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I've got kidney disease > Lecture 20 > Flashcards

Lecture 20 Flashcards

1
Q

1 out of every how many people have high blood presssure?

A

5

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2
Q

Is any Na+ actively secreted?

A

no, it is reabsorbed and excreted

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3
Q

How many mmol of Na+ does the proximal tubule receive per day and how much does it reabsorb? What percentage of filtered load of Na+ is this?

A
  • receives 27,000 mmol/day

- reabsorbs 18,000 mmol/day (67%)

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4
Q

How many mmol of Na+ does the loop of Henle (total from the thin and thick ascending limb) receive per day and how much does it reabsorb? What percentage of filtered load of Na+ is this?

A
  • receives 8,900 mmol/day

- reabsorbs 6750 mmol/day (25%)

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5
Q

How many mmol of Na+ does the distal tubule (early versus late distal tubule) receive per day and how much does it reabsorb? What percentage of filtered load of Na+ is this?

A

– receives 2,150 mmol/day

– reabsorbs 1,350 mmol/day (5% of filtered Na+)

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6
Q

How many mmol of Na+ does the collecting duct receive per day and how much does it reabsorb? What percentage of filtered load of Na+ is this?

A

– receives 800 mmol/day

– reabsorbs 700 mmol/day (2.5% of filtered Na+)

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7
Q

What is Na+ secretion equal to?

A

filtered Na+ - tubular reabsorption of Na+ (there is no active Na+ secretion)

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8
Q

What do the kidneys try to do to adjust secretion?

A

they try to adjust excretion to match ingestion of Na+

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9
Q

What is the formation of filtrate dependent on? (3)

A
  • changes in starling forces
  • the renin-angiotensin-aldosterone system
  • renal nerve activity
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10
Q

What are the starling forces?

A
  • hydrostatic and oncotic pressures can alter GFR
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11
Q

Where do the hydrostatic and oncotic pressures come from?

A

the hydrostatic pressure depends on the blood pressure and the oncotic pressure is the pressure from the osmotic particles in the blood

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12
Q

Give an example of the renal nerve activity

A

the sympathetic nerve stimulation to increase the constriction of the afferent arteriole results in reduced GFR, therefore increased proximal and distal Na+ reabsorption

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13
Q

What is the equation for the ultrafiltration pressure?

A

P(UF) = P(GC) - P(BS) - π(GC)

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14
Q

What happens if we constrict the afferent arteriole?

A

There is reduced GFR as the hydrostatic pressure in the glomerulus decreases and so there is less loss of Na+ so there is increased reabsorption

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15
Q

There is a relationship between changes in the ________ of either the _________ arteriole or _________ arteriole on _______ _______ _______ or _________

A 
resistance
afferent
efferent
renal blood flow
GFR
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16
Q

Describe the effect of constriction of the afferent arteriole on the renal blood flow and GFR

A

If the afferent arteriole is constricted, the pressure in the glomerular capillaries decreases. This means that GFR decreases and renal blood flow decreases. This means that more Na+ is retained in the blood and so there is less Na+ lost by filtrate

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17
Q

Describe the effect of constriction of the efferent arteriole on the renal blood flow and GFR

A

If the efferent arteriole is constricted, the pressure in the glomerular capillaries increases. This means that GFR increases and renal blood flow increases. This means that less Na+ is retained in the blood and so there is more Na+ lost by filtrate

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18
Q

Describe the effect of dilation of the efferent arteriole on the renal blood flow and GFR

A

If the efferent arteriole is dilated, the pressure in the glomerular capillaries decreases. This means that GFR decreases and renal blood flow decreases. This means that more Na+ is retained in the blood and so there is less Na+ lost by filtrate

19
Q

Describe the effect of dilation of the afferent arteriole on the renal blood flow and GFR

A

If the afferent arteriole is dilated, the pressure in the glomerular capillaries increases. This means that GFR increases and renal blood flow increases. This means that less Na+ is retained in the blood and so there is more Na+ lost by filtrate

20
Q

What are three other factors that are involved in Na+ reabsorption?

A
  • prostaglandins
  • atrial natriuretic peptide
  • inhibitors of Na+/K+ ATPase
21
Q

What is the effect of prostaglandins on Na+ reabsorption?

A

PGE2 inhibits tubular Na+ reabsorption by blocking ENaC

22
Q

What is the effect of ANP on Na+ reabsorption?

A

This is released from the cardiac atria in response to high blood pressure.
It reduces Na+ reabsorption by increasing cGMP in the collecting ducts which reduces the Na+/K+ ATPase activity. This decreases Na+ transport across the collecting duct cells (see Adam’s lectures)

23
Q

What is the effect of Na+/K+ ATPase on Na+ reabsorption?

A

This reduces Na+ reabsorption

24
Q

Which of the following statements is TRUE?
A. If the afferent arterioles are constricted the GFR will increase.
B. Atrial naturetic peptide decreases the tubular reabsorption of
Na +.
C. If the efferent arterioles are constricted the GFR will decrease.
D. Na+ can be actively secreted by the cells of the collecting ducts.

A

B. Atrial naturetic peptide decreases the tubular reabsorption of
Na +.

25
Q

What two things make up the juxtaglomerular apparatus

A

the macula densa cells and the granular (juxtaglomerular) cells

26
Q

Where are the macula densa cells and what is their functino?

A

These are in the thick ascending limb and they have osmoreceptor function

27
Q

Where are the granular (juxtaglomerular) cells located and what is their function?

A

These are smooth muscle cells of the afferent arteriole and they have baroreceptor function and they produce renin and angiotensin 2

28
Q

Where is renin produced and released from?

A

granular (juxtaglomerular) cells of the juxtaglomerular apparatus

29
Q

What is aldosterone, where is it produces and what it is stimulated by?

A

mineralocorticoid hormone produced by the adrenal cortex (zona glomerulosa cells); stimulated by angiotensin II

30
Q

As well as the granular (juxtaglomerular) cells of the juxtaglomerular apparatus producing renin, where else is it produced?

A

In the mast cells in the blood, the macrophages, ovaries and testes etc.

31
Q

What is the purpose of aldosterone?

Where does this occur?

A

it increases Na+ reabsorption at the level of the late distal tubule and collecting duct (as well as in the salivary glands, rectum and sweat glands

32
Q

What detects the flow rate?

A

the macula densa cells

33
Q

What three things stimulate the release of renin from the kidney?

A
  • decrease in afferent arteriolar blood pressure
  • increase in sympathetic activity
  • decrease in flow rate in the distal tubule
34
Q

Explain how aldosterone comes to be

A
  • angiotensinogen is released from the liver
  • renin is released from the kidney which converts sinogen to angiotensin I
  • when the blood travels through the lungs, angiotensin converting enzyme converts I to II
  • II is converted to aldosterone
35
Q

As well as being converted into aldosterone, what are the effects of angiotensin II?

A
  • it increases thirst
  • it increases ADH
  • it increases reabsorption of Na+ in the proximal tubule
  • and it affect blood pressure
36
Q

Where is the aldosterone receptor? What is it?

A

This mineralcorticoid receptor is inside the cell (eg. the principle cell of the cortical collecting tubule)

37
Q

What does aldosterone do to the cell?

A

it alters gene expression

38
Q

What is the effect does aldosterone altering gene expression?

A

It causes an upregulation of quiescent (not open) Na+ channels in the membrane and causes synthesis of new ENaC channels, Na+/K+ ATPases and other induced proteins. There could also be possible non-genomic effects

39
Q

What are the three locations of ENaC?

A
  • in the membrane
  • in vesicles near the membrane
  • in the membrane but quiescent
40
Q

What is the gene that aldosterone causes the expression of to have the effects?

A

Serum glucocorticoid stimulating kinase (SGK)

41
Q

What are the three phases of action of aldosterone and what is their time period?

  • phase 1, _______ period: this is ______ ________ synthesis and induced _______ (_______), _______ - ______ hr
  • phase 2, _______ response: ______ - ______ hour, activation of pre-existing ______ channels and _________ ________
  • phase 3, __________ response: ______ - ______ hours, induction of new _________ channels and __________ _________
A
  • phase 1, latent period: this is new protein synthesis and induced proteins (SGK), 0.5 - 1 hr
  • phase 2, early response: 1.5 - 3 hour, activation of pre-existing Na+ channels and Na+/K+ ATPases
  • phase 3, late response: 6 - 24 hours, induction of new Na+ channels and Na+/K+ ATPases
42
Q

What is the relationship between ENaC. Nedd4-2 and SGK?

A

Nedd4-2 is a ubiquitination enzyme which leads to the removal of channels from the membrane for recycling or degradation.
In response to low Na+, aldosterone is released which upregulates SGK to phosphorylate Ned4-2 so it can’t bind to ENaC to take it out of the membrane so ENaC remains in the membrane to increase Na+ reabsorption

43
Q

Which of the following statements is TRUE?
A. The macula densa cells function as baroreceptors.
B. Aldosterone is a steroid hormone and binds to a receptor on the basolateral membrane of Late Distal Tubule and Collecting Duct cells.
C. Angiotensin II is cleaved by renin to produce Angiotensin I.
D. Renin is released from the granular (juxtaglomerular) cells of the
afferent arteriole.

A

D. Renin is released from the granular (juxtaglomerular) cells of the
afferent arteriole.

44
Q

Where is a good summary slide found?

A

slide 23, 24

I've got kidney disease (43 decks)

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