Small Animal Clinical Pharmacology - CYF MEDICAL DISTRIBUTION

PARATHYROID DISEASE
Ipodate
Sodium or calcium ipodate, a cholecystographic contrast
agent that reduces thyroid hormone production,
has potential for the treatment of feline thyrotoxicosis,
although experience with the drug is limited and complicated
by lack of availability.
Mechanism of action
Although ipodate blocks the release of thyroid hormones
as a consequence of the iodine released during
its metabolism (ipodate is 63% iodine by weight), its
major effect is to inhibit the outer-ring 5’ deiodination
of T 4 to T 3. Consequently, although circulating T 4 concentration
may be unaffected by ipodate, there may be
some clinical response as T 3 production is suppressed.
Formulations and dose rates
• 100 mg/cat divided twice daily is the recommended starting
dose, administered orally
Adverse effects
No adverse side effects have been reported.
Stable iodine
Iodine is not indicated for the long-term medical management
of cats with hyperthyroidism, but has been
used (in combination with β-adrenergic blockers) for the
presurgical treatment of cats unable to tolerate thiamazole
or carbimazole. Its antithyroid effects are transient
and inhibition only lasts for a short time (approximately
2–3 weeks). Iodine can be administered in conjunction
with thiourylenes but this is rarely considered necessary
because of their potency and efficacy when used alone.
Mechanism of action
Large doses of stable iodine acutely inhibit thyroid
hormone synthesis (Wolff–Chaikoff effect) and thyroid
hormone release. The former effect is mediated through
inhibition of the enzyme thyroid peroxidase. These
effects are not consistent and serum thyroid hormone
concentrations, while often decreasing, rarely suppress
markedly. Stable iodine purportedly reduces the size and
vascularity of adenomatous thyroid tissue, although this
is controversial.
Formulations and dose rates
• The current recommendation is to use potassium iodate at a
dose of 21.25 mg three times daily for 10 days prior to surgery
in cats with prior (10 d) and concurrent propranolol treatment
Adverse effects
Side effects include ptyalism and inappetence resulting
from its unpleasant brassy taste. These can be minimized
by placing the tablets in gelatin capsules before
administration.
PARATHYROID DISEASE
Drugs used to treat parathyroid disease are rarely
directed at the parathyroid gland itself but rather correct
the derangements in calcium homeostasis resulting from
both parathyroid and nonparathyroid disorders. Irrespective
of cause, the principles of therapy for hypocalcemia
and hypercalcemia remain the same. In order to
understand the indications for and actions of the various
drugs used, an understanding of normal calcium homeostasis
and the diseases that potentially result in hypoand
hypercalcemia is important.
Relevant physiology/pathophysiology
Calcium homeostasis is controlled predominantly by
parathyroid hormone (PTH (parathormone)), and the
active form of vitamin D (1,25-dihydroxycholecalciferol
(1,25(OH) 2 D 3 ) or calcitriol) variously acting through
the kidneys, gastrointestinal tract and bone. Phosphate
homeostasis is similarly controlled although it is generally
considered to be secondary to calcium. Calcitonin,
produced by the parafollicular cells of the thyroid gland,
may also affect calcium homeostasis, although its physiological
role in dogs and cats is less clear.
Typically there are two parathyroid glands associated
with each thyroid lobe (cranial or external and caudal
or internal) although ectopic parathyroid tissue may
also be found in both dogs and cats. The chief (or principal)
cells form the major cell type of the parathyroid
glands and their primary function is to secrete PTH.
This hormone is an 84-amino acid, single-chain polypeptide
secreted in response to low plasma ionized
calcium concentration. Subsequently, calcium concentrations
are increased through a concerted action on
both bone and kidney, as follows.
● Stimulation of calcium and phosphate release from
bone with the permissive presence of 1,25(OH) 2 D.
● Increased calcium reabsorption from the
glomerular filtrate while phosphate reabsorption is
inhibited.
● Stimulation of the enzyme 1 α-hydroxylase located
in the proximal tubules of the kidney which in turn
increases the synthesis of 1,25(OH) 2 D.
● As circulating calcium is increased, PTH release is
inhibited.
Vitamin D is integral to normal calcium homeostasis.
Vitamin D is a fat-soluble vitamin. The first step in its
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