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Endocrinology > Exam 3 Lesson 20 > Flashcards

Exam 3 Lesson 20 Flashcards

1
Q

What does aldosterone regulate?

A

electrolyte transport across epithelial cells

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2
Q

what is electrolyte transport?

A

Na+ resorption and K+ secretion

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3
Q

what are the main target tissues of aldosterone?

A

kidney, intestine, salivary and sweat glands

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4
Q

How does low sodium diet affect aldosterone secretion?

A

it increases it.

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5
Q

what happens to zona glomerulosa with a low sodium diet?

A

it doubles in thickness in 3 weeks

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6
Q

how much does sodium have to decline in plasma for aldosterone secretion to be stimulated?

A

About 20 mEq/L

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7
Q

how much does plasma K+ have to increase to stimulate aldosterone secretion?

A

Only 1 mEq/L

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8
Q

what secondary messengers are involved in the regulation of aldosterone secretion?

A

ACTH, angiotensin II, K+

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9
Q

intracellular mediator ACTH?

A

cAMP, PKA

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10
Q

intracellular mediator angiotensin II?

A

DAG, PKC

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11
Q

intracellular mediator K+?

A

Ca2+ via v-gated Ca2+ channels

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12
Q

Four parts of kidney

A

cortex, medulla, renal pelvis, ureter

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13
Q

how does blood flow in and out of glomerulus?

A

afferent arteriole from renal artery flows into glomerulus and efferent arteriole to renal vein flows out

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14
Q

what does aldosterone bind to?

A

intracellular aldosterone receptor in principal cell of collecting duct

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15
Q

where does aldosterone stimulate Na+ reabsorption?

A

across luminal membrane through epithelial Na+ channels

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16
Q

How does aldosterone upregulate Na+ reabsorption?

A

It upregulates open Na+ channels and increases the no of Na+K+ ATPase pumps in basolateral membrane

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17
Q

how do spironolactone and eplerenone act to inhibit aldosterone?

A

they compete directly with aldosterone for receptor

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18
Q

how do amiloride and triamterene inhibit aldosterone?

A

they indirectly inhibit aldosterone by closing the epithelial sodium channels

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19
Q

aldosterone receptor: what binds to aldosterone receptor besides aldosterone?

A

cortisol

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20
Q

aldosterone receptor: what happens when ligand binds to aldosterone receptor?

A

it loses its inhibitor and dimerizes, then translocates into the nucleus, binds with RE, and promotes mRNA transcription

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21
Q

How do the isozymes of 11Beta-HSD interact with cortisol?

A

11Beta-HSD2 is an exclusive dehydrogenase that acts in classical aldosterone tissues. It excludes cortisol from otherwise nonselective mineralocorticoid receptors. It inactivates cortisol, turning it to cortisone. 11Beta-HSD1 is an 11beta reductase that activates cortisol to increase local intracellular glucocorticoid concentrations

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22
Q

Where does 11beta-HSD2 work?(Tissue)

A

kidney, colon, sweat glands, salivary glands, placenta

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23
Q

where does 11beta-HSD1 work (Tissue)

A

skin, liver, adipose, CNS, placenta

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24
Q

How much higher is cortisol concentration in circulation than aldosterone circulation?

A

100x

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25
Q

what is the active component of licorice? What does it do?

A

glycyrrhetinic acid/ inhibits 11beta OHSD

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26
Q

what can happen when cortisol is in excess in circulation?

A

it can saturate 11beta OHSD and then interacts with aldosterone receptor

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27
Q

Renin-angiotensin and aldosterone secretion: what does aldosterone in distal nephron stimulate?

A

it stimulates increases Na+ resorption and K+ secretion and stimulates the juxtaglomerular apparatus to make renin

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28
Q

renin-angiotensin and aldosterone secretion: What is the purpose of renin?

A

renin turns angiotensinogen into angiotensin I

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29
Q

Renin-angiotensin and aldosterone secretion: how does angiotensin I turn into angiotensin II?

A

angiotensin converting enzyme

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30
Q

renin-angiotensin and aldosterone secretion: what is the target of angiotensin II?

A

adrenal gland

31
Q

what part of the juxtaglomerular apparatus secretes renin?

A

juxtaglomerular cells

32
Q

what is the role of the macula densa?

A

it modulates renin secretion

33
Q

what does macula densa sense?

A

both flow and sodium delivery

34
Q

what does renin secretion do?

A

it helps maintain total body sodium and glomerular filtration rate at an acceptable level

35
Q

Feedback control by macula densa: what happens when macula densa senses increase in both flow and sodium delivery?

A

macula densa releases ATP (adenosine), which a. decreases GFR and maintains normal filtered load and b. decreases renin secretion and allows more sodium excretion

36
Q

feedback control by macula densa: what happens when macula densa senses decrease in both flow and sodium delivery?

A

it releases NO, prostaglandins which a. increase GFR and maintains normal filtered load and b. increases renin secretion and conserves body sodium.

37
Q

what are the two roles of the juxtaglomerular apparatus?

A

a. endocrine gland that secretes renin b. sensor of blood volume, tubular fluid composition

38
Q

how do juxtaglomerular cells determine the need for renin release?

A

they are pressure transducers. The sense stretch of afferent arteriolar wall, or renal perfusion pressure. This pressure helps determine renin release necessary.

39
Q

what makes up the macula densa?

A

a specialized group of convoluted distal tubular cells

40
Q

what do macula densa cells do?

A

they function as chemoreceptors to monitor sodium and chloride in distal tubule. b. they monitor flow rate of fluid

41
Q

how do macula densa cells work?

A

they release ATP, prostaglandin in a paracrine manner on neighboring jx. Cells

42
Q

how does an increase in blood volume affect juxtaglomerular cells?

A

it stretches the cells, which may be stimulus that stops renin secretion

43
Q

what works as substrate for renin?

A

angiotensinogen

44
Q

how large is angiotensinogen?

A

it has 13+ aa

45
Q

how large is angiotensin I?

A

it has 10 aa

46
Q

how large is angiotensin II?

A

it has 8 aa

47
Q

what three things stimulate the tubuloglomerular feedback system?

A

a. a depletion of the extracellular fluid compartment b. a decrease in renal blood pressure c. a decrease in NaCl concentration at the macula densa

48
Q

what is the first indicator to the tubuloglomerular feedback system that blood pressure is low?

A

the afferent arteriole, which is a pressure receptor and detects low blood pressure due to low blood volume. This will induce the secretion of renin.

49
Q

how does tubuloglomerular feedback mechanism work?

A

it links changes in NaCl concentration (sensed by macula densa) with the control of afferent and efferent arteriolar resistance to autoregulate renal blood flow and the GFR

50
Q

what does angiotensin II stimulate (4)?

A

a. aldosterone secretion by the adrenal cortex b. arteriolar vasoconstriction c. ADH secretion and thirst d. reabsorption of NaCl by the proximal convoluted tubule

51
Q

what does aldosterone stimulate?

A

the reabsorption of NaCl by the loop of Henle, the distal convoluted tubule, and the collecting tubule

52
Q

how does antidiuretic hormone help raise blood pressure?

A

it helps increase water reabsorption in the collecting tubule.

53
Q

why does prolonged action aldosterone require the continuous stimulation of renin secretion?

A

because both renin and aldosterone have short plasma half lives (approx 15 min).

54
Q

what is the half life of angiotensin II?

A

less than a minute

55
Q

three direct renal influences on cardiovascular system?

A

Red blood cell production, ECF volume, total peripheral resistance

56
Q

how do kidneys produce red blood cells?

A

via erythropoeitin

57
Q

what renal influences affect blood volume?

A

red blood cell production and control of extracellular fluid volume

58
Q

what controls blood pressure?

A

blood volume and total peripheral resistance

59
Q

what influences total peripheral resistance?

A

angiotensin II

60
Q

effect of low salt diet on ANP, vasopressin, aldosterone, renin, urine and plasma Na+?

A

ANP, low – vasopressin, low – aldosterone, high – renin, high – urine Na+ low – plasma Na+ high

61
Q

effect of normal salt diet on ANP, vasopressin, aldosterone, renin, urine and plasma Na+?

A

ANP, vasopressin, aldosterone all normal. Low renin. High Na+ in urine, normal plasma Na+.

62
Q

effect of high salt diet on ANP, vasopressin, aldosterone, renin, urine and plasma Na+?

A

ANP, high – VP, high – aldosterone, low – renin, low – high urine and plasma Na+

63
Q

what do natriuretic peptides do?

A

promote sodium excretion in urine

64
Q

what are the natriuretic peptides and what is their main source?

A

ANP, BNP – heart

65
Q

What does ANP inhibit?

A

a. renin release b. angiotensin II promotion of Na+ reabsorption c. medullary collecting dust Na+ absorption

66
Q

what increases natriuretic peptide secretion?

A

atria distension, which can be due to plasma volume expansion

67
Q

what is the fetoplacental unit concept

A

the placenta cannot make estrogen on its own, and the fetal adrenal gland cannot make progesterone. The placenta synthesizes progesterone, sends it to the fetal adrenal gland, which in turn makes DHEA/DHEAS, and resends that to the placenta. The placenta uses DHEA/DHEAS to make estrogen, which it the secretes.

68
Q

what is the luteal-placental shift?

A

chorionic gonadotropin maintains the corpus luteum of pregnancy after LH secretion stops.

69
Q

what molecules are imported by placenta (3)?

A

maternal immunoglobulins (intracellular R), ions (ATP dependent membrane R), glucose (facilitated diffusion)

70
Q

how is gas exchanged through placenta (O2 and CO2)

A

simple diffusion

71
Q

what does placenta excrete (3)

A

placental lactogen, estrogen, chorionic gonadotropin

72
Q

what is the purpose of lactogen?

A

together with chorionic gonadotropin, it stimulates the mammary gland for postpartum lactogenesis

73
Q

what are the layers of the placenta?

A

syncytiotrophoblast, cytotrophoblast

74
Q

functions of fetal adrenal cortex

A

a. DHEA production during early gestation b. production of glucocorticoids, which are responsible for functionl hypothalamopituitary development, induction of thymic involution, and production of surfactant by alveolar cells of lung

Endocrinology (21 decks)

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