Capstone - Burns and Sepsis Flashcards Preview

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Flashcards in Capstone - Burns and Sepsis Deck (35):
1

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

Superficial epidermis
Epidermis
Red and dry
Tenderness
Sveral Days

2

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

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

3

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

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

4

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

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

5

4th degree burn

bone and fascia exposed

6

Zone of coagulation

Surface coagulation necrosis - irreversible cell death
No cap blood flow

7

ZOne of stasis

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

8

Zone of hyperemia

Inflammatory response
Vasodiliation and increased cap permeability

9

Pathophys of large burns

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

10

Inflammatory phase of wound healing

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

Fibroblasts migrate into wound

Blood coagulates

11

Proliferative phase of wound healing

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

12

Maturation phase of wound healing

Collagen remodeling through cycle of synthesis and removal
Parallel and collagne fibers

13

SIRS criteria

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

14

Sepsis criteria

Evidence of infection
SIRS

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

15

Septic shock criteria

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

16

What can cause SIRS without systemic infection

Trauma, aspiration, pancreatitis, Burns

17

Management of Sepsis (in order)

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

Best drug to use against sepsis

Norepinephrine (alpha and B1 agonists)

19

Recombinant human act protein C

Promotes fibrinolysis and initiates thrombosis
Modulates procoagulant response that contributes to Organ dysfuncti

20

Antithrombin

Inactivates factor 2 and 10
Modulates procoagulant response

21

TLR 4 antagonists

Supress cytokine production

22

G-CSF

Enhances neutrophil production and functiomn

23

Anti-TNF monoclonal antibody and TNF receptor antagonists

Supress cytokine production leading to shock and clotting cascade activation

24

IL-1 receptor antagonist

Suppress acute phase reactant production contributing to shock

25

Glucocorticoids

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

Increase anti-inflam cytokines and decrease inflam cytokines

26

SIRS stage 1

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

IL -1

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

28

IL-6

Induces B and T cell differentiation
Fever
Acute phase reactant formation

29

TNF-alpha

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

30

IL-12

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

31

SIRS stage 2

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

IL-10

Inhibits activityof Th1 cells, NK cells, and macrophages

33

PGE2

Suppresses T-cell rceptor signlaing

34

IL-1 receptor antagonist

Inhibits IL-1 activity

35

SIR stage 3

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