Trauma: Thermal Injuries Flashcards

1
Q

Which 5 factors cause cell injury?

A
  1. Nutritional Deficit
  2. Mechanical Forces
  3. Chemical Injury
  4. Radiation Injury
  5. Extreme Temperature
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How does nutritional deficit cause cell injury?

A

Nutritional deficits are caused by a lack of vitamins, iron, and caloric deficit. The lack of nutrients will cause the cells to weaken in function and dysregulate.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does mechanical force cause cell injury?

A

Caused by an intense force that may inhibit perfusion and oxygenation to a body part and result in cell death. ex. fractures, bruising, impactful injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Define Chemical Injury.

A

Caused by intoxication, drugs, biological agents, and toxicity. The toxic chemical disrupts the cell membrane and promotes apoptosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Define Radiation Injury.

A

Damage to the cells at a molecular level.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Two Types of Radiation Injury.

A
  1. Ionizing Radiation: can cause electron displacement, break cellular bonds and affect cellular replication
  2. Ultraviolet Radiation: Can cause DNA damage or cellular necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Cellular Injury Pathophysiology.

A
  1. Inflammation: response to damaged tissue. (5 cardinal signs of inflammation; loss of function, heat, pain, redness, and swelling)
  2. Hypoxia: low oxygenation to the tissues
  3. Cellular Calcium Dysfunction
  4. Free Radicals
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Pathway of Cellular Injury.

A
  1. Electrolyte Pump Dysfunction causes fluid shift resulting in low intracellular K+, high intracellular Na+ and Ca+. Increasing cellular edema and decreasing function
  2. Decreased function leads to cell organ damage! The lack of oxygen leads to hypoxia and anaerobic metabolism
  3. Anaerobic respiration leads to the accumulation of lactic acid and lowers the body’s pH. Causing acidosis
  4. The cell organ damage causes mitochondrial dysfunction which results in ATP depletion
  5. There will be an increase in the free radical formation and injury to cell structures
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Pathological Sequelae of Cellular Injury.

A

Hypoxia-Ischemia-Necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Define Cellular Calcium Dysfunction.

A

Caused by cellular hypoxia. Due to the increased concentration in the intracellular space, there will be compensatory stimulation by the parathyroid gland to release calcium from the bone. This will lead to hypercalcemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Signs and Symptoms of Hypercalcemia.

A
  • CNS- confusion and lethargy
  • Muscle Weakness
  • Constipation
  • Bone weakness and joint pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Define Free Radicals.

A

Molecules containing an ‘unpaired’ electron are unstable and reactive. They impact cell membranes, enzymes, DNA and cellular function

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Define Oxidative Stress.

A

A normal cell that has been damaged due to free radicals. Cells with oxidative stress release cytokines and cause an inflammatory response!

  • They also alter cellular electrolytes
  • Alter intracellular fluid balance
  • Increase cellular membrane permeability
  • Alter depolarization and repolarization of the cell
  • Decrease mitochondrial function
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How do you treat oxidative Stress?

A

Antioxidants! Antioxidants can interrupt the propagation of free radicals by inhibiting the formation of free radicals and subsequently reducing oxidative stress!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Drugs that contribute to cellular injury.

A
  1. Tylenol: easily overdose and causes hepatic damage
  2. Aminoglycosides: narrow TI
  3. Arsenic: poisonous substance, causes cellular necrosis
  4. Carbon Monoxide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Treatment for Arsenic.

A

Chelation Therapy

17
Q

Define Polonium. (What are it’s effects on cellular damage)

A

An unstable and radioactive chemical agent. Binds to cellular electrons and causes cellular structure destruction and necrosis. It will directly ionize the cells (pull part the cell structure) it will also ionize water molecules, causing free radicals
-Half-Life: 140 days

18
Q

Define Sunburns.

A

damage caused by UV radiation

Epidermal and or dermal layers are affected and caused redness

19
Q

Prevention for sunburns.

A

Prevention: Sunscreen

-They absorb UVR (benzophenone and oxybenzone)

20
Q

Define a Burn.

A

A burn is an injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction or contact with chemicals.

21
Q

What are the 6 Types of Burns?

A
  1. Superficial
  2. Partial-Thickness
  3. Superficial Partial-thickness
  4. Deep
  5. Full-thickness
  6. 4th degree
22
Q

Superficial Burns.

A

Damage to the epidermal layer!

  • Does not blister
  • painful, dry, red
  • healing time: 6 days
23
Q

Partial Thickness Burn.

A

Damage to the epidermis and dermis!

-Classified as superficial partial-thickness OR deep

24
Q

Superficial Partial-Thickness

A

Type of Partial Thickness burn.

  • Blisters in 24 hours
  • painful, red, weeping
  • healing time: 7 to 21 days
25
Q

Deep Burns.

A

Type of Partial Thickness burn.

  • Damage to hair follicles and glandular tissue
  • Less painful, waxy appearance
  • healing time: up to 9 weeks
26
Q

Full thickness Burn.

A

Damage to the full dermis and subcutaneous tissue

  • No blisters
  • Waxy and black appearance
  • No pain, no tactile sensation, loss of function
27
Q

4th Degree Burn.

A

Underlying structures damaged

-Muscles, bones, joints

28
Q

How to treat Superficial Burns.

A

Cool the burn with cool water for 20 minutes

  • Cool compress decreases vascular flow, decrease inflammation and decrease nociceptor stimulation
  • Analgesics for pain relief
  • Protect with a loose cover over burn area with sterile gauze
  • Rehydration: Fluids + electrolytes
29
Q

What NOT to do with burns.

A

Do not apply ice, butter or oils

30
Q

Six Effects of Burns.

A
  1. Cell Injury
  2. Inflammation
  3. Increased capillary permeability
  4. Fluid Shift
  5. Hypoxia
  6. Necrosis of the affected tissue
31
Q

Complications of Burns.

A
Hemodynamic Instability (unstable BP) 
Hypermetabolic State
Respiratory Dysfunction
Immune Dysfunction (risk of sepsis and infection)
32
Q

Hypovolemic Shock and burns.

A

The first phase of severe burns. Loss of fluids and protein from cellular and interstitial compartments

a. Fluid shift
b. Total Fluid loss
c. Decreased cardiac output and respiratory dysfunction

33
Q

Hypermetabolic State and burns.

A

In response to the high levels of cytokine mediators, the body will overcompensate by increasing CO, high cellular metabolic rate and fever
Metabolic crisis: protein catabolism, extreme glucose mobilization but insulin resistance

34
Q

Immune Dysfunction and burns.

A

Depletion of WBCs increase risks of infection by up to 50%

35
Q

How to treat burn complications?

A
Maintain ABC’s
Maintain Fluid Balance (1st fluid resuscitation and albumin replacement) 
Assess for hypermetabolic state 
Thermoregulation 
Treat Lactic acidosis 
Manage Hyperglycemia
36
Q

Important Considerations for Pediatric patients in a Trauma SItuation.

A

Peds compensate well & then decompensate suddenly, respiratory failure happens 1st

37
Q

Important Considerations for Adult Patients in Trauma Situations.

A

Adults don’t compensate well d/t comorbidities & aging, cardiac failure occurs 1st