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N216 A/B > [216B] Trauma: Thermal Injury > Flashcards

[216B] Trauma: Thermal Injury Flashcards

1
Q

How well do pediatric patients compensate? Which failure happens first?

A
  • Compensate well but decompensate quickly

- Resp. failure

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2
Q

How well do adult patients compensate? Which failure happens first?

A
  • Not well due to comorbidities + aging

- Cardiac failure

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3
Q

What are 5 causes of thermal cell injury?

A
  • Nutritional deficits
  • Mechanical forces
  • Chemical injury
  • Radiation injury
  • Extreme temp.
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4
Q

What are the 4 main mechanisms of the pathophysiology of cellular injury?

A
  • Inflammation
  • Hypoxia
  • Cellular calcium dysfunction
  • Free radicals
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5
Q

What are some examples of damage caused by excessive inflammation?

A
  • Edema
  • Ischemia
  • Hypotension
  • Hypoperfusion
  • DIC
  • Metabolic/lactic acidosis
  • Hyperkalemia/glycemia
  • Necrosis
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6
Q

What is the difference between hypoxia, hypoxemia, and ischemia:

A

Hypoxia: Low tissue O2
Hypoxemia: Low blood O2
Ischemia: Impaired O2 delivery due to low perfusion

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7
Q

What are 4 causes of hypoxia?

A
  • Low air content
  • Constriction/obstruction
  • Altered cellular permeability
  • Hypermetabolic states
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8
Q

The brain will be injured in _ mins if hypoxia is present.

A

4 mins.

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9
Q

The kidneys will be injured in __-__ mins if hypoxia is present.

A

15-20 mins.

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10
Q

How will Na+, K+ and Ca2+ be impacted in cell damage?

A

High intracellular Na+ (hyponatremia).
Low intracellular K+ (hyperkalemia).
High intracellular Ca2+ (hypocalcemia).

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11
Q

Electrolyte imbalances d/t cell injury will result in a fluid shift into the ________ space, which we will see as:

A

intracellular; cellular edema.

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12
Q

Hypoxia will cause the cell to use _______ metabolism for energy. Why is this bad?

A

Anaerobic: lactic acid byproduct will cause acidosis.

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13
Q

List 3 causes of calcium dysfunction.

A
  1. Hypoxia.
  2. Stimulation of the parathyroid gland.
  3. Inflammation.
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14
Q

What happens when the parathyroid gland is stimulated?

A

Ca2+ released into blood from bone.

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15
Q

Why would we see stimulation of the parathyroid gland in cell damage?

A

To compensate for low blood calcium (hypocalcemia) (despite there being high intracellular calcium, but the parathyroid doesn’t know this)

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16
Q

Free radicals will react with endogenous substances such as (3):

A
  1. Lipids (cell membranes).
  2. Enzymes.
  3. Cell structures/mechanisms (ex: proteins, DNA).
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17
Q

When free radicals combine with endogenous substances, they create:

A

ROS (reactive oxygen species).

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18
Q

ROS are endogenous byproducts of (2):

A

respiration & cell metabolism.

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19
Q

ROS are balanced by (2); give an example of each.

A
  1. Antioxidants (ex: Vit C)

2. Endogenous scavengers (ex: catalase)

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20
Q

List 6 examples of acute causative agents of free radicals.

A
  1. Radiation.
  2. Drugs.
  3. Pathogens.
  4. Inflammation.
  5. Chemicals (cytokines).
  6. Nicotine.
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21
Q

Oxidative stress is direct damage to individual cells via:

A

electron reactions.

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22
Q

Oxidative stress results in (3):

A
  1. Decreased function.
  2. Cytokine release = inflammation.
  3. Alteration of cellular metabolites.
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23
Q

Chronic oxidative stress results in:

A

ageing.

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24
Q

List 3 antioxidant agents.

A
  1. Ascorbate (vitamin C).
  2. Flavonoids.
  3. Carotenes (vitamin A).
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25
Q

Name 4 types of drug exposures that can cause cell damage. Give an example of each.

A
  1. Overdoses (ex: Tylenol d/t toxic metabolites).
  2. Drugs with narrow TIs (ex: aminoglycosides).
  3. Toxic exposures (ex: arsenic).
  4. CO (carbon monoxide).
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26
Q

Arsenic causes cell necrosis by _________ cellular ATP production. List 4 ways it does so.

A

Decreasing cellular ATP production:

  1. Imitates/replaces cellular phosphate.
  2. Inhibits pyruvate production.
  3. Inhibits cellular glucose uptake & gluconeogenesis.
  4. Directly induces oxidative stress.
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27
Q

Why is chelation therapy helpful in substance poisonings (ex: arsenic)?

A

It binds with the substance to prevent further damage, then the compound is excreted.

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28
Q

Why is polonium harmful to our cells? (3)

A
  1. Binds cell electrons = destruction > necrosis.
  2. Ionizes cells & H2O molecules > ROS formation.
  3. Direct DNA damage d/t electron binding.
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29
Q

Polonium will affect cells that:

A

multiply quickly (ex: bone marrow, WBCs, hair).

30
Q

_______ is used in chelation therapy for polonium poisoning.

A

Dimercaprol.

31
Q

Half life of polonium:

A

140 days.

32
Q

Which UV rays are most skin damaging?

A

UVB.

33
Q

UVB causes cellular damage in (3):

A

Melanin, Langerhans cells & immune cells.

34
Q

UVB rays cause oxidative stress via:

A

ROS formation.

35
Q

List 4 s&s of a superficial sunburn.

A
  1. Erythema (redness).
  2. Peeling of damaged skin.
  3. Dryness.
  4. Itchiness.
36
Q

List 2 s&s of a moderate sunburn.

A
  1. Extensive blistering.

2. Oozing (“wet” appearance).

37
Q

List 4 systemic effects of severe sunburn.

A
  1. Fever.
  2. Chills.
  3. Malaise.
  4. Dehydration.
38
Q

How do we prevent sunburn?

A

Sunscreen!

39
Q

What are the 2 types of sunscreens?

A
  1. Absorb UVR.

2. Reflect UVR.

40
Q

What is the active ingredient in sunscreens that absorb UVR?

A

Benzones (ex: benzophenone, oxybenzone).

41
Q

What is the main ingredient in sunscreens that reflect UVR?

A

Zinc (or zinc-like materials).

42
Q

Are burns usually uniform in depth?

A

No :0

43
Q

How long can it take to classify a burn? Why?

A

Several days: burns are dynamic and may progress to deeper wounds as time goes on.

44
Q

Regeneration is present on _______ tissue. What should we do if this tissue is completely damaged or unavailable?

A

Dermal tissue: if none, graft.

45
Q

List the 4 burn classifications. Which layers do each of them involve?

A
  1. Superficial: epidermis.
  2. Partial thickness: epidermis & dermis.
  3. Full thickness: full dermis & subcutaneous tissue.
  4. 4th degree: underlying structures (ex: bone, muscle, joints).
46
Q

Which burn(s) blister?

A

Partial-thickness.

47
Q

Which burn(s) are the most painful? Why?

A

Superficial: only burn type where pain nociceptors will be fully intact.

48
Q

What is the healing time for superficial & partial thickness burns?

A

Superficial: 6 days.

Partial thickness: 7-21 days.

49
Q

Partial thickness burns can be further classified into 2 categories:

A

Superficial or deep.

50
Q

Dead black tissue in burns is called:

A

Eschar.

51
Q

List 5 “do”s with superficial burns.

A
  1. Stop the burning with cool water or a cool compress.
  2. Relieve pain with analgesics or soothing lotions.
  3. Protect by loosely covering.
  4. Rehydrate for fluids & electrolytes.
  5. Keep blisters intact.
52
Q

List 2 “don’t”s with superficial burns.

A
  1. No ice (further damage).

2. No oils/butter (trap heat, enhance burning).

53
Q

Which type of burn is not counted by the rule of 9’s.

A

Superficial burns.

54
Q

According to the rule of 9s, hypovolemia is present if >_% of the body is affected by the burn.

A

15%.

55
Q

According to the rule of 9s, severe burn effects are likely if >_% of the body is affected by the burn.

A

40%.

56
Q

List 3 severe burn effects in the burn zone.

A
  1. Direct cell membrane disruption > cell injury.
  2. Inflammation.
  3. Necrosis of affected tissue.
57
Q

List 7 consequences of inflammation d/t tissue damage (ex: burns).

A
  1. Vascular injury/permeability.
  2. Hypoxia.
  3. Cellular Ca2+ dysfunction.
  4. Oxidative stress.
  5. Insulin resistance.
  6. Fluid shift ( > hypovolemia, hypoproteinemia)
  7. Stimulation of platelets > coagulation.
58
Q

List 4 systemic severe burn effects.

A
  1. Hemodynamic instability (d/t loss of water & electrolytes).
  2. Hypermetabolic state (increased cell demand, stress response).
  3. Respiratory system dysfunction (ex: secondary inhalation injuries).
  4. Immune dysfunction > risk of infection/sepsis.
59
Q

Which will we see first in a burn pt: hemodynamic instability or the hypermetabolic state?

A

Hemodynamic instability.

60
Q

During hemodynamic instability, the pt is at risk for __________ ________, which will cause a ______ in CO.

A

hypovolemic shock; decrease in CO.

61
Q

What 3 endogenous substances are released in the hypermetabolic state?

A
  1. Catecholamines.
  2. Cortisol.
  3. Inflammatory mediators.
62
Q

List 5 inflammatory mediators released in a burn pt. Which is specific to burn stress?

A
  1. Bradykinin.
  2. Histamine.
  3. NO.
  4. Cytokines.
  5. Hydrogen sulfide (produced in liver in response to burns).
63
Q

When will the hypermetabolic state start? How long can it last?

A

Starts 24-72 hrs post-burn, but may last up to 2 years.

64
Q

What will the body do to overcompensate in a hypermetabolic state? (3)

A
  1. Have high CO.
  2. Induce high cellular metabolic rates.
  3. Induce fever.
65
Q

List 3 things we would see in a metabolic crises.

A
  1. Protein catabolism (breakdown) d/t injury.
  2. Hyperglycemia d/t extreme glucose mobilization but insulin resistance.
  3. Electrolyte imbalance.
66
Q

List 11 treatments for burns.

A
  1. ABCs.
  2. Oxygenation (possibly intubation).
  3. Hemodynamic stability via IV fluids & electrolytes.
  4. Thermoregulation (initial cooling, warm room after).
  5. Treat lactic acidosis (O2, sodium bicarb, glucose admin).
  6. Nutrition (enteral feeds).
  7. Manage hyperglycemia with insulin/oral antidiabetics.
  8. Prevent infection (sterile dressings, isolation).
  9. Escharotomy.
  10. Wound grafting asap.
  11. Manage hormonal imbalances d/t hypermetabolic responses (check labs & correct).
67
Q

Do we give prophylactic abx to burn pts?

A

No d/t risk of creating resistant organisms.

68
Q

What is escharotomy?

A

Debridement/making an incision in the eschar to relieve pressure & prevent compartment syndrome.

69
Q

What 3 additional txs might we need for electrical burns?

A
  1. Tx of the exit wound,
  2. Arrhythmias (asystole, heart block, vfib)
  3. Seizures (changes to CNS depolarization).
70
Q

List 3 possible associated injuries in burn pts. Which is most common?

A
  1. Fractures (most common: 50-60%).
  2. Head injuries (up to 25%).
  3. Inhalation injuries (ex: cyanide poisoning).

N216 A/B (26 decks)

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