Septicemia in foals

Question 1

Endotoxemia is the sum of total clinical signs caused by ____ response to circulating endotoxins

Answer 1

inflammatory

Question 2

SIRS is systemic inflamm. response syndrome and is what?

Answer 2

A physiologic response to non-specific insult, stimulated by presumed or true insult (infectious or non infectious)

Question 3

SIRS due to infectious insult =

Answer 3

SEPSIS

Question 4

MODS=

Answer 4

multiple organ dysfunction (in acutely ill patients that require intervention to maintain homeostasis)

Question 5

Sepsis – severe sepsis –

Answer 5

septic shock and MODS

Question 6

SIRS clinically manifests as two or more of the following:

Answer 6

o Abnormal body temp (fever/hypothermia)
o Tachycardia
o Abnormal RR (tachypnea/bradypnea)
o Abnormal leukogram (leukopenia, leukocytosis, LS)
o MM discoloration – “toxic line” (horse specific)

Question 7

LPS components:

“L”

Answer 7

L- lipid A
innermost, hydrophobic, anchors LPS to the outer cell wall
TOXIC principle, highly conserved

Question 8

LPS components:

“P”

Answer 8

Core polysaccharide, middle portion, linked to lipid A by KTO, more conserved than O chain, used to stimulate cross protective antibodies

Question 9

LPS components:

“O”

Answer 9

Specific side chain of outermost hydrophilic properties that has a lot of antigen diversity

Question 10

What is the most common Endotoxin source?

Answer 10

GIT- gram negative bacteria that normal occurs in GI lumen, short half life

Question 11

___ are apart of innate immunity and bind PAMPs

Answer 11

PRR

Question 12

____ is an impt PRR that recognizes ____ via cytoplasmic signals

Answer 12

TLR4; LPS

Question 13

Excess ___ mediated signaling= septic shock

Answer 13

TLR

Question 14

How does LPS cause pulmonary hypertension??

Answer 14

Mediated by thromboxanes–> Increased RR (also hypoxemia, dyspnea, pulmonary hypertension)
Prostaglandin I2 causes: discolored membranes, prolonged CRT, decreased venous return, decreased cardiac output, hypotension

Question 15

First part of LPS toxicity is ?

What happen after that?

Answer 15

1- pulm. hypertension

2. hyperdynamic phase with warm shock
3. vasoconstrictive phase with hypodynamic phase and decompensated shock and MODs

Question 16

What occurs during pulm. hypertension from LPS toxicity?

Answer 16

Increased RR, dyspnea, pulmonary hypertension, discolored membranes, prolonged CRT decreased venous return, decreased CO, decreased BP

Question 17

What occurs during the warm shock phase/hyperdynamic phase of LPS toxicity??

Answer 17

Vasodilation and peripheral vascular pooling, reduced diastolic pressure, warm extremities, INCREASEDDDD RR, CO, BP

Question 18

What occurs in the vasoconstrictive phase of LPS toxicity???

Answer 18

hypodynamic phase with systemic hypotension

Question 19

how can we diagnose LPS endotoxemia??

Answer 19

CS, leukopenia, leukocytosis, neutropenia then neutrophilia

Question 20

What are the goals for tx of endotoxemia?

Answer 20

stabilize, support, bind endotoxin and neutralize bacterial toxins (LPS), inhibit mediator synthesis/release, DIC therapy

Question 21

What can we use to bind endotoxin?

Answer 21

Biosponge (PO) – binds GI toxins–> decrease absorption
Hyperimmune plasma – Ab to gram (-) bacteria
Polymyxin B – irreversibly binds to lipid A

Question 22

how can we prevent mediator synthesis and release

Answer 22

pentocphylline, omega 3 FA, TNF-alpha, anti PAF receptors, A2 antagonists