Path 1 - Endocrine 2

drraythe's version from 2016-03-04 22:36

6.2 Endocinology: Pituitary Gland


Question Answer
Developmental disturbances → Adenohypophyseal aplasia/hypoplasia. Explain the genetic defect which results in this in cows & the related CSIt is a genetic defect in genetic defect in Guernsey & Jersey cattle, where the adenohypophysis is absent or hypoplastic. This causes hypoplasia of the target organs, which results in cessation of fetal development after 7 months! This results in a PROLONGED GESTATION bc cortisol levels of the fetus won't be ↑ enough to trigger the mom into labor
Developmental disturbances → Adenohypophyseal aplasia/hypoplasia. Explain the plant which causes this in ewes & the resulting problemIngestion of Veratrum Californicum by ewes in early pregnancy leads to both cranial malformation (cyclopia, CNS malformations, nasofacial defects) & also aplasia/hypoplasia of the fetal pituitary → hypoplasia of target endocrine organs in the fetus & prolonged gestation (fetus continues to grow though, unlike w/ the cattle genetic deformity)
Explain how Adenohypophyseal aplasia/hypoplasia leads to prolonged gestationDue to hypoplasia of the adrenal cortex → inadequate cortisol secretion & failure of the “estrogen surge” (stims PG synthesis in the uterus → smooth muscle contractions → parturition)
Developmental disturbances → Pituitary cyst & pituitary dwarfism: Who does this affect & what happens developmentally for this to happen?This is a problem in dogs (GSD, spitz, toy pinscher & Carelian bear dogs) where there is failure of the oropharyngeal ectoderm of Rathke's pouch to differentiate into trophic hormone-secreting cells of the Pars Distalis
Developmental disturbances → Pituitary cyst & pituitary dwarfism: What are the lesions which result from this developmental anomaly?There will be a large, multiloculated cyst in the Sella Turcica & the absence of an adenohypophysis. This leads to pituitary dwarfism w/ slower growth, stunting, bilaterally symmetric alopecia & hyperpigmentation of the skin
**Neoplasms → Explain the difference b/t a fxnal & non-fxnal neoplasm & how they both can still contribute to endocrine disordersFxnal: Produce trophic hormones that stimulate target organs
Non-fxnal: Don't secrete trophic hormones, but are destructive adjacent to the mass
What are 3 examples of problems caused by the impingement of non-fxnal neoplasms of the pituitary?Panhypopituitarism
Diabetes Insipidus
Neurologic disorders (e.g., CNS &/or cranial nerve dysfxn)
***Differentiate an Adenoma from Nodular Hyperplasia?Adenomas are usually larger & will have a capsule
**What is the most common pituitary tumor in EQUINES?Adenomas of the Pars Intermedia (2nd most common in dogs, rare in other species)
Adenomas of the Pars Intermedia → DOGS: What do the lesions grossly look like? What happens if the adenoma is INACTIVE? How about ACTIVE?It will look like moderate enlargement of the pituitary gland. If the adenoma is inactive, the resulting problems will be hypopituitarism & Diabetes Insipidus. If the adenoma is ACTIVE there will be excessive ACTH secretion → bilateral adrenal cortical hyperplasia → hypercortisolism (Cushing’s disease)
Explain the difference btwn the active & inactive adenomas of the Pars Intermedia in dogs, which result in different clinical appearances? Which is responsible for the active type tumor responsible for the Cushings?It depends on the cell population involved. There are 2 populations:
(1) Type A cell: stains strongly for α-MSH (α-Melanocyte-stimulating hormone)
(2) Type B cell: stains intensely for ACTH but not for α-MSH* syndrome of cortisol excess related to type B cell (This B the cell which causes you more problems)
**Adenomas of the Pars Intermedia → HORSES: What do the lesions grossly look like?Large yellow to white, multinodular neoplasms extending out of the Sella Turcica → compression of the hypothalamus
Adenomas of the Pars Intermedia → HORSES: what are the CS you will see w/ this?Polyuria, polydipsia, ravenous appetite, muscle weakness, somnolence (sleepiness), intermittent hyperpyrexia, generalized hyperhidrosis (excessive sweating), pro-opiomelanocortin (POMC) → cortisol excess → mild aderenocortical hyperplasia
****When I say POMC, you thinkHorse w/ an Adenoma of the Pars Intermedia & that it leads to adrenocortical hyperplasia
What are the 5 things that an adenoma of the Pars Intermedia in horses will secrete?Pro-opiomelanocortin (POMC), corticotropin-like intermediate lobe peptide (CLIP), α-MSH, β-MSH, β-endorphin
***What unique symptom happens to horses w/ an Adenoma of the Pars Intermedia?Hypertrichosis (**hirsutism) → failure to seasonally shed hair; the hair over most of the trunk & extremities is long (up to 10 to 12 cm), abnormally thick, wavy & often matted
What is Hirsutism & who gets this when?HORSES w/ an ADENOMA of the PARS INTERMEDIA. It is basically hypertrichosis where they have super long wavy hair
ACTH-secreting adenoma → Who does this happen to? Which cells are affected by this adenoma? What disease does this lead to & what are the main symptoms?This is a fxnally ACTIVE adenoma, which is derived from corticotroph (ACTH-secreting) cells in either the Pars Distalis or the Pars Intermedia of dogs. Specifically, ADULT to aged Boxers, Boston terriers, Dachshunds. The result is CUSHINGS DZ, which is characterized by gluconeogenic, lipolytic, protein catabolic, antiinflammatory activities
ACTH-secreting (corticotroph) adenoma → What are the gross lesions you'd see w/ this?(Fxnally active ACTH secreting) Enlarged pituitary gland + extension into the thalamus, bilateral adrenal cortical hyperplasia w/ nodules of yellow-orange cortical tissue outside the capsule & extending down into & compressing the adrenal medulla
Endocrinologically inactive chromophobe adenoma → Who does this usually affect? What are the lesions of this adenoma? What CS does this cause?Occurs in dogs, cats, laboratory rodents, parakeets...but is UNCOMMON in other species. This adenoma causes space-occupying lesions (chromophobes are inactive cells remember?) & compression atrophy. Bc of this, the CS are decreased spontaneous activity, incoordination, weakness & collapse after exercise & in chronic cases → blindness & dilated, fixed pupils due to compression of the optic nerves (dogs cats rats & keets are scared of color out on the streets)
**Craniopharyngioma → What cells is this neoplasm derived from? Who does this affect & w/ what lesions & resulting problems/CS?This tumor is derived from epithelial remnants of the oropharyngeal ectoderm of the craniopharyngeal duct (Rathke's pouch). This problem occurs in YOUNGER ANIMALS where the lesion is large & grows ventrally. The sequelae are panhypopituitarism & dwarfism, Diabetes Insipidus (release & synthesis of ADH disturbed), disturbances of the CNS/cranial nerves, 2º hypothyroidism & hypoadrenocorticism (NON-fxnal SOL of remnant cells of Rathke’s pouch in young animals)
**ADENOMAS & CARCINOMAS are more common in?ADULTS
**Craniopharyngioma are more common in?YOUNG
Pituitary abscesses most often occur in who? What are the usual agents? What CS will be seen?Sporadic in ruminants & swine, usually caused by bacteria (Arcanobacterium pyogenes) or mycotic agents. This most often results in neurological signs due to associated meningitis or encephalitis
**Explain the 2 different kinds of Diabetes Insipidus(1) **Hypophyseal form - (Central Diabetes Insipidus) where the problem lies in reduced secretion of ADH
(2) Nephrogenic form - Kidneys fail to concentrate urine despite adequate amounts of ADH
**Why might an animal develop the hypophyseal form of Diabetes Insipidus?Any lesion interfering w/ ADH synthesis or secretion, like neoplasms, granulomas, abscess, cysts or trauma (severed infundibular stalk), or **compression &/or destruction of the Pars Nervosa, Infundibular Stalk or Supraoptic Nucleus in the Hypothalamus
*What is the reason for the nephrogenic form of Diabetes Insipidus?This is a HEREDITARY DEFECT where there is a *LACK OF Adenylate Cyclase in the kidney cells. Bc of this, *cells fail to respond to normal or ↑ circulating ADH
What are the CS that both types of Diabetes Insipidus cause?PU, PD & urine of low osmolality (hypotonic urine) even after water deprivation
What can you do to try to tell if the Diabetes Insipidus is hypophyseal or nephrogenic?Administration of exogenous ADH will lead to a rapid increase in urine osmolality above that of plasma if it is the HYPOPHYSEAL form

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