Septicemia in foals Flashcards
Endotoxemia is the sum of total clinical signs caused by ____ response to circulating endotoxins
inflammatory
SIRS is systemic inflamm. response syndrome and is what?
A physiologic response to non-specific insult, stimulated by presumed or true insult (infectious or non infectious)
SIRS due to infectious insult =
SEPSIS
MODS=
multiple organ dysfunction (in acutely ill patients that require intervention to maintain homeostasis)
Sepsis – severe sepsis –
septic shock and MODS
SIRS clinically manifests as two or more of the following:
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)
LPS components:
“L”
L- lipid A
innermost, hydrophobic, anchors LPS to the outer cell wall
TOXIC principle, highly conserved
LPS components:
“P”
Core polysaccharide, middle portion, linked to lipid A by KTO, more conserved than O chain, used to stimulate cross protective antibodies
LPS components:
“O”
Specific side chain of outermost hydrophilic properties that has a lot of antigen diversity
What is the most common Endotoxin source?
GIT- gram negative bacteria that normal occurs in GI lumen, short half life
___ are apart of innate immunity and bind PAMPs
PRR
____ is an impt PRR that recognizes ____ via cytoplasmic signals
TLR4; LPS
Excess ___ mediated signaling= septic shock
TLR
How does LPS cause pulmonary hypertension??
Mediated by thromboxanes–> Increased RR (also hypoxemia, dyspnea, pulmonary hypertension)
Prostaglandin I2 causes: discolored membranes, prolonged CRT, decreased venous return, decreased cardiac output, hypotension
First part of LPS toxicity is ?
What happen after that?
1- pulm. hypertension
- hyperdynamic phase with warm shock
- vasoconstrictive phase with hypodynamic phase and decompensated shock and MODs
What occurs during pulm. hypertension from LPS toxicity?
Increased RR, dyspnea, pulmonary hypertension, discolored membranes, prolonged CRT decreased venous return, decreased CO, decreased BP
What occurs during the warm shock phase/hyperdynamic phase of LPS toxicity??
Vasodilation and peripheral vascular pooling, reduced diastolic pressure, warm extremities, INCREASEDDDD RR, CO, BP
What occurs in the vasoconstrictive phase of LPS toxicity???
hypodynamic phase with systemic hypotension
how can we diagnose LPS endotoxemia??
CS, leukopenia, leukocytosis, neutropenia then neutrophilia
What are the goals for tx of endotoxemia?
stabilize, support, bind endotoxin and neutralize bacterial toxins (LPS), inhibit mediator synthesis/release, DIC therapy
What can we use to bind endotoxin?
Biosponge (PO) – binds GI toxins–> decrease absorption
Hyperimmune plasma – Ab to gram (-) bacteria
Polymyxin B – irreversibly binds to lipid A
how can we prevent mediator synthesis and release
pentocphylline, omega 3 FA, TNF-alpha, anti PAF receptors, A2 antagonists
