Lec18 SIRS Flashcards

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1
Q

What is SIRS?

A
  • systemic inflammatory response syndrome
  • manifested by 2 or more of:
  • — temp > 38 or < 36
  • — HR > 90
  • — RR > 20 or pCO2 < 32
  • — WBC > 12K or < 4K or > 10% bands
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2
Q

What are blood pressure measures for SIRS definition?

A

BP not included in definition

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3
Q

What is the definition of sepsis?

A

SIRS and a high suspicion of or documented infection

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4
Q

What is the definition of severe sepsis?

A

sepsis associated with organ dysfunction or hypoperfusion

  • lactic acidsosis from tissue hypoxia
  • oliguria [not enough urine]
  • alteration in mental status
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5
Q

What is definition of sepsis with shock?

A

when hypotension not responsive to IV fluid

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6
Q

What is definition of multi-organ system failure [MOSF]?

A

results from shock, under-perfusion and tissue damage from cytokines and endothelial injury

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7
Q

What are initial treatments for sepsis?

A
  • fluids = mainstay treatment, give normal saline boluses
  • antibiotics: start broadly and narrow when you get culture results [cefalosporin, vanco]
  • give oxygen: O2 delivery is impaired in sepsis
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8
Q

What is the clinical pathophysiology of sepsis?

A
  • impaired end organ function due to:
  • injury to microvasculature [decreased vessel tone]
  • decreased blood volume [leak of plasma into tissues, bleeding, coagulopathy]
  • decreased O2 delivery [anemia, pulmonary edema, ventricular dysfunction]
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9
Q

What is the cellular pathophysiology of sepsis?

A
  • initated by immune system - T cells, PMNs
  • mediated by: cytokines, cell wall factors, coagulation cascade, complement
  • results in immune dysregulation and tissue injury
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10
Q

What is the normal response to infection/insult?

A
  • innate immune [T cells]

- adaptive immune [B cell]s

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11
Q

What are the physical barriers of the immune system?

A
  • skin
  • cornea
  • mucus layers
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12
Q

what are the chemical barriers or the immune system?

A
  • stomach acid
  • fatty acids on skin
  • lysozyme in tears
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13
Q

What are the active mech of immune system?

A
  • immune cells
  • intracellular [interferons, apoptosis]
  • organismal [complement, phagocytosis]
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14
Q

How does innate immune recognize pathogens?

A
  • toll like receptors recognize pathogen associated molecular patterns [PAMPS]
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15
Q

What are 3 examples of PAMPS?

A

LPS on gram-neg
lipotechoic acid on gram-pos
mannans on yeast

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16
Q

Which effector mech are activated as art of innate immune response?

A
  • activation of complement
  • activated NFkB
  • initiation pro-inflammatory cytokines [IL1 and IL6] to recruit other cellular components
  • activated adaptive immune response
  • initiation anti-inflammatory mediators to limit host tissue injury [IL10, resolvins, protectins]
17
Q

What are 3 hypotheses for sepsis:

A
  1. bacteria and products cause tissue injury and organ injury
  2. excessive host inflammatory response
  3. inadequate compensatory anti-inflammatory response causes dysregulated excessive pro-inflammatory response
18
Q

What are the consequences of innate immune that lead to DIC [disseminated intravascular coagulopathy]?

A
  • cytokines and antigens involved in immune response stimulate tissue factor release from blood vessel endothelium and activate coagulation cascade, suppress fibrinolysis
  • get clot formation –> –> DIC
19
Q

What is third spacing?

A
  • get endothelial injury from inflammatory response
  • endothelial injury causes plasma to leave vessel and go into interstitial space
  • get edema, hypovolemia
20
Q

What are mech of sepsis?

A
  • failure of negative feedback [IL10] to regulate innate immune response
  • high activity of inflammatory mediators –> leaky vessels, coagulation, direct/indirect tissue injury
  • low systemic vascular resistance, hypotension
  • oxygen delivery impairment
  • coagulopathy/thrombosis
21
Q

What two mediators cause decreases systemic vascular resisitance?

A

NO

TNF-alpha

22
Q

What causes cellular dysoxia/oxygen delivery impairment in sepsis?

A
  • have disordered lcal circulatory regulation
  • causes cells to need to undergo anaerobic metabolism
  • get metabolic acidsois
23
Q

The 3 main types of disturbances in sepsis?

A
  • micro-circulation [cell adhesion, vascular leak, DIC]
  • macro-circulation [V/Q, systemic vasodilation, cardiac depression]
  • inflammatory cascade [massive inflammation]
24
Q

What causes some patients to get sicker than others

A
  • co morbid illness or injury [chronic disease – liver disease or cancer]
  • pathogen type and dose [pseudomonas aeruginosa particularly known to cause sepsis]
  • genetic predisposition