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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
What happens with patients with excess cortisol (CUSHING's SYNDROME)
HYPERGLYCEMIA
26
What three hormones, workign together, promotes increase in blood glucose
Glucagon + Epinephrine + Cortisol
27
What is role of epi and NE? What must be present for effects to be fully manifested?
Epi and NE promote vasoconstriction and bronchodilation Cortisol must be present for these effects to be manifested
28
What happens to excretion of water load when cortisol is deficient?
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
29
Why do animals that are crotisol deficient unable to survive stress?
lack of cortisol facilitation of mobilizatino of energy stores, and to lack of cortisol-facilitation of catecholamin-induced peripheral vascualr restisance
30
What is stress a stimulator of
Potent stimulator of corticotropin releasing hormone (CRH), ACTH, and Cortisol
31
Which nucleus controls of teh time of day release of cortisol
Superchiasmatic nucleus (SCN)
32
Why is there excessive melanization (darkenign) of skin when cortisol secretion is deficient? (addison's desease)
Due to Beta- melanocyte stimulateing hormone activity of beta-lipotropin adn the alpha-MSH activity within the aa sequence of ACTH
33
What dooes POMS break down into?
ACTH and beta-lipotropin
34
What does beta endorphin bind to
Optiate recetpros and amy modulate perceptino of pain
35
What is relationship between rlease of ADH and ACTH
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
What happens to ADH secretion if there is a balloon in right atrium?
it decreases, b/c there is high BP --> tehrefore decrease release of ADH
37
What could be wrong with a patient if he/she is abonormally "tanned"?
ADH deficiency (no ADH to send negative feedback to CRH --> inc. POMC --> Inc ACTH & Beta Liptr[opi --> inc beta MSH
38
What is the major controller of Na content of ECF
Aldosterone
39
What is the cellular mechanism of alosterone actiion
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
What does aldosterone do to Na and K pumps on the lumenal membrane
Increases number of Na channels in lumenal membrane, thus increaseing passive movement of Na form filltrate into the cell
41
What does Aldosterone do to Type A intercalated cells of renal collectign duct
Secretes H+ into filtrate HCO3 moves into the renal ECF to e absorbed by blood
42
What causes primary hyperaldosteronism
Excessive secretino of aldosterone
43
What is an example cause of primary hyperaldosteronism
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
What are the consequencs of primary hyperaldosteronism
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
WHat happens to secretion of renin and ang II in Primary Hyperaldosteronism
Secretion of renin and Ang II low
46
What s acuse of hypertension in primary hyperaldosteronism?
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
What is the cause of Primary HYPOALDOSTERONISM
primary deficiency of aldosterone secretion = Addison's disease
48
What is the resutl of HYPOALDOSTERONISM
``` Na loss water loss reduced volume of ECF and Plasma Hypotention (hypovolumenic shock) Hyperkalemia Metabolic Acidosis ``` Ratio of Na/K abnormally low `
49
Why is aldosterone low in Hypoaldosteronism
Aldosterone secretion is low b/c of problem in medulla itself (autonomous destruction of adrenal cortex by TV or HIV virus)
50
What happens ot secretion of Renin and Ang Ii in Hypoaldosteronsim
Elevated
51
How is Renin Released?
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
What causes secondary hyperaldosteronism
PHSYIOLOGICAL STIMULUS Any event that decerases arterial BP or decreases BP in kidney will increase secretion of renin, Ang II and aldosterone
53
What does this increases in secondary hyperaldosteronism lead to
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
What conditions increase B-1 nonadrenergic input to kidney
hemorrhage, dehydration, vomiting, diarrhea Increasing renin, angiotesnin and aldosterone secretion
55
What other events increase aldosterone ssecretion via renin-angiotensin mechanism
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
What are examples that elevate renin secretion whihc, in turn, elicits increased aldosterone se retion (secondary hyperaldosteronism)
Congestive heart failture Partial obstruction of inferior vena cava Hepatic cirrhosis
57
What is secondary hypoaldosteronism
Stimuli that decrease aldosterone secretion by decreasing renin secretion
58
Why is aldosterone secretion decresion (and Na loss increased) by weightlessness?
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
Is aldosterone secretion increased or decreased by WEIGHTLESSNESS?
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
What happens to ADH and salt secretion during weightlessness
decrease in ADH and an increase in secretion of ANP --> contribute to loss of water and salt
61
what are the effects of bed rest
mimics weightlessness on teh secretion of the same hormones
62
what does pregnancy or esterogen-conetaining birth control do to aldosterone secretion?
it increases it
63
Why does increased plasma estrogen increase aldosterone secretion
b/c estrogen increases hepatic productino of angiotensiongen --> renesubstrate elevated --> --> therfore inc aldosterone
64
What is the effect of elevated K+ concentration (hyperkalemia) on aldosterone secretion
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
What controls the secretion of ACTH and cortisol
Circadian rhytm
66
How do you properly measure ACTh and cortisol secretion?
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
What is the cause of PRIMARY HYPOADLOSTERONISM= Addison's disease
destruction of adrenal gland (TB or HIV virus) makes it incapable of secreting cortisol
68
Consequences of hypoCORTICOLISM/ Addison's Disease
plasma conceration of cortisol low --> plasma concentraitn of ACTH will be high 2. All zones of adrenal cortex are desteroxyd, the signs of minearlcorticoid deficiency are manifested as well as those of glucocorticoid deficiency
69
What is the cause of seconary Hypoadrenocrotical function (SECONDARY HYPOADRENOCOTICOLISM0
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
What happens to secretion of aldosterone in secondary hypoadrenocorticolism
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
What happes to plasma cortisol and ACTH in secondary hypoadrenocortisolism
both are below nomral primary manifestation willb e hose of glucocorticoid deficiency (not minearlcorticoid)
72
What is cause of Hyperadrenocortical function (Cushing's syndorme)
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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