Path MT, Endo II

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Path MT, Endo II
2012-02-23 16:03:20
Path MT Endo II

Path MT, Endo II
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  1. What is an intracranial germ cell tumor? What embryological structure does it arise from? Common in young or old?
    • Craniopharyngioma = benign tumor from epithelial remnants of oropharyngeal ectoderm (Rathke's pouch)
    • younger animals (dwarfism w/low somatotropin/growth hormone)
  2. Where is a craniopharngioma? What are some clinical signs or craniopharyngioma?
    • grows on ventral aspect of brain (can extend into hypothalamus/thalamus/cranial nerves)
    • -subnormal fx of adrenal cortex due to lack of pituitary tropic hormone secretion
    • -failure to attain somatic maturation (lack of GH)
    • -disturbances w/water metabolism, PU/PD, low SG due to problems with ADH release
    • -cranial nerve deficits/CNS dysfunction
  3. What is etiology of pituitary abscesses seen in ruminants and swine? What are clinical signs?
    • bacteria (Arcanobacterium pyogenes) or mycotic agents
    • -neurological (meningitis/encephalitis)
  4. What are two types of inflammation associated with adenohypophysis?
    • pituitary abscesses (arcanobacterium/mycosis)
    • infiltration of mononuclear inflammatory cells (virus/protozoa)
  5. Diabetes insipidus is a disorder of which part of pituitary? what hormone is involved? What are two forms?
    • neurohypophysis
    • hypophyseal form (central DI w/intereference of ADH production/secretion) and nephrogenic form (hereditary failure to respond to ADH)
  6. Will exogenous ADH increase urine osmolality in patient with diabetes insipidus of central or nephrogenic form?
    central/hypophyseal form (diagnostic tool to distinguish)
  7. What developmental anomaly has small adrenal cortices with normal adrenal medulla and is secondary to maldevelopment of hypophysis?
    hypoplasia of adrenal cortex
  8. What can cause hemorrhage in adrenal medulla?
    trauma in newborn, severe stress, septicemia/toxemia
  9. What is Waterhouse-Friderichsen syndrome of adrenal cortex?
    • massive, diffuse bilateral hemorrhage in cortex
    • uncommon but fatal consequence of endotoxemic shock
  10. what species get nodular hyperplasia of adrenal cortex? If they are functional, what hormone is in excess?
    • old horses, dogs, cats, and female ferrets
    • androgen excess --> muscle mass, hypertrophy of clitoris, involution of mammary gland
  11. What do nodular hyperplastic lesions of adrenal cortex look like?
    multiple, well defined, yellow, spherical nodules in cortex or attached to capsule (often bilateral)
  12. What is 2nd most common neoplasia in adult ferrets? Females or males more? Those neutered early or late?
    • adrenal gland neoplasia
    • female > male
    • neutered early (2-4 mo) due to chronic trophic stimulation of zona reticularis by LH
  13. What are clinical signs seen w/functional proliferative lesions in ferrets?
    • vulvular enlargement
    • bilaterally symmetric alopecia (ventral abdomen/med rear legs)
    • PU/PD
    • palpable mass on cranial kidney
    • anemia/thrombocytopenia
    • pyometra
    • squamous metaplasia of prostate
    • incr. estradiol 17-B
  14. What are 4 pathogenic mechanisms of Cushing's Disease (hypercorticism)? What is prevalence of each?
    • primary hyperadrenocorticism (10-15%)
    • secondary (80%)
    • iatrogenic/pharmacological (5-10%)
    • ectopic ACTH syndrome/paraneoplastic syndrome
  15. What species get Cushing's?
    old dogs and sometimes horses
  16. What are clinical signs/lesions related to Cushing's? (consider effect on skin, muscles, liver, glucose levels, etc)
    • hyperglycemia (lipolysis, protein breakdown, glyconeogenic)
    • PU/PD/polyphagia
    • hepatomegaly (incr. glycogen in hepatocytes)
    • pendulous abdomen (mm. atrophy/hepatomegaly)
    • muscle wasting
    • skin lesions/alopecia/calcinosis cutis
    • immunosuppression
  17. What are cancerous tumors (some benign) that arise outside pituitary but produce ACTH?
    paraneoplastic syndrome (ectopic ACTH syndrome which can lead to Cushing's)
  18. What is secondary hyperadrenocorticism?
    • bilateral cortical hyperplasia due to increased ACTH from pituitary tumor
    • aka: pituitary dependent hyperadrenocorticism
  19. What are some ways the adrenal glands are affected by primary hypoadrenocorticism? Why can primary addison's be fatal?
    • bilateral idiopathic cortical atrophy (young to mid-aged female dogs)
    • bilateral destruction of adrenal gland
    • iatrogenic (sudden w/drawal after prolonged steroid admin)
    • -lack of mineralocorticoids can be lethal!
  20. What is secondary hypOadrenocorticism (which zones are effected)?
    ACTH deficiency due to atrophy of ONLY INNER 2 ZONES (fasciculata/reticularis)
  21. Can patients w/secondary Addison's regulate glucose levels? Are they at risk for Addisonian crisis?
    • glomerulosa not effected so mineralocorticoids still secreted --> no Addisonian crisis
    • but still unable to regulate glucose
  22. What are clinical signs in dogs with Addison's? (consider effect on heart, GIT, stress response, skin)
    • lethargy, stress intolerance, bradycardia, anorexia, V/D, dehydration/emaciation
    • hyperpigmented in long standing cases (excess MSH)