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Renal Regulation Flashcards

1
Q

What is Osmosis?

A

The movement of water across a semi-permeable membrane from an area of low solute concentration to an area of higher solute concentration until equilibrium is reached.

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2
Q

What is Osmotic pressure proportional to?

A

No. of solute particles

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3
Q

What is the formula for osmolarity?

A

Osmolarity = concentration x No. of dissociated particles = Osm/L or mOsm/L

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4
Q

Describe the distribution of fluids in the body

A

2/3 intracellular
1/3 extracellular

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5
Q

Unregulated water losses

A
  • Sweat
    • Faeces
    • Vomit
    • Water evaporation from respiratory lining and skin
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6
Q

Regulated water losses

A

renal - urine

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7
Q

When is there positive water balance?

A

High water intake = increased ECF volume in conjunction with low Na+ and low plasma osmolarity

This leads to hypoosmotic urine production which equilibrates osmolarity

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8
Q

When is there negative water balance?

A

Low water intake = reduced ECF volume and high Na+ in conjunction with high osmolarity.

This leads to hyperosmotic urine production —> equilibration of osmolarity

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9
Q

In what part of the nephron is the majority of water reabsorbed?

A

2/3s in the proximal convoluted tubule

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10
Q

In what part of the nephron can salt be reabsorbed but not water?

A

Ascending limb of the loop of Henle

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11
Q

In what part of the nephron is salt actively reabsorbed and where is it passively reabsorbed?

A

Actively in the thick portion of the ascending limb of the loop of Henle

Passively in the thin portion of the ascending limb of the loop of Henle

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12
Q

In what part of the nephron is water passively reabsorbed but not salt?

A

Descending limb of Loop of Henle

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13
Q

Why does the medullary interstitium need to be hyperosmotic?

A

To allow for an osmotic gradient to form, allowing PASSIVE reabsorption of water in the descending limb of the LOH and collecting duct

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14
Q

In what part of the nephron are variable levels of water reabsorbed?

A

DCT and Collecting duct

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15
Q

What is the name given to the process that results in the formation of a gradient in the medullary interstitium?

A

Countercurrent multiplication

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16
Q

Describe the process of countercurrent multiplication

A
  1. Active salt reabsorption in the thick ascending loop of Henle
    1. Passive water reabsorption in the thin descending loop of Henle

This process continues and results in an increase in osmolarity in the medullary interstitium

Concentration gradient is formed - most concentrated at the bottom of the loop of Henle

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17
Q

Describe the process of urea recyling

A
  1. Urea is moved out of the collecting duct
    a. Moved out of the apical side by UT-A1
    b. Moved out of the basolateral side by UT-A3
    1. It enters the interstitium -> increases osmolarity
    2. Then has 2 options
      a. One -> back into blood - by UT-B1
      b. Two -> renters into the thin descending loop of Henle - by UT-A2
      c. Some urea remains in the interstitium
    3. This concentrates urea - less water to remove
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18
Q

What is the purpose of urea recycling?

A

To increase the osmolarity of the interstitium ( allowing for urine concentration [ i.e less water loss] and secondly, urea excretion requires less water.)

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19
Q

Why does urea excretion requires less water?

A

A high tubular urea concentration will be matched with a high urea concentration in the interstitium and so rather than water entering the tubule, the urea equilibriates independently to minimise it’s effect on the osmolarity of the tubular fluid so water does not need to enter the tubule and urea can be excreted with less water

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20
Q

What effects does Vasopressin have on urea recycling?

A

Helps in boosting UTA1 and UTA3 as well as improving permeability in the collecting duct for urea.

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21
Q

What is ADH?

A

Anti-diuretic hormone, 9 amino acids long

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22
Q

What is the function of ADH?

A

Main function - Promotes water reabsorption from the renal collecting duct
Side quests - Urea and sodium reabsorption

23
Q
  • Specifically where is ADH produced?
A

Neurones in supraoptic and paraventricular nucleus of the hypothalamus

24
Q

Where is ADH stored?

A

Posterior pituitary

25
- What is the plasma osmolarity of a healthy adult (incl units)
275-290 mOsm/kg H2O
26
What are stimulatory factors influencing ADH production and release?
Increase in plasma osmolarity (sensed by osmoreceptors) Reduced blood pressure (Hypovolemia - baroreceptors can detect this once there is a change of 5-10%) Nausea Angiotensin II Nicotine
27
What are inhibitory factors influencing ADH production and release?
Hypervolemia (increased blood pressure) Ethanol —> dehydration Atrial Natriuretic peptide Decrease in plasma osmolarity
28
Describe the mechanism of action of ADH
ADH acts on the V2 receptor and this activates G protein to stimulate Adenylate Cyclase to convert ATP into cAMP cAMP activates Protein Kinase A and this allows the fusion of AQP2 and AQP3 channel vesicles into the apical membrane of CCD cells Water leaves the cells of the collecting duct via basolateral AQP4 channels
29
What is Diuresis?
Increased dilute urine excretion
30
What is Antidiuresis?
Concentrated urine in low volume excretion
31
What are the 3 ways through which ADH supports Na+ reabsorption in the kidney?
1) Thick ascending limb : increases Na+/K+/2Cl- symporter 2) Distal convoluted tubule : increased Na+/Cl- symporter 3) Collecting duct : increased sodium channels
32
What is the cause of central diabetes insipidus?
Decreased/negligent production and release of ADH Due to genetic reasons/ acquired reasons such as trauma.
33
What are the 2 main clinical features seen in CDI?
Polyuria and Polydipisa (excessive or abnormal thirst, accompanied by intake of excessive quantities of water or fluid)
34
How do you treat CDI?
External ADH
35
What is Syndrome of inappropriate ADH secretion? ( SIADH)
Increased production and release of ADH
36
What are the 3 main clinical features of SIADH?
Hyperosmolar urine Hypervolemia Hyponatremia
37
What is the treatment for SIADH?
Non-peptide inhibitor of ADH receptor (conivaptan and tolvaptan)
38
What is nephrogenic diabetes insipidus (NDI)?
Less/mutant AQP2 Mutant V2 receptor
39
- What are the clinical features of NDI?
Polyuria and Polydipsia
40
What is the treatment for NDI?
Thiazide diuretics —> reduce filtration rate at the Bowman's capsule so less blood filtered = lower urine production NSAIDs
41
What is the bicarbonate buffer system?
There is a net addition of metabolic acid and so to tackle this, bicarbonate buffers the decrease in pH
42
What is the role of the kidneys in maintaining an acid-base balance?
1) Secretion and excretion of H+ 2) Reabsorption of HCO3- 3) Production of new HCO3- - all to counter the net addition of metabolic acid ( 50-100 mEq/day)
43
What is occurring if the acid base disorder has a respiratory cause?
Changes in PCO2
44
What is occurring if the acid base disorder has a metabolic cause?
Changes in HCO3- concentration
45
Describe the distribution of reabsorption of the HCO3- ion in the nephron.
80% in PCT 10% in LOH 10% in DCT + CCD ( 4 and 6% respectively)
46
- What are the different intercalated cells in the DCT and CD and what is their function?
Alpha intercalated cells : HCO3- reabsorption and H+ secretion Beta intercalated cells : HCO3- secretion and H+ reabsorption
47
- When does the role of the beta intercalated cells become significant?
Alkalosis/ slight disbalance in the number of bicarbonate ions
48
Describe production of new HCO3- ions in the PCT.
1 glutamine gives rise to 2 ammonium ions and a divalent ion which gives rise to 2 bicarbonate ions which are transported back into the blood If the ammonia ions are not excreted, they will be taken in to the liver where they: 1 ammonia ion gives 1 urea ion and 1 proton in the liver The proton will again require the use of a bicarbonate ion for its neutralisation which nullifies the buffer it provides Therefore important that the 2 ammonia ions are excreted from the body and not returned into blood circulation Ammonia will either be excreted via Na+H+ antiporter or as Ammonia gas where it will form the ammonia ion again in the tubular fluid by binding to the proton
49
Describe production of new HCO3- ions in the DCT and CD.
Once proton reaches tubular fluid it can bind to non-bicarbonate base to act as a buffer for it e.g. Phosphate buffer system as seen above Bicarbonate is then rebsorbed via Cl-HCO3- antiporter The use of non-boicarbonate ion buffer systems, we can neutralise the protons in the tubular fluid = gain of a molecule of bicarbonate
50
Describe the characteristics of metabolic acidosis and the compensatory response associated with it.
Low pH and HCO3- Compensation involves Hyperventilation and increased reabsorption of HCO3-
51
Describe the characteristics of metabolic alkalosis and the compensatory response associated with it.
High pH and HCO3- Compensation involves hypoventilation and excretion of HCO3-
52
Describe the characteristics of respiratory acidosis and the compensatory response associated with it.
Low pH and high PCO2 Acute compensation : carbonic acid dissociates to form H+ and HCO3-, which then exits the RBC via the AE1 transporter. (Intracellular buffering) Chronic compensation : Increased HCO3- reabsorption and production
53
Describe the characteristics of respiratory alkalosis and the compensatory response associated with it.
High pH and low PCO2 Acute compensation : Intracellular buffering - more carbonic acid production Chronic compensation : Less HCO3- reabsorption and production

BRS Y2 (1 decks)

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