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AP EXAM 5 > LECTURE 33 11/30/22 (LECTURE 18 SLIDES: RENAL PHYSIOLOGY CONT.) > Flashcards

LECTURE 33 11/30/22 (LECTURE 18 SLIDES: RENAL PHYSIOLOGY CONT.) Flashcards

1
Q

Term that describe massive reabsorption of water and substance dissolved in water using both transcellular and paracellular pathways.

A

Bulk Flow (8:32)

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2
Q

What is the formula for the quantity of glucose filtered?

How much glucose is filtered from 10dL of filtrate with the concentration of glucose at 100 mg/dL?

A

Quantity of Glucose Filtered = Volume of fluid filtered (dL) * Concentration of glucose (mg/dL).

1000 mg of glucose filtered
(10 dL * 100 mg/dL = 1000 mg)

(15:02)

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3
Q

At what plasma glucose will there be glucose excretion in the urine?

A

> 200 mg/dL , threshold of kidneys.
(18:55)

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4
Q

What is the transport maximum for glucose?

A

375 mg/min. All reabsorption transporters are saturated.

Any further increase in plasma glucose past this point will result in a 1:1 correlation of excreted glucose.

(19:37)

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5
Q

Why is there no paracellular reabsorption of glucose?

A

Glucose is too big, will not fit.

(21:54)

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6
Q

Gliflozins are SGLT2 inhibitors, what does this do to transport maximum and threshold?

What happens to the glucose and Na+ after using a SGLT2 inhibitor?

A

The SGLT2 inhibitor will lower transport maximum and lower threshold level.

More Na+ and glucose will be left in the tubule which will result in water movement into the tubule. Natriuretic effect (getting rid of Na+ and H20). Lowers blood pressure.

(25:00)

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7
Q

Term that describes getting rid of both sodium and water.

A

Natriuretic Effect.

(25:00)

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8
Q

Describe the process of how bicarb is reabsorbed into our body through the proximal convoluted tubule?

Pharm Recall

A
  1. NHE starts the cycle in the PCT cell. Na+ reabsorption for a H+ secretion to the renal tubule.
  2. The H+ in the lumen/urine will bind to HCO3- and form H2CO3 (carbonic acid)
  3. On the luminal surface there is an enzyme called carbonic anhydrase (CA) which will facilitate the dissociation of H2CO3 to H2O and CO2
  4. CO2 is a gas and will freely diffuse into the cell.
  5. Once inside the cell, there is H2O. The CA works in both directions and convert H2O and CO2 to carbonic acid.
  6. Carbonic acid can exist in an equilibrium as H+ and HCO3-
  7. HCO3- can now be reabsorbed into blood, maintaining bicarb buffering system. (34:00)
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9
Q

What drug will indirectly reduce the cycling of NHE?

A

Acetazolamide (25:48)

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10
Q

What is the issue with using SGLT2 inhibitors and preventing glucose reabsorption?

A

More glucose being excreted into the kidney can increase UTI risk. (27:30)

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11
Q

How is GFR affected with a SGLT2 inhibitor?

A

More Na+ will be sensed by the Macula Densa. Which will lead to a reduction in ANG II, which will relax the efferent arteriole to decrease GFR. (28:00)

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12
Q

Where is new bicarb produced?

How is it produced and what byproducts are produced?

A

New bicarb is produced in the proximal tubular cells.

Glutamine is the precursor that will produce 2 HCO3- and 2 NH4+ as a byproduct that will go into the urine.

(30:30)

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13
Q

What acts as a buffer in the urinary system?

A

NH4+ and Phosphates

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14
Q

What does an anhydrase enzyme do?

A

Pulling the H2O out of a substance. (33:32)

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15
Q

What are two major functions of the NHE?

What governs the rate of the NHE?

A
  1. Secretion of H+
  2. Reabsorption of HCO3-

The Na+/K+ pump on the interstitial side that creates the concentration gradient for Na+.

(35:00)

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16
Q

How does NaHPO4- act as a urinary buffer?

Where does the phosphate come from?

A

The negative charge of the compound will attract H+ ions.

The phosphate comes off from bone during calcium release. Phosphate is freely filtered and stays in the tubule and as a buffering agent in the urinary system to increase pH.

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17
Q

What receptor does ANG II bind to on the proximal tubules?

What will result from ANG II binding to this receptor in the proximal tubules?

A

AT1 receptors.

The binding to ANG II to AT1 receptors will in:
1. Increasing the rate of the Na+/K+ pump which will increase the rate of the NHE. This will result in more H+ secretion.
2. There will also be an increase in Na+ cell wall permeability to increase Na+ reabsorption.
3. Increase sodium reabsorption will increase water reabsorption. Which will increase blood volume.

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18
Q

What will trigger ANG II release?

What is the rate limiting step in the formation of ANG II?

A

The Macula Densa will sense either a drop in GFR or drop in Na+. The granular cells will release renin which will lead to the formation of ANG II.

Renin is the rate limiting step to ANG II formation.

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19
Q

What will result from blocking AT1 receptors?

A

Reduction in the Secretion of H+
Reduction of Na+ Reabsorption
Decrease water reabsorption
Decrease BP.

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20
Q

What is the pathway to forming ANG II?

A

Angiotensinogen is produced by the liver.
Angiotensinogen is converted to Angiotensin I in the presence of Renin.
Angiotensin I is then converted to Angiotensin II via Angiotensin Converting Enzyme (ACE).

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21
Q

What can ANG II do?

A

ANG II regulate SVR or smooth muscle contractions in the systemic circulation.

ANG II is involved increasing fluid and electrolyte reabsorption.

ANG II can regulate as a growth factor/ growth of new blood vessels. (ie: heart remodeling after an MI)

(Select all that apply) (46:00)

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22
Q

What substance can only pass through the proximal tubule via paracellular route?

What substance can only pass through the proximal tubule via transcellular route?

what substance can pass through the proximal tubule via both paracellular and transcellular route?

A

Paracellular Route Only: Cl- ?

Transcellular Route Only: Glucose, Amino Acids

Both Routes: H2O, Ca2+, Na+

Needs clarification

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23
Q

How does Ca2+ enter the transcellular membrane from the lumen in the proximal tubule?

How does Ca2+ efflux the cell into the interstitium in the PCT?

A

Ca2+ channel.

Calcium will be transported out of the cell via PMCA (Plasma Membrane Calcium ATP-ase)/ Ca+ ATPase Pump and the NCX (Na+ Ca2+ Exchanger).

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24
Q

Calcium reabsorption is ___________ dependent.

What happens when this hormone is increased?

A

PTH

PTH is increased due to hypocalcemia, which will cause increase diet/renal Ca2+ reabsorption and increase Ca2+ release from bones in order to increase Ca2+ blood serum. (50:00)

**PTH does not affect the proximal tubule as much, it is more involved in the later parts of the tubular system. Nevertheless, there is a lot of Ca2+ reabsorbed at the proximal tubule. Just know that calcium management is regulated by PTH.

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25
Q

What percentage of water is left to be reabsorbed after the thin descending limb of the LOH.

A

approximately 13-15% of water left to be reabsorbed after the thin descending limb of the LOH.

-2/3 (65-67%) of water reabsorption happens at the proximal tubule.
-20% of water reabsorption happens at the descending LOH.

26
Q

What is the thin descending limb of the LOH impermeable to?

A

Ions

descending limb of the LOH is very permeable to water.

27
Q

What is the trend of the interstitial concentration going down the descending limb of the LOH? How does this affect water reabsorption?

A

Concentration gradient of the interstitium will increase as you go down the LOH, this will cause water to be reabsorbed from the nephron. (55:00)

28
Q

What is the osmolarity of the upper cortical interstitium?

A

300 mOsm, this will be similar to the osmolarity of blood.

29
Q

Why does the osmolarity in the proximal tubule remain consistently at 300 mOsm.

A

Solutes and water are reabsorbed at a proportional rate in the proximal tubule. (57:00)

30
Q

What two places will contribute to the high interstitium concentration in the LOH?

A
  1. Reabsorption of electrolytes in the thick ascending limb of the LOH
  2. Reabsorption of electrolytes and urea in the collecting duct.

(60:00)

31
Q

What happens if the rate of fluid moving through the LOH is too fast?

If there is reasonable flow rate what is the relationship between the concentration of the tubular fluid and concentration of the interstitium?

A

The rush of H2O leaving the nephron will destroy the concentration gradient of the interstitium resulting in less water being reabsorbed. (60:40)

If there is reasonable flow rate in the tubular system, it’s osmolarity should match the osmolarity of the interstitium as the tubular fluid travels down the LOH. (79:58)

32
Q

What is the limit of the renal interstitium concentration?

A

1200 mOsm (62:00)

This is the reason why you can’t drink ocean/sea water because the ocean water has a higher salt content than the ability of our kidneys to selectively hang on to water. The osmolarity of ocean/sea water is much greater than 1200 mOsm.

33
Q

What is the osmolarity of the tubular fluid at the end of the thick ascending limb of the LOH?

Why is it that number?

A

100 mOsm

The drop in osmolarity is due to reabsorption of electrolytes (NaCl) in the thick ascending part of the LOH.

34
Q

Where in the LOH will there be passive permeability to sodium and chloride?

Where in the LOH will there be active transporters of sodium and chloride?

A

Thin ascending limb of the LOH (passive transport)

Thick ascending limb of the LOH (active transport)

(81:20)

35
Q

What transporter is used on the apical side of the thick ascending limb of the LOH?

A

Na+/K+/2Cl- transporter. (NKCC2 Transporter)

NHE transporter (sodium proton exchanger)

36
Q

How are Na+, Cl-, and K+ transported into the renal interstitium from the tubular cell of thick ascending limb of the LOH?

A

Na+ will be transported into the renal interstitium via Na+/K+ ATPase

Chloride and Potassium will leave the tubular cell passively into the renal interstitium.

37
Q

What makes K+ unique in the thick ascending limb of the LOH?

What ions does K+ in the tubular fluid help reabsorb?

A

When K+ makes its way into the tubular cell of the thick ascending limb of the LOH. Some of the K+ can leave passively into the renal interstitium and some of the K+ can leak back into the tubular fluid.

The migration of K+ into the tubular fluid will cause the tubular lumen to have a positive electrical charge of +8mv. This positive charge will drive paracellular reabsorption of Mg2+ and Ca2+ from the thick ascending limb of the LOH.

38
Q

What diuretics will target the NKCC2 transporter in the thick ascending LOH?

A

Loop Diuretics:
Furosemide (Lasix)
Bumetanide (Bumex)
Ethacrynic Acid

(84:00)

39
Q

What happens to the concentration of the renal interstitium if a loop diuretic is used?

What will this ultimately result?

A

Renal interstitium concentration will decrease because less ions are being reabsorbed due to inhibition of the NKCC2.

If we decrease the concentration of the renal interstitium (renal interstitium “washout”), there is a reduction in water reabsorption. This will result in the body to concentrate urine and lead to massive loss of water to the renal tubules and excretion. (85:00)

40
Q

Which part of the nephron is known as the diluting segment?

A

Distal Convoluted Tubule.

It is called that because there is reabsorption of NaCl, but very little reabsorption of water. This leaves the tubule with an osmolarity of 100 mOsm. (88:00)

41
Q

What transporters at the distal convoluted tubule is responsible for Na+ reabsorption?

What drug will target this transporter?

What will be the result of this drug?

A

Na+/Cl- symporter

Thiazide diuretics

Increase urinary output due to more NaCl in the tubular fluid.

42
Q

PTH has a large effect on which part of the nephron?

What does PTH do in this part of the nephron?

A

Distal convoluted tubule

PTH will stimulate activation of Ca2+ channels on the luminal side of the nephron to facilitate Ca2+ reabsorption.

(89:00)

43
Q

How does Ca2+ efflux the cell into the interstitium in the distal convoluted tubule?

A

NCX

44
Q

What will happen to the NCX in the DCT if a thiazide diuretic is used?

A

Increase the cycling rate of the NCX.

By blocking the reabsorption of Na+ there will be a decrease in intracellular [Na+] that will increase the electrochemical gradient for Na+ which will speed up the NCX pump. Resulting in an increase in Ca2+ reabsorption. (91:30)

45
Q

What are the two types of cells in the late distal tubule and the collecting ducts?

What does each cell do?

A

Principal Cells and Intercalated Cells

Principal cells are used to control blood potassium levels.

Intercalated cells are set up to deal with acid/base issues.

46
Q

What hormone can affect water reabsorption that is independent of salt reabsorption. This hormone can affect both principal and intercalated cells in the nephron.

A

ADH (Vasopressin)

47
Q

How does principal cells control blood K+ level?

What hormone will regulate this process?

A

Na+/K+ ATPase pump will transfer 2 K+ into the tubular cell in exchange for 3 Na+ out to the interstitium. K+ will passively move through K+ channels into the tubular fluid to be excreted.

Aldosterone (steroid hormone, water soluble and can hang out inside the tubular cell)

48
Q

When aldosterone receptors are activated what 2 things does it do?

What will this lead to?

A
  1. Increase the amount of K+ channels placed on the tubular side of the nephron. Need to clarify
  2. Increase the rate of the cycling of the sodium potassium pump.

The end result will be more potassium being lost in the urine and more sodium reabsorption from the urine. (96:00)

49
Q

What drugs will act as aldosterone antagonist?

What drugs will block the ENaC (Epithelia Sodium Channel)?

A

Spironolactone and Eplerenone

Amiloride and Triamterene

50
Q

What drugs will be considered as potassium sparing diuretics?

A

Spironolactone
Eplerenone
Amiloride
Triamterene

51
Q

What is ratio of sodium reabsorption to potassium secretion in the principal cells of the distal tubule?

How will diuretics used upstream of the principle cell affect Na+ in tubular fluid?

A

For every 3 sodium that is reabsorbed, 2 potassium will be excreted.

Using diuretics upstream from the principal cells will result in more Na+ in the tubular fluid, this will result in more reabsorption of Na+ ions and more secretion of K+ ions from the principal cells.

(101:00)

52
Q

If you have a ridiculous amount of cortisol in your body, you may have problems with your blood pressure and keep a normal amount of potassium in the body. Why?

A

Structurally, cortisol looks a lot like aldosterone and will act like the compound if there is a high enough concentration of it in the body.

(102:00)

53
Q

What enzyme is located in the principal cell acts as a defense mechanism against cortisol?

How does this enzyme work?

What compound can inhibit this enzyme?

A

11β-HSD Type II or
11 β -hydroxysteroid dehydrogenase type 2.

This enzyme will take water out of cortisol and decrease the likelihood that it will interact with aldosterone receptors in principal cells. This enzyme can be overwhelmed if there is a massive amount of cortisol.

Licorice can inhibit 11β-HSD Type II

(104:00)

54
Q

What is another term for an aldosterone receptor?

A

Mineralocorticoid Receptor

55
Q

Where is the source of aldosterone?

A

Renal Cortex, specifically the outer portion of the cortex called the zona glomerulosa

56
Q

Which one is aldosterone?

A
57
Q

Which one is cortisol?

A
58
Q

What will trigger aldosterone release from the adrenal glands (2 ways).

A
  1. Increase in circulating blood potassium concentration
  2. ANG II binding to AT1 receptor on the adrenal cortex.
59
Q

What will dictate how much water will be reabsorbed in the collecting ducts?

A

Water reabsorption in the collecting ducts will be dictated by how much AQP-2 channels are available through vasopressin.

60
Q

How will ADH (vasopressin) be released from the brain?

What will control the release of ADH?

A

Increase in blood osmolarity or decrease in MAP

Osmoreceptors in the hypothalamus

61
Q

If an osmoreceptor is placed in an isotonic solution (300 mOsm/L), what is the net movement of water?

If an osmoreceptor is placed in a hypotonic solution (200 mOsm/L), what is the net movement of water? ADH response?

If an osmoreceptor is placed in a hypertonic solution (360 mOsm/L), what is the net movement of water? ADH response?

A

Isotonic = no net movement of water

Hypotonic = net movement of water into the cell (cell swells). Decrease amount of ADH release to reduce water reabsorption and allow water to leave the cell.

Hypertonic = net movement of water out of the cell (cell shrinks). Increase amount of ADH to retain water.
(118:00)

AP EXAM 5 (6 decks)

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