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Gut, metabolism and hormones > Water and salt balance - Renal 3 > Flashcards

Water and salt balance - Renal 3 Flashcards

1
Q

Control of water and salt balance:

❖Hormonal control of salt and water reabsorption
❖Role of renal system in maintaining blood pressure
❖Renin-angiotensin-aldosterone system

A
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2
Q

LEARNING OUTCOMES:
* Understand the importance of fluid balance
* ADH and water balance
* Renin-Angiotensin-Aldosterone System (RAAS)
* Aldosterone
* Atrial Natriuretic Peptide and salt balance

A
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3
Q

Fluid balance is regulated by?

A

Controlling the extracellular cellular fluid volume and osmolarity

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4
Q
  1. Total body fluid in L?
  2. TBF % of body fluid
  3. % of body weight?
A
  1. 42L
  2. 100%
  3. 60%
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5
Q
  1. Intracellular fluid in L?
  2. ICF % of body fluid
  3. % of body weight?
A
  1. 28 L
  2. 67%
  3. 40%
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6
Q
  1. Extracellular fluid in L?
  2. ECF % of body fluid
  3. % of body weight?
    Breakdown of plasma and interstitial fluid?
A
  1. 14 L
  2. 33%
  3. 20%

Plasma = 2.8L, 6.6% of body fluid which is 20% of ECF and 4% of body weight
Interstital fluid = 11.2L, , 26.4% of body fluid which is 80% of ECF and 16% of body weight

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7
Q

Water steady state is based on?

A

Amount ingested = amount eliminated

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8
Q

Pathological losses in regards to water steady state?

A

Vascular bleeding (H20, Na+ )
Vomiting (H20, H+)
Diarrohea (H20, HCO3-).

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9
Q

Fluid balance is maintained by regulating?

A

ECF volume and osmolarity

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10
Q

Why must ECF volume be closely regulated?
What is of primary importance in the long-term regulation of ECF volume?

A

To help maintain blood pressure
Maintaining salt balance

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11
Q

Why must ECF osmolarity be closely regulated?
What is of primary importance in regulating ECF osmolarity?

A

To prevent swelling or shrinking of cells
Maintaining water balance

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12
Q

What prevents changes in ICF volume?

A

Controlling ECF osmolarity

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13
Q

Slide 7
What is hypertonicity?
How does it happen?

A

Imbalance of water and sodium in the body
Individual loses water while retaining high concentration of electrolytes and then fluid that surrounds cells has a high sodium concentration
Water leaves cell and the cell shrinks

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14
Q

Symptoms of hypertonicity
Common?
As severity increases?
Rare?

A

Common: fatigue, dark urine, less frequent urination, dry skin/lips
As severity increases: low/reduced blood pressure, light headedness, muscle cramps, headaches or dizziness
Rare: Convulsions, loss of consciousness, hypovolemic shock, death

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15
Q

Causes of hypertonicity?

A

Loss of bodily fluids through:
Skin: sweating, overexposure to heat, development of burns, impaired thirst mechanisms, cognitive deficits
GI Tract: Diarrhea, vomiting, use of laxatives, gastric suctioning, ascites, abdominal infections
Urinary System: Kidney disease, post obstructive diuresis, salt wasting tubular disease, Addison disease, hypoaldosteronism, hyperglycemia, diabetics insipidus

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16
Q

Treatment of Hypertonicity?

A

Oral rehydration therapy
Intravenous fluids
Treating underlying conditions

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17
Q

Hypotonicity - what is it?

A

ECF is too dilute and low solute load which causes cells to swell

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18
Q

Causes of hypotonicity?

A

Inability to excrete a dilute urine (renal failure)
When water is rapidly ingested
When excess water is retained in body due to inappropriate secretion of vasopressin

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19
Q

Symptoms and effects of hypotonicity?

A

Swelling of neurons
Weakness due to swelling of muscle cells
Circulatory disturbances - hypertension and oedema (fluid retention)

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20
Q

Water reabsorption takes place via what hormone?

A

Vasopressin / anti-diuretic hormone (AH)

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21
Q

What does ADH do?
When does it increase/decrease?

A

Controls variable H20 reabsorption in the distal and collecting tubular segments
Increased in response to a H20 deficit: ECF = Hypertonic
Decreased in response to a H20 excess: ECF = Hypotonic

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22
Q

How is ADH made and secreted and then stopped?
6 STEPS

A
  1. High blood osmotic pressure stimulates hypothalamic osmoreceptors
  2. Osmoreceptors activate the neuro-secretory cells that make and release ADH
  3. Nerve impulses release ADH from axon terminals in the posterior pituitary into the bloodstream
  4. Kidneys retain more water which decreases urine output
  5. Low blood osmotic pressure inhibits hypothalamic osmoreceptors
  6. Inhibition of osmoreceptors reduces/stops ADH secretion
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23
Q

ADP is secreted from?

A

Posterior pituitary

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24
Q

ADH synthesis is where?

A

Paraventricular nucleus of hypothalamus

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25
Q

Osmoreceptors in hypothalamus are responsible for ADH secretion:
1. Low water intake?
2. High water intake?

A
  1. Low water intake (↑ plasma osmolality)
  2. High water intake (↓ plasma osmolality)
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26
Q

Final stage of ADH working how does water exit the cells?

A

Water exits the cell through different, always open water channels (either ACP-3/ACP-4) permanently positioned at the basolateral border and then enters the blood in this way being reabsorbed.

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27
Q

What is diabetes insipidus?

A

It is a rare disorder that causes the body to make too much urine.

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28
Q

Causes of Diabetes inspidus?
1. Central
2. Nephrogenic

A
  1. Idiopathic, head trauma, pituitary tumour, neurosurgery
  2. Lithium toxicity, renal disease, hypokalemia, medications, pregnancy: excessive vasopressinase activity, an enzyme expressed by placental trophoblasts
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29
Q

What happens if there is low ADH?

A

Kidneys stop conserving H2O -
Large volume of urine produced (polyuria)
Low water conservation
Thirst (polydipsia)
Dehydration
Hypernatremia if water limited

Damage to hypothalamus

30
Q

Treatment for central diabetes insipidus?

A

Desmopressin which is a manufactured version of ADH

31
Q

Salt balance is very important in regulating?

A

ECF volume

32
Q

Salt input occurs by?
It is maintained by?

A

Ingestion - often not well controlled
Outputs in urine - salt also lost in perspiration and faeces

33
Q

What account for 90% of ECG osmolality?

A

Na and accompanying Cl^- (passively reabsorbed following Na+)

34
Q
  1. By reabsorbing Na^+ and Cl^- what do the kidneys automatically conserve?
  2. The more salt in ECF, the more?
  3. Decrease in Na+ leads to?
  4. What determines ECF volume?
A
  1. H20 because H20 comes along osmotically
  2. Therefore, the retained salt solution is isotonic - the more salt in the ECF the more H2O.
  3. But a decrease in Na+ leads to a decrease in water retention – Reduced volume
  4. Na+ determines ECF volume
35
Q

Systems regulating water and salt balance?

A

Hypothalamic Osmoreceptors
RAAS system
Left atrial receptors

36
Q

How does hypothalamic osmoreceptors regulate water and salt balance?

A

Osmolarity control
Monitor osmolarity of plasma in CNS and stimulates the process of vasopressin secretion

37
Q

How does the RASS system regulate water and salt balance?

A

Volume control
Stimulates vasopressin secretion, thirst and increased reuptake of Na+

38
Q

How does left atrial recepytors regulate water and salt balance?

A

– Volume control
Myelinated vagal fibres, monitor pressure of venous return
Upon detection of increase in stretch of atria, drive reduction invasopressin secretion and release of ANP

39
Q

Regulation of GFR contributes to?

A

Na+ regulation

40
Q

Are DCT and PCT regulated?

A

DCT - regulated
PCT - unregulated

41
Q

What affect BP?

A

Hypernatraemia + Hyponatraemia

42
Q

Aldosterone and Atrial Natriuretic peptide effect on Na+?

A

Aldosterone (↑ Na+ reabsorption)
Atrial Natriuretic Peptide (↓ Na+ reabsorption)

43
Q

See slide 18 and 20

A
44
Q

Where is atrial natriuretc peptide (ANP) released by?
Secreted in response to?

A

Atria of the heart
Secreted by cells in the atria in response to stretch of the atrial wall due to an increase in plasma volume

45
Q

Renin-Angiotensin system
1. Angiotensinogen is made?
2. Renin enzyme is made?
3. Angiotensin 1 hormone is made?
4. Angiotensin converting enzyme (ACE) is made?

A
  1. Angiotensinogen produced - Liver.
  2. Renin (enzyme) produced - Kidney (JG cells).
    - Low BP and ↑ sympathetic activity stimulate renin secretion.
    - Decreased [Na+] in the tubular fluid stimulate renin secretion
  3. Angiotensin I (hormone) produced from angiotensinogen.
  4. Angiotensin converting enzyme (ACE) produced - Lungs
    - Converts AngI into AngII.
46
Q

JGA role in RAAS see slide 22

What role do:
1. Macula densa cells have?
2. Granular cells?

A
  1. Macula densa cells: detect [Na+] – major role in the control of BP (tubuloglomerular feedback)
  2. Granular cells – specialised smooth muscle cells, contain baroreceptors, innervated by SNS – synthesise, store and release renin for the control BP
47
Q

See slide 23+24

A
48
Q

Decreased MAP has what affect on afferent arteriole pressure and what does this lead to?

A

Decreased MAP, decreases afferent arteriole pressure which causes juxtaglomerular cells of afferent arteriole to increase Renin release

49
Q

Decreased MAP has what affect on baroreceptor reflex and what does this lead to?

A

Causes baroreceptor to increase sympathetic activity thus releasing beta1 adrenoreceptors causing juxtaglmerular cells of the afferent arteriole to increase renin release

50
Q

What effect does decreased MAP have on GFR and what does this lead to?

A

Decreased MAP decreased GFR, which causes a decrease in NA+ and Cl- concentrations in distal tubules which causes the macula densa to increase the chemical signal secretion of PGE2 which causes the juxtaglomerular cells fo the afferent arteriole to increase renin release

51
Q

How does Aldosterone work? 5 steps

What is to note here about when reabsorbing K+ what else is excreted?

A
  1. Aldosterone diffuses through the capillary membrane.
  2. Aldosterone binds to the mineralocorticoid receptor. The hormone receptor complex then diffuses into the nucleus.
  3. Transcription and translation of the epithelial sodium chloride channel and the Na-K ATPase pump.
  4. Transfer of sodium from the tubular lumen into the ductal cell.
  5. Transfer of sodium from the ductal cell to the interstitial fluid and then capillary.

Note here when reabsorbing sodium K+ or H+ is excreted! – normally excrete K+ however in acidotic situations H+ prevails which can have an effect on [K+]. And visa versa for alkalosis

52
Q

What does Aldosterone promote the expression of?

A

Renal outer medullary potassium (ROMK) channels

53
Q
  1. ECF volume is needed to regulate?
  2. Outcomes if the variable is not normal?
  3. Mechanism for regulating the variable?
A
  1. Important in the long term control of arterial blood pressure
  2. Decreased ECF volume causing decreased arterial blood pressure and increased ECF volume causes increased arterial blood pressure
  3. Maintenance of salt balance, salt osmotically “holds” H20, so the Na+ load determines the ECF volume. Accomplished primarily by aldosterone-controlled adjustments in urinary Na+ excretion.
54
Q
  1. ECF osmolarity is needed to regulate?
  2. Outcomes if the variable is not normal?
  3. Mechanism for regulating the variable?
A
  1. Important to prevent detrimental osmotic movement of H20 between the ECF+ICF.
  2. Increased ECF osmolarity (hypertonicity) causes H20 to leave the cells and cells shrink. Decreased ECF osmolarity (hypotonicity) causes H20 to enter the cells and causes cells to shrink.
  3. Maintenance of free H20 balance. Accomplished primarily by vasopressin-controlled adjustments in excretion of H20 in the urine.
55
Q

What is a diuretic?

A

Any substance that promotes diuresis, the increased production of urine.

56
Q

Loop diuretic examples?

A

Furosemide, bumetanide, ethacrynic acid

57
Q

Osmotic diuretics examples?

A

Mannitol, Acetazolamide

58
Q

Loop diuretics mechanism?

A

Block the Na+/K+/2Cl- co-transporter in the thick ascending limb of the Loop of Henle, hence increase the solute load of the filtrate and reduce water resorption.

59
Q

Effects of Loop diuretics?

A

Significant loss of water and Na+Cl- Ca2+, K+ and H+ excretion is also increased

60
Q

Loop diuretics act as treatment for?

A

Volume-mediated hypertension, nephrotic syndrome

61
Q

Mechanism of Osmotic diuretics?

A

Mannitol is a solute that is freely filtered at the glomerulus but poorly reabsorbed from the tubule, so it remains in the lumen and holds water by osmotic effect. The reduction in water reabsorption occurs
in the proximal tubule and loop of Henle and also slightly increases Na+ loss.

62
Q

Effects of Osmotic diuretics?

A

Mannitol can reduce brain volume and intracranial pressure by osmotically extracting water from the tissue into the blood.

63
Q

What are osmotic diuretics used as treatment for?

A

Glaucoma, elevated intracranial pressure

64
Q

Thiazide Diuretic example?

A

Thiazide and Metolazone and Indapamide

65
Q

Potassium-sparing diuretics example?

A

Amiloride, Spironolactone and Triamterene, eplerenone

66
Q

Mechanism of potassium sparing diuretics?

A

Spironolactone and eplerenone are aldosterone antagonists and hence inhibit the sodium-retaining action of aldosterone. Amiloride and triamterene block sodium channels in collecting tubules. Both types decrease K+ excretion.

67
Q

Effects of Potassium sparing diuretics?

A

They increase Na+ excretion and decrease K
+ and H+ excretion, there is a mild associated diuresis (risk of hyperkalaemia)

68
Q

Potassium-sparing diuretics can be used to treat?

A

Oedema and high BP due to heart failure or kidney disease, hypokalaemia that does not improve with supplementation

69
Q

Thiazide diuretics can be used to treat?

A

Volumetric hypertension and oedema and some conditions related to unbalanced calcium metabolism.

70
Q

Mechanism of thiazide diuretics?

A

They inhibit the Na+Clsymporter in the distal convoluted tubule, decreasing Na+Clresorption and hence increase water loss.

71
Q

Effects of thiazide diuretics?

A

Moderate increase in Na+ and Cl- excretion. They result in low urine Ca2+ by increasing urinary Ca2+ resorption (the opposite effect of loop diuretics). They can cause profound hypokalaemia due to excessive K + loss. Excretion of uric acid is reduced, and Mg2+
is increased.

Gut, metabolism and hormones (22 decks)

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