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Systemic Pathology > Endocrine Path > Flashcards

Endocrine Path Flashcards

1
Q

What is the difference between primary hyperfunction and primary hypofunction?

A

Primary hyperfunction: source is the endocrine organ itself;often neoplastic

Primary hypofunction:

  • Immune-mediated injury - ex: hypothyroidism
  • Failure of development - ex: pituitary dwarfism
  • Failure of hormone synthesis caused by genetic defect - ex: Congenital dyhormonogenic goiter in sheep, goats, and cattle
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2
Q

What is the difference between secondary hyperfunction and secondary hypofunction?

A

Secondary hyperfunction: a lesion in other organ (e.g. adenohypophysis) secretes an excess of trophic hormones

  • e.g. ACTH-secreting tumor in the pars distalis/intermedia in dogs –> stim of adrenal cortex

Secondary hypofunction: a destructive lesion in one organ such as pituitary, interferes w/ trophic hormone release

  • usually a large endocrinologically inactive tumor or dietary iodine deficiency (results in diffuse hyperplastic goiter)
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3
Q

What is an example of hypersecretion of hormones by non-endocrine tumors

A
  • Humoral hypercalcemia of malignancy (paraneoplastic syndrome) - clinical syndrome produced primarily autonomous secretion of PTHrP by cancer cells
    • T-cell lymphoma
    • Apocrine anal sac adenocarcinoma
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4
Q

What is an example of endocrine dysfunction resulting from failure of target cell response?

A

insulin resistance

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5
Q

Describe failure of fetal endocrine function and give some potential causes of this

A
  • subnormal function of fetal endocrine system, esp. in ruminants, may disrupt the normal fetal development –> prolonged gestation
  • genetic - failure of development (aplasia) of the adenohyposis
  • toxic plants e.g. ewes ingesting Veratum californicum
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6
Q

What are examples of endocrine dysfunction resulting from abnormal degradation of hormones, both increased and decreased degradation?

A
  • Incr degradation: long-term admin of xenobiotics (e.g. phenobarb) results in induction of liver enzymes –> incr degradation of T4
  • Decr degredation: blood hormone levels persistently elevated
    • Feminization resulting from hyperestrogenism assoc. w/ cirrhosis and decr hepatic degradation of estrogens
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7
Q

What hormones are secreted from the neurohypophysis (posterior lobe)?

A

Oxytocin, ADH

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8
Q

What hormones are secreted from the adenohypophysis (posterior lobe)?

A
  • Pars distalis (anterior lobe): ACTH, TSH, FSH, LH, LTH, GH
  • Pars intermedia (posterior lobe): ACTH in the dog
  • Pars tuberalis: capillaries; Influenced by releasing hormones from hypothalamus
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9
Q

Describe Juvenile Panhypopituitarism (Pituitary Dwarfism)

A
  • Due to a pituitary cyst - failure of Rathke’s pouch to differentiate into hormone secreting cells for pars distalis
  • deficiency in GH, TSH, prolactin, and gonadotropins; ACTH +/- decr
  • brachycephalic breeds, GSH, Spitz, Toy pinscher
  • Normal at birth until 2 mo
    • slower growth rate, retention of puppy coat, lack of primary guard hairs, bilateral symmetrical alopecia, delayed permanent dentition
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10
Q

Describe corticotroph (ACTH-secreting) adenomas

A
  • Derived from corticotroph cells in either pars distalis/intermedia
  • cortisol excess > pituitary dependent hyperadrenocorticism in dogs
  • severity of dz NOT related to tumor size, although larger tumors can cause compression and additional CNS signs, diabetes
  • Seen in Bostons, Boxers, Doxies
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11
Q

Describe pars intermedia (melanotroph) adenomas

A
  • Adenomas derived from cells of pars intermedia
  • most common pituitary tumor in horses
    • ​clinical syndrome of pituitary pars intermedia dysfunction (PPID)
  • ​produce a variety of POMC-derived peptides, incr frequency in older animals and females
  • C/S: PU/PD, laminitis, incr appetite, mm weakness, intermittent pyrexia, hyperhydrosis, hirsutism
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12
Q

What is a somatotropin adenoma?

A
  • Adenoma of growth hormone-secreting acidophils (somatotrophs) - very RARE
  • reported in cats, dogs, and sheep
  • these are functional adenomas (hypersecretion of GH) in cats and dogs
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13
Q

Describe acromegaly. What type of neoplasm do you often see these with?

A
  • Dz characterized by overgrowth of CT, incr appositional growth of bone, coarsening of facial features, gingival hyperplasia, incr separation of teeth, macro glossia, enlargement of viscera
  • in cats, get prognathia inferior
  • seen with somatotroph adenomas
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14
Q

Describe diabetes insipidus

A
  • Hypophyseal form - inadequate ADH > destruction of pars nervosa or infundibular stalk or hypothalamus from cyst, tumor, trauma, inflammation
  • Nephrogenic form - target cell defect
  • C/S: PU/PD, hypo-osmotic urine, cannot concentrate
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15
Q

What are the four layers of the adrenal gland are what is produced in each layer?

A
  • Zona glomerulosa - aldosterone
  • Zona fasciculata - glucocorticoids (ACTH-dependent)
  • Zona reticularis - sex steroids
  • Adrenal Medulla - catecholamines
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16
Q

What is the typical cortical to medullary ratio of an adrenal gland?

A

1:1-2:1

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17
Q

What are causes of Cushing’s Disease?

A
  • Functional ACTH producing pituitary adenoma
  • functional adrenocortical adenoma or carcinoma
  • idiopathic hyperplasia of adrenal cortex
  • iatrogenic from chronic corticosteroid administration
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18
Q

How do nodular and diffuse adrenal cortical hyperplasia differ from each other?

A

Nodular: Multiple discrete nodules of hyperplasia affecting any of 3 cortical zones, in older animals, often bilateral

Diffuse: bilateral, diffuse, uniform; in response to excessive ACTH from functional pituitary adenoma, results in Cushing’s

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19
Q

Describe adrenal cortical adenomas

A

Single, unilateral, well demarcated and histologically well differentiated

  • most often functional - contralateral adrenal cortical atrophy, associated with Cushing’s
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20
Q

Describe adrenal cortical carcinomas

A

Seen in older dogs, less common than adenomas, larger than adenomas, can be bilateral, often functional

  • contralateral gland atrophic if unilateral, highly invasive and able to metastasize
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21
Q

Describe Cushing’s disease

A
  • Slowly progressive condition resulting from cortisol excess
    • mostly dogs, sometimes cats
  • signs due to the gluconeogenic, lipolytic, protein catabolic and anti-inflammatory effects of cortisol
  • C/S:
    • hepatomegaly - steroid hepatopathy
    • delayed wound healing protein- catabolism
    • freq infections - lympocytolysis
    • incr appetite, CNS signs
    • pendulous abdomen - mm wasting
    • bilaterally symmetrical alopecia
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22
Q

Describe calcinosis cutis

A
  • Iatrogenic Cushing’s dz C/S
  • form of dystrophic calcification (Ca salts precipitate on degenerating collagen)
  • firm gritty, chalky plaques w/ ulceration
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23
Q

What is the clinical pathology you see with Cushing’s?

A
  • Neutrophilia with a left shift
  • lymphopenia
  • eosinopenia
  • monocytosis
  • elevated GLU, ALP
  • low USG
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24
Q

How does Cushing’s differ in the cat?

A
  • Not as common, but same mechanisms as the dog
  • liver lesions usually not present but can be
  • cutaneous fragility - severe atrophy, easily torn skin with poor healing > no calcinosis cutis
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25
Q

Describe hypoadrenocorticism (Addison’s)

A
  • Deficiency of glucocorticoids (ZF/ZR) and mineralocorticoids (ZG)
  • potentially fatal
  • grossly - adrenal glands are mainly medulla - abnormal cortex to adrenal ratio = 1:4
26
Q

What are the mechanisms of Addison’s dz?

A
  • Idiopathic adrenocortical atrophy
  • immune mediated destruction
  • abrupt cessation of long term steroid therapy (only ACTH zones)
  • tropic adrenal cortical atrophy - pituitary lesions, ACTH zones
27
Q

What are the general clinical signs of Addison’s?

A
  • Weight loss
  • non-specific gastroenteritis
  • impaired stress tolerance
  • hypotension shock
28
Q

What are the aldosterone deficiency-related signs of Addison’s disease?

A
  • Hyperkalemia/hypokaluria
  • hyponatremia/hypernaturia
  • hypochloremia/hyperchloruria
  • bradycardia (high K+)
  • Na/K ratio of 23:1 strongly suggestive
  • microcardia (hyperkalemia)
  • in a nut shell - K is retained and Na and Cl are loss and water goes with them!
29
Q

Describe pheochromocytomas

A
  • most common neoplasm of the adrenal medulla
    • composed of epi/norepi-secreting cells or both
  • small pheos - well encapsulated, stay in adrenal gland
  • large pheos- invade capsule, adjacent tissues, CVC, and aorta (malignant)
  • mets - 50% of cases to liver, reg l.n., spleen, lungs
  • functional pheos - catecholamine overproduction –> tachycardia, edema, cardiac hypertrophy
30
Q

How do pheochromocytomas differ grossly from cortical tumors?

A

pheos are red, while cortical tumors are tan, like the cortex

31
Q

What happens with adrenal hemorrhage?

A
  • occurs in newborns of any species - thought d/t birth trauma
  • Potential causes:
    • Exhaustion phase of the “stress response”
      • wild animals that die during restraint
      • horses that die from overexertion
    • Toxemia e.g. intestinal torsion in horses
    • Septicemia - injuring to endothelial lining of adrenal sinusoids
32
Q

What type of cells produce T3 and T4?

A

follicular cells of the thyroid

33
Q

What do parafollicular or thyroid C cells produce?

A

calcitonin (reduces blood Ca concentration)

34
Q

What occurs with ectopic thyroid tissue and where is it commonly found?

A
  • occurs from base of the tongue along the path of the developing glands, can migrate further caudally to diaphragm
  • dogs - functional nodules are common near the ascending aorta at the base of the heart
35
Q

Describe thyroglossal duct cysts

A
  • formed from thyroglossal duct remnants
  • cysts or sinus tracts along ventral midline of the neck
  • contain watery mucoid secretions
  • seldom exceed 1 cm in diameter
  • can become inflamed, rupture, and form fistulous tract to skin
  • rarely can undergo malignant transformation
36
Q

What is a goiter?

A
  • non-neoplastic enlargement of thyroid gland as a result of follicular cell hyperplasia
    • not always grossly apparent, can be diffuse or multinodular
37
Q

What is the difference between diffuse and multinodular goiters?

A
  • diffuse goiters - compensatory, TSH-induced response to hypothyroidism
  • multinodular goiters in old cats - function autonomously (independent of TSH) –> hyperthyroidism
38
Q

What are potential causes of a goiter?

A
  • iodine deficiency
  • iodine excess
  • goitrogens
  • defects in the synthesis of thyroid hormones (congenital dyshormonogenetic goiter)
39
Q

Describe what occurs with iodine deficiency

A
  • esp during fetal/neonatal period (need for thyroid hormone = the greatest) -> major cause of diffuse goiter
    • geographic areas - Pacific NW/Great Lakes
    • Need dietary iodine supplementation to prevent
  • Gross - diffusely enlarged and reddened
  • Histo - incr vascularity (red), follicles irregularly enlarged, decr luminal diameter, follicular cell hypertrophy (columnar), colloid paler
  • Fetus - myxedema in dermis, less hair
40
Q

What are goitrogens and what are some examples?

A

compounds including plants and drugs that cause hyperplastic goiters

  • marginal iodine deficiency incr sensitivity
  • excess iodine can also be goitrogenic
41
Q

What occurs when you end up with a colloid goiter?

A
  • follicular atrophy
  • it’s the involution stage after repletion of dietary iodine in cases of hyperplastic goiter
  • thyroid gland remains enlarged, but follicular cells have undergone atrophy b/c of decreased TSH
42
Q

What type of dogs typically get hypothyroidism, and what are a few potential causes?

A
  • middle age or older
  • acquired most common
  • >90% considered primary
  • Causes:
    • idiopathic follicular atrophy
    • lymphocytic thyroiditis
43
Q

What occurs with idiopathic follicular atrophy?

A
  • thyroid gland shrunken and pale
  • most parenchyma has been lost or replaced by adipose tissue
44
Q

Describe lymphoplasmacytic thyroiditis

A
  • autoimmune thyroid dz
  • infiltration of thyroid by reactive T lymphocytes
  • triggered by genetic and environmental factors
45
Q

Describe characteristics of follicular adenomas

A
  • aged cats >>> dogs
  • feline follicular adenomas are often functional > hyperthyroidism
    • not if unilateral
  • gross - discrete tan to brown nodules compress adjacent tissue
46
Q

Describe the characteristics of follicular carcinomas

A
  • mainly diagnosed in dogs
  • typically invasive
  • early metastasis –> lungs
  • most nonfunctional
  • arise from ectopic thyroid tissue
  • vascular
47
Q

Describe the characteristics of thyroid C-cell hyperplasia and neoplasia

A
  • Bulls, esp dairy bulls fed a high Ca diet, are prone to develop C-cell hyperplasia and neoplasia
  • C-cell neoplasms are more common with incr age
  • Affected bones have incr vertebral bone density
  • Types:
    • C-cell adenoma: most common equine thyroid tumor –> incidental finding at necropsy
    • C-cell carcinoma: bulls and dogs, mets to reg. l.n. or lungs
48
Q

What is the role of the chief cells in parathyroid glands?

A

release PTH in response to decr ionized Ca in peripheral blood –> mobilizes Ca by activating osteoclasts in bone, promoting Ca absorption from intestine, and blocking reabsorption of P in proximal tubules in kidney

49
Q

What causes hypoparathyroidism and what are the clinical signs and effects of this condition?

A

Causes:

  • insufficient PTH release by chief cells or inability of target cells (renal tubules) to respond to PTH
  • atrophy or destruction of parathyroid chief cells is a major cause
  • familial in mini schnauzers
  • cats post thyroidectomy

C/S: develop hypocalcemia + hyperphosphatemia

50
Q

What causes hyperparathyroidism?

A
  • Primary - autonomous hypersecretion of PTH by hyperplastic or neoplastic chief cells
  • Parathyroid (chief cell) adenomas - mainly dogs
  • Chief cell carcinomas - larger, more invasive
  • Idiopathic, multinodular hyperplasia of chief cells in dogs
51
Q

What causes secondary hyperparathyroidism?

A
  • More common than primary
    • ​typically diffuse and bilateral
  • Nutritional imbalances
    • ​excessive P –> most freq cause stimulates parathyroid gland indirectly by reciprocal lowering of blood Ca
    • deficient Ca, cholecalciferol deficiency
52
Q

Describe what occurs with nutritional hyperparathyroidism

A
  • increased PTH pulls Ca out of bone > bony remodeling with fibrous CT
    • fibrous osteodystrophy
53
Q

Describe the mechanisms of renal secondary hyperparathyroidism

A
  • if renal dz is severe enough to decr GFR, then P is retained –> hyperphosphatemia
  • incr P –> reciprocal decline in ionized blood Ca levels
  • chronic renal dz also impairs calcitriol synthesis –> decr intestinal absorption of Ca
  • incr PTH response to hyperphosphatemia, hypocalcemia, or low blood Ca
    • C/S: fibrous osteodystrophy (most severe in skull bones), “rubber jaw”
54
Q

Describe diabetes mellitus

A
  • deficiency of insulin production and secretion by islet beta cells or failure of target cells to respond to insulin
    • decr movement of glucose into insulin-sensitive cells (ie. hepatocytes, adipocytes, sk myocytes)
  • corresponding incr in hepatic glucose production and hyperglycemia
55
Q

What are some potential causes of diabetes mellitus?

A
  • aplasia or hypoplasia of pancreatic islets in diabetic puppies
  • degeneration or necrosis is more common
  • immune mediated lymphoplasmacytic inflammation can cause selective islet destruction
  • chronic pancreatitis destroys both endocrine and exocrine tissue
  • insulin resistant DM - most commonly in cats
56
Q

What are the clinical signs and effects of diabetes mellitus?

A
  • animals have a diminished resistance to infection
  • urinary tract infections
    • emphysematous cystitis
  • PU/PD
  • cataracts
  • hepatomegaly
  • glomerulopathy, retinopathy, and gangrene –> result of microangiopathy
57
Q

Describe insulinomas

A
  • beta cell (insulin-secreting) neoplasms
  • adenomas and carcinomas
    • are often functional
  • most commonly dog and ferret (benign)
    • also in cats, cattle
58
Q

Describe beta cell adenomas/insulinomas

A
  • solitary
  • yellow to red
  • small (< 3 cm) spherical nodules
  • sharply delineated from surrounding parenchyma
59
Q

Describe beta cell carcinomas

A
  • more common than adenomas in dogs
  • freq in duodenal (right) lobe of pancreas
  • larger, invasive –> omentum, mesentery
    • mets to liver, l.n.
  • C/S - neurologic from hypoglycemia
60
Q

Describe pancreatic nodular hyperplasia

A
  • multiple small nodules
  • gray to tan
  • aged cats and dogs
  • incidental finding

Systemic Pathology (8 decks)

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