Endocrine Pathology Examples Flashcards
if adrenal cortex is hyperfunctional what hormones are likely to be affected?
aldosterone
cortisol
adrenaline
what would occur to the pituitary with elavated cortisol?
ACTH would decrese
what would occur to the contralateral adrenal with increased cortisol
atrophy
what effects does overproduction of cortisol lead to
gluconeogenic
lipolytic
protein catabolic
anti-inflammatroy
what is the difference between pituitary dependent (PDH) and adrenal dependent (ADH) canine cushing’s
pituitary: increased ACTH from pituitary –> bilateral stimulation of adrenals –> increased cortisol from both adrenals ~85% of cases
adrenal dependent: adrenal tumour –> increased cortisol from diseased gland –> negative feedback –> less ACTH from pituitary ~15% of cases
what is the third cause of Cushing’s
iatrogenic
exogenous source of steroids act in lieu of adrenal cortex (prednisone)
alopecia, fragile skin syndrome
what is adrenal medulla hypofunction
rare
what is hyperfunction of adrenal medulla
associated with functional neoplasia –> pheochromocytoma
what hormones are effected if adrenal medulla is hyperfunctional
adrenaline, noradrenaline, catecholamines
what is pheochromocytoma
most common adrenal medullary tumour
usually non-functional
but if functional –> catecholamine release –> tachycardia, edema, cardiac hypertrophy
what are possible primary causes of hypothyroidism
idiopathic follicular atrophy
lymphocytic thyroiditis (immune-mediated)
what are secondary causes of hypothyroidism
decreased TSH from pituitary disease
what are the effects of hypothyroidism (3)
decreased basal metabolic rate
decreased T3, T4
increased cholesterol
what are the metabolic findings of hypothyroidism in dogs
- lethargy
- weight gain
- exercise intolerance
what are the dermatological findings of hypothyroidism in dogs (4)
- hair thinning
- poor quality coat
- hyperpigmentation
- pyoderma
what is the primary pathology of hypothyroidism in dogs
small, often pale thyroid
what is the secondary pathology of hypothyroidism (4)
- hyperkeratosis
- hyperpigmentation
- myxedema
- atherosclerosis
what does atherosclerosis in hypothyroid dog lead to
hyperlipidemia –> endothelial damage –> monocyte adhesion + infiltration, smooth muscle migration and proliferation –> lipid accumulation, extracellularly and intracellularly in macrophages and muscle cells
what is a goitre caused by
- iodine deficiency
- iodine toxicity
- goitrogenic plants
what does a goitre result in
inadequate T3/T4 synthesis
bilateral enlargement
why does inadequate synthesis of T3/T4 lead to bilateral enlargement of the thyroid glands
inadequate thyroxine synthesis –> decreased T3/T4 recognized by the hypothalamus and anterior pituitary –> increased TSH release
what are the 3 mechanisms for development of goitre
- dietary iodine deficiency
- block of iodine uptake
- enzyme defect
what is a goitrogen
compound which result in hyperplastic goitre
what are examples of goitrogens
plants: brassica (rape, kale) –> digestion leads to thiocyanate which competes with iodide ions for absorption by thyroid follicular cells
drugs: phenobarbitone, rifampin, increase breakdown of T4 and T3
excessive iodine in diet: foals of mares fed dry seaweed
how does enzyme defect cause hypothyroidism
dyshormogenesis due to enzyme defect –> impaired thyroglobulin biosynthesis
massive enlargement of thyroid
circulatory level of T3 and T4
what is hyperthyroidism
unilateral or bilateral
common in cats
what are the causes of hyperthyroidism
- hyperplastic nodules
- adenoma
- adenocarcinoma (less common)
what is primary hyperthyroidism
multi-nodular hyperplasia –> thyroid neoplasia –> feline hyperthyroidism –> increased T3/T4 levels –> increased metabolic rate –> cardiac hypertrophy –> sudden death
what is secondary hyperthyroidism
pituitary dysfunction (very rare) –> feline hyperthyroidism –> increased T3/T4 levels –> increased metabolic rate –> cardiac hypertrophy –> sudden death
what causes parathyroid hypofunction
rare
unless surgically removed –> causes hypocalcemia
what are the causes of hypocalcemia (4)
- decreased PTH concentration (primary hypoparathyroidism, pseudohypoparathyroidism) –> decreased PTH receptor responsiveness
- inadequate Ca mobilization from bone or absorption in intestine (hypovitaminosis D, chronic renal failure, milk fever)
- excess urinary excretion of Ca: ethylene glycol toxicosis
- unknown: acute pancreatitis in dogs, urinary tract obstruction
what is rickets
dietary Ca/P/Vit D imbalance –> relative hypocalcemia –> bone resorption and abnormalities of the growth plate
how does excess urinary retention lead to hypocalcemia and what is a common cause of this
ex. antifreeze
calcium oxalate crystals form –> crystals damage kidney –> renal tubular necrosis –> hypocalcemia
what are the 3 causes of secondary hyperparathyroidism
- renal (response to chronic hypocalcemia)
- nutritional (high dietary P, low dietary Ca)
- pseudohyperparathyroidism (tumours)
how does renal secondary hyerparathyroidism occur
- chronic renal disease
- decreased golmerular filtration rate
- phosphate retention
- continued stimulation of the parathyroid gland
- continued resorption of bone
–> fibrous osteodystrophy (bone replaced by fibroblastic tissue, bone remodelling, periosteal new bone formation)
how does the normal animal respond to relative hypocalcemia
resorption from bone –> phosphate excretion in kidney –> calcium resorption in kidney
describe the pathway of secondary renal hyperparathyroidism and chronic renal failure
how does nutritional secondary hyperparathyroidism occur
dietary imbalance of calcium and phosphorus (diets with low Ca or high oxalates, diets with high P and low or normal Ca, occasionally vitamin D deficiency)
leads to increased PTH production
how does pseudohyperparathyroidism occur
humeral hypercalcemia of malignancy (HHM) –> tumours of non-endocrine origin (lymphoma, multiple myeloma, adenocarcinoma of glands of anal sac)
–> PTHrP (parathyroid hormone related peptide)
–> affected animals have trophic atrophy of the parathyroid glands
how does humeral hypercalcemia of malignancy lead to
tumour in parathyroid produces parathyroid hormone related peptide –> increased intestinal absorption, resorption from bone and decreased renal excretion of Ca –> hypercalcemia
how does functional parathyroid neoplasm lead to hypercalcemia
increased PTH –> increased intestinal absorption and resorption of Ca from bone as well as decreased renal excretion of Ca –> hypercalcemia
what type of hyperparathyroidism is function parathyroid neoplasm cause
primary
what is the clinical syndrome of pancreatic islet hypofunction
diabetes mellitus
what is pancreatic islet hypofunction caused by (4)
- vacuolar degeneration
- amyloidosis (cats)
- immune-mediated destruction (dogs)
- secondary to pancreatitis
what does diabetes mellitus occur
when does diabetes mellitus occur in cats and dogs
common in cats and dogs
in dogs –> spontaneous diabetes (1:200), middle-aged, females 2x > males, some small dog breeds increased incidence (min. poodles, dachshunds, terriers)
what are islet cell tumours
often B-cell type (insulin secreting)
can still have non-functional neoplasms and hyperplasia of the pancreas
what is an insulinoma
B-cell (insulin secreting) pancreatic islet hyperfunction
increased insulin –> hypoglycemia –> decreased glucose bioavailabilty –> neurologic signs (weakness, lethargy, collapse, seizures, nervousness)
–> adrenal medulla secretes catecholamines –> increased blood pressure
