Endocrine – Anatomic Pathology Flashcards
Endocrine Pathologic Processes
- Proliferation
* Neoplasia
* Hyperplasia
> Diffuse (↑ stimulation or ↓ feedback)
> Multifocal (often idiopathic)
> Focal (often incidental) - Atrophy
* Lack of trophic hormone
* Idiopathic
* Compression - Inflammation
* Immune-mediated > infectious
Endocrine Neoplasia - functional vs non-functional effects
Functional
* Distant effects, in target tissue(s) of overproduced hormone(s)
> Size doesn’t always matter
<><><>
Non-functional
* Local effects, compression and destruction of adjacent tissues
> Size matters more
Pituitary gland Pathological Processes
Adenohypophysis (pars: distalis, intermedia, tuberalis) ie. anterior pituitary
* Cysts
* Neoplasia
* Inflammation
<><><>
Neurohypophysis (pars nervosa) ie. posterior
* Diabetes insipidus
* Neoplasia
> Pituicytoma
pituitary cysts
- where are they derived from
- anatomy
- importance? effects?
Derived from different aspects of pituitary gland
* Distal end of the craniopharyngeal duct
* Proximal end of the craniopharyngeal duct
* Failure of differentiation of the oropharyngeal ectoderm of Rathke’s pouch
> Remnants, common
<><><><>
* Typically incidental unless large, but can:
* Exert pressure on other structures
> Consequences dependent on affected structures
> Rupture can lead to inflammation and fibrosis
pituitary
Large or Invasive Tumour/Cyst Consequences
Lack of secretion of pituitary trophic hormones:
* Trophic atrophy and subnormal function adrenal cortex
and thyroid gland
* Gonadal atrophy
* Failure to attain somatic maturation
<><><>
Water metabolism disturbances
* Interference with the release and synthesis of antidiuretic hormone (ADH)
<><><>
* Deficits in cranial nerve function
* CNS dysfunction caused by extension into the overlying brain
Juvenile Panhypopituitarism
- what is this? what happens?
- Dx
- Pituitary dwarfism
<><><><> - Dogs, also seen in cats and other species
> German Shepherds most common - Deficiency in GH, TSH, prolactin, and gonadotropins
> ACTH = N or ↓ - Normal: birth up to ~2 mos, then…
> Slower growth rate, retention puppy hair, lack primary guard hairs
> Bilaterally symmetrical alopecia develops gradually
> Often progresses to complete alopecia (except for head and tufts of hair on legs)
> Progressive skin hyperpigmentation, until uniformly brown-black - Dx: compare littermates, radiographs (open epiphyseal lines), thyroid function tests, skin biopsy, serum GH or IGF-1
pituitary neoplasia:
Corticotroph (ACTH-secreting) adenoma
- where? effects? who?
- Pars distalis (or pars intermedia) -> produce ACTH -> ↑ cortisol from adrenal gland = pituitary dependent hyperadrenocorticism
- Dogs
pituitary neoplasia:
Pars intermedia (melanotroph) adenoma
- what happens? who?
- POMC-derived peptides
- Pituitary pars intermedia dysfunction
(PPID) - Horses
pituitary neoplasia:
Somatotroph adenoma
- what is it? effects?
- Growth hormone (GH)-secreting acidophils (somatotrophs)
- Infrequent in animals
- Large, indent hypothalamus, extend into overlying brain
- Hypersecretion of GH -> acromegaly
- Insulin-resistant diabetes mellitus in cats
> Increased GH -> downregulation of insulin receptors
pituitary neoplasia:
Suprasellar germ cell tumour (craniopharyngioma)
- what is it? who gets it? origins?
non-functional tumour
* Young animals
* Derived from epithelial remnants of the oropharyngeal ectoderm of the craniopharyngeal duct (Rathke’s pouch)
inflammation of the pituitary can occur how?
Systemic disease
* Bacterial septicemia in ruminants
<><><><>
Regional disease (extension)
* Suppurative meningitis
* Trauma from fighting or dehorning
* Inner ear
* Tooth root
* Sinuses
Diabetes Insipidus
- what is it?
- forms?
Large volumes of hypotonic urine with polydipsia
* Urine osmolality decreased below normal plasma osmolality
<><><><>
Hypophyseal form
* Inadequate antidiuretic hormone (ADH) production
> Compression and destruction of the pars nervosa, infundibular stalk, or supraoptic nucleus in the hypothalamus
=> Cysts, neoplasia, granulomas, skull trauma with hemorrhage
<><><>
Nephrogenic form
* Lack of response in target cells to normal or high ADH
Adrenalitis
- what causes it? why here?
- Infectious and parasitic agents
<><><><>
Why? - High local concentration of anti-inflammatory steroids in the adrenal cortex suppresses local cell-mediated immunity
> Permits the preferential progressive growth of certain fungi, protozoa, and bacteria
adrenal hemorrhage - when do we see it?
- Newborn animals
- Stress response
- Secondary infarct
> toxemia
> septicemia
Hyperplasia of the adrenal Medulla
- what we see, when
- Diffuse or nodular
> Can precede the development of pheochromocytoma in bulls with C-cell tumours
Hyperplasia of the adrenal Cortex
- types we see
- Nodular cortical hyperplasia (and accessory cortical nodules)
> Common, incidental, non-functional in aged dogs
<><> - Diffuse cortical hyperplasia
Hyperadrenocorticism (Cushing’s)
- origins, rates
- Pituitary (functional corticotroph adenoma) = 85%
- Adrenal (functional adrenal neoplasm) = 15%
> adenoma or carcinoma
Hyperadrenocorticism: Ferret
- anatomic variations
- what it produces
- associated with what other condition?
Adrenal enlargement
* Bilateral
> Diffuse or nodular hyperplasia
* Unilateral
> Adrenocortical adenoma/carcinoma
=> Carcinoma more common
=> More common on left
<><><><>
Overproduction of estrogenic steroids
* Estradiol 17-β
<><><><>
1⁄3 ferrets with adrenocortical tumours also have neoplasms derived insulin producing β-cells of the pancreatic islets
* Hypoglycemia
Hyperadrenocorticism: Ferret pathogenesis, clinical signs
Ferret, pathogenesis:
* Early gonadectomy -> loss of negative feedback on pituitary gonadotrophs -> increase LH secretion -> stimulation & proliferation of zona reticularis of the adrenal cortex -> sex steroids overproduction
<><><><>
Gross/Clinical signs:
* bilaterally symmetrical alopecia, sexual behaviour, swollen vulva
Neoplasias of the adrenal Cortex
- what types?
- species? anatomy?
Adenomas
* Dogs > years
> Sporadically in horses, cattle sheep
* Single nodules in cortex, can be bilateral
<><>
Carcinoma
* Less common than adenomas, larger than adenomas
* Invasion into surrounding tissues
> Metastasis to liver and lung
* Cattle and older dogs
<><>
Myelolipoma
* Cattle
<><><><>
*Adenomas and carcinomas can be functional or non-functional
neoplasia of the adrenal medulla
- Pheochromocytoma
> what is this?
> what does it do?
> anatomy
> species
Tumour of chromaffin cells
* Secrete: epinephrine, norepinephrine, or both
> If functional, norepinephrine -> constricts blood vessels -> systemic hypertension, tachycardia, cardiac hypertrophy
<><><><>
* Unilateral or bilateral
* Cattle and dogs
> Bulls can be concurrent with calcitonin-secreting C-cell tumours
of the thyroid gland
* Often large
Neoplasias of the adrenal medulla
- their anatomy and characteristics
Pheochromocytoma
<><><><>
Neuroblastoma
* Primitive neuroectodermal cells
* Younger animals
* Large intra-abdominal mass
<><><><>
Ganglioneuroma
* Tumour of multipolar ganglion cells and neurofibrils
* Often contain melanin pigment in cattle
* Small
<><><><>
Metastatic
* Common site
* Usually bilateral and in the medulla
Hypoadrenocorticism (Addison’s)
- primary definition / cause, general anatomy
- iatrogenic cause
Primary
* Idiopathic – possibly immune-mediate inflammatory destruction (other causes of destruction are uncommon)
* Unilateral – productive neoplasm in contralateral gland
<><><><>
Iatrogenic
* Exogenous glucocorticoids + abrupt cessation
* Overdose other drugs (mitotane)
Hypoadrenocorticism (Addison’s) pathogenesis (primary)
Destruction of adrenal cortex -> mineralocorticoid (aldosterone) & glucocorticoid deficiency -> excessive Na excretion in renal tubules & retention of K and H ions -> hyponatremia -> hypovolemia + hypotension + prerenal azotemia
* Hypovolemic crisis
