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Pharm exam 4
kidney pharmacotherapy
| Question | Answer |
|---|---|
| kidney disease worldwide prevalence | more than 697 million |
| 2017 kidney disease stats | 1.2 million deaths, 35.8 million disability-adjusted life years |
| etiology of kidney disease | Diabetic kidney disease (25-50%) Hypertension |
| most common cause of kidney disease | diabetes, type 1 and 2 |
| 2nd most common cause of kidney disease and why | HTN because pts don't feel bad when they have HTN so no reason to get checked out |
| Patients on dialysis have higher | mortality |
| most common types of pts needing kidney transplant | diabetes and HTN |
| main functional component of kidneys | glomerulus |
| normal urine output | 0.5-1ml/kg/hr 840-1680 ml/day |
| functions of the kidney | excretory functions endocrine functions metabolic functions |
| excretory function of kidney | Water Electrolytes Urea Medications |
| some electrolytes and medications are | actively secreted |
| kidney filters and reabsorbs | Water Electrolytes Urea Medications |
| endocrine function of kidney | Hormones – e.g. erythropoietin |
| erythropoietin | produced by kidney and promotes production of RBC |
| if kidneys can't make erythropoietin | then there will be a lack of RBC |
| metabolic function of kidney | Vitamin D Gluconeogenesis Insulin |
| metabolic function regarding insulin | kidneys aren't eliminating insulin as well so need to decrease dose of insulin, does NOT mean diabetes is getting better |
| assessment of kidney function using | creatinine, cystatin C, urinalysis |
| creatinine | product of creatine metabolism from muscle |
| normal Scr | 0.5-1.2 mg/dL |
| increased Scr suggests | kidney failure |
| equations | CrCl and eGFR |
| CrCl estimates | how much blood the kidneys clear of creatinine per minute |
| eGFR estimates | the overall filtering capacity of the kidneys |
| creatinine is higher in | men because they typically have a higher muscle mass |
| cystatin C | product of all nucleated cells |
| normal cystatin C | 0.55-1.18 mg/dL (women) 0.6-1.11 mg/dL (men) |
| cons to cystatin C | takes longer in the lab, more expensive |
| urinalysis | Albumin (normal <30mg/g Creatinine) Protein (normal <150mg/g creatinine) |
| staging of CKD | stage 2-5 |
| what level do you start dialysis | stage 5 |
| what is CKD staging based off | GFR (ml/min/1.73m2) |
| likely to identify CKD prior to | stage 2 |
| the lower the GFR | the more severe stage |
| albuminuria categories | A1, A2, A3 |
| albuminuria categories based off | Quantification (mg/g) |
| as you increase Quantification (mg/g), | the more severely increased the albuminuria |
| Sociodemographic factors impacting risk of CKD | Ethnic minority Older age Low income/education Environmental exposures |
| Clinical factors impacting risk of CKD | !!Diabetes !!Hypertension, cardiovascular dz Obesity Smoking Autoimmune dz Infection CAD h/o AKI |
| symptoms of CKD stage 4-5 | Fatigue Weakness Shortness of breath Confusion Nausea/vomiting Anorexia Itching Cold intolerance |
| why might someone with CKD 4-5 have SOB | due to the accumulation of fluid in lungs or anemia |
| signs of CKD | Edema Decreased Urine Output “foaming” of urine (albumin) Elevated blood pressure |
| edema in CKD due to | decreased urine output, seen in extremities and lungs |
| increased lab findings in kidney disease | Serum creatinine Blood Urea Nitrogen (BUN) Potassium (K+) Phosphorous (PO4) Parathyroid Hormone (PTH) Glucose/HbA1c LDL andTriglycerides |
| why is PTH high in CKD | because trying to decrease the high PO4 |
| decreased lab findings in kidney disease | eGFR Bicarbonate (metabolic acidosis) Hemoglobin/hematocrit Transferrin saturation Iron Vitamin D levels Albumin |
| treatment of kidney disease | treat underlying causes slow progression complications renal replacement therapy - dialysis |
| treatment of underlying disease like | diabetes, HTN and albuminuria |
| treatment of diabetes using | Glycemia control - early and constant! ACEI or ARB SGLT2i or GLP-1RA Finerenone Avoid sulfonylureas |
| why should a diabetic with CKD avoid sulfonylureas | because they will accumulate and cause hypoglycemia |
| ideal tx for diabetes in CKD | ARBs or ACEi |
| treatment of HTN using | Blood pressure control ACEI or ARB Thiazide diuretic, CCB Sodium restriction - in terms of volume |
| treatment of albuminuria using | ACEI or ARB preferred to decrease spilling of albumin into urine SGLT2i |
| slowing the progression of kidney disease using | ACEi, ARBs, SGLT2i, MRA, CCBs |
| ACEi example | lisinopril |
| ACEi: lisinopril SE | Hyperkalemia, cough; contraindicated in pregnancy |
| ARB example | valsartan |
| ARB: valsartan SE | Hyperkalemia; contraindicated in pregnancy |
| SGLT2i example | dapagliflozin |
| SGLT2i: dapagliflozin SE | Dehydration, GU fungal infections, DKA; contraindicated DM 1 |
| MRA example | finerenone |
| MRA: finerenone SE | Hyperkalemia |
| Non-dihydropyridine CCBs examples | verapamil, diltiazem |
| Non-dihydropyridine CCBs are fourth most effective because | not nearly as lowering ace ACEi |
| kidney disease complications | anemia, mineral bone disorder, hyperkalemia, hyperphosphatemia, n/v, itching |
| anemia of kidney disease | Increased Blood loss + Decreased erythropoietin production + Decreased RBC lifespan |
| target hemoglobin in anemia of kidney disease | less than or equal to 11 g/dL |
| treatment of anemia of kidney disease | Erythropoiesis Stimulating Agents (ESA) Iron supplementation HIF prolyl hydroxylase inhibitors (HIF-PHIs) |
| Erythropoiesis Stimulating Agents (ESA) | Erythropoietin or agents that mimic it like Darbepoietin |
| ESA: Darbepoietin SE | hypertension |
| Iron supplementation goal | Tsat U30%, Ferritin > 500ng/ml |
| oral Iron supplementation | many pts dont like because of the SE |
| oral Iron supplementation SE | constipation, nausea, and abdominal cramping |
| IV Iron supplementation SE | allergic reactions, hypotension, dizziness, dyspnea |
| HIF prolyl hydroxylase inhibitors (HIF-PHIs) example | daprodustat |
| go to other SS for IV iron and ESA | run bb run |
| Mineral and Bone Disorder of Kidney Disease goal | Prevent bone disease, CV and extravascular calcifications |
| Mineral and Bone Disorder of Kidney Disease treatment | Management of Parathyroid Hormone (PTH), phosphorus, and calcium |
| how to manage PTH, PO4 and Ca | Diet Phosphate-binding medications Vitamin D Calcimimetic therapy |
| diet | phosphorus restriction |
| Phosphate-binding medications SE | constipation, diarrhea, N/V, abdominal pain |
| Phosphate-binding medications examples | Calcium: acetate and carbonate Iron: Ferric citrate and Sucroferric oxyhydroxide Resin: sevelamer carbonate or hydrochloride (Renvela®) |
| Phosphate-binding medications should be given with | snack and meals |
| Vitamin D | calcifediol, calcitriol |
| Calcimimetic therapy | cinacalcet hydrochloride, etelcalcetide |
| risks for hyperkalemia | salt substitutes, kidney disease, medications (ACE (lisinopril), ARB (valsartan), MRA (finerenone), NSAIDs, trimethoprim/sulfamethoxazole, tacrolimus, cyclosporine, heparin) |
| presentation of hyperkalemia | Asymptomatic Heart palpitations ECG changes – peaked T waves |
| dietary considerations: high phosphorus content | Natural vs processed - natural better because less added phosphorus and less absorbable by the body Vegetable vs animal proteins - vegetable proteins better because produce less metabolic waste and have less added phosphorus |
| dietary considerations: high potassium content | Bananas Avocado Potatoes Leafy greens Pomegranate Beets Prunes, raisins, apricots |
| treatment of hyperkalemia is | emergent |
| treatment of hyperkalemia goals | Antagonize cardiac effects Restore normal body-stores of potassium (i.e. <5meq/L) |
| treatment of hyperkalemia examples | Calcium (gluconate or chloride) Regular Insulin (+/- glucose) B-2 receptor agonists (albuterol, terbutaline) Sodium bicarbonate Loop diuretics (furosemide) |
| Calcium (gluconate or chloride) effect | Stabilize cardiac membrane |
| Regular Insulin (+/- glucose) effect | Shift Potassium from extracellular to intracellular |
| Loop diuretics (furosemide) effect | Increase elimination |
| Dialysis effect | removes potassium fast |
| Exchange resins effect | removes potassium slow |
| Hyperkalemia meds | veltassa and lokelma |
| veltassa | cation exchange polymer that contains a calcium-sorbitol counterion - powder |
| SE of veltassa | constipation, hypomagnesemia, diarrhea, nausea, abdominal discomfort and flatulence |
| lokelma | sodium zirconium cyclosilicate – potassium binder |
| SE of lokelma | edema!! |
| pt counseling of veltassa and lokelma | Require separation from other medications |
| how long does veltassa have to be separated for | 3 hrs |
| how long does lokelma have to be separated for | 2 hrs |
| uremia symptoms | Altered mental status Nausea/Vomiting Itching |
| dialysis consideration | B-vitamins/folate removed by dialysis – supplementation “nephrovites” |
| Medication dosing/administration in kidney disease | Increased total body water Slower elimination Changes in binding |
| types of renal replacement therapy | Kidney transplant Intermittent Hemodialysis (IHD) Home Hemodialysis Peritoneal Dialysis Continuous Renal Replacement Therapy (CRRT) |
| Kidney transplant | least invasive long term, requires anti-rejection med |
| Intermittent Hemodialysis (IHD) | most traditional, 3x a week, 3-4 hrs intrusive and not flexible |
| Home Hemodialysis | pt and caregiver need to be trained, allows for flexibility |
| Peritoneal Dialysis | doesn't use needles, uses peritoneum cavity |
| Continuous Renal Replacement Therapy (CRRT) | used for critically ill pts in the hospital, runs 24hrs a day, runs much slower and gentler than dialysis as pts BP may not tolerate the high fluid like in dialysis |
Created by:
leh195