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RENAL II Exam 2 > Physiology Review II > Flashcards

Physiology Review II Flashcards

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

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

A

passive entry though channels
-regulated by PTH

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

23
Q

calbindin

A

distal tubule cells

  • facilitates calcium reabsorption
  • increased with vitamin D
24
Q

collecting duct

A

principal cells and intercalated cells

25
Q

principal cells

A

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
Q

aldosterone

A

increases ENaC and basolateral Na/K ATPase of principal cells

increased sodium reabsorption and increased K secretion

27
Q

ADH

A

aka AVP

  • acts on V2 receptors
  • increases aquaporins on principal cells

increased water reabsorption**

28
Q

intercalated cells

A

acid-base regulation

  • luminal H+ ATPase - pumps H+ into lumen
  • secreted H+ buffered via ammonia and phosphate
29
Q

aldosterone

A

stimulates H+ ATPase of intercalated cells

-excess - can lead to metabolic acidosis

30
Q

proximal renal tubular acidosis type II

A

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
Q

distal renal tubular acidosis type I

A

inability of distal nephron to secrete and excrete fixed acid

metabolic acidosis with high urine pH
-serum potassium low

32
Q

renal tubular acidosis type IV - hypoaldosterone states

A

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
Q

potassium balance

A

98% inside cells / 2% outside cells
>5 hyperkalemia / < 3.5 hypokalemia

gradient caused by the negative intracellular potential

34
Q

insulin and epinephrine

A

stimulate Na/K ATPase - can reduce plasma K

35
Q

activity of Na/K pump

A

3 Na out

2 K in

36
Q

acidosis

A

potassium from ICF to ECF
-hyperkalemia

also with cell shrinkage

37
Q

alkalosis

A

potassium from ECF to ICF
-hypokalemia

also with cell swelling

38
Q

potassium secretion

A

determined by filtrate flow and sodium reabsorption (negative luminal potential)

39
Q

increased potassium secretion

A

increased flow

increased aldosterone

40
Q

decreased potassium secretion

A

decreased flow

decreased aldosterone

41
Q

hyperkalemia

A

stimulates aldosterone

42
Q

H+ and K+ balance

A

to keep electroneutrality

  • administer bicarb - protons out of cell/ K into cell
  • results in hypokalemia
43
Q

insulin

A

increased Na/K ATPase

-more K into cells

44
Q

hyperkalemia clinical

A

muscle weakness and fatigue
high T wave - eventually to V-Fib
metabolic acidosis

45
Q

hypokalemia clinical

A

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
Q

diuretics

A

increased flow - hypokalemia

47
Q

acute renal failure

A

rapid loss of renal function - often reversible

increased BUN/Cr

48
Q

prerenal failure

A

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
Q

FeNa

A

fractional excretion of sodium

50
Q

intrarenal failure

A

tubular damage occurs

  • increased FeNa
  • casts in urine
  • low BUN/Cr
51
Q

postrenal failure

A

obstruction of outflow from kidney

  • early - decreased FeNa, increased BUN/Cr
  • late - pressure increases - to intrarenal failure - increased FeNa and decreased BUN/Cr
52
Q

chronic renal failure

A

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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