Anatomy System includes the kidneys and entire urinary tract 2 kidneys located behind the peritoneum, on either side of the spine Weighs about 8 oz and the left if longer and narrower than the right
Kidney Renal capsule- fibrous tissue Renal cortex- outer tissue Medulla-inner tissue with “fans” Pyramids-12-18/kidney Papilla-end of the pyramid Calyx-collects the urine at the end of the papilla Renal pelvis- calices form it and leads to ureter
Renal blood flow Kidneys receive 20-25% of the total cardiac output Blood flow is 600-1300 ml/min Renal artery comes off of the abdominal aorta Exits off the renal vein and into the IVC
Nephrons Functioning unit of the kidney Urine is formed from blood 1 million nephrons Blood comes from the afferent arterioles, enters the glomerulus Leaves by efferent arterioles
Nephron parts Bowman’s capsule surrounds the glomerulus Proximal convoluted tubule Loop of Henle Distal convoluted tubule Collecting ducts
Renin-angiotensin system Renin is produced by the macula densa cells note changes in the distal convoluted tubules Based on decreased BP, bld volume and bld NA levels Renin changes angiotensinogen into angiotensin I, ACE changes it to angiotensin II
Angiotensin II Leads to 4 main outcomes: – Increased Na concentration (aldosterone from adrenal cortex) – Increased serum Na level by tubular reabsorption of Na in ascending loop of Henle (constricts afferent arteriole to decrease GFR, if bld volume is low) – Allows fluid to be removed and increases Na concentration in the bld, if blood volume if normal (constricts efferent arteriole to increase GFR) – Enhances reabsorption of Na from DCT
Renal regulatory functions Glomerular filtration- water, electrolytes, Cr, urea N and glucose are filtered Blood, albuminis too large Forms 180 L of filtrate/day or GFR=125ml/min Regulated by constricting and dilating the afferent arteriole When SBP goes below 70mm Hg, GFR stops (MAP of 60)
Tubular reabsorption and Secretion Reabsorption – Most of the water and electrolytes are reabsorbed, 65% of filtrate to keep urine output at 1-3 L – Most of water reabsorption is in the PCT, some is in DCT – DCT is affected by ADH and aldosterone – ADH enhances water reabsorption by increasing membrane permeability – Aldosterone reabsorbs Na Solute Reabsorption – 50% of urea, no creatinine – Most Na, Cl is reabsorbed in the PCT, some in the collecting ducts by aldosterone – K is reabsorbed in the PCT and the ascending loop of Henle – Bicarb, Ca and Phosphate are in the PCT – Glucose is reabsorbed up to 220mg/dl > will be excreted Tubular secretion is substance need to be excreted, such as K and H
Renal hormones Renin= RAAS (renin-angiotensin-aldosterone system) Prostaglandins- PGE and PGI, regulate filtration and vascular resistance Bradykinins-dilates the afferent arteriole and increase capillary membrane permeability Erythropoetin-released when there is decreased oxygen, triggers RBC production in the bone marrow Vitamin D activation- converted to its active form in the kidney
Renal Assessment Personal history- what questions should we ask? What about diet, why is that important? What is a normal urine output? What types of medical conditions can affect the kidneys?
Renal Assessment Inspection- note any swelling or discoloration in the flank region, costovertebral angle is 12 th rib and vertebrae Auscultate for what? How do you palpate the kidneys?, not be done is suspect pheochromocytoma, what is that? Percuss what? Only the kidneys or bladder too?
Diagnostic tests Blood – Creatinine- end product of muscle and protein metabolism (0.6-1.2) – BUN- excretion of urea N from protein metab, liver failure, trauma will elevate (10-20 mg/dl – Ratio BUN/CR is 12-20:1, dehydration can cause BUN to be elevated, but not CR – Decreased ratio will occur with FVE Urine – Urinalysis for inspection, odor, cloudiness, pH, specific gravity – What is a normal S.G.? – What things would be abnormal in the urine? – How high is the bacterial count in order to be treated?
Diagnostic tests IVP- intravenous pyelogram, now called IV urography Given a contrast dye, should not give if pt has renal insufficiency Shows the size, shape and location of kidneys Patency of calices, pelves and ureters Detects obstructions and masses
Diagnostic Tests CT of the kidney Renal Arteriogram
Diagnostic Renal Biopsy – Check blood counts before procedure, may need to transfuse – Given procedural sedation – Monitor the site for bleeding 24 hours after, bruising on flank, H&H – Bedrest for 6 hours – Will have hematuria
Cystoscopy Visualize the bladder and any abnormalities
Urinary Tract Infections UTI’s are the most prevalent nosocomial infections, costing 1.6 billion/yr How can they be prevented in the hospital? What is the recommended length of time a catheter should remain in, in the acute care setting? What factors may contribute to a UTI? Which organisms are most commonly the cause of UTI’s?
Urinary Tract Infections Cystitis- inflammation of the bladder, interstitial cystitis, unknown etiology Can lead to urosepsis, has a high mortality and prolonged hospitalization Incidence is greater in women than men and increases by 50% in women over 80
Case Study- UTI 24 y.o. sexually active female, who arrives in the ED, complaining of frequency, urgency and dysuria. She has difficulty initiating a stream. This has been occurring for the past 3 days, but not she feels weak and has noticed some blood in her urine
Case Study What type of questions may you ask this patient? What type of urine sample would you get? The urine comes back with > 100,000 c./ml Should this be treated? What is the most common antibiotic that is given for an uncomplicated 3 day course?
Case Study What nursing diagnoses would be appropriate for this patient? What patient education should be done? Include diet and prevention therapy
Urinary Incontinence Incontinence- involuntary loss of urine Not a normal result of aging In the elderly, can be caused by: – Medications, disease, depression, unable to walk or get to the BR
Types of incontinence Stress- most common, occurs during coughing, sneezing, jogging or lifting, weakening of the bladder neck can occur with childbirth, can’t tighten the urethra enough to overcome the urge to void Urge- when they feel the “urge” to go, they can not hold it until they find a BR, called overactive bladder, can be caused by CVA, parkinson’s disease, MS, UTI, BPH, artificial sweeteners, caffeine, alcohol, diruetics, nicotine
Incontinence Overflow- when the detrusor muscle fails to contract, the bladder becomes overdistended, leaks out to prevent rupture, may be urethral obstruction, diabetic neuropathy, pelvic surgery Reflex- abnormal detrusor contractions r/t neurologic problems- CVA, spinal cord lesions, MS Functional- loss of cognitive function in patients with dementia
Incontinence 85% of all cases are women Contributing factors are: – Medications- diuretics, opioids – Diseases- CVA, arthritis, parkinson’s – Psychological disturbances Physical examination – Assess for bladder fullness- bladder scan, cystocele, note detrusor muscle
Incontinence- Interventions Exercise- kegel’s strengthen pelvic floor Weight reduction, decrease fluids at night Drug therapy- estrogen, antispasmodics- ditropan, probanthine, bentyl, detrol, antidepressants- tricyclics- anticholinergics and alpha-adrenergics, so decrease urination Vaginal cone- weighted cones to tighten muscles, pessary to hold bladder up in cases of cystocele
Incontinence- Surgery Vaginal or retropubic surgery Elevates the urethra, repairs cystocele Postop- monitor voiding, may have SP catheter, PVR should be less than 50ml, monitor for bleeding
Incontinence education What type of education should be provided for bladder training? How can you get the family to help? If the patient does need to straight cath or have a foley at home, what things should they monitor for?
Renal Calculi- Urolithiasis Nephrolithiasis- stones in the kidney Ureterolithiasis- stones in the ureter 75% of the stones contain Ca- Ca oxalate or Ca phosphate 15% struvite, 8% uric acid and 3% cystine 90% of patient have a metabolic risk factor for the stones Incidence is higher in men
Renal calculi Formation is from – Slow urine flow from the element, such as Ca – Damage to the lining of the tract – Decreased inhibitor substances in the urine that would dissolve
Renal Calculi Risk Factors Hypercalcemia- – Increased intake or renal failure – Hyperparathyroidism – Immobilization Hyperoxaluria- – genetic trait that overproduces – Excess intake from spinach, rhubarb, coca, beets, wheat germ, pecans, okra, chocolate Hyperuricemia- – Gout with purine metabolism disorder – Increased purines from cancers and thiazide diuretics Struvite- – Magnesium ammonium phosphate and carbonate, urea splitting bacteria causes Cystinuria- – Genetic defect of amino acids
Renal Calculi Symptoms: – Renal colic- what is that? – Oliguria vs anuria, what is the difference? What is the predominant nursing diagnosis? Interventions: – Drug therapy: Pain relief, what should be used? Besides opioids, what medication may be helpful? – Lithotripsy- Shock wave therapy to break up stones Monitor ECG, bleeding after Strain the urine for stone collection
Surgical interventions Nephrolithotomy and ureterolithotomy – Endoscope or lithotriptor to grasp and extract the stone – Nephrostomy tube is left in place – Keep the nephrostomy site sterile and never irrigate with more than 10 ml – May be performed as an open procedure if the stone is too large
Patient education How can the patient prevent getting more stones? What foods should be avoided if the patient has a calcium oxalate stone? A calcium phosphate stone? A struvite stone? A uric acid stone? How much fluid should the patient take in per day?
Renal Disorders Polycystic kidney disease- genetic disorder, cysts develop on the kidney, most patients are hypertensive, RAAS is activated As the patient ages, kidney is more damaged Controlled by monitoring the BP and using ACE inhibitors, control the cell proliferation of PKD, follow a low NA diet Control for pain, many need a transplant
Glomerulonephritis Third leading cause of ESRD Disorders that cause are often autoimmune, such as: – Lupus, Goodpasture’s syndrome, Wegener’s granulomatosis, amyloidosis, diabetes, HIV, hepatitis C, cirrhosis, sickle cell disease, endocarditis Infectious processes also cause, such as: – Beta-hemolytic streptococcus, Staph bacteremia, syphilis, pneumococcal mycoplasma or klebsiella, CMV, histoplasmosis, varicella, toxoplasmosis
Glomerulonephritis An infection may precipitate Symptoms occur 10 days 75% of patients have edema of face, hands, eyelids Fluid overload and circulatory congestion
Glomerulonephritis Urine is smoky or reddish brown with hematuria and oliguria HTN with wt. gain Fatigue, anorexia, N&V What kind of labs would be done? What lab would be done to assess for a strep infection? What type of 24 hour urine would be done?
Case Study- Nephrotic Syndrome 8 y.o. presents to the hospital with swelling of the face and hands. He has the sickle cell trait. His mother has noted a marked decrease in his urine output and it looks dark brown. He complains of feeling tired and not wanting to eat.
Case Study What process occurs with Nephrotic syndrome? What would you expect to see in his urine? What about his lab values? His mother asks if this condition can be cured, what would you say? What type of treatment may be prescribed? Medications and therapy
Benign Prostatic Hypertrophy Prostate become hyperplastic and enlarges with age Prostate extends upward into the bladder and inward, narrowing the urethral channel Obstructs urine flow, overflow incontinence Bladder becomes irritable and leads to urgency and frequency, muscles enlarge and can lead to hydroureters and hydronephrosis
BPH Symptoms: – Nocturia – Frequency, urgency – Reduced stream and force – Incomplete emptying and dribbling – Hematuria in elderly males Assessment: – Digital rectal exam – Urinalysis – PSA level, what is this for? What nursing diagnoses would be appropriate?
BPH Medications: – Shrink- Proscar, finasteride, lowers DHT, may take 6 months to lower, major side effect is ED and decreased libido – Alpha-adrenergic blockers- Hytrin, Cardura, Flomax, constricts the prostrate and reduces pressure Avoid medications that may cause urinary retention, such as anticholinergics, antihistamines and decongestants Don’t take in a large amounts of fluid, avoid alcohol and diuretics, that can cause overdistention
BPH Surgery TURP- transurethral resection of the prostate Can only remove pieces of the prostrate in chip form Suprapubic, Retropubic and Perineal prostatectomy- done when the prostate is large or the bladder also needs to be explored
BPH surgery Postop: – Assess incision site if applicable for bleeding – Continuous Bladder irrigation (CBI) done 24 hours post surgery – Monitor for FVE, running total of I & O – Bleeding is to be expected, but urine should not be “frank” blood, may have clots, monitor H&H – May have bladder spasms, ditropan or B&O supp.
Renal Failure Renal failure is the loss of function r/t nephron damage. In CRF, 90-95% of the nephrons are lost before failure is obvious ARF, only 50% decrease in nephrons can cause failure, ARF is a sudden onset and may last < 3 mo, good prognosis Most common causes of CRF are: – Diabetes (43%), HTN (25%), glomerulonephritis (8%)
Acute Renal failure- ARF Types of ARF: – Prerenal azotemia- correct by increasing BP, giving volume, improve C.O., prolonged damage can lead to intrarenal failure – Intrarenal- ATN- infections, drugs, NSAID’s, aminoglycosides, tumors, glomerulonephritis
Phases of ARF Onset: – Hours to days, precipitating event until oliguria, BUN and Cr increase Oliguric: – Urine output of 100-400ml/day, does not respond to diuretics or fluid challenges, BUN and CR increase, K, Magnesium and Phosphate increase, Na is retained, but masked with fluid, dilutional, lasts 8-15 days
Phases of ARF Diuretic: – Urine output increases rapidly, can be 10L/day of dilute urine, electrolyte losses occur, BUN decreases last, 2-6 weeks, until BUN falls, renal tubular function returns Recovery: – Functions at lower level, may take up to 12 months to return to normal In critically ill patients, 50-80% mortality rate for those who develop ATN
Case Study for ARF 25 y.o. male admitted to the ICU post MVA, he had multiple fractures, ruptured spleen and significant blood loss. He has been in the ICU for 24 hours and is ventilated. He has received blood transfusions and maintenance IV fluids, but his blood pressure continues to drop and is presently 80/44, his urine output has only been 100 ml for the past 12 hours. What do you expect is occurring?
Case Study for ARF What type of ARF is the patient experiencing? What phase is he in? What can be done to initially correct this problem? What nursing interventions should be done to monitor for patient improvement? The MD says that the patient has prerenal azotemia, what does that mean?
Case Study- ARF If the patient is in the oliguric phase, what would the lab values be? CR – Bun – Na – K – Phosphorus- Ca – Magnesium – Bicarbonate- pH-
Case Study- ARF Because of the disruption in electrolytes, what symptoms may the patient experience? Besides electrolytes, what other labs should the RN monitor? K- Na- Phosphate- Ca- H-
Case Study- ARF What are the main Nursing diagnoses for this patient? What medications may be given to this patient? Besides replacements, what other meds would be needed? What should his diet include? How much protein can he take in? How much fluid?
Case Study- ARF The patient remains oliguric and has persistent hyperkalemia, FVE and metabolic acidosis, the MD decides that he must begin dialysis to remove the end-products CRRT is ordered, what does this mean? Why is this done instead of Hemodialysis? What type of catheter would be inserted? Where is the cath inserted? Why not have a renal fistula done?
Case Study- ARF Prisma machine used for CRRT Can do hemofiltration, uses a double venous access, one catheter is arterial and one venous return Changes in fluid removal can be set for every 30-60 minutes and so they don’t remove as much as regular hemodialysis Set blood flow at 150ml/hr, dialysate rate at 1L/hr
Case Study- ARF After 5 days on CRRT, the patient’s kidneys begin to improve and his urine output is >30ml/hr, his BP has stabilized and he is off of all vasopressors. He is being transferred to the floor. What types of things should be still be careful of? What agents may be nephrotoxic to him?
Chronic Renal Failure Progressive, irreversible kidney disease Kidney function does not recover, ESRD Have azotemia (increased nitrogen wastes), uremia (azotemia with symptoms), uremic syndrome (clinical and labs r/t ESRD)
Chronic Renal Failure Stages of CRF: – Stage 1: Diminished Renal Reserve- renal function is reduced, but no accumulation of wastes, can’t concentrate urine polyuria and nocturia – Stage 2: Renal Insufficiency- wastes accumulate, no response to diuretics, oliguria and edema develop, decreased GFR – Stage 3: ESRD- excessive wastes, BUN and CR, H, treatment is dialysis
Chronic Renal Failure Metabolic changes: – BUN, CR elevated – Na elevated in later stages, may appear nl or low at first – K elevated, up to 7 or 8 mEq/L, can cause cardiac arrest – H is elevated metabolic acidosis, lungs try to blow off Kussmaul’s respirations – Ca is low, phosphorus is elevated stimulation of PTH, which causes Ca to be released form bone renal osteodystrophy, lack of vitamin D also makes it worse
Chronic Renal Failure Cardiac changes: – Hypertension- most have because of what? – Hyperlipidemia- changes fat metabolism elevated trigylcerides, cholesterol and LDL – Heart failure- resulting from increased cardiac workload r/t volume, HTN and CAD – Uremic pericarditis- pericardial sac becomes inflammed with toxins pericardial effusion, tamponade and death Hematologic: – Anemia occurs because of decreased erythropoetin and RBC’s GI changes: – Ammonia from urea breakdown causes halitosis and stomatitis – Anorexia, N & V occurs, PUD may occur
Chronic Renal Failure What are the common nursing diagnoses for the patient with CRF?
Chronic Renal Failure- Interventions Diet therapy: – Increase calories, but restrict Protein, Fluid, K, Na, Phosphorus, why restrict protein? If the patient is on peritoneal dialysis, protein may be increased – Take vitamins and minerals- return vitamin D, Ca, folic acid
Chronic Renal Failure- Interventions Drug therapy- – Diuretics- only if FVE that is not on dialysis – Biologic response modifiers- procrit – Phosphate binders- amphojel, alternagel, renagel, tums, oscal – Stool softeners- colace, miralax – Vitamins- folic acid, ferrous sulfate – Antihypertensives- ACE, Ca channel and betas may be used
Renal Replacement Therapies Hemodialysis – Better clearance – Short time for treatment – Have to leave home 3x/wk – Can cause disequilibrium syndrome, muscle cramps, hemorrhage – Restricted diet Peritoneal dialysis – Easy access – Fewer hemodynamic complications – Infections and adhesions can occur – Less effective – Protein loss and peritonitis – Uses intra-abdominal catheter
Hemodialysis Used in patients with: – Fluid overload – Pericarditis – Uncontrolled HTN – Uremic signs – Worsening anemia – Irreversible renal failure when other therapies are not possible
Hemodialysis Process: – Diffusion of molecules with the use of dialysate solution, high in electrolytes, water – Waste products move from the blood through the filters semipermeable membrane into the outflow resevoir – Water is also removed by osmosis as it follows the solutes
Hemodialysis Hemo filter- over 1 million fine hairs, act as nephrons Venous access AV shunt- only short term Can become dislodged, or bleed
Hemodialysis Venous access AV fistula or graft- artery and vein anastomosed, as it matures, blood flow increases and it enlarges Do not take BP or blood draws from that arm Assess pulses Palpate for thrill and listen for bruits No lifting of heavy objects
Hemodialysis Care Weigh the patient before and after, know the “dry wt” Measure BP, HR and Respirations Watch for orthostatic hypotension Watch for disequilibrium syndrome- after HD is completed, change in fluid and urea headache, N&V, change in LOC, cerebral edema, seizures, slowing down the fluid removal can prevent it Bleeding can occur, from heparinization of the lines and low blood counts Infectious diseases, such as hepatitis C and HIV through blood transmission
Peritoneal dialysis Silastic Catheter is inserted in the abdominal cavity Dialysate is inserted, dwells for 3-4 hours, allowing fluid to mix with dialysate Effluent or outflow is then opened and waste products and water are removed
Peritoneal dialysis Process is by diffusion and osmosis of products Dialysate has water and electrolytes, also glucose in 2.5, 5 or 10%, determines the amount of diffusion Heparin and antibiotics may be added to dialysate Can be done either throughout the day with a Y-set or at night with an automatic cycler
Peritoneal dialysis Complications – Peritonitis- contamination of catheter, cloudy outflow, fever, abdominal pain and cramping – Pain – Poor outflow and leakage- can be caused by constipation, fibrin clots in the catheter Tenckhoff, peritoneal catheter
Renal Transplantation Selection: – Free from medical problems, such as cancer, heart disease and diabetes ( should be under control) – Age is 2-70 – Use living and cadaver donors
Renal Transplantation Postoperative Care – Monitor urine output, should return to normal in 48 hours, color may be pink with some clots – Complications: Rejection – Hyperacute- within 48 hours, fever, pain and increased BP – Acute- 1 wk to 2 yrs, most common, oliguria, fever, enlarged kidney, elevated BUN, Cr – Chronic- months to years, gradual increase in BUN, Cr, fluid retention, fatigue
Renal Transplantation Complications – ATN- may have occurred due to damage to transplanted kidney – Thrombosis- renal artery or vein 2-3 days post – Renal artery stenosis- may lead to hypertension, can often be repaired with a stent – Infections- on immunosuppressives for life Cyclosporine, prednisone, imuran
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