Endocrine Pathology Flashcards
what are the mechanisms of endocrine disease
- hypofunction (primary and secondary)
- hyperfunction (think tumours, primary and secondary)
- endocrine dysfunction due to neoplasia
- failure of target cell response
- abnormal hormone degradation
what are the 3 types of intercellular signalling
- autocrine (target sites on same cell)
- paracrine (secretory cell –> adjacent target cell)
- endocrine (hormone secretion into blood by endocrine gland)
what are the clinical results of endocrine disease (4)
- skin: alopecia, hirsutism
- nervous system: seizures
- urinary system: polyuria
- skeletal: fractures
what hormones are released by the anterior (adenohypophysis)
growth hormone (GH)
adrenocorticotrophic hormone (ACTH)
thyroid-stimulating hormone (TSH)
follicle-stimulating hormone (FSH)
luteinizing hormone (LH)
melanocyte-stimulating hormone (MSH)
prolactin (PRL)
what hormones are released by the posterior pituitary (neurohypophysis)
anti-diuretic hormone (ADH)
oxytocin
what are the main reasons for hypofunction (2)
- failure to develop (aplasia, hypoplasia)
- damage to secondary disease (inflammation, neoplasia, trauma)
what are the causes of hyperfunction
tumour
benign hyperplasia
what are the causes primary anterior pituitary hypofunction
- aplasia/hypoplasia: congenital, toxic, viral –> destruction secondary to space occupying
- lesion: cystic Rathke’s pouch, abscess, neoplasm
what are the secondary causes of anterior pituitary hypofunction
hypothalamic malfunction
what are the various causes of anterior pituitary hypofunction (TSH, GH, ACTH, FSH/LSH)
- decreased TSH –> decreased T3/T4 –> hair coat alterations –> altered metabolism and growth
- decreased GH –> altered metabolism and growth
- decreased ACTH –> decreased cortisol –> altered metabolism and growth, delayed parturition
- decreased FSH/LSH –> infertility or sub-fertility
what are the causes of pituitary dwarfism
- decreased growth rate
- abnormal hair coat
- hypoplasia of gonads and genitalia
- delayed permanent dentition, epiphyseal closure
what can anterior pituitary dwarfism cause in certain breeds
congenital cysts of Rathke’s pouch (no/very little adenohypophysis)
what does posterior pituitary hypofunction cause
diabetes insipidus
what is primary diabetes insipidus caused by
- destruction of neurohypophysis –> no anti-diuretic hormone (ADH), trauma, neoplasia, congenital defects, immune mediated
- central diabetes insipidus
what is secondary diabetes insipidus caused by
- nephrogenic diabetes insipidus (renal tubules can’t respond to ADH)
what is the role of ADH
increased permeability of collecting tubules and ducts –> resorption of water –> concentration of urine
what is the most common cause of pituitary hyperfunction
functional neoplasms
- adenoma
- adenocarcinoma
what are other causes of pituitary hyperfunction
- pituitary hyperplasia
- pituitary dependent hyperadrenocorticism (PDH)
what does anterior pituitary hyperfunction lead to

when is pituitary hyperplasia common
in aged dogs
hyperplastic nodules/microadenomas
hyperadrenocorticism (cushing’s syndrome)
what are the clinical symptoms of pituitary hyperplasia
- non-pruritic alopecia
- comedones with dystrophic calcification
- flaccid abdominal wall due to muscle wasting
- canine cushings calcinosis cutis
- cushing’s: vascular hepatopathy –> increased glucose and glycogen metabolism –> increased deposits of lipid and glycogen
when is equine pituitary hyperplasia common
in aged horses (>15yo)
what are the causes of equine pituitary hyperplasia
adenomatous hyperplasia, microadenomas, adenomas of pars intermedia
what is equine pituitary pars intermedia dysfunction (PPID)
pathogenesis different to cushing’s disease in dogs
normal equine pars intermedia under dopaminergic control from hypothalamus, seasonal decrease in autumn allows hair coat growth and deposition of fat
dopamine is decreased all year without inhibition, melanotrophs of pars intermedia synthesize excessive hormones, hyperplasia, micro and macroadenomas develop
what are the signs related to deranged hypothalamic function in horses
- polyphagia, polyuria, polydipsia
- hyperglycemia
- laminitis
- generalized hyperhidrosis (sweating)
- somnolence
- striking hypertrichosis (hirsutism)
what is the pathogenesis of PPID
- pressure atrophy & degeneration of hypothalamus
- inability to control appetite (polyphagia)
- excessive food intake –> hypersinulinemia
- down-regulation of insulin receptors on target cells
- insulin-resistant hyperglycemia –> glycosuria

what is equine metabolic syndrome
younger horses/ponies
what does equine metabolic syndrome cause
- increased adiposity (regional –> neck crest, lumbar fat pads)
- insulin resistance
- laminitis
- altered E metabolism, adipocyte function, promote thrombosis, induce inflammation and oxidant stress, alter vascular endothelial cell function
how do you differentiate PPID from EMS
- age of onset (EMS –> younger)
- further clinical signs suggestive of PPID (delayed/failed coat shedding, hirsutism, excessive sweating, PUPD, skeletal muscle atrophy)
- positive diagnositc test for PPID (increased plasma ACTH without pain, stress)
what is adrenal cortical hypofunction
Addison’s disease
what does addison’s disease cause
adrenal cortical atrophy (idiopathic, any damage –> infectious, vascular, drug induced) or secondary to pituitary hypofunction
what is the pathogenesis of adrenal cortex hypofunction

what is adrenocrotical hemorrhage
waterhouse friderichsen syndrome
horses
massive, diffuse often bilateral hemorrhage in overwhelming sepsis
how is PPID diagnosed
increased plasma ACTH without pain, stress