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3/26 Lecture 9: Urinary Pathophysiology

Urinary Tract Infections (UTIs) Uncomplicated = normal urinary system Complicated = abnormal urinary system Causes Physical Urethral strictures a narrowing of the lumen occurs when infection, injury, or surgical manipulation produces a scar 1. Mostly occurs in men 2. Severity of obstruction is dependent on location, urethra length and diameter Causes 1. Prostate enlargement (prostatic hypertrophy) 2. Pelvic organ prolapse (ex: prolapsed uterus = uterus collapses) the abnormal descent from organ’s original position, or herniation of organs in the pelvic cavity 3. Bladder obstruction (stones, trauma, abdominal cavity) Prostate enlargement / hypertrophy : enlargement of prostate gland Detrusor Hyperflexia Partial obstruction of the bladder outlet / urethra urinary stones (Calculi plural Calculus) masses of crystals / protein most commonly made of calcium (calcium stone) located in kidneys, ureters, urinary bladder prevalence: women = 7% / men = 10% recurrence rate: 30 - 50% within 5 years most renal stones are unilateral most develop first stone > 50 years old risk factors: age, sex, geographical location on planet (temp, humidity, rainfall), seasonal factors,

fluid intake, diet, occupation —> women have shorter urethra = increased risk —> men secrete antimicrobial film = decreased risk most important formation factor: urine pH from urinalysis (UA) and temperature UA should be clear yellow, no protein, WBCs cause bleeding, micro-tears along urethra / bladder = blood clots = blocked urethra = incontinence Uric acid stone type of kidney stone urine becomes acidic and the filtrate contains low amounts of water, allowing uric acid to crystallize Bacterial capsular antigens resists phagocytosis hemolysin damages epithelium urease positive bacteria promote infection; Proteus and Klebsiella Adhesins: E. coli type 1 and P. fimbria bind to uroepithelium E. coli contamination from colon Klebsiella, Proteus G(-) bacteria produce beta-lactamases and carbapenemases —> cause penicillin, cephalopsorin, and carbapenem resistance Host factors kidney stones occur when your urine contains more crystalforming substances (calcium, oxalate and uric acid) than the fluid in your urine can dilute most common: calcium oxalate / calcium phosphate (70- 80%) urine pH > 7 (alkaline) second common: Struvite (magnesium ammonium phosphate) (15%)

urine pH < 5 (acidic) Diabetes Mellitus (DM) ureteral reflux immunosuppression pregnancy neurogenic bladder: lack of bladder control due to a brain, spinal cord or nerve problem P blood group antigens short urethra in women indwelling catheters Complications of UTI Acute Cystitis: an inflammation of the bladder is the most common complication of UTI some cases may show hemorrhage / pus formation (exudate) on epithelial surface of bladder = infection prolonged infection may lead to sloughing of the bladder mucosa with ulcer formation severe infections may cause necrosis of bladder wall infecting organisms: E. coli (most common), Staph saprophyticus (second most common) —> years of chronic infections can lead to cancer Interstitial cystitis an inflamed / irritated bladder wall, can lead to scarring of bladder caused by warm climates , fungus more common in people with autoimmune diseases Pyelonephritis: acute or chronic infection of one or both upper urinary tracts (ureter, renal pelvis, interstitium) can involve one or both sides —> Chronic pyleonephritis leads to scarring of one or both kidneys most common risk factors: urinary tract obstruction, reflux of urine from bladder predisposing risk factors: kidney stones, vesicoureteral reflex pregnancy neurogenic bladder, instrumentation, female sex trauma most common in women can change someones personality, microbes can affect frontal lobe of brain

Acute Pyelonephritis microorganisms: E. coli, Proteus & Pseudomonas (associated with Foley catheter / surgery) split urea molecule into ammonia = alkaline urine = increased risk stone formation Chronic Pyelonephritis persistent or recurrent kidney infection leading to scarring prevent elimination of bacteria = inflammation = renal pelvis and calyces alterations = tubule destruction = atrophy / dilation, diffuse scarring = impaired uterine ability = chronic kidney failure Symptoms of UTI urinary frequency edema in bladder all stimulates discharge of stretch receptors = sx of bladder fullness Antibiotic resistance in UTIs caused by antibiotic overuse risk for resistance highest in regions with highest rates of prescription pts who receive Bactrim (trimethoprim-sulfamethoxazole) treatment within last 3 months, have diabetes mellitus, have been recently hospitalized, have community-specific antibiotic resistance rates of > 20% TMP-SMX and fluoroquinolone have high rate of resistance multi-drug resistant extended spectrum beta-lactamase (ESBL) producing E. coli occurring with no known risk factors : under microscope, has glowing ring around microbe cause increased cost, hospitalization, morbidity, and mortality Prevention drug resistance awareness / knowledge Antibiotics (Anti-infective) Steps 1. Check culture report (3 days); know what your pt has and check that med if effective against microorganism (prevent superbugs and formation of resistant organisms) 2. Check temp q 4 hours, is temp > 101 consider holding med and ask provider of cultures should be redrawn (possible development of drug-resistant organism)

3. Instruct pt to use incentive spirometer q 1 hour, 10 times, while awake, to prevent pneumonia 4. Consider holding for new onset of dyspnea, wheezing, rash 5. If pt has diarrhea, ask provider if stool culture is needed (detection of hospital acquired clostridium difficile) —> before administering anti-infective for UTI, check culture report and temperature of pt Nursing actions with anti-infectives monitor / trend WBC, neutrophil differential percentage and increase / decrease determine if pt has previous allergic response, monitor for hypersensitivity obtain any ordered blood, urine, sputum cultures before giving first dose Urinary Incontinence definition: the involuntary passage of urine by a child who is beyond the age when voluntary bladder control should have been acquired (< 5 years old); influenced by cultural beliefs and parents Incontinence = inability to retain urine Sphincter dysenergia: Alpha 1 receptors control detrusor muscle Types Urge incontinence (Overactive Bladder, OAB): involuntary loss of urine occurring for no apparent reason associated with abrupt and strong desire to void (urgency), involuntary / hyperactive contraction of detrusor muscle —> Urge Incontinence = urine leakage + urgency Detrusor hyperreflexia: involuntary contractions associated with neurologic disorder Detrusor instability: no neurologic disorder exists, may be associated with decreased bladder wall compliance Associated with age, gender, surgeries most common in older adults affects more women than men Causes: detrusor instability (most common), bladder irritation from neoplasm, interstitial cystitis often accompanied by nocturia, damage to nerves in bladder from neurologic disease (MS, Parkinson’s, Alzheimer’s, stroke) Treatment: oxybutynin therapy (anticholinergic med

inhibits contraction of overactive bladder) Other conditions can cause similar symptoms such as UTI, BPH, bladder/prostate cancer Stress incontinence: involuntary loss of small amounts of urine during coughing, sneezing, laughing, physical activity associated with increased intra-abdominal pressure = increased pressure on bladder, reduced resistance —> is a type of urethral hypermobility Most common in women < 60 years old and men who have had prostate surgery Aggravating factors: obesity, pregnancy, COPD, smoking Post void cystometry will be normal Treatment: kegel exercsies (preferred), urethroplexy (preferred), estrogen (in post-menopausal women), weight loss, stop smoking Surgical treatment: Burch and Sling procedures, bladder neck suspension surgery Overflow incontinence: occurs when pt’s bladder is always full so that it frequently releases small amounts of urine from bladder over-distension and increased residual volume; associated with neurologic lesions below S1, pole neuropathies, urethral obstruction —> too little contraction Use post-void residual volume Causes: diabetic nephropathy, BPH, meds (ibuprofen), blockage of urethra (tumors, kidney stones) Treatment if medication induced: stop meds add Bethanechol to improve detrusor muscle action —> if control still not regained: intermittent catheterization to drain bladder Mixed incontinence: combo of both stress and urge incontinence Functional incontinence: involuntary loss of urine attributable to dementia or immobility similar to overflow incontinence urine comes out without sneezing / coughing Underactive bladder (Urinary retention): inability to

voluntarily void urine; characterized by a slow urinary stream, hesitancy, and straining to void, with or without a feeling of incomplete bladder emptying sometimes with storage symptoms —> the loss of usual sensation of the bladder filling and failure of the detrusor muscle to contract as forcefully as it should, resulting in incomplete bladder emptying Causes: peripheral nerve damage, diabetes (high blood sugar can damage nerves) Acute urinary retention: painful inability to void Chronic urinary retention: painless inability to start urine stream or inability to empty the bladder Sx: complete lack of voiding, strong urge to urinate, inability to start voiding, incomplete bladder emptying, frequent urination, lower abdominal bloating Causes: obstruction (BPH, tumors), infection, inflammation, meds (antidepressants, alpha adrenergic agonists, neurologic damage Treatment: bladder catheterization Causes UTIs, vaginal infection/irritation, constipation medicines neurologic disturbances congenital defects of the meatus urethra bladder neck allergies Causes for the elderly weak/overactive bladder muscles, damage to bladder nerves (MS, Parkinsons), blockage arthritis (make it difficult to reach bathroom intake) Associated conditions with incontinence: perinatal anoxia, CNS trauma, seizures, attention-deficit/hyperactivity disorder, developmental delay, imperforate anus, bladder trauma, surgery, obesity, hidden malformations of the spine —> kidney stones = bleeding in bladder / urethra = blood clots = blocked ureter Associated conditions with enuresis: altered sleep arousal,

obstructive sleep apnea Treatments drugs do not work because urinating involved both SNS and PNS Sympathetic NS: Parasympathetic NS Alpha blocker meds; Alpha 1 receptors contract detrusor muscles, block contractions Estrogen (with caution of cancer potential) Tests Urinalysis (UA): to check for bacteriuria (infection), glycosuria (diabetes), hematuria (kidney disease), proteinuria kidney, cardiac, blood disease), pyuria (infection) Post-void residual volume: repeated measurements of 100 200 mL or higher represent inadequate bladder emptying, repeated measurements are necessary Urodynamic testing: cystometry to measure the anatomic and functional status of the bladder and urethra —> if Urodynamic tasing fails, then go to endoscopy / imaging Endoscope tests: cystoscopy may be performed when urodynamic testing fails to duplicate sx, when the pt experiences new sx (ex: cystitis, pain), or when urinalysis reveals a disease process (ex: hematuria, oyuria) Cystoscopy identifies presence of bladder lesions Imaging: x-rays and ultrasounds may be used to evaluate anatomic conditions associated wit incontinence Inability to void / urinate Lesion above C2 involve pontine micturition disorder (UMN disorder) causes: detrusor hyperreflexia (urgency and leakage) diseases: stroke, traumatic brain injury, MS, hydrocephalus, cerebral palsy, Alzheimers, brain tumors Lesions between C2 and S1 (UMN disorder) causes: detrusor 1 hyperreflexia with vesicosphincter dyssynergia (functional bladder obstruction) diseases: spinal cord injury C2-T12, MS, transnerve myelitis, Guillain-BArre syndrome, disk problems

—> spinal cord injury associated with uncontrolled / premature contractions of detrusor muscle Lesions below S1 cauda equina syndrome (LMN disorder) causes: contractile detrusor, with or without urethral sphincter incompetence (stress urinary incontinence) diseases: myelodysplasiam peripheral poly neuropathies, MS, cauda equina syndrome, herpes may be 2 issues: failure to void & failure to retain Adaptive Immunity immune injury caused by activation of biochemical mediators or inflammation (complement and cytokines from leukocytes) and begins after the antigen-antibody complexes have deposited / formed in the glomerular capillary wall complement is deposited with antibodies and activation can cause cell lysis or serve as chemotaxis stimulus for attraction of neutrophils, monocytes, T lymphocytes phagocytes + activated platelets increase inflammatory reaction by releasing mediators that injure the glomerular filtration membrane, including epithelial cells glomerular basement membranes and endothelial cells the injury increases glomerular membrane permeability and decreases glomerular membrane surface area GFR decreases = increased serum creatinine levels = decreases glomerular blood flow = decreasing driving hydrostatic pressure, decreased GFR, and hypoxic injury End Stage Renal Disease (ESRD) leading cause = diabetes + hypertension affect the ability to contract / constrict / dilate the vessels in the kidney GFR (glomerular filtration rate): measures amount of blood passing through glomeruli each minute (filters) average: 90 - 120 > 120: no problem > 60: no need to change meds < 60 for more than 3 months: kidneys failure, need to change meds

< 15 end stage kidney failure < 10 uremia = increased waste in blood (organs pickle) BUN (blood urea nitrogen): evaluates kidney function average: 7 - 18 mg affected by protein / fluid Creatinine: waste product of normals breakdown of muscle tissue average: 0.6 - 1.2 mg more accurate than BUN bc it is not affected buy diet —> Sx of high BUN + creatinine: NV, lethargy, fatigue meds can also cause changes in BUN + creatinine —> if changes mentation look at BUN and creatinine levels, could be UTI, Renal failure,, or worsening RF Triglycerides: fat in the blood average: < 150 mg increased = defective carbohydrate metabolism, defective/ altered lipid metabolism increased insulin = increased triglycerides —> pt will be put on statin + Gemfibrozil (Lopid) to decreased triglyceride levels and fix LDL Key Terms Kegel exercises: tightens pelvic floor, helps urinary incontinence Urethropexy: abdominal procedure performed to correct stress urinary incontinence Post void cystometry: test used to look for problems with the filling and emptying of the bladder Post void residual volume: volume of urine left in bladder after urinating Acute glomerulonephritis: sudden onset of renal diseases that trigger inflammation and proliferation of glomerular tissue that can result in damage to the basement membrane, mesangium, or capillary endothelium Chronic glomerulonephritis: gradual occurrence of inflammation and proliferation of glomerular tissue Anuria / anuresis: kidneys aren't producing urine, linked to kidney disease Cystocele: occurs when when the bladder sags or presses into the vagina Detrusor areflexia: detrusor will be unable to contract, so the patient will not be able to urinate and urinary retention will occur Diabetic nephropathy: common kidney disease in people with diabetes

Treatment: Angiotensin converting enzyme inhibitors (ACEi),angiotensin receptor blockers (ARBs Low bladder wall compliance: impede bladder’s ability to stretch, attributable to increased detrusor muscle tone Obstructive uropathy: a condition in which the flow of urine is blocked, urine backs up and injures kidneys Oliguria: poor urine output 1. Which population group is at greatest risk for bladder tumors? The elderly (> 55 years old) + Caucasians 2. Why is cystitis more common in women? Shorter urethra 3. What diseases from the video (on blackboard) are the causes of incontinence? neurologic diseases (MS, Parkinson’s, Alzheimer’s, stroke) 4. What is glomerulonephritis? List two types. inflammation of the glomeruli (tiny filters in your kidneys). Glomeruli remove excess fluid, electrolytes and waste from your bloodstream and pass them into your urine. Glomerulonephritis can come on suddenly (acute) or gradually (chronic) 5. What immune mechanisms are operative in glomerulonephritis? immune dysregulation, adjuvant or bystander effects, epitope spreading, molecular mimicry, epitope conformational changes, and antigen complementarity 6. Explain how diabetes can affect urinary health. Diabetes impacts blood flow, nerves, and sensory functions of body Diabetics are prone to UTIs, bladder issues, sexual dysfunction.

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4/16 Lecture 10: Innate and Adaptive Immunity

Immunity: “internal monitoring system” What does it do? Senses for pathogens (bacteria, viruses, parasites, fungi, protozoa) Senses cellular changes Attacks abnormal cells (cancer / mutant), worn-out cells,

cellular debris (dying neutrophils) Sense tumor formation Homeostasis: promotes return to normal functioning after illness / injury First rule: body distinguishes between self and non-self Autoimmune issues: immune system attacks itself, recognizes bodily tissues as foreign invaders ex: allergies (IgE), autoimmune disorders (Lupus, rheumatoid arthritis), transplant rejection Pathogen: microbes that infect the body and cause illness Antigen: parts of the pathogen that alert the body to infection, immune cells recognize antigens Types Innate Immunity: defense mechanisms that appear immediately or within hours of antigen exposure immediate first response, non-specific Barriers: physical (skin), biochemical (mucosal membranes, stomach acid), resistance, mechanical, bacteria —> too much inflammation can interfere with healing meds that directly limit inflammatory response: ibuprofen, prednisone, Benadryl vasodilation + redness at site of injury is due to body’s vascular response to cell injury Gained at birth Against foreign bodies, injuries, pathogens Bacteria-killing substances, scavenger cells (tissue), pattern recognition proteins phagocytes eosinophils: kill antibody-coated parasites, release histamine granules and other pro-inflammatory mediators leukocytes / leukotrienes: acidic, sulfur containing lipid that has similar effects to histamine slow, reactive substance associated with anaphylaxis Ex: cough reflex, stomach acid, enzymes in tears, skin oils, mucus, epithelial barriers (includes GI, GU, respiratory tract), phagocytosis

Nursing interventions: skin protection (turning, moisture barriers), hand washing, labs, nutritional status Adaptive Immunity: immunity that has been introduced to the body by way of previous infection, ex: immunization (work by sensitizing your body ti prepare antibodies against the virus if exposed in the future to the same antigen), inoculation second response, specific (more complex than Innate) Initiated when innate immune system signals cells of adaptive immune system —> is weakened when health is decreased (old age, sickness, etc) elder people must get re-innocculated / revaccinated Against specific pathogens, changed body cells Defense cells can be active or inactive in blood: B lymphocytes (B-cells) / antibodies in tissue: T lymphocytes (T-cells) Antibodies Direct attachment agglutination: antigens clump precipitation: antigens become insoluble neutralization: antigens lose toxic properties Activation of Complement chemotaxis: attracts macrophages / neutrophils into region inflammation: promotes local tissue changes, prevents antigen spread lysis: cell membranes rupture Natural killer cells: release lytic granules that form complex to destroy microorganisms Cytokines: proteins secreted by cells that affect behavior of nearby cells creates a “memory” to make future responses more efficient Types

Naturally acquired (normal environmental exposure) Active: antigens enter body naturally, body induces antibodies / specialized lymphocytes few years - lifelong Passive: antibodies pass from mother to fetus via placenta or mothers milk weeks - months Artificially acquired (m...