Renal Part 2c Flashcards

(59 cards)

0
Q

Distal delivery is what percent of the filtered load of H2O? and NaCl?

A

10% of both H20 and NaCl

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1
Q

Distal nephron consists of what?

A

Distal convoluted tubule + collecting tubule (cortical –> papillary)

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2
Q

Distal transport of H2O is regulated by what hormone?

A
Antidiuretic hormone (ADH)
(Increase ADH --> Increase H2O reabsorption --> Decreased H20 Excretion)
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3
Q

What regulates distal nephron transport of NaCl?

A

Aldosterone

Increased Aldosterone –> Increased NaCl reabsorption –> Decreased NaCl excretion

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4
Q

In the presence of what hormone is the collecing tubule permeable to water?

A

ADH

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5
Q

A favorable osmotic gradient in collecting tubule (tubular fluid –> interstitium) promotes what?

A

Water reabsorption there by generating a small volume of concentrated (hypertonic) urine: ANTIDIURESIS

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6
Q

In the absence of ADH, the collecting tubule is permeable or impermeable to water?

A

Impermeable to water

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7
Q

What is occurring during diuresis in collecting tubule?

A

Reabsorption of some NaCl in the distal nephron continues to dilute the tubular fluid resulting in excretion of a large volume of hypotonic urine

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8
Q

Reabsorption of water by the collecting tubule system is dependent on the presence of what?

A

Water channels (aquaporins) in the luminal membrane

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9
Q

ADH stimulates insertion of pre-existing ________________ into the luminal membrane

A

AQP-2 channels (aquaporins)

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10
Q

What aquaporin channels are constitutively expressed in the basolateral membrane?

A

AQP-3 channels. AQP-2 are the channels that can be moved by action of ADH to the luminal side of the membrane

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11
Q

T or F, All nephron segments express basolateral aquaporins

A

True

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12
Q

How many isoforms of aquaporins are differentially distributed along the nephron?

A

3

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13
Q

What would explain water impermeability of the ascending limb?

A

Lack of luminal aquaporins

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14
Q

The cortical collecting tubule reabsorbs what? and secretes what?

A

Reabsorbs sodium

Secretes potassium

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15
Q

ALdosterone controls reabsorption of Na+ by: (3)

A
  1. Increased number of luminal membrane Na+ channels
  2. Increased Na+-K+-ATPase (de novo synthesis of pumps)
  3. Increased Krebs cycle enzyme synthesis (thus more ATP) –> increased ATPase activity
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16
Q

Aldosterone and cortisol have similar affinity for what receptor?

A

Mineralocorticoid receptor

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17
Q

How are higher circulating levels of cortisol prevented from affecting Na+ reabsorption?

A

By 11B hydroxysteroid dehydrogenase type 2

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18
Q

Mutations in 11B hydroxysteroid dehydrogenase type 2 can lead to what?

A

NaCl retention and hypertension

You can no longer suppress the actions of cortisol

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19
Q

What does Parathyroid Hormone stimulate in distal tubule?

A

Calcium reabsorption

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20
Q

Increased PTH –> Increased Ca2+ reabsorption in the distal tubule due to stimulation of:

A
  1. Ca2+ ATPase

2. Na-Ca2+ exchanger on the basolateral membrane

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21
Q

Step 1 of countercurrent multiplication

A
  1. Reabsorption of NaCl by the ascending limb; retention in interstitium
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22
Q

Step 2 of countercurrent multiplication

A
  1. reabsorption of NaCl by ascending limb; retention in interstitium
  2. reabsorption of H20 by the descending limb; removal by vasa recta
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23
Q

Step 3 of countercurrent multiplication

A
  1. reabsorption of NaCl by the ascending limb; retention in interstitium
  2. reabsorption of H2O by the descending limb ; removal by vasa recta
  3. isotonic fluid from proximal tubule into loop; hypertonic fluid into the ascending limb
24
T or F, Cortical/outer medullary collecting tubule reabsorbs urea
False, it cannot reabsorb urea
25
T or F, As tubular fluid flows into inner medullary collecting tubule, high urea concentration promotes passive reabsorption into interstitium
True
26
Does ADH promote permeability of inner medullary collecting tubule to urea?
Yes
27
With a decrease in ADH, do you excrete more or reabsorb more urea?
You excrete more urea. Without the permeability of the inner medullary collecting tubule, urea does not get reabsorbed and is excreted into urine. This tends to happen when you are hydrated
28
T or F, Plasma ADH levels control medullary interstitial urea but not NaCl concentrations
False, it controls both
29
Medullary blood supply essential for: (2)
1. Nutrient supply | 2. Removal of reabsorbed H20 and NaCl
30
Does the plasma flowing out of the medulla have a higher osmolality or lower osmolality than when it entered?
Higher osmolality
31
T or F, Exiting plasma flow rate will be lower than that entering the medulla (vasa recta)
False, It will be higher
32
What is the only water output that can be precisely controlled?
Urine output
33
Maximum Diuresis:
Urine volume: 20-25 L/day | Urine Osmolality: 50-75 mOsm/kg
34
Maximum ANTIDIURESIS:
Urine volume: 0.5 L/day | Urine Osmolality: 1200-1400 mOsm/kg
35
Where is ADH synthesized? | Where is it stored?
in neural cell bodies located in supraoptic and paraventricular nucleii of hypothalamus - Transported down axon, stored in nerve terminals in posterior pituitary
36
Which method of ADH secretion regulation is most sensitive?
Changes in plasma osmolarity (hypothalamic osmoreceptors) - Increases in plasma osmolarity will increase secretion of ADH so that the tubule will become more permeable and therefore reabsorb water
37
The lesser sensitive method to regulating ADH secretion is through what?
Volume receptors: Plasma volume (baroreceptors) | Changes in plasma volume will affect ADH secretion
38
T or F, Increase in osmolality = Decrease in urine volume
True
39
What are some causes of Syndrome of Inappropriate ADH secretion (SIADH)
Head trauma, encephalitis, meningitis ADH secreting tumors (lung, pancreas) Drug-induced (nicotine, morphine, chemotherapeutic agents)
40
What is the effect of Syndrome of Inappropriate ADH secretion (SIADH)?
Increase in ADH, Increase in H2O reabsorption --> Hyponatremia Decrease in serum Na --> Decrease in Plasma osm --> influx of H2O (into brain cells) --> Coma
41
What is the cause of Diabetes Insipidus (D.I.)
1. Hypothalamic (CENTRAL) D.I. --> decrease of production or release of ADH 2. Nephrogenic D.I. --> Renal unresponsiveness to ADH
42
What may cause nephrogenic D.I.?
- Mutations in the ADH receptor - Impaired synthesis/translocation of aquaporins - Drugs (lithium, tetracyclines); hypokalemia
43
What is the effect of Diabetes Insipidus
Lower ADH --> Lower H2O reabsorption --> Hypernatremia | Higer serum Na --> Higher plasma osm --> efflux of H2O (out of brain cells) --> Coma
44
What is Free Water clearance?
Represents the amount of distilled water that must be added to or removed from urine to create an isotonic fluid
45
What is the use for Free Water Clearance?
It provides a non-invasive assessment of diluting efficiency of the thick ascending limb
46
T or F, ECF volume is directly related to total body sodium (chloride)
True
47
ECF volume being directly related to total body sodium is due to what: (3)
1. H2O shifts extracellular intracellular 2. Effects on ADH secretion, thus distal nephron H2O reabsorption 3. Effects on thirst
48
How do kidneys maintain constant ECF volume?
by adjusting NaCl excretion to match NaCl intake
49
How much of filtered load of sodium is excreted?
1% or less of filtered load
50
Na excretion is primarily regulated by the action of what?
Aldosterone on the cortical collecting tubule
51
Aldosterone regulates the excretion of approximately how much percentage of the filtered load of sodium?
5%
52
Aldosterone controls reabsorption of Na+ by: (3)
1. Increased number of luminal membrane Na channels 2. Increase Na-K-ATPase 3. Increased Krebs cycle enzyme synthesis (more ATP)--> ATPase activity
53
Total body Na changes sensed as changes in?
Effective circulating volume (ECV)
54
The effective circulating volume (ECV) is monitored by what?
Baroreceptors - Cardiac atria, pulmonary vasculature - carotid sinus, aortic arch, juxtaglomerular apparatus
55
Rate limiting step in aldosterone release from adrenal cortex?
Renin (enzyme) release by kidney (Renin --> Angiotensin to Angiotensin I -> Converting enzyme from lungs converts Angiotensin I to Angiotensin II --> Angiotensin II to adrenal cortex --> Adrenal cortex releases Aldosterone to kidney)
56
Renin-angiotensin-aldosterone system can be pharmacologically controlled at several points: (4)
1. Renin inhibitors 2. ACE (angiotensin converting enzyme) inhibitors 3. Angiotensin II receptor antagonists 4. Aldosterone receptor antagonists
57
Renin is secreted by what cells?
Granular cells of the afferent arteriole
58
SUSTAINED increases in aldosterone secretion results in what?
Relatively transient Na retention - Increase in Aldosterone --> Increase ECV --> Increase blood pressure - This results in Pressure natriuresis and Pressure diuresis (Aldosterone Escape)