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IVECCS 2016 MDR: Physiology of the Endothelial Glycocalyx

IVECCS 2016 MDR: Physiology of the Endothelial Glycocalyx

IVECCS 2016 MDR: Physiology of the Endothelial Glycocalyx

Meghan Harmon, DVM, DACVECC
Meghan Harmon, DVM, DACVECC
on behalf of Veterinary Emergency and Critical Care Society

$ 40.00 $ 40.00 $ 40.00

$ 40.00 $ 40.00 $ 40.00

$ 40.00 $ 40.00 $ 40.00
$ 40.00 $ 40.00 $ 40.00
Normal Price: $ 40.00 $ 40.00

Review:

Launch date: 01 Nov 2016

Expiry Date:

Last updated: 26 Oct 2017

Reference: 166873

$ 40.00 $ 40.00 $ 40.00
$ 40.00 $ 40.00 $ 40.00
IVECCS 2016 MDR: Physiology of the Endothelial Glycocalyx
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No Exam Available

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Course Availability

This course is only available to trainees days after purchase. It would need to be repurchased by the trainee if not completed in the allotted time period. This course is no longer available. You will need to repurchase if you wish to take the course again.

Description

This lecture reviews the relevant anatomy and function of the endothelial glycocalyx. Specifically, this lecture will focus on the Revised Starling Model and how this newer model of fluid flux differs from the Classical Starling Model. In addition to fluid and solute transport across the membrane, this lecture will also discuss how common pathological conditions (e.g., inflammation, fluid loading, sepsis) impact the endothelial glycocalyx and further treatment of these critical patients.

Objectives

Understand Starling’s Classical Model of fluid filtration
Fluid movement between the interstitial and intravascular space occurs across a semi-permeable capillary membrane. Fluid movement between the two compartments depends on the hydrostatic pressure difference and the oncotic pressure gradient between the interstitial and circulatory space. In normal capillaries, fluid filtration occurs over the arterial end of the capillary, and reabsorption occurs over the venular end of the capillary, as capillary pressure decreases over the length of the capillary.
Learn the anatomy of the endothelial glycocalyx
The endothelial glycocalyx provides a structural framework for endothelial cells to interact with soluble plasma components, such as proteins and lipids. The EG is comprised of macromolecules, which include proteoglycans, glycosaminoglycans, glycoproteins, and polysaccharides. These macromolecules vary in the size of the core protein, number of glycosaminoglycan side chains, and location in the glycocalyx.
Learn the Revised Starling Principle
In the Revised Starling Model, the oncotic pressure within the interstitial space (πi) is replaced by the oncotic pressure of the interstitial fluid residing in the subglycocalyx space between endothelial cells (πg). Therefore, fluid filtration (Jv) depends on the transendothelial pressure difference (Pc – Pi) and the COP gradient between the plasma and subglycocalyx space (πp - πg). Therefore, the filtration force = (Pc-Pi) - σ (πp - πg).
Understand how the glycocalyx modulates inflammation and coagulation
In health, the glycocalyx prevents red blood cells, leukocytes and platelets from interacting with the endothelium. However, when the endothelium is damaged, leukocytes and platelets bind adhesion glycoproteins, enhancing inflammation.
Understand the importance of the endothelial glycocalyx in disease states (e.g., sepsis, trauma, fluid loading) and how components of the glycocalyx can serve as biomarkers of illness severity
Sepsis, trauma, and volume loading result in shedding of the endothelial surface layer (ESL). The end result of ESL shedding is tissue edema and multi-organ dysfunction. The ESL is home to many important anticoagulant proteins and enzymes, therefore, loss of this layer results in alterations in coagulation. Recently, studies have documented that serum hyaluronan and syndecan-1 concentrations may be useful biomarkers of illness severity in certain disease states.
Know the current literature regarding therapeutic interventions for glycocalyx shedding and destruction
In animal models of endothelial surface layer (ESL) damage, replenishment of the ESL occurred after 5-7 days. While numerous studies are attempting to discover how to repair the ESL once damaged, a better strategy may lie in prevention of ESL shedding. Current therapies include the replenishment of exogenous glycosaminoglycans, maintenance of normal plasma protein levels, inhibition of damaging proteases, and prevention of hyperglycemia and hypercholesterolemia. Other strategies involve altering the immune response through the action of antioxidants, inflammatory modulators, and inhalant anesthetics.
Meghan Harmon, DVM, DACVECC

Author Information Play Video Bio

Meghan Harmon, DVM, DACVECC
on behalf of Veterinary Emergency and Critical Care Society

Clinical Instructor, Small Animal Emergency and Critical Care. A graduate of the University of Indianapolis (BS) and University of Missouri (DVM), Meghan Harmon completed an internship at North Carolina State University and residency at Michigan State University. She joined the MU faculty in October 2014. Research interests: coagulation; trauma; immune-mediated disease. Clinical interests: post-operative critical case management; polytrauma; abnormalities in hemostasis

Current Accreditations

This course has been certified by or provided by the following Certified Organization/s:

  • AAVSB-Registry of Approved Continuing Education (RACE)
  • 0.25 Hours -
    Exam Attempts: 3
    -
    Exam Pass Rate: 70

Faculty and Disclosures

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