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Pathology 1 > Endocrine system > Flashcards

Endocrine system Flashcards

1
Q

what is normal thyroid function dependent on

A

trophic stimulation by TSH

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2
Q

what is TSH produced by

A

anterior pituitary

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3
Q

what is TSH production inhibited and stimulated by

A
  • inhibited by T4 and T3

- stimulated by TRH from hypothalamus

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4
Q

how is TRH transported to anterior pituitary

A

hypophyseal portal system

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5
Q

clinical signs of hypothyroidism (9)

A
  • lethargy
  • alopecia
  • weight gain
  • dry hair coat/shedding
  • anestrus
  • hyperpigmentation
  • cold intolerance
  • bradycardia
  • myxedema
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6
Q

clinical lab findings in hypothyroidism (6)

A
  • hypercholesterolemia
  • atherosclerosis
  • corneal lipidosis
  • anemia
  • low T4
  • abnormal TSH
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7
Q

2 causes of hypothyroidism

A
  • lymphatic thyroiditis

- idiopathic thyroid atrophy

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8
Q

how much of thyroid tissue must be lost to show signs of hypothyroidism

A

75%

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9
Q

lymphocytic thyroiditis

A
  • hypothyroidism cause
  • multifocal to diffuse accumulations of lymphocytes, plasma cells, macrophages in thyroid interstitium
  • remaining follicles are smaller
  • necrotic epithelial cells, fibrosis
  • autoantibodies against thyroglobulin and other thyroid antigens
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10
Q

idiopathic thyroid atrophy

A
  • hypothyroidism cause
  • loss of thyroid follicles, replacement by adipose tissue
  • can have inflammation in end stage
  • degenerate follicles are smaller, no colloid
  • epithelial cells may be necrotic
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11
Q

are all dogs affected with lymphocytic thyroiditis likely to be hypothyroid

A

no –> need 75% affected to be hypothyroid

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12
Q

define: goiter

A

non-neoplastic and non-inflammatory enlargement of the thyroid glands

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13
Q

dietary iodine deficiency

A
  • hypothyroidism
  • uncommon in most developed nations
  • reduces ability of thyroid to make T3/T4
  • goitrogenic plants and drugs can cause
  • infant mortality –> alopecia, myxedema, asphyxia from goiter
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14
Q

dietary iodine overload

A
  • hypothyroidism
  • causes hyperplastic goiter (fed lots of seaweed with iodine)
  • inhibition of thyroid peroxidase –> decreases organification of iodine –> decreased thyroxine formation
  • protects animal from massive thyroid hormone release
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15
Q

congenital dyshormonogenetic goiter

A
  • hypothyroidism
  • autosomal recessive condition in sheep, cattle, goats
  • unable to synthesize and secrete adequate quantities of thyroid hormones
  • hyperplastic goiter develops in response to continued TSH stimulation and lack of T3/T4 negative feedback
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16
Q

skin lesions of hypothyroidism

A
  • bilaterally symmetric hair loss
  • increased scales
  • hyperpigmentation
  • endocrine dermatosis (thin epidermis, hyperkeratosis)
  • myxedema
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17
Q

equine congenital hypothyroidism

A
  • iodine deficient soil
  • foals born hypothyroid
  • silky coat, delayed bone ossification, lax tendons, mandibular prognathism
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18
Q

hyperthyoidism clinical signs (8)

A
  • weight loss
  • hyperactivity
  • polyphagia
  • tachycardia
  • PU/PD
  • heart murmur
  • comiting
  • diarrhea
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19
Q

hyperthyroidism clinical lab findings

A
  • increased T4/T3

- CBC non-specific

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20
Q

thyroid pathology of hyperthyroidism

A
  • contain discreet adenomas

- nodular hyperplasia (one or both lobes) –> benign, non-invasive

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21
Q

thyroid glands with nodular hyperplasia

A
  • hyperthyroidism
  • may be normal sized or slightly enlarged
  • follicles with irregular shapes with varying sizes
  • follicles elsewhere in gland are atrophied
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22
Q

thyroid glands with adenomas

A
  • hyperthyroidism
  • enlarged, may be palpable (thyroid slip)
  • adenomas sharply deliniated from surrounding tissue
  • variable follicle structure, may be partially collapsed
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23
Q

cardiac lesions with hyperthyroidism

A
  • left ventricular concentric hypertrophy
  • mild to moderate cardiomegaly
  • may progress to left-sided congestive heart failure
  • reversible
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24
Q

canine hyperthyroidism

A
  • boxers, beagles, goldens
  • similar clinical signs
  • usually associated with thyroid carcinoma –> only some are functional (owners notice neck mass)
  • highly malignant neoplasms
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25
Q

canine hyperadrenocorticism basic info

A
  • chronic overproduction of cortisol by hyperactive cells of adrenal cortex
  • clinical signs related to effects of glucocorticoid hormone on organs
26
Q

clinical signs of canine cushing’s (8)

A
  • PU/PD
  • polyphagia
  • abdominal distension
  • muscular weakness
  • alopecia/acne/calcinosis cutis
  • increased panting
  • testicular atrophy/anestrus
  • myopathy
27
Q

clinical lab findings for cushing’s

A
  • CBC: mature neutrophilia, monocytosis, lymphopenia
  • serum chem: elevated ALP ALT, cholesterol, glucose, insulin, lipids - decreased BUN
  • ACTH stim is gold standard
28
Q

3 causes of canine cushing’s

A
  • pituitary dependent bilateral adrenal cortical hyperplasia/hypertrophy (85%)
  • primary functional adrenocortical adenoma/carcinoma
  • iatrogenic
29
Q

pituitary dependent bilateral adrenal cortical hyperplasia/hypertrophy and canine cushing’s

A
  • 85% of spontaneous cushing’s
  • associated with corticotrophs of pituitary
  • macroadenomas damage hypothalamus
  • rarely malignant
30
Q

primary functional adenocortical adenoma/carcinoma and canine cushing’s

A
  • 10-15% of cases

- non-neoplastic remnant adrenal cortical tissue atrophied from negative feedback inhibition

31
Q

liver problems and canine cushings’s

A
  • steroid hepatopathy
  • liver is grossly enlarged and pale
  • enlarged and vacuolated hepatocytes
32
Q

skin problems and canine cushing’s

A
  • endocrine dermatosis
  • calcinosis cutis
  • atrophy of sweat glands
33
Q

clinical signs of equine PPID (8)

A
  • chronic lameness and abscesses
  • PU/PD
  • polyphagia
  • muscle weakness/wasting
  • somnolence
  • hyperpyrexia
  • hyperhidrosis
  • hirsutism
34
Q

clinical lab findings for equine PPID

A
  • hyperglycemia and glucosuria

- plasma cortisol levels normal to slightly elevated

35
Q

etiology of equine PPID

A

pituitary tumor of pars intermedia

36
Q

type 1 DM

A
  • immune destruction of pancreatic islet beta cells
  • insulin therapy required to prevent ketoacidoss and death
  • influx of lymphocytes into pancreatic islets –> beta cell destruction
  • small number of canine cases, very rare in cats
37
Q

type 2 DM

A
  • cats and humans, not in dogs
  • insufficient insulin secretion relative to metabolic demand
  • insulin resistance
  • progressive loss of beta cells with concurrent deposition of amyloid (formed from islet amyloid peptide IAPP)
38
Q

secondary DM

A
  • may occur in dogs due to chronic relapsing pancreatitis with secondary (non-specific) destruction of pancreatic islets
  • may occur in cases of hyperadrenocorticism or growth hormone excess (acromegaly) due to growth hormone secreting pituitary tumor
39
Q

diabetic ketoacidosis

A
  • insulin deficiency and counter-regulatory hormone excess
  • insulin deficiency increases release of FFA from adipose cells –> FFA converted in liver to ketone bodies –> increased entry of FFA into liver –> fatty acid oxidation
  • excess ketone bodies lead to acidosis and ketonuria –> osmotic duiresis and dehydration
40
Q

cataracts

A
  • fairly common in diabetic dogs
  • due to conversion of glucose to sorbitol and fructose in the lens (aren’t freely permeable)
  • osmotic swelling and destruction of lens cells
41
Q

neuropathy

A
  • peripheral demyelinating neuropathy
  • diabetic cats with “lameness”
  • plantigrade stance on hind limbs due to reduced nerve conduction velocity
  • can manifest as megacolon with severe constipation
42
Q

primary hyperparathyroidism hormone info

A
  • not very common
  • PTH produced in parathyroid gland, secreted in response to decreased Ca ion concentrations in blood
  • PTH promotes increased Ca ions in blood
43
Q

features of primary hyperparathyroidism

A
  • older dogs and cats

- lethargy, hypercalcemia, hyperphosphatemia, increased PTH, PU/PD, demineralization of bone

44
Q

etiology of primary hyperparathyroidism

A
  • parathyroid (chief cell) ademonas: uncommon but most common cause of this (enlargement of one parathyroid gland)
  • parathyroid (chief cell) carcinomas: rare cause (invade surrounding tissue)
45
Q

features of humoral hypercalcemia of malignancy (HMM; pseudohyperparathyroidism)

A
  • similar to primary hyperparathyroidism
  • milder hypercalcemia
  • PTH levels may be within normal range
46
Q

etiology of humoral hypercalcemia of malignancy (HMM; pseudohyperparathyroidism) - basic info

A
  • many (usually malignant) neoplasms

- most often due to secretin of parathyroid hormone-related protein (PTHrP) –> binds to PTH receptor in bone and kidney

47
Q

3 primary mechanisms by which humoral factors can induce hypercalcemia in HMM

A
  • stimulation of osteoclastic bone resorption
  • increase in calcium reabsorption from kidney
  • increase in calcium reabsorption from intestines
48
Q

tumors associated with pseudohyperparathyroidism

A
  • dogs: apocrine adenocarcinoma or anal sac (95% metastasize), lymphosarcoma (usually T-cell - increased PTHrP), other neoplasms
  • horses: squamous cell carcinoma
49
Q

pancreatic endocrine neoplasia - cells affected and products

A
  • beta cells (insulin, IAPP)
  • alpha cells (glucagon)
  • gamma cells (somatostatin)
  • PP-cells (pancreatic polypeptide)
  • fetal cells (gastrin)
  • other: calcitonin gene-related peptide
50
Q

dogs and pancreatic endocrine neoplasias

A
  • uncommon in all breeds

- carcinomas more common than adenomas

51
Q

other domestic species and pancreatic endocrine neoplasias

A
  • ferrets: relatively common (adrenal cortical adenomas/carcinomas)
  • very rarely reported in other domestic species
52
Q

pathology of pancreatic endocrine neoplasias

A
  • firm, dense fibrous texture when cut
  • adenomas are well delineated and encapsulated
  • carcinomas are poorly delineated and invade surrounding tissues
  • polyhederal cells in lobular pattern
53
Q

insulinomas

A
  • hypoglycemia from inappropriate secretion of insulin

- muscle tremors and fasciculation, seizures, coma, death

54
Q

glucagonomas

A
  • rare in dogs

- associated with superficial necrolytic dermatitis

55
Q

gastrinomas

A
  • rare in dogs
  • associated with gastrin hypersecretion
  • GI issues
56
Q

pheochromocytoma

A
  • neoplasm from chromaffin cell of adrenal medulla
  • secretion of catecholamines (norepinephrine)
  • dogs and cattle
  • 50% show evidence of malognancy (adrenal vein –> caudal vena cava)
57
Q

hypoadrenocorticism (addison’s disease)

A
  • adrenal cortical insufficiency
  • causes: idiopathic (all layers affected), adrenitis (bacterial and parasitic agents), adrenocortical hemorrhage (sepsis)
58
Q

pathogenesis of addison’s disease

A
  • less potassium excreted –> hyperkalemia

- less Na/Cl reabsorbed –> hypernatremia, hyperchloriduria

59
Q

clinical signs of addison’s disease

A
  • result of deficient production of corticosteroids
  • non-specific symptoms, variety of them
  • circulatory collapse, hyporension, emesis, diarrhea, anorexia
60
Q

diabetes insipidus

A
  • inadequate production of ADH (hypophyseal/central form) OR when target cells in kidney fail to respond to ADH (nephrogenic form)
  • from compression/destruction of pars nervosa, infundibular stalk, or supraoptic nucleus in hypothalamus
  • nephrogenic form: ADH levels normal (body can’t repond)
  • produce large volumes of hypotonic/dilute urine –> PU/PD
61
Q

pituitary dwarfism (panhypopituitarism)

A
  • failure of the oropharyngeal ectoderm of rathke’s pouch to differentiate into trophic hormone secreting cells of pars distalis
  • result is progressively enlarging, multiloculated cyst and absence of adenohypophysis
  • autosomal recessive (german shepherds)

Pathology 1 (3 decks)

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