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RUSVM LAM1 > Endotoxemia > Flashcards

Endotoxemia Flashcards

1
Q

What is the progression of endotoxemia?

A

Disease -> sepsis -> endotoxemia -> systemic inflammatory response syndrome -> compensated anti-inflammatory response syndrome -> multiple organ dysfunction syndrome —> multiple organ failure

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2
Q

What are the primary causes multiple organ dysfunction syndrome?

A

Acute respiratory distress syndrome (ARDS)

Disseminated intravascular coagulation (DIC)

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3
Q

What are the criteria for diagnosis of systemic inflammatory response syndrome?

A

At least 2 of the following..

Leukopenia, leukocytosis, or >10% bands

Hyperthermia or hypothermia
Tachycardia
Tachypnea
Evidence of sepsis in foals

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4
Q

What is endotoxemia?

A

Presence of endotoxin in circulation
-LPS from the cell wall of gram negative bacteria

—> recognition of pathogen leads to inflammatory response that cannot be sufficiently controlled

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5
Q

What are the 3 structural domains of LPS?

A

Polysacchardie O region (polar) -> accounts for the serologic differentiation among bacterial species

Core acidic polysaccharide

Lipid A (hydrophobic) 
-> unique and well conserved
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6
Q

What part of LPS is most responsible for the toxic effect of endotoxemia?

A

Lipid A

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7
Q

What preventative mechanisms does the body have against endotoxemia?

A

Mucosal epithelial cells/ physical barrier

  • restrict bacterial transmural movement across the bowel wall
  • secrete lysozyme, enzymes, and antibodies

Circulation

  • liver removes endotoxin from portal blood (monocytes AKA kupffer cells)
  • intravascular macrophages
  • anti-endotoxin antibodies bind and remove
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8
Q

Where can bacteria breach physical barriers leading to endotoxemia?

A 
Digestive 
Respiratory 
Reproductive 
Integumentary 
Urinary
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9
Q

You do an abdominocentesis on a colic horse, what cbc and biochem results would indicate significant compromise of the GI system ?

A

High protein and high WBC

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10
Q

T/F: the larger the section of compromised bowel, the larger the chance of developing endotoxic shock

A

True

—> reperfusion injury due to ischemia and necrosis

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11
Q

How does an enteritis or colitis lead to endotoxemia?

A

Damage to the GI walls allowing bacterial translocation

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12
Q

What organism causes Potomac horse fever?

A

Neorickettsial

AKA equine monocytic ehrlichiosis

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13
Q

What pathology is associated with Potomac horse fever?

A

Acute entercolitis —> colic, fever, and diarrhea

Laminitis often appears due to systemic inflammation

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14
Q

What is a sand colic? What are methods of diagnosis?

A

Horse consumes sand, large amounts settle in large intestine

Auscultation of cranial abdominal cavity-> hear waves washing onto the shore

Passage of mineral oil and check for sand

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15
Q

How does carbohydrate overload lead to endotoxemia?

A

Carbohydrate overload-
> lowers pH -> bacterial overgrowth -> high amount of fermentation injury mucosa —> bacteria gains access to portal circulation

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16
Q

What drugs can induce a colitis?

A

Antibiotics

NSAIDS: Banamine (flunixin meglumine) or phenylbutazone

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17
Q

T/F: pleuropneumonia is most commonly viral

A

False

Bacterial

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18
Q

What is the usually the treatment for a pleuopneumonia?

A

Thoracotomy - provide drainage

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19
Q

Horse has watery green tinged nasal discharge

Dysphagia
Gagging

What is your dx?

A

Choke - esophageal obstruction with feed

Often leads to aspiration pneumonia -> Ecoli and Klebsiella

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20
Q

What gram positive organism of the skin can pass into the blood causing endotoxemia?

A

Clostridium myositis

21
Q

What reproductive disease most commonly leads to endotoxemia?

A

Retained placenta

Other causes

  • uterine rupture
  • severe metritis
22
Q

What disease of the urinary tract can lead to an endotoxemia?

A

Infection

Obstruction

23
Q

What is the pathophysiology of equine metabolic syndrome ?

A

Lipotoxicity (excessive conversion of glucose to fat)

  • disruption of insulin receptors progress until insulin resistance
  • associated with oxidative stress and inflammation
  • > increased IL6, IL8, IL10, and TNFa
  • > prolonged cytokine expression in circulatory leukocytes - increased inflammatory response (also lead to laminitis )
24
Q

Hyper-cortisolemic state is caused by what endocrine disease in horses?

A

Pituitary par intermedia dysfunction (PPID)

-> ACTH overstimulates adrenal glands —> cortisol synthesis

25
Q

What is the pathophysiology of endotoxemia?

A

Physical barrier breach

Endotoxin stimulate macrophages

Macrophages stimulates TXA2 and vasoconstriction
Macrophages synthesize cytokines

TNF and IL1 act on neutrophils and endothelial cells —> margination of neutrophils and emptying of granular content

Endothelial damage -> hypercoagulable state
Vasodilator substances from endothelium —> shock

Compromised organ perfusion

26
Q

What receptors on macrophages are responsible for binding LPS? And what pathway is activated in the macrophages?

A

Pathogen associated molecular pattern (PAMP; LBP which binds to CD14 cell surface and activation of pathogen recognition receptors (PRR) on toll like receptors

Toll like receptor 4
-> MyD88 pathway -> TNF and IL1 production (pro inflammatory)

27
Q

In the early stage of macrophage activation, it stimulates TXA2 causing ??

A

Vasoconstriction

—> pulmonary vasoconstriction results in increase in pulmonary arterial pressure

28
Q

In the later stages of macrophage activation, they synthesize cytokines (TNF and IL1) which results in??

A

Amplification of endotoxin signal

Endogenous pyrogens, cortisol, epi, procoagulant activity

NO -> vasodilation

29
Q

TNF and IL1 act on what cells and what response do they produce??

A

Neutrophils and endothelial cells

-> cytokine induced margination of neutrophils (leukopenia)

30
Q

___________ cells contribute to the procoagulant activity while ______ contribute to the procoagulant effect

A

Endothelial; platelets

31
Q

What substances produced by the endothelium are vasodilator?

A

Prostacyclin

NO

32
Q

Endotoxemia causes abnormal vascular tone. In the initial stage there is _________ shock, in later stages there s _________ shock

A

Hyperdynmaic (vasoconstriction); hypodynamic (vasodilation)

33
Q

What contributes to the compromised organ perfusion seen with endotoxemia?

A 
Vasodilation 
Vascular leakage and injury
Intravascular cellular plugging 
Coagulation 
Systemic arterial hypotension
34
Q

Damaged endothelium caused by extravasation of neutrophils causes leakage of??

A

Proteins

35
Q

In recovery from endotoxemia, LPS induces _____ which results in deactivation of mononuclear phagocytes and inhibits pro-inflammatory cytokines

A

IL10

36
Q

What clinical signs are associated with EARLY endotoxemia?

A 
Tachypnea and tachycardia 
(Associated with vasoconstriction) 
- depression, restlessness, inappetence, 
fever 
Pale MM colour and prolonged CRT 
Fever

Toxic line

37
Q

At 4-6hours what clinical signs do you see associated with endotoxemia?

A

Tachycardia and tachypnea
Fever

Circulatory failure and coagulopathy

Dehydration

  • dry MM
  • skin tenting
  • sunken eye
38
Q

At later stages of endotoxemia what are associated clinical signs?

A 
Decrease rectal temp 
Oliguria or anuria 
Rapid weak pulses 
Muscle tremors 
Hemostatic dysfunction  
-petechia, ecchymosis 
-hypercoagulable
39
Q

At 24hrs what clinical signs are associated with endotoxemia?

A

Ventral edema and laminitis

40
Q

T/F: horses have a higher sensitively to LPS compared to other species

A

True

41
Q

What is the equine-specific cellular response to flagellin?

A

Flagellin induces pro-inflammatory responses by neutrophils (TLR5)

42
Q 
Physical exam shows 
Increased HR (>48bpm) 
Toxic mucus membranes 
Cold extremities 
Poor pulse 
Fever

You suspect endotoxemia.. what diagnostics can you do to confirm?

A

CBC -> leukopenia, neutropenia and left shift

Arterial blood gas: hypoxemia and metabolic acidosis

Platelet and fibrinogen low due to DIC

Limulous ameobcyte lysate assay —> direct measurement fo circulating endotoxins

43
Q

When treating a horse for endotoxemia, you see on the biochem it has hyperglycemia. What is the prognosis for this animal

A

Poor

44
Q

How can endotoxemia be prevented?

A

Vaccination with S. Typhimurium mutant -> partial protection and little support

LPS repeated exposure -> diminish pro inflammatory response (short duration of tolerance)

45
Q

What are the goals in treatment of endotoxemia?

A 
Circulatory support 
Remove causes 
Neutralize endotoxin 
Inhibit inflammation 
Prevent laminitis
46
Q

What can you do to improve cardiovascular function in endotoxemia?

A

Balance polyionic solution

  • LRS or Normosol
  • volume and rate depend on the degree of hypovolemia

Hypertonic saline (7.5%) - always follow with balanced IV fluids

Plasma proteins

47
Q

What therapies can be used to neutralize circulating endotoxin?

A

Hyperimmune plasma -> antiLPS IgM and IgG antibodies (very $$$$)

Polymixin B - cationic polypenptide antibiotic -> interact with lipid A forms stable molecules and decrease TNFa

Endoserum from hyper-immune horses

48
Q

What therapies inhibit inflammation induced by endotoxins?

A

NSAIDS - flunixin meglumine prevents increase in TXA2 and PGI2

Glucocorticoids is controversial (immunosuppressive and laminitis)

Pentoxifylline: phosphodiesterase inhibition -> inhibit TNFa and IL6

DMSO -> decrease expression of TNFa, IL6, and macrophage inflammatory protein 1-a

Ketamine -> cytokine modulating activity (last choice)

Lidocaine CRI -> anti TNFa

Ethyl pyruvate -> down regulates TNFa, IL6, and COx2

49
Q

T/F: flunixin meglumine is more efffective in treating hemodynamic effects off LPS when combined with pentoxifylline

A

True

RUSVM LAM1 (17 decks)

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