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NSCC 7320 - Critical Care Theory 3 > Sepsis > Flashcards

Sepsis Flashcards

1
Q

what is the sepsis continuum

A

infection -> SIRS -> Sepsis -> septic shock -> MODS

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2
Q

what kind of a response is sepsis

A

dysregulated widespread systemic response to infection that injures own tissues/organs

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3
Q

What is SIRS

A

systemic inflammatory response

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4
Q

what can trigger sirs

A

infectious or non-infectious insult such as trauam, thermal injury, massive blood replacement, pancreatitis

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5
Q

How is SIRS defined

A 
2+ of the following criteria
Temp >39 or <36
HR > 90
RR >20 or PaCO2 <32
WBC >12 or <4
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6
Q

What is the term for a subset of sepsis where circulatory, cellular and metabolic alterations are associated with a higher mortality rate

A

septic shock

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7
Q

what are 4 criteria of septic shock

A

fulfills sepsis definition
persistent hypotension despite adequate fluid replacement
lactate >2
requires pressers to maintain MAP >65

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8
Q

when does MODS occur

A

if dysregulation worsens and organ dysfxn increases

inadequate cellular oxygenation results in organ dysfunction

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9
Q

can MODS occur in result to a non-infectious insult

A

yes

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10
Q

In MODS what 2 systems do we most often see dysfunction

A

resp and renal

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11
Q

What is the acronym VIPP for and what does it stand for

A 
acronym for normal inflammatory response
Vascular response
Immune Response
Platelet-related actions
Plasma protein response
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12
Q

what 5 things occur in the vascular response

A

increased permeability and vasodilation

release of histamine, bradykinin and prostaglandins

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13
Q

What Factor is activated when it comes in contact with collagen

A

Hageman Factor XII

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14
Q

Where is the Hageman Factor produced

A

liver

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15
Q

Haveman Factor stimulates what to produce what

A

Prekallkrien System to release Bradykinin

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16
Q

What does Bradykinin do

A

Potent vasodilator
Increases permeability
increases pain

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17
Q

what are the two things that can stimulate Prekallkrien system

A

Hageman Factor XII

Complement System

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18
Q

what is activated by damaged endoethelium

A

Hageman Factor XII

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19
Q

What type of cells does bradykinin stimulate

A

Mast cells

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20
Q

What 4 things are involved in the immune response portion of VIPP

A

neutrophils
monocytes/macrophages
antibodies
antigen

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21
Q

what are the of Platelet-related actions

A

coagulation and fibrinolysis

traps exudate, microorganisms and foreign bodies

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22
Q

what is the plasma protein repsonse

A

complement system

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23
Q

what does the complement system do

A

vasodilation

promote leukocyte chemotaxis and augments phagocytosis

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24
Q

what 3 cells are attracted to an area of cellular injury by chemical messengers

A

mast cells
neutrophils
monocytes

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25
Q

what do neutrophils do (3)

A

provide first wave of attack on invading organisms
phagocytosis
move out of vascular space and attack foreign organisms (extravasation/ emigration)

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26
Q

what do monocytes do

A

ass through membrane into tissues where they grow into macrophages
attach to certain tissue and destroy bacteria
phagocytosis

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27
Q

When cellular injury occurs what 3 things occur

A

mast cells, neutrophils and monocytes are attracted to area by chem messengers
release more chem mediators to call for help
increased cellular activity at area

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28
Q

what are the 3 complement pathways

A

classical
alternative
lectin

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29
Q

the three complement pathways activate what

A

C3

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30
Q

What are three cell derived mediators

A

(ways cells can call for more help)
histamine
cytokines
arachidonic acid pathways

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31
Q

what is histamine released from and what does it do

A

released from degranulated mast cells

promotes vasodilation and capillary permeability

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32
Q

what are cytokines and give 3 examples

A

chemical messengers

interleukins, tumor necrosis factor, interferons

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33
Q

T or F cytokines play a role in acquired immunity

A

true

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34
Q

what are the two components or arachidonic acid pathway

A

prostaglandins and leukotrienes

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35
Q

what does the bradkykinin cascade do

A

increase capillary permeability

stimulate pain receptors

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36
Q

what is the responsibility of the clotting cascade

A

tissue repair, platelet aggregation, clot formation

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37
Q

what is a main function of the complement system

A

opsonization

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38
Q

where do B and T lymphocytes originate from

A

stem cells in bone marrow

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39
Q

which cells produce antibodies

A

B-cells

40
Q

What does the acronym ABCCs of sepsis stand for

A

Arachidonic Acid (AA)
Bradykinin
Coagulation
Complement

41
Q

What does Arachidonic acid do

A

creates initial vasoconstriction around injury to keep localized then vasoidlation to increase bloodflow to area to bring inflammatory cells

42
Q

how does arachidonic acid exert its affects

A

prostoglandins - inc vasodilation and permeability

thromboxanes - promote platelet aggregation

43
Q

What are the systemic effects of AA (2)

A

vasoconstriction/vasodilation - maldistribution of blood
decreased afterload

widespread permeability - fluid shifts (edema)
decreased preload

44
Q

What activates the release of bradykinin

A

tissue injury

45
Q

what does bradykinin do (3)

A

vasodilation and increased permeability
stimulates mast cells to release histamine causing vasodilation
stimulates AA, coag cascade and complement cascade

46
Q

what are the systemic effects of bradykinin

A

profound vasodilation and widespread permeability - maldistribution of blood flow and fluid shifts
decreased preload and afterload

47
Q

what are the two pathways in the coagulation cascade and what are each of them triggered by

A

extrinsic - tissue factor from damaged tissues

intrinsic - proenzymes secreted in blood

48
Q

T or F the intrinsic and extrinsic pathway meet up at the main pathway in the coagulation cascade

A

False

commmon pathway

49
Q

what occurs in the common pathway of the clotting cascade

A

prothrombin is converted to thrombin
thrombin helps convert fibrinogen to fibrin
Fibrin forms mesh for platelets to adhere to forming a clot

50
Q

what does widespread permeability from AA cause in the lungs

A

fluid shifts into lungs - increased AC membrane thickness, decreased lung compliance and impaired ventilation and gas exchange

51
Q

what occurs in the vascular response

and what is it caused by

A 
vasodilation - warmth
capillary permeability - swelling
histamine
bradykinins
prostaglandins
causes pain and fever as well
52
Q

what is involved in the immune response and what do we see

A

neutrophils
monocytes/macrophages (secrete cytokines)
anitbodies
antigens

seen as PUS

53
Q

what is involved in the platelet phase what does it result in

A

coagulation cascade
fibrinolysis

results in clotting

54
Q

what 2 things are involved in the plasma protein response and what does it do

A

complement and bradykinin

promotes inflammatory response

55
Q

what releses histamine and what triggers it

A

released form MAST cells

triggered by phsyical injury, chemical agents and immunologic or infectius causes

56
Q

what are 3 things histamine does

A

increases vessel dilation and permability
increased gastric acid secretion
increased airway mucous secretion

57
Q

what are 2 important cytokines

what is another name for cytokines

A

leukocytes

interleukins & tumor necrosis factor

58
Q

what do interleukins do (2)

A 
type of cytokine
cause fever (effects hypothalamus)
recruits neutrophils and monocytes
59
Q

what does TNF do and what is it

A

type of cytokine
causes widespread destruction
causes fever, hypotension, decreased organ perfusion and increased capillary permability

60
Q

what are the two major branches of Arachidonic acid

A

lipoxygenase and clycloxygenase

61
Q

what enzyme are we concerned about in the lipoxygenase branch of AA

A

leukotrienes

causes bronchoconstriction vasoconstriction and vascular permeability

62
Q

what are the enzymes we are concerned about in the cycloxygenase pathway of AA

A

thromboxane and prostaglandins

63
Q

what does thromboxane do

A

causes vasoconstriction and promotes platelet aggretagion

ASA works on this

64
Q

what do prosglandins do in the AA pathway

A

vasodilation
permeability
pain

65
Q

what is AAs major effects in sepsis (6)

A 
vasodilation
inc cap permeability
edema
pain
fever
maldsitribution of blood flow!
66
Q

can AA cause fluid to shift into the lungs impairing gas exchange

A

yes

67
Q

how is bradykinin released

A

hageman factor stimultes prekallkrien system to release bradykinin

68
Q

what does bradykinin do

A

potent vasodilator
inc vascular permability
stimulates mast cells activating AA pathway
causes pain

69
Q

T or F the prekallkrien system cannot be triggered by anthing other than hageman Facto

A

False can be triggered by the complement system

70
Q

what is the hageman factor XII also invovled in? where is it produced and how is it activated

A

coagulation cascade

produced in the liver activates with tissue injury as it comes in contact with collagen

71
Q

what are the major effects of bradykinin in sepsis

A

potent vasodilation
increased permeability
pain

72
Q

what does bradykin do to afterload

A

decreased

73
Q

what occurs at the common pathway in coagulation

A

prothrombin is converted to thrombin

firbinogen to fibrin

74
Q

what are clots typically broken down by

A

plasmin

75
Q

what happens with plasmin in sepsis

A

plasmin production is blocked by circulating cytokines which leads to increased clotting and less breakdown of clots

76
Q

what happens in coagulation during sepsis

A

clotting and loss of clot breakdown leads to inappropriate blocking of blood flow in microvasculature contributing to maldistribution of blood flow leading to organ dysfunction

77
Q

what are the 3 main pathways in complement system

A

classical
alterniative
lectin

78
Q

what are the 3 outcomes of the complement pathways

A

opsonisation - stimulates phagocytosis
creation of MAC - pathogen destruction stimulating immune response
promotes inflammatory and immune response - histamine and chemotaxis

79
Q

what do the 3 complement pathways activate

A

C3

80
Q

what does C3 turn into and what does it do

A

C3B causes opsonization

81
Q

what does C3B do

A

combines with C5 to make MAC

82
Q

what is MAC

A

group of proteins that busts a hole through pathogens so water can rush in and cause pathogen to explode further triggering inflammation

83
Q

what does C5 do

A

chemotaxsis

stimuates mast cells to release histamine

84
Q

what is the major effect of complement in sepsis

A

intensifies inflammatory response

increased vasodilation and permeability cuases cell death

85
Q

what produces MDF

A

ischemic pancreas

86
Q

what does the acronym CHAOS stand for

A 
pathogens trigger CHAOS
C VS compromise
Homeostasis
Apoptosis
Organ dysfunction
Suppression of the immune system
87
Q

what is the 2016 sepsis guideliens definition of sepsis

A

life threatening organ dysfunction caused by dysregulated host response to infection

88
Q

what is septic shock defined as for 2016 sepsis guidelines

A

diagnosed with sepsis
required vasopressor therapy to maintain MAP >65
Lactate >2 despite fluid resus

89
Q

what is a tool to identify pts outside the ICU with known or suspected infections at risk of sepsis

A

qSOFA

90
Q

how is qSOFA scored

A

GCS <15
RR > 22
SBP < 100
need a score 2 or higher

91
Q

what is a scoring system used to assess the severity of organ dysfunction in a pt with known sepsis

A

SOFA

Sepsis related Organ Failure Assesment

92
Q

how is SOFE scored

A 
infection + change in SOFA
decreased PaO2
decrased GCS
dec BP
inc bili
decreased platelts
increased creatinien
93
Q

what is the 1 hour bundle (5)

A

measure lactate
obtain blood cx prior to abx
adminster abx
initate crystalloid for hypotension or lactte
apply pressers if hypotensive after fluid resus

94
Q

what is the 3 hour bundle

A

measure lactate
obtain blood cultures
administer Abx
initiate fluids

95
Q

what is the 6 hour bundle

A

apply pressors for hypotension
remeasure lactate
if persistant hypotension measure CVP SCvO2, bedside US
passive leg raise or fluid challenge

96
Q

ABCD’s for treatment of sepsis (O2 supply and demand

A 
A - airway or abx
B - breathing mech vent
C - cardiac output 
     preload - fluids CVP 8-12
     afterload - pressers MAP >65
     contractility - inotrops ScvO2 >70
D -decrease demand or drugs
97
Q

what other drugs might be necessary to decrease demand

A

glycemic control - insulin infusion
steroids - for pts in refractory shock
stress ulcer prophylaxis

NSCC 7320 - Critical Care Theory 3 (5 decks)

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