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Renal concentrating mechanisms Flashcards

1
Q

Where is the site of renin synthesis?

A

The juxtaglomerular apparatus.

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2
Q

What are the four components of the JGA?

A
  1. modified smooth muslce cells in 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

What causes angiotensiongen to be cleaved to angiotensin I?

A

Renin

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4
Q

What converts Angiotensin I to angiotensin II?

A

Angiotensin Converting Enzyme

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5
Q

What is the more potent vasoconstrictor in the body?

A

Angiotensin II

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6
Q

Where is angiotensin I converted to angiotensin II?

A

Lungs

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7
Q

What are the 5 actions of Angiotensin II?

A
  1. Vasoconstriction and increased blood pressure.
  2. Increased aldosterone synthesis and release
  3. Increased ADH
  4. Increased thirst
  5. Feedback inhibition of renin release
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8
Q

What does ACE inhibitor do?

A

Inhibits angiotensin I from converting to angiotensin II?

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9
Q

What helps maintain GFR in spite of constrictive effects of Angiotensin II?

A

Prostagladins

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10
Q

Where is aldosterone synthesized in the body?

A

Zona glomerulosa of the adrenal cortex

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11
Q

Chronic ACE inhibitors cause a patient to be refractory to what medications?

A

Epinephrine and neosynephrine and ephedrine

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12
Q

What medication would you use to ACE inhibitor caused refractory hypotension?

A

Vasopressin

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13
Q

What causes aldosterone release and synthesis?

A
  1. Increased K+ levels in the ECF
  2. Angiotensin II
  3. Decreased Na+ levels
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14
Q

Where does aldosterone act on in the nephron?

A

Distal tubule and collecting ducts

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15
Q

What is the net effect of aldosterone?

A

Get rid of K+ and H+

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16
Q

Name a steroid hormone that is synthesized in the zona glomerulosa of the adrenal cortex?

A

Aldosterone

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17
Q

Does aldosterone cause a marked reabsorption of secretion of Na+?

A

Reabsorption

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18
Q

What is exchanged for K+ and H+ by aldosterone?

A

Na+

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19
Q

Where is ADH made?

A

Hypothalamus

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20
Q

Where is ADH released from?

A

Pituitary gland

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21
Q

Atrial natriuretic peptide does what to the nephron?

A
  1. Increases GFR
  2. Decrease Na+ reabsorption
  3. Inhibits release of renin/aldosterone/ADH
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22
Q

What is Conn’s Syndrome?

A

Aldosterone secreting tumor

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23
Q

What three main things does Conn’s Syndrome cause?

A
  1. Hypertension
  2. Hypernatremia
  3. Hypokalemia
24
Q

What symptom of Conn’s Syndrome is most dangerous?

A

Hypokalemia can cause heart/muscle/nerve hyperpolarization

25
Q

What is maximum capable urine concentration?

A

1200mOsm/L

26
Q

What is the minimum daily urine output?

27
Q

Where are osmoreceptor cells located?

A

Anterior hypothalamus

28
Q

What effects does increase in extracellular fluid osmolarity have on osmoreceptor cells?

A

Causes them to shrink

29
Q

Shrinkage of osmoreceptor cells causes them to fire to the pituitary gland to do what?

A

Stimulates release of ADH

30
Q

Where does ADH work in the nephron?

A

Late distal tubules

31
Q

What stimuli cause ADH release?

A
  1. Osmoreceptor stimulation
  2. Angiotensin II
  3. Fright
  4. Nausea
  5. Pain
  6. Anesthesia
  7. Nicotine
32
Q

T/F: Alcohol inhibits ADH release?

33
Q

In the presence of dehydration, ADH is released or inhibited?

34
Q

In the presence of overhydration, ADH is released or inhibited?

35
Q

How does ADH work?

A
  1. Increases the permeability of the collecting system of water
  2. Increases urea permeability
36
Q

What three things are the basic requirements for forming a concentrated urine?

A
  1. High level of ADH
  2. High osmolarity of the renal medullary interstitial fluid
  3. Water moving by osmosis into the renal interstitium
37
Q

What is the osmolarity of the interstitial fluid in the medulla of the kidney?

A

1200-1400 mOsm/L

38
Q

What 4 major factors contribute to the buildup of solute concentration into the renal medulla?

A
  1. Active transport.
  2. Active transport
  3. Facilitated diffusion
  4. Diffusion
39
Q

What is an example of active transport?

A

Sodium ions and co-transport potassium/chloride/other ions out of the thick portion of the asecnding limb into the medullary interstitium

40
Q

What is an example of active transport?

A

Ions from the collecting ducts into the medullary interstitium

41
Q

What is an example of facilitated diffusion?

A

Urea from the inner medullary collecting ducts into the medullary interstitium

42
Q

What is an example of diffusion?

A

Small amounts of water from medullary tubules into medullary interstitium

43
Q

What is the role of urea?

A

Byproduct of amino acid metabolism consisting of 2 ammonia molecules.

44
Q

How much Urea is made per day by the liver?

A

25-30g/day

45
Q

What can high levels of ammonia cause?

A

Encephalopathy and coma

46
Q

Does the medullary interstitium have a high or low concentration of urea?

47
Q

What are the two functions of the vasa recta?

A
  1. Remove reabsorbed fluid from the interstitium.

2. Minimize solute uptake from the medulla.

48
Q

Why is vasa recta U-shaped?

A

Act as countercurrent exchangers to minimize solute washout.

49
Q

Where does RAAS system start?

A

Macula Densa

50
Q

Is urine hyper or hypo osmolar?

A

Hyper osmolar

51
Q

What is Central Diabeters insipidus?

A

An inability to produce or release ADH from the posterior pituitary

52
Q

What is treatment of central diabetes insipidus?

A

Administration of a synthetic analog of ADH (desmopressin)

53
Q

What receptor does demsopressin act on?

A

V2 receptor

54
Q

What does stimulation of the V2 Receptor cause?

A

Increase water permeability in the late distal and collecting tubules.

55
Q

What is Nephrogenic diabetes insipidus?

A

Normal or elevated levels of ADH are present, but the renal tubular segments cannot response appropriately.

Renal (5 decks)

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