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Endocrine Physiology > Adrenal Gland > Flashcards

Adrenal Gland Flashcards

1
Q

What are the general features of the adrenal gland?

A

Covered with a dense connective tissue capsule, Stroma consists mainly of reticular fibers, supporting secretory cells, & microvasculature, Adrenal cortex & Adrenal medulla

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2
Q

What types of hormones are secreted from the adrenal gland and from which part?

A

steroids in the cortex and catecholamines in the medulla

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3
Q

What is the make-up of the cortex?

A 
Parenchymal cells that synthesize and secrete steroid hormones. All hormones are synthesized from cholesterol. 3 concentric zones: 
Zona glomerulosa (15%), Zona fasciculate (80%), Zona reticularis (5-7%)
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4
Q

What is the cellular make up of the zona glomerulosa?

A

small columnar/pyramidal shaped cells are closely packed ovoid clusters

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5
Q

What is the cellular make up of the zona fasiculata?

A

long cords of large, polyhedral cells separated by fenestrated sinusoidal capillaries

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6
Q

What is the cellular make up of the zona reticularis?

A

smaller cells with deeply stained nuclei arranged in a network of irregular cords surrounded by wide capillaries; often dark with electron-dense cytoplasm

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7
Q

What hormones are produced/secreted from the zona glomerulosa?

A

secrete mineralocorticoids – compounds that function in the regulation of sodium & potassium homeostasis & water balance, Principle secretion is aldosterone which increases sodium resorption & stimulates potassium excretion, under the feedback of the renin-angiotensin-aldosterone system

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8
Q

What hormones are produced/secreted from the zona fasiculata?

A

secrete glucocorticoids which regulate gluconeogenesis & glycogenesis; cortisol
& corticosterone

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9
Q

What hormones are produced/secreted from the zona reticularis?

A

secrete weak androgens & some glucocorticoids but in smaller amounts than the fasciculata
dehydroepiandrosterone (DHEA)

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10
Q

What is the function of the zona glomerulosa?

A

controlling fluid and electrolyte balance

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11
Q

What is the function of the zona fasiculata?

A

control carbohydrate, fat and protein metabolism

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12
Q

What is the function of the zona reticularis?

A

weak, masculinizing hormones

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13
Q

What is the make-up of the adrenal medulla?

A

Functions as a modified sympathetic ganglion, completely invested by the adrenal cortex; Contains chromaffin cells innervated by myelinated, presynaptic sympathetic ganglion cells

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14
Q

What do the chromaffin cells do?

A

(pheochromocytes) function as modified postganglionic sympathetic neurons, secrete either epinephrine or norepinephrine, can only be distinguished histochemically; release stimulated by ACh from preganglionic sympathetic nerve terminals

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15
Q

What do the ganglion cells do?

A

innervate adrenal cortex to modulate secretory activity and innervate BV

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16
Q

What is the cellular characteristics of chromaffin cells?

A

large epitheloid, vesicles; high electron density of vesicles contain norepinephrine; low electron density vesicles contain epinephrine

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17
Q

What are the effect of epinephrine and norepinephrine?

A

increased alertness, increased heart rate, increase BP, mobilize fat for energy, increase glucose release, increase oxygen consumption, increase heat production, increase glucose release

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18
Q

How does the blood flow through the adrenal gland?

A

capsular artery to cortical arteriole into zona glomerulosa capillaries, short arterioles to medullary capillary to the medullary vein or cortical arteriole to medullary arteriole (long) to medullary vein

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19
Q

What is the purpose of the adrenal medulla?

A

fight or flight emergency response; 1st line: epinephrine and norepinephrine, 2nd line: ACTH-Cortisol, Vasopressin-ADH, Renin angiotensin (hours and days)

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20
Q

What are the components of the neuroendocrine system in the adrenal medulla?

A

splanchnic nerves secrete ACh on nicotinic receptors of Chromaffin cells which release epinephrine and norepineprine

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21
Q

How are catecholamines synthesized? What is the rate limiting steps?

A

Tyrosine hydroxylated by TH to DOPA which is decarboxylated to dopamine in the cytosol, it is then taken up into vesicles where it is hydroxylated by DBH to NE which is methylated by PMNT to Epi; rate limiting step is TH

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22
Q

What is stored in vesicles in the adrenal medulla?

A

EPI, NE, ATP, proteins, lipids, enkephalins, Ascorbic acid, DBH; Catecholamine:ATP ratio is 4:1

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23
Q

How are catecholamines metabolized?

A

large portion NE retaken up by presynaptic terminals and recycled, COMT is diffusely in all tissues but mainly responsible to metabolismin the liver and kidney, MAO metabolizes in sympathetic synapses (found in sympathetic nerve terminals

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24
Q

What are stimuli for catecholamine release?

A

danger, harm, anxiety, fear, pain, hypovolemia, hypotension, anoxia, extremes of temperature, hypoglycemia, and strenuous exercise

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25
Q

What is the method of action of epinephrine?

A

binds well to beta1 and beta2 receptors but porrly to alpha receptors; B receptors exert actions via cAMP protein kinase system;

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26
Q

What is the method of action of norepinephrine?

A

binds better primarily with alpha receptors, frequently decreases cAMP levels via a2, intracellular Ca via IP3 as second messenger via a1;

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27
Q

What effects do the catecholamines have?

A

increase HR, myocardial contractility and conduction velocity; vasoconstriciotn of all vessels except those of the liver and skeletal muscle (beta2); vasoconstriction of splanchnic, renal and cutaneous circulations, promote energy substrate mobilization and conserve glucose for use by CNS, stimulates renin, PTH and thyroid secretion

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28
Q

What are the features of hyposecretion of catecholamines?

A

minor effect on overall body functions except in young children where hypoglycemic episodes may result from epinephrine deficiency

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29
Q

What are the features of hypersecretion of catecholamines?

A

frequently resulting from chromaffin cell tumor or pheochromocytoma; generally results in hypertension or easily invoked hypertensive episodes; hyperglycemia and weight loss due to hypermetabolic state

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30
Q

Cholesterol is necessary for synthesis of adrenocorticoid hormones, how is the cholesterol transported into the cell? how is it regulated?

A

LDL receptor mediated endocytosis; it is metabolically regulated; clathirin coated pit internalizes, LDL in endosomefuses with lysosomes and the pit with receptors is recycled

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31
Q

What happens to the cholesterol in the adrenal cortex when the endosome fuses with the lysosome?

A

lppoprotein digested, lysosomal acid lipase hydrolyzes cholesteryl esters and free cholesterol exits to the cell cytoplasm, free cholesterol can be re-esterified or channeld to biosynthesis pathway

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32
Q

how does free cholesterol in the cytoplasm get into the mitochondria in the adrenal cortex?

A

through inner mitochondrial membrane via StAR (steroidogenic acute regulatory protein) and PBR (peripheral type benzodiazepine receptor; this is the rate limiting step of synthesis.

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33
Q

What regulates StAR?

A

AngII in zona glomerulosa and ACTH in zona fasciculate and reticularis

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34
Q

What enzyme is only found in the zona glomerulosa? What are they stimulated by? What reactions does it catalyze?

A

CYP11B2;IMM; induced by AngII and K+, DOC to cortisone (aldosterone synthesae/11B-hydroxylase), cortisone to 18-OH-corticosterone (aldosterone synthase/18-hydroxylase), 18-OH-corticosterone to aldosterone (aldosterone synthase/18-oxidase)

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35
Q

What enzyme is only found in the fasciculate? What does it catalyze?

A

CYP11B1 (11B-hydroxylase:IMM) induced by ACTH; 11-deoxycortisol to cortisol

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36
Q

What catalyzes cholesterol to pregnenolone in the adrenal cortex?

A

CYP11A1;

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37
Q

What does CYP17 (17a-hydroxylase do? Where is it found?

A

prenenolone to 17-OH-Pregnenolonemicrosome in fasciculata and reticularis

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38
Q

What does CYP17 (17,20-lyase) do? Where is it found?

A

17-OH-pregnenolone to DHEA and 17-OHprogesterone to androstenedione; microsome in zona fasciculata and reticularis

39
Q

What does 3B-hydroxysteroid dehydrogenase/isomerase catalyze? Where is it found?

A

pregnenolone to progesterone; 17-OH-pregnenolone to 17-OH-progesterone, DHEA to androstenedione; microsome of adrenal cortex cells

40
Q

What does CYP21A2 (21-hydroxylase) catalyze? Where is it found?

A

Progesterone to DOC, 17-OH-Progesterone to 11-deoxycortisol; SER in adrenal cortex cells

41
Q

What type of receptor is PBR?

A

multifunctional transmembrane protein associated with voltage-dependent anion channel; regulated cholesterol channel between the outer and inner mitochondrial membrane

42
Q

How does StAR worl?

A

transiently synthesized by respective stimuli and rapidly eliminated upon termination of the stimuli; StAR binds to PBR resulting in activation of PBR which opens at the center of the channel for passage of cholesterol to SCC site

43
Q

How does CYP11A1 work?

A

removes side chain of cholesterol; electron needed for enzyme function is donated by adrenodoxin which receives electron from cAMP regulated adrenodoxin reductase; both are present in the mitochondrial membrane

44
Q

What are the consequences of 21-hydroxylase (CYP21A2) deficiency?

A

95% of genetic abnormalities; Type I and II CAH, loss of sodium due to lack of aldosterone, virilization

45
Q

What are the consequences of 11B-hydroxylase (CYP11B1) deficiency?

A

type II CAH, excess 11-deoxycortisol, 11-DOC and androgen, salt and water retention, virilization effect; 2nd most frequent abnormality in adrenal steroid hormone synthesis

46
Q

What are the consequences of 3B-hydroxy steroid dehydrogenase, type 2 (3B-HSD2) deficiency?

A

Type IV CAH; block of post-DHEA adrenal steroid synthesis

47
Q

What are the consequences of 11B-hydroxysteroid dehydrogenase type 2 (11B-HSD 2) deficiency?

A

normally enzyme metabolizes cortisol to inactive cortisone in kidney, prevents cortisol activation of aldosterone receptors; cortisol activates Type I mineralocorticoid receptors in renal tubules; results in excess mineralocorticoid activity

48
Q

What are the consequences of StAR deficiency?

A

Type VI or congenital lipoid adrenal hyperplasia, excessive lipid accumulation; use just PBR

49
Q

Where are CBG and SHBG synthesized? What stimulates its synthesis? What increases it?

A

liver, estrogen, during pregnancy

50
Q

How does aldosterone travel in the blood?

A

binds more to albumin than to CBG, relatively large percentage of DOC binds to CBG and albumin which lowers DOC binding to type I receptor and lower mineralocorticoid activity; low rate of secretion also keeps plasma levels of free hormone at physiological concentrations

51
Q

How does androstenedione travel in the blood?

A

bound mostly to albumin and small percentage to other binding proteins

52
Q

What four methods are glucocorticoids metabolized by?

A

reduction, dehydrogenation, hydroxylation, conjugation, or removal of the side chain

53
Q

Which glucocorticoids are metabolized by reduction? How?

A

5a and 5b reductase (rate limiting step) forms 5a or 5b dihydrocortisol, further reduced to 5a or 5b-tetrahydrocortisol by 3a-HSD,; reduction reactions by 11Bhydroxysteroid dehydrogenase type 1 in liver convert cortisone to cortisol

54
Q

Which glucocorticoids are metabolized by dehydrogenation? How?

A

cortisol converted to inactive cortisone by 11B-hydroxysteroid dehydrogenase type 2

55
Q

Which glucocorticoids are metabolized by removal of side chain? How?

A

formation of crotolis acid or crotolonic acid from cortisone

56
Q

Which glucocorticoids are metabolized by hydroxylation? How?

A

cortisol to 6B-hydroxycortisol in the liver

57
Q

Which glucocorticoids are metabolized by conjugation? How?

A

tetrahydrocortisol conjugated with glucuronic acid to form glucuronates, highly water soluble and excreted in urine

58
Q

How is aldosterone metabolized?

A

reduction in the liver by 5B-reductase and 3a-HSD forming 3a, 5B-tetrahyroaldosterone which is conjugated to glucuronates in the liver

59
Q

Where are GCRs? What happens with binding?

A

in cytosol complexed with heat shock protein which dissociates upon steroid binding, ligand-activated GCR translocates into the nucleus where it induces or inhibits gene transcription; induce synth of anti-inflammatory proteins by binding to GRE, suppressed transcription of inflammatory genes via nGRE, transrepression through direct or indirect interaction with transcription factors, competition for nuclear coactivators btwn GC/cGCR complex and transcription factors

60
Q

What effects does cortisol have on glucose metabolism?

A

induction of gluconeogenic enzymes in liver, increased blood and hepatic glucose levels, activation of glycogen synthase in the liver, permissive effects on glucagon and epinephrine action, induction of peripheral insulin resistance, or the Randle mechanism

61
Q

How does cortisol induce peripheral insulin resistance?

A

acetyl co A from FA metabolized in kreb’s cycle, resulting in block of glycolysis, glucose utilization is suppressed; suppression of glut 4 transporter synthesis in muscle (glucose entry strongly inhibited) and decreased glucose uptake in fat cels and increased lipolysis due to increased activity of insulin sensitive lipase

62
Q

What enzymes in the liver involved in glucose metabolism are affected by cortisol?

A

G-6-Pase driving G6P to Glucose for secretion, glycogen synthase driving G1P to glycogen, phosphofructokinase deactived by phosphorylation preventing G6P to F1,6BisP (glycolysis), F2,6BisPase converts F6P to F2,6BisP which inhibits F1,6BisPase

63
Q

What can happen with chronic hyperactivity of cortisol?

A

may lead to loss of bone, muscle, skin and CT (collagen) mass

64
Q

How does cortisol affect protein metabolism?

A

decreased synthesis and increased catabolism in all except the liver, increased AA mobilization from muscle, decrease AA transport to extrahepatic tissues (to liver instead), increased synth in liver and elevation of plasma proteins, decreased collagen and glycosmainoglycans

65
Q

How does cortisol affect fat metabolism?

A

enhanced lipolysis in adipose (permissive to epi, gluc, and GH), decreased conversion of glucose to FA, increased oxidation FA in liver and muscle-> acetyl-CoA utilized by kreb’s to generate ATP

66
Q

How does cortisol affect the body in a starvation state?

A

low blood glucose=low insulin, activates hormone sensitive lipase in adipocytes-> breakdown of stored triglycerides to FA and glycerol and released to blood; C stimulates B-oxi for acetyl-CoA in mitochondria for Kreb’s

67
Q

How does cortisol affect the body in a fed state?

A

(stress, alcohol, cannabis) stimulates higher blood glucose which stimulates insulin which suppresses hormone-sensitive lipase and stimulates lipoprotein lipase (circulating TriG to FA and glycerol), FA and glycerol enter adipocytes and are reconverted to TriG

68
Q

What overall functions does cortisol have on tissues and organs?

A

maintains contractility and work output by cardiac and skeletal muscle, decrease bone formation, maintain blood volume, potentiate adrenergic vasoconstriction, increase GFR, modulate perception and emotion, stimulates surfactant synth in fetal devl., helps mature intestinal mucosa (neonates), suppresses immune response

69
Q

How does cortisol deficiency manifest clinically?

A

hypoglycemia, insulin sensitivity, weight loss, vasodilation, hypotension, hypovolemia, hyponatremia, hyperkalemia, likelihood of autoimmune, anemia, lymphocytosis, anorexia, fatigue, increased ACTH and pigmentation

70
Q

How does cortisol excess manifest clinically?

A

hyperglycemia, insulin resistance, decreased protein structure(bone, muscle, skin), poor wound healing, hyperlipidemia, redistribution of fat (trunk), hypertension, hypovolemia, hypernatremia, hypokalemia, decrease inflammatory response, increased susceptibility to infection, decreased fibrous tissue formation, erythrocytosis, lymphophenia, leukocytosis, euphoria, depression, decreased ACTH secretion (if excess secondary to HP drive then increase in ACTH)

71
Q

What regulates cortisol secretion?

A

ACTH, stress and trauma

72
Q

How is the specificity of aldosterone action achieved?

A

Type I receptors and presence of 11B-hydroxysteroid dehydrogenase (which inactivates cortisol

73
Q

What affect does aldosterone have on principal cells?

A

increasing expression of a subunit of ENaC, increase stability of ENaC in apical membrane by SGK-1 (serum glucocorticoid regulated kinase 1), SGK1 works by increasing ENaC insertion and inhibiting Nedd4-2 dependent degradation of ENaC and increases activity of ROMK and basolateral sodium-potassium ATPase; increase gene expression of ROMK and SGK1

74
Q

What does an inactivating mutation of ENaC subunit cause?

A

pseudohypoaldosteronism type I; causes aldosterone resistance and symptoms of aldosterone deficiency

75
Q

What causes Liddle syndrome?

A

mutations in ENaC subunits preventing Nedd 4-2 interaction, therefore not able to degrade; hypertension, hypokalemia and low levels of renin and aldosterone

76
Q

How does aldosterone affect ADH actions?

A

induces ADH regulated adenylyl cyclase

77
Q

What affect does aldosterone have on the colon, salivary glands, sweat glands and gastric glands?

A

increases sodium and water reabsorption and K excretion

78
Q

What affect does aldosterone have on CV system?

A

proinflammatory and profirbotic affect; promotes left ventricular hypertrophy and remodeleing; increases morbidity and mortality in patients with essential hypertension

79
Q

What are the major causes of Addison’s disease>

A

aka adrenal insufficiency; autoimmune adrenalitis often associated with T1DM, chronic lymphocytic thyroiditis and vitiligo; infection (TB, CMV induced damage by AIDS), hemorrhage, metastases, and surgery

80
Q

What are they symptoms and hormone level changes associated with primary adrenal insufficiency? Where is the problem?

A

High ACTH, Hyperpigmentation, fatigue, weakness, unexplained weight loss, Low Na, High K, hypotension, rarely headache or visual loss, low aldoseterone, adnrogens, and cortisol, no changes in GH gonadotropins or reponse to ACTH challenge; problem in adrenal gland

81
Q

What are they symptoms and hormone level changes associated with secondary adrenal insufficiency? Where is the problem?

A

low ACTH, pallor, frequently headache and visual loss, fatigue, weakness, variable weight loss, normal aldosterone, variable androgens, low cortisol, decreased GH and gonadotropins, sluggish response to ACTH challenge; problem in hypothalamus or pituitary

82
Q

What is Cushings? What are the major causes?

A

exogenous glucocorticoids, ACTH-producing pituitary tumors (Cushings disease), cortisol secreting adrenal adenoma or carcinoma, ectopic ACTH or CRH production by non-pituitary tumors,

83
Q

What are the signs and symptoms of Cushings syndrome?

A

weight gain, round faces, truncal obesity, weakness, hypertension (BP >150/90), hirsutism in women, amenorrhea, cuntaneous straie, ecchymosis, osteoporosis, hyperglycemia, and growth retardation in children; Acanthosis nigracans is cushings disease only

84
Q

What are the clinical features of primary cushings syndrome?

A

site of problem is adrenal, adrenal pathology (tumor) decreased ACTH secretion

85
Q

What are the clinical features of secondary cushings syndrome?

A

if hypothalamic pituitary source then bilateral hyperplasia of adrenals and increased ACTH; if ectopic tumors is the source then bilateral adrenal hyperplasia and a marked increase in ACTH

86
Q

What are the indications and applications of the low dose dexamethasone suppression test?

A

Cushings syndrome screening, can do just an overnight or a two day test or both; in cushings disease, syndrome and ectopic ACTH there will be increased cortisol in urine or saliva; obesity will have increase overnight but suppressed after the 2 day; if positive need to do a high dose test

87
Q

What are the requirements for ruling out a suspected diagnoses of Cushings syndrome?

A

atleast 2 24 hour urinary free cortisol tests atleast 2 late-night salivary cortisol tests or one dexamethasone suppression test

88
Q

What are the indications and applications of the high dose dexamethasone suppression test?

A

used to confirm Cushings syndrome and differentiate the etiology; Disease= suppressed overnight and 2 day, Syndrome and ectopic ACTH both will be increased; can tell the difference because adrenal is ACTH independent and will likely have lower levels

89
Q

What are the signs and symptotms of hyperaldosteronism?

A

hypertension, hypokalemia, suppressed renin activity, abnormal aldosterone supression

90
Q

What is the escape phenomenom in hyperaldosteroneism?

A

initial Na retention and volume expansion, ECF and vascular volume increase, GFR increases, which increases rate of Na delvery to nephron andthere fore rate of Na excretion which limits ability of aldoseterone to continue expanding ECF vol; increased vascular volume stimulates ANP secretion which suppresses ENaC activity causing natriuresis and H2O loss, ANP also inhibits renin secretion; prevents Na overload and edema but aldosterone secretion remains so depleted K and metabolic alkalosis persist

91
Q

What is familial hyperaldosteronism or glucocorticoid-remediable aldosteronis,?

A

CYP11B1 (cortisol) promoter region fuses with CYP11B2 (aldosterone) region; so CYP11B2 is expressed in the fasciculata and drives synthesis thereACTH stimulates CYP11B1 thus stimulating the CYP11B2 portion fused increasing aldosterone synthesisleading to Na retention and hypertension; aldosterone does not negatively feedback on ACTH so it remains uncontrolled; dexamethasone to manage

92
Q

What is AME?

A

apparent mineralocorticoid excess; defects in 11B-HSD2; cortisol binds to type I receptors and mimics aldosterone effects; can also occur due to consumption of glycyrrhizin which is hydrolyzed to glycyrrhetenic acid in the liver and blocks 11BHSD2 activity

93
Q

What is the result of 21-hydroxylase deficiencies?

A

90% of clinical CAH (congenital adrenal hyperplasia); blocks aldosterone and cortisol synthesis funneling precurosors to DHEA and ultimately androstenedione ; masculinization of external genetalia of female infantsclassic form oresent at birth can be salt wasting or simple virilization type 1-2% activity (rare); usually late onset, 20-30% activity rapid early growth but short stature in males, females hirsutism, oligomenorrhea and infertility

Endocrine Physiology (9 decks)

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