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BRS UROLOGY & RENAL > 1b Regulation of Water and Acid / Base > Flashcards

1b Regulation of Water and Acid / Base Flashcards

1
Q

What is osmotic pressure proportional to ?

A

the number of solute particles

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2
Q

What is the formula for osmolarity?

A

Concentration * number of dissociated particles

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3
Q

what is osmosis?

A

The movement of solute particles from an area of low concentration to an area of high concentration, across a semi permeable membrane

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4
Q

What proportion of the bodies fluid is intracellular and extracellular?

A

1/3 is ECF
2/3 is ICF

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5
Q

Of the Extracellular fluid, what proportion is intravascular and extravascular?

A

Intravascular = 25%
Extravascular = 75%

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6
Q

What are the four ways in which water leaves the body in an unregulated sense?

A

Sweat
Faeces
Vomit
water evapouration from respiratory lining and skin

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7
Q

What is the regulated method of water loss from the body?

A

renal regulation = urine production

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8
Q

Describe how renal regulation will normalise the osmolarity when there is a high water intake?

A

High water intake

Higher ECF volume, Lower Sodium conc.

Lower osmolarity

Hypoosmotic urine production

Osmolarity normalised

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9
Q

What is the first compartment which water enters into once it enters into the body?

A

ECF

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10
Q

Describe how renal regulation will normalise the osmolarity when there is a low water intake?

A

Low water intake

Lower ECF volume, Higher Sodium conc.

higher osmolarity

Hyperosmotic urine production

Osmolarity normalised

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11
Q

What does water require in order to be absorbed passively?

A

A gradient

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12
Q

What is the osmotic status of the medullary interstitium?

A

The medullary interstitium needs to be hyperosmotic for water reabsorption to occur from the Loop of Henle and Collecting Duct

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13
Q

What is /isnt absorbed in the descending loop of henle?

A

Water is passively reabsorbed

Salt is not reabsorbed

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14
Q

What is / isn’t absorbed in the ascending loop of henle?

A

Active and passive reabsorption of Salt

No Water reabsorption

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15
Q

Where does ADH act?

A

On the collecting duct and distal convoluted tubule

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16
Q

Describe the process of countercurrent multiplication?

A
  1. Active Salt reabsorption
  2. Passive water reabsorption

Firstly, there is active salt reabsorption from the thick ascending limb of the LOH. That leads to an increased salt conc. in the intermedullary interstitium —> water from the descending limb leaves the descending limb by osmosis.

Tubular fluid then reaches the thin ascending LOH and it is hyperosmolar and this means salt must passively be reabsorbed to reduce the osmolarity of the tubular fluid

Then the new filtrate arrives at the descending limb and the process starts again. There is multiplication each time it occurs.

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17
Q

What does counter-current multiplication generate?

A

Forms a gradient from the top of the loop of Henle to the bottom in the medullary interstitium

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18
Q

Describe the process of Urea recycling

A
  1. Urea enters into the collecting duct
  2. Some leaves via the UT-A1 (Apical membrane) and UT-A3 (Basolateral) transporters into the medullary interstitium
  3. Then, the urea is either reabsorbed into the blood (Vasa Recta) through the UT-B1 transporter, or reabsorbed into the THIN DESCENDING LIMB (LOH) using UT-A2
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19
Q

What is the result of Urea recycling?

A
  1. Urine concentration occurs
  2. Urea excretion requires less water
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20
Q

Describe the effect of vasopressin in Urea recycling?

A

Vasopressin boosts UT-A1 and UT-A3 numbers

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21
Q

Which membrane is UT-A1 in?

A

Apical

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22
Q

Which membrane is UT-A3 in?

A

Basolateral

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23
Q

What is the main function of ADH?

A

Promote water reabsorption from the collecting duct

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24
Q

Where is ADH stored?

A

Posterior Pituitary

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25
Q

Where is ADH produced?

A

Hypothalamus (neurones in supraoptic and paraventricular nuclei)

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26
Q

What are the main stimulatory factors for ADH release?

A

Increased plasma osmolarity

Decreased blood pressure

Nausea
Angiotensin II
Nicotine

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27
Q

What are the main inhibitory factors for ADH production and release?

A

decreased plasma osmolarity

Hypervolemia = high blood pressure

Ethanol
Atrial Natriuretic Peptide

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28
Q

What percentage change in blood pressure is required for detection by baroreceptors?

A

5-10%

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29
Q

What detects the fluctuation in plasma osmolarity?

A

osmoreceptors in the hypothalamus

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30
Q

Describe the mechanism of action of ADH?

A

ADH binds to V2 receptor

Binds G protein

This activates Adenylate cyclase - ATP-> cAMP

This activate protein kinase A

This leads to increased vesicle transport of Aquaporin 2 molecules to the apical membrane

Water then reabsorbed into the blood through AQP2 on the apical and AQP3 and AQP4 on the basolateral side into the blood

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31
Q

What is meant by diuresis?

A

Increased dilute urine excretion

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32
Q

During diuresis, how much ADH is present

A

Zero or small amounts

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33
Q

Describe how the reabsorption of salt in the thick ascending limb of the LOH contributes to diuresis?

A

Na+ K+ ATPase Pump on basolateral side pumps Na+ into blood

K+ Cl+ Symporter on basolateral - pumps both into the blood

Na+ k+ 2Cl- symporter on the apical side

All work to increase the absorption of Na and Cl into the blood

34
Q

How much water and salt is reabsorbed into the proximal collecting duct?

A

2/3 of salt and water

35
Q

The fluid which comes out the LOH is what osmotic state?

A

Hypoosmotic

36
Q

Describe how reabsorption in the distal convolute tubule contributes to diuresis?

A

Active Na + Cl reabsorption through ATPase pumps and symporters

37
Q

Describe how reabsorption in the principal cells contribute to diuresis

A

Na+ K+ ATPase Pumps pump sodium into the blood

Some water reabsorption into blood via paracellular pathways (as no ADH so no AQP) to counteract

38
Q

What type of urine is produced during diuresis?

A

Hypoosmotic - dilute urine, alot of water

39
Q

What is meant by anti-diuresis?

A

When concentrated urine is produced (low volumes)

40
Q

How much ADH is present in state of anti-diuresis?

A

Alot

41
Q

What are the three ways in which ADH supports Na+ reabsorption?

A
  1. Thick ascending limb = increasing Na+ K+ 2Cl- symporter
  2. Distal convoluted tubule = increased Na+ Cl- symporter
  3. Collecting duct = Increasing Na+ channels
42
Q

What are the three ADH related clinical disorders?

A

AVP deficiency (Cranial Diabetes Insipidus)

SIADH

AVP resistance (Nephrogenic diabetes Insipidus)

43
Q

What is the cause of central diabetes insipidus?

A

Decreased production / release of ADH

44
Q

What are the clinical features of CDI?

A

Polyuria and PolyDipsia

45
Q

What is the treatment for CNI?

A

external ADH

46
Q

What is the cause of SIADH?

A

Increased production and release of ADH

47
Q

What are the clinical features of SIADH?

A

Hyperosmolar urine
Hypervolemia
Hyponatremia

48
Q

What is the treatment for SIADH?

A

Non-peptide inhibitor of ADH receptor (Conivaptan & Tolvaptan)

49
Q

What is the cause of nephrogenic Diabetes Insipidus?

A

Less / mutant AQP2
Mutant V2 receptor

50
Q

What are the clinical features of Nephrogenic diabetes insipidus?

A

Polyuria and Polydipsia

51
Q

What is the treatment for nephrogenic diabetes insipidus

A

Thiazide diuretics + NSAIDs

52
Q

Describe how there is a net addition of metabolic acid in the body?

A

Diet + Metabolism -> Acid + Base -> Base then excreted in the faeces

53
Q

How is metabolic acid neutralised?

A

Through the bicarbonate buffer system

54
Q

what is the problem with the bicarbonate buffer system?

A

Only a certain amount of bicarbonate in the ECF compartment, therefore has to be replenished

55
Q

How do the kidneys have a role in acid base regulation?

A

Reabsorption of Bicarbonate

Production of new bicarbonate

56
Q

If the cause of an acid base disorder is the partial pressure of carbon dioxide, what is the type of disorder?

A

respiratory disorder

57
Q

If the cause of an acid base disorder is the concentration of bicarbonate, what is the type of disorder?

A

Metabolic

58
Q

Which part of the kidneys is most of the bicarbonate absorbed into?

A

The proximal collecting tubule

59
Q

What is the enzyme which is needed to convert carbon dioxide into bicarbonate?

A

Carbonic anhydrase

60
Q

Describe how bicarbonate is reabsorbed into the proximal convoluted tubule?

A

HCO3- is reabsorbed via the Na+ HCO3- symporter (3 x HCO3- for each Na+)

H+ back into the tubular fluid through Na+ - H+ antiporter (NHE3) and H+ ATPase pump (V-ATPase Pump)

61
Q

How does CO2 enter into the cells of the kidney?

A

Diffusion

62
Q

What happens in the alpha intercalated cells of the distal convoluted tubule?

A

HCO3- reabsorption and H+ secretion

63
Q

What happens in the beta intercalated cells of the distal convoluted tubule?

A

HCO3- secretion and H+ reabsorption

64
Q

Which cells of the distal convoluted tubule are active during alkalosis?

A

Beta cells

65
Q

Which cells of the distal convoluted tubule are active during acidosis?

A

Alpha intercalated

66
Q

How is bicarbonate reabsorbed in the alpha intercalated cells?

A

Cl- HCO3- antiporter

67
Q

How is bicarbonate excreted in the B-intercalated cells?

A

Through the Cl- HCO3- anti-porter on the apical side (into the tubular fluid)

68
Q

What needs to happen in the proximal convoluted tubule in order for new bicarbonate production to occur?

A

The ammonia which is generated as a result of the breakdown of Glutamine needs to be removed, otherwise they will just neutralise the bicarbonate produced

69
Q

What buffer system helps new bicarbonate to be produced in the distal convoluted tubule?

A

Phosphate buffer system

70
Q

How is new bicarbonate produced in the distal convoluted tubule?

A

Bicarbonate is absorbed into the blood via the Cl- and HCO3- anti-porter, and the H+ then reacts to form phosphoric acid, so it is unable to react with the bicarbonate

71
Q

What are the characteristics of metabolic acidosis?

A

Low bicarbonate and Low pH

72
Q

What are the characteristics of metabolic alkalosis?

A

high bicarbonate and high pH

73
Q

What are the characteristics of respiratory acidosis?

A

High pCO2 and Low pH

74
Q

What are the characteristics of respiratory alkalosis?

A

Low pCO2 and High pH

75
Q

Describe the compensatory response to metabolic acidosis?

A

respiratory compensation - Hyperventilation, so pCO2 decreases, H+ decreases and HCO3- reabsorption and production increases

76
Q

Describe the compensatory response to metabolic alkalosis?

A

respiratory compensation - Hypoventilation, so pCO2 increases, H+ increases and HCO3- excretion increases

77
Q

What is the acute compensatory mechanism which occurs in response to respiratory acidosis and alkalosis?

A

Intracellular buffering, where the H+ ions are neutralised by cellular proteins

78
Q

A patient reported to his GP complaining of stomach bloating, swelling in legs, headache, and fatigue. Urine dipstick test results showed high specific gravity, and further urine analysis showed high [Na+]. Blood tests showed decreased plasma [Na+]. What is the most plausible diagnosis and treatment?

A

Syndrome of Inappropriate ADH release, treat with non-peptide inhibitor of ADH

79
Q

What is the compensatory mechanism for chronic respiratory acidosis?

A

Increased bicarbonate reabsorption and production

80
Q

What is the compensatory mechanism for chronic respiratory alkalosis?

A

Decreased bicarbonate reabsorption and production

BRS UROLOGY & RENAL (11 decks)

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