Endocrine System Flashcards
What are endocrine glands?
collections of specialized cells that synthesize, store, and directly release their secretory products into the bloodstream, resulting in physiological effects on target cells distant from the glands
What are 3 major characteristics of the general anatomy of endocrine glands?
- small and widely spaced out throughout the body
- rich vasculature with interconnected cell clusters
- connected with the nervous system
What are the 4 major categories of substances secreted by endocrine glands?
- steroids
- polypeptides - insulin
- iodothyronines - T3, T4
- catecholamines - EPI, NE
What are the 3 major proliferative lesions in the endocrine system?
- NODULAR HYPERPLASIA - well-demarcated, non-encapsulated small nodule(s) that look like normal cells
- ADENOMA - well-demarcated, encapsulated solitary and unilateral nodule composed of cells that deviate from normal arrangement, but not by much
- CARCINOMA - poorly demarcated, non-encapsulated bilateral nodules with features of malignancy
What are the 3 features of malignancy?
- SIZE - large, bilateral, with rapid growth that typically leads to necrosis and hemorrhage
- MORPHOLOGY - pleomorphic, presence of mitotic figures, anisocytosis, anisokaryosis, multiple nuclei, or bizarre cells
- INVASION - invades intraglandular and intravascular through capsule and tissue (rich vasculature - tend to be lung or liver metastasis)
What is the difference between functional and nonfunctional lesions?
FUNCTIONAL - secrete excess hormones continuously or periodically causing atrophy of the contralateral gland due to decreased trophic hormone
NONFUNCTIONAL - do not secrete excess hormones and may destroy tissue, but doesn’t cause contralateral gland atrophy
Why are large lesions especially disruptive to the endocrine system?
whether functional or not, they can destroy the rest of the gland and cause deficiencies in hormones secreted by other populations of cells
What are the 2 secondary changes resulting from endocrine lesions?
- DIFFUSE ATROPHY - excess circulating hormones (negative feedback), decreased stimulatory hormones, autoimmune/toxic destruction
- DIFFUES HYPERPLASIA - excess stimulatory hormones from pituitary
What is the most common secondary effect of functional adrenocortical tumors?
increased cortisol from the tumor induces negative feedback and decreases ACTH from the pituitary, resulting in contralateral adrenocortical atrophy
What commonly occurs following the development of a non-functional tumor in the pituitary gland?
lack of stimulatory hormone causes endocrine glands to atrophy
- bilateral atrophy of adrenal cortex due to decreased ACTH
What commonly occurs following the development of a functional pituitary gland tumor?
increased stimulatory hormone causes endocrine glands to become hyperplastic
- Cushings: increased ACTH secretion causes adrenal cortex hyperplasia
What is the difference between aplasia, hypoplasia, and dysplasia?
APLASIA = never formed
HYPOPLASIA = formed, but small
DYSPLASIA = formed incorrectly
What is acute and chronic inflammatory commonly secondary to? What type of exudate is expected?
ACUTE = no endocrine signs, secondary to systemic disease (endotoxemia, septicemia) or local extension, rather than primary infection; suppurative
CHRONIC = secondary to systemic disease with immune-evading agents (fungi, Mycobacteria) or autoimmune disease; (pyo)granulomatous, lymphoplasmacytic
What hormones are produced by the adenohypophysis, neurohypophysis, adrenal cortex, adrenal medulla, thyroid, parathyroid, and Islets of Langerhans?
- GH, ACTH, TSH, FSH, LH
- ADH, oxytocin
- cortisol, aldosterone
- EPI, NE
- T3, T4, calcitonin
- PTH
- insulin, glucagon, gastrin
What are the general manifestations of hypothyroidism, Cushing’s, hyperthyroidism, hyperinsulinism, and hyperparathyroidism?
- alopecia
- alopecia
- weight loss with increased appetite
- seizures
- bone fracture
How do the neurohypophysis and adenohypophysis develop in the embryo?
ectoderm invaginates forming the neurohypophyseal bud (future posterior pituitary) and hypophyseal pouch (future anterior pituitary, from oral ectoderm)
Development of pituitary gland:
Pituitary gland:
ventral to hypothalamus
Pituitary anatomy:
Rathke’s pouch surrounded by the pars intermedia separates pars distalis (adenohypophysis) and pars nervosa (neurohypophysis)
What is the sella turcica? What is the largest part of the pituitary gland?
Turkish saddle - depression in the sphenoid bone where the pituitary sits
pars distalis - composed of several endocrine cell populations that secrete pituitary hormones
What is the function of the pituitary gland?
hormones produced by the hypothalamus act on the anterior and posterior pituitary gland to release trophic hormones that act on specific endocrine glands, stimulating them to release their own hormones that exert ultimate actions on downstream tissues
What hormones are produced by the posterior pituitary?
pars nervosa - ADH oxytocin
What are the 3 populations of cells in the adenohypophysis?
- basophil
- acidophils
- chromophobes (few secretory granules, may be stem cells)
What causes cystic Rathke’s pouch? What does it look like grossly? What does this lead to? In what animals is this seen?
failure of oropharyngeal ectoderm to develop into hormone-secreting cells of pars distalis
enlarged (gelatinous) cyst replaces almost all of the pituitary
pituitary dwarfism (juvenile panhypopituitarism)
dogs —> German Shepherds
Juvenile panhypopituitarism:
cystic Rathke’s pouch —> German Shepherds
Pituitary dwarfism:
- juvenile panhypopituitarism —> cystic Rathke’s pouch
- alopecia due to hypothyroidism, retention of puppy coat
- stunted growth (decreased GH)
- dwarf pups appear normal from birth until approximately 2 months
Pituitary dwarfism, puppy:
- alopecia
- retention of puppy hair coat
What are craniopharyngiomas? How do they act? In what animals are they most common?
suprasellar germ cell tumors derived from the epithelial remnants of the craniopharyngeal duct (Rathke’s pouch)
generally benign and nonfunctional, but can be locally invasive, causing neurological signs
young adult to middle-aged dogs
What do functional adenomas of pars distalis secrete? What happens when they become large? What disorder is commonly associated with this?
ACTH
can compress/efface optic chiasm, rest of the pituitary gland, and hypothalamus
Cushings —> most common in older dogs
What are 4 common pathologies associated with pars distalis adenomas?
- diffuse hypertrophy of adrenal cortices
- muscle atrophy and increased intra-abdominal fat deposits
- pulmonary thrombosis
- epidermal atrophy, flank alopecia, calcinosis cutis
Pars distalis adenoma, adrenal glands:
- cortical hyperplasia due to increased ACTH
- causes increased cortisol —> Cushings
What are 3 causes of the pendulous abdomen (potbelly) appearance associated with pars distalis adenomas?
- hepatomegaly due to increased gluconeogenesis
- muscle weakness and wasting
- redistribution of fat (obesity) due to increased protein and lipid metabolism
(increased ACTH causes an excess of cortisol)
What are 4 effects of excess cortisol on the immune system?
- reduces expression of inflammatory mediators (cytokines, prostaglandins, NO)
- inhibits inflammatory cell migration by inhibiting the expression of cell adhesion molecules
- promotes apoptosis of leukocytes
- affects wound healing due to inhibition of fibroblast proliferation and collagen synthesis that causes a decrease in scar tissue formation
What causes pulmonary thrombosis associated with pars distalis adenomas?
hypercoagulable state due to impaired fibrinolysis due to increase in plasminogen activator inhibitor and clotting factor production by liver
What are the most common dermatopathology associated with pars distalis adenomas?
- flank alopecia*
- epidermal atrophy
- calcinosis cutis: idiopathic mineralization (30%)
Are pars distalis carcinomas usually functional or nonfunctional? How do they act? In what animals are they most commonly seen?
nonfunctional —> if functional, secretes ACTH
invasive, commonly effaces the optic chiasm, rest of pituitary, hypothalamus, and along the base of the brain, and infiltrates sphenoid bone and metastasizes
dogs
Pars distalis carcinoma:
adrenocortical atrophy = nonfunctional (decreased ACTH = decreased cortisol)
What pituitary neoplasm is common in old horses? Is it typically functional or nonfunctional?
adenoma of pars intermedia
functional —> increased POMC = increased MCSH
How do adenomas of the pars intermedia typically affect the hypothalamus? What 2 pathologies are commonly associated?
large lesions compress it and disrupt homeostasis
- hirsutism - long, full coat in spring/summer due to failure in seasonal shedding
- laminitis - “equine Cushings” causes insulin-resistance hyperglycemia (adrenal unaffected)
Pars intermedia adenoma, hirsutism:
failure in seasonal shedding
Pars intermedia ademona, laminitis:
insulin-resistant hyperglycemia
What pituitary neoplasm is common in cats? What does it typically cause? What pathology is associated?
functional adenoma of pars distalis that secretes GH
acromegaly, insulin-resistant diabetes mellitus (liver produces insulin-stimulating protein)
coarse facial features (gangster jaw) with increased growth and enlarged viscera
Feline pars distalis ademona:
- broad face, large feet
- gangster jaw, enlarged mandible
What pituitary pathology is commonly seen in ruminants? What is it associated with? What are 2 common causes?
pituitary abscesses (ruminants and deer) with purulent exudate that can efface the pituitary gland
nose rings and headbutting
- Trueperella
- Pasteurella
Pituitary abscess:
- most common in ruminants and deer
- nose ring contamination = infection readily reaches vasculature and travels to the pituitary
What disorder is commonly associated with the pars nervosa? What are the 2 forms?
diabetes insipidus in dogs and cats
- hypophyseal (central) - any lesion that interferes with ADH synthesis and/or secretion, like compression/destruction of the pars nervosa, infundibular stalk, or supraoptic nucleus (responds to exogenous ADH)
- nephrogenic - target cells in the kidney lack the biochemical pathways necessary to respond to ADH (does not respond to exogenous ADH)
How do animals with diabetes insipidus respond?
excrete large amounts of hypotonic urine and are polydipsic, since ADH regulates the retention of water and a decrease will not allow the concentration of urine and cause a reduction in urine output
What are the layers of the adrenal cortex? What hormones are produced by each? What is produced by the medulla?
- glomerulosa: mineralocorticoids for water retention
- fasciculata: glucocorticoids, like cortisol (increased lipid vacuoles due to cholesterol)
- reticularis: sex hormones
chromaffin cells produce catecholamines (EPI, NE)
What does nodular adrenal cortical hyperplasia look like? In what animals is this most common?
multiple, discrete, nonencapsulated nodules that histologically resemble zona glomerulosa with lipid droplets
commonly incidental findings in older dogs, cats, and horses, possibly secondary to Cushings
What is unique about the gross presentation of nodular adrenal cortical hyperplasia in horses?
nodules protrude out of the capsule
What is the most common gross presentation of adrenal cortical adenomas? In what animals is this most common?
well demarcates single nodule —> can be difficult to distinguish grossly from hyperplasia, but it will be encapsulated and single (tan and yellowish confirms that it is cortical)
dogs —> second most common cause of Cushing’s
How can adrenal cortical carcinomas be differentiated from adenomas?
larger and more likely to be bilateral with extensive hemorrhage and necrosis, commonly invading the caudal vena cava
(more pleomorphic cells histologically)
What are the most common signs of adrenal cortical tumors?
if functional —> Cushing’s!
- bilateral symmetric alopecia
- pendulous abdomen
What are adrenal pheochromocytomas? What animals are they most common in? What are they originated from? What do they look like grossly?
chromaffin cell tumors that typically secrete catecholamines, like EPI and NE —> dogs and ruminants
neural crest
fleshy, pink red-brown nodule in the medulla
How do pheochromocytomas look histologically?
chromaffin cells are arranged in packets (neuroendocrine pattern) and surrounded by a delicate fibrovascular stroma
What are the 3 most common pathologies associated with pheochromocytomas?
- cardiac hypertrophy
- arteriosclerosis
- widespread arteriolar medial hypertrophy related to hypertension
Pheochromocytoma, dog:
- gray-red = medulla
- cortex origin would be yellow-tan
Where do malignant pheochromocytomas and adrenocortical carcinomas typically metastasize?
invade caudal vena cava
What is Addison’s disease? What are the 2 causes?
hypoadrenocorticism —> adrenal cortex atrophy
- PRIMARY (idiopathic) - likely immune-mediated destruction of cortex (lymphocytic adrenalitis)
- SECONDARY - nonfunctional pituitary tumor (lack ACTH), acute discontinuation of chronic corticosteroid administration or overdose of Mitotane for Cushing’s treatment (iatrogenic)
What are the 2 main clinical pathological signs of Addison’s disease?
- aldosterone deficiency - renal loss of sodium and retention of potassium = hyponatremia, hyperkalemia
- cortisol deficiency - failure of gluconeogenesis and increased sensitivity to insulin = hypoglycemia
What 3 conditions is adrenal hemorrhage commonly secondary to? In what animals is this most commonly seen
- septicemia, endotoxemia (Waterhouse-Friderichsen)
- traumatic birth
- terminal overexertion: trapped horse or chased wild animal
horses, ruminants
Why is adrenalitis common? What are the 8 most common causes?
good blood supply and high local concentration of anti-inflammatory steroids is permissive to growth of fungi, protozoa, and bacteria
- Gram -
- TB
- Toxoplasma
- Histoplasma
- Cryptosporidium
- Coccidioides
- Herpes
- hairy vetch toxicity
How does adrenalitis present grossly?
hyperemia with swelling due to inflammation and edema
Why are adrenal metastatic tumors common?
(lymphoma, hemangiosarcoma, carcinoma) —> rich blood supply
- dogs: 21%
- cats: 15%
- horses: 27%
- cattle: 31%
