Test 2 Steroid Hormone Physiology

Front 1

where does the adrenal cortex develop from?

Back 1

urogenital ridge mesoderm…. Accessory cortical nodules are common

Front 2

most common cuase of adrenal cortex hypoplasia

Back 2

anencephaly

Front 3

primary product of fetal adrenal

Back 3

androgen (dhea) synthesis

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right adrenal vein

Back 4

goes directly to vena cava, left adrenal joins left renal vein

Front 5

action of cytochrome p450

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all hydroxylases thus insert molecular o2 into hydrocarbon bond.

Front 6

aggregates of cells beneath capsule

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glomerulosa

Front 7

columns of cells rich in lipid

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fasiculata

Front 8

eosinophillic, sparse lipid COMPACT and many contain lipofuscin

Back 8

reticularis

Front 9

the hormonally regulated rate limiting first step in the syntheisis of all steroid hormones

Back 9

removal of side chain catalyzed by CYP11A1 in the mitochondria producing pregnenolone

Front 10

how is cholesterol transported to the adrenal

Back 10

80% ldl, 20% synthesized denovo from acetate

Front 11

How does acth stimulate ldl receptor production

Back 11

cAMP

Front 12

how is cholesterol stored

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as esters ACAT in lipid droplets

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cholesterol ester hydrolase

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stimluated by ACTH free's cholesterol

Front 14

P450scc is located

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in the inner mitochondrial membrane

Front 15

what stimulates cholesterol flux into the innter mito membrane

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StAR and P450scc6

Front 16

what regulates star

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ACTH

Front 17

is STAR in placenta or brain

Back 17

no but is found in gonads

Front 18

P450scc funciton

Back 18

terminal oxidase as part of a unique mitochondrial electron transport system

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adrenodoxin

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NADPH transfers electrons to adrenodoxin reducates to adrenodoxin then to P450scc

Front 20

3BHSD

Back 20

3B hydroxysteroid dehydrogenase/delta5-4 isomerase… conversts preg to prog and 17alpa preg to 17 alpha prog and dhea to andostenedione and androstendiol to testosterone

Front 21

CYP17

Back 21

P450c17 17 alpha hydroxylase 17,20 lyase… converst pregnnolole or progesterone to the 17 hydrogylated deriitives both then undergo scission of the C17 , C20 caron bond to yield DHEA or androstenedione…. But the MAJOR RXN IS FORMING DHEA

Front 22

21 hydroxylase CYP 21A2, P450c21

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the 21 position of progesterone and 17alpha hydroxyprogesterone can be hydroxylated by this microsomal enzyme to form DOC or 11 deoxy cortisol (S) respectively.

Front 23

#1 cause of CAH

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defect in CYP21A2

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CYP11B1

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11Bhydroxylase P450c11 93% identical to P450c11AS; CYP11B2 (aldosterone synthase) and both are mitochondrial in location. CYP11B1 DOC to corticosterone and S to cortisol (F) while CYP11B2 is found exclusively in the glomerulosa and catalyzes the final 3 steps in mineralocortcoid synthesis. Uses same chain as others

Front 25

17B HSD

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many forms exist it converts androstenedione to testosterone, dhea to androstenediol, estrone to estradiol… most active in extra adrenal tissue and can funciton in oxidative and reductive modes

Front 26

CYP19

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p450arom; aromatase the enzyme essential for estrogen biosynthesis and one enzyme carries out all the steps in converting testosterone to estradiol. The enzyme is present in the ovary and in many peripheral tissues especially in adipose tissue. Not in adrenaal

Front 27

11BHSD

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conversts cortisol and corticosterone to their inactive forms. Cortisone and 11 dehydroxycoriscosterone respecively. Two major types Typ3 and II

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Type 1 11BHSD

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high Km in many glucocorticoid target tissues and function in oxidase and reductase modes

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Type II 11BHSD

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low Km is present in mineralocorticoid target tissues and protects the minearlocorticoid receptor from glucocorticoid binding and functions in an oxidase mode

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Cortisol binding

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transcortin (AKA CBG), some to albumin, only 10% is free.

Front 31

T1/2 of Cortisol

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60-90 minutes

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Cortisol and estrogen

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estrogen increases CBG levels

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CBG manufactured

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in liver, kidney disease

Front 34

major secretory product of the adrenal

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dhea

Front 35

cortisol is metabolized in the

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liver… as are steroids (but steroids also have 11B hsd)

Front 36

aldosterone t1/2

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20 minutes and only slightly bound to protein

Front 37

what regulates glucocorticoid release

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HPA

Front 38

what stimulates glucocorticoid release

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CRH (stress and diurnal rhythm)

Front 39

acth release is from

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pomc cleavage in anterior pit

Front 40

acth stimulates the release of glucorticoids (primarily cortiso) through what

Back 40

cAMP mediated and calcium via t-type channel

Front 41

DHEA secretion is stiumatled by

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ACTH not gonadotropin

Front 42

are the effects of ACTH acute or cronic

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both, stimulates cholesterol to preg and chroni stimulates adrenal growt and maintains most of the enzymes along steroidogenic pathway

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SF-1

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orphan nulcear receptor necessary for P450 expression

Front 44

genomic effects o fsteroids take

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several hours or more,

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how do glucocorticoids stimulate gluconeogenesis

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avtivate gluconeogenic enzymes in the liver; mobilize amino acids from muscle; permisseve effects on glucagon and catecholamines; enhance glycerol release from fat cell by stimulating lipolysis

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glucocorticoid and glucose updtake

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inhibited glucose uptake and metabolism in periphery

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glucocorticoids and glycogen

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gets deposited in the liver

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glucocorticoids and lypolysis

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increased

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glucocorticoid and liver protein production

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stiulate protein and rna synthesis in liver but stimulate breakdown and inhibit protein syntheiss peripherally.

Front 50

cardiovascular effects of glucocorticoids

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maintain vascular reactivity to vasoactive agents; induce cardiac proteins (maintain contractilti); maintain ability to secrete a water load; moduleate electolytes (regulate gfr, adh, and anp)

Front 51

steroids and brain

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affects mood, behavior, neural activity and biochemisty

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steroids and fibroblasts

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inhibity fibroblasts (inhibit collagen synthesis)

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steroids and type ii pneumocytes

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stimulate

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steroids and ca2++

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absorption in guy reduced and reduced kidney reabsorption

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steroid and bone

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increase resorption, decrease linear growth

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immune supressinve effects of steroids

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decrease blood concentraions of eos, basos lymphocytes, t cell proliferation and activation,

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steroids and t cells

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decreas Th1, increase Th2

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steroids and inlammation

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inhibit annexin a-1, inhibit, nfkb, inhibit PGE2 and histamine and serotoniin release

Front 59

what is the affect of mineralocoticoids

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affect ion transport in epithelial tissues

Front 60

major mineralocorticoids

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aldosterone (glomerulosa) and DOC(fasciculata) aldosterone 24X more potent than DOC

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mechanisms of mineeralocorticoids

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1. ENaC (openining of pre-existing epithelial sodium channel by SGK (serum glucocorticoid kinase) on the apical membrae) 2. induciton of Na/K ATPase on the basolateral side 3. induction of mitochondrial proteins with resultant increases in energy

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Regulators of aldosterone

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1. RAS 2. K+ 3. ACTH (transient) also posture and circadian rhythm

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when is aldosteron highest

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in morning prior to awakening

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ANP aciton on renin

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inhibits and renin secretion and modulates glomerulosa response to angiotensin II

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in steroid action what stimulates or inhibits transcriptoion

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ligand receptor

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when is feedback overridden

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during stress (infection, surgery, hypoglycemia, trauma, anxiety and depression)

Front 67

acetylcholine, gaba, serotonin, NE do what to steroid axis

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stimulate

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Endophin and steroid axis

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inhibits

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adh and ssteroid axis

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cosecreted with CRH and augmets acth release

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crh cns effects

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stimulates sns and wakening, decreases fever, supresses food intake, supresses sexual activity

Front 71

what type of patern does cortisol have

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dirunal

Front 72

what alters the cortisol pattern

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altering sleep-wake cycle… also though has intrinsic rythim in suprrachiasmatic nucleus

Front 73

cortiosl effects on glucose

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activates glycogen synthase, inactivates phophorylase

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cortisol effects on insulen

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generally diabetogenic

Front 75

benefits of cortisol function during sres

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maintani cardiovascular system, mobilize energy. Cardio effects through catecholamines and angiotensin II, engergy mobilizaiton via glucagon, epi, GH

Front 76

how does AII stimulate alsdosterone production

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IP3 and CaM kinase

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high plasma K+

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deplolarize glomerulosa and allows ca2+ entry