Uremia Flashcards
Ways in which the GI system is affected in uremia? (including anything involving eating..)
Decreased appetite. Altered taste. Bad breath (uremic fetor). Esophagitis/motility problems. GI bleeding. Diverticular disease and constipation.
Simplest definition of uremia?
Symptomatic renal failure.
How is anemia caused by uremia characterized? (in MDTI terms, for cell size and color)
Normochromic normocytic anemia.
with hypoproliferative bone marrow and decreased reticulocytes.
3 primary drivers of anemia in uremia?
Reduced EPO production.
Shortened RBC lifespan.
Inhibitors of erythropoeisis accumulate.
What cells in the kidney actually make EPO?
A population of interstitial fibroblasts (Type I interstitial cells)
Several aggravating factors for anemia of uremia?
Fe or B12/folate deficiency. Blood loss (via GI tract or from dialysis). HyperPTH.
Drawback to EPO or synthetic EPO therapy for anemia of uremia?
There’s increased risk of adverse CV events…
One should aim for an Hg of 10-11, not 14.
Why do patients with uremic syndrome bleed more easily?
Impaired platelet aggregation.
Some toxin appears to be inhibiting IIb/IIIa, but we don’t know what that is
Treatment options for uremic syndromes with bleeding?
Treat anemia with EPO. DDAVP (synthetic AVP aka ADH) -> vWF release. Cryoprecipitate. Estrogens. Dialysis.
Unique CVD risk factors that uremic patients have? (they’re not all entirely unique…)
Anemia. Increased homocysteine. Thrombogenic state. Ca++ intake. HyperPTH. Persistent inflammatory state. Toxins.
Why are CV events often not aggresively treated in pts with CKD?
People are afraid of drugs / procedures in pts with CKD.
What’s the most common lipid abnormality associated with uremia?
High TGs - due to decreased clearance from bloodstream.
due to reduced function of lipoprotein lipase, reduced hepatic lipase, increased retention a lipase inhibitor…
Cholesterol changes in uremia?
Decreased HDL.
Increased apolipoprotein A1.
Is sexual dysfunction a big problem in CKD?
Yes. But you can still get pregnant with triplets sometimes.
Most important factor in predicting fetal outcome in CKD?
HTN
Is transplant or dialysis better if you want to have a baby?
Transplant, generally.
2 problems that occur more frequently in the pregnancies of women with CKD?
Pre-eclampsia.
Fetal growth retardation.
What happens to phosphate levels in CKD?
What does this lead to?
More phosphate is retained.
Hyperphosphatemia -> FGF-23 -> hypocalcemia and secondary hyperPTH -> Vit D activation.
Bone reabsorption, calcium deposition in tissues.
It wasn’t really emphasized in other lectures, but what enzyme activates 1-OH-D (calcidiol) to 1,25-(OH)2-D (calcitriol)?
1-alpha-hydroxylase
At the end of all the pathways… how are serum phosphate, FGF-23, calcium, Vit D, and PTH in advanced CKD?
(It’s confusing because there are mutually antagonistic effectors floating around.)
Phosphate: high FGF-23: high Calcium: low Vit D: very low PTH: very high
What high-turnover bone disease happens in pts with CKD? What mediates the disease?
hyperPTH -> osteitis fibrosa
What effect does low Vit D have on bone?
Osteomalacia.
Why is secondary hyperPTH from CKD especially bad for kids?
It causes really bad growth retardation.
4 ways to treat these mineral/hormone imbalances of CKD?
Restrict phosphate / give phosphate binders (which have lots Ca++). To suppress PTH: -Calcitriol. -Calcimimetics. (activate CaSR) -Parathyroidectomy.
