Endocrine 2 – Pituitary and Adrenal Flashcards
If have a tumor above pituitary (ex. in hypothalamus)
- Everything below it will be ‘stopped’/have complications
- *many effects
GnRH to Somatotrophin: metabolic actions
- Protein synthesis
- Lipid metabolism
- Increased insulin resistance
What can also stimulate somatotrophin production?
- Sleep stages III and IV
- Stress
- Many others
Pituitary congenital anomalies
- Aplasia or hypoplasia: RARE
- Pituitary cysts
- Pituitary dwarfism
Pituitary cysts
- Benign if NO changes to pituitary function
- *hard to get to cause surrounded by bone
o Not many places it can go
Pituitary dwarfism
- German shepherds
- *panhypopituitarism: effects all of the endocrine functions due to lack of signals to thyroid, adrenals and gonads
- Usually do not last to adulthood (especially in cats)
What are the 2 forms of diabetes insipidus?
- Hypophyseal form=central diabetes insipidus
- Nephrogenic form
Hypophyseal form (central diabetes insipidus)
- Any lesion that interferes with ADH synthesis OR secretion like damage to pars nervosa or hypothalamus
Nephrogenic form (diabetes insipidus)
- Hereditary defects in ADH receptor or water channels in kidneys
What does diabetes insipidus result in
- PU/PD
- Urine with low osmolality even after water deprivation
- *administration of exogenous ADH will lead to a rapid increase in urine osmolarity above that of plasma in hypophyseal form (BUT NOT in nephrogenic form)
Neutrophil inflammation=abscess
- Sporadic in ruminants and pigs
- Bacteria
- Fugus (pyogranulomatous)
Lymphoplasmacytic inflammation
- Smaller animals
- Viral or protozoan
Pituitary hyperplasia
- Old sheep
- Hyperplasia of pars intermedia
o Sometimes it may be an adenoma - *usually no clinical signs
- Compression of adjacent tissue
Corticotroph adenoma
- Pars distalis
- Secretes ACTH
- Bilateral hypertrophy of zona fasciculata (and zona reticularis) (CORTEX of adrenal glands)
- **TOO MUCH CORTISOL
- **Cushing’s disease
Chromophobe adenoma
- Tumor grew upwards and compressed tissue around it
- **very little adrenal cortex (bilateral)
o Other organs would be affected as well
Pituitary pars intermedia dysfunction (PPID): horse
- PI cells produce excess POMC derived peptides
o Varying levels of ACTH, CLIP, alpha-MSH, beta-endorphin
o ACTH: may be biologically inactive - Called Equine Cushing’s but it is NOT really Cushing’s
o Horses do NOT get Cushing’s - *it is a clinical syndrome
**PPID: clinical syndrome
- PU/PD/PP
- Muscle atrophy, weakness
- Laminitis
- Hirsutism: rough hair coat
- Crested neck: altered fat deposition
- Flop sweats
- Hyperglycemia or hyper-insulinemia
Craniopharyngioma
- Adenohypophysis and neurohypophysis destroyed
- Atrophy of thyroid and adrenal glands
o Thyroid appears normal size, but is mostly colloid NOT active follicles
Medulla : cortex ratio
- 1:2
Adrenal secretions: cortex
- Mineralocorticoids: aldosterone (SALT)
- Glucocorticoids: cortisol (SUGAR)
- Adrenal androgens (SEX)
Adrenal secretions: medulla
- catecholamines
o NE
o E
o Dopamine
Primary hypoadrenocorticism
- Bilateral idiopathic adrenal cortical atrophy
o Destruction of all 3 cortical layers - Bilateral destruction of adrenal glands
Secondary hypoadrenocorticism
- Destructive pituitary lesions
- Iatrogenic
o MOST COMMON CAUSE: sudden withdrawal of synthetic glucocorticoids treatment after prolonged usage
o *atrophy of inner 2 zones
What are the lesions of hypoadrenocorticism?
- Lethargy
- Stress intolerance
- Heart: bradycardia
- GI
- Skin: hyperpigmentation
- ***chemistry
o Hyponatremia * hyperkalemia=hallmarks of ADDISON’S - Metabolic: hypoglycemia, hemoconcentration
Hyperadrenocorticism
- COMMON endocrinopathy in DOGS
o Less in horses, rare in other animals - OLDER dogs
o Smaller with a big pot belly - Combined gluconeogenic, lipolytic, protein catabolic and immunosuppressive effects of corticosteroids
What are the lesions with hyperadrenocorticism?
- PU/PD/PP
- Hepatomegaly
- *pendulous abdomen
- Skin lesions: dermal atrophy, bilateral alopecia
- Dystrophic mineralization: lung, muscle, stomach
- Bacterial infections
- Clinical path test
o Hypercoagulability, eosinopenia, lymphopenia
What are the types of hyperadrenocorticisms?
- Primary: 10-15%, functional cortical neoplasm or hyperplasia
- Secondary: 80%
- Iatrogenic: 5-10%
Iatragenic Cushing’s
- Atrophy of cortex
- Long-term, daily administration of large doses of corticosteroids (exogenous)
- Decreased ACTH
- *why can get an Addisonian crisis if immediately remove the steroids=not able to function
Glucocorticoid-induced hepatopathy
- Very bubbly histology
o Glycogen being stored - Yellow, brown liver (NOT icteric)
- Enlarged
What is calcinosis cutis?
- White chalky material under the skin
- *mineral deposition
Cortical carcinoma
- Atrophy of contralateral organ=due to cortical tumor producing cortisol
- *enlarged (carcinoma=looks angry)
Pheochromocytoma
- Mainly in dogs, horses and cattle(seen in any species)
- Large and encapsulated
- *invades the vena cava and metastasize extensively (ex. liver cause that is where it goes first)
- Rarely functional, if so:
o Secrete E and/or NE
o Can cause tachycardia, edema and cardiac hypertrophy = how they present - If hasn’t invaded vena cava and only one=can be removed and submitted for biopsy