Jackson Lectures 3 Flashcards

1
Q

The adrenal medulla is a modified

A

sympathetic ganglion. Recall that the SNS includes preganglionic neurons that arise from the thoracic and lumbar regions of the spinal cord.

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2
Q

In the case of the adrenal medulla, the gland is the

A

ganglion and there are no postsynaptic neurons with axons. Instead, the postganglionic cells, or chromaffin cells, release epinephrine (80%) and norepinephrine (20%) into the blood. NE stronger of the two.

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3
Q

NE is —- than E

A

stronger

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4
Q

adrenal medulla contains significant amounts of the enzyme

A

phenyl-N-methyltransferase which converts NE to E.

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5
Q

E and NE from the adrenal medulla have effects similar to those of

A

SNS innervation of target organs, although β-adrenergic receptors have a greater affinity for E, and α-adrenergic receptors have a greater affinity for NE, so the responses to neural (NE) and endocrine (NE and E) stimulation can vary (see Table 6.11).

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6
Q

In summary, the adrenal medulla enhances the

A

sympathetic response by releasing hormones that can reach additional targets without using neural circuits. And because the endocrine signal is blood-borne, the responses may last longer.

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7
Q

The adrenal cortex is divided into three structurally and functionally different zones:

A

zona glomerulosa – outermost

zona fasciculata – middle

zona reticularis – innermost, adjacent to the medulla

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8
Q

zona glomerulosa –

A

outermost

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9
Q

zona fasciculata –

A

middle

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10
Q

zona reticularis –

A

innermost, adjacent to the medulla

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11
Q

Steroid synthesis and secretion are stimulated by

A

ACTH, with the exception that aldosterone is regulated more strongly by other signals discussed below.

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12
Q

Aldosterone is a

A

mineralocorticoid produced by cells in the zona glomerulosa;

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13
Q

the cells in the zona glomerulosa that produce aldosterone contain

A

high levels of aldosterone synthase, and are deficient in the enzymes that convert corticosterone to cortisol or androgens.

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14
Q

The principle action of aldosterone is to stimulate

A

Na+ and H2O retention by the kidney in order to maintain blood volume and blood pressure.

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15
Q

The mechanisms by which aldosterone helps reabsorb Na+ and H2O in the kidney results in an increase in

A

urinary excretion of K+ and H+.

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16
Q

. The effect of aldosterone include: more —– in apical membrane

A

more Na+ channels in apical membrane

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17
Q

. The effect of aldosterone include: more —— in basolateral membrane

A

more Na+-K+ ATPase in basolateral membrane –

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18
Q

. The effect of aldosterone include: increased

A

increased synthesis of mitochondrial enzymes used in oxidative phosphorylation (electron transport system) –

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19
Q

. The effect of aldosterone include: increased

A

increased synthesis of mitochondrial enzymes used in oxidative phosphorylation (electron transport system) –

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20
Q

The secretion of aldosterone is regulated by multiple factors (ACTH has a minor/negligible effect).
• stimulated by an increase in

A

plasma angiotensin II – angiotensin II is a hormone produced in response to renin, a hormone released by the kidney in response to a decrease in Na+ or blood pressure.

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21
Q

Aldosterone secretion is • stimulated by an increase in plasma

A

K+ -

22
Q

Aldosterone secretion is • • stimulated by a decrease in

A

plasma pH or increase in plamsa H+ -

23
Q

Aldosterone secretion is • • stimulated by a drop in

A

systemic blood pressure –

24
Q

Aldosterone secretion is • • inhibited by increased

A

Na+ intake –

25
Q

Glucocorticoids, cortisol and corticosterone, are secreted by the cells of the

A

zona fasciculata. In humans, cortisol is the physiologically important hormone.

26
Q

The major effects of glucocorticoids or cortisol are to increase

A

metabolic fuel availability and use in tissues.

27
Q

glucocorticoids or cortisol : increases —— in liver

A

• ↑ gluconeogenesis in liver -

28
Q

glucocorticoids or cortisol: • ↑ proteolysis in

A

muscle –

lots of AA used in liver*

29
Q

glucocorticoids or cortisol increases

A

• ↑ lipolysis –

30
Q

glucocorticoids or cortisol: • ↓ glucose uptake in

A

muscle and fat – inhibits gluc transport

31
Q

glucocorticoids or cortisol: • ↓

A

immune and inflammatory responses- inhibits cytokine production.

32
Q

glucocorticoids or cortisol: • ↓ growth and reproductive function via combo of

A

upstream inhibition and central effects.

33
Q

glucocorticoids or cortisol: • permissive action on ——– to reg BP

A

β-adrenergic receptors in vascular smooth muscle to regulate blood pressure. Increases receptor expression*

34
Q

Synthesis and secretion of glucocorticoids is stimulated by

A

ACTH.

35
Q

Cortisol has a

A

negative feedback action on both CRH and ACTH.

36
Q

Sex steroids (mostly androgens) are secreted by the

A

zona reticularis;

37
Q

the two major androgens are

A

dehydroepiandrosterone (DHEA) and androstenedione.

38
Q

DHEA is a precursor of

A

other sex steroids (see steroid biosynthetic pathway figure) so it can serve as a circulating reservoir for conversion in peripheral tissues containing steroidogenic enzymes.

39
Q

DHEA has relatively

A

weak androgenic action

40
Q

DHEA: peripheral concentrations reflect overall activity of the

A

adrenal cortex

41
Q

androstenedione is synthesized by enzymatic conversion of

A

DHEA

42
Q

Androstenedione is a

A

stronger androgen that DHEA

43
Q

Androstenedione provides a non-gonadal source of

A

testosterone and estradiol

44
Q

DHEA is an important source of

A

reproductive steroids prior to puberty and in postmenopausal women

45
Q

Adrenal sex steroids are important regulators of

A

mood and libido, hair growth, erythropoiesis, and acne.

46
Q

Synthesis and secretion of adrenal androgens is stimulated by

A

ACTH (not GnRH or LH….just because adrenal androgens are sex steroids doesn’t mean they are regulated by gonadotropin releasing hormone/GnRH or gonadotropins!)

47
Q

A stress response is a response of the

A

stress axis (hypothalamus – anterior pituitary – adrenal cortex) to a stressor that stimulates hypothalamic CRH neurons and inputs to the SNS.

48
Q

SNS activation →

A

specific organ responses and increased circulating epinephrine.

rapid response involving smooth muscle stimulation and inhibition

widespread effects of epinephrine

49
Q

activation of the stress axis →

A

increased secretion of cortisol → increases availability of metabolic fuel and other functions

50
Q

activation of stress axis: this is a

A

delayed response

51
Q

cortisol inhibits the actions of insulin, leading to fulfilling three goals:

A
  • maintain bp (insure delivery of o2 and glucose),
  • mobilize and increase metabolic fuel availability,
  • inhibit nonessential functions (decrease motility in gut, urinary and repro systems).
52
Q

In the short term, the stress response is

A

good, and it is shut off by removal of the stressor and negative feedback actions of cortisol on CRH and ACTH.