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RENAL II Exam 2 > Physiology Review II > Flashcards

Physiology Review II Flashcards

(52 cards)

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1
Q

proximal tubule

A

fluid that enters - isotonic

-concentration of substance equals plasma concentration for freely filtered substances

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2
Q

sodium in proximal tubule

A

2/3 filtered is reabsorbed

  • driven by basolateral Na/K ATPase
  • glomerulotubular feedback
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3
Q

catecholamine and ANG II

A

stimulate basolateral ATPase to increased Na reabsorption

-proximal tubule

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4
Q

water and electrolytes in proximal tubule

A

2/3 filtered H2O, K, and Cl (leaky) follow the sodium gradient

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5
Q

end of proximal tubule

A

osmolality of Na and K have not changed significantly

-but one third of filtered remains

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6
Q

SGLT-2

A

sodium-glucose linked transporter type 2

  • in the kidney
  • glucose and Na cotransport
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7
Q

metabolites in the proximal tubule

A

proteins, peptides, AAs, ketone bodies reabsorbed via secondary active transport
-linked to sodium transport

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8
Q

bicarbonate in the proximal tubule

A

80% reabsorbed

  • combines with H+ in lumen to CO2 and H2O
  • luminal carbonic anhydrase
  • H+ pumped into lumen, exchanged for sodium
  • also H + ATPase
  • CO2 - crosses luminal membrane - combines with water
  • reforms H and bicabonate
  • H pumped back into lumen and bicarb exits basolateral membrane
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9
Q

important factor for proximal tubule H+ secretion

A

concentration of H+ in cell

  • acidosis - increased H secretion and bicarb reabsorption
  • alkalosis - decreased H secretion and bicarb reabsorption
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10
Q

ANG II

A

stimulates Na/H antiporter

-volume depleted state - increased bicarb reabsorption

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11
Q

uric acid in the proximal tubule

A

breakdown of nucleotides - xanthine oxidase
-90% is reabsorbed in proximal tubule

low pH - urate > uric acid - precipitate out - stone (gout)

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12
Q

secretion in proximal tubule

A

organic anions/cations

-PAH, inulin, PCN, atropine, morphine

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13
Q

concentration of inulin along tubule

A

index of water reabsorption

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14
Q

inulin concentration

A

freely filtered - concentration in BS = plasma

  • water reabsorbed, inulin is not - [inulin] increases along tubule
  • 2/3 reabsorbed in PT - inulin concentration triples

[highest] in collecting duct

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15
Q

loop of henle

A

fluid entering is isotonic - but volume is 1/3 filtered

  • countercurrent mutliplier
  • creates concentrated medulla
  • predominantly NaCl and urea
  • caused by juxtamedullary nephrons (surrounded by vasa recta)
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16
Q

descending limb loop of henle

A

permeable to water (15% reabsorption here)

-impermeable to solute

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17
Q

ascending limb loop of henle

A

impermeable to water

-solutes transport out

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18
Q

Na/K/2Cl transporter

A

thick ascending limb of loop of henle

  • electroneutral
  • reabsorb 25% filtered Na, Cl, and K

there is a K channel - allows diffusion back into lumen

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19
Q

calcium sensing receptor

A

basolateral membrane - ascending thick limb

  • GPCR
  • net effect - inhibit Na/K/2Cl transporter
  • reduces positive luminal potential (less K back out)
  • in turn decreases calcium reabsorption

**high plasma calcium can reduce ascending thick limb calcium reabsorption

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20
Q

distal tubule

A

early distal tubule - reabsorbs Na, Cl, Ca

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21
Q

NaCl in dustal tubule

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A

crosses apical membrane via NaCl symporter

  • Na across basolateral - Na/K exchanger
  • Cl across basolateral through channels

impermeable to water - decreases osmolality further

22
Q

calcium in distal tubule

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A

passive entry though channels
-regulated by PTH

-basolateral transport - Ca ATPase or 3Na-Ca antiporter

23
Q

calbindin

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A

distal tubule cells

  • facilitates calcium reabsorption
  • increased with vitamin D
24
Q

collecting duct

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A

principal cells and intercalated cells

25
principal cells
luminal epithelial Na channels (ENaC) -sodium follows its gradient established by basolateral Na/K ATPase creates negative luminal potential - Cl left in lumen -results in potassium secretion reabsorption of sodium and secretion of K linked**
26
aldosterone
increases ENaC and basolateral Na/K ATPase of principal cells increased sodium reabsorption and increased K secretion
27
ADH
aka AVP - acts on V2 receptors - increases aquaporins on principal cells increased water reabsorption**
28
intercalated cells
acid-base regulation - luminal H+ ATPase - pumps H+ into lumen - secreted H+ buffered via ammonia and phosphate
29
aldosterone
stimulates H+ ATPase of intercalated cells | -excess - can lead to metabolic acidosis
30
proximal renal tubular acidosis type II
diminished capacity of proximal tubule to reabsorb bicarb - low plasma bicarb and acid urine - ex/ fanconi syndrome - serum potassium low bicarb lost in urine - lost as sodium bicarb - pulls water with it - creates osmotic diuresis - diuresis leads to loss of potassium in urine
31
distal renal tubular acidosis type I
inability of distal nephron to secrete and excrete fixed acid metabolic acidosis with high urine pH -serum potassium low
32
renal tubular acidosis type IV - hypoaldosterone states
cannot secrete potassium (hyperkalemia) -decreased H+ secretion - metabolic acidosis due to diabetic nephropathy (low renin) drug that (-) RAAS trimethoprim addisons disease - decreased aldosterone from adrenal cortex
33
potassium balance
98% inside cells / 2% outside cells >5 hyperkalemia / < 3.5 hypokalemia gradient caused by the negative intracellular potential
34
insulin and epinephrine
stimulate Na/K ATPase - can reduce plasma K
35
activity of Na/K pump
3 Na out | 2 K in
36
acidosis
potassium from ICF to ECF -hyperkalemia also with cell shrinkage
37
alkalosis
potassium from ECF to ICF -hypokalemia also with cell swelling
38
potassium secretion
determined by filtrate flow and sodium reabsorption (negative luminal potential)
39
increased potassium secretion
increased flow | increased aldosterone
40
decreased potassium secretion
decreased flow | decreased aldosterone
41
hyperkalemia
stimulates aldosterone
42
H+ and K+ balance
to keep electroneutrality - administer bicarb - protons out of cell/ K into cell - results in hypokalemia
43
insulin
increased Na/K ATPase | -more K into cells
44
hyperkalemia clinical
muscle weakness and fatigue high T wave - eventually to V-Fib metabolic acidosis
45
hypokalemia clinical
muscle weakness, general fatigue hyperpolarization - delays repolarization low T wave, high U wave decreased insulin response to carbohydrate load, decreased growth in children, nephrogenic DI, metabolic alkalosis
46
diuretics
increased flow - hypokalemia
47
acute renal failure
rapid loss of renal function - often reversible increased BUN/Cr
48
prerenal failure
decreased renal perfusion - decreased GFR - reduced FeNa - increased reabsorption - elevated BUN/Cr - however, increased water reabsorption > increased urea reabsorption > higher elevation of BUN compared to Cr
49
FeNa
fractional excretion of sodium
50
intrarenal failure
tubular damage occurs - increased FeNa - casts in urine - low BUN/Cr
51
postrenal failure
obstruction of outflow from kidney - early - decreased FeNa, increased BUN/Cr - late - pressure increases - to intrarenal failure - increased FeNa and decreased BUN/Cr
52
chronic renal failure
irreversible loss of nephrons - causes glomerular HTN to remaining glomeruli - leads to fibrosis/scarring - elevated BUN/Cr - volume overload and edema - hyperkalemia - metabolic acidosis - hyperphosphatemia - reduces plasma Ca - increased PTH (secondary hyperparathyroidism) - cannot hydroxylate Vit D enzmye - hypocalcemia - anemia - decreased erythropoietin most common cause*** - diabetic nephropathy second most common cause - HTN

RENAL II Exam 2 (10 decks)

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