Sunday, February 11, 2018

Acid Base Disorders, Calcium Disorders, Chloride-Bicarbonate Exchange

[Note: most of this page is quotes from the links they fall under.  Everything in italics and brackets are my notes, not quotes.]

Acid Base Disorders - Merck Manuals

From this article:
Acid-base disorders are pathologic changes in arterial pH and carbon dioxide partial pressure (Pco2), and in serum bicarbonate (HCO3).
  • Acidemia is serum pH < 7.35.
  • Alkalemia is serum pH > 7.45.
  • Acidosis refers to physiologic processes that cause acid accumulation or alkali loss.
  • Alkalosis refers to physiologic processes that cause alkali accumulation or acid loss.
Actual changes in pH depend on the degree of physiologic compensation and whether multiple processes are present.

Metabolic causes of Acidemia (acidic):
  • Insulin resistance
  • Inhibition of anaerobic glycolysis [production of lactic acid from glucose - hypoglycemia affect this?]
  • Reduction in ATP synthesis
  • Hyperkalemia - [high serum potassium levels]
  • Protein degradation
  • Bone demineralization (chronic)
[Some horses have hyperkalemia due to cellular breakdown after tying up.  Protein degradation - PSSM2 variant horses suffer from muscle atrophy and protein loss - will this push them into Acidemia?  During his period of exercise intolerance, my horse seemed to suffer from hypoglycemia - did this inhibit anaerobic glycolysis and cause Acidemia?]

Metabolic causes of Alkalemia (alkaline):
  • Stimulation of anaerobic glycolysis
  • Formation of organic acids
  • Decreased oxyhemoglobin dissociation
  • Decreased ionized calcium - [low serum calcium levels]
  • Hypokalemia - [low serum potassium levels]
  • Hypomagnesemia - [low serum magnesium levels]
  • Hypophosphatemia - [low serum phosphorous levels]
Increased anion gap is most commonly caused by metabolic acidosis in which negatively charged acids—mostly ketones, lactate, sulfates, or metabolites of methanol, ethylene glycol,or salicylate—consume (are buffered by) HCO3. Other causes of increased anion gap include hyperalbuminemia [an increased concentration of albumin in the blood. Typically, this condition is due to abrupt dehydration.  Albumin - a simple form of protein that is soluble in water and coagulable by heat, such as that found in egg white, milk, and (in particular) blood serum.]  and uremia (increased anions) and hypocalcemia or hypomagnesemia (decreased cations).

[Unfortunately I've learned that dehydration causes quite a bit of blood in urine.  Bloody urine is usually associated with muscle degradation and protein loss - is 'albumin' moving from muscle into blood serum part of that? Is this another hint that Acidemia is part of Jax's issues?]

Decreased anion gap is unrelated to metabolic acidosis but is caused by hypoalbuminemia (decreased anions); hypercalcemia, hypermagnesemia, lithium intoxication, and hypergammaglobulinemia as occurs in myeloma (increased cations); or hyperviscosity or halide (bromide or iodide) intoxication. The effect of low albumin can be accounted for by adjusting the normal range for the anion gap 2.5 mEq/L downward for every 1-g/dL fall in albumin.

Recognizing and treating disorders of calcium metabolism in horses - DVM 360

"Shifting leg lameness and stiffness have been reported with Ca/P imbalance as is seen with nutritional hyperparathyroidism."

[RER (including Px gene) is a defect in the calcium channel of muscles - the muscle won't release the calcium and won't relax - is this related in any way?]

"High blood calcium concentrations caused by inappropriate increase in PTH secretion from the parathyroid gland is termed primary hyperparathyroidism. Because parathyroid tissue is found up and down a horse’s neck from the thoracic inlet to the thyroid gland, identifying the causative tissue and removing it is often extremely difficult."

"Secondary hyperparathyroidism occurs when calcium is wasted and phosphorus is in excess. If this occurs via dietary imbalance, it is termed nutritional hyperparathyroidism. In instances of renal failure, the increased blood P due to decreased renal clearance results in increased PTH secretion. In extreme cases “big head”, or fibrous osteodystrophy can develop. In less severe cases, horses may present with indeterminate lameness and stiffness."

Chloride--bicarbonate exchange in red blood cells: physiology of transport and chemical modification of binding sites.

"About 80% of the CO2 formed by metabolism is transported from tissues to lungs as bicarbonate ions in the water phases of red cells and plasma. The catalysed hydration of CO2 to bicarbonate takes place in the erythrocytes but most of the bicarbonate thus formed must be exchanged with extracellular chloride to make full use of the carbon dioxide transporting capacity of the blood. The anion transport capacity of the red cell membrane is among the largest ionic transport capacities of any biological membrane. Exchange diffusion of chloride and bicarbonate is nevertheless a rate-limiting step for the transfer of CO2 from tissues to lungs. Measurements of chloride and bicarbonate self-exchange form the basis for calculations that demonstrate that the ionic exchange processes cannot run to complete equilibration at capillary transit times less than 0.5 s. The anion exchange diffusion is mediated by a large transmembrane protein constituting almost 30% of the total membrane protein. The kinetics of exchange diffusion must depend on conformational changes of the protein molecule, associated with the binding and subsequent translocation of the transported anion. We have characterized the nature of anion-binding sites facing the extracellular medium by acid-base titration of the transport function and modification of the transport protein in situ with group-specific amino acid reagents. Anion binding and translocation depend on the integrity and the degree of protonation of two sets of exofacial groups with apparent pK values of 12 and 5, respectively. From the chemical reactivities towards amino acid reagents it appears that the groups whose pK = 12 are guanidino groups of arginyl residues, while the groups whose pK = 5 are likely to be carboxylates of glutamic or aspartic acid. Our studies suggest that the characteristics of anion recognition sites in water-soluble proteins and in the integral transport proteins are closely related."

[So if the horse isn't getting enough chloride, they can't make bicarbonate, and will suffer acidemia.  Is this why baking soda has been helping my horse?  Also, arginyl residues, and carboxylates of glutamic or aspartic acid - Jax's feed that has really helped contains high levels of arginine, glutamic acid, and aspartic acid.]

About the Artist:

horse artist, equine artist, PSSM horse
Since starting my art business in 2004, I have been on a roller coaster ride that's taken me from art, to house flipping, to legal assistant, to horse trainer, and a full 180* back to my artworks.

I'm thankful to get back to my art, and also for the life experiences I've gained.

Things in life that matter the most!  Jen, husband Jared, and Jax

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