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endocrine gland and organ abnormalities
dysfunction originating in the peripheral endocrine gland (primary disorders)
pituitary gland
Hyperfunction: Hyperplasia or neoplasia
Hypofunction: autoimmune disorders, tumors, infections, vascular disorders, toxins
abnormal tissue responses to hormones
blockage of conversion from secretion to active form
treatment
hypofunction = replacement of peripheral endocrine hormone
hyperfunction = radiation therapy, surgery, drug to suppress hormone production
Thyroid
Iodine-dependent gland
triiodothyronine (T3) and thyroxine (T4)
regulate the body’s metabolism by stimulating cells in the body to produce proteins
increases cellular metabolism
calcitonin
physiological responses
tachycardia
tissue growth and development
thermoregulation
energy consumption
PE, patient history, and blood chemistry tests
normal thyroid gland function
Hypothalamus » releases Thyrotropin-Releasing Hormone (TRH)
TRH stimulates nearby pituitary gland
Pituitary gland is stimulated to release Thyroid-stimulating Hormone (TSH)
Pituitary TSH stimulates the thyroid gland to produce triiodothyronin (T3) or thyroxin (T4)
thyroid gland control
T3 and T4 are released into the blood and taken up by cells in the body to increase the body’s metabolic rate
T3 is the biologically active form of thyroid hormone (even though produced less than T4)
T4 is converted by enzymes in the body tissues to T3 (removing an iodine converts T4 → T3)
T4 acts as a circulating precursor reservoir of hormone to be converted to T3 as needed
T3 and T4 provides negative feedback
Hypothyroidism
low T4, high TSH
weight gain, bradycardia, lethargy, bilateral alopecia, dull/brittle hair, thin skin
treatment depends to T3 and T4 levels in the blood
free T4 level (fT4) » circulating in blood, not bonded to protein
will be low cause gland not responding
thyroid stimulating hormone (TSH)
pituitary keeps producing TSH which will be elevated cause keeps producing cause no thyroid hormones produced
synthetic hormone supplementation with regular hormone level monitoring
Levothyroxine
MOA:
synthetic T4
preferred over synthetic T3 (liothyronine)
has longer half life so needs to be dosed less frequency
Use:
hypothyroidism - treatment of choice
Forms:
Soloxine; Thyro-Tabs
Side Effects:
Rare
Notes:
therapeutic monitoring - make sure do not over supplement and cause hyperthyroidism
Hyperthyroidism
excessive TT4 or FT4
commonly caused by benign hyperplasia (adenoma on thyroid gland)
weight loss, polyphagia, tachycardia, polyuria/polydipsia
treatment options:
thyroidectomy, radioiodine therapy, anti-thyroid drug (ex: methimazole), iodine-limiting prescription diet
choice based upon:
cost
client ability/willingness to administer daily medication life long
anesthetic/surgical risk
Methimazole
MOA:
interferes with incorporation of iodine into precursors of T3 and T4
Use:
feline hyperthyroidism
Forms:
transdermal, oral liquid, or tablet
Felimazole
Tapazole
Side Effects:
v+, anorexia, facial irritation
Notes:
Carbimazole » another drug that is converted to Methimazole
therapeutic monitoring - make sure don’t over suppress and cause hypothyroidism
monitor renal values - hyperthyroidism causes hypertension and improves renal excretion and once controlled pressure normalizes and renal perfusion decrease to normal and can “unmask” renal disease
Radioactive Iodine
MOA:
beta emission destroys over-productive thyroid tissue
Use:
Feline Hyperthyroidism
Forms:
Radioactive iodine (I-131); SQ, IV
Notes:
Cat housed in special facility since will excrete radiation in feces, urine
after 3 days - 3 weeks cat is released
Limited number of facilities that perform procedure
Dietary Food
MOA:
prevent formation of T3/T4 by limiting iodine needed to create the hormones
clinically proven nutrition to restore thyroid health
improves thyroid health in 3 weeks
complete daily nutrition
Nursing Info
because iodine intake from other food sources - treats, another pet’s food, etc - can compromise the effectiveness of low-iodine nutrition, it’s critical that only y/d if fed exclusively