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2ND YEAR SYSTEMS: Urinary > ECF volume regulation > Flashcards

ECF volume regulation Flashcards

1
Q

The kidney regulates what important aspect of the ECF?

A

The volume - it does this by regulating Na+ in the body

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2
Q

What are the major ECF osmoles

A

Na+ and Cl-

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3
Q

What are the major ECF osmoles?

A

K+ salts

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4
Q

Distribution of body water

A

14 litres in ECF - 3 in plasma, 11 in interstitial fluid

28 litres in ICF

42 litres TBW

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5
Q

What impact does changing the Na+ content of the ECF have?

A

It changes the ECF volume and therefore will affect the vol of blood perfusing the tissues which is effectively the circulating volume. It therefor also affects BP

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6
Q

What is the regulation of Na+ basically dependent on?

A

high and low pressure baroreceptors

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7
Q

Describe the renal response to a decrease in ECF volume (hypovolaemia)

A

Increased salt and H2O loss caused by vomiting/ diarrhoea/excess sweating causes decreased plasma volume, decreased venous pressure, decreased venous return, decreased atrial pressure, decreased EDV, decreased SV, decreased CO, decreased BP which ultimately results in decreased carotid sinus baroreceptor inhibition of sympathetic discharge

This means an increased sympathetic discharge => increased total peripheral resistance - vessels constrict - BP increases

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8
Q

Which 2 renal responses to increased salt and water loss promote stimulation of ADH secretion?

A

Decreased atrial pressure

Decreased carotid sinus baroreceptor inhibition discharge

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9
Q

The nervous system responds to a decrease in carotid sinus baroreceptor discharge by bringing about vasoconstriction which increases total peripheral resistance. What effect does this have on the Kidney?

A

Increases renal arterial constriction

Increases renin production

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10
Q

As a result of renin production Angiotensin II levels increase.

What are the 2 major roles of Angiotensin II?

A

Increases reabsorption of NaCl and water at the proximal tubule

Increases aldosterone production which increases reabsorption of NaCl and water in the distal tubule

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11
Q

Specific response of the kidney to increased sympathetic discharge

A

Increased renal vasoconstricting nerve activity causes increased renal arteriolar constriction and an increase in renin.

Renin increases the conversion of Angiotensin II. Then the peritubular capillary hydrostatic pressure decreases due to constriction. Causing increased Na+ reabsorption from the proximal tubule and therefore less Na+ is excreted.

Increase in renin causes increase in angiotensin II which increases aldosterone and increases distal tubule Na+ reabsorption and therefore less Na+ excreted. Changes in proximal tubule Na+ reabsorption are due to changes in the rate of uptake by the peritubular capillaries.

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12
Q

Why is there increased Na+ reabsorption into the peritubular capillaries?

A

Due to greater reabsorptive forces in the peritubular capillaries

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13
Q

If a lot of NaCl and H20 is lost through vomiting etc which pressure increases even more than normal?

What does this mean for reabsorption?

A

Oncotic pressure

Can now reabsorb up to 75% of the filtrate into the blood at the proximal tubule.

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14
Q

How is GFR maintained when ECF volume changes?

A

Autoregulation maintains GFR and the vasoconstriction of afferent and efferent means there is little effect on GFR

This is the case until volume depletion is severe enough to cause a considerable decrease in MBP.

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15
Q

Where does the interstitial fluid lie?

A

Between the basement membrane of the tubules and the peritubular capillaries

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16
Q

In hypovolaemia what happens to starlings forces?

A

There is an automatic readjustment of starlings forces in the peritubular capillaries in order to increase the amount of NaCl and H20 being reabsorbed to correct the imbalance.

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17
Q

What % of filtrate can be reabsorbed in hypovolaemia vs normovolaemia?

A

hypovolaemia - 75%

Normovolaemia - 70%

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18
Q

In hypervolaemia what are the oncotic pressures and peritubular pressures like in comparison to normal

A

Peritubular pressure = higher than normal because the efferent arterioles are less constricted

Oncotic pressure is lower than normal because the plasma proteins are diltued by retention of salt and water in the blood

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19
Q

Which hormone controls Na+ reabsorption at the distal tubule?

A

Aldosterone

20
Q

Which two structures form the Juxtaglomerular apparatus?

A

Macula densa - histologically specialised loop of the distal tubule

Juxtaglomerular cells - in afferent arteriole

21
Q

Which hormone do Juxtaglomerular cells produce?

A

Renin

22
Q

Which protein does renin act on? Where is it found?

A

Angiotensinogen

It is always present in the plasma

23
Q

How does Angiotensin II affect the kidney?

A

Angiotensin II stimulates the aldosterone- secreting cells in the zona glomerulosa of the adrenal cortex (suprarenals)

24
Q

How does aldosterone reach the kidney?

A

Aldosterone passes in the blood to the kidney where it stimulates distal tubular Na+ ion reabsorption.

25
Q

How do JG cells respond to decreased pressure in the afferent arteriole?

A

They increase Renin production.

This is an intrinsic property meaning it occurs even if denervated.

26
Q

The rate of renin secretion is inversely proportional to the rate of what?

A

Delivery of NaCl at the macula densa

Decrease in NaCl delivery => increased renin production

27
Q

What feeds backs to inhibit renin?

A

Angiotensin II

28
Q

What inhibits renin release?

A

ADH

29
Q

How is angiotensin II funadmentally important in the body’s response to hypovolaemia? (4)

A

It stimulates aldosterone and therefore NaCl and H2O retention.

It is a very potent biological vasoconstrictor and contributes to increasing TPR

It acts on the hypothalamus to stimulate ADH secretion which increases H2O reabsorption from Collecting Duct.

It stimulates the thirst mechanism and the salt appetite (in the hypothalamus).

30
Q

How does the tubuloglomerular feedback work to maintain GFR

A

GFR increases

Flow through tubule increases. So, flow past macula densa increases.

Paracrine from macula densa to afferent arteriole

Afferent arteriole constricts

Resistance in afferent arteriole increases

Hydrostatic pressure in glomerulus decreases

GFR decreases

31
Q

Look

A

ADH will increase because of the baroreceptors, even though this is associated with hypoosmolarity.

32
Q

When does volume become the primary determinant of ADH concentration

A

Normally osmolarity is the main determinant of [ADH], but if there is a sufficient volume change to compromise brain perfusion, then volume becomes the primary drive.

So to conserve volume, we tolerate disturbed osmolarity. Once volume is restored in hypovolaemia - then osmolarity will be normalised and again becomes the main determinant of ADH

33
Q

If a patient has lost a large amount of salt and water what should be done to correct this?

A

Infuse or drink saline

REPLACE SALT AND WATER

34
Q

How does aldosterone cause weight gain?

A

because of retention of H2O with the increase in [Na+]blood

35
Q

Function of Atrial Natriuretic Peptide (ANP)?

A

Promotes Na+ excretion

36
Q

What stimulates the release of ANP from atrial cells?

A

Volume expansion

37
Q

What is the effect of aldosterone on potassium?

A

Causes potassium secretion

38
Q

How is ANP linked to aldosterone?

A

Aldosterone causes sodium reabsorption

Increase in weight because of retention of H2O with sodium reabsorption. Volume expansion causes increased atrial stretch which stimulates release of ANP from atrial cells

ANP overrides aldosterone effects on Na+ reabsorption because of volume expansion = “Aldosterone escape”.

39
Q

What are the imbalances in the blood present when the patient presents with conn’s syndrome? - Hyperaldosteronism

A

Potassium is depleted but the patient is not hypernatraemic (high [Na+])

ANP still works and causes loss of sodium in urine

40
Q

What part of the brainstem does ANP act on to reduce blood pressure?

A

Medulla oblongata

41
Q

In uncontrolled DM, what effect does the high plasma glucose level have on ECF volume and distribution? (4)

A
  1. Glucose remains in the tubule and exerts an osmotic effect to retain H2O in the tubule.
  2. [Na+] in tubule lumen decreases due to H20 retention. Glucose shares a symport with Na+. Na+ reabsorption decreases as normally Na+ moves into the proximal tubule cells by passive diffusion but because the concentration of Na+ has been altered this gradient has been lost and there is decreased Na+ reabsorption as a result meaning there is a decrease in the ability to reabsorb glucose too (stays in tubule)
  3. In the descending limb of the loop of Henle, movement of H2O out of the tubule into the interstitium is reduced because the glucose and excess Na+ exert an osmotic effect to retain H2O. Therefore fluid in the descending limb is not so concentrated.
  4. Fluid delivered to the ascending limb is less concentrated. Since the NaCl pumps in the ascending limb are gradient limited, the medullary interstitial gradient is much less. Therefore there is considerable reduction in the vol of NaCl and H2O reabsorbed from the loops of henle. A large vol of NaCl and H2O is delivered to the distal tubule and the interstitial gradient is gradually abolished
42
Q

Under normal conditions, what would happen if a large volume of NaCl and H2O is delivered to the distal tubule?

A

There would be excess ECF volume and therefore NaCl and H2O need getting rid of.

The macula densa will detect the high rate of delivery of NaCl so that renin secretion will be suppressed and Na+ reabsorption at the distal tubule will be decreased.

43
Q

What type of urine is excreted from diabetic patients?

A

A large volume of nearly isotonic urine will be excreted

This results in a decreased plasma volume

Patients with uncontrolled DM can produce urine volumes of up to 6-8 l/day, causing severe salt and water depletion.

If ingestion is not adequate, a raging thirst is one of the first signs of DM, then the hypotension may be so severe as to cause a hyperglycaemic coma

44
Q

What is the difference between a hyperglycaemic coma and a hypoglycaemic come?

A

Hyperglycaemic coma is due to inadequate blood flow to the brain

hypoglycaemic coma is due to inadequate glucose for the brain

45
Q

How is this problem in DM not self-limiting?

A

The liver keeps producing glucose

2ND YEAR SYSTEMS: Urinary (25 decks)

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