Manual of Equine Anesthesia and Analgesia. Группа авторов

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raises the serum indirect concentration.

       Reduced feed intake raises the serum indirect concentration as a result of slowed clearance of bilirubin from the blood rather than from its overproduction. However, the cause is uncertain.Ligandin, a protein responsible for bilirubin uptake into the liver may be decreased in the fasting horse, as has been demonstrated in rats.Free fatty acids may play a role in fasting hyperbilirubinemia, and horses develop significant hyperlipidemia during fasting. This may result in competition for carrier proteins.Increases in unconjugated bilirubin occur after 12 hours of fasting.

       Neonates have higher bilirubin values due to immaturity of liver processing.This can lead to kernicterus, resulting from unconjugated bilirubin causing neurologic damage. However, this condition is extremely rare in foals, and may be more likely to occur in a foal with neonatal isoerythrolysis.

      G Serum bile acids (SBA)

       Bile acids are synthesized and secreted by the liver.

       Bile acids are removed from the portal blood by hepatocytes, and SBA concentrations increase as hepatic function decreases.

       Increase in SBA concentration is an indicator of hepatic dysfunction.

       Reference range: 0–20 μmol/l.

       Bile acids are not affected by fasting.

       Only a single blood sample is required instead of pre‐ and post‐feeding samples, as bile is released continuously because the horse lacks a gallbladder.

      H Blood urea nitrogen (BUN) andcreatinine(Cr)

       Increased BUN and or Cr indicates that the horse suffers from either pre‐renal, renal, or post‐renal azotemia.

       Reference range for BUN is 4.2–8.9 mmol/l and for Cr is 80–130 μmol/l.

       In contrast to urea nitrogen, Cr is not reabsorbed within the tubules, so serum Cr concentrations provide a more accurate measurement of glomerular filtration rate (GFR) than does BUN.

       Neonates have higher Cr values, and the value declines over the first week of life.

       Pre‐renal azotemia

       Occurs when the increases in BUN and Cr results from a decrease in renal blood flow and the associated decrease in GFR.

        Significant (>75%) decreases in GFR are required before the BUN is increased, especially early in disease.Most commonly results from dehydration and circulatory shock.

       When renal function is adequate (pre‐renal), azotemia is accompanied by a urine specific gravity (USG) > 1.025.This indicates that the kidney has the ability to concentrate the urine.

       Uroperitoneum secondary to bladder rupture in foals also causes pre‐renal azotemia.

       Renal azotemia

       Occurs when the GFR is low due to acute or chronic kidney injury.

       BUN may be low because less of the filtered urea is re‐absorbed in the proximal tubule.

       Serum Cr increases as filtration decreases.

       Diagnosed by concurrently measuring the USG.The presence of azotemia in a patient that cannot concentrate their urine (USG < 1.020) indicates kidney injury.

       Post‐renal azotemia

       Is associated with mechanical (e.g. uroliths) or functional (e.g. neurogenic bladder dysfunction) obstruction of the urinary tract.

       It is uncommon in horses.

      III Plasma proteins

       Blood consists of plasma and solid components.

       Plasma comprises about 55% of the blood volume.

       Plasma contains about 90% water, and the remaining 10% consists of ions, proteins, dissolved gases (primarily nitrogen, oxygen, and carbon dioxide), nutrients, and wastes.

       Total protein reference range for adult horse: 6.5–7.5 g/dl.Plasma protein value is approximately 0.3–0.5 g/dl greater than serum protein.

       The proteins in plasma include the globulins, albumin, fibrinogen, and coagulation factors.

       A hand‐held refractometer can be used to measure total solids, which are an estimate of total protein; however, the readings can be affected by other substances in the plasma.This is because refractometer scales are calibrated against normal serum, and values of many non‐protein solutes (e.g. electrolytes) vary in the population.Thus, it may be prudent to evaluate albumin and globulin concentrations separately in some disease states.

      A Albumin

       Albumin is the main protein present in plasma.

       The reference range is 2.7–3.7 g/dl.

       Its main function is the regulation of the colloidal osmotic pressure (COP) of blood.

       It accounts for 75–80% of the COP of normal plasma, although it only comprises 50–60% of the total protein content of plasma.

       The oncotic effect of albumin is enhanced by its ability, due to its negative charge, to attract cations, particularly Na+.This is termed the Gibbs‐Donnan effect.

        Albumin is the smallest plasma protein in molecular weight (~66 kDa).

       Albumin binds water, ions, fatty acids, hormones, bilirubin, and therapeutic compounds.

       It is synthetized by the liver and has a plasma half‐life of approximately 19 days in the horse.

       Albumin is classified as a negative acute phase reactant because its production is down‐regulated during inflammation.

       Hypoalbuminemia can result from:

       Increased loss (most common cause).Gastrointestinal (GI) (e.g., bacterial‐induced colitis).Vasculitis, peritonitis, and pleuritis.Renal – due to glomerular disease.

       Reduced synthesis.End‐stage or diffuse liver disease.Chronic inflammation.

       Excessive catabolismMost likely due to starvation.Plasma proteins are a rapid source

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