Path 1 - Endocrine

drraythe's version from 2016-03-06 17:32

Endocrine Quick & Dirty

Be familiar w/ this chart of fxnl neoplasms!


Question Answer
**Neoplasms → Explain the difference btwn 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
***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 → HORSES: What do the lesions grossly look like?Large yellow to white, multinodular neoplasms extending out of the Sella Turcica → compression of the hypothalamus
****When I say POMC, you thinkHorse w/ an Adenoma of the Pars Intermedia → Adrenocortical Hyperplasia → Hirsutism
***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
**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
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
**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 amts 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 is a CONSISTENT finding in the case of fxnal proliferative lesions in ferrets?↑ plasma concentrations of estradiol-17β (ferrets are moody bc of all the estrogen)
**What is the cz of 1⁰ HYPERadrenocorticism?Usually czd by a Cortical Neoplasm, especially Adenoma OR an Idiopathic Adrenocortical Hyperplasia (MOST COMMON)
**What is happening in 2⁰ HYPERadrenocorticism?Bilateral Cortical Hyperplasia due to ↑ ACTH from pituitary tumor (Pituitary Dependent Hyperadrenocorticism (PDH))
**Explain what Ectopic ACTH syndrome is?This is a PARANEOPLASIA! Can spontaneously produce ACTH which can result in HypERcortisolism

Various cancers:
Small Cell Lung Cancer
Carcinoid tumor
Pancreatic Islet Cell Tumors
Medullary Carcinomas of the Thyroid
***CS of HypERcortisolism are dependent on the general effects of cortisol itself. Effects on proteins, sugars & fats & Role in inflammation?Cortisol is Glyconeogenic
Protein Catabolic → MUSCLE WASTING (so, makes sugar but breaks down proteins & fats)
Anti-inflammatory effects (Corticosteroids)
**How does hypercortisolism affect the liver?HEPATOMEGALY! Due to steroid hepatopathy, ie. ↑ glycogen in hepatocytes bc gluconeogenesis
**How does hypercortisolism affect the skin?It czs dermal atrophy (catabolic processes, affects elasticity of skin & makes it thinner)
Bilateral Symmetric Alopecia (atrophy of hair follicles & sebaceous glands)
Dystrophic Mineralization of the skin ("Calcinosis Cutis"), lung, mm & stomach (due to altered collagen & elastin)
*Which cz of 1⁰ HYPOadrenocorticism is most common?Bilateral Idiopathic Adrenal Cortical Atrophy
**Bilateral Idiopathic Adrenal Cortical Atrophy → Who is this most common in? Why does this happen? What are the main results of this on the adrenal gland & what is most concerning? (Not clinical signs yet)MOST COMMON type of 1⁰ Addison’s & its most common in young to middle-age female dogs. This is an autoimmune/inherited disorder which can result in destruction of ALL 3 CORTICAL LAYERS → deficient production of all cortical hormones. Why does this matter? Bc deficiency of mineralocorticoids can be lethal
***Lymphocytic Infiltration in Adrenal Cortex w/ destruction of cortical tissue czing Adrenalitis can lead to?Idiopathic Atrophy & Addison's Dz
*Which type of HYPOadrenocorticism affects MINERALCORTICOID PRODUCTION?1⁰!! (Not 2⁰)
**What is the hallmark clinical sign of Addison’s?HYPERKALEMA! (cortisol is sodium saving & potassium losing. so no cortisol means sodium losing & potassium saving)
**What is the general energy level of an animal w/ Addison’s?Lethargic w/ stress intolerance
**How does Addison’s affect the GI?Anorexia
Vomiting/Diarrhea (non-specific gastroenteritis) → dehydration & emaciation
***What are 3 main electrolytes affected by Addison’s & how are they affected?K - HYPERKALEMIA (hypokaluria) → Weakness & Bradycardia
Na - HYPONATREMIA (hypernaturia)
Cl - HYPOCHLORIDEMIA (hyperchloriduria)
**How does Addison’s affect the skin?In chronic cases, you will see hyperpigmentation due to an excess of pituitary MSH that develops reciprocally to a ↓ of an inhibitory cortisol (reduced negative feed-back)
**What are the 4 pathogenic mechanisms for developing a goiter?(1) Iodine deficient diet
(2) Excess dietary
iodide (NOT iodine)
(3) Goitrogenic compounds interfering w/ thyroxinogenesis
(Brassica & Cruciferae plants)
(4) Genetic enzyme defects in hormone synthesis
**What are the lesions associated w/ a colloid goiter?Follicles are larger (Macrofollicles) & have densely eosinophilic colloid & less vascularized (colloid likes color, but not blood red)
***Follicular cell adenoma → Most common in who?More common in CATS than in dogs & horses
**How does hyperthyroidism affect the cardiovascular system? How does it affect electrolytes?Hypertrophic Cardiomyopathy in CATS due to increased heart rate. This might be complicated by the fact there can be disturbances in calcium homeostasis
****What are 5 etiological czs of HYPOthyroidism (KNOW ALL!)?(1) Idiopathic follicular atrophy (“collapse”)
(2) Lymphocytic thyroiditis
(3) Bilateral nonfunctional tumors
(4) Chronic pituitary lesions (compression/destruction)
(5) Severe prolonged iodine def (prevents production of both T4 & T3)
*What's the clinical expression of hypothyroidism he super emphasized w/ colors?Hypercholesterolemiaatherosclerosis
**How does HYPOthyroidism affect body weight? How does it affect energy, growth & metabolismTRAGIC FACE
Can cz a reduction in basal metabolic rate! this leads to:
Weight gain
Muscular weakness & slow reflexes
Cretinism (stunted growth) in young animals
*How does hypothyroidism affect the musculoskeletal system?Due to the ↓ in basal metabolic rate → muscular weakness, slow reflexes, joint pain & effusion
*How does hypothyroidism affect the skin?Hyperkaratosis (so see lots of skin flakes)
Bilateral symmetric alopecia (telogen hairs....lack of thyroid hormone keeps hairs in the telogen which is the resting phase where hair is more easily epilated)
Follicular keratosis
(also calcinosis cutis/atropy)
*HypOthyroidism czs HYPERCHOLESTEROLEMIA!!! This results in...(4)Atherosclerosis
Glomerular & corneal lipidosis
**Hyperthyroidism is czd by what general kind of problem? 3 situations which fall under this cz?1⁰ hyperfxn!! It happens w/ Thyroid Carcinoma in dogs & Thyroid Adenoma or Multinodular Hyperplasia in CATS
**Chronic Renal Dz in dogs is occasionally associated w/ persistent HyERrcalcemia why?Kidney is unable to degrade PTH (along w/ ↓ urinary excretion of Ca+ = ↑ PTH & ↑ Ca)
***If I say Hyperparathyroidism, what 2 conditions do you think?Fibrous Osteodystrophy & Hypercalcemia
**Parturient paresis (milk fever) → Due to a prob w/ HYPO or HYPER parathyroidism?HYPO! Cow will be down w/in a few hours!!
**What are the 3 neoplasms which are seen in 1º hyperparathyroidism? Which is more common & happens most commonly in who?(1) Parathyroid Hyperplasia
(2) Parathyroid Adenomas = MORE COMMON (occur in older dogs; usually single, encapsulated & fxnal)
(3) Parathyroid Carcinomas (rarely)
**Explain what is happening in 1º hyperparathyroidism which leads to lameness?Tumor produces excess PTH → osteolytic & osteoclastic bone → fibrous osteodystrophy → lameness due to fractures
**Dietary 2º hyperparathyroidism happens in who? Which species in which dietary circumstances, specifically?This can occur in all species, but especially in:
Dogs & cats on all-meat diets
Horses on ↑ grain/poor quality roughage or all-bran diets (Miller's Dz)

Nonhuman primates
**In general terms, which kind of diets lead to dietary 2º hyperparathyroidismGenerally, ↓ Ca ↑ P diets
*Which type of diet puts CATS/DOGS at a risk for 2º hyperparathyroidism?All-meat diets
*Which type of diet puts HORSES at risk for 2º hyperparathyroidism?↑ grain/poor quality roughage or all-bran diets
**Explain how renal failure leads to 2º hyperparathyroidismRenal dz, the kidney has impaired activation of Vit D3 (unable to absorb Ca from the gut). due to ↓ GFR P starts building up in the system. The low Ca, stimulates PTH to be produced. Impaired activation of Vit D3 also ↓ renal degradation of PTH, so PTH also builds up = the body sucks more Ca out of bones → RUBBER JAW IN DOGS & CATS


Question Answer
**Manifestations of hypothyroidism in the dog could include each of the following EXCEPT:
   A. epidermal atrophy
   B. dermal myxedema
   C. atherosclerosis
   D. abnormal estrus cycles
   E. elevated basal metabolic rate
E. elevated basal metabolic rate
**Which of the following lesions would NOT result in Diabetes Insipidus?:
   A. tumor metastasis into the pituitary gland
   B. destruction of hypothalamic neurosecretory cells
   C. pituitary gland abscess czing destruction of the pars nervosa
   D. adrenocortical atrophy w/ destruction of the zona glomerulosa
   E. traumatic severance of the infundibular stalk of the pituitary gland
D. adrenocortical atrophy w/ destruction of the zona glomerulosa
**Which 1 of the following features would NOT be expected w/ a very large fxnl tumor arising from the pars intermedia in the horse?:
   A. hirsutism from interference w/ cyclic shedding
   B. abnormal ACTH plasma levels
   C. diabetes insipidus
   D. hyperglycemia
   E. decreased susceptibility to bacterial infxns
E. decreased susceptibility to bacterial infxns
**A horse w/ Hirsutism from interference w/ cyclic shedding is due to:
   A. pars intermedia tumor
   B. widespread tumor metastasis
   C. a fxnl adrenocortical adenoma
   D. epidermal atrophy
   E. abnormal estrus cycle
A. pars intermedia tumor

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