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Uro > Renal regulation of water and acid-base balance > Flashcards

Renal regulation of water and acid-base balance Flashcards

1
Q

How do you calculate osmolarity?

A

Concentration x No. of Dissociated Particles
size of molecule doesn’t matter

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2
Q

What is osmotic pressure directly proportional to?

A

No. of Solute Particles

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2
Q

What are the units for osmolarity?

A

Osm/L or mOsm/L

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2
Q

Calculate the osmolarity for 100mmol/L of glucose

A

Osmolarity = 100 x 1 particle = 100 mOsm/L

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3
Q

Calculate the osmolarity for 100mmol/L of NaCl

A

Osmolarity = 100 x 2 particles (Na+, Cl-) = 200 mOsm/L

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4
Q

Osmolarity

A

Osmoles per 1L of solvent

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5
Q

Osmolality

A

number of solute particles in 1 kg of solvent
Can be measured

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6
Q

Body fluid distribution

A

1/3 - Extracellular fluid
1/4 - intravascular (plasma)
3/4 - extravascular
95% interstitial fluid
5% transcellular fluid
2/3 - Intracellular fluid

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7
Q

What are some examples of unregulated water loss?

A

Sweat, released for temp homeostasis
Faeces, to allow easy excretion
Vomit,
Water evaporation from resp lining and skin

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8
Q

What is an example of regulated water loss?

A

Renal urine production

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9
Q

Explain how renal regulated water loss works for a positive water balance

A

Positive water balance = too much water in blood, decreased osmolarity -> hypoosmotic urine production

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10
Q

Explain how renal regulated water loss works for a negative water balance

A

Negative water balance = too little water in blood, increased osmolarity -> hyperosmotic urine production

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11
Q

Explain how countercurrent multiplication in the loop of henle works?

A

Water passively diffuses out of descending limb. Ions are actively pumped out of ascending limb. This leads to even more water passively diffusing out of descending limb. The remaining fluid is even higher in concentration, so more ions are actively pumped, until the highest concentration of medulla (1200 mOsm) is reached - at the base of loop of henle. Top of loop of henle is less concentrated as ions are actively pumped out from the bottom of the ascending loop first.

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12
Q

Explain how urea recycling works

A

Urea is freely filtered in the PCT. Urea passively enters the descending loop of henle via the UT-A2 transporter. Urea cannot leave the ascending loop nor DCT. In the collecting duct, ADH stimulates UT-A1 and UT-A3 transporters to bind to cell membrane, allowing urea to leave the collecting duct. The remaining urea re-enters the descending loop of henle (hence recycling), or enters blood supply via UTB-1 (vasa recta)

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12
Q

Why is it beneficial for vasopressin to stimulate urea reabsorption in the collecting duct?

A

Urea recycling requires less water than urea remaining in the urine - net positive effect and blood water levels

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13
Q

Role of NaCl and urea in the interstitium

A

Responsible for generating a hyperosmotic medullary interstitium

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14
Q

Where is vasopressin produced?

A

Supraoptic and Paraventricular Nuclei of Hypothalamus

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15
Q

How much change in blood volume is required for the hypothalamus to be alerted, and through what receptor does this occur?

A

5-10% plasma osmolarity, through baroreceptors

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16
Q

What are examples of stimulatory stimuli for ADH production and release?

A

Increased plasma osmolarity, decreased blood pressure, hypovolemia, nausea, ang II, nicotine

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17
Q

What are examples of inhibitory stimuli for ADH production and release?

A

Decreased plasma osmolarity, increased blood volume, hypervolemia, ethanol, Atrial Natiuretic Peptide

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18
Q

Explain the mechanism of action of ADH

A

ADH binds to V2 receptor on collecting duct (attached to G protein). G protein activates adenyl cyclase converts ATP to cAMP, leading to protein kinase A upregulating expression of aquaporin 2. Attach both to apical cell membrane for more water reabsorption

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19
Q

Explain how NaCl reabsorption occurs in the thick ascending loop of henle

A

Na+.K+.2Cl- Symporter moves all of these ions from lumen into cell.
Na+/K+ ATPase pump moves sodium into blood.
K+.Cl- Symporter moves these ions into blood

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20
Q

Explain how NaCl reabsorption occurs in the distal convoluted tubule

A

Na+.Cl- Symporter moves these ions from lumen into cell. Na+/K+ATPase pump moves sodium into blood. K+.Cl- Symporter moves ions into blood. (ONLY DIFFERENCE is Na+.Cl- Symporter)

20
Q

Main function of ADH aka AVP

A

promotes water reabsorption form the collecting duct

20
Q

Explain how Na+ reabsorption occurs in the collecting duct

A

Na+ diffuses into principal cell. Enters blood via Na+/K+ ATPase Pump (NOTICE how only sodium)

21
Q

What is Central diabetes insipidus otherwise known as?

A

AVP deficiency

22
Q

What is nephrogenic diabetes insipidus otherwise known as?

A

AVP resistance

23
Q

Causes of AVP deficiency

A

Decreased production and release of AVP(ADH)

24
Q

Clinical features of AVP deficiency

A

Polyuria
Polydipsia

25
Q

Treatment of AVP deficiency

A

External AVP(ADH)

26
Q

Causes of AVP resistance

A

Less/mutant AQP2
Mutant V2 receptor

27
Q

Clinical features of AVP resistance

A

Polyuria
Polydipsia

28
Q

Treatment of AVP resistance

A

Thiazide diuretics - help w/ symptom control
NSAIDs

29
Q

When would a change in loop of henle/DCT/collecting duct cause antidiuresis?

A

Supported Na+ and Cl- reabsorption in any of these areas (water follows ions)

30
Q

What is a condition where ADH is in excess?

A

SIADH - Syndrome of Inappropriate ADH Release

31
Q

Cause of SIADH

A

increased production/release of ADH

32
Q

Clinical features of SIADH

A

Hyperosmolar urine
Hypervolemia - due to fluid retention
Hyponatremia
Hypoosmotic blood - fluid release via urine

33
Q

Treatment of SIADH

A

ADH receptor antagonists

34
Q

What does ADH regulate

A

the number of AQP2 channels on both the apical and basolateral membranes of the principal cells.

35
Q

Role of kidneys in acid-base balance

A

secretion/excretion of H+
Reabsorption of HCO3-
Production of new HCO3- (in the case of respiratory acidosis)

36
Q

What causes respiratory disorders

A

CO2 partial pressure changes

37
Q

What causes metabolic disorders

A

HCO3- concentration changes

38
Q

Where does the majority of HCO3- reabsorption occur

A

proximal convoluted tubule

39
Q

How does HCO3- act as a buffer?

A

Binds to free H+ ions, forming carbonic acid (H2CO3), which can dissociate to water and CO2

40
Q

Cells controlling AB homeostasis in the DCT/CD

A

alpha-intercalated cell and beta intercalated cell

41
Q

Role of alpha-intercalated cell

A

HCO3- reabsorption/H+ secretion

42
Q

Role of beta intercalated cell

A

HCO3- secretion/H+ reabsorption

43
Q

How does resorption of HCO3- occur at the alpha-intercalated cell?

A

Convert water and CO2 to H+ and HCO3-, H+ leaves cell into tubule via H+ ATPase pump and H+/K+ ATPase pump. HCO3- enters blood via HCO3-/Cl- antiporter (no sodium transporter as too far across nephron)

44
Q

How does resorption of H+ occur at the beta-intercalated cell?

A

Convert water and CO2 to H+ and HCO3-, HCO3- leaves cell into tubule via HCO3-/Cl- antiporter. H+ enters blood via H+ ATPase pump

45
Q

How is new HCO3- produced in the PCT

A

Glutamine converted into NH4+ and HCO3-
Both leave via diffusion

46
Q

How is new HCO3- produced in the DCT/CD

A

alpha intercalated cells use carbonic anhydrase to convert H20 + CO2 -> HCO3-

47
Q

Metabolic acidosis

A

low bicarbonate/ low pH
Increase ventilation and HCO3- reabsorption and production

48
Q

Metabolic alkalosis

A

Increased bicarbonate/high pH
Decreased ventilation and increase HCO3- excretion

49
Q

What is the acute compensatory response to respiratory acidosis/alkalosis?

A

Intracellular buffering (basically proteins that hold onto the H+ temporarily)

50
Q

What is the chronic compensatory response to respiratory acidosis/alkalosis?

A

Respiratory acidosis: Increased HCO3- resorption, production (reverse for respiratory alkalosis)

Uro (7 decks)

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