Page 168 - Basic Monitoring in Canine and Feline Emergency Patients

Dietary intake Passive
phosphorus
VetBooks.ir calcitriol Kidney
diffusion
Phosphorus
Active GI filtered
mucosal
transport
Inorganic FGF-23
phosphorus --
bloodstream PTH
80–90% (or 0–20% (or
more) more) lost in
reabsorbed
Cell urine
membranes
Other ATP Bone

Fig. 8.3. Basic phosphorus (P) metabolism. Inorganic phosphorus is ingested in the diet and then either diffuses
into the bloodstream or is actively transported across gastrointestinal (GI) mucosal cells into the bloodstream from
the gastrointestinal lumen. Active transport of phosphorus from the GI lumen is upregulated in the presence of
calcitriol. Once in the bloodstream, the inorganic phosphorus can be incorporated into multiple structures including
cell membranes, ATP, and the bony matrix, in addition to playing a role in the coagulation system and white blood
cell function. Phosphorus in turn is filtered at the level of the kidney where it is either reabsorbed or lost in the urine.
Phosphorus loss in the kidney is increased in the presence of parathyroid hormone. Osteocyte production of fibroblast
growth factor 23 (FGF-23) in response to hyperphosphatemia also increases renal excretion of phosphorus. See
Fig. 8.2 for more information about regulation of PTH and calcitriol. ATP, adenosine triphosphate; GFR, glomerular
filtration rate; PTH, parathyroid hormone.

leukocytes, and compromised platelet functional- of vomiting, lethargy, or polyuria/polydipsia attrib-
ity/lysis of platelets. Red blood cells also have less utable to kidney failure.
2,3 diphosphoglycerate (2,3 DPG – see Chapter 4)
and cannot release oxygen as readily to the tissues.
If muscle cells lyse due to hypophosphatemia Potassium
(rhabdomyolysis), patients can be weak or in pain, Potassium is the primary cation found within cells.
and eventually decreases in cellular energy (ATP) Its concentration is similar to the extracellular con-
will alter brain functions and lead to encephalopa- centration of sodium, helping to maintain the elec-
thies and mentation changes. Changes in heart mus- trochemical balance. The majority of potassium
cle functions and/or arrhythmias can also occur in (66–75%) is contained within muscle cells. The
severe hypophosphatemia, as can GI signs includ- primary role of potassium is maintaining the rest-
ing ileus, vomiting, and diarrhea. ing membrane potential of the cell, specifically
In contrast, hyperphosphatemia leads to a playing an important role in repolarization of mus-
decrease in the serum calcium concentration by cle and nerve cells during each action potential.
reducing the activity of 1-α hydroxylase (and there- Therefore, alterations in potassium (especially
fore reducing calcitriol production; see Fig. 8.2) as hyperkalemia) can lead to arrhythmias which can
the body attempts to prevent the phosphorus × potentially be life threatening. See Fig. 8.4 for an
calcium product from exceeding 60–70 which will overview of potassium metabolism.
place the animal at risk for calcification of tissues. It is important to understand that the potassium
Therefore, the clinical signs seen with hyperphos- concentration in the bloodstream is in proportion
phatemia are typically related to hypocalcemia to the potassium levels in the intracellular compart-
(see the Calcium section). Since hyperphosphatemia ment. Therefore, when blood potassium levels are
is often associated with calcification of tissues low, it means the intracellular compartment is
and resulting disruption of tissue function, espe- also depleted of potassium. Similarly, if a patient
cially in the kidneys, patients may also display signs is hyperkalemic, the intracellular compartment is

160 E.J. Thomovsky