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Endocrine > Adrenal gland, continued (L6) > Flashcards

Adrenal gland, continued (L6) Flashcards

1
Q

What is the primary action of mineralocorticoids?

A

Promote sodium retention by the kidney

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2
Q

Secondary result of sodium retention

A

Water retention

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3
Q

Primary endogenous MC

A

Aldosterone

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4
Q

11-deoxycorticosterone

A

Precursor of aldosterone that also has MC action

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5
Q

Aldosterone synthase - location

A

Primarily located in the zona glomerulosa of the adrenal cortices

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6
Q

Sites of action of aldosterone

A

Kidney
Colon
Salivary glands
Sweat ducts

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7
Q

Aldosterone effects on the kidney

A

Primary target. Retains sodium and water, excretes more potassium

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8
Q

Four steps in the renin-aldosterone-angiotensin pathway

A
  1. Decreased blood volume stimulates renin production from the juxtaglomerular apparatus
  2. Renin cleaves angiotensinogen to angiotensin I
  3. Angiotensin I is converted to angiotensin II by ACE
  4. AT-II is a vasoconstrictor and stimulates release of aldosterone
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9
Q

Aldosterone vs AVP

A

Aldosterone is a primary regulator of the blood volume, whereas AVP is more focused on free water volume

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10
Q

Primary high-affinity receptor for aldosterone

A

MR (nuclear receptor superfamily)

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11
Q

To what does the MR bind with high affinity?

A

Both MCs and GCs

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12
Q

Relative concentrations of GCs to MCs

A

GCs are 100-1000x higher than MCs, but over 95% are bound and aldosterone has no specific binding protein

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13
Q

Inactivation of glucocorticoids

A

Conversion of cortisol to cortisone by 11beta-HSD type 2 in the kidneys

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14
Q

Carbenoxolone

A

Inhibits 11beta-HSD type 2

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15
Q

Excessive licorice consumption

A

Licorice is also a natural inhibitor of 11-beta HSD type 2 and will lead to increased sodium and water retention if eaten too much

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16
Q

Adrenal androgen

A

DHEA(S): dehydroepiandosterone (sulfate)

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17
Q

What does DHEA get converted into?

A

Testosterone and estrogen

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18
Q

How many of total androgens come from the adrenal cortex in the prostate?

A

50%

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19
Q

When does androgen peak?

A

Between 20-30 years old

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20
Q

“Weak” androgens

A

DHEA: low affinity for androgen receptor

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21
Q

Pregnenolone

A

First compound in the synthesis of androgens; converted from cholesterol in the mitochondria

22
Q

Cholesterol ester hydrolyase

A

Converts cholesterol ester to free cholesterol; enzyme is stimulated by ACTH

23
Q

Rate-limiting step in steroid hormone biosynthesis

A

StAR protein moving cholesterol from the outer to the inner mitochondrial membrane; regulated by ACTH

24
Q

Desmolase/P450scc

A

Converts cholesterol to pregnenolone

25
Q

21-alpha-hydroxylase deficiency - hormone levels

A

Causes excess DHEA, no glucocorticoids, no mineralocorticoids

26
Q

21-alpha-hydroxylase deficiency - clinical manifestations

A

Masculinization, ambiguous genitalia at birth, sodium loss

27
Q

11-beta hydroxylase deficiency - hormone levels/gene involvement

A

CYP11B1 deficiency. Excess DHEA, no cortisol

28
Q

11-beta hydroxylase deficiency - clinical manifestations

A

Salt and water retention due to excess MR activity

Low aldosterone due to low renin, high ANP

29
Q

17-alpha hydroxylase deficiency - hormone levels

A

No adrenal androgens, decreased glucocorticoids, excess MCs

30
Q

17-alpha hydroxylase deficiency - clinical manifestations

A

Feminization, sodium and water retention due to excess MR activity

31
Q

What will all the adrenal enzyme deficiencies result in?

A

High ACTH levels due to lack of feedback

32
Q

CYP11B2 stimulation

A

Stimulated by angiotensin II, not ACTH

33
Q

Innervation of the adrenal medulla

A

Splanchnic nerve

34
Q

Cellular architecture of the adrenal medulla

A

Cords of polyhedral epithelial cells

35
Q

What is epinephrine released in response to?

A

Acute stress (pain, cold, perceived danger)

36
Q

Speed of movement of epinephrine

A

Rapid release, rapid return

37
Q

Locations of catecholamine synthesis

A

Dopamine can be converted to norepinephrine in the peripheral nerves, but epinephrine is ONLY made in the adrenal medulla

38
Q

What stimulates conversion of NE to epi?

A

Cortisol

39
Q

Through what types of receptors does epi act?

A

Both alpha and beta adrenergic receptors

40
Q

Arousal effects of epi

A

Pupil dilation, sweating, GI and bronchial relaxation

41
Q

Metabolic effects of epi

A

Increased glucose mobilization, increased BMR

42
Q

Cardiovascular effects of epi

A

Vasoconstriction, tachycardia

43
Q

Three main targets of epi

A

Muscle, liver, and fat

44
Q

Half life of catecholamines

A

Very short: 10-90 seconds

45
Q

Degradation of catecholamines

A

COMT or MAO

46
Q

Metabolic byproduct of catecholamine breakdown

A

Vanillymandelic acid (VMA)

47
Q

What is the clinical significance of VMA?

A

Has a longer half-life; can be used to detect tumors secreting NE or epi

48
Q

Pheochromocytomas

A

Tumors in the chromaffin cells

49
Q

Symptoms of pheochromocytomas

A

Hypertension without response to meds, headaches, tachycardia

50
Q

Diagnosis of pheochromocytomas

A

Measurements of urinary metanephrines

51
Q

Treatment of pheochromocytomas

A

Surgery. (Presurgery: alpha/beta blockers)

52
Q

What is the nickname of pheochromocytomas?

A

The “10% tumor”

Endocrine (11 decks)

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