation?
Impaired physical and mental development (teratogenic)
35
What are radiation-induced cytologic atypia and why is this an issue?
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