Sepsis Flashcards
1
Q
what is the sepsis continuum
A
infection -> SIRS -> Sepsis -> septic shock -> MODS
2
Q
what kind of a response is sepsis
A
dysregulated widespread systemic response to infection that injures own tissues/organs
3
Q
What is SIRS
A
systemic inflammatory response
4
Q
what can trigger sirs
A
infectious or non-infectious insult such as trauam, thermal injury, massive blood replacement, pancreatitis
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
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
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
8
Q
when does MODS occur
A
if dysregulation worsens and organ dysfxn increases
inadequate cellular oxygenation results in organ dysfunction
9
Q
can MODS occur in result to a non-infectious insult
A
yes
10
Q
In MODS what 2 systems do we most often see dysfunction
A
resp and renal
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
12
Q
what 5 things occur in the vascular response
A
increased permeability and vasodilation
release of histamine, bradykinin and prostaglandins
13
Q
What Factor is activated when it comes in contact with collagen
A
Hageman Factor XII
14
Q
Where is the Hageman Factor produced
A
liver
15
Q
Haveman Factor stimulates what to produce what
A
Prekallkrien System to release Bradykinin
16
Q
What does Bradykinin do
A
Potent vasodilator
Increases permeability
increases pain
17
Q
what are the two things that can stimulate Prekallkrien system
A
Hageman Factor XII
Complement System
18
Q
what is activated by damaged endoethelium
A
Hageman Factor XII
19
Q
What type of cells does bradykinin stimulate
A
Mast cells
20
Q
What 4 things are involved in the immune response portion of VIPP
A
neutrophils
monocytes/macrophages
antibodies
antigen
21
Q
what are the of Platelet-related actions
A
coagulation and fibrinolysis
traps exudate, microorganisms and foreign bodies
22
Q
what is the plasma protein repsonse
A
complement system
23
Q
what does the complement system do
A
vasodilation
promote leukocyte chemotaxis and augments phagocytosis
24
Q
what 3 cells are attracted to an area of cellular injury by chemical messengers
A
mast cells
neutrophils
monocytes
25
what do neutrophils do (3)
provide first wave of attack on invading organisms
phagocytosis
move out of vascular space and attack foreign organisms (extravasation/ emigration)
26
what do monocytes do
ass through membrane into tissues where they grow into macrophages
attach to certain tissue and destroy bacteria
phagocytosis
27
When cellular injury occurs what 3 things occur
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
28
what are the 3 complement pathways
classical
alternative
lectin
29
the three complement pathways activate what
C3
30
What are three cell derived mediators
(ways cells can call for more help)
histamine
cytokines
arachidonic acid pathways
31
what is histamine released from and what does it do
released from degranulated mast cells
| promotes vasodilation and capillary permeability
32
what are cytokines and give 3 examples
chemical messengers
| interleukins, tumor necrosis factor, interferons
33
T or F cytokines play a role in acquired immunity
true
34
what are the two components or arachidonic acid pathway
prostaglandins and leukotrienes
35
what does the bradkykinin cascade do
increase capillary permeability
| stimulate pain receptors
36
what is the responsibility of the clotting cascade
tissue repair, platelet aggregation, clot formation
37
what is a main function of the complement system
opsonization
38
where do B and T lymphocytes originate from
stem cells in bone marrow
39
which cells produce antibodies
B-cells
40
What does the acronym ABCCs of sepsis stand for
Arachidonic Acid (AA)
Bradykinin
Coagulation
Complement
41
What does Arachidonic acid do
creates initial vasoconstriction around injury to keep localized then vasoidlation to increase bloodflow to area to bring inflammatory cells
42
how does arachidonic acid exert its affects
prostoglandins - inc vasodilation and permeability
| thromboxanes - promote platelet aggregation
43
What are the systemic effects of AA (2)
vasoconstriction/vasodilation - maldistribution of blood
decreased afterload
widespread permeability - fluid shifts (edema)
decreased preload
44
What activates the release of bradykinin
tissue injury
45
what does bradykinin do (3)
vasodilation and increased permeability
stimulates mast cells to release histamine causing vasodilation
stimulates AA, coag cascade and complement cascade
46
what are the systemic effects of bradykinin
profound vasodilation and widespread permeability - maldistribution of blood flow and fluid shifts
decreased preload and afterload
47
what are the two pathways in the coagulation cascade and what are each of them triggered by
extrinsic - tissue factor from damaged tissues
| intrinsic - proenzymes secreted in blood
48
T or F the intrinsic and extrinsic pathway meet up at the main pathway in the coagulation cascade
False
| commmon pathway
49
what occurs in the common pathway of the clotting cascade
prothrombin is converted to thrombin
thrombin helps convert fibrinogen to fibrin
Fibrin forms mesh for platelets to adhere to forming a clot
50
what does widespread permeability from AA cause in the lungs
fluid shifts into lungs - increased AC membrane thickness, decreased lung compliance and impaired ventilation and gas exchange
51
what occurs in the vascular response
| and what is it caused by
```
vasodilation - warmth
capillary permeability - swelling
histamine
bradykinins
prostaglandins
causes pain and fever as well
```
52
what is involved in the immune response and what do we see
neutrophils
monocytes/macrophages (secrete cytokines)
anitbodies
antigens
seen as PUS
53
what is involved in the platelet phase what does it result in
coagulation cascade
fibrinolysis
results in clotting
54
what 2 things are involved in the plasma protein response and what does it do
complement and bradykinin
promotes inflammatory response
55
what releses histamine and what triggers it
released form MAST cells
| triggered by phsyical injury, chemical agents and immunologic or infectius causes
56
what are 3 things histamine does
increases vessel dilation and permability
increased gastric acid secretion
increased airway mucous secretion
57
what are 2 important cytokines
| what is another name for cytokines
leukocytes
interleukins & tumor necrosis factor
58
what do interleukins do (2)
```
type of cytokine
cause fever (effects hypothalamus)
recruits neutrophils and monocytes
```
59
what does TNF do and what is it
type of cytokine
causes widespread destruction
causes fever, hypotension, decreased organ perfusion and increased capillary permability
60
what are the two major branches of Arachidonic acid
lipoxygenase and clycloxygenase
61
what enzyme are we concerned about in the lipoxygenase branch of AA
leukotrienes
| causes bronchoconstriction vasoconstriction and vascular permeability
62
what are the enzymes we are concerned about in the cycloxygenase pathway of AA
thromboxane and prostaglandins
63
what does thromboxane do
causes vasoconstriction and promotes platelet aggretagion
| ASA works on this
64
what do prosglandins do in the AA pathway
vasodilation
permeability
pain
65
what is AAs major effects in sepsis (6)
```
vasodilation
inc cap permeability
edema
pain
fever
maldsitribution of blood flow!
```
66
can AA cause fluid to shift into the lungs impairing gas exchange
yes
67
how is bradykinin released
hageman factor stimultes prekallkrien system to release bradykinin
68
what does bradykinin do
potent vasodilator
inc vascular permability
stimulates mast cells activating AA pathway
causes pain
69
T or F the prekallkrien system cannot be triggered by anthing other than hageman Facto
False can be triggered by the complement system
70
what is the hageman factor XII also invovled in? where is it produced and how is it activated
coagulation cascade
| produced in the liver activates with tissue injury as it comes in contact with collagen
71
what are the major effects of bradykinin in sepsis
potent vasodilation
increased permeability
pain
72
what does bradykin do to afterload
decreased
73
what occurs at the common pathway in coagulation
prothrombin is converted to thrombin
| firbinogen to fibrin
74
what are clots typically broken down by
plasmin
75
what happens with plasmin in sepsis
plasmin production is blocked by circulating cytokines which leads to increased clotting and less breakdown of clots
76
what happens in coagulation during sepsis
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
what are the 3 main pathways in complement system
classical
alterniative
lectin
78
what are the 3 outcomes of the complement pathways
opsonisation - stimulates phagocytosis
creation of MAC - pathogen destruction stimulating immune response
promotes inflammatory and immune response - histamine and chemotaxis
79
what do the 3 complement pathways activate
C3
80
what does C3 turn into and what does it do
C3B causes opsonization
81
what does C3B do
combines with C5 to make MAC
82
what is MAC
group of proteins that busts a hole through pathogens so water can rush in and cause pathogen to explode further triggering inflammation
83
what does C5 do
chemotaxsis
| stimuates mast cells to release histamine
84
what is the major effect of complement in sepsis
intensifies inflammatory response
| increased vasodilation and permeability cuases cell death
85
what produces MDF
ischemic pancreas
86
what does the acronym CHAOS stand for
```
pathogens trigger CHAOS
C VS compromise
Homeostasis
Apoptosis
Organ dysfunction
Suppression of the immune system
```
87
what is the 2016 sepsis guideliens definition of sepsis
life threatening organ dysfunction caused by dysregulated host response to infection
88
what is septic shock defined as for 2016 sepsis guidelines
diagnosed with sepsis
required vasopressor therapy to maintain MAP >65
Lactate >2 despite fluid resus
89
what is a tool to identify pts outside the ICU with known or suspected infections at risk of sepsis
qSOFA
90
how is qSOFA scored
GCS <15
RR > 22
SBP < 100
need a score 2 or higher
91
what is a scoring system used to assess the severity of organ dysfunction in a pt with known sepsis
SOFA
| Sepsis related Organ Failure Assesment
92
how is SOFE scored
```
infection + change in SOFA
decreased PaO2
decrased GCS
dec BP
inc bili
decreased platelts
increased creatinien
```
93
what is the 1 hour bundle (5)
measure lactate
obtain blood cx prior to abx
adminster abx
initate crystalloid for hypotension or lactte
apply pressers if hypotensive after fluid resus
94
what is the 3 hour bundle
measure lactate
obtain blood cultures
administer Abx
initiate fluids
95
what is the 6 hour bundle
apply pressors for hypotension
remeasure lactate
if persistant hypotension measure CVP SCvO2, bedside US
passive leg raise or fluid challenge
96
ABCD's for treatment of sepsis (O2 supply and demand
```
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
what other drugs might be necessary to decrease demand
glycemic control - insulin infusion
steroids - for pts in refractory shock
stress ulcer prophylaxis
