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Large Animal Medicine > Endotoxemia > Flashcards

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
Q

What is happening to the evins in the HYPOdynamic state?

A

Overall vasodilated

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26
Q

Describe the T,P,R, MM, CRT, and extremities of a hyperdynamic patient.

A 
T - high
P - strong, tachycardic
R - tachypnic
MM - injected (more blood flow, brighter)
CRT - normal
Extremities - warm
27
Q

Describe the T,P,R, MM, CRT, and extremities of a hypodynamic patient.

A 
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
Q

What is the gold standard in diagnosing endotoxemia?

A

Limulus test

NOTE: Really only used in research

29
Q

What do you expect in your hemogram with endotoxemia?

A

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
Q

What do you expect in your hemogram with stress?

A

Leukocytosis, neutrophilia and lymphopenia

31
Q

What do you expect in your hemogram with stress and endotoxemia?

A

Total WBC and Neutrophils WNL, lymphopenia.

32
Q

What should you call a minimum database in large animal?

A

Chemistry profile

Know what you want and know what you expect to get from it.

33
Q

Why would you ask for a chemistry profile?

A

Ensure normal organ fxn because we probably have cardiovascular compromise and organ dysfunction.

Helps guide our fluid therapy.

34
Q

What is the first step to endotoxemia therapy?

A

Remove the cause (usually surgery to correct a volvulus)

Antimicrobials in systemic dz

35
Q

Why do you withhold antimicrobials in the endotoxemic foal?

A

Because the bacterial death causes release of MORE endotoxin

36
Q

What are the 2 antimicrobials used in endotoxemia?

A

Ceftiofur

Amikacin

37
Q

Which antimicrobial is better to use in endotoxemia and why?

A

Amikacin is better because Ceftiofur causes more endotoxin release

NOTE: If you HAVE to use Ceftiofur, use Amikacin as well

38
Q

What 2 things do you need to provide to help with cardiovascular support?

A

Fluids

Protein (if TP

39
Q

When providing fluid support, what type of fluids would you use (3 things)?

A

High volume crystalloids
Hypertonic saline
Combo of both

40
Q

What is the 3rd step in treating endotoxemia?

A

Neutralize the circulating endotoxin

41
Q

What do you give to neutralize the circulating endotoxin?

A

Endoserum

Polymixin B infusions

42
Q

What si the 4th step in treating endotoxemia?

A

Inhibit the endotoxin-associated inflammation and mediators

43
Q

What is the number 1 NSAID choice to inhibit the inflammation and mediators?

A

Flunixin meglumine (Banamine) low dose

NOTE: Low dose Banamine is anti-endotoxic, higher dose is anti-inflammatory

44
Q

What are other NSAIDs that can be used to inhibit inflammation and mediators?

A

Ketoprofen, Phenylbutazone, Ibuprofen

45
Q

What is Pentoxyfylline used for?

A

Used to limit amount of mediators produced. Only minimal effects, better when combined with Banamine

46
Q

What is DMSO used for?

A

As an antioxidant, anti-inflammatory
Inhibits neutrophil adhesion and reduced platelet aggregation

Also very good at reducing edema

47
Q

What type of dose of DMSO would you use?

A

Low dose for GI (20mg/kg)

48
Q

Why is lidocaine also used in endotoxemia cases (3 reasons)?

A

Inhibits hemodynamic and cytokine responses to endotoxin profoundly.
Provides pain relief
Enhances gut motility and reduces post-op illeus

49
Q

How do Omega-3 Fatty Acids help with endotoxemia?

A

Reduces inflammatory mediators

50
Q

What is an anti-oxidant that you will not see really used?

A

Allopurinol (becaues variable results)

51
Q

What can you use to combat the altered coagulability in endotoxemia?

52
Q

What does DIC stand for in equine medicine?

A

Death Is Coming (really the normal DIC… this is just also applicable)

53
Q

What happens to the effectiveness of Heparin is you don’t have sufficient AT3?

A

Won’t really help.

54
Q

How can endotoxemia be prevented?

A

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
Q

What are 4 typical clinical complications of endotoxemia?

A

GI problems
Laminitis
Renal failure
Coagulopathies

56
Q

What sort of GI problems can arise as a complication to endotoxemia?

A

Most typically illeus

Hypoperfusing the gut, acid/base balance and electrolyte distrubances

57
Q

When do you see renal failure in the horse?

A

Not often. Endotoxemia is the classic case.

58
Q

What sort of coagulopathies do you see as a complication to endotoxemia (2 things)?

A

Jugular thrombosis

DIC

59
Q

Why is it so common to see jugular thrombosis in endotoxemia cases?

A

Because horse is hypercoagulable,and getting poked a lot.

60
Q

Why can bilateral jugular thrombosis be so serious?

A

Head swells quickly and can progress to airway obstruction and death because they are obligate nasal breathers

61
Q

How can you minimize the negative effects of bilateral jugular thrombosis (2 ways)?

A

Keep head UP above chest height

35cc syringe cases into nostrils to hold airway open

62
Q

What 4 things do you look at to dx DIC?

A

PLT count
Prothrombin time
Fibrinogen
FDPs

NOTE: Need 3/4 of these

63
Q

Why are Fibrinogen and FDPs not really the greatest indicators of DIC?

A

It’s not a very exact measurement and is also probably elevated because it is secondary to another issue

Large Animal Medicine (5 decks)

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