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Pathopharm Final > 10: Adult Burns & Shock (Part 2) > Flashcards

10: Adult Burns & Shock (Part 2) Flashcards

30-58

1
Q

Secondary MODS
definition

A

excessive inflammatory reaction during latent period after the initial injury in organs distant from the original injury site

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2
Q

Secondary MODS
cause

A

host response to a second insult
not a direct result of the primary injury

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3
Q

T/F
Secondary MODS is a direct result of the primary injury.

A

False
Host response to a second insult

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4
Q

Secondary MODS
Second insult characteristics

A
  • mild but immensely disproportionate response
  • produced because of the previous priming of leukocytes
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5
Q

Secondary MODS
substances released

A

Barrage of mediators-particularly the cytokines:
* tumor necrosis factor (TNF)
* interleukin 1 (IL-1)

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6
Q

Interaction of injured organs leads to a self-perpetuating inflammation decsribes what phenomenon?

A

Secondary MODS

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7
Q

T/G
Inflammation in Secondary MODS is self-limiting.

A

False
self-perpetuating

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8
Q

MODS
responses

A
  • Stress response!
  • Complement, coagulation, kinin release
  • vascular endothelium changes
  • inflammation mediated by substances released from activated neutrophils and macrophages
  • Proteases
  • Activated neutrophils accumulate in the organs, playing a key role in the pathogenesis of MODS.
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9
Q

Proteases in MODS response

A
  • from neurophils
  • Directly damage endothelium & neighboring cells = ↑ permeability
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10
Q

Proteases cause (↓/↑) vascular permeability.

A

increased!

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11
Q

Plays a key role in the pathogenesis of MODS

A

Activated neutrophils accumulate in the organs

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12
Q

MODS response’s numerous inflammatory processes are mediated by…

A

substances released from activated neutrophils and macrophages
ie: proteases

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13
Q

In MODS, maldistribution of blood flow causes an uneven distribution of flow to various organs and between the….

A

large vessels & capillary beds

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14
Q

Maldistribution of blood flow
neutrophils role

A
  • Adhere & migrate through the endothelium
  • aggregate in damaged tissue
  • amplify inflammation
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15
Q

T/F
In MODS, Activated neutrophils alter blood flow by increasing the production and release of nitric oxide, causing vasodilation.

A

False
Activated endothelial cells

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16
Q

What causes the changes in blood flow in MODS?

A
  • vasodilation
  • increased vasopermeability
  • selective vasoconstriction
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17
Q

T/F
Vasoconstriction and vasodilation both occur during MODS and contribute to maldistribution of blood flow.

A

True
* vasodilation
* selective vasoconstriction
* increased vasopermeability

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18
Q

MODS
Hypermetabolism

A

excessive & injuring endocrine response:
↑ circulating catecholamines & cortisol

results:
tachycardia, hypermetabolism, ↑O2 consumption

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19
Q

MODS Hypermetabolism is mediated by…

A

actions of TNF and IL-1

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20
Q

MODS Hypermetabolism causes alterations in metabolism of…

A

carbohydrate, fat, & lipids

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21
Q

T/F
MODS Hypermetabolism increases demand on the entire body.

A

True

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22
Q

MODS
The 4 Plasma Cascades that are activated

A
  • Complement
  • kallikrein-kinin
  • coagulation
  • fibrinolytic
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23
Q

MODS presults in a net ____ state.

A

procoagulant

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24
Q

MODS
Myocardial depression
(3 things happen)

A
  • myocardial depressant factors (MDF) TNF & IL-1 affect cardiac contractility
  • myocardial hypoxia
  • Alters 🩷 α-adrenergic receptors
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25
Q

Reperfusion injury

A
  • Follwing a period of ischemia, restoring blood flow can cause organ damage.
  • Oxygen radicals attack already damaged tissues
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26
Q

MODS
Oxygen consumption
(3)

A
  • Imbalance in oxygen supply & demand
  • Reserve exhausted
  • oxygen consumed depends on how much circulation can deliver
  • If inadequate, tissue hypoxia
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27
Q

MODS
Clinical manifestations

A
  • Encephalopathy
  • mental status changes ranging from confusion to deep coma
  • can occur at any time
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28
Q

MODS manifestations
how quickly does the sequence occur?

A

can rapidly evolve or evolve over weeks

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29
Q

MODS manifestations
timeline

A
  • 24 H: Low fever, tachycardia, tachypnea, dyspnea, AMS, hyperdynamic, hypermetabolic
  • 24-72 H: lung failure starts; ARDS?
  • 7-10 D: hepatic, intestinal, & renal failure
  • 14-21D: worse renal & liver failure; death?
  • Later: Hematologic & myocardial failure
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30
Q

What would we expect to see 1 week into MODS?
A) altered mental status
B) Beginning of lung failure
C) Start of renal failure
D) Death
E) None of these

A

C) Start of renal failure

  • 24 H: Low fever, tachycardia, tachypnea, dyspnea, AMS, hyperdynamic, hypermetabolic
  • 24-72 H: lung failure starts; ARDS?
  • 7-10 D: hepatic, intestinal, & renal failure
  • 14-21D: worse renal & liver failure; death?
  • Later: Hematologic & myocardial failure
31
Q

Death is likely to occur how long after MODS starts?

A

14-21 days

  • 24 H: Low fever, tachycardia, tachypnea, dyspnea, AMS, hyperdynamic, hypermetabolic
  • 24-72 H: lung failure starts; ARDS?
  • 7-10 D: hepatic, intestinal, & renal failure
  • 14-21D: worse renal & liver failure; death?
  • Later: Hematologic & myocardial failure
32
Q

Myocardial failure is seen how long after MODS starts?

A

After ~21 days

33
Q

MODS
Prevention vs Treatment

A
34
Q

MODS
treatment

A
  • Respiratory: MV (Low Vt, high O2, PEEP)
  • GI: Enteral feed or hyperalimentation, POCT 80-110 mg/dl; Calories for hypermetabolic state
  • Renal: HD or continuous hemofiltration
  • CV: Inotropes or vasopressors (Steroids controversial)
35
Q

T/F
A MODs pt would require excess calories.

A

True
Calories for hypermetabolic state

36
Q

Optimal glucose range for MODS patient

A

Tight glucose control
80 - 110 mg/dl

37
Q

T/F
The use of steroids in MODS is controversial.

A

True

38
Q

Best vent settings for MODS

A
  • Low tidal volumes
  • high oxygen [ ]
  • PEEP
39
Q

Burn
definition

A
  • general term
  • cutaneous injury as a result of thermal, chemical, or electrical causes
  • either thermal or nonthermal
40
Q

Burns are Multisystem injuries with interactions of…(3)

A
  • shock
  • inflammation
  • immunocompromised state
41
Q

Vesicants

A

cause blistering of the epithelial surfaces

42
Q

Burn wound depths

A
  • Partial-thickness: only epidermis; no dermal or subQ injury
  • Superficial partial-thickness: Thin-walled, fluid-filled blisters develop within a few minutes
  • Deep partial-thickness: entire dermis; sparing hair follicles & sweat glands
  • Full-thickness: Entire epidermis, dermis, and often subQ
43
Q

T/F
Deep partial-thickness burn injures are painless because nerve endings have been destroyed.

A

False
Full-thickness injury

44
Q

Which type of burn injury produces fluid-filled blisters?

A

Superficial partial-thickness injury

45
Q

T/F
Only Full-thickness injury
involves the entire dermis.

A

False
Deep partial-thickness: entire dermis
&
Full-thickness: Entire epidermis, dermis, and often subQ

46
Q

Rule of Nines

A

Head and neck: 9%
Each arm and hand: 9%
Chest: 9%
Stomach: 9%
Upper back: 9%
Lower back: 9%
Each leg and foot: 18%
Genital area: 1%

47
Q

A 25 year old female patient has sustained burns to the back of the right arm, posterior trunk, front of the left leg, anterior head and neck, and perineum.
Body surface area percentage that is burned?

A

37%

Back of right arm (4.5%)
posterior trunk (18%)
front of left leg (9%)
anterior head and neck (4.5%)
perineum (1%)

48
Q

Burns exceeding ___% in most adults are considered major burn injuries.

A

20%

49
Q

Burns exceeding 20% of TBSA
Are associated with ….

A
  • massive evaporative water losses
  • flux of large amounts of fluid & electrolytes
  • Generalized edema
  • Circulatory hypovolemia
50
Q

Burns
Pathophysiology (Phases)

A
  • Immediate/acute phase: burn shock; hypovolemic shock; immunologic disruption
  • Ebb phase: ↓contractility
51
Q

Indicates the end of burn shock

A

Capillary seal

52
Q

Burn shock in the immediate (acute) phase

A
  • Life-threatening hypovolemic shock
  • cellular & immunologic disruption
  • within a few hours of the burn
53
Q

Ebb phase

A
  • Cardiac contractility diminished during the initial 24-hour resuscitation period
  • shunts blood away from liver, kidney, gut
54
Q

Burns
Systemic response

A

Massive edema
* associated with burn shock
* inevitable with fluid resuscitation
* in unburned and burned areas
* mechanical airway obstruction = ETT
* worsens interstitial pulmonary edema associated with inhalation injury

55
Q

Failure to administer fluid resuscitation results in…

A

irreversible hypovolemic shock and death

56
Q

Lung pathology associated with inhalation injury

A

interstitial pulmonary edema

worsened by edema created by: systemic response to burn & the fluid resuscitation

57
Q

Burns
Metabolic response

A
  • ↑ Metabolic activity
  • ↑ body catabolism
  • Extensive burn injury: Initiates the most significant alterations in body metabolism associated with any illness.
58
Q

Initiates the most significant alterations in body metabolism associated with any illness

A

Extensive burn injury

59
Q

Burns
Cellular response

A
  • Transmembrane potential changes in cells not directly damaged
  • Intracellular: ↑ Na & water; ↓Mag & Phos
60
Q

Electrolyte shifts in burns

A

Intracellular:
↑ Na & water
↓Mag & Phos

61
Q

Evaporative water loss in burns

A

Ability of the skin to regulate evaporative water loss is totally disrupted

62
Q

Burns
Immunologic response

A
  • Immunosuppressio
  • susceptible to potentially fatal wound sepsis
  • Release of cytokines, oxygen radicals, systemic inflammatory response: chemotactic factors, and eicosanoids
63
Q

Burns
Release of these 4 leads to a systemic inflammatory response

A
  • cytokines
  • oxygen radicals
  • chemotactic factors
  • eicosanoids
64
Q

The Burn Response Cascade

A
65
Q

Clinical manifestations
by injury extent/thickness

A
  • Partial: Local pain; erythema; blisters 24H AFTER injury
  • Superficial partial: painful; blisters in minutes
  • Deep partial: Waxy, white; skin may peel off in sheets
  • Full: White/cherry red/black; delineation has no significant color change; dry and leathery
66
Q

_____ injury is indistinguishable from a full-thickness injury until 7 to 10 days, at which time skin buds and hair appear.

A

Deep partial-thickness injury

67
Q

T/F
Blisters are expected in Full-thickness injury.

A

False
rare

Superficial partial-thickness: thin-walled and fluid-filled blisters develop within a few minutes

68
Q

Treatment
First-degree burns

A

Usually no treatment

69
Q

Treatment

A
  • Burn units
  • Meticulous wound management
  • Massive amounts of IV fluid
  • Give LR faster than the loss of circulating volume
  • Early enteral feeding
  • antibiotic catheters
  • glycemic mgmt
  • Anabolic agents
  • Pain control
70
Q

The most reliable criterion for adequate fluid resuscitation

A

Urine output

71
Q

Early surgical excision and grafting

A

Excision, followed by grafting of the person’s unburned skin (autograft)

72
Q

Early enteral feeding reduces the potential of…

A

gut-mediated sepsis

73
Q

Anabolic agents for Burns

A
  • recombinant human growth hormone
  • agents that modulate inflammatory & endocrine mediators (ibuprofen, propranolol): Showing promise
74
Q

Burns
Pain control

A
  • Opioid-based agents
  • antianxiety agents
  • Hypnosis & relaxation
  • Virtual reality systems

Pathopharm Final (8 decks)

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