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33 Cards in this Set

  • Front
  • Back
ESRD can be caused by damage to the ___1___ or ___2___
glomerulus
tubulointerstitium
Urea serves as a direct uremic toxin and a......
marker of the buildup of other nitrogenous wastes
1) Most important symptom of CKD that we need to manage in order to slow damage.
2) How do we do this?
1) HTN

2) ACE-I or ARB
Name 7 complications of CKDB
1) __emia
2) ___kalemia
3) metabolic ____osis
4) Alterations in the metabolism of
5) ____disorders
6) _____ dysfunction
7) altered _____ metabolism
1) Anemia
2)Hyperkalemia
3) Metabolic acidosis
4) Alterations in Ca/PO4 metabolism
5) Nutritional Disorders
6) Endocrine dysfunction
7) ALtered drug metabolism
How is the anemia of CKD described?
Normocytic, normochromic, with low reticulocyte count.
Why does CKD cause anemia
1) primary reason
2) secondary reasons
1) Insufficienct productio of erythropoietin
2) Bone marrow fibrosis due to hyperparathyroidism
3) Shortened RBC lifespan due to unidentified uremic factors
4) repeated Blood loss due to dialysis
1) What secondary deficiency is caused in CKD anemia
1) Iron deficiency
1) How to we Tx CKD anemia?
2) WHat is the target Hemoglobin levels
1) With Recombinant Erythropoietin (Erythropoiesis stimulating agents) (Procrit, Epogen)
2) 11-12
1) What symptoms of anemia are reduced by ESAs?
2) WHat is the only known side effect of using ESAs to increase hemogobin?
1) Decreased bleeding tendancy
Increased exercise tolerance
Nurtition
Cognitive Fxn
Reduced LVH
enhanced sex function (menses and Erection)

2) loss of BP control
1) Why do people on dialysis have low iron?

2) How do we Tx?
1) low dietary iron
frequent blood draws
blood loss due to dialysis
2) Iron supplementations
1) Poor response of anemia to ESA signals what problem?
1) Iron deficiency
in CKD,
1) one kind of high turnover osteosystrphy can occur. describe
2) two kind of low turnover osteosystrphy can occur. describe
Osteitis fibrosis cystica- Due to High PTH. both osteoclasts and blasts are stimulated. They lay haphazardly formed bone.

2)Osteomalacia- osteoid deposition exceeds mineralization
Adynamic bone disease- bothosteoid and mineralization are severely rreduced
Levels after homeostatic response in early secondary hypoparathyoidism
1) PTH
2) PO4
3) Ca++'
4) D3
1) high
2) WNL
3) WNL
4) high
The latter two are kept WNL by increasing PTH.
Describe how Renal deficit causes a change in PO4, Ca++, PTH, and D3
1) As REnal function declines, PO4 excretion is impaired. This causes high phosphate
2) High phosphate complexes Ca++ and leads to low free Ca++.
3) Low Ca++ and high PO4- cause PTH secretion.
4) PTH inhibits PO4 reabsorbtion by the PCT, and increases Ca++ reasborbtion in the C and MCD.
5) By favoring Vitamin D hydroxylation in the kidney, it also causes Ca++ reabsorption in the gut
6) PTH also stimualte Ca++ release from the bone matrix.
What can a person with CKD do to prevent secondary hyperparathyrodism?
Phosphate restricted diet
1) Why does D3 fall in moderate-severe kidney failure?
2) What is the consequence of this?
3) What causes PTH to go up even more here?
1) Inhibitory effect of PO4 on PCT cells and reduced renal mass.
2) decreased Gut absorption of Ca++
3) Hyperphosphatemia causes resistance of parathyroid chief cells to D3 inhibition. They will hypertrophy.
1( WHat effect, other than Ca++ liberation, does PTH have on bone?
2) what bone condition does this combo cause?
1) Increases bone collagen deposition
2) Osteitis fibrosis cyctica and fibrosis of marrow cavity
What two things must be elevated to cause Calciphylaxis?
Ca x P must be >55-60

Note: This is not just free Ca++ here, it counts the stuff complexed to PO4.
How can CKD cause LOW bone turnover disease
1) Low D3
2) Aluminum deposition at the mineralization front
3) poor response to PTH
4 steps in controlling Ca++/PO4 metabolic problems in CKd
1) Lower PO4 with diet and phosphorus binders. CaCO3 at meal time.
2) Increase free Ca++. Use CaCO3 between meals
3) Vitamin D replacement or analog to enhance gut Ca++ absorbtion
4) Surgical parathyroidectomy for levels of PTH >1000
Target levels in CKD
1) Phosphate
2) Ca++
3) PTH should be below this or parathyroidectomy is indicated
1) 3.5-4,5
2) 9-9.5
3) 1000
risk of calcium supplementation
hypercalciemia
How does low D3 contribute to high PTH aside from its inability to allow Ca++ reabsorbtion.
Decreased Ca++ feedback receptors on parathyroid chief cells so PTH is unregulated. No amount of Ca++ iberated will be enough to shut off PTH.
Under what circumstances is surgical parathyroidectomy indicated
Cannot supress PTH using medical therapy
PTH >1000
OR
Calciphylaxis
1) CKD can give rise to chronic metabolic ___osis.
2) If this is early the __1__osis will be __2__
3) Later is can be ___3___
4) Tx?
1) Acidosis
2) Hyperchloremic
3) Anion Gap
4) NaBicarb
1) __1__kalemia is common in CKD
2) Wishy-washy cause
3) Tx?
1) Hyperkalemia
2) Inadequate filtration and global dysfunction
(goes along with metabolic acidosis)
3) Dietary restriction, Loop diuretic
Nutritional recommendations in CKD
Reduce Salt
Reduce K
Reduce Phosphate
0.8 g/kg/protein/day until dialysis
1.2 kg/day on hemodialysis
1.5 g/kg/day on peritoneal dialysis
Why do we increase protein intake in people on dialysis?
It can cause protien loss in the fluid

0.8 g/kg/protein/day until dialysis
1.2 kg/day on hemodialysis
1.5 g/kg/day on peritoneal dialysis
Low dietary protein is supposed to lower uremic symptoms, and thus delay CKD preogression? Why is a low proetein diet controversial?
Doctors worry about malnutrition which predisposes to infection an hospitalization
Why do we manage obesity (restrict calories) in people with CKD?
because obesity predisposes to DMIII and HTN which both worsen CKD.
Why do we give Statins to people with CKD?
The are predisposed to high choleterol and triglycerides.
What is the GFR cutoff where we switch from diet/lifestyle, vaccines (pneumococcus, HEPB, flu), and education to more insensive course with dialysis and transplant?
<30 mL/min
Indications for dialysis
1) uremic syndreom
2) pericarditis
3) intractable fluid overload
4) Intractable metabolic acidosis
5) Poor nutrition of unexplained weight loss
6) Intractable hyperkalemia