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Auburn ECC > Sepsis/SIRS/MODS > Flashcards

Sepsis/SIRS/MODS Flashcards

1
Q

Risk factors for nosocomial VAP?

A

age, obesity, chronic lung disease, previous pneumonia, sepsis, head trauma, stress ulcer prophylaxis, paralytics, enteral nutrition, multiple transfusions, immunosuppression, tracheostomy, reintubation, frequent vent circuit changes, multi central lines, u cath, post op infection

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2
Q

Guidelines for initiating empirical abs for suspected CRBSI

A

indwelling cath >48h, evidence of cath site infection, fever, hypotension, tachycardia, leukocytosis

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3
Q

In gram negative sepsis, LPS binds?

A

TLR-4

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4
Q

In gram positive sepsis, lipoteichoic acid binds?

A

TLR-2

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5
Q

Examples of PAMPs?

A

LPS, lipopeptides, lipoteichoic acid, flagellin, micobial DNA, microbial RNA

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6
Q

What are the downstream effects of activating PAR-1

A

synthesis of platelet activating factor, IL-6, IL-8, P-selectin, and adhesion molecule expression

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7
Q

Each hour delay in effective antimicrobial administration AFTER 6 HOURS of spetic shock decreases survival by what %?

A

7.6%

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8
Q

PRR stands for?

A

pattern recognition receptor

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9
Q

Major findings of CORTICUS NEJM 2008 study of hydrocortisone therapy in septic shock?

A

Hydrocortisone did NOT improve survival or reversal of shock in patients with septic shock, overall of in patients who did not have a response to corticotropin.
BUT, reversed shock faster in whom shock was reversed.

Increased incidence of superinfection, including new episodes of sepsis or septic shock, in the hydrocortisone group. Higher glucose in steroid group

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10
Q

What are caspases? Why they important?

A
  • Cysteine proteases: degrade cellular proteins at aspartic acid sites along protein sequences
  • Mediate programmed cell death
  • Part of inflammasome signaling pathway
  • Contribute to synthesis of mature IL-1
  • Caspase dependent apoptosis of B and T cells
  • Central to pathogenesis of sepsis-induced immunosuppression
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11
Q

List the criteria used to define SIRS in clinical patients

A 
dogs- must have at least 2/4 criteria
cats- must have at least 3/4 criteria
temp: dogs 102.6, cats 104
HR: dogs >120, cats 225
RR: dogs >20, cats >40
WBC: dogs 16 or >3% bands, cats >19
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12
Q

what is the specificity and sensitivity of using the proposed SIRS criteria (temp, wbc, rr, hr) in dogs

A

sensitivity 97%

specificity 64%

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13
Q

list some factors from gram - & gram + bacteria and fungi that are known to induce inflammation via stimulation of monocytes and macrophages

A

LPS (gram -), lipoteichoic acid (gram +), peptidoglycan (gram +), flagellin (gram -), mannan (fungi)

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14
Q

list some pro-inflammatory mediators responsible for SIRS

A

TNFa, IL-6, prekallikreins, bradykinin, platelet activating factor

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15
Q

Name some anti-inflammatory mediators that are released in response to pro inflammatory mediators such as TNFa with SIRS

A

IL10, TGFb, IL13, reduction of B and T lymphocyte production, production of TNFa receptor antagonists

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16
Q

what type of disruptions of homeotasis occur with SIRS

A

loss of vascular tone, disruption of endothelial permeability barrier, stimulation of coagulation

17
Q

what is the mechanism of loss of vascular tone in SIRS

A

excessive inducible nitric oxide synthase production, possible deficiency of vasopressin, possible cortisol deficiency

18
Q

what is the mechanism of disruption of endothelial permeability barrier in SIRS?

A

cytokine production

19
Q

list some reasons why hypercoagulability occurs with SIRS

A
  • induced by cytokine-mediated tissue factor expression on leukocyte surface
  • leads to fibrin deposition on microvascular surface
  • anticoagulation factors such as protein C, TFPI, and AT are consumed and may be impaired as well
  • TNFa downregulates protein C, which is an anti-inflammatory & anticoagulant protein
20
Q

What 2 biomarkers are listed in hopperstein “SIRS” chapter that are extensively studied in human medicine to differentiate sepsis vs sirs?

A

C reactive protein

procalcitonin

21
Q

what does the acronym PIRO stand for in regards to sepsis?

A

predisposition, insult/infection, response, organ dysfunction

22
Q

describe CRP and its potential use for ID of sepsis

A
  • acute phase protein, produced by hepatocytes in response to TNFa, IL-1b
  • peaks 36-50 hrs after secretion; half life 19 hours
  • increase in CRP in sepsis but also trauma, surgery, pancreatitis, myocardial infarction
  • non-specific, not ideal marker
23
Q

describe procalcitonin and its potential use for ID of sepsis

A
  • precursor to calcitonin
  • normally produced by thyroid gland; in sepsis may originate from mononuclear leukocytes after endotoxin/cytokine stimulation
  • released hours after stimulation; peak up to 24 hrs
  • increases nitric oxide release
  • superior to CRP for biomarker of sepsis
  • appears to be related to severity of inflammation and may have prognostic value in septic shock and sepsis
24
Q

T/F: antagonist of TNFa, IL1, PAF have failed to show a survival benefit in people with sepsis

A

true; some studies show detrimental effects

25
Q

which of the following have shown potential survival benefit with sepsis?

a-ibuprofen
b-steroids
c-IVIG
d-statins
e- recombinant human activated protein C
A

C & E
Statins have not been extensively studied yet
E- Protein C has had mixed results; some show no benefit, no longer available on market

26
Q

in one study, dogs with and without SIRS (when compared to healthy controls) showed which coagulation abnormalities?

A

prolonged PT; PTT
reduced AT
reduced protein C

27
Q

Name the diseases in small animals in which CRP has been shown to be elevated

A

IMHA, MMVD, neoplasias, pyometra

28
Q

what are some biochemical abnormalities assoc with sirs?

A

hyper or hypoglycemia, hypoalbuminemia, elevated ALT and AST, +/- hyperbilirubinemia, evidence of tubular and glomerular dysfxn

29
Q

what are the proposed mechanisms for increased t bili in SIRS?

A

cholestasis, immune mediated hemolysis

30
Q

proposed mechanisms for hypoalbuminemia in SIRS?

A

negative acute phase protein, losses thru changes in endothelial permeability

Auburn ECC (26 decks)

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