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
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)
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
4
Q
What is an example of endocrine dysfunction resulting from failure of target cell response?
A
insulin resistance
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
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
7
Q
What hormones are secreted from the neurohypophysis (posterior lobe)?
A
Oxytocin, ADH
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
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
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
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
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
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
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
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
16
Q
What is the typical cortical to medullary ratio of an adrenal gland?
A
1:1-2:1
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
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
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
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
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
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
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
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
25
Describe hypoadrenocorticism (Addison’s)
* Deficiency of glucocorticoids (ZF/ZR) and mineralocorticoids (ZG)
* potentially fatal
* grossly - adrenal glands are mainly medulla - abnormal cortex to adrenal ratio = 1:4
26
What are the mechanisms of Addison’s dz?
* 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
What are the general clinical signs of Addison’s?
* Weight loss
* non-specific gastroenteritis
* impaired stress tolerance
* hypotension shock
28
What are the aldosterone deficiency-related signs of Addison’s disease?
* 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
Describe pheochromocytomas
* **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
How do pheochromocytomas differ grossly from cortical tumors?
pheos are red, while cortical tumors are tan, like the cortex
31
What happens with adrenal hemorrhage?
* 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
What type of cells produce T3 and T4?
follicular cells of the thyroid
33
What do parafollicular or thyroid C cells produce?
calcitonin (reduces blood Ca concentration)
34
What occurs with ectopic thyroid tissue and where is it commonly found?
* 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
Describe thyroglossal duct cysts
* 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
What is a goiter?
* non-neoplastic enlargement of thyroid gland as a **result of follicular cell hyperplasia**
* not always grossly apparent, can be diffuse or multinodular
37
What is the difference between diffuse and multinodular goiters?
* diffuse goiters - compensatory, **TSH-induced response to hypothyroidism**
* multinodular goiters in old cats - **function autonomously** (independent of TSH) --\> hyperthyroidism
38
What are potential causes of a goiter?
* iodine deficiency
* iodine excess
* goitrogens
* defects in the synthesis of thyroid hormones (congenital dyshormonogenetic goiter)
39
Describe what occurs with iodine deficiency
* 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
What are goitrogens and what are some examples?
**compounds including plants and drugs that cause hyperplastic goiters**
* marginal iodine deficiency incr sensitivity
* _excess iodine can also be goitrogenic_
41
What occurs when you end up with a colloid goiter?
* **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
What type of dogs typically get hypothyroidism, and what are a few potential causes?
* middle age or older
* acquired most common
* \>90% considered primary
* Causes:
* idiopathic follicular atrophy
* lymphocytic thyroiditis
43
What occurs with idiopathic follicular atrophy?
* thyroid gland shrunken and pale
* most parenchyma has been _lost or replaced by adipose tissue_
44
Describe lymphoplasmacytic thyroiditis
* autoimmune thyroid dz
* **infiltration of thyroid by reactive T lymphocytes**
* triggered by genetic and environmental factors
45
Describe characteristics of follicular adenomas
* aged cats \>\>\> dogs
* **feline follicular adenomas are often functional** \> hyperthyroidism
* not if unilateral
* gross - discrete tan to brown nodules compress adjacent tissue
46
Describe the characteristics of follicular carcinomas
* mainly diagnosed in dogs
* **typically invasive**
* early metastasis --\> lungs
* **most nonfunctional**
* arise from ectopic thyroid tissue
* **vascular**
47
Describe the characteristics of thyroid C-cell hyperplasia and neoplasia
* 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
What is the role of the chief cells in parathyroid glands?
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
What causes hypoparathyroidism and what are the clinical signs and effects of this condition?
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
What causes hyperparathyroidism?
* 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
What causes secondary hyperparathyroidism?
* **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
Describe what occurs with nutritional hyperparathyroidism
* increased PTH pulls Ca out of bone \> bony remodeling with fibrous CT
* fibrous osteodystrophy
53
Describe the mechanisms of renal secondary hyperparathyroidism
* 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
Describe diabetes mellitus
* 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
What are some potential causes of diabetes mellitus?
* 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
What are the clinical signs and effects of diabetes mellitus?
* animals have a diminished resistance to infection
* urinary tract infections
* emphysematous cystitis
* PU/PD
* cataracts
* hepatomegaly
* glomerulopathy, retinopathy, and gangrene --\> result of microangiopathy
57
Describe insulinomas
* beta cell (insulin-secreting) neoplasms
* adenomas and carcinomas
* are often functional
* most commonly dog and ferret (benign)
* also in cats, cattle
58
Describe beta cell adenomas/insulinomas
* solitary
* yellow to red
* small (\< 3 cm) spherical nodules
* sharply delineated from surrounding parenchyma
59
Describe beta cell carcinomas
* 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
Describe pancreatic nodular hyperplasia
* multiple small nodules
* gray to tan
* aged cats and dogs
* incidental finding
Systemic Pathology
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