Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Boards: Skin > Burns (JVECC review 1+2, Henrikkson papers, CCM 130) > Flashcards

Burns (JVECC review 1+2, Henrikkson papers, CCM 130) Flashcards

1
Q

How do you differentiate local burn injury versus severe burn injury?

A

severe burn injury involves >20-30% TBSA and results in burn shock with systemic involvement

local burn injury does not typically cause systemic disease

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

What are the 2 phases of burn shock?

A
  • resuscitation phase (immediately after injury, lasts 24-72 hours)
  • hyperdynamic hypermetabolic phase (begins 3-5 days after injury, can last up to 24 months)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

name 4 types of burn injury most commonly encountered in small animals

A
  • thermal injury
  • radiation injury
  • chemical injury
  • electrical injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What are the different classifications of burn depth, list the dermal layers involved, wound characteristics and healing

A

Superficial
* Epidermis only
* erythematous desquamation, dry flaky appearance, may not be immediately visible
* heals within 3-5 days via re-epithelialization, minimal scar formation

Superficial partial thickness
* Epidermis + upper 1/3 of dermis (papillary layer)
* erythematous, moist blances, painful blisters, edema may present eschar formation
* heals in 1-2 weeks via re-epithelialization, minimal scar formation

Deep partial thickness
* Epidermis + all dermis
* red-waxy white, reduced pain sensation, blisters, eschar
* heals in 2-3 weeks, surgical intervention recommended to prevent significant scar formation

Full-thickness
* Epidermis + dermis + subcutaneous tissue
* bloodless pearl-white eschar formation
* hair easily plugged
* requires surgical intervention for healing

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

What are the 3 zones of burn injuries?

A

Zone of coagulation
* area of initial and most severe thermal injury
* most cellular damage
* thermal injury –> coagulation of constituent proteins –> irreversible tissue loss –> primary location of eschar formation

Zone of stasis
* capillary vasoconstriction –> decreased tissue perfusion –> ischemia
* mixture of viable and nonviable cells
* tissue damage potentially reversible (need to restore blood flow, e.g., fluid therapy) –> otherwise becomes zone of coagulation

Zone of hyperemia
* viable cells
* local inflammatory mediators –> vasodilation

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

What main mediators are implicated in the development of the resuscitation phase of severe burn injuries?

A
  • Prostaglandins, prostacycline
  • TXA-2
  • ROS
  • NFK-b, TNF-alpha, IL-1, IL-6
  • Histamine
  • caspases (myocardial apoptosis!)
  • macrophage migration inihbitor factor
  • kallikrein-kinin system&raquo_space; bradykinin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How much does the CO in the hyperdynamic phase of patients with severe burn injuries increase?

A

1.5 x CO of a healthy person

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the metabolic rate of a patient in the hyperdynamic phase of a patient with severe burn injuries?

A

3 x basal metabolic rate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

List the 3 counterregulatory hormones driving the hypermetabolic state in severe burn injury patients

A
  • cortisol
  • glucagon
  • catecholamines
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Explain how burn patients develop hyperglycemia and the risk factors associated with hyperglycemia in patients with severe burn injury

A

hyperdynamic and hypermetabolic phase
* increased gluconeogenesis
* cortisol, glucagon, catecholamines –> insulin resistance

  • hyperglycemia + high insulin cc for up to 4-5 weeks after SBI

hyperglycemia –> increased risk of bacterial or fungal infection, decreased wound healing, increased mortality

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

How does severe burn injury lead to hepatomegaly?

A

hypermetabolic state during the hyperdynamic state:
counteregulatory hormones (cortisol, glucagon, catecholamines) –> lipolysis –> increased triglyceride –> fatty liver –> hepatomegaly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the pathophysiology of airway injury from smoke inhalation (include time line)

A
  • direct thermal injury to the upper airway - effects seen within 24 hours
  • soot adheres to the respiratory mucosa –> irritant binding
  • inflammation –> edema –> airway obstruction and bronchospasms (peaks at 24 hours, can resolve over a few days)
  • damaged mucosal cells –> exudate rich in protein, inflammatory cells, necrotic debris
  • neutrophilic chemotactic response within 4 hours of injury –> inflammation –> inhibits the mucociliary apparatus
  • exudate, mucus, cellular debris etc can move distally –> obstruction of lower airways
  • within 3-5 day - exfoliation of the tracheal and bronchi lining –> pseudomembrane casts –> block lower airways –> inactivate surfactant –> segmental atelectasis (48-72 hours after smoke inhalation)
  • bronchiolar obstruction peaks at 72 hours
  • distal migration of particulate matter + bacteria –> pneumonia (in 50% of people with smoke inhalation injury)

Note: often appear better initially and full extend of injury take 24-36 hours to show

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

Besides Hb binding, what complications are associated with CO poisoning?

A
  • induction of lipid peroxidation
  • direct cellular damage
  • reperfusion injury
  • CNS demyelination&raquo_space; delayed neurologic sequelae - 2 to 40 days after initial improvement
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the expected timing of pharyngeal edema post burn injury with smoke inhalation?

A

occurs within first 24-48 hours and resolved after a few days

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

What is the time frame of pesudomembrane cast formation and secondary lower airway obstruction in patients with smoke inhalation?

A

48-72 hours

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the two causes for neurologic signs after a patient sustained burn injuries or smoke inhalation?

A

carbon monoxide toxicity
cyanide toxicity

17
Q

During carbon monoxide poisoning, what are the expected SpO2 and PaO2 findings

A

falsely higher peripheral oxygen saturation reading –> SpO2 cannot differentiate between oxyhemoglobin and carboxyhemoglobin

normal PaO2, unless pulmonary disease present as well

18
Q

What is the likely diagnosis in a patient sustaining burn injuries with neurologic signs, normal co-oximetry, lactic acidosis, and normal PaO2?

A

Cyanide toxicity

19
Q

What ocular injuries may occur from burn exposure?

A

exposure keratopathy
corneal ulceration
less common: corneal burn

orbital compartment syndrome (subsequent optic neuropathy and blindness)

20
Q

What is the half-life of carboxyhemoglobin on room air, 100% oxygen administration, or 100% in hyperbaric conditions (HBOT)?

A
  • 5 hours
  • 1 hour
  • 20 min
21
Q

How soon after burn injury does hemodynamic instability typically ensue?

A

1-2 hours later

22
Q

Describe the “Parkland” aka “Censensus” formula for fluid therapy in burn patients

A

administer 4mL/kg/%TBSA burned
50% of this over first 8 hours, rest 50% over next 16 hours

reduce by 25 to 50% in cats

e.g., cat 5kg 40% TBSA burned –> 4mL x 5 x 40 = 800 mL - 25% reduction 600 mL –> 300/8 = 37 mL/hr first 8 hours, then 300/16 = 19 mL/hr next 16 hours

23
Q

What are the antimicrobial properties of honey?

A
  • low pH
  • hydrogen peroxide production
  • high osmolality
24
Q

Why is an elevated temperature not a reliable marker for secondary infections in patients with severe burn injury?

A

because during the hyperdynamic hypermetabolic phase, the set point temperature may be elevated by 2 C or 3.6 F

25
Q

How do you define “burn shock”?

A

caused by severe burn injuries –> characterizes by
* intravascular volume depletion
* reduced CO
* increased systemic vascular resistance
* decreased peripheral blood flow

26
Q

Describe the Resuscitation phase

A
  • 24-72 hours after SBI
  • hemodynamic instability
  • increased vascular permeability&raquo_space; ECV loss and plasma protein loss into interstitium&raquo_space; edema formation
  • reduced CO that’s poorly responsive to therapy
27
Q

In a patient 40% TBSA burn, how much plasma water can be lost in 2-3 hours?

A

50%

28
Q

Characterizie the changes in the hyperdynamic phase of SBI that leads to increaed CO

A
  • decreased vascular permeability (ECV resotred)
  • increaed HR
  • decreaed PVR
29
Q

How does cyanide toxicity occur in poeple/animals exposed to fired?

A

combustion of nitrogen-containing products&raquo_space;> hydrogen cyanide forms

cyanide binds to cytochrome oxidase&raquo_space;> impairs tissue oxygenation&raquo_space;> anaerobic metabolism

30
Q

What are possible complications from HBOT?

A
  • pneumothorax
  • gas embolism
  • barotrauma
  • oxygen toxicity-induced seizures
  • pulmonary edema and hemorrhage
  • oxidative stress
31
Q

When patients experience not just SBI but also smoke inhalation, how does this change the initial fluid requirements?

A

has shown to increase requirements by 30-50%

32
Q

What is the gold standard topical treatment for burn wounds?

A

silver sulfadiazide (SSD)

33
Q

Why is vitamin C suspected to help in burn victims?

A

reduces lipid peroxidation (i.e., oxidative injuries)

may also reduce microvascular leakage and lower IV fluid requirements

34
Q

What intraabdominal pressure is considered elevated, and when are therapeutic interventions recommended?

A

over 10 cm H2O

over 20 cm H2O

35
Q

Which vascular structures supply what layers of the skin?

A

layers:
* epidermis
* dermis
* hypodermis or SQ

superficial plexus and middle plexus supply dermis with capillary loops from the superficial plexus also reaching the epidermis

both of these origniate from the subdermal plexus from the SQ layer

36
Q

When after burn injury does an eschar form?

A

7-10 days after

37
Q

What is the Rule of Nine in people?

A

Body surface area distribution

  • 9% head/neck
  • 9% each arm
  • 18% torso
  • 18% trunk
  • 18% each pelvic limb
  • genitalia 1%
38
Q

What is the BSA of mesocephalic dogs compared to the rule of 9?

A

head 14%
neck 9%
thorax 18%
abdomen 14%
thoracic limbs 9% each
pelvic limbs 11% each
tail and pelvic 5%

39
Q

What is the BSA of cats compared to the rule of 9?

A
  • head 13%
  • neck 5%
  • thorax 20%
  • abdomen 15%
  • thoracic limbs 7% each
  • pelvic limbs 12% each
  • tail and pelvis 9%

Boards: Skin (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions