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Physiology 2 > Renal concentrating mechanisms and urine formation - Quiz 3 > Flashcards

Renal concentrating mechanisms and urine formation - Quiz 3 Flashcards

1
Q

Where is renin synthesized?

A

Juxtaglomerular apparatus

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2
Q

What are the 4 components of the juxtaglomerular apparatus?

A
  1. modified smooth musc cells in the afferent arteriole
  2. Modified smooth muscle cells in the efferent arteriole
  3. Extraglomerular mesangial cells
  4. macula densa cells in the distal tubule
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3
Q

Most potent vasoconstrictor known

A

Angiotensin II

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4
Q

What are the actions of Angiotensin II?

A
  1. Profound vasoconstriction –> increased BP
  2. Increased aldosterone synthesis and release
  3. Increased ADH (vasopressin) release
  4. Increased thirst
  5. Feedback inhibition of renin release
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5
Q

How does angiotensin II work on the afferent and efferent arterioles?

How does this affect GFR?

A

Ag2 constricts the afferent and efferent arterioles

Ag2 also releases prostaglandins that maintain GFR inspire of the arteriolar constriction (autoregulation)

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6
Q

Where does aldosterone work?

A

distal tubule and collecting ducts

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7
Q

What does aldosterone do?

A

causes K secretion and also H in exchange for Na

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8
Q

What is the net effect of aldosterone?

A

gets rid of K and H

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9
Q

What is aldosterone and where is is made?

A

Steroid hormone

synthesized in zona glomerulosa of the adrenal cortex

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10
Q

3 factors that stimulate aldosterone release and synthesis

A
  1. Increased K in the ECF
  2. Ag2
  3. Decreased Na levels
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11
Q

What is Conn’s syndrome?

A

An aldosterone secreting tumor that causes:

  1. HTN
  2. HyperNa
  3. HypoK
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12
Q

What is the physiologic process of Conn’s syndrome?

A

The increased Na load eventually exceeds the distal tubule and collecting duct ability to reabsorb the Na But in its effort to pump all the Na back into the interstitial, it kicks all the K into the urine, causing hypoK.

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13
Q

What is the result of hypokalemia?

A

hyper polarization of nerve in muscle cells (will probably be manifested in the heart)

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14
Q

4 renal concentrating and diluting mechanisms

A
  1. ADH (vasopressin)
  2. ANP (atrial natriuretic peptide)
  3. Countercurrent multiplier
  4. Urea
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15
Q

Why is the ability to concentrate or dilute urine important?

A

In order for cells to fx, they must be bathed in ECF with a fairly stable concentration of electrolytes and solutes

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16
Q

What is the maximal urine concentration a human kidney can produce?

A

1200-1400 mOsm/L

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17
Q

a normal 70 kg human must excrete _____ mOsm of solute each day and therefore must excrete _____L/day
(if the concentrating ability is assumed to be 1200 mOsm/L)

A

600 mOsm

0.5 L/day

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18
Q

Where is ADH synthesized?

A

in the hypothalamus

FYI: it is an octapeptide

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19
Q

Where is ADH stored and released?

A

posterior pituitary

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20
Q

How does ADH play a major role in conserving water?

A

by concentrating the urine

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21
Q

What factors stimulate ADH release?

A
  1. Osmoreceptors in the hypothalamus (increased osmolality stimulates ADH release)
  2. Mechanoreceptors in the atria and aorta (decreased volume stimulates ADH release)
  3. AG2
  4. Fright
  5. Nausea
  6. Pain
  7. Anesthesia
  8. Nicotine
  9. Morphine
  10. Hypoxia
22
Q

What inhibits ADH release?

A

ETOH
Clonidine
Haldol

23
Q

Will anesthesia cause increased or decreased UOP? Why?

A

Decreased.

Anesthesia stimulates ADH release, therefore the body conserves water and doesn’t let the kidneys excrete as much.

24
Q

How will the following affect ADH release?

  1. Plasma osmolarity
  2. Blood volume
  3. BP
A

Plasma osmolarity

  • increased –> increased ADH
  • decreased –> decreased ADH

Blood volume and BP

  • increased –> decreased AHD
  • decreased –> increased ADH
25
Q

How does ADH work?

A

It increases the permeability of the collecting system to water.
It also increases urea permeability in the medullary collecting ducts

26
Q

What must be present for ADH to work?

A

Hypertonic interstitium

a driving force to move water out of the tubules into the interstitium

27
Q

Key features of the countercurrent multiplier

A
  1. U-smaped loop of Henle - allows flow in opposite directions
  2. differences in permeability of certain nephron segments which flow in opposite directions
  3. Energy from ATP in NaK pumps
28
Q

3 important anatomical aspects that enable the countercurrent multiplier system

A
  1. Juxtamedullary nephrons with long loops of Henle and vasa recta reaching into the medulla
  2. Arrangement of the Juxtamedullary nephrons and collecting ducts - critical for countercurrent mechanism
  3. The hyper-osmotic gradient in the renal medulla interstitium which is creased by the anatomical relationships of the components
29
Q

How does the countercurrent multiplier work?

A
  1. Active Na and Cl transport out of the TAL –> increased osmolarity of the interstitial space
  2. Fluid entering the descending limb is iso-osmotic but is reabsorbed from the descending limb –> tubular fluid is more concentrated
  3. Fluid delivered to the TAL has a high concentration of NaCl, and the solute is pumped into the interstitium –> increased interstitial osmolality
30
Q

What is the osmolarity the interstitial fluid around the loop and vasa recta? (hypo, hyper, or iso?)

A

Hyperosmolar

31
Q

What is the osmolarity of the tubular fluid if ADH is present?
If ADH is nor present?

A

ADH present - tubular fluid is more concentrated

ADH absent - tubular fluid stays dilute

32
Q

How does ADH cause urine to be concentrated?

A

ADH makes collecting duct more permeable to water –> tubular fluid equilibrates with the hyperosmolar interstitum –> concentrated urine

33
Q

The TAL is located in the outer medulla. Where is the osmotic gradient at its maximum? Why?

A

Inner medulla

Urea

34
Q

What is urea?

A

byproduct of amino acid metabolism; 2 ammonia molecules stuck together

35
Q

How much urea is made daily, and where is it made?

A

25-30 g/day

in the liver

36
Q

In liver failure what causes encephalopathy and coma?

A

increased ammonia levels

37
Q

Is the concentration of urea in the medullary interstitium high or low?

A

high

38
Q

What role does the high concentration of urea in the medullary interstitium play?

A

generates a hypertonic interstitium

39
Q

Which limb of the loop of henle is permeable to urea?

A

Thin ascending limb

40
Q

Is the TAL permeable to urea?

A

No. It is not permeable to water or urea.

41
Q

When is the inner medulla permeable to urea? How does this affect urea?

A

in the presence of ADH

urea diffuses into the interstitium and becomes trapped there

42
Q

Urea contributes _____% of the osmolarity of the renal medulla gradient during max urine concentration.

A

40%

43
Q

Urea passively diffuses from the medullar collecting duct during water deficits when ADH is present. Where does the reabsorbed urea go?

A

It is recirculated from the medulla interstitium into the loop of Henle and retired to tubular fluid.

44
Q

2 fx’s of the vasa recta

A
  1. remove reabsorbed fluid froth interstitium

2. minimizes solute uptake from the medulla

45
Q

How does the vasa recta maintain medullary hypertonicity?

A

by minimizing solute uptake from the medulla

46
Q

What aspects of the medullary blood flow contribute to solute concentration?

A
  1. low medullary blood flow

2. U-shaped Vasa recta

47
Q

How does low medullary blood flow contribute to solute concentration?

A

sluggish flow minimizes solute loss

48
Q

How does the U-shaped vasa recta contribute to solute concentration?

A
  1. acts as a countercurrent exchange to minimize solute wash out
  2. little net dilution of interstitium by U-shaped vessels
49
Q

In the descending VR, what happens to fluid?

A

fluid leaves because of the rapid flow; more fluid leaves than solute enters

50
Q

in the ascending VR, what happens to fluid?

A

decreased hydrostatic pressure and increasing osmolality of blood –> fluid reabsorption into vessels (opposite of descending VR)

51
Q

Over all is more fluid lost or reabsorbed in the VR?

A

more fluid is reabsorbed

52
Q

How much can ADH increase the osmolality of the interstitium?

A

from 400-1200 mOsm

Physiology 2 (8 decks)

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