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2 - Infection and Immunity > Sepsis > Flashcards

Sepsis Flashcards

1
Q

What is sepsis?

A

Life-threatening organ dysfunction due to a dysregulated overwhelming immune host response to infection

Triggered by infection in susceptible patients (can not occur in the absence of infection)

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2
Q

What tool is used to identify high risk patients and what is the critera?

A

qSOFA
Respiratory ≥ 22 breaths/min
Altered mentation (Glasgow Coma Scale <15)
Systolic blood pressure ≤ 100 mm Hg

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3
Q

What is the baseline for qSOFA?

A

Baseline qSOFA = 0 unless patient has pre-existing organ dysfunction BEFORE onset of infection

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4
Q

What is an important critera to aid diagnosis of infection (not specific to sepsis) and what does it measure?

A

SIRS
SIRS refers to the body’s inflammatory response to a non-specific insult, which can be either infectious or non-infectious in origin

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5
Q

What does the GCS assess?

What is the threshold?

A

mentation

<15 for altered mentation

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6
Q

What causes sepsis?

A

any infection (bacterial, viral, fungal) can trigger sepsis

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7
Q

Where is the most common site of infection?

A

lungs

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8
Q

What type of bacteria triggers sepsis the most?

A

gram negative bacteria (E-coli, p.gingivalis)

(LPS toxin)

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9
Q

Who gets sepsis most?

A

Sepsis disproportionately affects medically and immune- compromised patients
* Cancer
* Cirrhosis
* Autoimmunity
* HIV/AIDS
* Organ transplantation
* Diabetes

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10
Q

What system activations is the immunopathogenesis of sepsis associated with?

A
  • Innate immunity
  • Complement system
  • Vascular endothelium
  • Coagulation System
  • Adaptive Immunity

Excessive inflammation and immune suppression

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11
Q

What is the pathophysiology of sepsis?

A
  • Body-wide blood clotting and ‘leaky vessels’
  • Organ failure
  • Hypotension
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12
Q

What receptors activate inflammatory signaling pathways in sepsis and how?

A

Pattern Recognition Receptors (PRRs)

recognise

Pathogen-Associated Molecular Patterns (PAMPs)
Damage-Associated Molecular Patterns (DAMPs)

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13
Q

Examples of PAMPS VS DAMPS

what are examples?

A

PAMPS
Exogenous (non-self) factors expressed by pathogens
(LPS, peptidoglycan, nucleic acids)

DAMPS
Endogenous (host) factors released following cell damage
(Heat-shock proteins, nucleic acid)

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14
Q

What does TNFalpha do when released systemically?

A

TNF⍺ coordinates local containment of infection but drives sepsis when released systemically

Systemic vasodilation
Increased vascular permeability
Loss of blood pressure
Systemic blood clotting in the microvasculature

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15
Q

What does TNFalpha stimulates expression of in controlling local infections?

A
  • Adhesion molecules on endothelial cells
  • Proteins that trigger blood clotting
  • Recruits immune cells to site of infection
  • Prevents pathogen spreading via blood
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16
Q

What system is a hallmark of sepsis?

A

complement

17
Q

How is the complement system activated and what does it generate?

A

Activated immediately upon recognition of PAMPs and DAMPs

Generation of peptides C3a and C5a

18
Q

What does C5a do?

A
  • C5a drives immunopathogenesis
  • Potent chemoattractant
  • Further amplifies inflammation
  • Contributes to vasodilation, tissue damage and organ failure
19
Q

What happens in the endothelial barrier during sepsis?

A

dysfunction
Changes in the vascular endothelium in response to inflammatory stimuli during sepsis

20
Q

What state does sepsis result in?

A

hypercoagulative state

21
Q

What is the hypercoagulative state characterised by?

A
  • Microvascular thrombi
  • Fibrin deposition
  • Neutrophil extracellular trap
    formation
  • Endothelial injury
22
Q

What organ systems does sepsis usually affect and what are the common signs?

A
  • Neurological (altered mental status)
  • Pulmonary (hypoxaemia) – Acute Respiratory Distress Syndrome (ARDs)
  • Cardiovascular (shock)
  • Renal (oligouria)
23
Q

As well as excessive inflammation, what do patients with sepsis show?

A

immune supression

24
Q

How is innate immunity activated?

A

via PAMPs and DAMPs

25
Q

How is the immune system supressed during sepsis?

A
  • Both innate and adaptive immunity
  • Apoptosis of T cells, B cells
  • Dysfunctional DCs (impairs activation of T/B cells)
  • Delayed apoptosis of immature dysfunctional neutrophils
26
Q

What are the best treatments for sepsis?

A

Intravascular antibiotics
Source control
Fluids/vasopressors
Supportive care (ventiliation)

27
Q

What are the NICE guidelines regarding healthcare professionals and sepsis?

A

all healthcare staff involved in assessing people’s clinical condition are given appropriate training in identifying people who may have sepsis

28
Q

What 2 key factors make dental abscesses a risk factors for sepsis?

A

live bacteria (highly infectious)
risk of spread to other sites

29
Q

What do dental abscesses contain and how do they happen?

A
  • Develop during immune response to acute bacterial infection of pulp space
  • Contain immune cells, dead tissue and LIVE bacteria
  • Highly infectious and can spread
30
Q

How are dental abscesses treated?

A
  • Treated promptly by excision and drainage
  • Periapical abscesses require root canal or extraction
  • Antibiotics ineffective (in the absence of spreading dental infection)
31
Q

What are important signs and symptoms of spreading dental infection?

A
  • Temp <36 or > 38
  • Elevated breathing rate (> 20 breaths/min)
  • Elevated or reduced heart rate
  • Varying degrees of facial swelling
  • Trismus
  • Dehydration
32
Q

What should be done if the signs and symptoms of spreading dental infection are recognised?

A

potential diagnosis of sepsis
* Refer to oral or maxillofacial surgeon in a hospital setting without delay
* qSOFA criteria associated with signs of infection – medical emergency

33
Q

Organ dysfunction can be identified as an acute change in total SOFA score of 2 or greater. Which criteria would score 1 using the quick SOFA criteria?

A
  • Pre-existing and poorly controlled diabetes (preexisting conditon organ dysfunction)
  • Score of 14 on Glasgow Coma Scale
  • Elevated respiratory rate
34
Q

The immunopathogenesis of sepsis is associated with strong activation of innate immunity. Which cell types express pattern-recognition receptors?

A
  • macrophages
  • neutrophils
  • epithelial cells
  • mast cells
  • NK cells
  • dendritic cells
35
Q

Which system most significantly contributes to the amplification of systemic inflammation in sepsis?

A

Complement

C5a is one of the most potent inflammatory cytokines in sepsis, which functions to significantly amplify inflammation

36
Q

Leaky vessels and blood clotting are significant pathological events occurring during sepsis and septic shock. These pathologies are driven by excessive inflammation activating which 2 systems?

A

coagulation
vascular endothelium

2 - Infection and Immunity (12 decks)

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