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Block 1 > Tubular Processing and Electrolyte Balance > Flashcards

Tubular Processing and Electrolyte Balance Flashcards

1
Q

At which part of the nephron does the majority of water and sodium reabsorption take place?

A

Proximal convoluted tubule

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2
Q

How is glucose reabsorbed in the PCT?

A

Na+/K+ATPase creates a negative concentration gradient between the lumen of the PCT and the epithelial cells, causing Na+ to move down its concentration gradient into the cells via SGLT(usually SGLT2), taking glucose with it.

Glucose is transported from the cell to the blood across the basolateral membrane via GLUT transporters.

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3
Q

How are amino acids reabsorbed in the PCT?

A

Following the concentration gradient created by Na+/K+ATPase on the basolateral membrane, Na+ moves down its concentration gradient from the lumen into the cell, using co-transporters that also take up amino acids.

Amino acids then diffuse out of the basolateral membrane into the blood.

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4
Q

How can glucose appear in the urine?

How does this cause increased urine output?

A

High levels of blood glucose can cause SGLT transporters in the PCT to reach their transport maximum where they cannot facilitate reabsorption any faster.

Excess glucose is not reabsorbed and is lost in the urine. Glucose is osmotically active so causes water retention in the lumen. This causes osmotic diuresis.

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5
Q

How is Na+ reabsorbed in the PCT?

A
  • SGLT with glucose
  • Amino acid co-transporter
  • Na+/H+ exchanger
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6
Q

How is sodium reabsorbed in the thick ascending loop of Henle?

How are other solutes reabsorbed

A

Primarily mediated by Na+/K+/2Cl- co-transporter

K+ moves freely out of the cell causing a positive charge in the lumen encouraging paracellular reabsorption of cations (Mg2+, Ca2+)

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7
Q

How are water and solutes reabsorbed in the early distal convoluted tubule?

A

Via Na+/Cl- co-transporter

Water permeability controlled by ADH:

  • Water permeable when ADH present
  • Impermeable when ADH not present
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8
Q

What are the 2 main epithelial cell types in the late distal convoluted tubule and cortical collecting duct?

What are their roles?

A

Principal cells:

  • Sodium reabsorption
  • Potassium excretion

Intercalated cells:

  • Potassium reabsorption
  • H+ secretion
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9
Q

How is sodium reabsorption controlled in principal cells?

A
  • Enters the cell through Na+ (ENaC) channels
  • Na+/K+ATPase moves sodium out of the cell to maintain concentration gradient.

Number of ENaC channels and activity of Na+/K+ATPase is under hormonal control of aldosterone.

Sodium is reabsorbed at the expense of potassium, therefore aldosterone has an important role in sodium and potassium homeostasis.

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10
Q

What is the role of aldosterone? Where is its site of action?

A

Collecting tubule and duct

  • Increases NaCl and H2O reabsorption
    • Increases production of proteins (ENaC, Na+/K+ATPase)
  • Increases K+ secretion
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11
Q

What is the role of angiotensin II in the kidneys? Where is its site of action?

A
  • Proximal convoluted tubule
  • Thick ascending loop of Henle
  • Distal convoluted tubule
  • Collecting duct

Increases NaCl and H2O reabsorption

Increases H+ secretion

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12
Q

What is the role of antidiuretic hormone in the kidney?

What is its site of action?

A
  • Distal convoluted tubule
  • Collecting tubule and duct

Increases H2O reabsorption

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13
Q

What is the role of atrial natriuretic peptide in the kidney?

What is its site of action?

A
  • Distal convoluted tubule
  • Collecting tubule and duct

Decreases NaCl reabsorption

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14
Q

What are the roles of parathyroid hormone in the kidney?

What are its sites of action?

A
  • Proximal convoluted tubule
  • Thick ascending loop of Henle
  • Distal convoluted tubule

Decreases PO4 reabsorption

Increases Ca2+ reabsorption

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15
Q

What are the main osmotically active cations in intracellular and extracellular fluid?

A

Intracellular: Potassium

Extracellular: Sodium

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16
Q

How do the kidneys maintain extracellular fluid volume?

A

By controlling sodium reabsorption and secretion:

  • Local control (pressure diuresis/natriuresis)
  • Hormonal control (RAAS system)
  • Neural control (sympathetic activation)
17
Q

What is pressure diuresis?

A

Kidneys excrete more sodium in response to raised arterial blood pressure.

18
Q

Describe the hormonal control of extracellular fluid volume

A

Renin release is triggered by:

  • Low afferent arteriolar pressure
  • Activation of sympathetic nerves that supply JGA
  • Low [NaCl] in distal convoluted tubule

All of these are markers of drop in blood pressure/ extracellular volume

19
Q

Describe the renin-angiotensin-aldosterone system

A
  1. Renin is released in response to:
    • Low afferent arteriole pressure
    • Activation of sympathetic nerves that supply JGA
    • Low [NaCl] in late DCT.
  2. Renin converts angiotensinogen from the liver into angiotensin I
  3. Angiotensin I is converted to angiotensin II by angiotensin coverting enzyme (ACE) in the lungs.
  4. Angiotensin II:
    • Causes vasoconstriction to raise BP
    • Increases sodium and water reabsorption in kidneys
    • Triggers release of aldosterone from adrenal glands.
  5. Aldosterone increases sodium and water retention in kidneys.
20
Q

What are the actions of angiotensin II?

A

Direct effects:

  1. Binds to intracellular mineralocorticoid receptors
  2. Transported to and binds to nucleus
  3. Increases production of proteins (e.g. ENaC, Na+/K+ATPase) which increase the cell’s ability to absorb sodium.

Indirect effects (to increase BP)

  1. Increases thirst, release of ADH and aldosterone
21
Q

What are the actions of atrial natriuretic peptide?

A

Released by atrial muscle fibres in the heart in response to stretch (e.g. due to excessive blood volume)

  • Inhibits NaCl (and therefore water) reabsorption by the kidney.
  • Causes small increases in GFR
  • Decreases renal absorption

Opposite effect to angiotensin II

22
Q

What electrolyte is a major determinant of resting membrane potential?

What are the consequences of changes to extracellular concentration?

A

Potassium

Changes in extracellular concentration can cause cardiac arrhythmias

23
Q

Where is the majority of potassium located in the body?

A

Intracellular compartment

(98%)

24
Q

How is short term control of extracellular potassium regulated?

A

By moving potassium between the extracellular and intracellular compartments

25
Q

Which factors decrease extracellular potassium by moving it to the intracellular compartment?

How do they do this?

Which of these is used as part of emergency treatment of hyperkalaemia?

A
  • Insulin
  • Aldosterone
  • B-adrenergic stimulation
  • Alkalosis

Increase Na+/K+ATPase activity and encourage cellular uptake of potassium

Insulin used as part of emergency treatment of hyperkalaemia

26
Q

How does aldosterone decrease levels of extracellular K+?

A

Increases urinary excretion

27
Q

What factors increase extracellular K+ by moving it into the extracellular compartment?

A
  • Insulin deficiency (DM)
  • Aldosterone deficiency (Addison’s disease)
  • B-adrenergic blockade
  • Acidosis
  • Cell lysis
  • Increased ECF osmolarity
  • Strenuous exercise
28
Q

How does acidosis increase extracellular K+?

A

Decreases the activity of Na+/K+ATPase

29
Q

How does increased extracellular fluid osmolarity increase extracellular K+ concentration?

A

Increased ECF osmolarity causes cellular dehydration therefore increased intracellular concentration of K+.

This results in a larger concentration gradient to move K+ out of the cell.

30
Q

What causes the majority of renal potassium excretion?

A

The amount of secretion in the late DCT and cortical collecting tubule

  • Under the control of aldosterone
31
Q

How is renal excretion calculated?

A

Renal excretion = filtration - reabsorption + secretion

32
Q

How is potassium secreted into the tubular lumen?

What is the rate controlled by?

A
  • Na+/K+ATPase moves sodium out of the cell and potassium in, creating a high intracellular K+ concentraiton.
  • K+ then flows out of BK and ROMK channels in the tubular lumen following its concentration gradient.

Rate controlled by:

  • Activity of Na+/K+ATPase
  • K+gradient between blood, principal cell and lumen
  • Permeability of luminal membrane to K+
33
Q

What are the 4 factors that regulate potassium secretion?

A

Increases K+ secretion:

  • Increased plasma K+ concentration:
    • Increases concentration gradient between blood, cell and lumen.
    • Increases activity of Na+/K+ATPase
    • Increases aldosterone release
  • Increased aldosterone:
    • Increases permeability of luminal membrane to K+
    • Increases Na+/K+ATPase activity
  • Increased luminal flow rate:
    • Increases permeability of luminal membrane to K+
    • Increases K+ concentration gradient between principal cell and lumen

Decreases K+ secretion:

  • Increased H+ concentration:
    • Decreases Na+/K+ATPase activity
    • (why acidotic conditions are often accompanied by hyperkalaemia)
34
Q

What is the effect of increased plasma potassium concentration on aldosterone?

A

Increasing plasma concentration of potassium increases the effects of aldosterone.

35
Q

How can tubular flow rate be increased?

A
  • Volume expansion
  • High sodium intake
  • Diuretics
36
Q

How does a high tubular flow rate maintain K+ excretion when aldosterone release is reduced by high Na+ levels?

A

High Na+ will reduce aldosterone levels reducing K+ secretion, however it also:

  • Increases GFR
  • Decreases proximal tubular Na+ reabsorption

These increase the distal tubular flow rate which increase K+ secretion by reducing the concentration of K+ in the lumen and increasing permeability of luminal membrane to K+.

Some excretion of potassium therefore is maintained, meaning the overall excretion of potassium is relatively unchanged.

37
Q

What is the normal extracellular (serum) K+ range?

A

3.5-5.3 mmol/L

38
Q

What are the common causes and symptoms of hypokalaemia?

How is it treated?

A

Causes:

  • Low dietary intake
  • Excessive losses e.g. diarrhoea, aldosterone excess, diuretics
  • Altered body distribution

Symptoms:

  • Muscle weakness
  • Cardiac arrhythmias
  • (Often asymptomatic)

Treatment:

  • Address underlying cause
  • Potassium supplementation if needed
39
Q

What are the causes, symptoms and treatment approaches to hyperkalaemia?

A

Causes:

  • High dietary intake
  • Inadequate losses e.g. kidney disease, aldosterone deficiency
  • Altered distribition e.g. acidosis

Symptoms:

  • Often asymptomatic
  • Cardiac arrhythmias (tall T waves on ECG)

Treatment:

  • Restrict intake
  • Address underlying cause
  • Calcium gluconate to stabilise myocardium
  • Insulin (with glucose) to drive potassium into cells
  • Aid excretion: fluids, ion-exchange resins, dialysis.

Block 1 (31 decks)

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