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BRS2 Term 2 > Sodium and potassium balance > Flashcards

Sodium and potassium balance Flashcards

1
Q

What is osmolarity?

A

measure of solute (particle) concentration in a solution (mOsm/L)
- the greater the number of dissolved particles, the greater the osmolarity

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2
Q

How does increased dietary sodium lead affect blood pressure?

A
  • inc. dietary sodium
  • inc. total body sodium
  • inc. osmolarity (but this can’t happen)
  • inc. water intake and retention
  • inc. ECF volume
  • inc. blood volume and pressure
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3
Q

What is the central mechanism involved in the regulation of sodium intake?

A
  • lateral parachrachial nucleus in brainstem
  • in euvolemia, serotonin and glutamate suppress basal sodium intake
  • during sodium deprivation/hypovolemia?, GABA and opioids drive inc. appetite for sodium
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4
Q

What is the peripheral mechanism involved in the regulation of sodium intake?

A

TASTE
low sodium in food= appetising
high sodium= fairly unpleasant taste

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5
Q

Where in the nephron is most of the sodium reabsorbed?

A

proximal convoluted tubule- 67%

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6
Q

Where is the macula densa?

A

in the juxtaglomerular apparatus of the distal convoluted tubule (in contact w/ cells around the glomerulus)

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7
Q

How do the cells in the macula densa respond to increased tubular sodium?

A
  • high sodium in tubular fluid
  • inc. sodium/chloride uptake via triple transporter
  • adenosine release from macula densa cells
  • triggers extraglomerular mesangial cells
  • promotes afferent smooth muscle cell contraction
  • so reduced flow into glomerulus–> reduced renal perfusion pressure and GFR (and so less sodium coming into tubular system)
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8
Q

What is the best way to retain sodium?

A

filter less!
lower efferent arteriole pressure–> more flow through–> lower filtration pressure–> better retention of sodium and water

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9
Q

How does atrial natriuretic peptide (ANP) decrease sodium reabsorption?

A
  • vasodilator
  • reduces sodium reuptake in PCT, DCT and collecting ducts
  • suppresses production of renin by JGA
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10
Q

How does beta-1 sympathetic activity increase sodium reabsorption/retention (and so inc. bp and fluid volume)?

A
  • directly stimulates SMC of afferent arteriole (reduces GFR)
  • stimulates sodium uptake in PCT
  • stimulates renin production by JGA–> cleaves angiotensinogen to angiotensin 1–> cleaved by ACE to angiotensin 2–> stimulates sodium uptake in PCT and stimulates adrenal glands (zona glomerulosa) to produce aldosterone (through inc. expression aldosterone synthase, needed for last 2 steps of conversion from cholesterol)–> stimulates sodium uptake in DCT and collecting duct
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11
Q

What are the functions of aldosterone in the kidney?

A
  • simulates sodium reabsorption
  • increases potassium secretion
  • increases H+ ion secretion
  • excess aldosterone–> hypokalaemic alkalosis
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12
Q

What are the consequences of hypoaldosteronism?

A
  • reduced reabsorption of sodium in distal nephron
  • leads to inc. urinary loss of sodium (and so inc. loss of water)
  • ECF volume falls–> inc. renin, angiotensin 2 and ADH
  • low bp–> dizziness
  • low salt–> salt cravings, palpitations
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13
Q

What are the consequences of hyperaldosteronism?

A
  • inc. reabsorption of sodium in distal nephron
  • leads to dec. urinary loss of sodium (and so dec. loss of water)
  • ECF volume inc. (hypertension)–> dec. renin, angiotensin 2 and ADH
  • inc. ANP and BNP production
  • high bp
  • muscle weakness
  • thirst, polyuria
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14
Q

What is Liddle’s syndrome?

A
  • inherited disease of high blood pressure
  • however normal or low aldosterone levels
  • mutation in the aldosterone-activated ENaC sodium channel–> always ‘on’–> inc. reabsorption of sodium (so inc. water retention and hypertension)
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15
Q

What is the effect of spironolactone on blood pressure?

A
  • mineralocorticoid antagonist
  • reduces effect of aldosterone
  • so decreases sodium reabsorption and water retention
  • leads to reduced blood pressure
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16
Q

What receptor does ANP bind to?

A

guanylyl cyclase

17
Q

What are the actions of ANP?

A
  • released in response to atrial stretch (high bp)
  • causes vasodilation of renal and other blood vessels (N.B. inc. GFR by relaxing SMCs in afferent arteriole)
  • inhibits sodium reabsorption in PCT and collecting ducts
  • inhibits renin and aldosterone production
  • -> reduces bp
18
Q

How do ACE inhibitors reduce blood pressure?

A

reduces angiotensin 2 production

  • -> leads to vasodilation (as A2 contracts vessels), so inc. vascular volume and dec. bp
  • -> renal effects: dec. sodium reuptake in PCT, so dec. water reabsorption
  • -> adrenal effects: dec. aldosterone production–> indirect renal effects (dec. sodium reuptake in collecting duct, so inc. sodium in distal nephron, so reduced osmotic gradient across tubular wall and dec. water reabsorption
  • ——-> reduced water volume, ECF volume and bp
19
Q

How do osmotic diuretics work?

A

put in something in PCT that doesn’t get reabsorbed, so it increases the osmolarity here–> so less water reabsorption here (region where most is reabsorbed) –> dec. bp

20
Q

How do carbonic anhydrase inhibitors work as diuretics?

A
  • block carbonic anhydrase, which is most active in PCT
  • protons not produced, so sodium/proton exchange activity reduced, so dec. net reabsorption of sodium –> inc. sodium in distal nephron, and dec. water reabsorption
  • N.B. also fewer protons pumped out, so reduced acidity of urine
21
Q

How do loop diuretics work?

A
  • block triple transporter (Na+/Cl-/K+) in thick ascending limb of loop of Henle
  • so reduced sodium reuptake–> inc. sodium in distal nephron and reduced water reabsorption–> dec. bp
22
Q

How do thiazide diuretics work?

A
  • block sodium chloride uptake transporter in DCT
  • so reduced sodium reuptake–> inc. sodium in distal nephron–> reduced water reabsorption–> dec. bp
  • N.B. also inc. calcium reabsorption, as sodium-calcium anti porter on basolateral side of DCT cells–> so more calcium pumped out of cell, due to sodium gradient
23
Q

How do potassium sparing diuretics work?

A
  • e.g. spironolactone
  • bind to mineralocorticoid receptor, inhibit aldosterone function–> block sodium reuptake–> inc. sodium in distal nephron–> dec. water reabsorption and dec. bp
  • in collecting duct
  • potassium sparing, as less potassium secreted through antiporters(?)
24
Q

What is the main intracellular ion?

A

potassium (150mmol/L)

25
Q

What stimulates potassium uptake into tissue?

A
  • insulin (also aldosterone and adrenaline)
  • insulin stimulates sodium-proton exchanger, increasing sodium coming into tissue cells, so inc. activity of Na+/K+ ATPase, to get rid of the sodium
26
Q

Where is potassium secreted if there is normal or inc. potassium intake?

A

DCT and collecting ducts

27
Q

Where is potassium reabsorbed in the kidney under normal conditions?

A
  • 67% in PCT
  • 20% in thick ascending limb of loop of Henle
  • Na+/K+/Cl- transporter
28
Q

What factors stimulate potassium secretion?

A
  • inc. plasma K+
  • inc. aldosterone
  • inc. tubular flow rate
  • inc. plasma pH
29
Q

How does increased tubular flow lead to increased potassium secretion?

A

w/ inc. flow, primary cilia on distal cells stimulate PDK1

–> inc. calcium conc. in cell–> stimulates openness of K+ channels, so more moves out

30
Q

What are the causes of hypokalaemia?

A
  • inadequate dietary intake (too much processed food)
  • diuretics (due to inc. tubular flow rate)
  • surreptitious vomiting
  • diarrhoea
  • genetics (Gitelman’s syndrome- mutation in Na/Cl transporter in distal nephron)
31
Q

What are the causes of hyperkalaemia?

A
  • in response to K+ sparing diuretics
  • ACE inhibitors
  • elderly
  • severe diabetes
  • kidney disease

BRS2 Term 2 (14 decks)

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