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Advanced A&P I > Final Exam - Renal 3 > Flashcards

Final Exam - Renal 3 Flashcards

1
Q

Describe angtiotensin II effects on the proximal tubule?

A

Binds to AT II receptors causing:
1. Increase in activity of Na/K ATPase, decreasing [Na+] inside the cell
2. This drives the increase in the NHE transporter, because now Na+ has a greater gradient to enter the cell
3. Increases activity of Na+/HCO3 co-transporter, driven by [HCO3-] intracellularly

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2
Q

Why is paracellular reabsorption prominent in the PCT?
What compound travels by this route and how?

A

The tight junctions are fairly wide, allowing easy passage of solutes.
Cl- is reabsorped this way and follows the positve charge of the Na+ ions that are being reabsopred transcellularly.

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3
Q

What is bulk flow?

A

They movement of filtrate into the paratubular capillaries set up the capillary starling forces

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4
Q

What drives the movement of water into the PT capillaries?

A

The highly concentrated renal interstitum drives osmosis of water. The primary solute responsible for the renal interstitum osmolarity is urea.

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5
Q

Describe the structure of the luminal tubular cells and its importance?

A

Contains a brush border, long extensions that increase the surface area of the cells 20x allowing placement of the many transporters.

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6
Q

What is the PCT cell membrane potential? What does this drive?
What is the PCT lumen membrane potential? What causes it?

A

-70mV, promotes Na+ reabsorption
-3mV, caused by dissolved solutes (Na+, K+, primarily Cl-)

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7
Q

Describe Na+ and Cl- concentration as they move through the PCT?

A

Na+ concentrations stay the same throughout the tubule because it’s reabsorption follows water reabsoprtion.
Cl- ion reabsorption is delayed, causing its concentration to increase along the tubule until enough Na+ ions have been reabsorped then Cl- follows it.

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8
Q

How much protein is filtered each day in a healthy patient?
How much is reabsorped? How is it reabsorped?

A

1.8g filtered (mostly peptides, few albumin)
1.7g reabsorped
Reabsoped by tubular cells only in the PCT via endocytosis(pinocytosis) where the proteins are broken down to amino acids to be recycled (this process cannot be sped up)

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9
Q

What is the primary way Na+ is reabsorped in the PCT?

A

The NHE

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10
Q

Explain acid-base balance in the PCT?

A

The NHE secretes a H+ into the tubule lumen with each cycle. This H+ can bond with HCO3- to create carbonic acid. Carbonic acid dissociates into CO2 + H2O, both of which freely cross the tuble cell membrane. Once inside the cell, CO2 and H20 combine again forming carbonic acid, which dissociates into HCO3- and H20. HCO3- can then be reabsorped and H+ secreted again via the NHE.

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11
Q

Describe the role of carbonic anhydrase?

A

Found intracellularly and on the luminal wall. Speeds up the conversion of carbonic acid. Can either break down carbonic anhydrase into CO2 and H2O or create carbonic anhydrase from CO2 and H2O. The direction is driven by the reactants available (HCO3- and H+, or CO2 and H2O)

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12
Q

What are the effects of carbonic anhydrase inhibition?

A

Decreases the speed of the NHE, reducing H+ in the tubule, preventing HCO3- reabsorption, causing HCO3- loss in the urine leading to acidosis. Also, prevents Na+ reabsorption, causing decreased H2O reabsorption leading to diuresis and decreased BP.

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13
Q

Where does glutamine come from?
What is it’s role in the PCT?

A

Produced by the liver; patient’s in liver failure have difficulty with acid base balance.
Broken down into 2 HCO3- and 2 NH4+ in the tubular cells.

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14
Q

What is ammonium’s role in the tubules?

A

NH4+ is a urinary buffer because H+ can bind to NH3 (ammonia) and be excreted as NH4+

We don’t want protons being excreted unbound because it would be very damaging to the tubules and urinary tract

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15
Q

What role does phosphate play in the PCT?

A

Uriniary buffer, combines wih H+ in the tubule and then excreted.

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16
Q

How is calcium reabsorped in the PCT?

A
  1. Via paracellular route by following water
  2. From lumen via transcellular route by Ca++ channels, To renal interstitum via Ca++ ATPase and NCX.
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17
Q

What can reduce calcium reabsorped?

A

Calcium can be more protein bound if blood pH is more basic, preventing it from being reabsorption.

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18
Q

How are serum calcium levels managed?

A

The parathyroid gland releases PTH when calcium is low. PTH causes: 1) increased Vitamin D activation, increasing intestinal Ca reabsorption. 2) Increased renal calcium reabsorption 3) Increased Ca release from bones

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19
Q

How does PTH cause Ca release from the bones?
How is this related to osteoporosis?

A

Increases osteoclast activity, which breaks down bones (Ca + PO4).
Decreases activity of osteoblasts which build bones from Ca and PO4

In osteoporosis there is chronically low Ca levels. So PTH is very active inhibiting bone building and promote bone break down. This causes the bones to become porous overtime.

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20
Q

How are organic cations secreted by the PCT?

A

Leave the PT capillaries and are in the renal interstitum. The cation enters the cell via specialized transporter and moves into the lumen via cation proton antiporter

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21
Q

How are organic anions secreted by the PCT?

A

Alpha-ketoglutarate (aKG) is uptaken into tuble cells with 3 Na+ creating a high concentration of aKG inside the cell. A different transporter can exchange aKG for the organic anion bringing it into the cell. Once in the cell, it its moved into the lumen by an anion transporter.

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22
Q

What are some endogenous organic cations?

A
  • ACh
  • Creatinine
  • Dopamine
  • Epinephrine
  • Histamine
  • Serotonin
  • Norepinephrine
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23
Q

What are some exogenous organic cations?

A
  • Atropine
  • Isoproternol
  • Morphine
  • Procaine
  • Quinine
  • TEA
24
Q

What are some endogenous organic anions?

A
  • Bile salts
  • Hippurates
  • Oxalate
  • Prostaglandins
  • Urate
25
Q

What are some exogenous organic anions?

A
  • Furosemide
  • Penicillin
  • Salicylates
26
Q

Why was penicillin given with hippurates?

A

Penicillin is heavily secreted in the kidneys. Hippurates use the same secretion transporter as penicillin. Giving enough hippurate would competitively inhibit the transporter allowing PCN levels to remain at a higher level in the body.

27
Q

What occurs in the descending limb of the loop of Henle?

A

Water reabsorption occurs because the filtrate is descending into medulla where the renal interstitum has a increasingly high osmolarity.

28
Q

What occurs in the thin ascending limb of the loop of henle?

A

Impermeable to water
Na+/Cl- ATP transporters here are reabsopring Na+ and Cl- from the filtrate

29
Q

Describe cation reabsorption in the thick ascending loop of henle?

A

Still impermeable to water.
Cations can be reabsorped via paracellular routes. Ca++ and Mg++ reabsorption is driven by K+ leaking from tubular cells that create a tubule membrane potential of +8mV.

30
Q

What transporters are present at the apical side of the thick ascending loop of henle?
Why are these important?

A

NHE
NKCC2
Responsible for generating the highly concentrated renal interstitum.

31
Q

Why is furosemide the most powerful diuretic?

A

Furosemide inhibits the NKCC2
This decreases the concentration of the renal interstitum, causing decreased water reabsorption, increasing diuresis.

32
Q

What is the most concentrated the renal interstitum can be?
What compouds make up the osmolarity?

A

1200 mOsm
Dissolved ions and urea

33
Q

What would it mean if the urine concentration was 1200 mOsm?

A

It would mean that the body is trying to conserve water by removing as much water as possible from the urine.

34
Q

What drives urine osmolarity?

A

The concentration of the renal interstitum.
The urine concentration will match the renal interstitum concentration because water will be reabsorbed via osmosis until interstitum and lumen to have the same concentration.

35
Q

How does PTH increase Ca reabsorption in the kidney?

A

PTH increases the number of Ca channels in the lumen of the distal tubule.

36
Q

What transporter is at the distal tubule?
What drugs inhibit it?

A

Na/Cl transporter
Thiazides

37
Q

What cells are sensitive to aldoseterone and ADH in the distal tubule?

A

Principal cells: Aldosterone and ADH
Intercalated cells: ADH

38
Q

What effects does aldosterone have at the principal cells?

A

Aldosterone can enter the cell can bind to the ALDO receptor intracellularly bc aldosterone is a cholesterol derivative.
Binding causes increase in the Na+/K+ pump, lowering the intracellular Na+ which increases the activity of Na+ channels. This increases Na+ reabsoprtion which increases H2O reabsporption. This also results in increased K+ secretion.

39
Q

How much of the filtered water is reabsorped in the think descending loop of henle?
How much of the total water has been reaborped by this point?

A

20%
85% (65% filtered in the PCT)

40
Q

How much of the filtered ions are reabsorped in the thick ascending loopd of henle?

A

25%

41
Q

Where is the last place in the nephron that solutes and water can be reabsorped?

A

The collecting duct via principal and intercalated cells

42
Q

What two areas of the nephron have the highest metabolic rate?

A

The PCT and the thick ascending limb of the loop of henle
Lots of reabsorption occuring via transporters here (requires energy)

43
Q

How is calcium primarily transported from distal tuble cells to the interstitum?
What drives this pump?

A
  • NCX
  • The Na+/K+ ATPase pump
44
Q

Describe how a thiazide diuretic can increase calcium reabsorption?
When would this be useful?

A

Thiazides inhibit the Na+/Cl- pump in the DCT
This reduces Na+ entry into the cell, and reduces the activity of the Na+/K+ ATPase, causing a increased driving force for Na+ entry from the interstitum
This increases Na+ entry via NCX which in turn increases calcium reabsorption

Useful in osteoporosis and preventing kidney stones (reduces calcium build up in the urine)

45
Q

What class of drug is aldosterone?

A

Mineralcorticoid

46
Q

What are the effects of aldosterone on Na+ and K+ channels at the apical wall of principal cells?

A
  • Increases the number of ENaC channels
  • Increases number of K+ channels by increasing their placement on the wall by ROMK and by opening BK channels (Big Potassium) which are normally closed.
47
Q

What drugs inhibit ENac channels?
What are it’s effects?

A
  • Amiloride and triamterene
  • Decreased Na+ entry via ENaC which also results in decreased secretion of K+
48
Q

What drug is an aldosterone antagonist?
What are it’s effects?

A
  • Spirinolactone
  • Blocks the effects of aldosterone which decreases the Na+/K+ ATPase, and decreases Na+ reabsorption and K+ secretion (potassium sparing)
49
Q

Describe the process of how upstream diuretics cause potassium wasting?

A

Upstream diuretics block the reabsorption of Na+ and or Cl-. This causes there to be an increased amount of Na+ that arrives at the collecting tubule principal cells. The increased concentration of Na+ increases the rate of it’s reabsorption via ENaC channels. Because the Na+/K+ ATPase is responsible for moving Na+ from the prinicipal cells to the interstitum, it’s increased cycling increases the entry of K+ and its secretion into the tubule.

50
Q

What is 1?
What is produced here?

A
  • Zona glomerulosa of adrenal gland
  • Aldosterone
51
Q

What is 2 and 3?
What is produced here?

A
  1. Zona fasciculata of adrenal gland
  2. Zona reticularis of adrenal gland
    Cortisol and androgens
52
Q

What class is cortisol in?
Why is it called this?

A
  • Glucocorticoid
  • Helps maintain glucose levels
53
Q

What is 4?
What is produced here?
How much?

A
  • Medulla
  • Epinephrine and Norepinephrine
  • 4:1; Epi:Norepi
54
Q

What causes release of aldosterone from the zona glomerulosa?

A
  • Increased potassium levels
  • Angtiotensin II binding to AT I receptors
55
Q

What enzyme produces aldosterone in the zona glomerulosa?

A

Aldosterone synthase

56
Q

Why does taking steroids increase blood pressure?

A

Many of the steroid compounds in the body have a very similar structure. Two of these are aldosterone and cortisol. Steroids increase cortisol levels and because cortisol looks a lot like aldosterone, it can bind to the aldo receptor, causing the same effects as aldosterone (Increased Na+ and H2O reabsorption = increased BP, and increased K+ secretion)

57
Q

How do our bodies prevent cortisol form binding to aldo receptors at baseline?

A

The enyme 11\beta

Advanced A&P I (11 decks)

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