renal regulation Flashcards

1
Q

What is osmosis? What is the force involved? What is it dependent on?

A

Flow of water from low solute concentration to high solute concentration till equillibrium is reached. Force is osmotic/oncotic pressure & depends on number of solute particles not size

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2
Q

How do you calculate osmolarity?

A

Osmolarity (mOsm/L) = concentration x number of dissociated particles (for glucose 1 for NaCl 2)

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3
Q

What is the body fluid distribution in the body?

A

2/3 intracellular, 1/3 ECF (intesrstitial, plasma, transcellular)

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4
Q

What will a high water intake cause?

A

Increase volume of ECF and decrease osmolarity. Kidneys will produce hypoosmotic urine to lose excess water and normalize ECF.

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5
Q

What will dehydration cause?

A

Decrease volume of ECF, osmolarity increased. Kidneys produce hyperosmolar (concentrated) urine to reabsorb more water

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6
Q

What are methods of unregulated water loss?

A

Sweat, faeces, vomit, water evaporation from respiratory lining and skin

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7
Q

How is water reabsorbed in the kidney? Where is it reabsorbed?

A

Most of water reabsorbed in PCT (67%). In descending limb of loop of henle water passively reabsorbed (15%). No water reabsorbed in rest of loop. Variable amounts of water reabsorbed at collecting duct.

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8
Q

What is needed for water to be passively reabsorbed

A

equires a gradient so medullary interstitium must be hypertonic to allow water reabsorption in loop of henle and collecting duct

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9
Q

Where is salt reabsorbed/how in the kidney?

A

In PCT (67%), passively in thin ascending loop and actively reabsorbed in thick ascending loop in order to make medullary interstitium hypertonic, to allow water to be passively reabsorbed

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10
Q

What is the countercurrent multiplier process and what does it achieve?

A

Salt actively reabsorbed in thick ascedning limb so sodium falls inside and rises in medullary interstitium making it hypertonic. Water will flow out into medullary interstitium via descedning limb passively to equilibrate this.

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11
Q

What are vasa recta?

A

Series of capillaries that surround nephron

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12
Q

How is urea recycled?

A

Urea filtered through bowman’s capsule & reaches collecting duct where it moves with transporters UT-A1 & UT-A3 into the medullary interstitium. From here it can either go into vasa recta via UT-B1 or enter thin ascedning limb via UT-A2 to be recycled.

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13
Q

how does urea recycling affect water reabsorption?

A

Some of urea enters medullary interstitiuma and increases osmolarity so water passively reabsorbed. Urea excretion requires less water.

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14
Q

How does ADH affect urea reabsorption?

A

ADH increases UT-A1 & UT-A3 numbers so has role in urea reabsorption.

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15
Q

What is mechanism of ADH? What is it stimulated by and inhibited by?

A

Acts on V2 receptor (activated G protein activates protein kinase A) and signalling cascade causes secretion of aquaporin-2 channels inserted into apical membrane so water reabsorbed from collecting duct. Stimulated by increased plasma osmolarity, decreased blood pressure/volume, nausea, angiotensin II, nicotine. Inhibited by decreased plasma osmolarity, increased blood pressure/volume, ethanol, atrial natriuretic peptide (ANP)

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16
Q

What happens during diuresis?

A

Diuresis is dilute urine excretion. Isoosmotic fluid enters loop and hypo-osmotic fluid leaves loop. In DCT salt gets reabsorbed but water channls closed because no acquaporin and same in collecting duct. So when urine exists its more hypoosmolar than plasma

17
Q

What happens during anti-diuresis?

A

ADH high, salt actively reabsorbed in thick ascedning, DCT, collecting duct. ADH supports sodium reabsorption by increasing symporters/channels in these places. Water reabsorbed in DCT and collecting duct (ADH) so urine leaves is hyperosmolar compared to plasma

18
Q

How does ADH support sodium reabsorption?

A

By increasing symptorters/channels in following places. Na-K-Cl transporter in thick ascedning limb. Na-Cl symporter in DCT. Na channel in collecting duct.

19
Q

What is central diabetes inspirius? Presentation? Treatment?

A

Decreased/no release of ADH. Polyuria/polydypsia/hypernatraemia. Desmopressin (external ADH)

20
Q

What is syndrome of inappropriate ADH secretion SIADH? presentation? treatment?

A

Incrreased production/release of ADH. Hyperosmolar urine, hypervolemia, dilutional hyponatreamia. Non-peptide inhibitor of ADH (conlvaptan & tolvaptan)

21
Q

What is nephrogenic diabetes inspididus? Presentation? Treatment?

A

Less/mutant AQP2, mutant V2 receptor. Polyuria/polydypsia. Thiazide diuretics + NSAIDS

22
Q

What is the role of bicarbonates?

A

neutralises metabolic acid

23
Q

how do kidneys ensure we can deal with metabolic acid?

A

Reaabsorption of almost all bicarbonate ions, production of new bucarbonate ions by kidney, secretion & excretion of H+ to prevent acidosis

24
Q

Where are bicarbonate ions reabsorbed in kidney?

A

Most in PCT, some in thick ascedning loop of henle, DCT & collecting duct

25
Q

How is bicarbonate reabsorbed in PCT and loop of henle?

A

CO2 reaction with carbonic anhydrate makes proton + bicarbonate. Proton ion enters tubular fluid by either 1. sodium-hydrgen antiporter using energy of sodium travel 2. proton-ATPase pump. Bicarbonate ion reabsorbed into blood via sodium-bicarbonate symporter.

26
Q

How is bicarbonate reabsorbed in DCT & collecting duct?

A

Proton pumped into tubular fluid by proton ATPase pump and proton potassium ATPase in a-intercalated cell and bicarbonate back into blood via choride-bicarboante antiproter.

27
Q

How do a-intercalated cells & β-intercalated cells work?

A

A-intercalated cells are for bicarbonate reabsorption and proton excretion so excrete proton to tubular fluid via proton ATPase pump & proton-potassium ATPase, and reabsorb bicarbonate into blood via chloride-bicarbonate antiporter. Β-intercalated do opposite, in alkalosis, use chloride-bicarbonate antiporter to excrete bicarbonate into tubular fluid and reabsorbs protons by proton-ATPase pump.

28
Q

How is new bicarboanate ion produced in PCT? What is net gain?

A

gluamine converted to 2 ammonium ions & 2 bicarbonate ions. ammonium ions are excreted into tubular fluid. net gain of 2 bicarbonate ions that are reabsorbed into blood

29
Q

How is new bicarbonate produced in DCT & collecting duct? Net gain?

A

proton going into tubular fluid (potassium-proton antiporter) neutralised by non-bicarbonate buffer (eg phosphate buffer system) to exit body. So we gain molecule of bicarbonate that enters blood to be used

30
Q

What happens in metabolic acidosis and how do we compensate?

A

Low bicarbonate so low pH. Hyperventilation, increased bicarbonate reabsorption + production

31
Q

What happens in metabolic alkalosis and how do we compensate

A

High bicarbonate high pH. Hypoventilation, increased bicarbonate excretion

32
Q

What happens in respiratory alkalosis and how do we compensate?

A

Low CO2- high pH. Acutely via intracellular buffering. Chronically - decreased bicarbonate production & reabsorption

33
Q

What happens in respiratory acidosis and how do we compensate?

A

High CO2 - low pH. Acutely intracellular buffering. Chronically increased bicarbonate reabsorption & production