Endocrine 2 – Pituitary and Adrenal Flashcards

1
Q

If have a tumor above pituitary (ex. in hypothalamus)

A
  • Everything below it will be ‘stopped’/have complications
  • *many effects
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2
Q

GnRH to Somatotrophin: metabolic actions

A
  • Protein synthesis
  • Lipid metabolism
  • Increased insulin resistance
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3
Q

What can also stimulate somatotrophin production?

A
  • Sleep stages III and IV
  • Stress
  • Many others
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4
Q

Pituitary congenital anomalies

A
  • Aplasia or hypoplasia: RARE
  • Pituitary cysts
  • Pituitary dwarfism
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5
Q

Pituitary cysts

A
  • Benign if NO changes to pituitary function
  • *hard to get to cause surrounded by bone
    o Not many places it can go
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6
Q

Pituitary dwarfism

A
  • 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)
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7
Q

What are the 2 forms of diabetes insipidus?

A
  1. Hypophyseal form=central diabetes insipidus
  2. Nephrogenic form
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8
Q

Hypophyseal form (central diabetes insipidus)

A
  • Any lesion that interferes with ADH synthesis OR secretion like damage to pars nervosa or hypothalamus
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9
Q

Nephrogenic form (diabetes insipidus)

A
  • Hereditary defects in ADH receptor or water channels in kidneys
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10
Q

What does diabetes insipidus result in

A
  • 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)
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11
Q

Neutrophil inflammation=abscess

A
  • Sporadic in ruminants and pigs
  • Bacteria
  • Fugus (pyogranulomatous)
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12
Q

Lymphoplasmacytic inflammation

A
  • Smaller animals
  • Viral or protozoan
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13
Q

Pituitary hyperplasia

A
  • Old sheep
  • Hyperplasia of pars intermedia
    o Sometimes it may be an adenoma
  • *usually no clinical signs
  • Compression of adjacent tissue
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14
Q

Corticotroph adenoma

A
  • Pars distalis
  • Secretes ACTH
  • Bilateral hypertrophy of zona fasciculata (and zona reticularis) (CORTEX of adrenal glands)
  • **TOO MUCH CORTISOL
  • **Cushing’s disease
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15
Q

Chromophobe adenoma

A
  • Tumor grew upwards and compressed tissue around it
  • **very little adrenal cortex (bilateral)
    o Other organs would be affected as well
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16
Q

Pituitary pars intermedia dysfunction (PPID): horse

A
  • 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
17
Q

**PPID: clinical syndrome

A
  • PU/PD/PP
  • Muscle atrophy, weakness
  • Laminitis
  • Hirsutism: rough hair coat
  • Crested neck: altered fat deposition
  • Flop sweats
  • Hyperglycemia or hyper-insulinemia
18
Q

Craniopharyngioma

A
  • Adenohypophysis and neurohypophysis destroyed
  • Atrophy of thyroid and adrenal glands
    o Thyroid appears normal size, but is mostly colloid NOT active follicles
19
Q

Medulla : cortex ratio

20
Q

Adrenal secretions: cortex

A
  • Mineralocorticoids: aldosterone (SALT)
  • Glucocorticoids: cortisol (SUGAR)
  • Adrenal androgens (SEX)
21
Q

Adrenal secretions: medulla

A
  • catecholamines
    o NE
    o E
    o Dopamine
22
Q

Primary hypoadrenocorticism

A
  • Bilateral idiopathic adrenal cortical atrophy
    o Destruction of all 3 cortical layers
  • Bilateral destruction of adrenal glands
23
Q

Secondary hypoadrenocorticism

A
  • Destructive pituitary lesions
  • Iatrogenic
    o MOST COMMON CAUSE: sudden withdrawal of synthetic glucocorticoids treatment after prolonged usage
    o *atrophy of inner 2 zones
24
Q

What are the lesions of hypoadrenocorticism?

A
  • Lethargy
  • Stress intolerance
  • Heart: bradycardia
  • GI
  • Skin: hyperpigmentation
  • ***chemistry
    o Hyponatremia * hyperkalemia=hallmarks of ADDISON’S
  • Metabolic: hypoglycemia, hemoconcentration
25
Q

Hyperadrenocorticism

A
  • 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
26
Q

What are the lesions with hyperadrenocorticism?

A
  • 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
27
Q

What are the types of hyperadrenocorticisms?

A
  1. Primary: 10-15%, functional cortical neoplasm or hyperplasia
  2. Secondary: 80%
  3. Iatrogenic: 5-10%
28
Q

Iatragenic Cushing’s

A
  • 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
29
Q

Glucocorticoid-induced hepatopathy

A
  • Very bubbly histology
    o Glycogen being stored
  • Yellow, brown liver (NOT icteric)
  • Enlarged
30
Q

What is calcinosis cutis?

A
  • White chalky material under the skin
  • *mineral deposition
31
Q

Cortical carcinoma

A
  • Atrophy of contralateral organ=due to cortical tumor producing cortisol
  • *enlarged (carcinoma=looks angry)
32
Q

Pheochromocytoma

A
  • 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