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Physiology Adrenal > Adrenal Gland Hormones > Flashcards

Adrenal Gland Hormones Flashcards

1
Q

What is 95% of Cortisol in plasma bound to?

A

Protein, an alpha-2 globulin-

CBG (cortisol-bidning globulin) that is synthesized in teh liver

CBG bound cortisol is in equilibrium with ree (unbound) cortisol

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2
Q

Do free or bound coritsol diffuse into cortisol target cells ?

A

ONLY FREE cortisol can diffuse into cortisol target cells

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3
Q

What hormone causes the increase of hepatic synthesis of CBG?

What kind of people does this happen to ofen?

A

Elevated plasma concentration of estrogen

As in pregnant women or women taking oral contraceptives

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4
Q

What dos liver damage do to syntehsis of CBG?

A

Decreases synthesis of CBG

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5
Q

Wht dos renal disease do to CBG

A

Renal disease causes loss of CBG in urine

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6
Q

In liver damage and renal disease, what happens to plasma concentration of CBG ?and the concentration of free cortisol?

A

Total plasma concentration of CBG decrases

Concentration of free cortisol remains normal

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7
Q

Does free coritsol of CBG-cortisol inhibit ACTH?

A

Only free cortisol inhibits ACTH secretion by pituaitry corticotrophs

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8
Q

Does changes in plasmca concentration of CBG produce changes in plasma concentration of cortisol?

A

Only temporarily!

Individualswith altered

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9
Q

Do individuals with altered CBG levels show symptoms of hyper or hypocorticosolism?

A

Niether!

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10
Q

What conditions cause increased synthesis of CBG? Decreased synthesis or plasma concentration?

Does free cortisol reain normal? What bout CBG ?

A

Increased syntesis- pregnancy or oral contraceptives (when estrogen level is higher)

Decreased concentration of CBG- liver disese and renal disease ((incresed excretion in urine)

Change in total plasma cortisol but NOT FREE CORTISOL

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11
Q

What percent of aldosterone is free?

A

1/2 (unbound to protein

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12
Q

Is aldosterone soluble in plasma?

A

Yes, its polarity makes it more soluble in plasma than other steroid hormones

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13
Q

What kind of cortisol is excreted?

A

Free cortisol only (cortisol not bount to CBG)

Thus the amt of cortisol in a “day’s woth” of urine approximates adrenal synthesis of cortisol on that day

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14
Q

What happens to DHEAS not bount to albumin (2%)

A

it is excreted int eh urine as DHEAS

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15
Q

How much more effective is cortisol as a glucocorticoid than corticosterone moleucle?

A

5x more effecitve than corticosterone

Therefore, the only impt glucocorticoid in humans is cortisolW

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16
Q

What is the general metabolic action of CORTISOL

A

opposite those of insulin

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17
Q

What are the functions of cortisol

A
  1. Promote mobilization of energy stores
    - aa from body protein
    - fatty acids and glycerl from adipose tissue
  2. Inhibit Glucose Uptake
    - in most ttissues, to spare plasma glucose for brain and RBC, tissues that require gluocse for survivat
  3. Inhibit amino acid uptake and protein syntehsis in most tissue, while promoting preotien breakeown
    - for GLUCONEOGENIC enzymes and Glucose 6 Phosphate –> increased generatino of glucose from noncarb sources
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18
Q

When cortisol is present in excess, what happens to hepatic glucose 6 phosphate production?

A

it increased so much that hepatic GLYCOGEN FORMATION is also INCREASED (this action is not opposite to insulin)

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19
Q

What are the effects of excess cortisol in the liver? (mechanism?

A

Increased plasma amino acids

Increased gluconeogenic enzymes

Increased G6P

Increased Glycogen formation

Increased Glucose 6 Phosphatase

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20
Q

What are the effects of excess coritsol in musce

A

Decrease protein synthesis

Increase protein breakdown

Decreased glucose uptake by muscle

Decrewased amino acid uptake by muscle

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21
Q

What are the effects of excess cortisol in Adipose Tissue

A

Increased Lipolysis

Decreased glucose uptake by adipose tissue

Increased plasma FFA and glycerol

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22
Q

What does it mean by saying there are “permissive” actinos of cortisol

A

By itself, cortisol is not a strong promoter of glycogenolysis, lipolysis, vasoconstrcition, or bronchodilations;

However it strongly enhances the capacity of ther hormones (glucagon, epinephrine, NE) to stimulate these processes

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23
Q

Describe action of glucagon and Epi, and how it depends on cortisol

A

Glucagon and Epi promote glycogenolysis and lipolysis, but CORTISOL must be present for these hormones to exert their full glycogenolytic and liipolytic effects

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24
Q

What happnes to patients that have inadequate cortisol secretion and fast

A

Cortisol promotes breakdown of gluocse from muscle/fats, so without cortisol

iwll be SEVERELY HYPOGLYCEMIC when fasting

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25
Q

What happens with patients with excess cortisol (CUSHING’s SYNDROME)

A

HYPERGLYCEMIA

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26
Q

What three hormones, workign together, promotes increase in blood glucose

A

Glucagon + Epinephrine + Cortisol

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27
Q

What is role of epi and NE? What must be present for effects to be fully manifested?

A

Epi and NE promote vasoconstriction and bronchodilation

Cortisol must be present for these effects to be manifested

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28
Q

What happens to excretion of water load when cortisol is deficient?

A

Excretion of water load is seriously impaired

B/c ADH secretion is not suppressed in spite of decreased osmolalit evoked by absorbing hypo-osmolar fluids.

Water is retained, ad ECF may remain hypotonic for a day or emore

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29
Q

Why do animals that are crotisol deficient unable to survive stress?

A

lack of cortisol facilitation of mobilizatino of energy stores, and to lack of cortisol-facilitation of catecholamin-induced peripheral vascualr restisance

30
Q

What is stress a stimulator of

A

Potent stimulator of corticotropin releasing hormone (CRH), ACTH, and Cortisol

31
Q

Which nucleus controls of teh time of day release of cortisol

A

Superchiasmatic nucleus (SCN)

32
Q

Why is there excessive melanization (darkenign) of skin when cortisol secretion is deficient? (addison’s desease)

A

Due to Beta- melanocyte stimulateing hormone activity of beta-lipotropin adn the alpha-MSH activity within the aa sequence of ACTH

33
Q

What dooes POMS break down into?

A

ACTH and beta-lipotropin

34
Q

What does beta endorphin bind to

A

Optiate recetpros and amy modulate perceptino of pain

35
Q

What is relationship between rlease of ADH and ACTH

A

The ADG = argininte vaopressin hormone (AVP) also stimulates secretion of ACTH

secretion of ADH is often seen as elevated in response to stres, thus this peptide also promotes ACTH secretion

36
Q

What happens to ADH secretion if there is a balloon in right atrium?

A

it decreases, b/c there is high BP –> tehrefore decrease release of ADH

37
Q

What could be wrong with a patient if he/she is abonormally “tanned”?

A

ADH deficiency (no ADH to send negative feedback to CRH –> inc. POMC –> Inc ACTH & Beta Liptr[opi –> inc beta MSH

38
Q

What is the major controller of Na content of ECF

A

Aldosterone

39
Q

What is the cellular mechanism of alosterone actiion

A

Aldosterone binds to nuclear receptors of princial cells int eh cortical collecting duct of the kidney

These activated receptors initiate proceses that increased fucntion fo basolateral Na/K ATPAse that pump Na out of principal cell and into renal ECF in excahgne of K

40
Q

What does aldosterone do to Na and K pumps on the lumenal membrane

A

Increases number of Na channels in lumenal membrane, thus increaseing passive movement of Na form filltrate into the cell

41
Q

What does Aldosterone do to Type A intercalated cells of renal collectign duct

A

Secretes H+ into filtrate

HCO3 moves into the renal ECF to e absorbed by blood

42
Q

What causes primary hyperaldosteronism

A

Excessive secretino of aldosterone

43
Q

What is an example cause of primary hyperaldosteronism

A

Tumor of zona glomerulosa (conn’s syndrome)

Excessive sectino is NOT occuring in rsponse to a physiological stimulus

There is a problem in adrenal itself (tumor) or becuase of excessive exogenous aldosterone is being administered

44
Q

What are the consequencs of primary hyperaldosteronism

A

Na retention, water retention, enlarged ECF volume and PV

Hypertenstion
Hypokalemia
Metabolic Acidosis
Ratio of Na/K is abnormally high

B/c increased BP, secretion of renin and ang II low

45
Q

WHat happens to secretion of renin and ang II in Primary Hyperaldosteronism

A

Secretion of renin and Ang II low

46
Q

What s acuse of hypertension in primary hyperaldosteronism?

A

Not really known!

Because ther eis Na escape, blood volume expands by no more than 0.5 L

Might be becuse of increase in TPR

47
Q

What is the cause of Primary HYPOALDOSTERONISM

A

primary deficiency of aldosterone secretion = Addison’s disease

48
Q

What is the resutl of HYPOALDOSTERONISM

A 
Na loss
water loss
reduced volume of ECF and Plasma
Hypotention (hypovolumenic shock)
Hyperkalemia 
Metabolic Acidosis

Ratio of Na/K abnormally low `

49
Q

Why is aldosterone low in Hypoaldosteronism

A

Aldosterone secretion is low b/c of problem in medulla itself (autonomous destruction of adrenal cortex by TV or HIV virus)

50
Q

What happens ot secretion of Renin and Ang Ii in Hypoaldosteronsim

A

Elevated

51
Q

How is Renin Released?

A

Decreased pressure in renal afferent arteriole
Decreased Na delivery to macula densa of distal convoluted tubule

Incrased b1 noradrenergic input to the juxtaglomerular cells

Juxta cells (baroR) secretes renin

52
Q

What causes secondary hyperaldosteronism

A

PHSYIOLOGICAL STIMULUS

Any event that decerases arterial BP or decreases BP in kidney will increase secretion of renin, Ang II and aldosterone

53
Q

What does this increases in secondary hyperaldosteronism lead to

A

promotes increased renal reabsorpation of Na, therefore water reabsorption

Partially restores plasma and V, helping maintain cardiac output and BP

Direct vasoconstrictive action of An II helps restore blood pressure

54
Q

What conditions increase B-1 nonadrenergic input to kidney

A

hemorrhage, dehydration, vomiting, diarrhea

Increasing renin, angiotesnin and aldosterone secretion

55
Q

What other events increase aldosterone ssecretion via renin-angiotensin mechanism

A

Prolonged sweating, esp. if accompanied by loss of Na

Going quickly fro lying down position to standing postiino

Sequestering of blood on venous side of systemic circulation (venous sequesteration of blood decreases cardiac output, thus ecresing pressure in renal artery –> inc renin secrtion)

56
Q

What are examples that elevate renin secretion whihc, in turn, elicits increased aldosterone se retion (secondary hyperaldosteronism)

A

Congestive heart failture

Partial obstruction of inferior vena cava

Hepatic cirrhosis

57
Q

What is secondary hypoaldosteronism

A

Stimuli that decrease aldosterone secretion by decreasing renin secretion

58
Q

Why is aldosterone secretion decresion (and Na loss increased) by weightlessness?

A

b/c blood no longer pools int eh extremities when standing or sitting

Portion of redistributed blood ends up int eh atria and large veins of chest, where it stimualtes baroreceptors

59
Q

Is aldosterone secretion increased or decreased by WEIGHTLESSNESS?

A

decreased –> b/c blood no longer pools in extremities when standing or sitting

Portion of redistributed blood ends up in atri and large veins of chest where it stimualtes baroreceptors –> decrease symp output (B1 Noradrenergic) –> less renin secreted

60
Q

What happens to ADH and salt secretion during weightlessness

A

decrease in ADH and an increase in secretion of ANP –> contribute to loss of water and salt

61
Q

what are the effects of bed rest

A

mimics weightlessness on teh secretion of the same hormones

62
Q

what does pregnancy or esterogen-conetaining birth control do to aldosterone secretion?

A

it increases it

63
Q

Why does increased plasma estrogen increase aldosterone secretion

A

b/c estrogen increases hepatic productino of angiotensiongen –> renesubstrate elevated –> –> therfore inc aldosterone

64
Q

What is the effect of elevated K+ concentration (hyperkalemia) on aldosterone secretion

A

Directly INCREASES aldosterone secretion

incraseing extracelllar K+ conecetration wil make equilibrium potenential less nagative (chagnes Tm)

Elevated K+ partially depolarizes the aldosterone secreting cells of hte zona glomerulosa –> act VG Ca cahnels –> stimualte aldosterone secretion

65
Q

What controls the secretion of ACTH and cortisol

A

Circadian rhytm

66
Q

How do you properly measure ACTh and cortisol secretion?

A
  1. only measure plasmt CTH and cortisola t 8am and compare the measured concentration to normal 8am values
  2. measure total amt of cortisol in one day’s collection of urin. 24 urineary free cortisol is direclty proprotional to the total cortisol secreted during entrie day, not as greatly affected by time of day or by sigle stressful event

also since only “free cortisol” is filtered through the glomerulus, urinary cortisol is not affected by factosr that alter plasma concentration of CBG –> URinary cortisol is more accurate

67
Q

What is the cause of PRIMARY HYPOADLOSTERONISM= Addison’s disease

A

destruction of adrenal gland (TB or HIV virus) makes it incapable of secreting cortisol

68
Q

Consequences of hypoCORTICOLISM/ Addison’s Disease

A

plasma conceration of cortisol low –> plasma concentraitn of ACTH will be high

  1. All zones of adrenal cortex are desteroxyd, the signs of minearlcorticoid deficiency are manifested as well as those of glucocorticoid deficiency
69
Q

What is the cause of seconary Hypoadrenocrotical function (SECONDARY HYPOADRENOCOTICOLISM0

A

Loss of adrenocortical function is secondary to a deficiency of pituiatry ACTH secretion

can cocur as a result of pituitary turmor that prevents corticotrophs from secreting ACTH, or from hypohtlamic tumor that prevents CRH from reaching corticotrophs

70
Q

What happens to secretion of aldosterone in secondary hypoadrenocorticolism

A

stays relavely normal, b/c stimulus of aldosterone secretion (ANG II) is still seceted

If BP drops due to cortisol def , secretion of renin and ang II may increase

71
Q

What happes to plasma cortisol and ACTH in secondary hypoadrenocortisolism

A

both are below nomral

primary manifestation willb e hose of glucocorticoid deficiency (not minearlcorticoid)

72
Q

What is cause of Hyperadrenocortical function (Cushing’s syndorme)

A

major pathophysiological manifestations are those produced by excessive cortisol

  1. Loss of musculature in arms and legs , resulting in weakenss
  2. Striae and purple blotches on sin of abds and legs
  3. Abdominal (central obesity)- yet spindly arms and legs
  4. bndomral glucose-tolerance tst
  5. hypertenstion

Physiology Adrenal (2 decks)

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