Sodium Balace and Diuretics Flashcards

1
Q

Amount of Na+ excreted/day

A

100mEq/mL

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2
Q

Water follows _____ only in the _______ _____

A

Salt! Proximal tubule!
Coupled reabsorption.

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3
Q

Sodium cotransport coupling

A

Utilising the concentration gradient to perform secondary active transport of other molecules.

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4
Q

Na+ absorption over the early proximal tubule (3)

A

Overall absorption
Apical
- SGLT - cotransport of glucose
- NHE - antiport of H+
Basolateral
- Na+ pump

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5
Q

Active reabsorption of glucose in the proximal tubule

A

Apical 2ndary active with Na+, passive transport across the basolateral membrane (GLUT)

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6
Q

Starling forces into the capillary

A

Drive fluid movement from the interstitial space.
Greatest contribution from the colloid osmotic (oncotic) pressure of the peritubular blood.

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7
Q

Na+ absorption in the late proximal tubule

A

Apical:
- NHE
Basolateral
- Na/K ATPase
Paracellular
- Driven by transepithelial [Cl-] gradient (higher in lumen, want to flow to blood, sodium follows)

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8
Q

Na+ in the ascending loop of henle (25%)

A

Apical
- NKCC: Na, K, Cl cotransporter
Basolateral
- Na/K ATPase

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9
Q

Furosemide (loop diuretic)

A

Inhibits NKCC in the loop of henle to inhibit sodium reabsorption to favour higher urine volume.

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10
Q

Na+ absorption in the early distal tubule (5%)

A

Apical:
- NCC (Na, Cl cotransporter)
Basolateral:
- Na/K ATPase

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11
Q

Thiazide diuretics

A

Inhibits NCC in distale tubule
Decreases Na reabsorption

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12
Q

Na absorption in the late distal tubule and the collecting duct (3%)

A

Apical:
- ENaC (constituitively open Na+ channel)
Basolateral:
- Na/K ATPase

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13
Q

K+ sparing diuretics

A

Acts on ENaC (inhibitory) to decrease Na reabsorption, subsequently K secretion decreases.
in late distal tubule and collecting duct

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14
Q

Increase in sodium on blood pressure

A

Osmolarity increases in blood, renal system adjusts within an hour by retaining water. Water retention decreases osmolarity but increases blood volume, blood pressure.
Higher blood pressure indicates more sodium must be excreted.

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15
Q

4 systems in controlling Na+ excretion

A

SNS, ANP, πc, Renin-angiotensin- aldosterone.

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16
Q

SNS in sodium excretion

A

Stimulated by change (-) in EFV, modulates afferent arteriolar resistance to change GFR, amount of fluid passing through then determines the amount of sodium available for secretion.

17
Q

Colloid osmotic pressure in sodium excretion

A

Isoosmotic reabsorption in the proximal tubule.
If EFV goes up, πc goes down due to concentration dilution, causes lower driving force across to the peritubular capillary, increased sodium secretion.

18
Q

Renin-angiotensin-aldosterone

A

Favours sodium reabsorption

19
Q

ANP

A

Favours sodium excretion

20
Q

Angiotensin II effect

A

On kidneys (indirect) - adrenal gland secretes aldosterone, triggers kidneys
On pituitary - secretion of ADH

21
Q

Renin origin, stimulated by ____

A

Released by juxtaglomelular cells, released directly into renal circulation
Stimulated by low pressure in the afferent arteriole, a decrease in EFV.
Decreased EFV, decreased Na, want to absorb more sodium

22
Q

Angiotensin II effect on kidneys

A

Acts of AT1 receptors of tubular epithelial cells, increases transport protein activity, increases reabsorption. (N/KA, NHE, NBC)

23
Q

Aldosterone effect on kidneys

A

Increases ENaC activity in the collecting duct
Increases expression of ENaC and Na/K ATPase genes
Increases sodium reabsorption.

24
Q

ANP secretion

A

From the heart in response to volume expansion (high blood volume, high Na concentration)
Acts antagonistically to the RAA system

25
ANP effects
Dilates the afferent arteriole, constricts efferent arteriol, large increase in GFR, sodium filtration and subsequent secretion. Directly inhibits the secretion of renin.
26
How does urine volume change in response to diuretic drug therapy?
Only about one extra liter. Decrease in blood volume then triggers the regulatory systems that triggers the sodium reabsorption to restore balance. Just maintain a lower EFV.
27
ENaC Na channel mutations
Pseudohypoaldosteronism Liddle’s syndrome
28
Pseudohypoaldosteronism
“loss-of-function” Increased Na+ secretion, reduced EFV, hypotension.
29
Liddles syndrome
Hyperactive ENaC channels, hyper absorption, increased EFV, hypertension