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

Lecture 11/20: Renal Physiology Cont'd Flashcards

Final (93 cards)

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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
What is the enzyme needed to aldo synthesis? Where would we expect to find this?
Aldosterone synthase Around the zona glomerulosa
26
What cholesterol derative has cross activity with aldo-R? Why?
Coristol They have a very similar structure
27
What effect can increase coristol have on the body?
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
28
What enzyme breaks down cortisol in the body? Why is this important?
11Beta HSD Type II enzyme (HSD = hydroxysteroid dehydrogenase) This decreases likelihood of aldo-R interaction
29
Describe the pathology of an ACTH secreting lung tumor
Secretes cortisol & overwhelms 11Beta HSD Type II enzymes --> increased cortisol --> increase aldo-R activity --> increased BP/hypokalemia
30
What inhibits 11Beta HSD type II?
Licorice **Cause increased BP/hypokalemia**
31
T/F: We cant prevent glucocorticoids from have a direct impact on BP
F We can prevent this.
32
T/F: There are place to reabsorb K+ in the DCT and collecting tubule
F
33
T/F: It is almost impossible to have increased K+ if you have healthy kidneys & adrenal gland
T
34
How does increased plamsa K+ effect aldo?
Increases aldo --> increase K+ secretion/excretion
35
What are the 2 types intercalated cells?
Type A: Secrete protons Type B: reabsorb protons/secrete bicarb
36
Where are intercalated cells located? What do they deal with?
location: collecting duct Acid/base balance and water reabsorption
37
What are the majority cells in the DCT?
principal cells
38
Intercalated cells are sensitive to _____
ADH
39
ADH =
Antidiuretic hormone (vasopressin)
40
T/F: Vasopressin is the exogenous version of ADH
T
41
What 2 cells are sensitive to ADH/Vaso?
principal intercalated
42
What are the Vasopressin receptors in the Kidneys? In the peripheries?
Kidneys: V2 Peripheries: V1
43
What does vasopressin/ADH do?
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
What Aquaporin channels are always in the cell wall? which side of the cell wall are they in?
AQP3 AQP4 Basolateral
45
Explain the pathology of Nephrogenic DI
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
Differential between Nephrogenic DI & central DI
Nephrogenic DI: problem with PKA/Phosphorlation of AQ2 channels --> getting them to cell wall Central DI: problem with release of vasopressin/ADH
47
What hormone prevents us from peeing very often?
ADH
48
What type of pumps are in intercalated Type A cells?
1. Hydrogen Potassium ATPase -1H+, 1K+, 1 ATP cotransporter 2. Hydrogen ATPase -1H+, 1 ATP -helps concentrate protons in urine
49
What medication can induce Nephrogenic DI? What is this medication commonly used for?
Lithium Commonly used for psycological disorders
50
Lithium can induce __________ which causes ________
Nephrogenic DI Urine dumping
51
What is the lowest urine osmolarity you can have?
50 mOsm/L
52
What is the urine osmo we expect to see in pt who take HIGH doses of lithium?
50 mOsm/L
53
What can causes central DI?
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
The movement of water is associated with ______
Vasopressin/ADH
55
What happens to vaso/ADH levels if we need to hold on to more water? get rid of?
Need more water: Vaso/ADH increases Get rid of water: Vaso/ADH decreases
56
What things trigger release of ADH/Vaso?
1. increase in plasma osmolarity 2. decrease in arterial BP 3. decrease in blood volume
57
How do barorecptors work?
Sense a drop in BP/Blood volume --> feedback info to CNS to release ADH --> reabsorbs more water --> BP increases
58
What is the primary way that ADH is release?
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
What is the major sensory/regulatory area in the brain?
hypothalamus **Controls temperature**
60
If you have a head injury, and began to start peeing alot, what should you expect?
Damage to the hypothalamus central DI
61
Where is ADH released from?
Pituitary gland
62
What are the neurons responsible for ADH secretion? How much? What is their location?
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
Where do the supraoptic & paraventricular neurons both meet?
**Neurohypophysis** Posterior pituitary gland Posterior lobe
64
What are all the names of the posterior pituitary gland?
Neurohypophysis Posterior lobe
65
What is the another name for the anterior lobe of the pituitary gland?
adenohypophysis
66
______ are cells that are specialized in sensing osmolarity changes in plasma. They are also connected to the cell bodies of
osmoreceptors
67
What type of neurons are supraoptic & paraventricular neurons?
Multipolar
68
A hypotonic solution is ______; a hypertonic solution is __________
diluted concentrated
69
What type of IV fluid is most like blood plasma?
Isotonic fluid
70
What will happen if we give hypotonic fluid?
Cell will swell Slows the rate of of AP sent to ADH production area --> Decreases ADH release
71
What happens if you give a hypertonic fluid?
Cell will shrink Increase rate of AP sent to ADH production area --> Increases ADH release
72
______ controls how much urea is reabsorbed in the loop of henle
vaso
73
What is the diluting segment?
Late thick ascending limb Early distal tubule
74
What can low levels of ADH in the nephron cause? high levels?
low: dilute urine --> low urine osmo --> urine dumping high: concentrated uring --> high urine osmo --> decreased urine excretion
75
Urea is a waste product of _________ but is used for water ________
metabolism osmosis (creates renal ISF gradient)
76
What are the Urea transporters? Where are they located?
UT-A1 UT-A3 Collecting duct
77
What are all the things at the collecting duct that helps us reabsorb water?
1. ADH 2. AQ2 3. UT-A1; UT-A3 4. V2
78
Increasing ______ levels helps urea absorption at the collecting duct
ADH
79
T/F: ADH allows for the reabsorption of water without salt
T
80
What hormone is the primary controller of plasma osmolarity?
ADH
81
What would happen if we lost control of the pituitary gland?
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
What 2 things decrease ADH release from the brain?
Alcohol Caffeine
83
What are things that decrease thirst?
-Decreased plasma osmolarity -increased blood volume -increased BP -decreased ANGII -gastric distention
84
What are things that increase thirst?
-increased plasma osmolarity -decreased blood volume -decreased BP -increased ANGII -dryness of mouth
85
What is the importance of keeping a pt mouth moist in the ICU?
It helps with thirst Dry mouth = increaed thirst
86
What decreases ADH release? Drugs?
-Decreased plasma osmolarity -increased blood volume -increased BP Drugs: Alcohol Clonidine Haloperidol
87
What increases ADH release? Drugs?
-increased plasma osmolarity -decreased blood volume -decreased BP -N/V -hypoxia Drugs: -morphine -nicotine
88
Increased thirst = _______ ADH levels
Increased
89
Decreased thirst = ________ ADH levels
Decreased
90
T/F: If adrenal & kidneys are working fine, should not have a problem with K secretion
T
91
What is the urine osmo in a completely healthy person?
600 mOsm/L
92
What is the urine osmo of a person trying to conserve fluid?
1200 mOsm/L
93
Are you supposed to drink distilled water? Why?
No Decreases plasma osmo --> decreases ADH --> Decreases urine osmo --> BIG URINE INCREASE

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