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33 Cards in this Set
- Front
- Back
ESRD can be caused by damage to the ___1___ or ___2___
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glomerulus
tubulointerstitium |
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Urea serves as a direct uremic toxin and a......
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marker of the buildup of other nitrogenous wastes
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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 |
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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 |
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How is the anemia of CKD described?
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Normocytic, normochromic, with low reticulocyte count.
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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 |
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1) What secondary deficiency is caused in CKD anemia
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1) Iron deficiency
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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 |
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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 |
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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 |
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1) Poor response of anemia to ESA signals what problem?
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1) Iron deficiency
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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 |
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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. |
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Describe how Renal deficit causes a change in PO4, Ca++, PTH, and D3
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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. |
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What can a person with CKD do to prevent secondary hyperparathyrodism?
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Phosphate restricted diet
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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. |
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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 |
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What two things must be elevated to cause Calciphylaxis?
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Ca x P must be >55-60
Note: This is not just free Ca++ here, it counts the stuff complexed to PO4. |
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How can CKD cause LOW bone turnover disease
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1) Low D3
2) Aluminum deposition at the mineralization front 3) poor response to PTH |
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4 steps in controlling Ca++/PO4 metabolic problems in CKd
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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 |
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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 |
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risk of calcium supplementation
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hypercalciemia
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How does low D3 contribute to high PTH aside from its inability to allow Ca++ reabsorbtion.
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Decreased Ca++ feedback receptors on parathyroid chief cells so PTH is unregulated. No amount of Ca++ iberated will be enough to shut off PTH.
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Under what circumstances is surgical parathyroidectomy indicated
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Cannot supress PTH using medical therapy
PTH >1000 OR Calciphylaxis |
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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 |
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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 |
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Nutritional recommendations in CKD
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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 |
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Why do we increase protein intake in people on dialysis?
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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 |
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Low dietary protein is supposed to lower uremic symptoms, and thus delay CKD preogression? Why is a low proetein diet controversial?
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Doctors worry about malnutrition which predisposes to infection an hospitalization
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Why do we manage obesity (restrict calories) in people with CKD?
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because obesity predisposes to DMIII and HTN which both worsen CKD.
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Why do we give Statins to people with CKD?
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The are predisposed to high choleterol and triglycerides.
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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?
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<30 mL/min
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Indications for dialysis
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1) uremic syndreom
2) pericarditis 3) intractable fluid overload 4) Intractable metabolic acidosis 5) Poor nutrition of unexplained weight loss 6) Intractable hyperkalemia |