Endotoxemia Flashcards

1
Q

What 3 things make up an endotoxin?

A

Polysaccharide O
Lipid A
Core sugar

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2
Q

Which part of an endotoxin is the antigenic part?

A

Polysaccharide O

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3
Q

What is the big problem with endotoxins in the horse?

A

Host’s own response, because does everything possible to get rid of it, and ends up hurting itself.

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4
Q

What is the normal cause of endotoxemia in the horse?

A

G- infections

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5
Q

What is the number 1 source of endotoxemia?

A

GI disturbance

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6
Q

What 2 parts of the GI do you worry about the most with endotoxemia?

A

Colon

Cecum

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7
Q

Why are horses not endotoxemic all the time?

A

Normally, not enough coming through and also going through liver first.

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8
Q

What barrier helps protect from endotoxemia?

A

Skin and mucosal surfaces

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9
Q

Besides mucosa, what else normally helps keep endotoxins at bay?

A

They bind to bile salts

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10
Q

What 3 ways are endotoxins removed from circulation normally?

A

Bind to LPS antibodies
Removed by RES in liver
Bind to LBP (LPS binding protein)

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11
Q

What is LBP?

A

A shuttle protein, not a bad guy or a good guy.

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12
Q

What cell type is the major target of endotoxins?

A

Pulmonary macrophages

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13
Q

What is the first parameter altered in endotoxemia?

A

Increased pulmonary alveolar pressure

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14
Q

What is the shock organ in the horse?

A

The lungs

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15
Q

What are 3 triggered responses to endotoxemia?

A
Vasoactive substances
Endothelial disruption
Systemic Inflammatory Response Syndrome (SIRS)
-Neutrophil adhesion
-Monocyte/Macrophage activation
-Platelet adhesion
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16
Q

What is shock?

A

Failure of the circulatory system to maintain adequate blood flow

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17
Q

What are the 2 most common types of shock that we see?

A
Distributive shock (Maldistribution)
Septic shock
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18
Q

Define sepsis.

A

SIRS induced by infection

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19
Q

Define septic shock.

A

Sepsis associated with organ dysfunction, hypoperfusion or hypotension

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20
Q

What is MODS?

A

Multiple Organ Dysfunction Syndrome

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21
Q

What is CARS?

A

Compensatory Anti-inflammatory Response Syndrome

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22
Q

What is MOFS?

A

Multiple Organ Failure Syndrome

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23
Q

What are the 2 clinical phases of shock?

A

Hyperdynamic state

Hypodynamic state

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24
Q

What is happening to the veins in the HYPERdynamic state?

A

Overall vasoconstricted

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25
What is happening to the evins in the HYPOdynamic state?
Overall vasodilated
26
Describe the T,P,R, MM, CRT, and extremities of a hyperdynamic patient.
``` T - high P - strong, tachycardic R - tachypnic MM - injected (more blood flow, brighter) CRT - normal Extremities - warm ```
27
Describe the T,P,R, MM, CRT, and extremities of a hypodynamic patient.
``` T - low P - weak, tachycardic R - tachypnic MM - congested (circulation getting there, but blood staying longer d/t peripheral vasoconstriction) CRT - prolonged Extremities - cold ```
28
What is the gold standard in diagnosing endotoxemia?
Limulus test NOTE: Really only used in research
29
What do you expect in your hemogram with endotoxemia?
Leukopenia, Neutropenia with normal lymphocytes *NOTE: Neutrophils are the major component of the white cell count, so if they change the whole white cell count changes.
30
What do you expect in your hemogram with stress?
Leukocytosis, neutrophilia and lymphopenia
31
What do you expect in your hemogram with stress and endotoxemia?
Total WBC and Neutrophils WNL, lymphopenia.
32
What should you call a minimum database in large animal?
Chemistry profile Know what you want and know what you expect to get from it.
33
Why would you ask for a chemistry profile?
Ensure normal organ fxn because we probably have cardiovascular compromise and organ dysfunction. Helps guide our fluid therapy.
34
What is the first step to endotoxemia therapy?
Remove the cause (usually surgery to correct a volvulus) | Antimicrobials in systemic dz
35
Why do you withhold antimicrobials in the endotoxemic foal?
Because the bacterial death causes release of MORE endotoxin
36
What are the 2 antimicrobials used in endotoxemia?
Ceftiofur | Amikacin
37
Which antimicrobial is better to use in endotoxemia and why?
Amikacin is better because Ceftiofur causes more endotoxin release NOTE: If you HAVE to use Ceftiofur, use Amikacin as well
38
What 2 things do you need to provide to help with cardiovascular support?
Fluids | Protein (if TP
39
When providing fluid support, what type of fluids would you use (3 things)?
High volume crystalloids Hypertonic saline Combo of both
40
What is the 3rd step in treating endotoxemia?
Neutralize the circulating endotoxin
41
What do you give to neutralize the circulating endotoxin?
Endoserum | Polymixin B infusions
42
What si the 4th step in treating endotoxemia?
Inhibit the endotoxin-associated inflammation and mediators
43
What is the number 1 NSAID choice to inhibit the inflammation and mediators?
Flunixin meglumine (Banamine) low dose NOTE: Low dose Banamine is anti-endotoxic, higher dose is anti-inflammatory
44
What are other NSAIDs that can be used to inhibit inflammation and mediators?
Ketoprofen, Phenylbutazone, Ibuprofen
45
What is Pentoxyfylline used for?
Used to limit amount of mediators produced. Only minimal effects, better when combined with Banamine
46
What is DMSO used for?
As an antioxidant, anti-inflammatory Inhibits neutrophil adhesion and reduced platelet aggregation Also very good at reducing edema
47
What type of dose of DMSO would you use?
Low dose for GI (20mg/kg)
48
Why is lidocaine also used in endotoxemia cases (3 reasons)?
Inhibits hemodynamic and cytokine responses to endotoxin profoundly. Provides pain relief Enhances gut motility and reduces post-op illeus
49
How do Omega-3 Fatty Acids help with endotoxemia?
Reduces inflammatory mediators
50
What is an anti-oxidant that you will not see really used?
Allopurinol (becaues variable results)
51
What can you use to combat the altered coagulability in endotoxemia?
Heparin
52
What does DIC stand for in equine medicine?
Death Is Coming (really the normal DIC... this is just also applicable)
53
What happens to the effectiveness of Heparin is you don't have sufficient AT3?
Won't really help.
54
How can endotoxemia be prevented?
A vaccine is available, but it is controversial because the Lipid A molecule is responsible for the signs, but it's not very antigenic.
55
What are 4 typical clinical complications of endotoxemia?
GI problems Laminitis Renal failure Coagulopathies
56
What sort of GI problems can arise as a complication to endotoxemia?
Most typically illeus Hypoperfusing the gut, acid/base balance and electrolyte distrubances
57
When do you see renal failure in the horse?
Not often. Endotoxemia is the classic case.
58
What sort of coagulopathies do you see as a complication to endotoxemia (2 things)?
Jugular thrombosis | DIC
59
Why is it so common to see jugular thrombosis in endotoxemia cases?
Because horse is hypercoagulable,and getting poked a lot.
60
Why can bilateral jugular thrombosis be so serious?
Head swells quickly and can progress to airway obstruction and death because they are obligate nasal breathers
61
How can you minimize the negative effects of bilateral jugular thrombosis (2 ways)?
Keep head UP above chest height | 35cc syringe cases into nostrils to hold airway open
62
What 4 things do you look at to dx DIC?
PLT count Prothrombin time Fibrinogen FDPs NOTE: Need 3/4 of these
63
Why are Fibrinogen and FDPs not really the greatest indicators of DIC?
It's not a very exact measurement and is also probably elevated because it is secondary to another issue