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A/P > Lecture 11/20: Renal Physiology Cont'd > Flashcards

Lecture 11/20: Renal Physiology Cont'd Flashcards

Final

1
Q

When you think principal cells think ______

A

Aldo

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2
Q

Principal cells help regulate what 2 ions?

A

Na
K

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3
Q

Aldosterone is a _________ that help manage _______ balance

A

Mineralocorticoid

mineral

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4
Q

What are the effects of Aldo?

A
  1. Increases the speed of the Na/K ATP –> Increases K secretion & Na through eNaC
  2. Increases # on Na channels (eNaC channels) on apical side for entry into tubular cell
  3. Increase # of K channels (ROMK/BK) on apical side for secretion then excretion
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5
Q

Aldo increases secretion of ________ in the tubular lumen and increases _________ into the tubular cells

A

K

Na

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6
Q

What effects does increased K+ have on Aldo?

A

Increased K+ –> Increases Aldo –> Increases K+ channels (ROMK/BK) to the cell –> increased K+ secretion –> Increased K+ excretion

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7
Q

What are the K+ channels that aldo move to the cell wall?

A

ROMK (Renal outer Medulla K+)
BK (Big K+)

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8
Q

Where are principal cells located?

A

Late DCT
Collecting Tubule

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9
Q

Decreased K+ = ________ Aldo = __________ K channels

A

decreased

decreased

This is to hold on to K

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10
Q

Potassium maintaince is associated with what type of cells? where are these cells located?

A

principal cells

late DCT & collecting tubule

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11
Q

Describe the mechanism of the ROMK/BK channels

A

BK: Always in the principal cell wall (But closed)
-opens during high levels of K+/aldo
-helps facilitate high levels of K+ secretion

ROMK: floating inside principal the cell
-comes to cell wall/open (& stays open) under normal K+ levels/aldo stimulation

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12
Q

Describe ROMK & BK channels at low, normal, and high K+

A

Low: BK: In cell wall closed
ROMK: floating in cell

Normal: BK: in cell wall closed
ROMK: In cell wall open

High: BK: in cell wall open
ROMK: In cell wall open

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13
Q

What are your K+ sparing diuretics? What is the MOA? What do we need to be mindful of?

A

-Spironolactone
-Eplerenone

MOA:
-Aldo Antagonist
-Block the aldo-R which decrease Na/K ATP activity –> decrease K secretion & Na into the cell

Considerations: If you are taking a K+ supplement

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14
Q

What are your Na+ channel blockers? What is the MOA? What do we need to be mindful of?

A

-Amiloride
-Triamterene

MOA: block EnaC in the principal cells –> slows down the Na/K ATP –> decreases K+ secretion

Considerations: If you are taking a K+ supplement

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15
Q

What happens when you take a diuretic that work upstream of the the DCT/Collecting tubule? What kind of medication can we give for this?

A

All of the Na+ being pulled in goes downstream in the nephron to be excreted

But the principal cells in the Late DCT/Collecting tubule have eNac/NaKATP/K channels that will cause K+ wasting

Tx:
-Na+ channel blocker: Amiloride/Triamterene
-K+ sparing diuretic: spirolactone/eplerenone

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16
Q

What is the main Na+ channel blocker given with hydrocholothiazide? Where this drug work? where does hydrocholothiazide work?

A

Triamterene: principal cells in the late DCT/collecting tubule

hydrochlorothiazide: thiazide diuretic that inhibits the NCC pump in the DCT

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17
Q

What are the 4 layers of the adrenal gland in order?

A

-Zona Glomerulosa: outer
-Zona Fasciculata
-Zona Reticularis
-Medulla: deepest

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18
Q

Where is Aldo produced?

A

Zona Glomerulosa in the adrenal gland

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19
Q

Where is estrogen produced?

A

Zona Fasciculata in the adrenal gland

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20
Q

where is cortisol & androgens produced?

A

Zona reticularis in the adrenal gland

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21
Q

Where are catecholamines produced? Whare are the most common ones?

A

Medulla

Epi/NE

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22
Q

What is the Epi/NE ratio?

A

4:1

Adrenal gland produced 4 epi’s for every NE
More EPI than NE

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23
Q

T/F: Renin causes Aldo release

A

T

There are AT1 receptors in the Zona glomerulosa

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24
Q

Epi/NE ratio is __:1

A

4

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25
Q

What is the enzyme needed to aldo synthesis? Where would we expect to find this?

A

Aldosterone synthase

Around the zona glomerulosa

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26
Q

What cholesterol derative has cross activity with aldo-R? Why?

A

Coristol

They have a very similar structure

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27
Q

What effect can increase coristol have on the body?

A

Cortisol is a stress hormone derived from cholesterol & secreted from the zona fasciculate of the adrenal gland

-similar structure to Aldo
-can bind to aldo-R

Increased cortisol can increase aldo-R activity
Increasing K secretion /Enac activity

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28
Q

What enzyme breaks down cortisol in the body? Why is this important?

A

11Beta HSD Type II enzyme
(HSD = hydroxysteroid dehydrogenase)

This decreases likelihood of aldo-R interaction

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29
Q

Describe the pathology of an ACTH secreting lung tumor

A

Secretes cortisol & overwhelms 11Beta HSD Type II enzymes –> increased cortisol –> increase aldo-R activity –> increased BP/hypokalemia

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30
Q

What inhibits 11Beta HSD type II?

A

Licorice

Cause increased BP/hypokalemia

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31
Q

T/F: We cant prevent glucocorticoids from have a direct impact on BP

A

F

We can prevent this.

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32
Q

T/F: There are place to reabsorb K+ in the DCT and collecting tubule

A

F

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33
Q

T/F: It is almost impossible to have increased K+ if you have healthy kidneys & adrenal gland

A

T

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34
Q

How does increased plamsa K+ effect aldo?

A

Increases aldo –> increase K+ secretion/excretion

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35
Q

What are the 2 types intercalated cells?

A

Type A: Secrete protons

Type B: reabsorb protons/secrete bicarb

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36
Q

Where are intercalated cells located? What do they deal with?

A

location: collecting duct

Acid/base balance and water reabsorption

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37
Q

What are the majority cells in the DCT?

A

principal cells

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38
Q

Intercalated cells are sensitive to _____

A

ADH

39
Q

ADH =

A

Antidiuretic hormone (vasopressin)

40
Q

T/F: Vasopressin is the exogenous version of ADH

A

T

41
Q

What 2 cells are sensitive to ADH/Vaso?

A

principal
intercalated

42
Q

What are the Vasopressin receptors in the Kidneys? In the peripheries?

A

Kidneys: V2

Peripheries: V1

43
Q

What does vasopressin/ADH do?

A

When bound to its receptor:

increase cAMP –> PKA phosphorylates AQP2 channels –> moves AQ2 channels to apical side of the cell wall –> increases water REABSORPTION –> body hold on to tinkle

44
Q

What Aquaporin channels are always in the cell wall? which side of the cell wall are they in?

A

AQP3
AQP4

Basolateral

45
Q

Explain the pathology of Nephrogenic DI

A

There’s an issue with PKA & the phosphorylation of the AQP2 channels getting to the apical side of the cell wall –> Not able to reabsorb urine –> urine dumping

46
Q

Differential between Nephrogenic DI & central DI

A

Nephrogenic DI: problem with PKA/Phosphorlation of AQ2 channels –> getting them to cell wall

Central DI: problem with release of vasopressin/ADH

47
Q

What hormone prevents us from peeing very often?

A

ADH

48
Q

What type of pumps are in intercalated Type A cells?

A
  1. Hydrogen Potassium ATPase
    -1H+, 1K+, 1 ATP cotransporter
  2. Hydrogen ATPase
    -1H+, 1 ATP
    -helps concentrate protons in urine
49
Q

What medication can induce Nephrogenic DI? What is this medication commonly used for?

A

Lithium

Commonly used for psycological disorders

50
Q

Lithium can induce __________ which causes ________

A

Nephrogenic DI

Urine dumping

51
Q

What is the lowest urine osmolarity you can have?

A

50 mOsm/L

52
Q

What is the urine osmo we expect to see in pt who take HIGH doses of lithium?

A

50 mOsm/L

53
Q

What can causes central DI?

A

Alcohol

-Decreases levels of ADH released from the brain
-impairs kidneys response at the V2-R

Think about yourself… alcohol makes you want to tinkle

54
Q

The movement of water is associated with ______

A

Vasopressin/ADH

55
Q

What happens to vaso/ADH levels if we need to hold on to more water? get rid of?

A

Need more water: Vaso/ADH increases

Get rid of water: Vaso/ADH decreases

56
Q

What things trigger release of ADH/Vaso?

A
  1. increase in plasma osmolarity
  2. decrease in arterial BP
  3. decrease in blood volume
57
Q

How do barorecptors work?

A

Sense a drop in BP/Blood volume –> feedback info to CNS to release ADH –> reabsorbs more water –> BP increases

58
Q

What is the primary way that ADH is release?

A

Osmoreceptors in the hypothalamus sense changes in plasma osmolarity –> feeds that info the the CNS

Osmoreceptors –> AP to Supraoptic & Paraventricular neuron –> they both lead to the posterior pituitary gland –> they release ADH into surrounding vessels

59
Q

What is the major sensory/regulatory area in the brain?

A

hypothalamus

Controls temperature

60
Q

If you have a head injury, and began to start peeing alot, what should you expect?

A

Damage to the hypothalamus

central DI

61
Q

Where is ADH released from?

A

Pituitary gland

62
Q

What are the neurons responsible for ADH secretion? How much? What is their location?

A

2x Supraoptic Nuclei:
-5/6 of ADH release
-in front of hypothalamus

2x Paraventricular Nuclei:
-1/6 of ADH release
-on side of 3rd ventricle (thyroid gland)

63
Q

Where do the supraoptic & paraventricular neurons both meet?

A

Neurohypophysis

Posterior pituitary gland
Posterior lobe

64
Q

What are all the names of the posterior pituitary gland?

A

Neurohypophysis

Posterior lobe

65
Q

What is the another name for the anterior lobe of the pituitary gland?

A

adenohypophysis

66
Q

______ are cells that are specialized in sensing osmolarity changes in plasma. They are also connected to the cell bodies of

A

osmoreceptors

67
Q

What type of neurons are supraoptic & paraventricular neurons?

A

Multipolar

68
Q

A hypotonic solution is ______; a hypertonic solution is __________

A

diluted

concentrated

69
Q

What type of IV fluid is most like blood plasma?

A

Isotonic fluid

70
Q

What will happen if we give hypotonic fluid?

A

Cell will swell

Slows the rate of of AP sent to ADH production area –> Decreases ADH release

71
Q

What happens if you give a hypertonic fluid?

A

Cell will shrink

Increase rate of AP sent to ADH production area –> Increases ADH release

72
Q

______ controls how much urea is reabsorbed in the loop of henle

A

vaso

73
Q

What is the diluting segment?

A

Late thick ascending limb
Early distal tubule

74
Q

What can low levels of ADH in the nephron cause? high levels?

A

low: dilute urine –> low urine osmo –> urine dumping

high: concentrated uring –> high urine osmo –> decreased urine excretion

75
Q

Urea is a waste product of _________ but is used for water ________

A

metabolism

osmosis (creates renal ISF gradient)

76
Q

What are the Urea transporters? Where are they located?

A

UT-A1
UT-A3

Collecting duct

77
Q

What are all the things at the collecting duct that helps us reabsorb water?

A
  1. ADH
  2. AQ2
  3. UT-A1; UT-A3
  4. V2
78
Q

Increasing ______ levels helps urea absorption at the collecting duct

A

ADH

79
Q

T/F: ADH allows for the reabsorption of water without salt

A

T

80
Q

What hormone is the primary controller of plasma osmolarity?

A

ADH

81
Q

What would happen if we lost control of the pituitary gland?

A

We would lose control over blood osmolarity

Blood plasma (Na+) would continue to increase and go unchecked
-There would be no release in ADH to help reabsorb water to balance this out.

82
Q

What 2 things decrease ADH release from the brain?

A

Alcohol
Caffeine

83
Q

What are things that decrease thirst?

A

-Decreased plasma osmolarity
-increased blood volume
-increased BP
-decreased ANGII
-gastric distention

84
Q

What are things that increase thirst?

A

-increased plasma osmolarity
-decreased blood volume
-decreased BP
-increased ANGII
-dryness of mouth

85
Q

What is the importance of keeping a pt mouth moist in the ICU?

A

It helps with thirst

Dry mouth = increaed thirst

86
Q

What decreases ADH release? Drugs?

A

-Decreased plasma osmolarity
-increased blood volume
-increased BP

Drugs:
Alcohol
Clonidine
Haloperidol

87
Q

What increases ADH release? Drugs?

A

-increased plasma osmolarity
-decreased blood volume
-decreased BP
-N/V
-hypoxia

Drugs:
-morphine
-nicotine

88
Q

Increased thirst = _______ ADH levels

A

Increased

89
Q

Decreased thirst = ________ ADH levels

A

Decreased

90
Q

T/F: If adrenal & kidneys are working fine, should not have a problem with K secretion

A

T

91
Q

What is the urine osmo in a completely healthy person?

A

600 mOsm/L

92
Q

What is the urine osmo of a person trying to conserve fluid?

A

1200 mOsm/L

93
Q

Are you supposed to drink distilled water? Why?

A

No

Decreases plasma osmo –> decreases ADH –> Decreases urine osmo –> BIG URINE INCREASE

A/P (33 decks)

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