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AP Kidneys 2024 > Lecture 7 Final > Flashcards

Lecture 7 Final Flashcards

1
Q

How many % of water and electrolytes are reabsorbed in the PCT?

A

65%

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2
Q

How much water gets reabsorbed in the thin descending limb?

A

20%; approximately 85% of the 2/3, remaining 15% is reabsorbed in the DCT and collecting duct.

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3
Q

In the TAL how many ions are reabsorbed (NKCL2)?

A

25%

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4
Q

The remaining 15% of reabsorption is decided in the…

A

DCT/collecting duct via principal cells.

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5
Q

What regulates the water reabsorption in the DCT/collecting duct?

A

ADH

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6
Q

The PTH moves the Ca++ from the lumen to the cell and then?

A

It is reabsorbed to the interstitium via Na/Ca exchanger (3:1) with the primary force of the N/K pump.

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7
Q

Explain how the speed of Ca reabsorption in the DCT is sped up.

A

With the N/K pump keeping it low + charge inside the cell, the Na/Ca exchanger wants to come in even faster. Na influx and Ca into the interstitium!

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8
Q

How else can you speed up the Ca++ reabsorption process in the DCT?

A

By using Thiazides, it’ll block the NCl channel from coming back in the DCT. Keeping it low + charged, causing N/CaE to move faster.

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9
Q

How does thiazide diuretics help treat osteoporosis?

A

It helps the kidneys reabsorb more Ca++.

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10
Q

What should you be careful in taking while on thiazide diuretics?

A

K supplements bc the kidneys ends up holding onto more K while on thiazide diuretics.

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11
Q

What other therapeutic effects can thiazide diuretics do?

A

Helps prevent future kidney stones bc reabsorbing Ca reduces the amount in the urine.

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12
Q

What is aldosterone also a type of, other than a cholesterol? What does it act on?

A

It is a mineralocorticoid; acts on principal cells to retain Na and h2o while excreting more K+. It also speeds up the Na/K pump promoting the secretion of Na through the ENac, K channels to work faster.

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13
Q

increased aldosterone leads to more ____ channels in the DCT

A

Na+ (ENaC = endothelial Na channels)

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14
Q

What are the types of K channels mediated by aldosterone?

A

(1st) ROMK = Renal Outer Medullary K+ channel. It’s sequestered so if not needed it just hangs out in the cell and moves to cell walls when needed.

(2nd) BK = Big K+ channels come into the cell wall if there’s a huge amount of K+ needed to be excreted.

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15
Q

Which cells are the main cells used for K+ maintenance in the DCT/collecting tubules?

A

Intercalated cells

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16
Q

Which meds work on the ENac of the DCT?

A

Amiloride and Triamterene and it also indirectly slows down the K secretion.

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17
Q

How does Spironolactone work in the DCT?

A

It is an aldosterone receptor antagonist, it’ll slow down the Na/K pump > slows ENac > slows K+ secretion

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18
Q

If you have more Na in the PCT, there is ___ in the DCT, which indirectly ______ secretion of _____.

A

even more Na+; increase; K+

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19
Q

What can you do to balance the amount of Na being reabsorbed (PCT) and K+ secreted in the DCT?

A

Give loop diuretics with K sparing diuretics.
(ex. HCTZ with Triamterene)

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20
Q

Where does aldosterone come from?

A

Adrenal Cortex:
Zona glomerulosa

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21
Q

Where does cortisol and androgens come from?

A

Zona Fasciculata and Zona reticularis

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22
Q

What is released from the adrenal gland?

A

Cortisol, glucocorticoids, estrogen (zona fasciculi)

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23
Q

Structure of adrenal gland from the outside - in.

A

Zona glomerulosa, zona fasciculata, Zona reticularis, medulla (catecholamines)

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24
Q

What is released in the adrenal medulla?

A

Epi/Norepi (4:1)

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25
Q

What is aldosterone sensitive to?

A
  • The more K+ levels, the more aldosterone is released via zona glomerulosa.
  • Low K+, lower aldosterone released.
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26
Q

What’s the process of aldosterone release?

A

The RAAA (renin angiotensin aldosterone axis) > Ang II > aldosterone

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27
Q

What enzyme works on aldosterone?

A

Aldosterone synthase

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28
Q

ACTH secreting lung tumor leads to…

A

increase cortisol (glucocorticoid) > HTN

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29
Q

How does cortisol balance glucose?

A

It is a glucocorticoid released under stress to help the body “figure things out” per Schmidt

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30
Q

What prevents the cortisol from interacting with the aldosterone inside the principal cell?

A

There’s a specific enzyme “11B HSD type II” that eats (dehydrogenase) all of the cortisol (steroid) inside the principal cell.

(11 Beta Hydroxy steroid dehydrogenase Type II)

31
Q

What happens when you have ACTH tumor?

A

Increase cortisol production > (Cushing’s syndrome) > enzyme 11B HSD type II overwhelmed > HTN > low K+

32
Q

What is the inhibitor for 11B HSD type II?

A

Licorice; also used for tobacco taste

cause HTN > low K+
(smoking leads to HTN)

33
Q

Aldosterone OD is similar to?

A

ACTH and Licorice exposure. (HTN, low K+)

34
Q

Which cells works more on the acid/base balance in the renal system?

A

Intercalated cells

35
Q

Are there specific intercalated cells for acids and bases?

A

Type A - Acids

Type B - Bicarb

36
Q

What channels does Type A intercalated cells work with?

A

H+ atp-ase pump

H+/K+ atp-ase pump

37
Q

Type B channel?

A

It is just a bicarb channel, no atp

38
Q

What are intercalated cells and principal cells sensitive to?

A

Vasopressin, ADH, water

39
Q

Vasopressin works on specific receptors in the late DCT/collecting tubule such as,

A

VP2.

VP1 is located in the periphery blood vessels

40
Q

Describe the process of Vasopressin in the kidneys

A

Vasopressin (AVP) > binds to VP2 > increase cAMP > activates Protein kinase A > phosphorylate AQP2 (aquaporins) lumen side; AQP3/4 interstitial side > moves to cell walls > water influx

41
Q

What disease cancels the protein kinase A in the late DCT/CT?

A

Diabetes Insipidus

42
Q

T/F:
We always have ADH floating around to control UOP.

A

True

43
Q

Problem with secretion of ADH or response of the kidney to ADH is called?

A

DI

44
Q

If it’s a problem at the kidney to release ADH is called?

A

Nephrogenic DI

(ex. Lithium induced)

45
Q

If it’s a problem with the release of ADH, this is called?

A

Central DI

46
Q

The DCT can also be known as?

A

the diluting segment

47
Q

What effects does alcohol have on the renal system?

A

Less ADH released from the brain; impairs the kidneys response to ADH

48
Q

Risks for head injury?

A

Hypothalamus Central DI

49
Q

ADH can be controlled by…

A

(Primary) Osmolarity, BP, blood volume

50
Q

What are osmoreceptors for?

A

In charge of balancing the osmolarity of the blood via vasopressin/ADH

51
Q

What are baroreceptors for?

A

Works on the pressures in the CV system

52
Q

What is the nuclei in front of the thalamus?

A

Supraoptic neuron = in charge of 5/6 of ADH released

53
Q

What is the nuclei on the side of the 3rd ventricle?

A

Paraventricular Neuron = in charge of 1/6 of ADH released

54
Q

Where does ADH go after released from the nuclei?

A

Posterior pituitary gland and into the blood vessels

55
Q

What’s another name for the posterior lobe of the pituitary gland?

Anterior lobe?

A
  • Neurohypophysis
  • Adenohypophysis
56
Q

what would happen if…
RBC is in
Isotonic solution?
Hypotonic?
Hypertonic?

A
  • No change d/t equal balance.
  • RBC swells
  • RBC shrinks
57
Q

APs and its relation to intracellular fluid levels

A

Swelling of cells - decrease APs

Shrunken cells - increased APs

58
Q

In the descending loop of Henle, solutes are

A

highly concentrated (1200) d/t water permeability as it goes down the medulla

59
Q

In the ascending loop osmolarity

A

decreases as the dilution part of the tubule is here

60
Q

In the late DCT/CT dilution is solely based on…

A

ADH

61
Q

T/F:
Vasopressin is in control of reabsorbing water and urea as well

A

True

62
Q

Does urea have special transporters in the DCT/CT?

A

Yes, UT-A1, UT-A3

63
Q

What is the main thing that makes the interstitium highly concentrated?

A

Urea, and it allows us to hang on to water via osmosis.

64
Q

If we needed to hang onto more water what does our body use to retain more water in the CT?

A

AQPs and UTs

65
Q

What is our primary controller of plasma osmolarity?

A

ADH

66
Q

What does caffeine do to ADH?

A

Lowers ADH

67
Q

Reasons for decrease thirst

A

Low plasma osmolarity
high blood volume
htn
low ang II
gastric distention

68
Q

Reasons that increase thirst

A

high plasma osmolarity
low blood volume
low bp
high ang II
dry mouth

69
Q

causes of decrease ADH

A

low plasma osmolarity
high bp/volume

drugs:
alcohol
haldol
clonidine

70
Q

causes of increase ADH

A

high plasma osmolarity
low bp/volume
nausea/vomiting

drugs:
Morphine
nicotine

71
Q

When is the only time that our body struggles with controlling K levels?

A

Renal failure

72
Q

Physiology:
drink 1L distilled water

A

osmolarity is reduced > lowers ADH > increase UOP > urine osmolarity decrease

after all the 1L fluid is excreted > urine osmolarity increases

73
Q

Normal urine osmolarity

A

600 mOsm

AP Kidneys 2024 (9 decks)

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