Exam 2 Renal Flashcards
anuria
no urine output or less than 50mL in 24 hours
oliguria
less than 400mL in 24 hours or less than 20mL per hour
azotemia
accumulation of nitrogenous waste in blood; BUN and creatinine (nitrogen in blood)
uremia
accumulation of nitrogenous waste in urine
gerontologic changes with kidney and urine
aging kidney less able to compensate for fluid changes, solute load, and CO; number of functioning nephrons decrease; decreased renal clearance; creatinine slowly increases; enlarged prostate; incontinence d/t decreased bladder innervation and weakened muscular tone; risk for malnutrition; thirst suppression; confusion
normal renal functions
maintenance of blood volume or pressure (RAAS); concentrates ions like bicard and hydrogen; maintains long term acid base balance (become acidic without); metabolic gluconeogenesis (liver backup); excrete metabolic waste; produce erythropoietin and renin; convert vitamin D to active form
Kidney function: Very Clever People Make Exciting Explorers
Volume, Concentration, pH balance, make gluconeogenesis or change amino acids, excretion, endocrine creates erythropoietin and renin
types of AKI
prerenal: blood flow to kidney; intrarenal: problem in kidney; postrenal: ureteral blockage; overall 50% mortality with treatment
chronic renal insufficiency/Chronic renal failure
GFR < 60mL/min; ESRD < 15mL/min; need dialysis or kidney transplant
Acute kidney injury
sudden decrease in renal function resulting from injury or toxins; causes accumulation of nitrogenous waste; if not corrected then can cause irreversible tubular necrosis
risk factors for AKI
over age of 65, INFECTION/SEPSIS, cardiac failure, respiratory failure, HX of leukemia or lymphoma, HYPOTENSION, nephrotoxic agents, liver disease
labs associated with AKI
increased fluid, increased BUN, increased creatinine, decreased urine output (<400mL/day), acidosis
stages of AKI
initiation -> oliguric (1-7 days) -> diuretic -> recovery
interventions for AKI
dialysis if needed,
electrolyte changes with AKI
hyperphosphatemia, hypernatremia, hypermagnesemia, hyperkalemia (causes peaked T waves)
assessment for kidney function
HPI, questions like what did they come in for?, what are their daily meds?, what is the urine color?, any pain when urinating?, blood present?, recent antibiotics?, recent infections?; physical exam; diagnostic tests
diagnostic testing for AKI
CT, MRI, UA, C&S, KUB, ultrasound, cystography; these are looking for structural changes in kidney
assessing an AKI
urine output volume over 24 hours, GFR, BUN: creatinine ratio (usually 10-20:1)
BUN normal values
10-20mg/dL
Creatinine normal values
adult men: 0.74-1.35mg/dL
adult women 0.59-1.04mg/dL
early manifestations of AKI
decreased creatinine clearance; increased BUN and Creatinine values; proteinuria (protein passing through glomerulus NOT GOOD)
later manifestations of AKI
fluid retention causing edema and oliguria; anemia due to reduced erythropoietin, acidosis, increased electrolytes and waste products
best indicators of kidney function
creatinine and urine output
prerenal AKI causes
decreased perfusion to the kidneys causing decreased perfusion and O2; d/t cardiac damage, vasodilation, hemorrhage, burns, GI losses, stenosis, constriction
causes of intrarenal AKI
damage in kidneys caused by prolonged ischemia; d/t myoglobinuria, hemoglobinuria, rhabdomyolysis, nephrotoxic drugs (NSAIDs, dye, antibiotics ending in mysin), infections, acute tubular necrosis
postrenal AKI
damage after the kidneys; caused by obstruction or blockage of urinary tract causing increased pressure in kidney and decreased filtration; due to renal calculi, blood clots, retriperitoneal issues, BPH, tumors, neuro damage (stroke), spinal cord damage, occluded catheter, urethral strictures
treatment of prerenal AKI
IV hydration and PO intake; renal protection before IV contrast; avoid fluid volume deficit; trauma and stenosis need OR; treat infection
diagnosis of intrarenal AKI
creatinine > 1.3 (bad kidney)
treatment of intrarenal AKI
remove the underlying cause; supportive therapy consisting of IV fluids or dialysis; if caused by med then discontinue med
acute tubular necrosis
destroyed tubular segment of nephron causing uremia and renal failure; blood flow to kidney is disrupted; caused by ischemic injury, nephrotoxic injury, blood transfusion reaction, rhabdomyolysis, hypotension, major surgery (kidney transplant), septic shock
diagnosing post renal AKI
xray for finding calculi or hydronephrosis, US to look for obstruction, CT without dye for obstruction and viewing of renal perfusion
treatment for postrenal AKI
remove underlying cause if possible, IV hydration, supportive measures; urinary catheter, ureteral stent, nephrostomy tube, lithotripsy, cytoplasty, prostate resection
AKI nursing management
daily weights at same time and same clothing, monitor IOs, maintain map of 60-70, fluid or sodium restriction, avoid nephrotoxins, nutritional support for electrolytes and protein, skin care, monitor WBCs and temp
examples of nephrotoxins
vancomycin, gentamycin, amphotcerin B
treating volume overload
diuretics and dialysis
treating hyperkalemia
kayexalate to bind and excrete; unstable pt get D50, insulin, calcium
treating hyponatremia
give sodium
treating hyperphosphatemia
PhosLo binds to excess phosphate; give prior and after meals; calcium should increase as phos goes down
treating impaired drug clearance
renal dosed meds d/t decreased excretion
treating metabolic acidosis
bicarb admin
treating uremia
removal of toxins via dialysis
indications for temporary dialysis
volume overload that is unresponsive to diuretics (high dose lasix 40-80), hyperkalemia, metabolic acidosis, progressive azotemia (BUN > 100)
options for temporary hemodialysis
intermittent hemodialysis: done via fistula or port, done 3 days a week; continuous renal replacement therapy (CRRT): constant dialysis when in ICU, run through port; peritoneal dialysis: hypertonic saline into peritoneal cavity that sits for a while to remove waste and then is removed
preventing AKI
recognize those at risk such as HTN and diabetics, maintain adequate circulating blood volume, limit exposure to toxins, minimize risk of infection
CKD
gradual irreversible condition of the kidney that can lead to end stage renal disease (ESRD); kidney damage present for > 3 mo indicated by structural or functional abnormality of kidney with decreased GFR, abnormal components of blood urine or imaging; GFR < 60mL for 3 months with or without kidney damage
kidney damage asymptomatic until…
> 40% of nephrons lost; dialysis begins when >90% of nephrons lost
risk factors for developing CKD
diabetes, HTN, nephrosclerosis (exacerbates renal damage), ACE/ARBs, glomerulonephritis
CKD casused by
untreated AKI, metabolic disorders, renal vascular disorders, immunological disorders like lupus, infections like UTI or pyelonephritis, primary tubular disorders, urinary tract obstruction, congenital disorders like polycystic kidney disease; most frequent causes are DM and HTN
nephrotic syndrome
leaking of albumin into the urine; kidney is not filtering out albumin back into blood; leads to hypoalbuminemia and edema
causes of nephrotic syndrome
bacteria or viral infection, cancer, genetic predispositions, systemic diseases like lupus or diabetes, NSAIDs; lupus causes direct renal damage
signs and symptoms of nephrotic syndrome
hypoalbuminemia: causes edema, fatigue, loss of appetite, hyperlipidemia; Proteinuria greater than 3g/day, large amount of protein in urine; may see clots
pathology of nephrotic syndrome
inflammatory response in glomerulus causes damage to membrane and causes loss of protein (albumin) that regulates oncotic pressure; leads to hypoalbuminemia
signs ans symptoms of CKD
decreased UOP, proteinuria, hematuria, lethargy, altered LOC/confusion, seizures, HTN, hypervolemia, HF, anorexia, N/V, uremic fetor (ammonia breath), metallic taste, impaired immune/inflammatory response, anemia, increased risk of bleeding, amenorrhea, erectile dysfunction, decreased libido, uremic frost, pruritis
CKD associated lab values
increase BUN, increased creatinine, increased K, increased magnesium, decreased calcium, increased phosphate
different types of UTIs
upper: pyelonephritis (kidney), uretitis (ureter infection); lower: cystitis (bladder), urethritis (urethra), prostatitis (prostate)
patho of UTI
can occur in any area of urinary tract; mostly acute (fast and serious), some can have chronic
chronic UTI
3+ UTIs in 12 months, bacteria persistent after 2 weeks of treatment
more at risk for developing UTI
women 4x more likely d/t short urethra and closer proximity of urethral opening to anus; diabetes increased risk d/t increased sugar and decreased WBC and decreased circulation (bacteria like sugar); pt who rely on catheters to void
when male has UTI…
more likely to be structurally related and associated with impaired flow of urine
signs and symptoms of UTIs
frequent painful urgent burning urine, urine is red dark milky or cloudy, foul smelling, flank pain if uretitis or pyelonephritis, pressure in pelvic area, fever, fatigue, altered mental status, confusion in older adults
gross hematuria
visible blood in urine to the eye
diagnosing UTI
UA with culture: will show 2 or more WBCs, 15+ bacteria in high powered field, >10000 colony forming units of one bacteria, + for nitrates, + hematuria, + proteins
pharmacological treatment for UTI
simple- trimethoprim/sulfamethazine aka bactrim, nitrofurantoin; complex- ciprofloxacin (can cause tendon rupture); pyridium analgesic for pain (may cause orange urine)
glomerulonephritis
bilateral inflammation of the glomeruli following a previous streptococcal infection; can be acute or can be chronic
causes of glomerulonephritis
epithelial layer of the glomerular membrane is disturbed
signs and symptoms of glomerulonephritis
pitting edema, increased BP, strep infection (common cause), electrolyte imbalance, sore throat, foamy/bubbly pink/red urine
complications associated with glomerulonephritis
CKD, ESRD, fluid overload, pulmonary edemat
treatment of glomerulonephritis
chronic treated with anitbx, diuretics, vasodilators, corticosteroids; may need plasmapheresis, dialysis, or transplant
renal calculi
can occur anywhere in the renal tract such as renal pelvic or calices; risk for development when too much of stone component like Calcium
renal calculi predisposing factors
dehydration, infection, obesity, exercise, male
types of stones
calcium oxalate and phosphate (associated with high calcium), struvite (associated with UTI), uric acid, cystine (seen in cystinuria)
signs and symptoms of renal calculi
N/V, agonizing flank pain that radiates to groin abdomen or testicles, sharp sudden severe pain, hematuria, dysuria, urinary frequency
diagnosing renal calculi
ultrasound, IVP (intravenous pyelogram to look at ureter and kidneys), renal stone analysis, KUB xray (kidney ureter bladder scan), serum (calcium oxalate and uric acid)
treatment for renal calculi
calculi </= 4mm have 80% chance of passing with vigorous hydration (will hurt), removal of stone via lithotripsy (ultrasonic waves to break up) or nephrolithotomy (invasive procedure going into kidney to break up or remove); admin analgesics, diuretics, thiazides (decrease calcium excretion in urine)
after renal calculi has passed
want to determine composition of stone and consult dietary for change of diet
hemodialysis
removal fluid, electrolytes, toxins from blood across a semipermeable membrane; loosens and separates impurities from blood; most efficient form of dialysis
indications for hemodialysis
ESRD, metabolic acidosis, poisonings to clear drug or toxins, AKI, hyperkalemia unresponsive to therapy, FVE in anuric patient
End stage renal disease
GFR < 5-10mL/min (GFR<15); BUN > 80-100mg/dL
Creatinine >/= 8
Vascular access for hemodialysis
central venous line, AV fistula, AV graft
central venous line for HD
acute access but temporary, use subclavian or internal jugular or femoral; cons- thrombosis, hematoma, not enough blood flow
AV fistula
rapid blood flow that is surgically created; connects artery and vein; takes 2-3 months to mature and lasts 3 years; pros- long lasting, not prone to infection, excellent blood flow, can shower, less likely to form clots; cons- needs to mature before use and requires direct needle into skin
AV graft for HD
used when unable to create fistula; inadequate blood vessel, 2-5 weeks to mature, lasts 2 years; pros- excellent blood flow, shower after heals; cons- less time than fistula, more prone to infection, 2 weeks before using, clotting
fistula pt education
Do: lanolin for dry skin, check bruit frequently, report bleeding or oozing of patch, wear medic alert bracelet, hold pressure for 20 min following access; DONTs: no blood draw/IV/BP, no tight clothing/jewelry, no lifting heavy items, do not bump, no itching or picking scabs
length of dialysis treatment
can be continued for 5-10 years
requirements for HD
anticoagulation and BP sufficient enough to remove 1 pint of blood at one time
peritoneal dialysis
dialysis takes place across peritoneal membrane; dialysate solution is warmed to body temp and infused into peritoneum; can be intermittent (3-5x a week for 8-12hr), continuous ambulatory (infused, dwells for 4-5 hrs, drains for 4-5 hrs), or cyclic continuous (intermittent night time cycling with day time ambulatory); collection bag must be below
complications of PD
peritonitis or infection at site, obstruction of flow, abdominal or discomfort, bleeding, HTN encephalopathy, ESKD, electrolyte disorders, dysrhythmias, resp. distress
continuous renal replacement therapy (CRRT)
used for hemodynamically unstable patients like those in ICU setting; slow continuous microfiltration; need A line for accurate pressure readings
kidney transplantq
used for those who cannot receive dialysis; human donor to recipient; tissue matching and immunosuppression is essential (type and screen)
tissue matching prior to kidney transplant
type and screen, Physical exam (papsmear), tissue typing, antibody screen, CXR, EKG, GI, cardiac workups, hep B, hep C, HIV, CMV
post-op care of recipient (kidney transplant)
immunosuppression, monitor for and prevent infection, monitor incision, monitor vitals, assess cardiac and respiratory, monitor urine output and labs, maintain semi-fowlers, pain management, manage urinary catheter; surger is about 3-4 hrs
kidney rejection
hyperacute- during surgery, acute- right after surgery, chronic- months to years after surgery; kidney will turn grey; detected via symptoms, rising creatinine, US for kidney size, biopsy
ongoing concern with kidney transplant recipients
chronic immunosuppression put patient at high risk for developing infection
contraindications to hemodialysis
inability to be anticoagulated, severe cardiac disease, hemodynamic instability
peritoneal dialysis drainage should be…
light yellow clear drainage
normal BUN, creatinine, GFR
GFR want >90mL/min; BUN normally 10-20
creatinine for men 0.74-1.35 mg/dL
creatinine for women 0.59-1.04 mg/dL; BUN to creatinine ratio usually 10-20:1
