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Foundations Test 4 > Capstone - Burns and Sepsis > Flashcards

Capstone - Burns and Sepsis Flashcards

1
Q

1st degree - description, layer, clinical, associated, healing

A 
Superficial epidermis 
Epidermis 
Red and dry 
Tenderness
Sveral Days
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2
Q

2nd degree superficial partial thickness - layer, clinical, association, healing

A

Papillary dermis
Red, fluid filled blisters
Tenderness
2-3 weeks

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3
Q

2nd degree deep partial thickness - layer, clinical, associated, healing

A

Reticular dermis
Blanched white and pink fluid-filled blisters
Decreased sensation and no capillary refill
3-6 weeks with hypertrophic scar

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4
Q

3rd degree burn - description, layer, clinical, associated, healing

A 
Full thickness
Subq fat
White, leathery, black and charred 
No sensation or capillary refill
No spont healing
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5
Q

4th degree burn

A

bone and fascia exposed

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6
Q

Zone of coagulation

A

Surface coagulation necrosis - irreversible cell death

No cap blood flow

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7
Q

ZOne of stasis

A

Injured, but viable cells
Sluggish cap flow
Susceptible to hypoperfusion injury, infection

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8
Q

Zone of hyperemia

A

Inflammatory response

Vasodiliation and increased cap permeability

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9
Q

Pathophys of large burns

A

Loss of fluid and protein (heat injured capillaries and vasoactive amine increasing permeability)
Systemic inflamm response (cytokines)
Hypermetabolic response
Dysregulated immune response (suppression)_

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10
Q

Inflammatory phase of wound healing

A

Hemostasis…macrophage nad neutrophil migratrion and release of grwoth factors, collagenases, and elastases

Fibroblasts migrate into wound

Blood coagulates

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11
Q

Proliferative phase of wound healing

A

Epitheliazation - basal epidermal cells migrate laterally
Fibroplasia - fibroblast proliferation (secrete procollagen, elastin, fibronectin…form new ECM)
Angiogenesis
Create granulation tissue

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12
Q

Maturation phase of wound healing

A

Collagen remodeling through cycle of synthesis and removal

Parallel and collagne fibers

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13
Q

SIRS criteria

A 
Temperature more than 38 or less than 36 
HR> 90
RR> 20 
PaCO2 < 32 mmHg
Inflammatory response 
WBC greater than 12000 or less than 4000
greater than 10% band form neutrophils
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14
Q

Sepsis criteria

A

Evidence of infection
SIRS

Organ dysfunction which is
RR>22
Altered mentation
SBP<100 mmHG

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15
Q

Septic shock criteria

A

Evidence of infection
SIRS
Sepsis
Despite adequate fluid restoration attempts,
Vasopressor therapy necessary to maintain MAP>65 mm Hg
Lactate>2

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16
Q

What can cause SIRS without systemic infection

A

Trauma, aspiration, pancreatitis, Burns

17
Q

Management of Sepsis (in order)

A

Reverse hypoxia by adding volume to increase perfusion and added oxygen to increase blood O2

Control the septic source (think urinary, blood, pneumonia) and administer antibiotics

Manage hypotension with vasopressors

18
Q

Best drug to use against sepsis

A

Norepinephrine (alpha and B1 agonists)

19
Q

Recombinant human act protein C

A

Promotes fibrinolysis and initiates thrombosis

Modulates procoagulant response that contributes to Organ dysfuncti

20
Q

Antithrombin

A

Inactivates factor 2 and 10

Modulates procoagulant response

21
Q

TLR 4 antagonists

A

Supress cytokine production

22
Q

G-CSF

A

Enhances neutrophil production and functiomn

23
Q

Anti-TNF monoclonal antibody and TNF receptor antagonists

A

Supress cytokine production leading to shock and clotting cascade activation

24
Q

IL-1 receptor antagonist

A

Suppress acute phase reactant production contributing to shock

25
Q

Glucocorticoids

A

No benefit in patients with SIRS or sepsis but maybe septic shock

Increase anti-inflam cytokines and decrease inflam cytokines

26
Q

SIRS stage 1

A

Activate innate immune system
PAMPs activate dendritic cells and macophages
Heat shock proteins produce in response to stress
Macrophage releases (IL-1, IL-6, TNF-alpha along with prostaglandins, leukotrienes and PGF)
Dendritic release (IL-12) then move to help activate T cells

27
Q

IL -1

A

Neutrophil and macrophage migration
Upregulates adhesion molecules
Fever
Acute phase reactant formation

28
Q

IL-6

A

Induces B and T cell differentiation
Fever
Acute phase reactant formation

29
Q

TNF-alpha

A 
Enhances NK cell and CD8 cell cytotoxicity 
Increase vascular permeability 
Fever
Shock
Pro-inflam cytokine production
30
Q

IL-12

A

Activates NK cells
Induces T differentiation
Supress IL-17 formation
Increase IFN-gamma

31
Q

SIRS stage 2

A

Pro-inflamm cytokines released into systemic circulation (leuko and lymph cytes)…stimulate acute phase reactant formation

Balanced by endogenous anti-inflamm mediators (IL-10, PGE2, IL-1 receptor antagonist)

32
Q

IL-10

A

Inhibits activityof Th1 cells, NK cells, and macrophages

33
Q

PGE2

A

Suppresses T-cell rceptor signlaing

34
Q

IL-1 receptor antagonist

A

Inhibits IL-1 activity

35
Q

SIR stage 3

A

Uncontrolled
Hypotnesion - decreased perfusion and shock…cytokines cause vasodilators
TIssue edema - permeability of endothelium
Maldistribution of microvascular blood flow - seuqestration of lymphocytes and platelets…activation of coag cascade
Impaired cellular oxygen utilization leads to cell death

Foundations Test 4 (12 decks)

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