Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
36 Cards in this Set
- Front
- Back
|
Common causes of chronic kidney disease |
Diabetes
Hypertension |
|
|
Dialysis
|
Hemodialysis
*Connected to machine through vascular access *Blood leaves body and is pump through dialysis circuit in the machine *Cleaned blood is returned to the patient *3-4 hour process, usually done 3x/wk Peritoneal dialysis *Glucose solution (the dialysate) is pumped into the peritoneal cavity, and the peritoneal membrane acts as the dialyzer membrane *Solution is left in cavity, then drained *Cycle is repeated throughout the day, everyday *Performed at home by patient |
|
|
Factors affecting drug removal during dialysis
|
Molecular size --- smaller molecules pass through more easily
Protein binding --- highly protein bound drugs will generally not be removed Volume of distribution --- if a drug has a large VD, dialysis is not as effective at removing the drug Plasma clearance --- the more a drug is renally eliminated ,the better dialysis will work to clear that drug The dialysis membrane --- low-flux vs high flux; high flux has the largest pore size |
|
|
The level of _____________ in the urine can be used to gauge the severity of kidney damage in patients with kidney disease or nephropathy
|
Albumin
- If the glomerulus is damaged, some of the albumin passes into the urine |
|
|
Creatinine
|
Waste product of muscle metabolism
Filtered through the glomerulus If nephrons are damaged, the filtration of creatinine is reduced and the SCr increases |
|
|
BUN
|
Blood urea nitrogen
Measures the amount of nitrogen that comes from the waste product urea Increases w/ renal impairment; CANNOT be used independently to measure declines in renal function as it is affected by other factors |
|
|
Primary function of aldosterone
|
To increase water and sodium retention
To lower potassium |
|
|
Common drugs that require dosing changes in decreased renal function
|
Amphotericin
AMGs --- increase dosing interval Azole antifungals Digoxin, procainamide Aztreonam Cyclosporine Dabigatran Famotidine, ranitidine Gabapentin, pregabalin LMWHs Metoclopramide --- DO NOT use in elderly Morphine, codeine --- lower starting dose PCNs Quinolones Statins Vancomycin --- acyclovir, allopurinol, amantadine, anti-TB meds, beta lactams, colchicine, ganciclovir, NRTIs, macrolides, maraviroc, Bactrim, tramadol, venlafaxine, zoledronic acid |
|
|
DO NOT use in severe renal impairment
|
Bisphosphonates
Chlorpropamide Dabigatran Fondaparinux Glyburide Lithium Meperidine Metformin Nitrofurantoin NSAIDs K-sparing diuretics Ribavirin Voriconazole IV -- avanafil, cidofovir, dofetilide, foscarnet, rivaroxaban, tadalafil, tenofovir, tramadol ER |
|
|
Stages of CKD
|
Stage 1 --- GFR > 90
Stage 2 --- GFR 60-89 Stage 3 --- GFR 30-59 Stage 4 --- GFR 15-29 Stage 5 --- GFR < 15 or dialysis dependent |
|
|
Anemia of Chronic Kidney Disease
|
Erythropoietin is produced by kidneys; stimulates production of reticulocytes in the bone marrow
Production of erythropoietin decreases as kidney function declines ---> anemia results CKD is a proinflammatory disease that can result in anemia of chronic disease May require iron, folate, or vitamin B12 supplementation |
|
|
Bone metabolism abnormalities
|
Require screening for abnormalities associated w/ parathyroid hormone, phosphorus, calcium, and vitamin D
Therapeutic targets for P, Ca, and PTH are dependent on the severity of CKD |
|
|
Treatment of hyperphosphatemia
|
Bone metabolism abnormalities are initially caused by elevations in phosphorus
Tx: *Restrict dietary phosphorus --- dairy products, dark colored sodas, chocolate, nuts *Phosphate binders --- bind meal-time phosphate in the gut that is coming from the diet |
|
|
Aluminum based phosphate binders
|
Potent; aluminum can accumulate in CKD; toxic to nervous system and bone
Should only be used short-term; not currently used SE - ***constipation***, poor taste, nausea, aluminum intoxication, osteomalacia ***NEUROTOXIN*** Aluminum hydroxide --- 300-600 mg TID w/ meals |
|
|
Calcium based phosphate binders
|
**1st line therapy for hyperphosphatemia of CKD**
Many renal patients are taking vitamin D, which raises calcium levels, and cannot tolerate additional calcium SE - constipation, hypercalcemia, nausea Acetate binds more dietary phosphorus compared to carbonate |
|
|
Calcium acetate
|
PhosLo, Phoslyra
Calcium-based phosphate binder 667-1334 mg TID w/ meals |
|
|
Calcium carbonate
|
Tums
Calcium-based phosphate binder 500 mg TID w/ meals, chewable or not |
|
|
Aluminum free, calcium free phosphate binders
|
Effective; DO NOT cause any problems w/ excess aluminum or calcium load
MOST expensive |
|
|
Lanthanum carbonate
|
Fosrenol --- aluminum and calcium free phosphate binder
500-1000 mg TID w/ meals (chewable) --- MUST CHEW THOROUGHLY SE - N/V/D/C, abdominal pain CONTRA - bowel obstruction, fecal impaction, ileus |
|
|
Sevelamer Info
|
Non-calcium, non-aluminum based phosphate binder
*NOT systemically absorbed* Lowers TC and LDL by 15-30% Carbonate has advantage over HCL by maintaining bicarbonate concentration SE - N/V/D/C, abdominal pain CONTRA - bowel obstruction |
|
|
Renvela
|
Sevelamer carbonate
800-1600 mg TID w/ meals |
|
|
Renagel
|
Sevelamer hydrochloride
800-1600 mg TID w/ meals |
|
|
Treatment of Vitamin D deficiency and Secondary Hyperparathyroidism
|
Secondary hyperparathyroidism is caused by hyperphosphatemia
After controlling hyperphosphatemia, 2nd hyper-PTH is tx through use of vitamin D May need to supplement Vitamin D2; dosing depends on severity of deficiency; treatment may result in hypercalcemia or hyperphosphatemia |
|
|
Vitamin D
|
Two forms:
*Vitamin D3 - cholecalciferol; synthesized in the skin *Vitamin D2 - ergocalciferol; produced from plant sterols; primary dietary source of Vit. D Calcitriol - active form of vitamin D3 --- used to increase calcium absorption from the gut, raise serum calcium conc., and inhibit PTH secretion |
|
|
Vitamin D analogs
|
Increase intestinal absorption of calcium; provides a negative feedback to the parathyroid gland
CONTRA - hypercalcemia; vitamin D toxicity SE - N/V/D, hypercalcemia, hyperphosphatemia TAKE w/ food or shortly after meal to decrease GI upset |
|
|
Rocaltrol, Calcijex
|
Calcitriol --- vitamin D analog
CKD - 0.25 mcg PO TIWk to QD Dialysis - 0.5-1 mcg PO QD or 0.5-4 mcg IV TIWk |
|
|
Hectorol
|
Doxercalciferol --- vitamin D analog
CKD - 1 mcg PO TIWk to QD Dialysis - 2.5-10 mcg PO TIWk; 1-4 mcg IV TIWk |
|
|
Zemplar
|
Paricalcitol --- Vitamin D analog
CKD - 1 mcg PO TIWk to QD DIalysis - 2.8-7 mcg IV TIWk; 2-4 mcg PO TIWk |
|
|
Calcimimetic
|
MOA - increases sensitivity of calcium-sensing receptor on the parathyroid gland, thereby reducing PTH, Ca, Phos, and preventing progressive bone disease
Cinacalcet (Sensipar) --- 30-180 mg PO daily w/ food CONTRA - hypocalcemia SE - hypocalcemia, N/V/D TAKE WHOLE, do NOT crush or chew |
|
|
Tx of Vitamin D Deficiency in CKD
|
Serum < 5 --- 50K units PO Qwk x 12 wks, then Qmonth for 6 months total; measure levels after 6 months
Serum 5-15 --- 50K units PO Qwk x 4 wks, then Qmonth for 6 months total; measure levels after 6 months Serum 16-30 --- 50K units PO Qmonth x 6 months; measure levels after 6 months |
|
|
Hyperkalemia
|
K levels > 5 mEq/L
K is most abundant intracellular cation Most common cause --- decreased renal excretion d/t renal failure; can be combo w/ high K intake or use of drugs that interfere w/ K excretion S/S --- muscle weakness, bradycardia, fatal arrhythmias may develop |
|
|
Treatment of hyperkalemia
|
Remove dietary sources
Enhance potassium uptake by the cells via: *Glucose - stimulates insulin secretion *Insulin - shifts K into the cells If metabolic acidosis -- admin Na bicarb IV calcium to stabilize cardiac tissue prn Beta agonists (ex. nebulized albuterol) Increase renal excretion w/ loop diuretic *Can use fludrocortisone as well to increase excretion Kayexelate -- cation exchange resin Emergency dialysis |
|
|
Kayexelate
|
Sodium polystyrene sulfonate
Works w/in 2 hrs Can decrease K by 2 mEq/L w/ a single enema GIVEN PO or rectal; rectal is preferred in emergency tx DO NOT mix PO Kayexelate w/ sorbitol d/t risk of GI necrosis SE - decreased appetite, N/V/C |
|
|
Metabolic acidosis and CKD
|
Kidney generates bicarbonate; ability decreases as CKD progresses, resulting in metabolic acidosis
Bicarb < 22 mEq/L Use sodium bicarbonate or sodium citrate/citric acid |
|
|
Sodium bicarbonate
|
1-2 tabs PO 1-3x/d
CONTRA - alkalosis, hypernatremia, hypocalcemia, pulmonary edema Caution in HTN, CV disease, fluid retention issues SE - N/V/D, increased sodium |
|
|
Sodium citrate/citric acid
|
Bicitra, Cytra-2, Oracit, Shohl's solution
10-30 mL PO w/ water after meals and at bedtime CONTRA - alkalosis, Na restricted diet, hypernatremia SE - N/V/D, increased sodium *May not be effective in liver failure - metabolized to bicarb by the liver* Avoid use w/ aluminum containing products Take after meals to avoid laxative effect Chill to improve taste |
