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Systemics- Repro and Endocrine > Endocrine > Flashcards

Endocrine Flashcards

1
Q

What is emiocytosis vs exocytosis

A

Secretion of entire secretory granules into extracellular space vs fusion of granules with cell membrane

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2
Q

What hormone types utilize secretory granules?

A

Polypeptide and catecholamine-secreting endocrine cells only

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3
Q

Features of polypeptide producing endocrine cells

A

ER with ribosomes, prominent golgi, secretory granules

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4
Q

Features of steroid producing endocrine cells

A

Large lipid vacuoles that contain cholesterol esters and other precursors, smooth ER, large mitochondria with cytochrome p450 systems
*Lack secretory granules, don’t store product

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5
Q

How do peptide hormones signal? steroids?

A

Peptides- GPCR (cell membrane)
Steroids- lipid soluble, travel through membrane and bind receptors in cytoplasm, travel to nucleus

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6
Q

Half life of peptide vs steroid hormones

A

Short vs long

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7
Q

Features of catecholamines and iodothyronine hormones

A

Tyrosine derivatives
Catecholamines from adrenal medulla, iodothyronines from follicular cells of thyroid
Catecholamines act like polypeptide hormones
Iodothyronines act like steroid hormones

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8
Q

Mechanism of humoral hypercalcemia of malignancy

A

Cancer cells produce PTHrp, which activates PTH receptors in bone and kidney, producing hypercalcemia

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9
Q

Common tumors that cause humoral hypercalcemia of malignancy

A

T cell lymphoma
AGASACA

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10
Q

Clin path findings with HHM

A

Hypercalcemia
Hypophosphatemia
Hypercalciuria
Osteoclastic bone resorption

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11
Q

How do NWPs differ in their vitamin D requirements

A

Require higher levels of vitamin D3, so prone to Vit D Resistant Rickets (type II) and osteomalacia

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12
Q

Causes of prolonged gestation in ruminants

A

Guernsey and Jersey cattle- adenohypophyseal aplasia causes hypoplasia of target organs (Adrenal cortex, thyroid follicular cells, gonads)
Ewes ingesting veratrum californicum- CNS malformations, so no hypothalamic stimulus for pituitary

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13
Q

Types of cells in the pituitary following Pit1 action and GATA2 expression

A

Somatrophs- GH
Lactotrophs- Prolactin
Thyrotrophs- TSH

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14
Q

Type of cells in the pituitary that are Pit1 independent, via Tbx19 and Sf1

A

Corticotrophs- POMC –> ACTH
Melanotrophs- POMC –> MSH
Gonadotrophs- LH/FSH

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15
Q

What cells in the pituitary are acidophilic?

A

Somatotrophs
Lactotrophs

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16
Q

What cells in the pituitary are basophilic? Additional positive stain?

A

Gonadotrophs
Thyrotrophs

PAS

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17
Q

What cells do not have obvious secretory granules (are not acidophilic or basophilic)

A

Chromophobes- corticotrophs and melanotrophs

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18
Q

What does the neurohypophysis do?

A

Contains terminal, unmyelinated axons from neurosecretory neurons from the hypothalamus that secrete oxytocin and ADH

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19
Q

Who is most likely to get juvenile pan hypopituitarism; associated genetic defect in dogs

A

Dogs- GSD, Spitz, Toy Pinscher, Wolfdogs
Eurasian badger; LHX3 gene, autosomal recessive

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20
Q

Which hormones are deficient in panhypopituitarism? Which are not?

A

GH, TSH, prolactin, gonadotropins; ACTH normal maybe

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21
Q

Remnant of distal craniopharyngeal duct- location and who gets it

A

Brachycephalic dogs, periphery of pars tuberalis and distalis

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22
Q

Remnant of proximal craniopharyngeal duct- location and who gets it

A

Brachycephalic dogs, dorsal oral cavity/nasopharynx

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23
Q

Rathke’s pouch ectoderm differentiation failure- location and who gets it

A

Entire pars distalis replaced, causes pituitary dwarfism in GSDs

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24
Q

Most common cause of Cushing’s

A

Corticotroph pituitary adenoma in pars distalis or pars intermedia

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25
Q

Cause of clinical signs in Cushing’s

A

Hyperplasia of adrenal cortices and chronically high cortisol

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26
Q

Which zones are hyperplastic in Cushing’s?

A

Zona fasciculata and reticularis

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27
Q

Who gets adenomas of the pars distalis? Pars intermedia?

A

Brachycephalic; nonbrachycephalic

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28
Q

Difference between adenomas of pars intermedia and pars distalis?

A

Intermedia has numerous colloid-filled follicles between neoplastic cells

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29
Q

Most common pituitary tumor in the horse? Clinical syndrome?

A

Pars intermedia adenoma; Pituitary pars intermedia dysfunction

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30
Q

Who gets PPID more?

A

Females, older

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31
Q

Key histo with equine pars intermedia adenoma

A

Spindle to polygonal eosinophilic cells; Follicles lined by cuboidal cells with colloid

32
Q

Clinical signs with PPID; pathogenesis?

A

PU/PD, hirsutism, hyperhidrosis, laminitis; Most signs due to compression of hypothalamus, also elevated POMC and MSH, CLIP, beta endorphin

33
Q

Most common pituitary tumor in cats; predisposes to

A

Somatotroph; acromegaly, diabetes mellitus

34
Q

Most common pituitary tumor in rats

A

Lactotroph

35
Q

What pituitary tumor do budgies get?

A

Somatotroph

36
Q

Where is the adrenal cortex derived from? Medulla?

A

Mesoderm; neural crest ectoderm

37
Q

Role of zona glomerulosa, fasciculata, and reticularis

A

G- Mineralocorticoids, columns
F- Glucocorticoids, abundant lipid, most of cortex (70%)
R- Sex steroids

38
Q

Effects of glucocorticoids

A

Sparing of glucose, hyperglycemia, increased gluconeogenesis
Suppress inflammation and immune system
Phagocyte inhibition
Stability of lysosomal membranes
Decreased wound healing

39
Q

Renin-angiotensin system summary

A

Renin produced by juxtaglomerular apparatus, cleaves angiotensinogen to angiotensin I, which is then converted to angiotensin II
Angiotensin II is a vasoconstrictor and trophic for glomerulosa, increasing aldosterone

40
Q

What does ACTH do?

A

Stimulates Fasciculata and reticularis through melanocortin 2 receptors (adenylyl cyclase and cAMP)

41
Q

Difference between idiopathic adrenocortical atrophy and trophic atrophy secondary to pituitary lesion with decrease in ACTH stimulation?

A

Idiopathic adrenocortical atrophy affects all layers of cortex, whereas trophic atrophy only affects inner two layers of cortex, so no electrolyte disturbances

42
Q

Layers affected by nodular hyperplasia of adrenal cortex

A

G and F

43
Q

Layers affected by diffuse adrenal cortical hyperplasia; cause?

A

Corticotroph adenoma, causes hyperplasia of Fasciculata and reticularis

44
Q

Associated lesion with adrenal cortical carcinoma; most common in who?

A

Extension into caudal vena cava; Cattle*, occurs in dogs but adenoma more common

45
Q

Most common adrenal tumor in ferrets

A

Cortical carcinoma, usually in left adrenal

46
Q

Clinical signs with ferret adrenal tumor; pathogenesis

A

PU/PD, vulvar enlargement, alopecia; overproduction of estrogenic steroids (estradiol-17beta)

47
Q

Associated lesion in ferrets with adrenal tumors

A

Insulin-producing islet cell tumors

48
Q

Predisposing factors for ferret adrenal tumors

A

Female, early gonadectomy (elevated LH secretion due to lack of negative feedback)

49
Q

Role of adrenal medulla; IHCs for medulla

A

Synthesis of catecholamines- NE and Ep; Chromogranin A

50
Q

Catecholamine pathway

A

Tyrosine–>Dopamine–>norepinephrine–>epinephrine

51
Q

Tumor that commonly accompanies pheochromocytoma

A

C cell thyroid adenoma

52
Q

Key histo with pheochromocytoma

A

Fine granular cytoplasm,

53
Q

Clinical signs with pheochromocytoma

A

Tachycardia, edema, cardiac hypertrophy, arteriolar sclerosis and medial hyperplasia

54
Q

Apicomplexan that commonly localizes to adrenal cortex

A

Toxoplasma gondii

55
Q

How is PTH regulated? Role of phosphorus?

A

When blood Ca is high, PTH release inhibited, when low, PTH released; Hyperphosphatemia decreases Ca, stimulating parathyroids

56
Q

Major inhibitors of PTH synthesis and release?

A

Calcium and calcitriol

57
Q

Actions of PTH

A

Stimulate calcitriol production in kidney
Increase reabsorption of Ca in kidney, and excretion of phosphorus
Mobilize Ca (and phos) from bone
Upregulates RANKL on osteoblasts (stimulate differentiation of osteoclasts)

58
Q

RANKL is on which cell? RANK is on which cell? Osteoprotegerin is what?

A

Osteoblasts; osteoclasts; soluble decoy receptor to regulate resorption

59
Q

Vitamin D activation pathway

A

Cholecalciferol from diet and skin–>In hepatocyte ER, cholecalciferol-25-hydroxylase converts to 25-hydroxycholecalciferol–> in kidney PCT mitochondria, 1 alpha hydroxylase converts to calcitriol (rate-limiting)

60
Q

PTH role in vitamin D activation

A

PTH stimulates 1 alpha hydroxylase, increasing production of calcitriol

61
Q

What other factors influence calcitriol?

A

Phosphate- inhibits 1 alpha hydroxylase
FGF23 inhibits 1 alpha hydroxylase

62
Q

Calcitriol’s main role; how

A

Increase absorption of Ca and phosphate from intestine; increases calcium binding protein on luminal enterocyte

63
Q

Other roles of calcitriol (in bone)

A

Upregulates RANKL on osteoblasts (stimulating differentiation of osteoclasts)
Stimulates release of FGF23 by osteocytes

64
Q

Roles of FGF23

A

Inhibits 1 alpha hydroxylase
Inhibits PTH secretion
Increases renal phosphate excretion

65
Q

Calcitonin’s role in Ca regulation; what stimulates its release?

A

Lowers plasma Ca; concentration of Ca in plasma and ECF stimulates C cells (same receptor as Chief cells)

66
Q

What causes C cell hyperplasia?

A

Long-standing hypercalcemia

67
Q

Actions of calcitonin

A

Inhibit osteoclastic bone resorption
Prevents postprandial hypercalcemia and excessive loss during pregnancy

68
Q

What causes diffuse parathyroid hyperplasia?

A

Chronic renal failure, dietary imbalances

69
Q

Key histo with parathyroid adenoma; who is predisposed?

A

Karyomegaly and anisokaryosis, fibrous capsule, compressed rim of normal tissue; keeshonds

70
Q

Associated lesion with primary hyperparathyroidism

A

Hyperostotic fibrous osteodystrophy

71
Q

Where does thyroid carcinoma often metastasize to first?

A

Pulmonary, then lymph nodes, because drains directly into brachiocephalic trunk

72
Q

Thyroid hormone synthesis pathway

A

Tyrosine–>incorporated into thyroglobulin protein–>thyroperoxidase oxidizes iodide into iodine–> iodine bound to tyrosine–>thyroxine (T4) and triiodothyronine (T3)

73
Q

How is iodine transported to follicular lumen?

A

Cotransported into follicular cell as iodide via NIS, then passively transported via pendrin into lumen

74
Q

What happens to follicles with sustained TSH?

A

Follicular cells become more columnar, lumina become smaller, increased endocytosis of colloid

75
Q

What happens to follicles with decreased TSH?

A

Follicular cells become flattened/cuboidal, follicles become enlarged and distended, decreased endocytosis of colloid

76
Q
A

Systemics- Repro and Endocrine (3 decks)

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