Acute and Chronic Kidney Disease: Understanding Renal Dysfunction, Exams of Nursing

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RNSG 2432 Exam 2: AKI and CKD All 207

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Renal cortex - ANSWER- outer area of kidney renal medulla - ANSWER- inner area of kidney⟶ renal columns, pyramids, papilla renal capsule - ANSWER- sausage casing minor calyx - ANSWER- small cuplike extensions where urine collects before flowing into urinary bladder⟶ several of these make up the major calyx major calyx - ANSWER- made up of several minor calyces⟶ urine flows through here before entering bladder renal column - ANSWER- delineates lobes of the kidney; part of the renal medulla renal pyramid - ANSWER- part of the renal medulla renal papilla - ANSWER- part of the renal medulla; base of the renal pyramid, projects into minor calyx hilus - ANSWER- pushed in center spot where blood vessels, lymphatic vessels, nerves, and ureter penetrate the kidney renal pelvis - ANSWER- dilated part of ureter in kidney⟶ formed by convergence of calyces and leads to ureter ureter - ANSWER- urine flows from kidney to bladder through here nephrons are - ANSWER- small filters in the kidney⟶ filter blood and create urine Kidney filtration process - ANSWER- 1. unfiltered blood enters the kidney

2. nephrons filter blood
3. urine drains into central collection
4. urine exits the kidney through the ureter
5. filtered clean blood leaves the kidney how many nephrons are in the kidney - ANSWER- >1 million Glomeruli - ANSWER- Tiny clusters of looping blood vessels; comes from the Greek word meaning filter.

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Nephron - ANSWER- Functional unit of the kidney; structure that actually produces urine in the process of removing waste and excess substances from the blood. Major functions of the kidney - ANSWER- regulate electrolyte balance⟶ continually filtering blood collect and excrete waste⟶ ammonia, bilirubin, creatinine, drugs, toxins (NSAIDs are esp harsh) secrete hormones regulate BP activate vitamin D & calcium reabsorption maintain Acid/base balance hormones secreted by the kidney - ANSWER- ADH⟶ holds fluids in erythropoietin⟶ RBC production prostaglandins renin⟶ part of RAAS system calcitrol⟶ vitamin D synthesis BP regulation⟶ RAAS system - ANSWER- renin-angiotensin-aldosterone-system hormone system that regulates BP, F&E balance, systemic vascular resistance kidneys maintain acid-base balance by - ANSWER- excreting H+ ions conserving HCO3 (bicarbonate) urea - ANSWER- waste product of protein metabolism protein⟶ ammonia⟶ urea uric acid - ANSWER- product of nucleotides creatinine - ANSWER- waste product of creatinine; muscle bilirubin - ANSWER- breakdown of RBC⟶ excreted in bile azotemia - ANSWER- too much nitrogen malproduction of kidney and waste system uremia - ANSWER- too much urea simple steps of RAAS system - ANSWER- kidneys sense ↓ in BP⟶ release renin⟶ secrete angiotensinogen⟶ converts to angiotensin I⟶ converts to angiotesin II angiotensin II causes vasoconstriction (↑ BP) and activates aldosterone⟶ holds on to H2O & Na+ but loses K+⟶ Na+ retention causes ↑ BP

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Activated Vit D is required for - ANSWER- absorption of Calcium in AKI/CKD Vit D is inactivated d/t kidney deficiencies and - ANSWER- does not allow for Calcium/phosphorus exchange in the kidney inability to convert vit D means - ANSWER- ↓ absorption of Ca⟶ && Ca⟶ ↑ PTH secretion⟶ calcium/phosphorus released from bones = demineralization low calcium and high phosphorus levels low calcium and high phosphorus levels cause - ANSWER- very soft or malformed bones regulation of acid-base imbalance is primarily controlled by - ANSWER- lungs⟶ regulate carbonic acid through respiration kidneys⟶ regulate bicarbonate by retention or excretion causes of metabolic acidosis - ANSWER- inability to excrete H+ ions and metabolic end products buffering of acidic hydrogen ions & metabolic end products ↓ bicarb production acute kidney injury (AKI) usually pertains to - ANSWER- a short term kidney problem but may lead to chronic kidney problems most pts can return to normal kidney fx What is acute kidney injury - ANSWER- umbrella term describing rapid decline in renal function spectrum of mild to severe with sudden onset leads to accumulation of nitrogenous waste⟶ azotemia Kidneys unable to remove urea from the blood⟶ uremia common causes of AKI - ANSWER- dehydration trauma drugs⟶ nephrotoxins infection Types of AKI - ANSWER- pre-renal intra-renal post-renal determined by where the damage/assault is happening

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pre renal AKI (before the kidney) examples - ANSWER- Problem with forward flow, low blood flow/hypovolemia: sepsis, dehydration *hypotension/decreased vascular resistance: CHF, MI *Arterial Obstruction: renal artery stenosis/obstruction ↑ BUN/Crt⟶ most common lab feature intra renal AKI (within the kidney) examples; aka Acute Tubular Necrosis (ATN) - ANSWER- Nephrotoxins, Drugs: Aminoglycosides, contrast, arsenic, antibiotics Prolonged Ischemia, direct injury: trauma Infections: UTI, Acute glomerulonephritis/Acute pyelonephritis Hgb from hemolyzed RBC: blood transfusion (hemolytic reaction) Myoglobin from necrotic muscle cells: Rhabdomyolysis post renal AKI (after the kidney) - ANSWER- Downstream Obstruction: trauma, BPH, hydro-nephrosis, strictures, cancer Neuromuscular disease: neurogenic bladder, retention renal trauma (intra-renal AKI) causes - ANSWER- blunt vs penetrating renal trauma (intra-renal AKI) diagnosis - ANSWER- IV pyelogram, renal US, CT, renal angiogram labs for renal trauma (intra-renal AKI) - ANSWER- BUN, Cr, CBC, RBC, H&H, UOP (color, output, clots in urine) and bladder scan why do we have strict hourly monitoring of UOP - ANSWER- to help identify AKI and further progression of kidney issues oliguria, anuria, hematuria s/sx of renal trauma - ANSWER- flank or abd pain, localized swelling, tenderness, ecchymosis, Turner's sign treatment of renal trauma - ANSWER- rest, observation, embolization vs open surgery for bleeding/repair, partial or total nephrectomy what is rhabdomyolysis - ANSWER- when the breakdown of muscle tissue releases intracellular contents into the blood⟶ can cause kidney damage signs of rhabdo - ANSWER- muscle pain, weakness, dark urine ELEVATED creatine kinase levels K+, BUN/Cr, myoglobin may be ↑ or ↓ myoglobin may occlude structures of the kidney and - ANSWER- break down into toxic compounds⟶ acute tubular necrosis or acute renal failure⟶ clogs the kidneys

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CK levels - ANSWER- tell how severe the rhabdo is renal biopsy indications - ANSWER- dx AKI, CKD or mass may be used on living donor to assess match nephrectomy indications - ANSWER- Renal tumor Massive trauma Polycystic kidney disease Donating a healthy kidney post op nephrectomy or renal biopsy management - ANSWER- MONITOR FOR BLEEDING⟶ v high risk Strict I&O: drains/foley TCDB & IS Incision in flank area, most done laparoscopically Pain control Renal Vein Thrombosis (clot in kidney) causes - ANSWER- trauma extrinsic compression d/t tumor, aortic aneurysm renal cell cancer pregnancy contraceptive use nephrotic syndrome diagnostics for renal vein thrombosis - ANSWER- kidney US, Doppler US, MRA/MRV Manifestations of renal vein thrombosis - ANSWER- flank pain, hematuria, fever, nephrotic syndrome treatments for renal vein thrombosis - ANSWER- Corticosteroids Anticoagulation Thrombectomy nephrotic syndrome is a - ANSWER- kidney disorder that causes your body to pass too much protein in your urine nephrotic syndrome is usually caused by - ANSWER- damage to the clusters of nephrons GFR tells us - ANSWER- how well kidneys are filtrating Sometimes acute kidney failure causes no s/sx because - ANSWER- we have so many nephrons the kidneys can absorb a lot of damage before it is noticed

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often detected through labs done for other reasons RIFLE defines - ANSWER- 3 grades of ↑ severity of AKI and 2 outcome classes RIFLE - ANSWER- severity: risk class⟶ at risk of AKI RIFLE - ANSWER- severity: injury class⟶ kidney is injured RIFLE - ANSWER- severity: failure class⟶ in kidney failure RIFLE - ANSWER- outcome: loss class⟶ loss of kidney function RIFLE - ANSWER- outcome: ESRD class⟶ in end stage renal disease 4 phases of AKI - ANSWER- onset⟶ hours to days oliguric⟶ 1 - 7 days (can last 10 days to months) diuretic⟶ until UOP improves recovery⟶ until concrete proof is shown in labs AKI: oliguric phase timeline - ANSWER- 1 - 7 days, but can last 10 days to months AKI: oliguric phase is defined by - ANSWER- UOP <400mL/day *but some pts can be non-oliguric AKI: oliguric phase diagnostics - ANSWER- UA: RBC, WBC, proteinuria, casts UOP: <400ml/day GFR: abrupt decline BUN/Cr: elevated Cr Clearance: >50% decreased Spec Grav: High & fixed at 1.010⟶ kidney loses ability to concentrate urine Na: potential for hypernatremia⟶ cannot excrete K: potential for hyperkalemia⟶ cannot excrete ABG: potential for metabolic acidosis⟶ && HCO3 production Calcium/Phos: ↓ Ca/↑ Phos⟶ no vit D = no calcitonin 24hr Urine Collection⟶ shoes how much Cr clears through kidneys in a day normal BUN levels - ANSWER- 10 - 20mg/dL critical level is > normal Cr levels - ANSWER- female 18-41y: 0.5-1.0 mg/dL female 41-61y: 0.5-1.1 mg/dL male 18-41y: 0.6-1.2 mg/dL male 41-61y: 0.6-1.3 mg/dL

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AKI: manifestations of oliguric phase - ANSWER- Oliguria (~50% of cases NON- oliguric) Edema, Pulmonary Effusion, HTN, HF, CP, JVD Peaked T wave⟶ hyperkalamia HA, anxiety, AMS, seizures, coma⟶ severe hypernatremia Kussmaul respirations⟶ indicates trying to blow off CO AKI: oliguric phase is a HIGH RISK for - ANSWER- fluid overload AKI: oliguric phase treatment - ANSWER- determine the cause Fluids to "blast out" tubules (most AKI fixes) If fail ⟶ Diuretics (Mannitol/Lasix) If fail ⟶ fluid restriction (UOP past 24hrs + 600ml) Treat fluid/electrolyte imbalances Daily weights, monitor labs, UOP CRRT: continuous renal replacement therapy Longer this phase lasts, poorer outcome why to we ↑ fluids when fluid overload is a high risk? - ANSWER- dehydration is the most common cause blasting w/ fluids can "jumpstart" the kidneys AKI: diuretic phase diagnostics - ANSWER- ↑ UOP⟶ can be up to 1-5L/day nothing definitive in other labs AKI: diuretic phase manifestations - ANSWER- Kidneys recover ability to excrete waste, but cannot concentrate urine Hypovolemia/hypotension may occur from massive volume loss AKI: diuretic phase treatment - ANSWER- Monitor for ↑↓Na, ↓K, dehydration MONITOR BP for hypotension Treat fluid/electrolyte imbalances Daily weights, monitor labs, UO Persistent HypoTN ⟶ vasopressors CRRT AKI: recovery phase is defined by - ANSWER- shows concrete proof in labs GFR ↑, BUN/Cr normalizes AKI: recovery phase diagnostics - ANSWER- labs begin to stabilize⟶ concrete proof of recovery phase AKI: recovery phase outcome depends on - ANSWER- overall health, severity of kidney injury, degree of complications

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w/ aggressive tx most pts achieve normal kidney fx w/o complications some have no recovery and progress to ESRD pt teaching for recovery phase of AKI - ANSWER- avoid NSAIDs and other nephrotoxins AKI treatments - ANSWER- Phosphorus Calcium Hypertension Anemia Nutritional Considerations Emergency dialysis Phosphorus - ANSWER- Renagel, Sevelamer hydrochloride Nephrox (phospate binders) Calcium - ANSWER- Phoslo, Calcium Acetate Oscal, Calcium Carbonate Hypertension - ANSWER- Lasix Norvasc (Amlodipine), Lopressor (Metoprolol) ACE inhibitors Anemia - ANSWER- epogen/Procrit ⟶ erythropoietin PRBC for Hgb < 7 Nutritional Considerations - ANSWER- Fluid: depends on fluids status ('blasting' vs restriction) Diet: K? Na? Protein? Normal 30-35Kcal/kg Emergency dialysis - ANSWER- K> 6 ⟶ usually reserved for this, often non-responsive to other meds Fluid overload (decompensated) Uremia Metabolic acidosis HCO3 < why do we see metabolic acidosis in AKI/CKD? - ANSWER- ↓ HCO3 production how do we treat metabolic acidosis - ANSWER- NaBicarb, NaCitrate, fluids, dialysis, CRRT what do respirations oiften look like in metabolic acidosis - ANSWER- Kussmaul respirations to try to blow off Co

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if they become slow/shallow⟶ decompensation⟶ intermediate intervention required treatment for hyperkalemia: C BIG K Drop - ANSWER- given in this order Calcium gluconate⟶ protects heart Beta-agonists (alButerol)or Bicarbonate⟶ shifts K+ into cell Insulin (second) + Glucose (first)⟶ shifts K+ into cell, avoids ↓ glucose Kayexalate⟶ binds w/ K+ in gut Diuretics⟶ furosemide (Lasix) Renal unit for dialysis of patient major side effect of dialysis - ANSWER- hypotension What is CRRT - ANSWER- continuous renal replacement therapy basically a slower continuous form of hemodialysis when is CRRT used - ANSWER- when patients are unstable or hypotensive and cannot handle hemodialysis usually for progressive AKI w/ certain criteria progressive AKI - ANSWER- Cr 3x baseline or acute rise >4mh/dL CrCl ↓ >75% hypotension volume overload w/ compromised cardiac/pulmonary status hyperkalemia (refractory to medical tx) metabolic acidosis mental status △'s dialyzable toxins⟶ lithium, toxic alcohols, salicylates AKI treatment goals - ANSWER- Determine/treat cause Manage s/sx Prevent complications treating primary underlying condition of AKI - ANSWER- Pre-renal, Intra-renal, Post- renal Determine cause! AKI tx: manage fluid balances - ANSWER- Strict I&O, daily weights relevant labs⟶ BUN/Cr, GFR, UOP, Na, K+, WBC, urine specific gravity Fluids during oliguric phase⟶ BLAST THEM if fluids fail⟶ diuretic therapy if diuretics fail⟶ restrict fluids

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How to we determine AKI fluid restriction - ANSWER- UOP last 24h + 600mL = fluid limit AKI complication prevention - ANSWER- Watch for early s/sx AKI⟶ oliguria <400mL Caution with contrast dye, nephrotoxic agents and other risk factors Nursing implications for AKI - ANSWER- Strict I&O, daily fluid volume replacement vs restriction Daily weights Monitor labs: Na, K, GFR, BUN/Crt, WBC, Specific Gravity, UOP Physical Exam: mental status, LOC, dysrhythmias, crackles, cardiac rub, murmur, signs of dehydration vs fluid overload Caution/Education: NSAIDS, ACE inhibitors, contrast dye, other nephrotoxins Pt admitted w/ crush injury to legs. serum myoglobin level 115.4 (ref 5-70) CK 960 (ref 22 - 198) What is your biggest concern? - ANSWER- rhabdo d/t ↑ myoglobin Pt admitted w/ crush injury to legs. serum myoglobin level 115.4 (ref 5-70) CK 960 (ref 22 - 198) What assessment findings might you see? - ANSWER- dark urine, muscle pain, weakness ↑ K+, ↓ UOP, ↑ CK Pt admitted w/ crush injury to legs. serum myoglobin level 115.4 (ref 5-70) CK 960 (ref 22 - 198) What are your priorities/treatment? - ANSWER- monitoring UOP, s/sx of AKI, fluids, diuresis PRN to prevent hyperkalemia, further renal injury, monitor for compartment syndrome, monitor EKG primary goals w/ chronic kidney disease (CKD - ANSWER- identify CKD, prevent further progression CKD is defined by - ANSWER- progressive, irreversible loss of kidney function AEB: Presence of kidney damage GFR <60 for longer than 3 months GFR stands for - ANSWER- glomerular filtration rate GFR estimates - ANSWER- how much blood passes through glomeruli filters each minute 5 stages of CKD in GFR - ANSWER- Stage 1 GFR >90⟶ normal kidney function

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Stage 2 GFR 60- 89 ⟶ early stage kidney disease Stage 3 GFR 30- 59 Stage 4 GFR 15- 29 Stage 5 GFR <15⟶ kidney failure what eGFR indicates need for dialysis - ANSWER- < most common causes of CKD - ANSWER- DM, HTN, glomerulonephritis, cystic disorders, developmental/congenital, infectious disease CKD stage is defined by - ANSWER- lab results GFR is not diagnostic in stages 1 and 2 in stage one and two of CKD, patients may be asymptomatic because - ANSWER- the other nephrons are handling renal matters CKD stage 1 labs - ANSWER- GFR ≥90⟶ not diagnostic Cr doubles CKD stage 1 manifestations - ANSWER- kidney damage w/ GFR ↑ or WNL 50% nephron loss may be asymptomatic CKD stage 1 plan - ANSWER- dx/treat risk reduction has slow progression CKD stage 2 labs - ANSWER- GFR ≥60- 89 GFR not diagnostic CKD stage 2 manifestations - ANSWER- kidney damage w/ ↓ GFR 50% nephron loss may be asymptomatic CKD stage 2 plan - ANSWER- estimate progression CKD stage 3 labs - ANSWER- GFR ≥30- 59 CKD stage 3 manifestations - ANSWER- Presence of kidney damage with mod. ↓ in GFR Malnutrition: ↓ Nutrition ⟶ anorexia, N/V, uremia, hormone imbalance, acidosis Anemia: EPO reduction LVH: Arterial HTN ⟶ pressure/volume overload ⟶ rapid atherosclerosis (80%) Renal Osteodystrophy: alterations in calc/phos metabolism = skeletal changes

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CKD stage 3 plan - ANSWER- evaluating & treating complications CKD stage 4 labs - ANSWER- GFR ≥15- 29 ↑ triglycerides ↑ phosphorus d/t not excreting ↑ K+ d/t not excreting CKD stage 4 manifestations - ANSWER- Significant ↓ GFR and solute clearance Can't concentrate urine, abnormal hormone secretion Metabolic acidosis: Kidneys not excreting acid, cannot retain adequate bicarbonate Uncompensated metabolic acidosis⟶ ↓ pH, normal CO2, ↓ HCO CKD stage 4 plan - ANSWER- prepare for kidney replacement CKD stage 5 labs - ANSWER- GFR <15 ↑ nitrogenous waste, ↑ BUN/Cr, ↑ urea, ↑ Phos, ↓ H&H, ↓ Ca CKD stage 5 is - ANSWER- ESRD CKD stage 5 manifestations - ANSWER- residual function <15% of normal GFR under 15 - ANSWER- excretory, regulatory, hormonal fx are severely impaired⟶ 90% have renal bone disease metabolic acidosis azotemia, uremic syndrome neuro: confused, ↓ LOC, fatigue CV: ↑ HR, swelling, OH fluid overload⟶ fatal if not treated CKD stage 5 plan - ANSWER- kidney replacement flow of renal failure malabsorption to renal osteodystrophy - ANSWER- ↓ vit D⟶ ↓ Ca absorption⟶ hypocalcemia⟶ ↑ PTH⟶ bone demineralization releases Ca into blood⟶ renal osteodystrophy lab results we see in renal failure malabsorption - ANSWER- hyperphosphatemia hypocalcemia ↑ PTH ↓ vit D PTH controls - ANSWER- reabsorption of phosphorus⟶ it is excreted through kidneys

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with CKD you see an ↑ in - ANSWER- PTH⟶ phosphorus builds up and vit D metabolism ↓ in the body CKD clinical manifestations in the urinary system - ANSWER- Early stages ⟶ no △'s in UOP If diabetes present may have polyuria Progressing stages ⟶ fluid retention ESRD ⟶ anuria CKD metabolic disturbances (clinical manifestations) - ANSWER- Waste production accumulation (BUN/Creatinine ↑) Carbohydrate intolerance Hyperlipidemia Kussmaul breathing Uncompensated Metabolic Acidosis ○ ↓ pH, normal CO2, ↓ HCO CKD electrolyte & acid-base imbalances - ANSWER- Hyperkalemia Na normal or low Calcium low Phosphorous high Hypermagnesemia Metabolic acidosis CKD hematologic implications - ANSWER- Anemia r/t ↓ in EPO production Bleeding tendencies r/t platelet dysfunction Infection r/t changes in leukocyte function CKD endocrine and reproductive manifestations - ANSWER- Hyperparathyroidism d/t vit D chain reaction Thyroid abnormalities Amenorrhea Erectile dysfunction CKD musculoskeletal manifestations - ANSWER- Vascular and soft tissue calcifications Renal Osteodystrophy Osteomalacia (bone softening) r/t parathyroid secreting PTH Osteitis fibrosa Osteitis fibrosa cystica (OFC) is a disorder involving the bone which results from - ANSWER- excessive production of PTH d/t PT gland hyperactivity CKD diagnostic studies - ANSWER- urinalysis renal US

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GFR

CKD diagnostics: UA - ANSWER- protein⟶ persistent proteinuria: 1+ on dipstick 2+ times over 3mo period RBCs WBCs Glucose CKD diagnostics: renal US - ANSWER- examines size, looks for obstruction CKD diagnostics: GFR calculation is considered best index to - ANSWER- estimate kidney function as it accounts for the specific criteria to individualize the filtration rate: ○ Serum creatinine ○ Gender ○ Ethnicity ○ Age ○ Weight treatment options for CKD - ANSWER- Correction of ECF overload or deficit Nutrition therapy EPOGEN (epoetin alfa) therapy Calcium supplements Antihypertensive therapy ACE inhibitors Treat hyperlipidemia Decrease Potassium⟶ ↓ intake or C BIG K DROP Adjust medications for renal doses Renal replacement therapy (RRT) ⟶ dialysis, transplant What do we need to manage with CKD - ANSWER- hyperkalemia⟶ limit foods high in K+ HTN⟶ ↓ Na+ intake Hyperphosphatenemia⟶ low phos diet, phosphate binding meds Hyperparathyroidism⟶ can cause renal osteodystrophy anemia⟶ procrit/epogen, takes 2 - 3w to see results hyperglycemia dyslipidemia hypothyroidism⟶ hormone replacement phosphate binding medications - ANSWER- Ca acetate (Phoslo) Ca carbonate (Caltrate) dialysis is - ANSWER- procedure used to correct F&E imbalances and remove waste products in renal failure

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dialysis acts as - ANSWER- artificial kidney to filter toxins, waste, and fluid from blood through semipermeable membrane types of dialysis - ANSWER- hemodialysis and peritoneal dialysis both types use dialysate solution filtering process to remove unwanted substances not everybody is a candidate for both peritoneal dialysis - ANSWER- natural lining of peritoneum acts as semipermeable membrane to filter blood done daily less effective, more flexibility hemodialysis - ANSWER- artificial membrane (cellulose or synthetic) is used to filter blood 4 hours, 3x weekly what is the purpose of dialysis - ANSWER- procedure used to correct fluid/electrolyte imbalances & remove waste products in renal failure how dialysis works - ANSWER- Osmosis Diffusion Ultrafiltration osmosis in dialysis - ANSWER- Movement of fluid from area of lesser concentration to area of greater concentration diffusion in dialysis - ANSWER- Movement of solutes across membrane from area of higher concentration to area of lower concentration ultrafiltration in dialysis - ANSWER- (water & fluid removal) results when there is an osmotic gradient or pressure gradient across the membrane what GFR indicates a need for hemodialysis - ANSWER- < peritoneal dialysis summary - ANSWER- 12% of dialysis in the US High concentration of glucose in dialysate Creates hypertonic solution, draws wastes in through osmosis & diffusion Wastes & electrolytes diffuse into dialysate until equilibrium achieved Automated vs Continuous Ambulatory Peritoneal dialysis solution should look - ANSWER- clear and straw colored if its cloudy that could indicate infection⟶ peritonitis⟶ possible sepsis

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which type of dialysis has an ↑ r/o infection - ANSWER- peritoneal peritoneal dialysis phases - ANSWER- fill⟶ fluid is infused into peritoneal cavity dwell⟶ the time fluid remains in peritoneal cavity drain⟶ time fluid drains from peritoneal cavity Advantages of peritoneal dialysis - ANSWER- Independence for patient easier on the body system No needle sticks Better blood pressure control Some diabetics add insulin to solution Fewer dietary restrictions ○ Protein loses in dialysate ○ Generally need ↑ potassium ○ Less fluid restrictions complications of peritoneal dialysis - ANSWER- Site infection Peritonitis ⟶ #1 priority ASSESS for abd pain/tenderness Hernia Lower back problems Bleeding Pulmonary complications⟶ drain fluid if patient having resp distress to allow for diaphragm expansion, △ position Protein loss nursing assessments for patients on peritoneal dialysis - ANSWER- Daily weights Lung sounds Presence of edema Total I & O s/sx of infection ⟶ peritonitis Blood pressure s/sx of dehydration or fluid overload Electrolytes △'s in BGL in diabetics from use of dextrose based dialysate △'s in appearance of effluent⟶ cloudy indicates infection pt teaching for peritoneal dialysis - ANSWER- Asepsis Empty bladder first Monitor urine output Monitor s/s of infection Monitor s/s of fluid volume overload

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PD catheter dressings - ANSWER- reinforce exit site on new ones, do not remove original dressing unless trained to do so be alert to tubing getting kinked or caught under pt because - ANSWER- it will prevent infusion or draining of fluid what to do if a dialysis patient experiences cramping - ANSWER- slow the infusion/draining, reposition what to do if a dialysis patient has less output than input during treatment - ANSWER- check for kinks, change position, roll them side to side what to do if the fluid in peritoneal dialysis is cloudy - ANSWER- abd assessment (pain, tenderness, rigidity), take vitals, call HCP why do we use warm sterile solution for peritoneal dialysis - ANSWER- warm to prevention vasoconstriction and sterile to prevention infection hemodialysis process - ANSWER- Blood removed from patient into extracorporeal circuit⟶ external kidney Diffusion and ultrafiltration take place in dialyzer Cleaned blood returned to patient hemodialysis access requires special access for - ANSWER- large volume hemodialysis access types - ANSWER- emergency catheter AV fistula AV graft what is an AV fistula - ANSWER- artery and vein are joined in surgery to create a bigger vessel for greater flow through the vein⟶ takes weeks to months to "mature" for use for hemodialysis fewer complications than other devices hemodialysis nursing implications - ANSWER- NO BP's or needle sticks to arm with vascular access⟶ includes finger sticks Place ID bands on other arm whenever possible Palpate thrill and listen for bruit⟶ these are good, you WANT these Document findings AND report loss of thrill or bruit Teach patient to wear nothing constrictive on that arm nursing care for a bleeding fistula (leaking, oozing, blood) - ANSWER- High volumes of blood can be lost quickly Prioritize patient w/ bleeding fistula!

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complications of hemodialysis - ANSWER- Hypotension most common⟶ r/t Hypovolemia and ↓ CO Disequilibrium syndrome ⟶ neuro s/sx d/t rapid removal of urea during hemodialysis Muscle Cramps Loss of Blood⟶ r/t blood incompletely rinsed from dialyzer Hepatitis from transfusions urea & protein are end products of - ANSWER- protein metabolism education for patients on dialysis - ANSWER- Monitor BP/HR before/after⟶ will be on tele Medications⟶ hold until after Daily weights Alleviate fears/reassurance Dialysis process Fistula/catheter care Diet: ↓K, ↓protein, ↑carb Diabetic teaching a kidney transplant is a treatment and not a - ANSWER- cure kidney transplant statistics - ANSWER- Only 4% ESRD get transplant 1 year survival rate ○ 90% for deceased donor ○ 95% for live donor advantages of kidney transplant - ANSWER- Restoration of "normal" renal function Freedom from dialysis Return to "normal" life Reverses pathophysiological changes r/t Renal Failure Less expensive than dialysis after 1st year disadvantages of a kidney transplant - ANSWER- lifelong medications⟶ immunosuppressants to ↓ rejection side effects from medications ↑ risk of cancer d/t immunosuppressants MAJOR SURGERY goal of immunosuppressants post-transplant - ANSWER- balance of suppression w/ maintenance of adequate defense side effects of immunosuppressant drugs - ANSWER- Infection Malignancies Toxicity

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considerations of immunosuppressants post-kidney transplant - ANSWER- Require frequent monitoring Teach food/drug interactions Strict med schedule Goal: Lowest dose for response that causes least side effects 2 categories of immunosuppressant medications - ANSWER- Induction agents⟶ powerful antirejection medications used at time of transplant Maintenance agents⟶ long-term antirejection meds most common combos of immunosuppressant drugs - ANSWER- Tacrolimus Mycophenolate Mofetil Prednisone monitoring transplant function - ANSWER- intra-renal AKI accurate I&O⟶ critical to avoid dehydration, output 100-500ml/Hr potential for volume deficit and/or overload labs⟶ K+, Na+, blood sugar US, renal scans, renal biopsy daily weights⟶ 2lbs/24h BAD assessment of renal fx and F&E balance INFECTION PREVENTION prevention & mgmt of rejection transplant rejection stages - ANSWER- hyperacute accelerated acute chronic hyperacute transplant rejection - ANSWER- Function ceases within 24hrs, Preformed antibodies to donor antigen Rx = removal accelerated transplant rejection - ANSWER- 1st week to one month, same as hyperacute but slower Rx = removal acute transplant rejection - ANSWER- First 6 months, 50% experience rejection vs cyclosporine toxicity Weight gain, ↑BUN/Cr, site tenderness, fever, ↓UOP, HTN, increased infx risk Rx = Usually reversible with additional immunosuppressants chronic transplant rejection - ANSWER- Gradual process months to years

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Irreversible Repeated rejection episodes not completely resolved with treatment Rx = return to dialysis or re-transplantation A patient is diagnosed with chronic renal failure and told she must start hemodialysis. Patient teaching would include which of the following instructions? A. Follow a high potassium diet B. Strictly follow the hemodialysis schedule C. There will be a few changes in your lifestyle D. Use alcohol on the skin and clean it due to integumentary changes. - ANSWER- B. Strictly follow the hemodialysis schedule A patient is undergoing peritoneal dialysis. The dialysate dwell time is completed, and the dwell clamp is opened to allow the dialysate to drain. The nurse notes that the drainage has stopped and only 500 ml has drained; the amount the dialysate instilled was 1,500 ml. Which of the following interventions would be done first? A. Change the patient's position B. Call the physician C. Check the catheter for kinks or obstruction. D. Clamp the catheter and instill more dialysate at the next exchange time. - ANSWER- C. Check the catheter for kinks or obstruction. A patient receiving hemodialysis treatment arrives at the hospital with a blood pressure of 200/100, a heart rate of 110, and a respiratory rate of 36. Oxygen saturation on room air is 89%. He complains of shortness of breath, and 2+ pedal edema is noted. His last hemodialysis treatment was yesterday. Which of the following interventions should be done first? A. Administer oxygen B. Elevate the foot of the bed C. Restrict the patient's fluids D. Prepare the patient for hemodialysis. - ANSWER- A. Administer oxygen