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LSS 2 > Urinary System 6 - Sodium and Potassium Balance > Flashcards

Urinary System 6 - Sodium and Potassium Balance Flashcards

1
Q

How does a high sodium diet affect body weight?

A
  • Eventually, over time, body weight will increase
  • This is because of decreased osmolarity of the tissues causing water to follow.
  • There is increased ECF volume
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2
Q

What is the effect of high dietary sodium on the blood volume and pressure?

A
  • High sodium results in increased ECF volume
  • This in turn causes increased blood volume and pressure, due to the increased water that has to be in the blood to maintain the osmolarity
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3
Q

List the percentages of sodium reabsorption in the different parts of the nephron

A
  • 65% in the PCT
  • 25% in the THICK ascending loop of henle
  • 8% in the distal convoluted tubule
  • 2% in the collecting duct (variable)
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4
Q

How does glomerular filtration rate affect sodium reabsorption?

A
  • Increased GFR results in increased sodium reabsorption
  • This is because the same proportion of sodium is absorbed at each point, but with that proportion being equal to a different volume.
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5
Q

Which processes, mediated by ion, occur when decreased sodium is detected at the juxtaglomerular apparatus?

A
  • Increased angiotensin II production causes increased sodium reabsorption at the PCT and increased aldosterone
  • Increased aldosterone causes increased reabsorption at the collecting duct and DCT
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6
Q

Which processes, mediated by the SNS are the result of increased sodium ion concentration in the blood?

A
  • Increased sympathetic activity
  • Increases reabsorption in the PCT and stimulates the juxtaglomerular apparatus
  • Causes vasoconstriction
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7
Q

List the functions of atrial naturietic peptide.

A
  • Increases GFR by affecting diameter of afferent and efferent arterioles
  • Inhibits renin and aldosterone release
  • Reduces blood pressure (vasodilation)
  • Inhibits sodium reabsorption at the PCT and in the collecting ducts
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8
Q

Describe the pathway from renin to aldosterone

A
  • Renin produced by the kidney
  • Catalyses conversion of angiotensinogen to angiotensin I in the liver
  • Angiotensin I converted to angiotensin II by ACE in the liver
  • Angiotensin II stimulates aldosterone release from the adrenal gland
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9
Q

List the stimulations of renin production

A
  • Decreased blood pressure
  • Increased sympathetic stimulation
  • Decreased fluid volume
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10
Q

List the effects of angiotensin II

A
  • Increased sodium uptake and water reabsorption at the proximal tubule
  • Results in increased ECF, and increased blood pressure
  • Also causes vasoconstriction
  • Also stimulates production of aldosterone at the adrenal gland
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11
Q

List the actions of aldosterone

A
  • Decrease in blood pressure via baroreceptors
  • Decreased osmolarity of the ultrafiltrate
  • Increased sodium reabsorption, and potassium/hydrogen ion secretion
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12
Q

What happens in aldosterone excess?

A

Hypokalaemic alkalosis

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13
Q

How does aldosterone work?

A
  • Diffuses through the cell membrane
  • Binds to receptors, releasing them from heat shock proteins
  • Two receptors form a complex, which acts as a transcription factor.
  • Increased sodium/potassium ATPase, increased sodium channels on the apical side of the membrane.
  • Also increases activation of channels
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14
Q

List the effects of hypoaldosteronism in the kiney

A
  • Reduced reabsorption of sodium in the distal nephron
  • Increased urinary loss of sodium
  • ECF falls and as a result there is increased renin, angiotensin II and ADH
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15
Q

List the symptoms that will be experienced in hypoaldosteronism

A
  • Dizziness
  • Low blood pressure
  • Salt craving
  • Palpatations
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16
Q

List the effects of hyperaldosteronism on the kidney

A
  • Increased reabsorption of sodium in the distal loop of Henle
  • Reduced urinary loss of sodium
  • ECF increases
  • Reduced renin, angiotensin II and ADP
  • Increased atrial natriuretic peptide and brain natriuretic peptode
17
Q

List the symptoms that will be experienced in hyperaldosteronism

A
  • High blood pressure
  • Muscle weakness
  • Polyurea
  • Thirst
18
Q

What is Liddles syndrome?

A
  • A disease of high blood pressure
  • Mutation in the aldosterone activated sodium channel, causing the channel to always be open
  • Results in sodium retention and hypertension
19
Q

List the baroreceptors that before the left ventricle

A
  • Atria
  • Right ventricle
  • Pulmonary vasculature
20
Q

List the baroreceptors after the left ventricle

A
  • Carotid sinus
  • Aortic arch
  • Juxtaglomerular apparatus
21
Q

Describe the process that happens when there is detection by receptors on the low pressure side

A
  • Low pressure causes signal through afferent fibres to the brainstem causes ADH release
  • Also recognise high pressure, resulting in ANP and BNP release
22
Q

Describe the process that happens when there is stimulation of receptors on the high pressure side

A
  • Detect low pressure only
  • Increase sympathetic activity
  • Release ADH
  • Renin secretion by JGA cells
23
Q

When and where is ANP made?

A
  • Made in the atria

- Released in response to atrial stretch

24
Q

List the different types of diuretic drugs

A
  • Osmotic diuretics (glucose and mannitol)
  • Carbonic anhydrase inhibitors
  • Loop diuretics (furosemide)
  • Thiazides (block Na/Cl cotransport)
  • K+ sparing diuretics
25
Q

How do carbonic anhydrase inhibitors work as loop diuretics?

A
  • Prevents entry of sodium into the cell via the Na/H+ antiporter
  • Therefore increases water in the tubular fluid
26
Q

How does furosemide work?

A

Blocks the triple cotransporter in the ascending loop of henle (sodium, calcium, potassium transporter)

27
Q

List the effects of extracellular potassium ions

A
  • High potassium depolarises membranes in action potentials

- Low potassium results in heart arrythmias

28
Q

What happens following potassium being absorbed after a meal?

A
  • Increased plasma potassium
  • Increased insulin, aldosterone and adrenaline
  • Causes tissue uptake via the sodium potassium pump, as well as increasing potassium channels on the basal membrane
29
Q

List the factors that stimulate potassium secretion

A
  • High plasma potassium concentration
  • High aldosterone
  • High tubular flow rate
  • High plasma pH
30
Q

Which cells are responsible for potassium secretion?

A

Principal cells

31
Q

How does aldosterone increase potassium secretion?

A
  • Stimulates production of sodium and potassium channels on the basal membrane
  • Stimulates sodium/potassium ATPase
32
Q

How does high tubular flow rate cause increased potassium reabsorption?

A

Cilia in the collecting tubules stimulate PK1 to increase potassium ion channels

33
Q

List the possible causes of hypokalemia

A
  • Diuretics
  • Surreptitious vomiting
  • Diarrhoea
  • Genetics (mutation in Na/Cl transporter)
34
Q

List the causes of hyperkalemia

A
  • In response to K+ sparing diuretics
  • ACE inhibitors
  • Elderly
35
Q

How do potassium sparing diuretics work?

A
  • Amiloride - block Na channels

- Spironolactone - aldosterone antagonist

LSS 2 (32 decks)

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