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Genitourinary > Integration Salt & Water Balance > Flashcards

Integration Salt & Water Balance Flashcards

1
Q

What is the most important hormone for salt and water balance?

A

Anti-diuretic hormone (ADH)

aka vasopressin or arginine vasopressin

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2
Q

What is diuresis?

A

Diuresis is the production of urine

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3
Q

What is the purpose of anti-diuretics?

A

To reduce the production of urine, so reabsorb H2O from tubule to retain in the body.

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4
Q

What is Anti-diuretic hormone associated with?

A

Aquaporins reabsorbing water in the distal convoluted tubule.

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5
Q

What process occurs with dehydration/low blood volume, 8 part?

A

Water deficit or low blood volume

  1. a - Increased extracellular osmolarity sensed by osmoreceptors
  2. b - decreased blood pressure as a result of low blood volume sensed by baroreceptros.
  3. Increased ADH secretion from posterior pituitary.
  4. Increased plasma ADH (in blood stream)
  5. V2 receptors on interstitial surface of tubule receive ADH.
  6. Signal transmitted for insertion of aquaporins on tubular lumen side.
  7. Increased H2O permeability in distal tubule and collected ducts
  8. Increased H2O reabsorption/reduced H2O secretion
  9. Negative feedback created by increased H2O re-absorption, and ADH secretion reduces.
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6
Q

Where is ADH synthesised and stored?

A

Synthesised in the hypothalamus, the central player in regulating Na/H2O balance.
Stored in the pituitary.

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7
Q

What are osmoreceptors?

A

Cells in neurons that are sensitive to osmolarity, and if osmolarity is high the they stimulate ADH release.

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8
Q

How do osmoreceptor neurons sense osmolality?

A

The architecture/building blocks of osmoreceptive neurons are such that they are affected by a change in osmolality.
Change in firing pattern depends on how large or small the neurons get hypo-osmotic fluid will move out. ???

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9
Q

Under what two physiological conditions is ADH released?

A
  1. Increased osmolality (less than 1% change) - so ADH released, H2O reabsorbed, and decreased osmolality.
  2. Decreased ECF volume (greater than 10% change) - decreased ECF volume causes a change in pressure which is sensed by the baroreceptors which also influence the release of ADH so that fluid will be reabsorbed to increase volume.
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10
Q

What are examples of non-physiological conditions that cause ADH to be released?

A
  1. Pain, stress
  2. Some drugs - medicinal
  3. Carcinomas
  4. Pulmonary disorders and CNS disorders
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11
Q

How does alcohol affect ADH?

A

Alcohol inhibits the secretion of ADH, so urine output is increased and ECF becomes dehydrated.

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12
Q

What process occurs in the kidney with ADH, 5 part?

A
  1. Increased osmolarity
  2. Increased secretion of ADH from pituitary (made in hypothalamus) into the blood stream.
  3. V2 receptors on interstitial side receive AHD
  4. Insertion of aquaporins on apical surface of tubular cells
  5. When there’s H2O it will pass through gradient.

Note - gradient is always present but H2O is stopped from passing through due to the absence of aquaporins.

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13
Q

What is the overall function of ADH?

A

ADH plasma levels are continually fluctuating -

effectively regulating osmolarity by altering the amount of H2O that’s reabsorbed or excreted.

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14
Q

Why is ADH important , what condition results from low levels of ADH?

A

Diabetes insipidus (central or nephrogenic) can result, because of low ADH levels it’s not possible to reabsorb water and urine production is high.

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15
Q

How does diabetes insipidus compare to diabetes mellitus?

A

Diabetes is the general term to describe increased urine output.
Insipidis relates to ADH where as mellitus is associated with insulin (from pancrease) not taking affect on glucose, so glucose passes and takes H2O with it so urine output is increased.

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16
Q

How does central diabetes insipidus compare to nephrogenic diabetes insipidus?

A

Central is an issue with the production of AHD.
Nephrogenic is an issue with the receptors.
Both conditions are related to ADH, but central is more treatable than nephrogenic.

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17
Q

What are some causes of central diabetes insipidus?

A

Inadequate ADH secretion.
Brain injury, tumour or infection.
Problems with hypothalamus or posterior pituitary.
AKA - neurogenic DI or pituatary DI

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18
Q

What are some causes of neurogenic diabetes insipidus?

A

Collecting tubule tubule unresponsive to ADH

Some drugs can damage kidneys, including lithium.

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19
Q

Describe an effective test to determine if the issue is central (AHD production) or nephrogenic (receptors)?

Note: If blood glucose levels are normal than it’s not diabetes mellitus.

A

Water deprivation test.

  1. Deprive the patient of water for a number of hours.
  2. Administrer a synthetic analogue of vasopressin (ADH)
    3a. If vasopressin causes a change in urine level then it’s central DI (ADH production).
    3b. If no change in urine level then it’s nephronic DI (ADH receptors).
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20
Q

What is SIADH?

A

Syndrome of inappropriate ADH secretion.

  1. Plasma ADH levels are higher than normal.
  2. Patient absorbs more water than needed.
  3. Very low osmolarity which can damage hypothalamus.
  4. SIADH may be causes by brain injury or tumour, or certain anti-cancer drugs.
  5. So patients are restricted from drinking water.
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21
Q

Which of the following statements is true:

A) The descending limb of the loop of Henle is permeable to water.

B) An increase in osmolarity will lead to an increase in ADH levels.

C) A decrease in blood volume will lead to an increase in ADH levels.

D) An increase in ADH levels results in dilute urine.

A

A) True
B) True
C) True
D) False - an increase in ADH levels results in concentrated urine.

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22
Q

In the study using rabbits as the study subject, kidneys were crushed and injected and then it was found that BP increased - what do they think caused the increase in BP?

A

Increase in renin levels from the crushed kidneys.

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23
Q

Salt is used as a proxy for blood flow - what senses a change in salt concentration and where is it sensed?

A

Macula densa cells, located near the vascular pole of the glomerus.

Macula densa are specialised epithelial cells in the distal convoluted tubule.

24
Q

What is released in response to low salt levels and what releases it?

A

Low salt

  1. Sensed by macula densa
  2. Renin released from JG cells (afferent arterioles).
25
Q

What three factors promote renin secretion?

A
  1. Reduced afferent arteriolar pressure
  2. Increased sympathetic activity
  3. Reduced macula densa NaCl delivery
26
Q

What does increased renin secretion cause?

A
  1. Renin promotes the production of angiontensin I

2. Angiotensin I is a prerequisite for angiotensin II

27
Q

What does angiotensen II do?

A
  1. Increases aldosterone production
  2. Vasoconstriction - and here constriction of efferent arteriole
  3. Reabsorption of Na, and so H2O will follow.
28
Q

Discuss ACE inhibitors?

A
  1. Angiotensen Converting Enzyme is inhibitied so angiotensin I is not converted to angiotensin II.
  2. Because angiotensin II is a vasoconstrictor then it is a good target for high blood pressure and heart failure.
29
Q

What are the two receptors involved in the renin-angiotensin system?

A
  1. AT1 - vasoconstriction, increased ADH, decreased RBF but maintains GFR.
  2. AT2 - vasodilation.

AT1 are more abundant than AT2, more durgs targetting AT1 receptors

30
Q

Which of the following statements is true:

A) An increase in macula densa NaCl concentration leads to a decrease in renin secretion.

B) Increased production of angiontensin II inhibits the sodium-hydrogen exchanger.

C) An increase in angiotensin II levels results in excretion of salt and water in the urine.

A

A) True
B) False
C) False

31
Q

High levels of angiotensin II are indirectly related to what three conditions?

A
  1. Hypertension
  2. Hearth failure
  3. Kidney disease
32
Q

Question:
If the right renal artery becomes abnormally constricted, what will happen to renin secretion by the right kidney and the left kidney?

A

Right kidney:
1. Low renal perfusion sensed by intrarenal
baroreceptors.
2. Low salt/flow to the macula densa.
3. SO increased renin, increased angiotensin II, and increased BP.
4. AND flow to kidney increases as a result of higher BP, but not usually up to 100%.

Left kidney:
1. Decreased renin secretion due to kidney sensing higher BP and increased blood flow.

One kidney increases renin and the other reduces renin, acutely sit in situation where renin angiotensin and pressure will be higher for flow past the obstruction to be close to normal before renin can begin to come down - but flow never goes back to 100%.

If high BP in renal vasculature the patient tolerates the high BP to ensure that flow in this kidney is near normal. Renal levels could be high just as a result of a small constriction in arteries.

33
Q

In summary, what occurs when you want to address osmolarity?

A

Use ADH to shift water.

34
Q

In summary, what occurs when you want to address total amount of fluid?

A

Move salt around and H2O follows.

35
Q

Provide a flow diagram on how renin is activated and what its effects are.

A

Diagram

1a. Low salt sense by macula densa cells
1b. Decreased afferent arteriolar pressure
1c. Increased sympathetic activity
2. Renin released from juxtaglomerular cells in the afferent arteriole
3. Renin is carried through the blood stream and together with angiotensinogen from the liver it forms angiotensin I
4. In the presence of Angiotensin Converting Enzyme (ACE) angiotensin I forms angiotensin II.
4. Angiotensin II targets AT1 receptors and AT2 receptors (AT1 are more populous) and causes vasoconstriction.
5. Vasonconstriction occurs vessels including efferent arterioles to slow blood down, thereby increasing blood pressure and increasing glomerula filtration rate.

36
Q

Provide a flow diagram on how aldosterone is activated and what its effects are.

A

1a. Low blood flow, low blood pressure is sensed by the macula densa cells as well intrarenal baroreceptors and the juxtaglomerula cells release renin which promotes the production of angiotensen II.
1b. High K+
2. The above are sensed by the AT1 receptors on the adrenal gland.
3. Aldosterone is released.

37
Q

What is the primary function of aldosterone?

A

To shift salt (Na+), which then also moves water.

38
Q

What happens when aldosterone is circulating in the blood stream?

A
  1. Aldosterone circulating in blood stream.
  2. Aldosterone binds to the mineral-corticoid receptor.
  3. To increase reabsorption of salt through ENaC channels on the tubular lumen side.
  4. Activates Na/K+ ATPase on the renal interstitial side.
  5. So high aldosterone > increased activation of mineral-corticoid receptors > high reabsorption of Na from ENaC channel and activated Na/K+ ATPase.
  6. Increased Na is reabsorbed from the lumen by ENaC channels and then into the ECF by Na/K+ATPase.
  7. The Na/K+ ATPase has exchanged the Na+ for K+ and so potassium levels decrease.
  8. Water follows Na+ and so ECF water also increases.
39
Q

What happens when potassium levels are high?

A

Aldosterone can be activated to exchange K+ for Na+ and so K+ is excreted and levels return to normal.

40
Q

What happens to aldosterone if you are treating a patient with angiotensin blockers (targeting the AT1 receptors)?

Seek confirmation from James - refer to page 107????

A

Aldosterone (that’s produced in response to angiotensin II) levels will decrease, so the body will find other mechanisms to drive production of aldosterone including an increase in potassium (which will be absorbed from the distal convoluted tubule). High K+ also activates adrenal gland for aldosterone.

41
Q

Why is it important to be aware of the effects of medication on potassium (K+) levels?

A

Increased potassium levels can cause arrhythmia’s.

High K+ hyperpolarises the potassium channels which control myocyte (maintain membrane potential of cardiomyocyte).

42
Q

Aldosterone can be blocked by medications including spironolactone - what effect does this have on potassium levels?

A
  1. Blocked aldosterone
  2. No mineral-corticoid receptor activation of Na+ reabsorption through the ENaC channels or the Na/K ATPase
  3. Not able to exchange out and excrete K+ so high potassium levels in plasma (hyperkalemia).
43
Q

Amiloride (K+ sparing diuretic) blocks ENaC channels - what does this do and what effect does it have on potassium levels?

A

If ENaC channels are blocked then there is less Na to drive the Na/K+ ATPase - so reduced extrusion of K+ and so K+ levels in the blood can increase.

44
Q

For cardiac failure there is evidence that an increase in spirolactone can help increase survival, also ARB (angiotensin receptor blockers), or ACE inhibiters and betablokers may give additional effects.

Why is it important to think and know about these?

A

As you start to prescribe you need to consider mechanisms.

  1. Think about what is causing increased blood pressure and the mechanisms, this will help determine which medications are best.
  2. The drugs that are most effective might differ for patients.
  3. Should you prescribe calcium blockers, ARBs (angiotensin receptor blockers) or ACE inhibitors.
45
Q

Question 1
Normally aldosterone stimulates the reabsorption of approximately 33g of sodium chloride/day. If a patient loses 100% of adrenal function, will 33g of sodium chloride be excreted per day indefinitely?

A

No - compensation will occur to help counter the decreased aldosterone-dependent sodium reabsorption.
For example reduced glomerular function rate and other factors that promote tubular sodium reabsorption.

46
Q

Regulation of osmolality - what is regulated, how tightly is it regulated and what is the mediator?

A

Regulated by changes in renal water handling (shifting water).
It is tightly regulated +-1-2%.
Mediated by ADH (aka arginine vasopressin AVP).

47
Q

Regulation of ECF volume - what is regulated, how tightly is it regulated and what is the mediator?

A

Regulated by changes in renal Na+ handling (shifts sodium around).
Varies throughout the day (increasing and decreasing).
Mediated by renin-angiotensin and sympathetic nervous system.

48
Q

Why does ECF osmolality need to be constant?

A

If osmolality of ECF is higher than ICF (hypertonic) then water is drawn out of ICF and cells can shrink.
If osmolality of ECF is lower than ICF (hypotonic) then water is drawn in to the ICF and cells may swell and explode.

49
Q

Changes in ECF volume are compensated by changes in Na+ reabsorption by the kidney.

How is decreased ECF compensated?

A

Decreased ECF is compensated by increased renal reabsorption of Na+, with which water follows.

This is achieved by by the renin-angiotensen-aldosterone system (AT1 receptor) and the sympathetic nervous system.

50
Q

Changes in ECF volume are compensated by changes in Na+ reabsorption by the kidney.

How is increased ECF compensated?

A

Increased ECF is compensated by decreased reabsorption of Na+.

This is achieved by atrial natriuretic peptide (ANP) hormone and reduced renin-angiotensen-aldosterone and sympathetic nervous system activity.

51
Q

ANP is a factor that inhibits Na+ reabsorption - draw a flow diagram of how ANP is activated and works?

A
  1. Increased ECF/Increased Na+
  2. Increased filling pressure and increased atrial stretch (consider Frank Starlings law)
  3. ANP released from atria
  4. ANP binds to receptors to increase cGMP
  5. Blocking ENaC and inhibiting Na/K ATPase
  6. Decrease of Na+ absorption in distal tubule and outer medullary CT
  7. a) Inhibits release of aldosterone
  8. b) Inhibits renin release
  9. c) Vasodilates afferent arterioles to increase GFR.
52
Q

What happens during dehydration?

What are the sensors?
What are the signals?
What are the effectors?
What is the eventual response?

Check with James - angiotensen and/or ADH pg 110 and pg 90

A
  1. Increased osmolarity (leads to increased thirst)
  2. Increased angiotensen II (and/or ADH)
  3. Increased H2O reabsorption
  4. Increased blood volume to correct osmolarity
  5. Then try and activate renin-angiotensin system to expel both Na/H2O
53
Q

Why do some people not take their medication?

A
  1. Side effects - including coughing and angioedema.
    2 Unable to see the benefits - with high BP there are no symptoms.
  2. Drugs unnaturally control BP - they clamp BP down so if one goes for a walk (which naturally lowers BP) they can fell ill.
  3. Some people are resistant to the drugs.
54
Q

Clinical scenario
A 67 year old woman is brought to the hospital after a fall on the stairs. She had a past medical history of high BP and atrial fibrillation, for which she took a calcium channel blocker and a beta blocker. She reported climbing a flight of stairs with a glass of water in her hand. The next moment she was lying on the ground not remembering what had happened. She apparently had a normal diet with normal salt intake. She was diagnosed with SIADH.

  1. Normal ADH levels can range from 1-5 picograms per milliliter (pcg/mL). What would you expect ADH levels to be in this patient? (10%).
  2. Normal plasma osmolality levels range between 275 to 295 milli osmosles per kilogram. What would you expect the osmolality levels in this patient to be an why? (20%).
  3. Draw a flow diagram explaining the renal excretory response in this patient to ingestion of 500ml of water. (30%)
A
  1. High ADH levels due to Syndrome of Innapropriate Anti-Diuretic Hormone.
  2. Would expect osmolality levels to be lower than normal because of the increased water reabsorption due to the high levels of ADH.

3.
1. 500ml of water ingested & and high ADH
2. increase blood volume, blood flow, and Na+ sensed by macula densa cells
GIVE FURTHER THOUGHT

55
Q

Clinical scenario
A 48 year old woman presents to emergency room with headache and a blood pressure of 188/104. Se has a history of hypertension that was previously well-controlled with anti-hypertensives including an ACE inhibitor. However, she stopped taking her medication because she didn’t like being dependent on drugs. She reports no other symptoms. Further investigations reveal that she has unilateral atherosclerotic renal artery stenosis.

  1. In her unmedicated state, what effect would this have on her angiotensin II levels and why?
  2. After resuming her medication, her creatinine levels rise, why?
  3. What will be the effects of surgical removal of the atherosclerotic kidney on blood pressure levels and why?
A
  1. a. Low perfusion past the stenosis due to atherosclerosis
    b. Low Na sensing by macula densa cells
    c. Increased renin
    d. Increased angiotensen II, so
    d. Angiotensin levels will be higher.
  2. a. Reduced BP
    b. Increased creatinine levels - the more aggressive the treatment the more damage that’s sustained to the kidney
    c. Need to balance - high BP and increased risk of stroke, or lowering BP and increasing risk of kidney damage.

3.
We think usually normal, but possible that there’s increased BP due to all the compensatory mechanisms.

James ??????

56
Q

Which of the following statements are true/false:

  1. A high salt pasta meal will lead to a decrease in angiotensin II levels.
  2. Dehydration will lead to a decrease in ADH levels
  3. The angiotensin response to haemorrhage is decreased if renal nerves to the kidney are denervated.
  4. An increase in angiotensin II levels results in excretion of salt and water in the urine.
  5. Angiotensin II is released by the juxtaglomerular cells when renal perfusion pressure increases.
  6. Stenosis of the renal artery will lead to increased sodium and water reabsorption
A
  1. True
  2. False
  3. True - JAMES
  4. False - ang II results in vasoconsriction and increased ADH
  5. False - ang II is not released by JG cells
  6. True - JAMES

Genitourinary (5 decks)

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