Endocrine Pathology Examples Flashcards

1
Q

if adrenal cortex is hyperfunctional what hormones are likely to be affected?

A

aldosterone

cortisol

adrenaline

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2
Q

what would occur to the pituitary with elavated cortisol?

A

ACTH would decrese

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3
Q

what would occur to the contralateral adrenal with increased cortisol

A

atrophy

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4
Q

what effects does overproduction of cortisol lead to

A

gluconeogenic

lipolytic

protein catabolic

anti-inflammatroy

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5
Q

what is the difference between pituitary dependent (PDH) and adrenal dependent (ADH) canine cushing’s

A

pituitary: increased ACTH from pituitary –> bilateral stimulation of adrenals –> increased cortisol from both adrenals ~85% of cases

adrenal dependent: adrenal tumour –> increased cortisol from diseased gland –> negative feedback –> less ACTH from pituitary ~15% of cases

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6
Q

what is the third cause of Cushing’s

A

iatrogenic

exogenous source of steroids act in lieu of adrenal cortex (prednisone)

alopecia, fragile skin syndrome

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7
Q

what is adrenal medulla hypofunction

A

rare

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8
Q

what is hyperfunction of adrenal medulla

A

associated with functional neoplasia –> pheochromocytoma

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9
Q

what hormones are effected if adrenal medulla is hyperfunctional

A

adrenaline, noradrenaline, catecholamines

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10
Q

what is pheochromocytoma

A

most common adrenal medullary tumour

usually non-functional

but if functional –> catecholamine release –> tachycardia, edema, cardiac hypertrophy

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11
Q

what are possible primary causes of hypothyroidism

A

idiopathic follicular atrophy

lymphocytic thyroiditis (immune-mediated)

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12
Q

what are secondary causes of hypothyroidism

A

decreased TSH from pituitary disease

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13
Q

what are the effects of hypothyroidism (3)

A

decreased basal metabolic rate

decreased T3, T4

increased cholesterol

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14
Q

what are the metabolic findings of hypothyroidism in dogs

A
  1. lethargy
  2. weight gain
  3. exercise intolerance
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15
Q

what are the dermatological findings of hypothyroidism in dogs (4)

A
  1. hair thinning
  2. poor quality coat
  3. hyperpigmentation
  4. pyoderma
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16
Q

what is the primary pathology of hypothyroidism in dogs

A

small, often pale thyroid

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17
Q

what is the secondary pathology of hypothyroidism (4)

A
  1. hyperkeratosis
  2. hyperpigmentation
  3. myxedema
  4. atherosclerosis
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18
Q

what does atherosclerosis in hypothyroid dog lead to

A

hyperlipidemia –> endothelial damage –> monocyte adhesion + infiltration, smooth muscle migration and proliferation –> lipid accumulation, extracellularly and intracellularly in macrophages and muscle cells

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19
Q

what is a goitre caused by

A
  1. iodine deficiency
  2. iodine toxicity
  3. goitrogenic plants
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20
Q

what does a goitre result in

A

inadequate T3/T4 synthesis

bilateral enlargement

21
Q

why does inadequate synthesis of T3/T4 lead to bilateral enlargement of the thyroid glands

A

inadequate thyroxine synthesis –> decreased T3/T4 recognized by the hypothalamus and anterior pituitary –> increased TSH release

22
Q

what are the 3 mechanisms for development of goitre

A
  1. dietary iodine deficiency
  2. block of iodine uptake
  3. enzyme defect
23
Q

what is a goitrogen

A

compound which result in hyperplastic goitre

24
Q

what are examples of goitrogens

A

plants: brassica (rape, kale) –> digestion leads to thiocyanate which competes with iodide ions for absorption by thyroid follicular cells
drugs: phenobarbitone, rifampin, increase breakdown of T4 and T3

excessive iodine in diet: foals of mares fed dry seaweed

25
Q

how does enzyme defect cause hypothyroidism

A

dyshormogenesis due to enzyme defect –> impaired thyroglobulin biosynthesis

massive enlargement of thyroid

circulatory level of T3 and T4

26
Q

what is hyperthyroidism

A

unilateral or bilateral

common in cats

27
Q

what are the causes of hyperthyroidism

A
  1. hyperplastic nodules
  2. adenoma
  3. adenocarcinoma (less common)
28
Q

what is primary hyperthyroidism

A

multi-nodular hyperplasia –> thyroid neoplasia –> feline hyperthyroidism –> increased T3/T4 levels –> increased metabolic rate –> cardiac hypertrophy –> sudden death

29
Q

what is secondary hyperthyroidism

A

pituitary dysfunction (very rare) –> feline hyperthyroidism –> increased T3/T4 levels –> increased metabolic rate –> cardiac hypertrophy –> sudden death

30
Q

what causes parathyroid hypofunction

A

rare

unless surgically removed –> causes hypocalcemia

31
Q

what are the causes of hypocalcemia (4)

A
  1. decreased PTH concentration (primary hypoparathyroidism, pseudohypoparathyroidism) –> decreased PTH receptor responsiveness
  2. inadequate Ca mobilization from bone or absorption in intestine (hypovitaminosis D, chronic renal failure, milk fever)
  3. excess urinary excretion of Ca: ethylene glycol toxicosis
  4. unknown: acute pancreatitis in dogs, urinary tract obstruction
32
Q

what is rickets

A

dietary Ca/P/Vit D imbalance –> relative hypocalcemia –> bone resorption and abnormalities of the growth plate

33
Q

how does excess urinary retention lead to hypocalcemia and what is a common cause of this

A

ex. antifreeze

calcium oxalate crystals form –> crystals damage kidney –> renal tubular necrosis –> hypocalcemia

34
Q

what are the 3 causes of secondary hyperparathyroidism

A
  1. renal (response to chronic hypocalcemia)
  2. nutritional (high dietary P, low dietary Ca)
  3. pseudohyperparathyroidism (tumours)
35
Q

how does renal secondary hyerparathyroidism occur

A
  1. chronic renal disease
    - decreased golmerular filtration rate
    - phosphate retention
    - continued stimulation of the parathyroid gland
    - continued resorption of bone

–> fibrous osteodystrophy (bone replaced by fibroblastic tissue, bone remodelling, periosteal new bone formation)

36
Q

how does the normal animal respond to relative hypocalcemia

A

resorption from bone –> phosphate excretion in kidney –> calcium resorption in kidney

37
Q

describe the pathway of secondary renal hyperparathyroidism and chronic renal failure

A
38
Q

how does nutritional secondary hyperparathyroidism occur

A

dietary imbalance of calcium and phosphorus (diets with low Ca or high oxalates, diets with high P and low or normal Ca, occasionally vitamin D deficiency)

leads to increased PTH production

39
Q

how does pseudohyperparathyroidism occur

A

humeral hypercalcemia of malignancy (HHM) –> tumours of non-endocrine origin (lymphoma, multiple myeloma, adenocarcinoma of glands of anal sac)

–> PTHrP (parathyroid hormone related peptide)

–> affected animals have trophic atrophy of the parathyroid glands

40
Q

how does humeral hypercalcemia of malignancy lead to

A

tumour in parathyroid produces parathyroid hormone related peptide –> increased intestinal absorption, resorption from bone and decreased renal excretion of Ca –> hypercalcemia

41
Q

how does functional parathyroid neoplasm lead to hypercalcemia

A

increased PTH –> increased intestinal absorption and resorption of Ca from bone as well as decreased renal excretion of Ca –> hypercalcemia

42
Q

what type of hyperparathyroidism is function parathyroid neoplasm cause

A

primary

43
Q

what is the clinical syndrome of pancreatic islet hypofunction

A

diabetes mellitus

44
Q

what is pancreatic islet hypofunction caused by (4)

A
  1. vacuolar degeneration
  2. amyloidosis (cats)
  3. immune-mediated destruction (dogs)
  4. secondary to pancreatitis
45
Q

what does diabetes mellitus occur

A
46
Q

when does diabetes mellitus occur in cats and dogs

A

common in cats and dogs

in dogs –> spontaneous diabetes (1:200), middle-aged, females 2x > males, some small dog breeds increased incidence (min. poodles, dachshunds, terriers)

47
Q

what are islet cell tumours

A

often B-cell type (insulin secreting)

can still have non-functional neoplasms and hyperplasia of the pancreas

48
Q

what is an insulinoma

A

B-cell (insulin secreting) pancreatic islet hyperfunction

increased insulin –> hypoglycemia –> decreased glucose bioavailabilty –> neurologic signs (weakness, lethargy, collapse, seizures, nervousness)

–> adrenal medulla secretes catecholamines –> increased blood pressure