HORMONE LOGIC
This hormone class is water-soluble stored in vesicles and acts via second messengers after binding membrane receptors
what are peptide/protein hormones
the step in thyroid hormone synthesis that is directly inhibited by methimazole
iodination of tyrosine residues via thyroid peroxidase
the single laboratory abnormality most consistent with euthyroid sick syndrome
low total t4 with normal tsh
the intracellular signal that links glucose metabolism to insulin secretion
increased atp closing potassium channels
a dog with low tt4 low ft4 and elevated tsh most likely has
primary hypothyroidism
these hormones are lipid-soluble bind carrier proteins in blood and exert effects primarily by altering gene transcription
what are steroid hormones and thyroid hormones
explain why iodine deficiency leads to goiter formation despite low circulating thyroid hormone levels
increased tsh causes thyroid follicular hyperplasia
why tsh alone is insufficient to diagnose hypothyroidism in dogs
tsh secretion is episodic and may remain normal in true hypothyroidism
why glucagon has minimal effect on skeletal muscle
muscle lacks glucose-6-phosphatase
a cat with polyphagia weight loss tachycardia hypertension and vomiting has changes in this receptor population
increased beta-adrenergic receptors
a hormone that is lipid-soluble but does not follow the classic steroid synthesis pathway
thyroid hormones
most circulating t3 originates from this location rather than direct thyroid secretion
peripheral tissues via deiodination of t4
a hospitalized dog with severe systemic illness has a low total t4 but normal free t4 and normal tsh. explain why thyroid supplementation is not indicated
thyroid gland function is normal and hormone suppression is illness related
explain how insulin resistance can exist despite normal or elevated insulin concentrations
decreased receptor sensitivity or post-receptor signaling defects
explain why hypothyroid animals often have dermatologic changes before neurologic signs
hair follicles and skin have high dependence on thyroid-regulated protein synthesis
explain why binding to plasma proteins increases hormone half-life but decreases immediate biologic activity
only free hormone is biologically active while bound hormone acts as a circulating reservoir
a patient has normal total t4 but decreased free t4 explain the most likely physiologic mechanism
increased binding proteins or altered protein affinity
why hyperthyroid cats commonly develop systolic murmurs without primary valvular disease
increased cardiac output and decreased blood viscosity
a diabetic patient develops ketone bodies despite hyperglycemia explain the paradox
lack of insulin prevents cellular glucose uptake causing reliance on fat metabolism
a diabetic patient is treated aggressively with insulin and develops weakness and arrhythmias
hypokalemia due to intracellular potassium shift
insulin secretion is best categorized under this feedback configuration rather than a classic axis
what is physiological response-driven feedback
why total t4 may be normal while clinical hypothyroidism is still present
altered protein binding or non-thyroidal illness affecting hormone availability
explain why treatment of hyperthyroidism may unmask chronic kidney disease
restoration of normal gfr reveals previously masked renal insufficiency
why cats are more prone than dogs to type ii diabetes mellitus
beta-cell amyloidosis combined with insulin resistance
integrate hormone classification receptor location and feedback to explain why thyroid hormones have delayed but prolonged effects
lipid solubility intracellular receptors gene transcription and protein synthesis