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Infection and Immunity BDS2 > Immunopathology of Sepsis > Flashcards

Immunopathology of Sepsis Flashcards

1
Q

what is sepsis

A

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

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2
Q

what is sepsis triggered by?

A

infection in susceptible patients

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3
Q

what is a qSOFA

A

quick sequential organ failure assessment - tool used to clinically characterise patients at risk of sepsis

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4
Q

what is the baseline qSOFA

A

0 unless the patient has pre-existing organ dysfunction before the onset of infection

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5
Q

what is SIRS

A

systemic inflammatory response syndrome

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6
Q

what does the Glasgow Coma Scale assess?

A

level of consciousness of patients, checks ability to communicate properly, assign a score according to the highest responses

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7
Q

what score on the Glasgow Coma Scale signifies an altered mentation rate?

A

15

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8
Q

what is the source of sepsis infection?

A

gram+ bacteria (staph aureus), gram negative bacteria, or fungal (candida)

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9
Q

who gets sepsis?

A

aging population and medically and immunocompromised patients (cancer, cirrhosis, HIV/AIDS, diabetes)

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10
Q

what is immunopathogenesis associated with?

A

innate immunity, complement system, vascular endothelium, coagulation system, adaptive immunity

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11
Q

how is sepsis differentiated from infection?

A

due to the overwhelming immune response triggered by infection that leads to tissue damage and organ failure

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12
Q

what is the pathophysiology of sepsis?

A

body-wide blood clotting and leaky vessels due to excessive release of inflammatory mediators, one or more organs begin to fail due to lack of blood flow, persistent hypotension

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13
Q

what are pattern recognition receptors (PRRs)

A

receptors expressed on innate immune cells but also the epithelia, endothelia and fibroblasts. They include TLRs and each receptor has specificity for one or more molecules - PAMPS and DAMPS

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14
Q

what are PAMPS

A

pattern associated molecular patterns - conserved exogenous factors expressed by pathogens

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15
Q

give examples of PAMPS

A

LPS, peptidoglycan, nucleic acids

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16
Q

what are DAMPS?

A

damage associated molecular patterns, endogenous factors, released following cell damage

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17
Q

give examples of DAMPS

A

heat shock proteins, nucleic acid

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18
Q

what causes the activation of inflammatory signalling pathways?

A

PAMPS and DAMPS

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19
Q

describe the activation of inflammatory signalling pathways

A

1 - cell surface and intracellular receptors detect PAMPS and DAMPS
2 - TLR4 recognises some DAMP molecules
3 - both PAMPS and DAMPS activate multiple signalling pathways
4 - each transcription factor regulates transcription of genes
5 - once the cytokines are released by cells, they further activate immune responses and initiate a cascade of other cytokines and chemokines

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20
Q

what does TNF alpha do?

A

coordinate local containment of infection but drives sepsis when released systematically, recruits immune cells to site of infection, prevents pathogen spreading via blood

21
Q

what does TNF alpha stimulate the expression of?

A

adhesion molecules on endothelial cells, proteins that trigger blood clotting

22
Q

how does TNF alpha contribute to the onset of sepsis and septic shock?

A

due to the systemic release of TNFa as it causes systemic vasodilation, increased vascular permeability, loss of blood pressure, systemic blood clotting of microvasculature

23
Q

describe how TNF alpha works?

A

1 - TNF released by macrophages
2 - TNF acts on blood vessels
3 - local release allows influx of fluid, cells, and proteins to allow host defence
4 - if this is not successful there can be macrophages in the liver and spleen activated and releasing TNF into circulation which leads to intravascular coagulation preventing blood flow to organs causing organ failure and death

24
Q

when is complement activated?

A

immediately upon recognition of PAMPS and DAMPS

25
Q

what complement proteins are involved in sepsis?

A

C3a and C5a

26
Q

what does C5a do?

A

it drives immunopathogenesis - potent chemoattractant, further amplifies inflammation, contributed to vasodilation, tissue damage and organ failure

27
Q

what is endothelium barrier dysfunction?

A

changes in the vascular endothelium in response to inflammatory stimuli during sepsis

28
Q

when does endothelial barrier dysfunction occur?

A

very early in sepsis and septic shock in particular

29
Q

what does the endothelial barrier dysfunction do?

A

mediates loss of fluid throughout tight junctions, leaky capillary membranes create massive loss of proteins, poor tissue perfusion and ultimately septic shock, contributes to activation of coagulation system

30
Q

what is the hypercoagulative state of sepsis characterised by?

A

microvascular thrombi, fibrin deposition, neutrophil extracellular trap formation, endothelial injury

31
Q

what can widespread anticoagulation lead to?

A

uncontrolled bleeding due to consumption of clotting factors

32
Q

what are the presenting signs and symptoms of sepsis?

A

neurological (altered mental status), pulmonary (hypoxaemia, acute respiratory distress syndrome), cardiovascular (shock), renal (oliguria - significantly reduced urine output)

33
Q

where does ARDS present

A

as sepsis in the lungs

34
Q

how does ARDS present?

A

lungs fill with inflammatory infiltrate and cannot get enough oxygen to the blood, consequence and common death of COVID

35
Q

what two things doe patients with sepsis demonstrate?

A

inflammation and immune suppression

36
Q

what is involved with excessive inflammation?

A

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

37
Q

what is involved with immune suppression?

A

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

38
Q

what does excessive inflammation and immune suppression lead to?

A

infectious complications, increasing frequency of blood cultures and shift to infection, increased rates of reactivation of latent viruses, profound changes to adaptive and innate immunity, predisposition to later infections, long term profound changes to immune function

39
Q

how do you treat sepsis?

A

early administration of antibiotics through IV within the first hour of diagnosis to get infection under control, vasopressors to maintain BP and dialysis for patients whose kidneys are failing

40
Q

why should dentists care about sepsis?

A

serious complication of acute dental infections

41
Q

when do dental abscesses develop?

A

during immune response to acute bacterial infection of pulp space

42
Q

what do dental abscesses contain?

A

immune cells, dead tissue and LIVE bacteria

43
Q

how are abscesses treated?

A

by excision and drainage although periapicals require root canal or extraction

44
Q

what is a common dental cause of sepsis?

A

dental abscesses

45
Q

what is the severe local consequence of dental abscesses?

A

neurotic submandibular abscess

46
Q

what is a severe systemic consequence of a dental abscess?

A

fluid extending from neck to aortic arch, diagnosis of sepsis with respiratory and renal dysfunction

47
Q

what are the red flag signs and symptoms of sepsis?

A

temperature below 36 or above 38, elevated breathing rate, elevated or reduced heart rate, varying degrees of facial swelling, trismus, dehydration

48
Q

what do you do if you notice red flag signs and symptoms?

A

refer the patient to oral or maxillofacial surgery in a hospital setting without delay

Infection and Immunity BDS2 (7 decks)

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