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BDS2 BAMS infection & immunity > sepsis > Flashcards

sepsis Flashcards

1
Q

what is sepsis?

A

life-threatening organ dysfunction due to dysregulated host response to infection

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2
Q

what is sepsis triggered by?

A

infection

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3
Q

what differentiates sepsis from infection?

A

organ dysfunction

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4
Q

what causes the organ dysfunction?

A

overwhelming immune response

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5
Q

how is organ dysfunction identified?

A

acute change in total SOFA score of >_ 2 points

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6
Q

what is SOFA?

A

a tool to clinically characterise px at risk of sepsis (prolonged ICU or death)

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7
Q

what is the SOFA criteria?

A

resp >_ 22 breaths/min
altered mentation (ggow coma scale <15)
systolic bp

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8
Q

what is baseline SOFA?

A

0, unless px has pre-existing organ dysfunction before onset of infection

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9
Q

what are the common sites of infection causing sepsis?

A

lungs
abdomen
bloodstream
urinary system

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10
Q

what are the common sources of infection causing sepsis?

A 
gram + bacteria
-staph aureus
gram - bacteria
fungal
-candida
-associated with higher mortality
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11
Q

who is more likely to get sepsis?

A 
older people
medically/immune compromised px
cancer
cirrhosis
autoimmunity
HIV/AIDS
organ transplantation
diabetes
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12
Q

what inflammatory pathways are activated?

A 
innate immunity
complement system
vascular endothelium
coagulation system
adaptive immunity
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13
Q

what is the pathophysiology of sepsis?

A

body-wide blood clotting and leaky vessels
one or more organs begin to fail
persistent hypotension

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14
Q

describe PRRs

A

pattern recognition receptors
-can be specific to one or more molecules
activated by PAMPs/DAMPs
leads to activation of inflammatory signalling pathways

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15
Q

what are PAMPs?

A 
pattern-associated molecular patterns
conserved exogenous (non-self) factors expressed by pathogens
eg LPS, peptidoglycan, nucleic acids
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16
Q

what are DAMPs?

A

damage-associated molecular patterns
endogenous (host) factors released following cell damage
eg heat-shock proteins, nucleus acid

17
Q

what does TNF-alpha coordinate?

A

local containment of infection, but drives sepsis when released systemically

18
Q

what does TNF-a do?

A 
stimulates expression of:
-adhesion molecules on endothelial cells
-proteins that trigger blood clotting
recruits immune cells to site of infection
prevents pathogen spreading via blood
19
Q

how does systemic release of TNF-a contribute to onset of sepsis and septic shock?

A

systemic vasodilation
increased vascular permeability
loss of blood pressures
systemic blood clotting of microvasculature

20
Q

what is the hallmark of sepsis?

A

complement

21
Q

how does complement contribute to sepsis?

A

activated immediately upon recognition of PAMPs and DAMPs
generation of peptides C3a and C5a
C5a drives immunopathogenesis
potent chemoattractant
further amplifies inflammation
contributes to vasodilation, tissue damage and organ failure

22
Q

why do changes in vascular endothelium occur during sepsis?

A

response to inflammatory stimuli

-endothelial barrier dysfunction

23
Q

what are the characteristics of a hypercoagulative state?

A 
microvascular thrombi
fibrin deposition
neutrophil extracellular trap
formation
endothelial injury
24
Q

what effect does sepsis have on the coagulation system?

A

results in a hypercoagulative state

25
Q

what organ systems are commonly affected?

A 
neurological
-altered mental status
pulmonary
-hypoxaemia
-ARDs
cardiovascular
-shock
renal
-oligouria
26
Q

how does sepsis affect adaptive immunity?

A

excessive inflammation and immune suppression

27
Q

describe excessive inflammation

A

sustained inflammation causes tissue injury
strong activation of innate immunity via PAMPs and DAMPs
sustained hyperinflammation
activation of complement system, coagulation system and vascular endothelium

28
Q

describe immune suppression

A

both innate and adaptive immunity
apoptosis of T cells, B cells
dysfunctional DCs
delayed apoptosis of immature dysfunctional neutrophils

29
Q

what are the current treatments for sepsis?

A 
enteral feeding
insulin therapy
urinary catheter
lung protective ventilation
antibiotics
fluids
vasopressors
-norepinephrine
-epinephrine
-vasopressin
30
Q

why is a dental abscess highly infectious?

A

develop during immune response to acute bacterial infection of pulp space
contain immune cells, dead tissue and live bacteria

31
Q

how are dental abscesses treated?

A

promptly with excision and drainage
periapical abscesses require root canal or extraction
antibiotics ineffective

32
Q

what can happen if dental abscesses spread?

A

severe local and systemic consequences

33
Q

what are red flag signs and symptoms of spreading dental infection?

A 
temp < 36 or > 38
elevated breathing rate (>20 breaths/min)
elevated or reduced HR
varying degrees of facial swelling
trismus
dehydration

BDS2 BAMS infection & immunity (6 decks)

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