Alterations of Renal & Urinary Tract Function PDF

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Alterations of Renal & Urinary Tract Function...

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Alterations of Renal & Urinary Tract Function Urinary Tract Infection o UTI is inflammation usually caused by infection of the urinary epithelium & occurs in: urethra, prostate, bladder, ureter, kidney o 2nd most common bacterial disease  8 million office visits a year  Direct cost 1.8 billion/year  100,000 people hospitalized per year  >15% of patients who develop gram - bacteremia die & 1/3 of these cases are caused by bacterial infections originating in the urinary tract o Most common bacterial infection in women  Pregnant women @ increased risk of infection o Organisms:  Escherichia coli (most common pathogen)  Fungal & parasitic UTI, very hard to treat  Uncommon  Immunosuppressed patients  Diabetes mellitus  Multiple antibiotics  Persons living in certain developing countries o Classifications:  Lower UTI: bladder, urethra  Upper UTI: renal parenchyma, renal pelvis, ureters o Terms:  Pyelonephritis: inflammation usually due to infection on the renal parenchyma, renal pelvis, & collecting system  Cystitis: inflammation of the bladder wall  Urethritis: inflammation of the urethra  Urosepsis: UTI that has spread into systemic circulation, life threatening, requires emergency treatment  Uncomplicated: UTI that occurs in an otherwise normal urinary tract & only involve the bladder  Complicated: coexisting presence of obstruction, stones, or catheters, existing diabetes, or neurologic diseases, pregnancy-induced changes, & recurrent infection  At risk for pyelonephritis, urosepsis, & renal damage o Classification by natural history:  Initial: 1st/initial infection; remote from any previous infection  Recurrent: reinfection caused by 2nd pathogen; previous infection was successfully eradicated  Unresolved bacteriuria: bacteria is initially resistant to antibiotics  Antibiotics fail to achieve adequate concentrations  Drug before bacteriuria is completely eradicated o Etiology & pathophysiology  Defense mechanisms: maintaining sterility in urinary tract & preventing UTI  Normal voiding w/ complete emptying of bladder; bacteria are washed out during micturition  Peristaltic activity that propels urine toward the bladder  Ureterovesical junction competence; closes during bladder contraction: prevents urine reflux  Antibacterial characteristics of urine are maintained by acidic pH (< 6.0) & high urea concentration

Alterations of Renal & Urinary Tract Function Male urethra longer, prostatic secretions, location Presence of Tamm-Horsfall protein Secretions from the uroepithelium (bactericidal) Abundant glycoproteins that interfere w/ the growth of bacteria  Diabetes Mellitus  Neurogenic bladder (muscle isn't contracting & emptying)  Menopause: lower estrogen levels cause vaginal atrophy, decrease in lactobacilli & increase in vaginal pH = overgrowth of bacteria = increase in UTI  Antibiotic treatment: disrupted vaginal flora  Organisms introduced via the ascending route from urethra & originate in the perineum  Blood stream: rarely does a blood-borne infection invade the kidney, ureters, or bladder (must be prior injury from obstruction, stone, or scars)  Instrumentation  Catheterization (trauma, openings for bacteria)  Cystoscopic exam  Allows bacteria normally present @ the opening of the urethra to enter the urethra/bladder  Sexual intercourse  Multiple partners  Spermicide use  Women urethra length & location (shorter & closer to anus)  Habitual delay of urination "nurse's" or "teacher's" bladder  Health care associated infections are an important source of UTIs  Catheter acquired UTI are the most common HAIs  Development of bacterial biofilms that are found on the inner surface of the catheter  Underrecognized & undertreated  Lead to complications  Renal abscesses  Bacteremia  Important to remove all lines & catheters as early as possible Pathology:  Retrograde movement of bacteria into the urethra & bladder, then ureter & kidney  Inflammatory response & edema in the bladder wall (symptoms of lower UTIs)  Discharge of stretch receptors  Initiates symptoms of bladder fullness w/ small volumes of urine  Result: urgency & frequency of urination Lower UTI  Symptoms are related to bladder storage or bladder emptying  Dysuria  Frequency (urination more than Q2 hours)  Urgency  Suprapubic discomfort/pressure  Hesitancy  Intermittency  Post void dribbling  Nocturia  Nocturnal enuresis (loss of urine during sleep)  Incontinence    

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Alterations of Renal & Urinary Tract Function Hematuria (grossly visible blood) Cloudy urine (sediment in urine) Elderly: overall abdominal pain, cognitive impairment, change in level of consciousness, generalized clinical deterioration  Urethritis: inflammation of the urethra, often times sexually transmitted  Etiology:  Bacterial infection (gonococcal infection, trichomonas infection, chlamydial infection)  Viral infection  Diagnostic studies & treatment:  Dipstick urinalysis: identify nitrites that indicate bacteriuria, WBC, & leukocyte esterase (enzyme indicating pyuria); pyuria/pus in the urine  Urine culture: clean catch  Sensitivity: bacteria susceptibility to a variety of antibiotics; select an antibiotic capable of destroying the bacteria  IVP  CT  Renal ultrasound  Treatment is based on identifying & treating the cause & providing symptomatic relief: antibiotics &/or urinary analgesics  Interstitial cystitis (Painful Bladder Syndrome):  Nonbacterial infectious cystitis: viral & fungal  Non-infectious cystitis: radiation treatment to pelvic area, autoimmune, hypersensitivity reactions  Clinical manifestations: most common in women 20-30 years old, negative urine cultures, bladder fullness, frequency, small urine volume, chronic pelvic pain  Treatment: no single treatment effective, symptom relief Upper UTI  Pyelonephritis: acute infection of the renal parenchyma & collecting system including the renal pelvis  Most common cause: bacterial, fungal, protozoa, or viruses  Preexisting factors contribute:  Retrograde/backward movement of urine  Obstruction (enlarged prostate-BPH)  Stricture (congenital, scar tissue)  Urinary stone  Indwelling catheters & urinary tract catheterization  Pregnancy induced change in the urinary system  Colonization & infection of the lower urinary tract via ascending urethral route  Ascending microorganisms along the ureters  Acute pyelonephritis commonly starts in the renal medulla & spreads to adjacent cortex  Inflammatory process: renal pelvis, calyces, & medulla  Medullary infiltrate of WBC: renal edema & purulent urine  Spread may occur to blood stream  Clinical manifestations: fever, chills, flank pain, lower urinary tract symptoms, costovertebral tenderness on affected side, vomiting from the pain, malaise  Diagnostic studies:  Urinary frequency   

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Alterations of Renal & Urinary Tract Function

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 Hematuria  CBC will show an increase in immature neutrophils (bands)  Urine culture  WBC cast in urine  Pyuria (pus in urine)  May require blood cultures  IVP  CT w/ contrast  Ultrasonography Acute pyelonephritis: Commonly starts in the renal medulla Spreads to the adjacent cortex Recurring episodes of pyelonephritis (especially in the presence of obstructive abnormalities) Result: scarred, poorly functioning kidney(s) Leads to chronic pyelonephritis Chronic pyelonephritis: The outcome of recurring infections involving the upper urinary tract  Kidney(s) become small atrophic & shrunken  Loss of function due to scarring & fibrosis Risk of chronic pyelonephritis increases w/ obstructive pathologic condition  Renal stones & reflux May occur in the absence of infection  Interstitial nephritis, chronic atrophic pyelonephritis, or reflux nephropathy Pathology:  Chronic urinary tract obstruction  Starts a process of progressive inflammation of interstitial spaces between tubules  Altered renal pelvis, calyces, destruction of tubules (atrophy/dilation)  Diffuse scarring  Impaired urine concentrating ability  One/both kidneys may be affected determining the level of renal function  Chronic renal failure Diagnostic studies: radiologic imaging & histologic testing  Image studies reveal small, contracted kidney w/ thinned parenchyma  Pathologic analysis: loss of functioning nephrons, inflammation, & fibrosis Clinical manifestations:  Mild fatigue depending on the severity  Sudden onset of chills, fever, vomiting, malaise, flank pain  LUTS: dysuria, urgency, & frequency  Costovertebral tenderness (CVA pain on affected side)  Urinary analysis: pyuria, bacteriuria, & hematuria indicating renal parenchyma involvement  Progression leads to renal failure

Glomerulonephritis

Alterations of Renal & Urinary Tract Function o

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Immunologic processes involving the urinary tract predominately affect the renal glomerulus  Inflammation of the glomeruli  Affects both kidneys equally Glomerulonephritis is the 3rd leading cause of renal failure in the US Inflammation of the glomeruli caused by:  Immunologic abnormalities (most common): SLE, scleroderma, good pasture syndrome  Drugs/toxins  Kidney infections: microbial infections (streptococcal)  Viral causes (hepatitis, rubella)  Ineffective endocarditis  Illegal drug use  Hypertension Most common cause of chronic & end-stage renal failure 1st type of immune process:  Antibodies have specificity for antigens w/in the glomerular basement membrane (GBM) termed anti-GBM antibodies  Immunoglobulins & complements are deposited along the GBM  The mechanism that causes the development of the antibodies against his/her own GBM is unknown  May be stimulated by a structural alteration in the GBM or by a reaction of the basement membrane w/ an exogenous source (virus) 2nd type of immune process:  Antibodies reaction w/ circulating non-glomerular antigens & are randomly deposited as  On microscopic evaluation the deposits appear "lumpy & bumpy" In this immune complex process the antigens come from endogenous circulating DNA or exogenous sources (bacteria, viruses, chemicals, drugs)  Bacterial source: poststreptococcal glomerulophiritis  Viral source: Hepatitis B & C or rubella (measles) Common in children & young adults Associated w/ streptococcal infection  5-21 days after infection (throat/skin)  Commonly affects children  Person produces antibodies to the streptococcal antigen Streptococcal antigen-antibody complexes deposit in the GBM  Formation of antibodies against the GBM  Inflammatory mediators damage the GBM  Causes glomerulonephritis Pathology:  Accumulation of antigen, antibody, & complement in the glomeruli  Immune complexes activate complement  Results in the release of chemotactic factors that attract polymorphonuclear leukocytes, histamine, & other inflammatory mediators  End result of these processes is glomerular injury Damage to the glomerulus = changes in GFR = proteinuria & hematuria Glomerular filtration rate: amount of blood filtered by the glomeruli, normal range is 125 mL/min, best index to estimate kidney function Clinical manifestations:  Hematuria (range is microscopic to gross) 

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 Urinary excretion of elements (RBC, WBC, casts)  Proteinuria  Elevated BUN & serum creatinine  Hypertension Recover from acute illness is complete, if progressive involvement occurs = destruction of renal tissue & ESRD develop Assess history:  Exposure to drugs  Immunization  Microbial infection  Viral infections (hepatitis, rubella)  Generalized immune disorders (SLE, systemic sclerosis) Recovery usually occurs w/out significant loss of renal function or recurrence  5%-15% develop chronic glomerulonephritis  1% irreversible renal failure Chronic glomerulonephritis: syndrome that reflects the end stage of glomerular inflammatory disease  Most types of glomerulonephritis & nephrotic syndrome can eventually lead to chronic glomerulonephritis  Characterized by: proteinuria, hematuria, slow development of uremia  Progresses insidiously toward renal failure over years (few-30 years)  Often coincidentally found b/c increased BP or abnormal urinary analysis  Diagnostic tests: ultrasound, CT, biopsy

Nephrotic Syndrome o Results when the glomerulus is excessively permeable to plasma protein, causing proteinuria that leads to low plasma albumin & tissue edema  Low protein levels in the blood leaves fluid or pushes fluid into the tissues o 1/3 of patients w/ nephrotic syndrome have a systemic disease such as: diabetes mellitus or SLE o Pathology (1):  Increased glomerular membrane injury causes massive excretion of protein in the urine (> 3.5 g protein/24 hours of urine)  Hypoalbuminemia: decreased serum protein (serum albumin < 3g/dL)  Massive peripheral edema (anasarca)  Ascites o Pathology (2):  Decreased serum proteins stimulates hepatic lipoprotein synthesis  Hyperlipidemia (serum cholesterol) = coronary artery disease  Increased phospholipids, triglycerides  Lipiduria (fat bodies present in urine)  Vitamin D deficiency  Hypertension o When nephrotic proteinuria, loss of clotting factors (anti-coagulant proteins) can result in a relative hypercoagulable state  Hypercoagulability: thromboembolism is a serious complication, renal vein most common site for thrombus, pulmonary embolism occur in 40% of patients o Immune responses (both humoral & cellular) are altered = infection is the primary cause of morbidity & mortality o Hypocalcemia (skeletal abnormalities & risk for fracture)

Alterations of Renal & Urinary Tract Function Phosphate & calcium bind together, causing the bone to release calcium trying to of set it Clinical manifestations:  Peripheral edema (massive anasarca)  Massive proteinuria (excretion of > 3.5 g or more of protein in the urine per day)  Hypertension  Hyperlipidemia  Hypoalbuminemia  Serum blood test:  Decreased serum albumin & total serum protein  Elevated serum cholesterol (triglycerides)  Hypocalcemia  Fat bodies appear in urine Treatment plan: normal protein diet, low fat diet, salt restrictions, immunosuppression, diuretics 

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Urinary Tract Obstruction o An interference w/ the flow of urine @ any site along the urinary tract (congenital/acquired) o Any anatomic or functional condition that blocks/impedes the flow of urine  Impedes the flow of urine proximal to the blockage  Dilates the urinary system  Increases the risk for infection  Compromises renal function o Severity based on:  Location  Completeness  Involvement of 1 or both urinary tracts  Duration  Cause o Damaging effects from urinary tract obstruction system above the level of obstruction o Common causes:  Ureter blockage from stone  Stricture  Congenital compression of a calyx  Abdominal inflammation/scarring  Malignancy: renal pelvis, ureter, lower urinary tract (bladder, prostate) o Hydroureter: accumulation of urine in the ureter  Dilation of the ureter caused by upper urinary tract obstruction  Ureteral dilation & distention o Hydronephrosis: dilation/enlargement of the renal pelvis & calyces caused by proximal obstruction o Mechanism of action:  Obstruction  Accumulation of urine  Enlargement & fibrosis (7 days)  Distal/proximal nephron parts affected (14 days)  Glomeruli of the kidney affected (28 days)  Renal cortex & medulla reduced in size  Decreased ability to concentrate urine

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 Increase in urine volume  Decrease GFR Nephrolithiasis: calculi or urinary stones  Masses of crystals, protein, or other substances that form w/in & may obstruct the urinary tract  Risk factors:  Gender, race, geographic location, seasonal factors, life style, fluid intake, diet, occupation, & metabolic (urine acid production/urine calcium levels)  Temperature & pH of urine  Alkaline urine contributes to the formation of stone  Acidic urine inhibits stone formation  Kidney stones are classified according to the minerals comprising the stones  Calculus: refers to stone  Lithiasis: refers to stone formation  5 major categories of stones: calcium phosphate, calcium oxalate, uric acid, cystine, struvate (magnesium ammonium phosphate)  Stone formation:  Ions precipitate from solution in the urine forming salts  Higher pH = calcium & phosphate stones  Lower pH = uric acid & cystine stones  Salts form crystals that grow into stones  Crystallization: the process by which crystals grow from small to larger stones  Crystals in a supersaturated concentration can precipitate & unite to form a stone  Keeping urine dilute & free flowing reduces the risk of recurrent stone formation  Urinary pH & solute load of the urine affect the formation of stones  Clinical manifestation:  Severe pain that develops suddenly; moderate to severe flank pain that may be associated w/ nausea & vomiting  Pain can be referred to different parts of the body depending on the location of the stone  Renal colic: sharp severe pain caused by the stretching, dilation, & spasms of the ureter in response to the obstructing stone  Pain in the groin  Lateral flank pain  Kidney dance (patient will walk, sit, lay down & repeat; unable to get comfortable)  ♂: testicular pain  ♀: labial pain  Lower urethral obstruction = urgency, frequent voiding, urge incontinence  Diagnostic tests:  History: previous stones, age of onset, presenting symptoms, OTC meds, diet, family history  Stone & urine analysis  Urine pH  24 hour urine  Intravenous pyelogram (IVP  Kidney, ureter, & bladder x-ray (KUB)

Alterations of Renal & Urinary Tract Function

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 Ultrasound  Spiral abdominal CT  Cystoscopy  Labs  BUN  Creatine levels Lower urinary tract stricture  Urethral stricture: narrowing of the lumen, resistance to urine flow, result of fibrosis or inflammation of the urethral lumen caused by surgery, adhesion, scar  ♂: prostatic enlargement  ♀: pelvic organ prolapse (cystocele, bladder outlet obstruction)  Urethritis infection: gonococcal particularly  Injury: previous catheterizations  Surgery: adhesions &/or scar tissue  Congenital defect  If obstruction persist…  Increased collagen w/in the smooth muscle of the detrusor muscle  Bladder wall loses its ability to stretch & accommodate urine  Detrusor loses its ability to contract efficiently  Results: hydroureter, hydronephrosis, impaired renal function  Clinical manifestations:  Diminished force of urinary stream  Straining to void  Sprayed stream  Post void dribbling  Split urine stream  Feeling of incomplete bladder emptying (urinary frequency, nocturia)  Acute urinary retention  Evaluation:  History & physical  Assess the efficiency in evacuating urine through micturition  Post void urine measurement  Catheterization 5-15 minutes after urination  Bladder scanner (ultrasound): height & width of bladder, provides approximation of urine amount  Uroflowmetry: force of urinary stream (milliliters voided per second)  Evaluate renal function (serum creatine)  Treatment:  Surgery  Urethral dilation  Intermittent catheterization  Condom catheter  Urinary diversion  Urostomy/suprapubic catheter  Long term catheterization Upper urinary tract stricture  Ureteral strictures: affects the entire length of the ureter  Usually an unintended result of surgical intervention  Secondary to adhesions &/or scar tissue

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Depending on severity ureteral stricture can threaten the function of the kidney  If the pressure in the kidney remains low to moderate & develop pyelonephritis b/c of urinary stasis & reflux Clinical manifestations: similar to renal stone Treatment:  Dilation  Stent (progressively enlarged)  Divert urinary flow via nephrostomy tube inserted into the renal pelvis  Dilate w/ a balloon/catheter  Endouretertomy (incised via endoscopy)  ...