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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
The compliment system is represented by the acute phase synthesis of
C3a C3b C4a C4b C5a C5b-C9 Factor B C1 inhibitor
26
What do the compounds of the complement system do?
1- Induce bacteriolysis 2 - Increase vascular permeability 3 - Chemotaxis for neutrophils 4 - Enhance opsonisation for microbes and damaged host cells
27
Reactive oxygen species encompass all oxygen-derived toxic mediators that originate from what
Mononuclear phagocytes or neutrophils
28
The rxns and re-pairing of free radicals causes what to occur
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
29
SIRS criteria in horse
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
30
Cut off value for Lactate (SIRS criteria)
2.06mmol/L
31
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
3
32
A nn. foal born at 300-310 days of gestation will have a sepsis score of?
2
33
A nn. foal born under 300 days will have a sepsis score of?
3
34
A nn. foal with a temp of >39*C will have a sepsis score of
2
35
NN. Foals with anterior uveitis, diarrhoea, respiratory distress, swollen joints, open wounds earns a sepsis score of
3
36
What neutrophil count scores a sepsis score of 3 in a nn. foal
<2,000/uL
37
What neutrophil count scores a sepsis score of 2 in a nn. foal
2,000-4,000/uL or >12,000/uL
38
What neutrophil count scores a sepsis score of 1 in a nn. foal
8,000-12,000/uL
39
How many bands per uL scores a 3 and a 2 in nn. foal sepsis score
3 - >200 2 - 50-200
40
What is necessary for a nn. foal to score 4 on the nn foal sepsis score
Marked toxic change in neutrophils IgG <200mg/dL
41
A score of what predicts sepsis in a nn. foal according to the sepsis scoring system
>11
42
What is MODS
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
Describe primary MODS
Any disease process inducing a well-defined injury that affects the function of organs at the initial site of insult
44
Describe secondary MODS
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
What are the pathophysiological events that drive MODS
1 - Immune mediated inflammatory injury 2 - Altered hemodynamics 3 - Dysfunction of the autonomic nervous system 4 - Reduced tissue perfusion
46
The major elements that define dysfunction of the coagulation system associated with the development of MODS are?
1- Excessive pro coagulation 2 - Loss of controlled fibrinolysis 3 - Loss of natural anticoagulant activities
47
What occurs in DIC
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
What % of horses with acute colitis fit the diagnostic criteria for DIC at admission
30%
49
What % of horses with large colon volvulus fit the diagnostic criteria for DIC at admission
70%
50
What % of septic foals fit the diagnostic criteria for DIC at admission
25%
51
What is the primary mechanism for the initial hypercoagulative state of DIC
Activation of the extrinsic coagulation cascade via enhanced expression of membrane tissue factors
52
In horses endotoxin favours activation of which tPA or PAI?
PAI (Plasminogen activator inhibitor)
53
Consequences of low Protein C and AT
Increased clot formation and heightened inflammatory response - resulting in further thrombus formation
54
Which horses are likely to have increased y-glutamyltransferase activity? Small strangulating lesions or proximal enteritis
Proximal enteritis - 12 times more likely
55
Acute renal failure is described as what
The presence of azotemia or oliguria or both in a normovolemic patient that does not have signs of post renal obstruction
56
What is the primary mechanism leading to acute renal failure
Acute tubular necrosis
57
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?
Hypoxemia Diffuse bilateral pulmonary infiltrates on thoracic radiographs in the absence of left atrial hypertension
58
When do ALI and ARDS develop
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
Triggers for ALI and ARDS in horses are
Sepsis Aspiration of GI content Smoke Severe trauma Transfusion run
60
What is the term CIRCI, Critical illness related corticosteroid insufficiency used to describe
Cortisol response is insufficient for the degree of stress induced by the illness
61
ALR and ADRS can be suspected in horses that meet what criteria
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
DIC can be suspected in the presence of
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
What are the most commonly recognised clinical abnormalities of the coagulation system in horses with acute GI disease?
Thrombocytopenia Prolongation of the prothrombin time
64
What is the mean urine production in foals?
6ml/kg/hr
65
Liver specific indices in the horse?
Persistently increased: serum sorbitol dehydrogenase y-glutamyltransferase serum bile acid conc
66
What is normal fraction shortening for most light breed adult horses?
28-45%
67
Define septicemia
Microbial invasion into the bloodstream with a concurrent systemic host response.
68
In what % of horses with acute colitis does bacteremia occur in?
29%
69
What do PRRs (Pattern recognition receptors) do?
Detect microbial ligands called PAMPs - pathogen associated molecular patterns
70
What are PAMPs?
Ligands unique to microbes - usually essential for microbial survival or virulence. Eg - bacterial cell wall extracts
71
Examples of PAMPs
Bacterial cell wall extracts such as endotoxin, peptidoglycan lipoteichoic acid prokaryotic DNA
72
What are the 3 types of PRRs
1- Defensins (Secreted) 2 - Cell membrane PRRs (involved in phagocytosis) 3 - Cell membrane PRRs (signal transduction)
73
Example of a well-characterised cell signalling PRR-ligand relationship
CD14-Toll like receptor (TLR) and its PAMP Endotoxin
74
Characteristics of endotoxin
Heat stable G- Lipopolysaccharide = 75% of outer cell membrane
75
What are the 3 structural domains of endotoxin?
1. Core - Monosaccharides 2. Core - Lipid A (Highly toxic) 3. Outer - polysaccharide "O-Antigenic" region
76
How does endotoxin manifest its pathologic effects
Once in the blood forms aggregates resembling micelles
77
What is an LBP Lipopolysaccharide binding protein and what does it do?
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
What is CD14
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
What is the most important TLR in the recognition of endotoxin?
TLR4
80
What does TLR2 recognise?
Gram positive bacteria
81
What is thought to be responsible for some violent runs to endotoxin?
Polymorphism of TLR4
82
What is the easy hyper dynamic phase of endotoxemia characterised by
Pulmonary hypertension and ileus associated with increased levels of Thromboxane A2
83
What is the easy hypodynamic phase of endotoxemia characterised by
Fever and hypotension Decreased systemic vascular resistance due to PG release
84
What is the gold standard test for Endotoxemia
The LAL - Limulus Amebocyte Lysate assay But not clinically practical
85
What is the cardinal diagnostic marker for endotoxemia?
Profound neutropenia with toxic neutrophil morphology with a left shift
86
How long after the onset of endotoxemia will neutropenia occur
1 hour
87
Dose of smectite orally for endotoxemia
4 ounces orally twice daily
88
The effectiveness of Antiendotoxin antibodies and Polymyxin B is a factor of what
Their dose and the amount of free unbound circulating endotoxin
89
What is Endoserum and how is it used?
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
What is Polymyxin B
A cationic antibiotic which also binds to and neutralises endotoxin through direct molecular interactions with the lipid A region.
91
Cons of Polymyxin B
Nephrotoxic Neurotoxic when used at bactericidal doses
92
Recommended dose of Polymyxin B
1000-6000 IU/Kg BWT IV every 8-12 hours
93
Doses of DMSO used for endotoxemia
0.1-1g/kg bw diluted to 10% in isotonic fluids
94
Flunixin in endotoxemia tx
Prevents endotoxin induced Prostanoid synthesis

Eq ACVS Phase 1 (72 decks)

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