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LA DX & TX I > Exam 3 - Endotoxemia > Flashcards

Exam 3 - Endotoxemia Flashcards

1
Q

what is endotoxemia?

A

clinical manifestation of a systemic inflammatory response to a circulating endotoxin

subset of sepsis

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2
Q

what makes the endotoxin in gram negative bacteria?

A

LPS

o specific chain

core region

lipid A - most antigenic part

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3
Q

T/F: 30% of horses with endotoxemia will not have detectable levels of endotoxins

A

true

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4
Q

what is the difference between an endotoxin & an exotoxin?

A

endotoxin - LPS attached to the outer membrane of bacterium which is liberated when the cell wall is broken

exotoxin - proteins are produced inside the bacterium & are secreted or liberated upon cell death

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5
Q

what are the 3 steps of the cellular cascade of endotoxemia?

A
  1. LBP-LPS binding to TLR
  2. NF-kB activation
  3. gene expression & products release
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6
Q

when there is activation of NF-kB, what cytokines are involved in causing clinical signs including: fever, tachypnea, leukocytosis, leukopenia, & obtundation?

A

TNF-a, IL-1, & IL-6

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7
Q

why can you see thrombosis, hemorrhage, & DIC in horses with endotoxemia?

A

activation of TF & factor VIII - these both activate intrinsic & extrinsic pathways & impair fibrinolysis which activates coagulation leading to the clinical signs

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8
Q

NF-kB activation activates ICAM-1, VCAM-1, B2 integrins, e-selectin, & chemokines leading to what cascade?

A

endothelial damage!!!! neutrophils become activated & cause release of ROS, RNS, & proteolytic enzymes which cause endothelial activation/injury leading to increased endothelial permeability (tissue injury)

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9
Q

what is the major player in vasodilation as a part of the endotoxemia cascade in NF-kB activation?

A

nitric oxide - causes hypotension, cardiovascular hyporeactivity, tissue hypoperfusion, & hypoxia

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10
Q

what do reactive oxygen species cause in endotoxemia?

A

endothelial damage & potentiation of inflammation

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11
Q

what is the major vasoactive mediator?

A

nitric oxide

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12
Q

what are the major inflammatory cytokine mediators of endotoxemia?

A

IL-1, IL-6, & TNF-a

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13
Q

what are the major procoagulant mediators in endotoxemia?

A

tissue factor & factor VIII

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14
Q

which is not produced as a result of NF-kB activation:
a. IL-10
b. TNF-a
c. IL-6
d. iNOS

A

a. IL-10

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15
Q

what 3 components make up virchow’s triad?

A
  1. hypercoagulable state
  2. endothelial damage
  3. abnormal blood flow
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16
Q

on a cellular level, what’s going wrong in endotoxemia?

A
  1. endothelial adhesion by neutrophils & reduced chemotaxis - low WBC because they are sequestered
  2. increased metabolic demands by the cell
  3. impaired oxygen use by the cell - mitochondria is not acting like the normal powerhouse
17
Q

what cardiovascular effects are seen in early endotoxemia?

A
  1. decreased preload
  2. left ventricular dysfunction
  3. arterial vasodilation
18
Q

what is the major cause of death in endotoxemia?

A

myocardial depression!!!!!!

19
Q

what 3 components of hemodynamic stability are affected in endotoxemia?

A
  1. hypovolemia
  2. abnormal perfusion distribution
  3. myocardial depression
20
Q

when comparing infection, SIRS, sepsis, severe sepsis, & septic shock, how do they differ?

A
  1. infection - microbial invasion
  2. SIRS - exaggerated inflammation, doesn’t have to have bacteria present, can be sterile
  3. endotoxemia/sepsis - exaggerated inflammation with infection
  4. severe sepsis - exaggerated inflammation with infection with organ failure
  5. septic shock - exaggerated inflammation with infection with organ failure & hemodynamic compromise
21
Q

what are the criteria for SIRS in the adult? how many must be met to be classified as SIRS?

A
  1. hypo/hyperthermia
    - <98
    - >101.5
  2. leukopenia or leukocytosis
    - <5,000/uL
    - > 14,500/uL
  3. tachycardia
    - >50 bpm
  4. tachypnea
    - > 25 bpm

just need to meet 2!!!

22
Q

what is the major other organ manifestation of endotoxemia seen in horses?

A

laminitis!!!!

23
Q

what are some examples of abnormalities seen on physical exam in a horse with endotoxemia?

A

mental dullness, congested or toxic mucus membranes, prolonged CRT, cool extremities, prolonged jugular refill, & fever

24
Q

what are some examples of clinicopathologic abnormalities seen in a horse with endotoxemia?

A
  1. early & profound leukopenia - neutropenia, left shift, toxic change, & lymphopenia
  2. glucose derangements
  3. prolonged clotting times
  4. hyperlactatemia
  5. hypocalcemia
25
Q

what is the prognosis for endotoxemia?

A

guarded at best

26
Q

what are the 5 steps of treatment for endotoxemia?

A
  1. cardiovascular resuscitation
  2. laminitis prevention
  3. eliminate cause
  4. neutralize circulating endotoxin
  5. inhibit inflammation
27
Q

what treatment components make up cardiovascular resuscitation in horses with endotoxemia?

A

early goal directed therapy!!!

expansion of blood volume - balanced polyionic crystalloid

with little improvement - retention of iv fluids, colloids

improved blood pressure - inotrope/vasopressin

28
Q

what are some risk factors of a horse with endotoxemia developing laminitis?

A

pony, BCS >5/9, > 24 hours of endotoxemia, & temp higher than 101.5

29
Q

what therapy can be used for laminitis prevention in a horse with endotoxemia?

A

prompt fluid resuscitation, NSAIDS, & cryotherapy (ice on the feet)

30
Q

what therapy can be used for eliminating the cause in a horse with endotoxemia?

A

drainage/lavage, surgical removal, antimicrobials (broad spectrum, bactericidal, but controversial with developing colitis)

31
Q

what therapy can be used for neutralizing the circulating endotoxin in a horse with endotoxemia?

A

smectite - if gut level

polymixin b - bloodstream, will only work if the toxin isn’t bound!!!

32
Q

what is the dose for flunixin for inhibiting inflammation in a horse with endotoxemia?

A

0.25 mg/kg IV every 6-8 hours

33
Q

T/F: if a foal shows up at the hospital, and you’re suspicious of endotoxemia, you should immediately provide oxygen supplementation

A

true

LA DX & TX I (45 decks)

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