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Pathology 1 > Endocrine system > Flashcards

Endocrine system Flashcards

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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
canine hyperadrenocorticism basic info
- chronic overproduction of cortisol by hyperactive cells of adrenal cortex - clinical signs related to effects of glucocorticoid hormone on organs
26
clinical signs of canine cushing's (8)
- PU/PD - polyphagia - abdominal distension - muscular weakness - alopecia/acne/calcinosis cutis - increased panting - testicular atrophy/anestrus - myopathy
27
clinical lab findings for cushing's
- CBC: mature neutrophilia, monocytosis, lymphopenia - serum chem: elevated ALP ALT, cholesterol, glucose, insulin, lipids - decreased BUN - ACTH stim is gold standard
28
3 causes of canine cushing's
- pituitary dependent bilateral adrenal cortical hyperplasia/hypertrophy (85%) - primary functional adrenocortical adenoma/carcinoma - iatrogenic
29
pituitary dependent bilateral adrenal cortical hyperplasia/hypertrophy and canine cushing's
- 85% of spontaneous cushing's - associated with corticotrophs of pituitary - macroadenomas damage hypothalamus - rarely malignant
30
primary functional adenocortical adenoma/carcinoma and canine cushing's
- 10-15% of cases | - non-neoplastic remnant adrenal cortical tissue atrophied from negative feedback inhibition
31
liver problems and canine cushings's
- steroid hepatopathy - liver is grossly enlarged and pale - enlarged and vacuolated hepatocytes
32
skin problems and canine cushing's
- endocrine dermatosis - calcinosis cutis - atrophy of sweat glands
33
clinical signs of equine PPID (8)
- chronic lameness and abscesses - PU/PD - polyphagia - muscle weakness/wasting - somnolence - hyperpyrexia - hyperhidrosis - hirsutism
34
clinical lab findings for equine PPID
- hyperglycemia and glucosuria | - plasma cortisol levels normal to slightly elevated
35
etiology of equine PPID
pituitary tumor of pars intermedia
36
type 1 DM
- 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
type 2 DM
- 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
secondary DM
- 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
diabetic ketoacidosis
- 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
cataracts
- 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
neuropathy
- 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
primary hyperparathyroidism hormone info
- 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
features of primary hyperparathyroidism
- older dogs and cats | - lethargy, hypercalcemia, hyperphosphatemia, increased PTH, PU/PD, demineralization of bone
44
etiology of primary hyperparathyroidism
- 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
features of humoral hypercalcemia of malignancy (HMM; pseudohyperparathyroidism)
- similar to primary hyperparathyroidism - milder hypercalcemia - PTH levels may be within normal range
46
etiology of humoral hypercalcemia of malignancy (HMM; pseudohyperparathyroidism) - basic info
- many (usually malignant) neoplasms | - most often due to secretin of parathyroid hormone-related protein (PTHrP) --> binds to PTH receptor in bone and kidney
47
3 primary mechanisms by which humoral factors can induce hypercalcemia in HMM
- stimulation of osteoclastic bone resorption - increase in calcium reabsorption from kidney - increase in calcium reabsorption from intestines
48
tumors associated with pseudohyperparathyroidism
- dogs: apocrine adenocarcinoma or anal sac (95% metastasize), lymphosarcoma (usually T-cell - increased PTHrP), other neoplasms - horses: squamous cell carcinoma
49
pancreatic endocrine neoplasia - cells affected and products
- beta cells (insulin, IAPP) - alpha cells (glucagon) - gamma cells (somatostatin) - PP-cells (pancreatic polypeptide) - fetal cells (gastrin) - other: calcitonin gene-related peptide
50
dogs and pancreatic endocrine neoplasias
- uncommon in all breeds | - carcinomas more common than adenomas
51
other domestic species and pancreatic endocrine neoplasias
- ferrets: relatively common (adrenal cortical adenomas/carcinomas) - very rarely reported in other domestic species
52
pathology of pancreatic endocrine neoplasias
- 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
insulinomas
- hypoglycemia from inappropriate secretion of insulin | - muscle tremors and fasciculation, seizures, coma, death
54
glucagonomas
- rare in dogs | - associated with superficial necrolytic dermatitis
55
gastrinomas
- rare in dogs - associated with gastrin hypersecretion - GI issues
56
pheochromocytoma
- 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
hypoadrenocorticism (addison's disease)
- adrenal cortical insufficiency - causes: idiopathic (all layers affected), adrenitis (bacterial and parasitic agents), adrenocortical hemorrhage (sepsis)
58
pathogenesis of addison's disease
- less potassium excreted --> hyperkalemia | - less Na/Cl reabsorbed --> hypernatremia, hyperchloriduria
59
clinical signs of addison's disease
- result of deficient production of corticosteroids - non-specific symptoms, variety of them - circulatory collapse, hyporension, emesis, diarrhea, anorexia
60
diabetes insipidus
- 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
pituitary dwarfism (panhypopituitarism)
- 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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