Electrolyte balance Flashcards

1
Q

What is pressure diuresis / natriuresis?

A

When the kidneys respond to increased arterial blood pressure and increased renal perfusion pressure by increasing urine output / increasing sodium excretion

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2
Q

Which cells release renin?

A

Granular (juxtaglomerular) cells

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3
Q

What is the aim of the release of renin?

A

Increase sodium reabsorption and therefore water reabsorption

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4
Q

What is the location of granular cells in the kidney?

A

Afferent arteriole

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5
Q

What are the 3 main triggers of renin release by granular cells?

A

Low afferent arteriole pressure

Low NaCl in distal tubule

Activation of sympathetic nerves that supply the JGA

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6
Q

What does renin convert?

A

Converts angiotensinogen into angiotensin I

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7
Q

Where is angiotensinogen made?

A

Liver

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8
Q

Where is ACE made?

A

Lungs

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9
Q

What are the 3 main effects and 2 minor effects of angiotensin II?

A

Main - Vasoconstriction

Increase sodium & water reabsorption in the kidneys

Stimulate aldosterone release from the adrenal gland

Minor – increase thirst

Stimulate ADH release from the posterior pituitary

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10
Q

Describe how angiotensin II increases sodium reabsorption in the kidney (which receptor it binds to and which transporters are effected and on which membranes).

A

Binds to AT1 receptor

Stimulates Na+K+ATPase and Na+HCO3- co-transporter on the basolateral membrane

Stimulates NHE (sodium-hydrogen exchanger) on luminal membrane

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11
Q

Which cells does aldosterone exert its effects on and what is their location in the nephron?

A

Principal cells in the late distal tubule + cortical collecting duct

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12
Q

Where is aldosterone released from?

A

Zone glomerulosa (adrenal cortex)

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13
Q

Which 2 things trigger aldosterone release?

A

Increased angiotensin II

Increased extracellular potassium concentration

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14
Q

Which receptors does aldosterone bind to?

A

Intracellular mineralocorticoid receptors (MR)

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15
Q

How does aldosterone increase reabsorption of sodium?

A

Increases number of Na+K+ATPase on the basolateral membrane and increases number of ENaC channels on the luminal membrane

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16
Q

ANP is released in response to what?

A

Increased BP / volume

17
Q

What is the effect of ANP?

A

Inhibits sodium (and water) reabsorption by increasing excretion by the kidneys

18
Q

In heart failure, what will the level of ANP be like?

A

Raised ANP

19
Q

Which 4 things shift potassium into cells (decrease extracellular potassium)?

A

Insulin

Aldosterone

B-adrenergic stimulation

Alkalosis

20
Q

Which 7 things shift potassium out of cells (increase extracellular potassium)?

A

Insulin deficiency (diabetes mellitus)

Aldosterone deficiency (Addison’s disease)

B-adrenergic blockade

Acidosis

Cell lysis

Strenuous exercise

Increased extracellular fluid osmolarity

21
Q

Which 3 factors determine the rate of potassium secretion in the distal convoluted tubule and early collecting duct?

A

Activity of Na+K+ATPase

Potassium gradient between blood, principal cells, & lumen

Permeability of luminal membrane to potassium

22
Q

What are the 2 potassium channels on the luminal membrane of principal cells?

A

BK channels

ROMK channels

23
Q

Which 4 factors regulate potassium secretion?

A

Increased plasma potassium concentration

Increased aldosterone

Increased tubular flow rate

Increased H+ concentration

24
Q

How does increased tubular flow rates in the nephron affect potassium excretion?

A

Increased potassium excretion

25
Q

By which 2 mechanisms does increased tubular flow rates in the nephron increase potassium excretion?

A

Higher tubular flow ‘flushes out’ potassium in the lumen, creating a steeper concentration gradient, encouraging more potassium to leave the cell and into the lumen

Increased flow physically stimulates potassium channels in the luminal membrane of the principal cells, making them more permeable to potassium ions and allowing potassium to exit more easily

26
Q

How does high sodium intake affect tubular flow rate in the nephron?

A

Increases tubular flow rate

27
Q

Why is increased tubular flow rate in the nephron a particularly useful mechanism for controlling potassium excretion?

A

Potassium secretion is typically controlled by aldosterone.

Increased tubular flow rate allows for independent potassium excretion even when aldosterone levels are decreased due to increased sodium intake

28
Q

What effect does acutely increased H+ have on potassium excretion and how?

A

Decreased potassium secretion by inhibiting the Na+K+ATPase pump on the basolateral membrane

29
Q

What is the characteristic ECG feature of hyperkalaemia?

A

Tall T waves

30
Q

What is the overall effect of high aldosterone on sodium reabsorption or secretion, and potassium reabsorption or secretion?

A

High aldosterone stimulates sodium reabsorption.

Stimulates potassium secretion