Chronic kidney disease part 2 Flashcards

1
Q

treatment of reversible causes

A

give fluids to correct hypovolemia

Discontinue or minimize nephrotoxic medications

Relieve obstruction

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2
Q

prevention or delay progression

A

Primary goals are lowering of blood pressure and proteinuria

Glycemic control

Correction of metabolic acidosis

Smoking cessation

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3
Q

elevated blood pressure: pathogenesis

A

↑ sodium retention

↑ renin-angiotensin system activity

↑ sympathetic nervous system activity

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4
Q

elevated blood pressure: management

A

With proteinuria, ACE inhibitor or ARB

With volume overload, diuretic

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5
Q

the presence or absence of diabetes does not does not affect

A

KDIGO recommendations for how to treat your patient with CKD.

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6
Q
elevated blood pressure: goals, 1st line, additional
proteinuric
volume overload 
non volume overload 
non-proteinuric 
volume overload 
non volume overload
A

proteinuric
< or equal to 130/80 mmHg, ace or arb, Diuretic then
Non-dihydropyridine CCB (IN ORDER)
< or equal to 130/80 mmHg, ace or arb, Non-dihydropyridine CCB (IN ORDER)
non-proteinuric
< or equal to 140/90 mmHg, diuretic, then ACEi or ARB or
Dihydropyridine CCB (NO SPECIFIC ORDER)
< or equal to 140/90 mmHg, ACEi or ARB or
Dihydropyridine CCB (NO SPECIFIC ORDER)

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7
Q

cutoff for considering someone proteinuric

A

30 mg/day

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8
Q

Non-dihydropyridine CCB examples

A

diltiazem and verapamil

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9
Q

proteinuria

A

Goal PCR 500 to 1000 mg/g

ACE inhibitor or ARB as for elevated blood pressure (G3-G5D)

Protein restriction < 0.8 g/kg/day (G4-G5)

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10
Q

control hyperglycemia to prevent CKD

A

Goal HbA1C ~7%

With type 2 diabetes, SGLT2 inhibitors

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11
Q

metabolic acidosis

A

Sodium bicarbonate or sodium citrate

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12
Q

anemia

A

Erythropoiesis-stimulating agents

  • SQ without dialysis
  • IV with dialysis

iron therapies

red blood cells
lower limit 10 g/dl without dialysis, 9 g/dl with dialysis

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13
Q

increased parathyroid hormone

A

increased P, decreased Na and calcitriol. will help counteract P and Na level dysfunction. but this increased level can become pathologic

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14
Q

CaR

A

calcium sensing receptor senses hypercalcemia. downregulates secretion of PTH in the setting of excess calcium.

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15
Q

when PTH is released

A

it works to promote activity of osteoclasts. breaks down bone in order to mobilize calcium into body.
so when you experience hypocalcemia, pth helps to mobilize calcium from bone.

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16
Q

patients who had mild to moderate CKD

A

P was not elevated, but calcitriol was decreased.

17
Q

fibroblast growth factor (FGF23)

A

molecule released in response to increasing phosphate, PTH, or calcitriol levels. improves release of phosphate by kidneys and decreases PTH and calcitriol levels. KLOTHO is needed.

18
Q

in CKD, klotho is decreased so less ability for

A

fgf23 to bind to PTH and to act. therefore, excessive levels of PTH.

19
Q

CKD-Mineral and Bone Disorder: Goals
goal 1
goal 2
goal 3

A

Goal 1/2: lower elevated phosphate towards normal range, avoid hypercalcemia (G3a-G5D)

Goal 3: reserve PTH-directed pharmacotherapy for severe and progressive secondary hyperparathyroidism (G3a-G5D)

20
Q

patients with severe and progressive secondary hypoparathyroidism (g4/g5)
pth therapies

A

(before dialysis) calcitriol, vitamin D

(during dialysis) calcimimetics

21
Q

treatment of hypoparathyroidism

Cinacalcet

A

Initiate 30 mg po qday and titrate to max 180 mg po qday

Administer with or shortly after meal

22
Q

treatment of hypoparathyroidism/lowers calcium

Etelcalcitide

A

Initiate 5 mg iv push thrice weekly and titrate from min 2.5 to max 15 mg iv push three times weekly
Administer post-dialysis