MCP 3 Flashcards

1
Q

function of steroid hormones

A

travel in blood from point of synthesis to target using nonspecific and specific carrier proteins. once they reach the target, the hormone enters the cell and binds receptor in cytoplasm or nucleus. alters transcription

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2
Q

synth of steroid hormones

A

involves shortening the hydrocarbon chain of cholesterol and hydroxylating the steroid nucleus. rate limiting step is conversion of cholesterol to the 21 carbon pregnenolone. Catalyzed by desmolase, CYP11A, and P450scc

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3
Q

CYP11A

A

cytochrome P450 mixed function oxidase located on the inner mitochondrial membrane. reaction requires NADPH and O2. cholesterol moves to inner MM through StAR

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4
Q

congenital adrenal hyperplasias

A

metabolic imbalances due to enzyme deficiencies in the steroid hormone production pathway

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5
Q

3-B-Hydroxysteroid dehydrogenase deficiency

A

no gluco or mineralocorticoids, active androgens, or estrogens. salt in urine. female like genitalia

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6
Q

17-A-hydroxylase deficiency

A

virtually no sex hormones or cortisol. increased production of mineralocorticoids causing Na and fluid retention and hypertension. female like genetalia

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7
Q

21-A-hydroxylase deficiency

A

most common form. partial and virtually complete deficiencies known. mineralo and glucocorticoids absent (classic) or deficient (nonclassic). overproduction of androgen leading to masculinization of external females and early virilization in males

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8
Q

11-B1-Hydroxylase deficiency

A

decrease in serum cortisol, aldosterone, and corticosterone. increased production of deoxycorticosterone causes fluid retention. overproduction of androgen causes masculinizations and virilization

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9
Q

cortisol

A

made in middle layer (zona fasciculata) of the adrenal cortex. production and secretion is controlled by hypothalamus to which the pituitary gland is attached. helps body respond to stress through effects on metabolism and immune/inflamm response.

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10
Q

ACTH/CRH in response to stress

A

CRH is produced and gets to anterior lobe of pituitary. there it causes production of ACTH, the stress hormone. causes adrenal cortex to synth and secrete cortisol. cortisol increase causes inhibition of CRH and ACTH release

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11
Q

ACTH in cortisol synth

A
  1. ACTH binds G-prot receptor and turns onn PKA.
  2. PKA activates lipase (which converts CE to cholesterol) and StAR prot
  3. Pregnenolone is returned to cytosol where it is turned to progesterone
  4. in ER membrane, progesterone –> 11-deoxycortisol
  5. 11-deoxycortisol goes to inner MM where CYP11B1 catalyzes production of cortisol
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12
Q

functions of aldosterone

A

made in outer layer of adrenal cortex (glomerulosa). production stimulated by a decrease in plasma Na/K ration and angiotensin II. Aldosterone enhances Na and water uptake and K efflux in kidney tubules. increases blood pressure. ACE inhibitors are used to treat renin dependent hypertension

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13
Q

androgens

A

made by inner (reticularis) and middle layers of adrenal cortex. adrenal androgens are converted to testosterone and estrogen in peripheral tissues.

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14
Q

GRH, LH, and FSH chain

A

gonadotropin releaseing hormone, GRH, made in testies/ovaries. stimulates anterior pituitary to release lutenizing hormone LH and follicle stimulating hormone FSH

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15
Q

LH and FSH functions

A

LH stimulates testes to make testosterone and overaies to make estrogens and progesterone. FSH regulates growth of ovarian follicles and stims spermatogenesis within testes

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16
Q

aromatase

A

enzyme that converts testosterone to estrogen. used to help women with estrogen responsive breast cancer

17
Q

excretion of steroid hormones

A

conjugation with glucuronic acid or sulfate makes excretion more soluble. 20-30% are secreted into bile and excreted in feces. remainder go to kidneys and are filtered into the urine

18
Q

D vitamin basics

A

group of sterols that function like hormones. active molecule is calcitriol enhances or represses transcription of a coordinated set of genes. regulates plasma levels of calcium and phosphorous

19
Q

sources of vitamin D

A

exogenous source: ergocalciferol from plants and cholecalciferol found in animal tissues.

endogenous source: 7-dehydrocholesterol –> cholecalciferol when we are exposed to sun. happens in dermis and epidermis

20
Q

converting inactive vitamin D to active vitamin D

A

vitamin D2 and D3 are converted through two steps

  1. in liver, 25 hydroxylase yields calcidiol. this is major form of D in the plasma and major storage form
  2. calcidiol is further hydroxylated in kidney ot make calcitriol
21
Q

25-hydroxycholecalciferol 1-hydroxylase regulation

A

increased directly by low plasma phosphate and indirectly by low plasma calcium.

low calcium causes PTH secretion which upregulates the enzyme. elevated calcitriol inhibits enzyme activity and PTH secretion through negative feedback

22
Q

intestinal calcium absorption

A

calcitriol binds VDR, vitamin d receptor, in cytoplasm of intestinal cell. this complex enters nucleus where it forms a dimer with RXR. This activates coactivators which bind DNA sequences, which diminishes or enhances transcripts influencing the expression of specific proteins

23
Q

vitamin D and calcium reabsorption from bones

A
  1. low plasma calcium causes increased calcitriol and PTH, which increase calcium absorpt. and bone resorpt. and inhibit calcium excretion
  2. high Ca blocks PTH which causes conformational change of calcitriol. elevated calcitonin causes inhibition of bone resorption and enhanced calcium excretion
24
Q

rickets

A

in children. formation of collagen matrix but insufficient mineralization resulting in soft and pliable bones

25
Q

osteomalacia

A

in adults. demineralization of existing bones makes them more susceptible to fracture

26
Q

Vitamin D toxicity

A

loss of appetite, nausea, thirst, and stupor. enhanced Ca absorption and bone resorption results in hypercalcemia, leading to Ca deposits in organs and kidneys and arteries