endocrine diseases Flashcards

1
Q

explain the etiology, clinical signs, diagnosis, and treatment of hypothyroidism

A

etiology:
-low levels of circulating T4 hormone (high TSH, low T4)
-acquired disease
-most common in middle-aged female canine

Clinical signs:
-weight gain w/o change in diet
-lethargy
-bilateral alopecia on back
- “rat tail” (hair loss in tail)
-recurrent skin/ear infections
-darkening of skin around groin/armpit

Diagnosis:
-serum chemistry (low T3 and T4, high serum cholesterol, mild anemia)
-TSH stimulation testing (tests negative feedback mechanism)
-IMMULITE/Equilibrium dialysis (test of free T4; separates bound and unbound T4)

treatment:
-supplement thyroid replacement hormone (levothyroxine sodium)

good prognosis; routine blood tests necessary

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2
Q

explain the etiology, clinical signs, diagnosis, and treatment of hyperthyroidism

A

etiology:
-common in middle-aged/older cats
-increase in T3 and T4 despite lack of stimulation from pituitary gland
-thyroid gland enlargement

Clinical signs:
-polyphagia (increased appetite)
-weight loss (due to increase metabolism)

Diagnosis:
-characteristic look: weight loss and muscle wasting (esp. in face)
-enlarged thyroid gland
-serum chemistry (increase T4, liver enzymes and metabolic products)

treatment:
-surgery: remove thyroid
-radioactive therapy: radioactive iodine-131 (destroys thyroid tissue=> decrease T4 concentration)
-anti-thyroid drugs: bind to iodine; stop the incorporation into T4

good prognosis; routine bloodwork necessary to ensure effectiveness of medication

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3
Q

explain the etiology, clinical signs, diagnosis, and treatment of goiter

A

etiology:
-small ruminants, avian, equine
-acquired or congenital
-enlargement of thyroid gland
-associated w/ iodine deficiency=> triggers thyroid follicular cells=> increase size of thyroid

Clinical signs:
-enlarged thyroid
-dry skin
-tendon laxity
- poor reproductive function

Diagnosis:
-enlargement of thyroid gland
-history of low dietary iodine
-salt fortified w/ iodine

treatment:
-supplement iodine in diet

good prognosis

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4
Q

explain the etiology, clinical signs, diagnosis, and treatment of diabetes mellitus

A

etiology:
-middle-aged/older female canines
-all age MN feline
-autoimmune destruction of beta cells in pancreas => decrease/stop insulin production
-after meal=low/no insulin => increase glucose (hyperglycemia)

Clinical signs:
-polydipsia/polyuria
-weight loss
-polyphagia (increase appetite)
-cataracts
-infections
-hepatomegaly
-plantigrade posture in cats (back legs fully planted on ground)

Diagnosis:
-PE
-serum chemistry (fasting blood glucose >200 mg/dL
-urine glycosuria (urinalysis)

treatment:
-diet
-insulin hormone injection

good prognosis with treatment:
-type 1 requires lifelong insulin therapy
-regular monitoring of glucose levels to avoid insulin overdose

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5
Q

explain the etiology, clinical signs, diagnosis, and treatment of equine metabolic syndrome

A

etiology:
-similar to type 2 diabetes
-genetic predisposition
-middle-aged horses

Clinical signs:
-generalized obesity/regional adiposity (crest-y neck/fat at base of tail)
-insulin resistance (hyperinsulinemia)
-laminitis (inflammation of hoof)

Diagnosis:
-fasting insulin >20 uU/mL
-oral sugar test to confirm diagnosis/insulin resistance (fast for 3-12 hrs)

treatment:
-low starch diet
-muzzle to prevent grazing
-exercise

good prognosis with proper diet and exercise

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6
Q

explain the etiology, clinical signs, diagnosis, and treatment of hypoadrenocorticism/Addison’s Disease

A

etiology:
-damaged adrenal gland
-low cortisol and aldosterone production
-increase ACTH production
-hyponatremia (low sodium in the blood)
-secondary: pituitary stops producing ACTH

Clinical signs:
-depression
-lethargy
-weakness
-anorexia
-vomiting/diarrhea
-polyuria
-bradycardia
-dehydration

Diagnosis:
-serum chemistry: decrease in circulating aldosterone, hyponatremia (low sodium), hyperkalemia (high potassium)
-urinalysis
-ACTH stimulation test (injection given to stimulate ACTH production, cortisol levels then tested)

treatment:
-IV fluid therapy & sodium
-oral glucocorticoids
-prednisolone (corticosteroid): prevent nausea, weakness, muscle pain

good prognosis; life-long treatment and veterinary monitoring

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7
Q

explain the etiology, clinical signs, diagnosis, and treatment of hyperadrenocorticism/Cushing’s Syndrome

A

etiology:
-pituitary gland tumor= hypersecretion of ACTH and cortisol
-possible adrenal tumor

Clinical signs:
-increased thirst and urination
-polyphagia
-alopecia and hyperpigmentation
-panting
-potbelly/abdominal enlargement
-muscle weakness
-abnormal gonad (testes/ovary) function

Diagnosis:
-serum chemistry: increase cortisol, liver enzymes, cholesterol, glucose
-ACTH stimulation test: exaggerated cortisol response
-dexamethasone suppression test: stops ACTH secretion=reduces circulating cortisol

treatment:
-surgical removal of tumor
-medications for pituitary tumor (decrease cortisone and progesterone production, precursors to cortisol)
-radiation therapy

guarded prognosis; 2-5 yr expectancy w/ or w/o treatment

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8
Q

explain the etiology, clinical signs, diagnosis, and treatment of Pituitary Pars Intermedia Dysfunction (PPID) EQUINE

A

etiology:
-tumor of pars intermedia (section between anterior and posterior pituitary gland) =decrease dopamine production=increase ACTH and cortisol
-high circulating cortisol reduces immune response, loss of muscle mass, increase metabolism and weight loss

Clinical signs:
-weight loss/muscle wasting
-thick curly haircoat that doesn’t shed
-lethargy
-abnormal sweating
-increase urination and drinking
-recurring laminitis
-insulin resistance
-persistent infection and hoof abscesses

Diagnosis:
-clinical signs
-dexamethasone suppression test
-ACTH in blood sample
-serum insulin

treatment:
-good husbandry practices
-daily pergolide: decrease ACTH and cortisol

good prognosis with treatment; horses may require body clipping

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9
Q

explain the etiology, clinical signs, diagnosis, and treatment of Primary Hyperparathyroidism

A

etiology:
-keeshond congenital disease
-parathyroid adenoma or carcinoma=enlargement of parathyroid gland=increase PTH and hypercalcemia (high blood calcium levels

Clinical signs:
-hypercalcemia
-anorexia
-vomiting
-constipation
-increased thirst and urination
-lethargy, exercise intolerance
-urinary calculi (kidney stones), cystitis (inflammation of bladder), incontinence

Diagnosis:
-serum chemistry: increase PTH and calcium levels
-enlargement of parathyroid gland
-keeshond genetic testing

treatment:
-surgical removal of affected parathyroid gland
-supplement vit D and Ca for life

guarded prognosis; depends on severity and progression of disease

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10
Q

explain the etiology, clinical signs, diagnosis, and treatment of nutritional secondary hyperparathyroidism

A

etiology:
-livestock with poor diets
-imbalance Ca:P ratio

Clinical sings:
-intermittent lameness
-loose teeth
-random bone fractures
-enlarged bones of the skull from fibrous tissue

Diagnosis:
-clinical signs and history
-radiographs: thinning of bone, enlarged skull, fibrous tissue replacing bone tissue
-decrease excretion of Ca in urine

treatment:
-correct Ca:P ratio in diet (5:1 initially and then 1:1 or 2:1)
-mineral supplementation in fortified feed

good prognosis with treatment

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11
Q

explain the etiology, clinical signs, diagnosis, and treatment of milk fever/hypocalcemia

A

etiology:
-blood Ca deficiency around calving time
-<8.0 mg/dL
-decrease in blood calcium=hyperexcitability of NS=muscle contractions=tetany (muscle spasms) and paralysis

Clinical signs/Diagnosis:
-down cows
-cold extremities
-muscle tremors
-rumen atony, stasis, bloat
-increase HR

treatment:
-IV calcium gluconate (stop treatment when HR returns to normal)

good prognosis with treatment

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