renal lecture 2 Flashcards

1
Q

where does reabsorption happen?

A

through renal epithelial tubular cells

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2
Q

what are the two sides of renal epithelial tubular cells?

A

apical (lumen/urine) and basolateral (capillary/blood)

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3
Q

what direction does absorption and secretion happen?

A

absorption - apical -> basolateral
secretion - basolateral -> apical

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4
Q

what are the two types of reabsorbtion?

A

transcellular (often active - through membranes) and paracellular (passive transport between cells through tight junctions)

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5
Q

how is Na+ transported in the early proximal tubule?

A

Na+-dependent cotransporters (Na+/glucose) and countertransporters/exchangers (NHE - Na+/H+) that move across apical membrane, and ATPase pumps on basolateral (with facilitated transporters for the other substances)

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6
Q

what is the tonicity of Na+ absorption?

A

isotonic, so it changes the concentration of other things as water moves with it (because of starling forces)

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7
Q

how is Na+ absorbed in the late proximal tubule?

A

NHE countertrasnports Na+ and H+ on the aprical membrane, and ATPase countertransports Na+ and K+ on basolateral membrane, NaCl also moves between cells by the transpeithelial Cl- concentration gradient

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8
Q

how is Na+ reabsorbed in the ascending loop of henle?

A

NKCC (NaKCl cotransporter) moves Na+ in through the apical membrane, ATPase pumps Na+ out and K+ in, and K+ and CL- leave basolaterally (passively)

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9
Q

what is furosemide?

A

diuretic that targets NKCC to inhibit Na+ reabsorbtion to increase water excretion in the loop of henle

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10
Q

what diuretic targets the ascending loop of henele?

A

furosemide

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11
Q

how is Na+ reabsorbed in the early distal tubule?

A

NCC (sodium chloride cotransporter) moves Na+ and Cl- on apical membrane, ATPase contransports Na+ out and K+ in on basolateral (Cl- leaves passively)

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12
Q

what diuretic targets the early distal tubule?

A

thiazide

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13
Q

what is thiazide?

A

diuretic that blocks NCC in early distal tubule

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14
Q

how is Na+ reabsorbed in the late distal/collecting duct?

A

ENaC (epithelial Na+ channel) brings Na+ in on apical, and ATPase brings Na+ out and K+ in through basolateral (K+ leaves through apical)

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15
Q

what diuretic targets the late distal and collecting duct?

A

K+ sparing diuretic

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16
Q

what is the K+ sparing diuretic?

A

blocks ENaCs and doesnt promote K+ in urine (like other diuretics) in late distal/collecting duct

17
Q

why is sodium balance important?

A

it controls extracellular fluid volume (and blood pressure)

18
Q

what happens when sodium intake changes?

A

sodium excretion changes to match (but lags a bit causing sodium retention or sodium loss)

19
Q

what happens in sodium retention?

A

osmolarity increases, extracellular fluid increases (to balance), and blood pressure increases

20
Q

what happens in sodium loss?

A

osmolarity decreases, extracellular fluid decreases (to balance) and blood pressure decreases

21
Q

what happens when there is a higher extracellular fluid volume?

A

sympathetic activity decreases, afferent arteriole dilates, Na+ reabsorption decreases (through increased GFR in duct, decreased PIc in prox, and decreased renin-angiotensin-aldesterone in prox and duct) which all serves to increases excretion

22
Q

how does angiotensin II increase excretion?

A

increases Na+ transporter proteins and increases Na+ reabsorption, stimulate aldosterone (which increases activity of ENaCs)

23
Q

how does ANP affect Na+ reabsorbtion?

A

released from heart to increase GFR by dilating afferent arteriole and constricting efferent arteriole, decreasing renin/angiotensin II/aldosterone/ADH, and decreases Na+ reabsorption and increases excretion

24
Q

what is the relationship between angiotensin II and ANP?

A

opposites - angio increases Na+ reabsorption and ANP decreases Na+ reabsorption

25
how do pharmacological diuretics work?
decrease Na+ reabsorption, which decreases ECF volume, which decreases blood pressure!
26
what are the three main types of diuretics?
loop diuretics thiazide diuretics K+-sparing diuretics
27
what are some pathological ENaC issues?
psuedohypoaldosteronism liddle's syndrome
28
what is psuedohypoaldosteronism?
loss of function of ENaCs, which increases Na+ excretion, lowers ECF volume, causes predisposition to hypotension
29
what is Liddle's syndrome?
gain of function of ENaCs, lowers Na+ excretion, increases ECF volume, causes predisposition to hypertension