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Renal Hormones Flashcards

1
Q

What is a hormone?

A

a chemical substance made in one or more locations which is carried by the blood to other areas where it has an effect on cellular function

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2
Q

What is an autacoid?

A

• Substance produced in an area that has an effect on tissue in the same area.

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3
Q

What is the GFR?

A

the total volume of fluid that is filtered from the plasma into the nephrons per unit time

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4
Q

What are the two intrinsic mechanisms of regulating GFR?

A
  1. Myogenic mechanism

2. Tubuloglomerular feedback machanism

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5
Q

What is the myogenic mechanism of GFR control?

A

The rise in pressure in the afferent arteriole of the glomerulus causes the arteriole to vasoconstrict and vice versa

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6
Q

Usually the GFR remains autoregulated (i.e. relatively constant) despite the fluctuations in arterial pressure that occur during a person’s normal activities. When can this fail?

A

At extremes of blood pressure, autoregulation fails and GFR and RBF vary directly with the systemic blood pressure.

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7
Q

What is the MOA of the tubuloglomerular feedback mechanism?

A

Macula densa senses increased flow (and [NaCl]) from increased filtration rate, and changes arteriole resistance through chemical mediators

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8
Q

What is the function of adenosine in the kidney?

A

decreases GFR

Decreased renin

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9
Q

What are the two things that the macula densa is sensing?

A

Flow

Na delviery

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10
Q

What is the chemical released by the macula densa in response to increased flow? What does this cause?

A

Adenosine

Lowers GFR and lower renin (to lower BP)

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11
Q

What is the effect of renin?

A

Increase BP by reabsorbing Na and causing angiotensin II formation

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12
Q

What is the chemical released by the macula densa in response to decreased flow? What does this cause?

A

NO, prostaglandins

Increases GFR and renin

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13
Q

How are afferent and efferent arterioles regulated relative to one another (directly or inversely)?

A

Inversely

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14
Q

Why do we want to uncouple BP and excretion regulation?

A

Sudden BP changes could interfere in fluid and electrolyte balance.

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15
Q

True or false: the proximal tubule almost always removes about 2/3 of the solutes from the tubule?

A

True

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16
Q

What is pressure diuresis?

A

Increased loss of fluids when BP increases

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17
Q

What is pressure natriuresis?

A

Increased loss of fluids when plasma Na increases

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18
Q

What are the two ways the kidneys are related to HTN? What is the consequence of this?

A
  1. Hypertension (for any reason) can cause renal damage and increased nephron flow
  2. Any form of renal damage tends to cause hypertension

=bad feedback

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19
Q

What is the effect of PGE2 and PGI production when angiotensin II/norepi/vasopressin is released? What is the effect on the kidney?

A

Increases,

thus can oppose vasoconstrictors produced by the macula densa

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20
Q

What is the mechanism through which chronic aspirin or IBU use can lead to renal damage?

A

If you reduce the amount of PGE2 and PGI2 synthesized unopposed vasoconstriction might cause renal damage

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21
Q

What happens to a pt with kidney damage when they take NSAIDs?

A

Inhibit vasodilation (which would be up in a damaged kidney), leads to ischemic nephrons

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22
Q

Which part of a kidney is particularly susceptible to ischemia? What is the consequence of this?

A

medullary blood flow

If there is damage, one sign may be the inability to produce concentrated urine (since this is where juxtaglomerular nephrons are)

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23
Q

What is the effect of norepi and epi on the adrenal medulla?

A

Constrict both the afferent and efferent arterioles thus decreasing renal blood flow and GFR.

More alpha 1 on afferent arterioles

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24
Q

What is the effect of angiotensin II generally? On the kidneys?

A

Vasoconstrictor in the systemic circulation

preferentially constricts the efferent arteriole under most physiological conditions

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25
Q

Angiotensin II preferentially constricts the efferent arteriole under most physiological conditions How is the afferent arteriole protected from this?

A

Vasodilator release by macula densa

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26
Q

What is the effect of unopposed angiotensin II? How?

A

Increased GFR b/c efferent arterioles constricted while afferent not

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27
Q

What is the relationship of efferent arteriole resistance relative to GFR and renal blood flow?

A

Direct with GFR

Inversely with renal blood flow

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28
Q

What is the relationship of afferent arteriole resistance relative to GFR and renal blood flow?

A

Inverse with both GFR and renal blood flow

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29
Q

What is glomerular tubular balance?

A
  1. Renal tubules increase their reabsorption rate when GFR increases
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30
Q

If the number of nephrons is decreased, the kidneys compensate how? How is this effected?

A

by increasing the filtration of each nephron

increasing PGE2 and PGI2 thus dilating afferent arterioles and increasing single nephron GFR.

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31
Q

What are the effects of Epi and norepi on the kidneys?

A

Constricts both the afferent and efferent arterioles thus decreasing renal blood flow and GFR

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32
Q

What is the effect of angiotensin II on the kidneys? (3)

A

preferentially constricts the efferent arteriole under most physiological conditions

Increase Na reuptake from tubules

Increases Aldosterone synthesis

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33
Q

What does the kidney do in response to low BP?

A

Releases renin

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34
Q

What is the function of renin?

A

Breaks angiotensinogen from liver into angiotensin I.

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35
Q

What converts angiotensin I to II?

A

ACE

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36
Q

What is the function of juxtaglomerular cells?

A

Release renin in response to BP changes in the kidney

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37
Q

What is the effect of aldosterone synthesis?

A

Increases renal reabsorption of sodium which can also raise blood pressure

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38
Q

What are the steps that the kidney takes in reposne to BP changes? (3)

A
  1. Changes renin from juxtaglomerular cells
  2. Renin converts Angiotensinogen to angiotensin I
  3. Angiotensin II increases aldosterone
39
Q

What are the two things that cause thirst?

A
  1. Angiotensin II

2. Increased blood osmolality

40
Q

Increased blood osmolality or decreased blood volume causes what?

A

increased release of ADH

41
Q

What is ADH’s effect on BP? How?

A

Increases via vasoconstriction

42
Q

What are the two natriuretic peptides in the heart?

43
Q

What is the signal for more ADH to be released?

A

Increased stretch on the right atrium

44
Q

What is the effect ANP has on ADH, Renin?

A

Decreases both

45
Q

What are the effects of ANP/BNP on the GFR?

A

Relaxes Arteriole to increase GFR

46
Q

What are the effects of ANP/BNP on angiotensin II?

A

Decrease/inhibits

47
Q

What are the effects of ANP/BNP on the Na/water reabsorption on the medullary collecting duct?

48
Q

What are the effects of ANP/BNP on aldosterone?

49
Q

What is the overall effect of ANP/BNP?

A

Decreased BP

50
Q

Where is erythropoietin mainly produced?

51
Q

What is the function of erythropoietin?

A

Goes to bone marrow to stimulate RBC production

52
Q

What is the enzyme that creates calcitriol from 25-hydroxycholecalciferol?

A

1alpha- Hydroxylase

53
Q

Where does the conversion of vit D3 take place?

54
Q

What is the prohormone of vit D that we take in via our diet? What is the first step to convert it to previt D?

A

7-dehydrocholesterol

Exposure to sunlight

55
Q

After previt D is converted to Vit D3 via sunlight, what happens?

A

25-hydroxylase converts it to 25 hydroxycholecalciferol

56
Q

What is the step after formation of 25 hydroxycholecalciferol?

A

1alpha hydroxylase converts it to calcitriol

57
Q

What is the active form of Vit D?

A

Calcitriol

58
Q

What are the effects of calcitriol? (3)

A

Stimulates renal tubule reabsorption of Ca and PO3

Suppresses PTH synthesis in the parathyroid

Stimulates FGF3 in bone

59
Q

The final hydroxylation step of vit D is stimulated by what?

60
Q

What is the effect of PTH?

A

controls plasma calcium concentration

61
Q

What controls [PTH]? What is the relationship?

A

[Ca], inversely

62
Q

What are the chemical reaction in the body that take place in response to lower [Ca]?

A

Increase PTH, Increasing Vit D activation, increasing Ca reabsorption/release from bones

63
Q

What is the relationship between PO3 and PTH?

A

inverse relationship

64
Q

Why is it important that PO3 an Ca vary inversely?

A

CaPO3 could precipitate out and cause renal stones

65
Q

What is the effect of PTH on PO3 reabsorption in the kidneys and intestines?

A

Decreases PTH reabsorption in the kidneys

Increases in intestines

66
Q

Where is the Ca drawn from bone via PTH?

A

The labile bone part

67
Q

What are the three rapid responses to PTH synthesis?

A

Decreased renal PO3 reabsorption

Increased renal Ca reab

Increase bone Ca withdrawl

68
Q

What are the two slow responses to PTH?

A

Increased osteoclast action

Increased intestinal Ca reabsorption

69
Q

What is fibroblast growth factor 23 (FGF23)? (what makes it, what does it do [2])?

A

a peptide hormone that is made by osteoblasts and osteocytes in bone

Decreases PO3 reabsorption in the kidney, and decreases production of calcitriol

70
Q

What stimulates FGF23 release?

A

Increased PO3 levels,

71
Q

What is the effect of PTH on calcitriol synthesis? FGF23?

A

Increased by PTH

Decreased by FGF23

72
Q

What is the effect of PTH on phosphate excretion? FGF23?

A

Both increase excretion

73
Q

What is the effect of CKD on [PO3]? What is the consequence of this?

A

Lowers GFR, increasing [PO3]. This increases PTH, increasing bone reabsorption. =osteodystrophy

74
Q

What is the effect of PTH on the kidney? Intestines?

A

Kidney = Increases Ca reabsorption, decreases PO3

Intestines = Increases Ca reabsorption, increases PO3

75
Q

What cells synthesize FGF23?

A

Osteoblasts/clasts

76
Q

What inhibits PTH?

77
Q

What is the feedback mechanism for Vit D synthesis?

A

Increased Ca inhibits PTH. PTH no longer activates 1alpha hydroxylase

78
Q

1alpha-hydroxylase is found where?

79
Q

25alpha hydroxylase is found where?

80
Q

What are the two hormones that ANP inhibits?

81
Q

Where is angiotensinogen produced?

82
Q

What type of sympathetic adrenoceptors are found on the kidney? What do they do?

A

B1, stimulate renin release

83
Q

Where are osmoreceptors found/what do they synapse to?

A

In the hypothalamus, synapsing on the paraventricular and supraoptic nerves

84
Q

How can tubuloglomerular feedback help prevent excessive fluid losses if there is damage to kidney proximal tubules?

A

Can redirect blood to other, “good” nephrons

85
Q

What is the effect of angiotensin II on vascular smooth muscle?

86
Q

What is the effect of angiotensin II on the adrenal cortex?

A

Stimulates aldosterone release

87
Q

What is the effect of angiotensin II on the afferent and efferent arterioles?

A

Vasoconstricts efferent.

88
Q

What is the effect of angiotensin II on the thirst center?

A

Increases thirst

89
Q

What is the effect of angiotensin II on ADH release?

90
Q

What is the effect of angiotensin II on sympathetic tone?

91
Q

What are the two organs that make erythropoietin?

A

Liver and kidney

92
Q

What is the major stimulus for erythropoietin secretion?

A

Hypoxia to kidneys

93
Q

What is more important, the effect of vit D on the intestines or the kidneys?

A

Intestines

94
Q

What is the effect of PTH on the kidney?

A

Increases PO3 secretion

Physiology (75 decks)

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