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P&T Block 5 Renal > L57 > Flashcards

L57 Flashcards

1
Q

Is Cr or BUN (urea) produced at a constant rate?

A

Cr

BUN det by protein intake and catabolism: unreliable marker of GFR

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2
Q

What happens to Cr as GFR drops?

A

HYPERBOLIC curve

Large ↓GFR is masked by small changes in Cr

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3
Q

What is eGFR?

A

Estimated GFR
Takes Cr, age, gender, weight and race into account
ONLY use in steady state

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4
Q

What lab value is used to stage CKD?

A

eGFR

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5
Q

What is the Cr during CKD stage 1?

A

eGFR = 90+
Early CKD - Cr may not change at all (L hyperbolic curve)
Realize small changes = large losses in fxn
The healthy nephrons hypertrophy to take the load from damaged ones

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6
Q

What does Cr tell you in late CKD?

A

Large shifts in Cr for small changes GFR

R side hyperbolic curve

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7
Q

How does the kidney’s handling of Na change in CKD?

A

Goal is the same during healthy or disease: Na in = Na out
See ↑FE Na
FE Na - same Na / less filtered load
You must excrete more of the filtered load because you’re now less effective

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8
Q

How does a CKD do to adapt to high Na intake?

A

Can elim the excess Na but takes longer

Leave you in +Na balance = edema

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9
Q

What does a CKD kidney do to adapt to low Na?

A

↓U Na - takes longer

Excess restriction = (-)Na balance -> hypovolemia

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10
Q

How does water excretion change in CKD?

A

Can’t max [ ] or dilute
If you can’t [ ] urine, you must pee more volume to get the same amt solute out
↑Minimum daily urine vol

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11
Q

Why does high urine volume NOT imply good renal fxn in CKD?

A

B/c less urine [ ] means more volume is need to excrete a normal amt solute

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12
Q

Which part of the nephron determines L homeostasis?

A

CD
All K is reabsorbed at PCT
Therefore depends on the ability to secrete K @ CD

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13
Q

Do you become alkalotic or acidemic during CKD progression? 3 reasons why

A

Metabolic acidosis

  1. Can’t reclaim bicarb (PCT)
  2. Can’t NH4 (PCT)
  3. Can’t generate pH gradient (CD)
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14
Q

What is the best measure of kidney H+ secretion?

A

U NH4 > pH

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15
Q

Is the metabolic acidosis during CKD gap or non-gap?

A

Early: non-gap
Late: gap b/c not excreting titratable acids

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16
Q

How does acidemia effect the bones? Treat

A

Osteodystrophy

+ PO bicarb

17
Q

Why does 1,25 vit D drop as ↓GFR?

A

B/c kidney does the 1 hydroxylation
Can’t make 1,25 vit D = calcitriol
↓Reabsorption of Ca from gut
Fails early in CKD

18
Q

3 normal fxn PTH

A
  1. Release Ca2+ from bone
  2. ↑25 -> 1,25 vit D @ kidney
  3. ↓Phosphate reabsorption by kidney
19
Q

What are the 2 factors that lead to ↓P Ca in CKD?

A

↓1,25 vit D - ↓Ca from gut

↓PO4 excretion - ↑ in plasma

20
Q

What are the effects of ↓Ca?

A

↑PTH

  1. ↑Osteoclast = ↑P Ca
  2. Reabsorb @ kidney (dysfxn)
21
Q

What is FGF23? How does it effect PTH + phosphate?

A

Phosphatonin = stim phosphate excretion via urine to raise blood Ca
↓FGF23 in CKD: ↓PTH, ↑phosphate

22
Q

Signs + symptoms of renal osteodystrophy

A 
Pain: low back, hips, knees
Pathologic fx
Pruritis
Vasc + tissue calcification 
Rickets + growth retardation - kids
23
Q

What is a negative SE of tissue calcification?

A

Calciphylaxis = thrombosis + skin necrosis

24
Q

What is osteitis fibrosa cystica? Appearance on XR

A

PTH excess: bone formation + reabsorption

XR: subperiosteal bone reabsorption

25
Q

Treat osteitis fibrosa cystica

A
  1. ↓Phosphate intake//bind whatever is in diet @ GI
  2. +1,25 vit D
  3. Ca receptor antag
    Extreme: parathyroidectomy
26
Q

What happens if you suppress PTH too much?

A

Adynamic bone disease - too brittle, can’t adapt

27
Q

What is osteomalacia?

A

Failure to mineralize new osteoid

Artifact of old meds - not as relevant

28
Q

Treat CKD anemia

A

Recombinant EPO

29
Q

Treat slowly progressing CKD

A

BP + diabetes/glucose control

ACE I or AGT receptor blockers

P&T Block 5 Renal (30 decks)

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