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Eq ACVS Phase 1 > Ch.2 Systemic Inflammatory Response > Flashcards

Ch.2 Systemic Inflammatory Response Flashcards

1
Q

What is SIRS

A

An incongruous and exaggerated systemic inflammatory reaction as response to infection and injury

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2
Q

What is CARS

A

Compensatory Anti-inflammatory Response Syndrome
Over recruitment of the anti-inflammatory processes
A state of anergy, increased susceptibility to infection and inability to repair damaged tissues.

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3
Q

What occurs in MARS - Mixed anti-inflammatory response syndrome

A

Surges of both CARS and SIRS coexist

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4
Q

What is the key event in the initiation and propagation of SIRS

A

Release of endogenous molecular substances by the hosts innate immune system

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5
Q

What are PAMPs

A

Pathogen associated molecular patterns - products released or associated with invading microorganisms

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6
Q

What are DAMPs

A

Damage associated molecule pattern - Products released from damaged cells

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7
Q

Function of PRRs (pattern recognition receptors)

A

Recognise PAMPs and DAMPs and initiate downstream release of endogenous mediators that drive the inflammatory response.

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8
Q

Proinflammatory cytokine examples

A

TNF - Tumour necrosis factor
Interleukin 1 IL-1
Interleukin 6 IL-6
Interleukin 8 IL-8
IFN-y - Interferon-y

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9
Q

Universal sources for proinflammatory cytokines

A

Macrophages and monocytes
Other cell types contributing
Neutrophils - TNF
Endothelial cells - IL-1, IL-8
Fibroblasts
Keratinocytes
Lymphocytes - IL-1, IL-6
Natural Killer Cells - TNF, IFN-y

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10
Q

Main functions of TNF, IL-1 and IL-6

A

Initiate coagulation,
Fibrinolysis,
Complement activation,
Acute phase response,
Neutrophil chemotaxis
TNF&IL-1 - Pyrogenic activities, augment further cytokine production

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11
Q

What is phospholipase A2 responsible for?

A

Cleavage of arachidonic acid

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12
Q

What up regulates phospholipase A2

A

IL-1, TNF, Endotoxin

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13
Q

What is arachidonic acid metabolised by and what are the metabolites

A

Lipoxygenase - Leukotrienes
Cyclooxygenase - Prostanoids ; Thromboxane A2(TxA2) and Prostaglandins (Pgs)

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14
Q

Which prostanoids are vasoconstrictors?

A

TxA2 (Thromboxane A2)
PGF2Alpha

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15
Q

Which prostanoids are vasodilators?

A

PGI2
PGE2

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16
Q

Role of prostanoids in primary homeostasis

A

TxA2 - promotes platelet aggregation
PGI2 - inhibits platelet aggregation

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17
Q

Which prostanoid is a pyrogen

A

PGE2

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18
Q

Action of leukotrienes in horses

A

Chemoattractants and increase vascular permeability

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19
Q

Where does PAF (Platelet Activating Factor) come from?

A

Released from cell membrane by phospholipase A2

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20
Q

Biologic effects of PAF?

A

1 - Vasodilation
2 - Increased vascular permeability
3 - Platelet aggregation
4 - Recruitment and activation of phagocytes

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21
Q

What is the expected SAA conc in healthy horses and foals?

A

<27mg/L

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22
Q

What test is used to determine SAA levels

A

Latex agglutination immunoturbidimetric assay

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23
Q

What test is used to determine C-Reactive protein (CRP)

A

Radial immunodiffusion

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24
Q

What is the expected CRP conc in healthy horses and foals?

A

5-14mg/mL

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25
Q

The compliment system is represented by the acute phase synthesis of

A

C3a C3b
C4a C4b
C5a C5b-C9
Factor B
C1 inhibitor

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26
Q

What do the compounds of the complement system do?

A

1- Induce bacteriolysis
2 - Increase vascular permeability
3 - Chemotaxis for neutrophils
4 - Enhance opsonisation for microbes and damaged host cells

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27
Q

Reactive oxygen species encompass all oxygen-derived toxic mediators that originate from what

A

Mononuclear phagocytes or neutrophils

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28
Q

The rxns and re-pairing of free radicals causes what to occur

A

1 - Molecular damage
2 - Loss of protein function
3 - Cross-linking of DNA
4 - Lipid per oxidation
5 - Vasoconstriction
6 - Pain

Oxygen free radicals also:
7 - Cytokine production
8 - Endothelial adhesion models

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29
Q

SIRS criteria in horse

A

Temp >38.5 (101.3) or <37 (98.6)
HR >52
Resp >20 or PaCO2<32mmHg
WBC >12,500 cells/uL or <5000 cells/uL or >10% bands

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30
Q

Cut off value for Lactate (SIRS criteria)

A

2.06mmol/L

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31
Q

In the Sepsis score system for neonatal foals; a nn. foal
from a mare with hx of placentitis, valvular dc, dystocia, Long transport of mare, sick mare, induced parturition, prolonged gestation >365 days will score where on the scale

A

3

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32
Q

A nn. foal born at 300-310 days of gestation will have a sepsis score of?

A

2

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33
Q

A nn. foal born under 300 days will have a sepsis score of?

A

3

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34
Q

A nn. foal with a temp of >39*C will have a sepsis score of

A

2

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35
Q

NN. Foals with anterior uveitis, diarrhoea, respiratory distress, swollen joints, open wounds earns a sepsis score of

A

3

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36
Q

What neutrophil count scores a sepsis score of 3 in a nn. foal

A

<2,000/uL

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37
Q

What neutrophil count scores a sepsis score of 2 in a nn. foal

A

2,000-4,000/uL or >12,000/uL

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38
Q

What neutrophil count scores a sepsis score of 1 in a nn. foal

A

8,000-12,000/uL

39
Q

How many bands per uL scores a 3 and a 2 in nn. foal sepsis score

A

3 - >200
2 - 50-200

40
Q

What is necessary for a nn. foal to score 4 on the nn foal sepsis score

A

Marked toxic change in neutrophils
IgG <200mg/dL

41
Q

A score of what predicts sepsis in a nn. foal according to the sepsis scoring system

A

> 11

42
Q

What is MODS

A

Multiple organ disfunction syndrome
Presence of altered organ function in an acutely ill patient such that hemostasis cannot be maintained without intervention.

A dynamic process that is a continuum of pathophysiologic change over time.

An extension and possible consequence of SIRS

43
Q

Describe primary MODS

A

Any disease process inducing a well-defined injury that affects the function of organs at the initial site of insult

44
Q

Describe secondary MODS

A

Any disease process inducing a well-defined injury that affects the function of organs remotely positioned from the primary injury, not as a direct response to the insult but as a consequence of the host’s response to the injury.

45
Q

What are the pathophysiological events that drive MODS

A

1 - Immune mediated inflammatory injury
2 - Altered hemodynamics
3 - Dysfunction of the autonomic nervous system
4 - Reduced tissue perfusion

46
Q

The major elements that define dysfunction of the coagulation system associated with the development of MODS are?

A

1- Excessive pro coagulation
2 - Loss of controlled fibrinolysis
3 - Loss of natural anticoagulant activities

47
Q

What occurs in DIC

A

prolonged or excessive thrombi formation results in platelets, coagulation factors, anticoagulant factors and fibrinolytic factors being consumed - balance is lost and haemorrhage may ensue

48
Q

What % of horses with acute colitis fit the diagnostic criteria for DIC at admission

A

30%

49
Q

What % of horses with large colon volvulus fit the diagnostic criteria for DIC at admission

A

70%

50
Q

What % of septic foals fit the diagnostic criteria for DIC at admission

A

25%

51
Q

What is the primary mechanism for the initial hypercoagulative state of DIC

A

Activation of the extrinsic coagulation cascade via enhanced expression of membrane tissue factors

52
Q

In horses endotoxin favours activation of which tPA or PAI?

A

PAI (Plasminogen activator inhibitor)

53
Q

Consequences of low Protein C and AT

A

Increased clot formation and heightened inflammatory response - resulting in further thrombus formation

54
Q

Which horses are likely to have increased y-glutamyltransferase activity? Small strangulating lesions or proximal enteritis

A

Proximal enteritis - 12 times more likely

55
Q

Acute renal failure is described as what

A

The presence of azotemia or oliguria or both in a normovolemic patient that does not have signs of post renal obstruction

56
Q

What is the primary mechanism leading to acute renal failure

A

Acute tubular necrosis

57
Q

Acute lung injury (ALI) and (ARDS) Acute respiratory distress syndrome are defined as the clinical conditions of acute respiratory failure, what are they characterised by?

A

Hypoxemia
Diffuse bilateral pulmonary infiltrates on thoracic radiographs in the absence of left atrial hypertension

58
Q

When do ALI and ARDS develop

A

When injury to the alveoli and pulmonary endothelium cause thromboembolism and protein rich pulmonary oedema
Type II pneumocytes and fibroblasts are recruited to replace damaged areas in the aleveoli

59
Q

Triggers for ALI and ARDS in horses are

A

Sepsis
Aspiration of GI content
Smoke
Severe trauma
Transfusion run

60
Q

What is the term CIRCI, Critical illness related corticosteroid insufficiency used to describe

A

Cortisol response is insufficient for the degree of stress induced by the illness

61
Q

ALR and ADRS can be suspected in horses that meet what criteria

A

1 - Acute onset <72hrs of respiratory distress or tachypnea at rest

2 - Patient has a known risk factor

3 - Pulmonary capillary leakage w/o increased pulmonary capillary pressure

4 - There is inefficient gas exchange

62
Q

DIC can be suspected in the presence of

A

1 - Thrombocytopenia
2 - Prolonged prothrombin; activated prothrombin time
3 - Decreased fibrinogen concentration or prolonged thrombin time
4 - Increased fibrin degradation products or D-dimer concentrations
5 - Decreased antithrombin activity

63
Q

What are the most commonly recognised clinical abnormalities of the coagulation system in horses with acute GI disease?

A

Thrombocytopenia
Prolongation of the prothrombin time

64
Q

What is the mean urine production in foals?

A

6ml/kg/hr

65
Q

Liver specific indices in the horse?

A

Persistently increased:
serum sorbitol dehydrogenase
y-glutamyltransferase
serum bile acid conc

66
Q

What is normal fraction shortening for most light breed adult horses?

A

28-45%

67
Q

Define septicemia

A

Microbial invasion into the bloodstream with a concurrent systemic host response.

68
Q

In what % of horses with acute colitis does bacteremia occur in?

A

29%

69
Q

What do PRRs (Pattern recognition receptors) do?

A

Detect microbial ligands called PAMPs - pathogen associated molecular patterns

70
Q

What are PAMPs?

A

Ligands unique to microbes - usually essential for microbial survival or virulence. Eg - bacterial cell wall extracts

71
Q

Examples of PAMPs

A

Bacterial cell wall extracts such as
endotoxin,
peptidoglycan
lipoteichoic acid
prokaryotic DNA

72
Q

What are the 3 types of PRRs

A

1- Defensins (Secreted)
2 - Cell membrane PRRs (involved in phagocytosis)
3 - Cell membrane PRRs (signal transduction)

73
Q

Example of a well-characterised cell signalling PRR-ligand relationship

A

CD14-Toll like receptor (TLR) and its PAMP Endotoxin

74
Q

Characteristics of endotoxin

A

Heat stable
G-
Lipopolysaccharide = 75% of outer cell membrane

75
Q

What are the 3 structural domains of endotoxin?

A
  1. Core - Monosaccharides
  2. Core - Lipid A (Highly toxic)
  3. Outer - polysaccharide “O-Antigenic” region
76
Q

How does endotoxin manifest its pathologic effects

A

Once in the blood forms aggregates resembling micelles

77
Q

What is an LBP Lipopolysaccharide binding protein and what does it do?

A

Lipid transfer protein synthesised by the liver
Acute phase protein
Extracts molecules of endotoxin from aggregated micelles in the blood and transports them to various locations.

78
Q

What is CD14

A

53-kDa Glycoprotein exists as a cell membrane receptor(mCD14) and a soluble form in circulation(sCD14)

sCD14 - Binds and neutralises circulating endotoxins

Does not structurally cross the cell membrane so associates with TLR

79
Q

What is the most important TLR in the recognition of endotoxin?

A

TLR4

80
Q

What does TLR2 recognise?

A

Gram positive bacteria

81
Q

What is thought to be responsible for some violent runs to endotoxin?

A

Polymorphism of TLR4

82
Q

What is the easy hyper dynamic phase of endotoxemia characterised by

A

Pulmonary hypertension and ileus associated with increased levels of Thromboxane A2

83
Q

What is the easy hypodynamic phase of endotoxemia characterised by

A

Fever and hypotension
Decreased systemic vascular resistance due to PG release

84
Q

What is the gold standard test for Endotoxemia

A

The LAL - Limulus Amebocyte Lysate assay
But not clinically practical

85
Q

What is the cardinal diagnostic marker for endotoxemia?

A

Profound neutropenia with toxic neutrophil morphology with a left shift

86
Q

How long after the onset of endotoxemia will neutropenia occur

A

1 hour

87
Q

Dose of smectite orally for endotoxemia

A

4 ounces orally twice daily

88
Q

The effectiveness of Antiendotoxin antibodies and Polymyxin B is a factor of what

A

Their dose and the amount of free unbound circulating endotoxin

89
Q

What is Endoserum and how is it used?

A

Hyperimmune serum from horses vaccinated with the Salmonella typhimurium Re mutant

It is diluted with sterile isotonic saline 1:10 or 1:20 and administered iv over 1-2 hours

90
Q

What is Polymyxin B

A

A cationic antibiotic which also binds to and neutralises endotoxin through direct molecular interactions with the lipid A region.

91
Q

Cons of Polymyxin B

A

Nephrotoxic
Neurotoxic when used at bactericidal doses

92
Q

Recommended dose of Polymyxin B

A

1000-6000 IU/Kg BWT IV every 8-12 hours

93
Q

Doses of DMSO used for endotoxemia

A

0.1-1g/kg bw diluted to 10% in isotonic fluids

94
Q

Flunixin in endotoxemia tx

A

Prevents endotoxin induced Prostanoid synthesis

Eq ACVS Phase 1 (72 decks)

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