COTAC EXAM 4

CHAPTER 55 (Management of Patients with Urinary Disorders)

10 Questions

CHAPTER 37 (Assessment and Management of a Patient with Allergic Disorders)

12 Quesitons

CHAPTER 35 (Assessment of Immune Function)

12 Question

CHAPTER 54 (Management of Patients with Kidney Disorders)

16 Questions

Allergy skin testing o appropriate nursing interventions o contraindications for

Allergy skin testing: Diagnostic evaluation of the patient with allergic disorders commonly includes blood tests, smears of body secretions, skin tests, and the serum-specific IgE test. Results of laboratory blood studies provide supportive data for various diagnostic possibilities; however, they are not the major criteria for the diagnosis of allergic disease. Complete Blood Count With Differential The white blood cell (WBC) count is usually normal except with infection and inflammation. Eosinophils, which are granular leukocytes, normally make up 2% to 5% of the total number of WBCs. They can be found in blood, sputum, and nasal secretions. A level greater than 5% to 10% is considered abnormal and may be found in patients with allergic disorders. Eosinophil Count An actual count of eosinophils can be obtained from blood samples or smears of secretions. During symptomatic episodes, smears obtained from nasal secretions and sputum of patients with allergies usually reveal an increase in eosinophils, indicating an active allergic response. Total Serum Immunoglobulin E Levels High total serum IgE levels support the diagnosis of allergic disease. In the majority of cases, the antibody typically responsible for an allergic reaction belongs to the IgE isotype. Patients with this disorder are said to have an IgE-mediated allergic disease. Skin Tests Skin testing entails the intradermal injection or superficial application (epicutaneous) of solutions at several sites. Depending on the suspected cause of allergic signs and symptoms, many different solutions may be applied at separate sites. These solutions contain individual antigens representing an assortment of allergens most likely to be implicated in the patient's disease. Positive (wheal-and-flare) reactions are clinically significant when correlated with the history, physical findings, and results of other laboratory tests. Skin testing is considered the most accurate confirmation of allergy. The results of skin tests complement the data obtained from the history. They indicate which of several antigens are most likely to provoke symptoms and indicate the intensity of the patient's sensitization. The dosage of the antigen (allergen) injected is also important. Most patients are hypersensitive to more than one allergen. Under testing conditions, they may not react (although they usually do) to the specific allergens that induce their attacks. In cases of doubt about the validity of the skin tests, a serum-specific IgE test or a provocative challenge test may be performed. If a skin test is indicated, there is a reasonable suspicion that a specific allergen is producing symptoms in a patient with allergies. However, several precautionary steps must be observed before skin testing with allergens is performed: Testing is not performed during periods of bronchospasm. Epicutaneous tests (scratch or prick tests) are performed before other testing methods, in an effort to minimize the risk of systemic reaction. Emergency equipment must be readily available to treat anaphylaxis. Appropriate nursing interventions: get history of manifestations; comprehensive allergy history. Have oxygen, epinephrine, histamines, and corticosteroids available while performing allergy tests to treat possible anaphylaxis. Contraindications for: Corticosteroids and antihistamines, including over-the-counter allergy medications, suppress skin test reactivity and should be stopped 48 to 96 hours before testing, depending on the duration of their activity. False-positive results may occur because of improper preparation or administration of allergen solutions. Skin prick testing should be used with caution in people with significant co-morbidities such as cardiovascular disease or arrhythmias and also in elderly people. Patients with skin conditions such as dermographism, because the results may be falsely positive.

Describe anaphylaxis o What are the priority assessments? o What are the potential causes? o What are the treatments? o What laboratory values would you anticipate being altered/abnormal? o Identify potential complications

Describe anaphylaxis: Anaphylaxis is a clinical response to an immediate (type I hypersensitivity) immunologic reaction between a specific antigen and an antibody. The reaction results from a rapid release of IgE-mediated chemicals, which can induce a severe, life-threatening reaction. What are the priority assessments: Airway, breathing pattern and vital signs are assessed. The patient is observed for signs of increasing edema and respiratory distress. Prompt notification of the rapid response team and provider are required. What are the potential causes: foods (peanuts, tree nuts, shellfish, fish, eggs soy, wheat), medications (antibiotics, especially penicillin and sulfas, anesthetic agents, vaccines, hormones, aspirin, NSAIDS), animal serums, antigens used in skin testing, insect stings, latex products. What are the treatments: Management depends on the severity of the reaction. Initially, respiratory and cardiovascular functions are evaluated. If the patient is in cardiac arrest, cardiopulmonary resuscitation (CPR) is instituted. Supplemental oxygen is provided during CPR or if the patient is cyanotic, dyspneic, or wheezing. Epinephrine, in a 1:1000 dilution, is given subcutaneously in the upper extremity or thigh and may be followed by a continuous intravenous infusion. Most adverse events associated with administration of epinephrine (i.e., adrenaline) occur when the dose is excessive or is given intravenously. Patients at risk for adverse effects include older patients and those with hypertension, arteriopathies, or known ischemic heart disease. Antihistamines and corticosteroids should not be given in place of epinephrine. However, they may also be given as adjunct therapy. Intravenous fluids (e.g., normal saline solution), volume expanders, and vasopressor agents are given to maintain blood pressure and normal hemodynamic status. In patients with episodes of bronchospasm or a history of bronchial asthma or chronic obstructive pulmonary disease, aminophylline and corticosteroids may also be given to improve airway patency and function. Patients who have experienced anaphylactic reactions and received epinephrine should be transported to the local emergency department (ED) for observation and monitoring because of the risk for a "rebound" or delayed reaction 4 to 8 hours after the initial allergic reaction. However, the observation time should be individualized based on the severity of the anaphylaxis. Longer periods of observation should be considered for patients who ingested the allergen, required more than one dose of epinephrine, had hypotension or pharyngeal edema, or have a history of asthma What laboratory values would you anticipate being altered/abnormal: elevated iGE serum, mast cell Tryptase protein that is released during anaphylaxis, low oxygen sat levels. Identify potential complications: rebound or delayed reaction 4 to 8 hours after the initial allergic reaction.

Renal surgery o Nursing assessment o Potential complications

Renal surgery: Surgery is performed only after a thorough evaluation of renal function. Patient preparation to ensure that optimal renal function is maintained is essential. Fluids are encouraged to promote increased excretion of waste products before surgery unless contraindicated because of pre-existing renal or cardiac dysfunction. If kidney infection is present preoperatively, broad-spectrum antimicrobial agents may be prescribed to prevent bacteremia. Antibiotic agents must be given with extreme care because many are toxic to the kidneys. Coagulation studies (prothrombin time, partial thromboplastin time, platelet count) may be indicated if the patient has a history of bruising and bleeding. Because many patients facing kidney surgery are apprehensive, the nurse encourages the patient to recognize and verbalize concerns. Confidence is reinforced by establishing a relationship of trust and by providing expert care. Patients faced with the prospect of losing a kidney may think that they will have to depend on dialysis for the rest of their lives. The nurse reassures the patient and family that normal function may be maintained by a single healthy kidney. Nursing assessment: Immediate postoperative care of the patient who has undergone surgery of the kidney includes assessment of all body systems. Respiratory and circulatory status, pain level, fluid and electrolyte status, and patency and adequacy of urinary drainage systems are assessed. Respiratory Status As with any surgery, the use of anesthesia increases the risk of respiratory complications. Noting the location of the surgical incision assists the nurse in anticipating respiratory problems and pain. Respiratory status is assessed by monitoring the rate, depth, and pattern of respirations. The location of the incision frequently causes pain on inspiration and coughing; therefore, the patient tends to splint the chest wall and take shallow respirations. Auscultation is performed to assess normal and adventitious breath sounds. Circulatory Status and Blood Loss The patient's vital signs and arterial or central venous pressure are monitored. Skin color and temperature and urine output provide information about circulatory status. The surgical incision and drainage tubes are observed frequently to help detect unexpected blood loss and hemorrhage. Pain Postoperative pain is a major problem for the patient because of the location of the surgical incision and patient's position on the operating table to permit access to the kidney. The location and severity of pain are assessed before and after analgesic medications are given. Abdominal distention, which increases discomfort, is also noted. Urinary Drainage Urine output and drainage from tubes inserted during surgery are monitored for amount, color, and type or characteristics. Decreased or absent drainage is promptly reported to the primary provider because it may indicate obstruction that could cause pain, infection, and disruption of the suture lines. Potential complications: Bleeding is a major complication of kidney surgery. If undetected and untreated, it can result in hypovolemia and hemorrhagic shock. The nurse's role is to observe for these complications, to report their signs and symptoms, and to administer prescribed parenteral fluids and blood and blood components. Monitoring of vital signs, skin condition, the urinary drainage system, the surgical incision, and the level of consciousness is necessary to detect evidence of bleeding, decreased circulating blood, and fluid volume and cardiac output. Frequent monitoring of vital signs (initially monitored at least at hourly intervals) and urinary output is necessary for early detection of these complications. If bleeding goes undetected or is not detected promptly, the patient may lose significant amounts of blood and may experience hypoxemia. In addition to hypovolemic shock due to hemorrhage, this type of blood loss may precipitate a myocardial infarction or transient ischemic attack. Bleeding may be suspected when the patient experiences fatigue and when urine output is less than 0.5 mL/kg/hr. As bleeding persists, late signs of hypovolemia occur, such as cool skin, flat neck veins, and change in level of consciousness or responsiveness. Transfusions of blood components are indicated, along with surgical repair of the bleeding vessel. Pneumonia may be prevented through the use of an incentive spirometer, adequate pain control, and early ambulation. Early signs of pneumonia include fever, increased heart and respiratory rates, and adventitious breath sounds. Preventing infection involves using asepsis when changing dressings and handling and preparing catheters, other drainage tubes, central venous catheters, and IV catheters for administration of fluids. Insertion sites are monitored closely for signs and symptoms of inflammation: redness, drainage, heat, and pain. Special care must be taken to prevent UTI, which is associated with the use of indwelling urinary catheters. Catheters and other invasive tubes are removed as soon as they are no longer needed. Antibiotics are commonly given postoperatively to prevent infection. If antibiotic agents are prescribed, serum creatinine and BUN values must be monitored closely because many antibiotic agents are toxic to the kidney or can accumulate to toxic levels if renal function is decreased. Preventing fluid imbalance is critical when caring for a patient undergoing kidney surgery, because both fluid loss and fluid excess are possible adverse effects of the surgery. Fluid loss may occur during surgery as a result of excessive urinary drainage when the obstruction is removed, or it may occur if diuretic agents are used. Such loss may also occur with GI losses, with diarrhea resulting from antibiotic use, or with nasogastric drainage. When postoperative IV therapy is inadequate to match the output or fluids lost, a fluid deficit results. Fluid excess, or overload, may result from cardiac effects of anesthesia, administration of excessive amounts of fluids, or the patient's inability to excrete fluid because of changes in renal function. Decreased urine output may be an indication of fluid excess. Astute assessment skills are needed to detect early signs of fluid excess (such as weight gain, pedal edema, urine output below 0.5 mL/kg/hr, and slightly elevated pulmonary artery wedge pressure if available) before they become severe (appearance of adventitious breath sounds, shortness of breath). Fluid excess may be treated with fluid restriction and administration of furosemide (Lasix) or other diuretic agents. If renal insufficiency is present, these medications may prove ineffective; therefore, dialysis may be necessary to prevent heart failure and pulmonary edema. Deep vein thrombosis (DVT) may occur postoperatively because of surgical manipulation of the iliac vessels during surgery or prolonged immobility. Antiembolism stockings are applied, and the patient is monitored closely for signs and symptoms of thrombosis and encouraged to exercise the legs. Heparin may be given postoperatively to reduce the risk of thrombosis.

Polycystic kidney disease o Pathophysiology o Nursing management

Pathophysiology: Polycystic kidney disease (PKD) is a genetic disorder characterized by the growth of numerous fluid-filled cysts in the kidneys, which destroy the nephrons. PKD cysts can profoundly enlarge the kidneys while replacing much of the normal structure, resulting in reduced kidney function and leading to kidney failure. PKD can also cause cysts in the liver and problems in other areas, such as blood vessels in the brain and heart. The number of cysts and the resulting complications help distinguish PKD from the usually harmless cysts that can form in the kidneys in later years of life. In the United States, PKD and cystic diseases are a leading cause of kidney failure. Two major inherited forms of PKD exist: Autosomal dominant PKD is the most common inherited form. Symptoms usually develop between 30 and 40 years of age, but they can begin earlier, even in childhood. About 90% of all PKD cases are autosomal dominant PKD. Autosomal recessive PKD is a rare inherited form. Symptoms of autosomal recessive PKD begin in the earliest months of life or in utero. When autosomal dominant PKD causes kidneys to fail, which usually happens after many years, the patient requires dialysis or kidney transplantation. Approximately one half of individuals with autosomal dominant PKD progress to stage 5 CKD, requiring renal replacement therapy. Clinical Manifestations: Signs and symptoms of PKD result from loss of renal function and the increasing size of the kidneys as the cysts grow. Kidney damage can result in hematuria, polyuria (excessive urine production), hypertension, development of renal calculi and associated UTIs, and proteinuria. The growing cysts are noted with reports of abdominal fullness and flank pain (back and lower sides). Nursing management: PKD has no cure, and treatment is largely supportive and includes blood pressure control, pain control, and antibiotic agents to resolve infections. Once the kidneys fail, renal replacement therapy is indicated (see later discussion in chapter). Genetic linkage studies and counseling may be indicated, particularly when screening family members for potential kidney donation. Following a low-salt diet and eating less protein might allow kidney cysts to respond better to the increase in fluids. Monitor vitals, monitor I&O's, monitor electrolyte balance, monitor daily weights, monitor for edmea, check skin integrity.

Urinary incontinence o Types o Treatments

Urinary incontinence: More than 25 million adults in the United States are estimated to have urinary incontinence (involuntary or uncontrolled loss of urine from the bladder), with most of them experiencing overactive bladder syndrome, making this disorder more prevalent than diabetes or ulcer disease. Despite widespread media coverage, urinary incontinence remains underdiagnosed and underreported. Patients may be too embarrassed to seek help, causing them to ignore or conceal symptoms. Many patients use absorbent pads or other devices without having their condition properly diagnosed and treated. Health care providers must be alert to subtle cues of urinary incontinence and stay informed about current management strategies. The costs of care for patients with urinary incontinence include the expenses of absorbent products, medications, and surgical or nonsurgical treatment modalities, as well as psychosocial costs (i.e., embarrassment, loss of self-esteem, and social isolation). Although urinary incontinence is commonly regarded as a condition that occurs in older multiparous women, it can occur in young nulliparous women, especially during vigorous high-impact activity. Age, gender, and number of vaginal deliveries are established risk factors that explain, in part, the increased incidence in women (see Chart 55-6). Men can have urinary incontinence, especially those with certain comorbid conditions. One group of researchers, for example, reported that 40% of men with Parkinson disease reported urinary incontinence. Urinary incontinence is a symptom of many possible disorders. Types: There are many types of urinary incontinence, including the following: Stress incontinence is the involuntary loss of urine through an intact urethra as a result of sneezing, coughing, or changing position. It predominantly affects women who have had vaginal deliveries and is thought to be the result of decreasing ligament and pelvic floor support of the urethra and decreasing or absent estrogen levels within the urethral walls and bladder base. In men, stress incontinence is often experienced after a radical prostatectomy for prostate cancer because of the loss of urethral compression that the prostate had supplied before the surgery, and possibly bladder wall irritability. Urge incontinence is the involuntary loss of urine associated with a strong urge to void that cannot be suppressed. The patient is aware of the need to void but is unable to reach a toilet in time. An uninhibited detrusor contraction is the precipitating factor. This can occur in a patient with neurologic dysfunction that impairs inhibition of bladder contraction or in a patient without overt neurologic dysfunction. Functional incontinence refers to those instances in which lower urinary tract function is intact but other factors, such as severe cognitive impairment (e.g., Alzheimer dementia), make it difficult for the patient to identify the need to void or physical impairments make it difficult or impossible for the patient to reach the toilet in time for voiding. Iatrogenic incontinence refers to the involuntary loss of urine due to extrinsic medical factors, predominantly medications. One such example is the use of alpha-adrenergic agents to decrease blood pressure. In some people with an intact urinary system, these agents adversely affect the alpha receptors responsible for bladder neck closing pressure; the bladder neck relaxes to the point of incontinence with a minimal increase in intra-abdominal pressure, thus mimicking stress incontinence. As soon as the medication is discontinued, the apparent incontinence resolves. Mixed urinary incontinence, which encompasses several types of urinary incontinence, is involuntary leakage associated with urgency and also with exertion, effort, sneezing, or coughing. Only with appropriate recognition of the problem, assessment, and referral for diagnostic evaluation and treatment can the outcome of incontinence be determined. All people with incontinence should be considered for evaluation and treatment. Treatments: Management depends on the type of urinary incontinence and its causes. Management of urinary incontinence may be behavioral, pharmacologic, or surgical.

Urinary retention o Causes o Nursing interventions

Urinary retention: Urinary retention is the inability to empty the bladder completely during attempts to void. Chronic urine retention often leads to overflow incontinence (involuntary urine loss associated with overdistention of the bladder). Residual urine is urine that remains in the bladder after voiding. In a healthy adult younger than 60 years, complete bladder emptying should occur with each voiding. In adults older than 60 years, 50 to 100 mL of residual urine may remain after each voiding because of the decreased contractility of the detrusor muscle. Urinary retention can occur postoperatively in any patient, particularly if the surgery affected the perineal or anal regions and resulted in reflex spasm of the sphincters. General anesthesia reduces bladder muscle innervation and suppresses the urge to void, impeding bladder emptying. Causes: Urinary retention may result from diabetes, prostatic enlargement, urethral pathology (infection, tumor, calculus), trauma (pelvic injuries), pregnancy, or neurologic disorders (e.g., stroke, spinal cord injury, multiple sclerosis, or Parkinson disease). Some medications cause urinary retention either by inhibiting bladder contractility or by increasing bladder outlet resistance. Nursing interventions: Strategies are instituted to prevent overdistention of the bladder and to treat infection or correct obstruction. However, many complications can be prevented with careful assessment and appropriate nursing interventions. The nurse explains to the patient why normal voiding is not occurring and monitors urine output closely. The nurse also provides reassurance about the temporary nature of retention and successful management strategies. Promoting Urinary Elimination Nursing measures to encourage normal voiding patterns include providing privacy, ensuring an environment and body position conducive to voiding, and assisting the patient with the use of the bathroom or bedside commode, rather than a bedpan, to provide a more natural setting for voiding. If his condition allows, the male patient may stand beside the bed to use the urinal; most men find this position more comfortable and natural. Additional measures include applying warmth to relax the sphincters (i.e., sitz baths, warm compresses to the perineum, showers), giving the patient hot caffeine free beverage and offering encouragement and reassurance. Simple trigger techniques, such as turning on the water faucet while the patient is trying to void, may also be used. Other examples of trigger techniques are stroking the abdomen or inner thighs, tapping above the pubic area, and dipping the patient's hands in warm water. After surgery or childbirth, prescribed analgesic agents should be given because pain in the perineal area can make voiding difficult. A combination of techniques may be necessary to initiate voiding. When the patient cannot void, bladder scanning is used to assess for distension, then straight catheterization (as prescribed) is used to prevent overdistention of the bladder (see later discussion of neurogenic bladder and catheterization). In the case of prostatic obstruction, attempts at catheterization (by the urologist) may not be successful, requiring insertion of a suprapubic catheter (catheter inserted through a small abdominal incision into the bladder). After urinary drainage is restored, bladder retraining is initiated for the patient who cannot void spontaneously. Promoting Home, Community-Based, and Transitional Care In addition to the strategies listed for promoting urinary continence found in Chart 55-9, modifications to the home environment can provide simple and effective ways to assist in treating urinary incontinence and retention. For example, the patient may need to remove obstacles, such as throw rugs or other objects, to provide easy, safe access to the bathroom. Other modifications that the nurse may recommend include installing support bars in the bathroom; placing a bedside commode, bedpan, or urinal within easy reach; leaving lights on in the bedroom and bathroom; and wearing clothing that is easy to remove quickly.

Urinary tract infections o Signs and symptoms o Nursing roles/ responsibilities & Patient education o Risk factors

Urinary tract infections: Urinary tract infections (UTIs) are caused by pathogenic microorganisms in the urinary tract (the normal urinary tract is sterile above the urethra). UTIs are generally classified as infections involving the upper or lower urinary tract and further classified as uncomplicated or complicated, depending on other patient-related conditions (see Chart 55-1). Lower UTIs include bacterial cystitis (inflammation of the urinary bladder), bacterial prostatitis (inflammation of the prostate gland), and bacterial urethritis (inflammation of the urethra). Acute or chronic nonbacterial causes of inflammation in any of these areas can be misdiagnosed as bacterial infections. Upper UTIs are much less common and include acute or chronic pyelonephritis (inflammation of the renal pelvis), interstitial nephritis (inflammation of the kidney), and kidney abscesses. Upper and lower UTIs are further classified as uncomplicated or complicated, depending on whether the UTI is recurrent and the duration of the infection. Most uncomplicated UTIs are community acquired. Complicated UTIs usually occur in people with urologic abnormalities or recent catheterization and are often acquired during hospitalization. A UTI is the second most common infection in the body. Most cases occur in women; one out of every five women in the United States will develop a UTI during her lifetime. The urinary tract is the most common site of nosocomial infection, accounting for greater than 40% of the total number reported by hospitals and affecting about 600,000 patients each year. In most of these hospital-acquired UTIs, instrumentation of the urinary tract or catheterization is the precipitating cause. More than 250,000 cases of acute pyelonephritis occur in the United States each year, with 100,000 patients requiring hospitalization. Approximately 8.1 million women are diagnosed with uncomplicated UTIs in the United States annually. For infection to occur, bacteria must gain access to the bladder, attach to and colonize the epithelium of the urinary tract to avoid being washed out with voiding, evade host defense mechanisms, and initiate inflammation. Many UTIs result from fecal organisms ascending from the perineum to the urethra and the bladder and then adhering to the mucosal surfaces Signs and symptoms: Signs and symptoms of UTI depend on whether the infection involves the lower (bladder) or upper (kidney) urinary tract and whether the infection is acute or chronic. Signs and symptoms of an uncomplicated lower UTI include burning on urination, urinary frequency (voiding more than every 3 hours), urgency, nocturia (awakening at night to urinate), incontinence, and suprapubic or pelvic pain. Hematuria and back pain may also be present. In older adults, these symptoms are less common (see Gerontologic Considerations section). In patients with complicated UTIs, manifestations can range from asymptomatic bacteriuria to gram-negative sepsis with shock. Complicated UTIs often are caused by a broader spectrum of organisms, have a lower response rate to treatment, and tend to recur. Many patients with catheter-associated UTIs are asymptomatic; however, any patient with a catheter who suddenly develops signs and symptoms of septic shock should be evaluated for urosepsis (the spread of infection from the urinary tract to the bloodstream that results in a systemic infection). Nursing roles/ responsibilities & Patient education: pharmacologic therapy, relieving pain, monitoring and managing potential complications such as sepsis, obstructions and kidney disease, performing perineal care, inspecting urine, monitor labs for signs of infection. Patient eduction should include information on performing daily hygiene, such as showing instead of baths and cleaning the perineum and urethral meatus from front to back. Increasing fluid intake to help flush out bacteria and drink cranberry juice. Avoid coffee, teas, and cola that are urinary tract irritants. Void every 2-3 hours and completely empty the bladder. Void after sexual intercourse. Take medications as prescribed, take vitamin C or cranberry supplement to acidify urine, notify provider if fever occurs. Risk factors: Contributing conditions such as: Female gender, Diabetes, Pregnancy, Neurologic disorders Gout, Altered states caused by incomplete emptying of the bladder and urinary stasis, Decreased natural host defenses or immunosuppression, Inability or failure to empty the bladder completely, Inflammation or abrasion of the urethral mucosa, Instrumentation of the urinary tract (e.g., catheterization, cystoscopic procedures). Obstructed urinary flow caused by: Congenital abnormalities, Urethral strictures, Contracture of the bladder neck, Bladder tumors, Calculi (stones) in the ureters or kidneys, Compression of the ureters. Gerontologic Considerations The incidence of bacteriuria in older adults differs from that in younger adults. Bacteriuria increases with age and disability, and women are affected more frequently than men. UTI is the most common infection of older adults and increases in prevalence with age. UTIs occur more frequently in women than in men at younger ages but the gap between the sexes narrows in later life, which is due to reduced sexual intercourse in women and a higher incidence of bladder outlet obstruction secondary to benign prostatic hyperplasia in men. In older adults, structural abnormalities secondary to decreased bladder tone, neurogenic bladder (dysfunctional bladder) secondary to stroke, or autonomic neuropathy of diabetes may prevent complete emptying of the bladder and increase the risk of UTI. When indwelling catheters are used, the risk of UTI increases dramatically. Older women often have incomplete emptying of the bladder and urinary stasis. In the absence of estrogen, postmenopausal women are susceptible to colonization and increased adherence of bacteria to the vagina and urethra. Oral or topical estrogen has been used to restore the glycogen content of vaginal epithelial cells and an acidic pH for some postmenopausal women with recurrent cystitis. The antibacterial activity of prostatic secretions that protect men from bacterial colonization of the urethra and bladder decreases with aging. The use of catheterization or cystoscopy in evaluation or treatment for prostatic hyperplasia or carcinoma, strictures of the urethra, and neuropathic bladder may contribute to the higher incidence of UTIs in men. The incidence of bacteriuria also increases in men with confusion, dementia, or bowel or bladder incontinence. The most common cause of recurrent UTIs in older males is chronic bacterial prostatitis. Resection of the prostate gland may help reduce its incidence.

Urolithiasis o Causes o Signs and symptoms o Post-treatment complications ESWL

Urolithiasis: Urolithiasis is when stones form in the urinary tract when urinary concentrations of substances such as calcium phosphate, uric acid and calcium oxalate increase. Stones can vary in size and they can be found anywhere from the bladder to the kidney. 80% of stones are composed of calcium oxalate or phosphate. Stones occur due to varying factors that favor their formation, including urinary stasis, infection, and periods of immobility, which slows kidney drainage and alters calcium metabolism. Hyperparathyroidism, renal tubular acidosis, dehydration, cancers, excessive vitamin D intake, and excessive milk intake can all cause hypercalcemia, which in return can cause urolithiasis Causes: Certain factors favor the formation of stones, including infection, urinary stasis, and periods of immobility, all of which slow kidney drainage and alter calcium metabolism. In addition, increased calcium concentrations in the blood and urine promote precipitation of calcium and formation of stones. Causes of hypercalcemia (high serum calcium) and hypercalciuria (high urine calcium) may include the following: Hyperparathyroidism, Renal tubular acidosis, Cancers (e.g., leukemia, multiple myeloma), Dehydration, Granulomatous diseases (e.g., sarcoidosis, tuberculosis), which may cause increased vitamin D production by the granulomatous tissue, Excessive intake of vitamin D, Excessive intake of milk and alkali, Myeloproliferative diseases such as polycythemia vera, which produce an unusual proliferation of blood cells from the bone marrow. For patients with stones containing uric acid, struvite, or cystine, a thorough physical examination and metabolic workup are indicated because of associated disturbances contributing to the stone formation. Uric acid stones (5% to 10% of all stones) may be seen in patients with gout or myeloproliferative disorders. Struvite stones account for 15% of urinary calculi and form in persistently alkaline, ammonia-rich urine caused by the presence of urease-splitting bacteria such as Proteus, Pseudomonas, Klebsiella, Staphylococcus, or Mycoplasma species. Predisposing factors for struvite stones include neurogenic bladder, foreign bodies, and recurrent UTIs. Several conditions, as well as certain metabolic risk factors, predispose patients to stone formation. These include anatomic derangements such as polycystic kidney disease, horseshoe kidneys, chronic strictures, and medullary sponge disease. Urinary stone formation can occur in patients with inflammatory bowel disease and in those with an ileostomy or bowel resection because these patients absorb more oxalate. Medications known to cause stones in some patients include antacids, acetazolamide (Diamox), vitamin D, laxatives, and high doses of aspirin. However, in many patients, no cause may be found. Signs and symptoms: Signs and symptoms of stones in the urinary system depend on the presence of obstruction, infection, and edema. When stones block the flow of urine, obstruction develops, producing an increase in hydrostatic pressure and distending the renal pelvis and proximal ureter. Infection (pyelonephritis and UTI with chills, fever, and frequency) can be a contributing factor with struvite stones. Some stones cause few, if any, symptoms while slowly destroying the functional units (nephrons) of the kidney; others cause excruciating pain and discomfort. Stones in the renal pelvis may be associated with an intense, deep ache in the costovertebral region. Hematuria is often present; pyuria may also be noted. Pain originating in the renal area radiates anteriorly and downward toward the bladder in the female and toward the testes in the male. If the pain suddenly becomes acute, with tenderness over the costovertebral area, and nausea and vomiting occur, the patient is having an episode of renal colic. Diarrhea and abdominal discomfort are due to renointestinal reflexes and the anatomic proximity of the kidneys to the stomach, pancreas, and large intestine. Stones lodged in the ureter (ureteral obstruction) cause acute, excruciating, colicky, wavelike pain that radiates down the thigh and to the genitalia. Often, the patient has a desire to void, but little urine is passed, and it usually contains blood because of the abrasive action of the stone. This group of symptoms is called ureteral colic. Colic is mediated by prostaglandin E, a substance that increases ureteral contractility and renal blood flow and that leads to increased intraureteral pressure and pain. In general, the patient is able to pass stones 0.5 to 1 cm in diameter. Stones larger than 1 cm in diameter usually must be removed or fragmented (broken up by lithotripsy) so that they can be removed or passed spontaneously. Stones lodged in the bladder usually produce symptoms of irritation and may be associated with UTI and hematuria. If the stone obstructs the bladder neck, urinary retention occurs. If infection is associated with a stone, the condition is far more serious, with the potential for urosepsis developing. Medical Management The goals of management are to eradicate the stone, determine the stone type, prevent nephron destruction, control infection, and relieve any obstruction that may be present. The immediate objective of treatment of renal or ureteral colic is to relieve the pain until its cause can be eliminated. Opioid analgesic agents are given to prevent shock and syncope that may result from the excruciating pain. Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective in treating kidney stone pain because they provide specific pain relief. They also inhibit the synthesis of prostaglandin E, reducing swelling and facilitating passage of the stone. Generally, once the stone has passed, the pain is relieved. Hot baths or moist heat to the flank area may also be helpful. Unless the patient is vomiting or has heart failure or any other condition requiring fluid restriction, fluids are encouraged. This increases the hydrostatic pressure behind the stone, assisting it in its downward passage. A high, around-the-clock fluid intake reduces the concentration of urinary crystalloids, dilutes the urine, and ensures a high urine output. Post-treatment complications: ESWL: If the stone does not pass spontaneously or if complications occur, common interventions include endoscopic or other procedures. For example, ureteroscopy, extracorporeal shock wave lithotripsy (ESWL), or endourologic (percutaneous) stone removal may be necessary. Ureteroscopy (see Fig. 55-6A) involves first visualizing the stone and then destroying it. Access to the stone is accomplished by inserting a ureteroscope into the ureter and then inserting a laser, electrohydraulic lithotriptor, or ultrasound device through the ureteroscope to fragment and remove the stones. A stent may be inserted and left in place for 48 hours or more after the procedure to keep the ureter patent. Length of hospital stay is generally brief, and some patients can be treated as outpatients. ESWL is a noninvasive procedure used to break up stones in the calyx of the kidney (see Fig. 55-6B). After the stones are fragmented to the size of grains of sand, the remnants of the stones are spontaneously voided. In ESWL, a high-energy amplitude of pressure, or shock wave, is generated by the abrupt release of energy and transmitted through water and soft tissues. When the shock wave encounters a substance of different intensity (a kidney stone), a compression wave causes the surface of the stone to fragment. Repeated shock waves focused on the stone eventually reduce it to many small pieces that are excreted in the urine.

Hemodialysis

Hemodialysis: Hemodialysis is used for patients who are acutely ill and require short-term dialysis for days to weeks until kidney function resumes and for patients with advanced CKD and ESKD who require long-term or permanent renal replacement therapy. Hemodialysis prevents death but does not cure kidney disease and does not compensate for the loss of endocrine or metabolic activities of the kidneys. More than 90% of patients requiring long-term renal replacement therapy are on chronic hemodialysis. Most patients receive intermittent hemodialysis that involves treatments three times a week with an average treatment duration of 3 to 5 hours in an outpatient setting. Hemodialysis can also be performed at home by the patient and a caregiver. With home dialysis, treatment time and frequency can be adjusted to meet optimal patient needs. The objectives of hemodialysis are to extract toxic nitrogenous substances from the blood and to remove excess fluid. A dialyzer (also referred to as an artificial kidney) is a synthetic semipermeable membrane through which blood is filtered to remove uremic toxins and a desired amount of fluid. In hemodialysis, the blood, laden with toxins and nitrogenous wastes, is diverted from the patient to a machine via the use of a blood pump to the dialyzer, where toxins are filtered from the blood and the blood is returned to the patient. Diffusion, osmosis, and ultrafiltration are the principles on which hemodialysis is based. The toxins and wastes in the blood are removed by diffusion—that is, they move from an area of higher concentration in the blood to an area of lower concentration in the dialysate. The dialysate is a solution that circulates through the dialyzer, made up of all the electrolytes in their ideal extracellular concentrations. The electrolyte level in the patient's blood can be brought under control by properly adjusting the electrolytes in the dialysate solution. The semipermeable membrane impedes the diffusion of large molecules, such as RBCs and proteins. Excess fluid is removed from the blood by osmosis, in which water moves from an area of low concentration potential (the blood) to an area of high concentration potential (the dialysate bath). In ultrafiltration, fluid moves under high pressure to an area of lower pressure. This process is much more efficient than osmosis for fluid removal and is accomplished by applying negative pressure or a suctioning force to the dialysis membrane. Because patients with disease requiring dialysis usually cannot excrete water, this force is necessary to remove fluid to achieve fluid balance. The body's buffer system is maintained using a dialysate bath made up of bicarbonate (most common) or acetate, which is metabolized to form bicarbonate. The anticoagulant heparin is given to keep blood from clotting in the extracorporeal dialysis circuit. Cleansed blood is returned to the body with the goal of removing fluid, balancing electrolytes, and managing acidosis. Complications: Although hemodialysis can prolong life, it does not alter the natural course of the underlying CKD, nor does it completely replace kidney function. The CKD complications previously discussed will continue to worsen and require treatment. With the initiation of dialysis, disturbances of lipid metabolism (hypertriglyceridemia) are accentuated and contribute to cardiovascular complications. Heart failure, coronary artery disease, angina, stroke, and peripheral vascular disease may occur and can incapacitate the patient. Cardiovascular disease remains the leading cause of death in patients receiving dialysis. Anemia is compounded by blood lost during hemodialysis. Gastric ulcers may result from the physiologic stress of chronic illness, medication, and pre-existing medical conditions (e.g., diabetes). Patients with uremia report a metallic taste and nausea when they require dialysis. Vomiting may occur during the hemodialysis treatment when rapid fluid shifts and hypotension occur. These contribute to the malnutrition seen in patients on dialysis. Poor calcium metabolism and renal osteodystrophy can result in bone pain and fractures, interfering with mobility. As time on dialysis continues, calcification of major blood vessels has been reported and linked to hypertension and other vascular complications. Phosphorus deposits in the skin can occur and cause itching. Many people undergoing hemodialysis experience major sleep problems that further complicate their overall health status. Early-morning or late-afternoon dialysis may be a risk factor for developing sleep disturbances. Other complications of dialysis treatment may include the following: Episodes of shortness of breath often occur as fluid accumulates between dialysis treatments. Hypotension may occur during the treatment as fluid is removed. Nausea and vomiting, diaphoresis, tachycardia, and dizziness are common signs of hypotension. Painful muscle cramping may occur, usually late in dialysis as fluid and electrolytes rapidly leave the extracellular space. Exsanguination may occur if blood lines separate or dialysis needles become dislodged. Dysrhythmias may result from electrolyte and pH changes or from removal of antiarrhythmic medications during dialysis. Air embolism is rare but can occur if air enters the vascular system. Chest pain may occur in patients with anemia or arteriosclerotic heart disease. Dialysis disequilibrium results from cerebral fluid shifts. Signs and symptoms include headache, nausea and vomiting, restlessness, decreased level of consciousness, and seizures. It is rare and more likely to occur in AKI or when BUN levels are very high (exceeding 150 mg/dL).

Define: Gammopathy

A benign condition in which there is a higher-than-normal level of a protein called M protein in the blood. Patients with monoclonal gammopathy of undetermined significance are at an increased risk of developing cancer. Also called MGUS. This abnormal protein is formed within your bone marrow, the soft, blood-producing tissue that fills in the center of most of your bones. The disorder occurs most commonly in older men. MGUS usually causes no problems. But sometimes it can progress to more-serious diseases, including some forms of blood cancer. If you have high amounts of this protein in your blood, it's important to have regular checkups so that you can get earlier treatment if it does progress. If there's no disease progression, MGUS doesn't require treatment.

Acute Kidney Injury o Pathophysiology o Clinical manifestations o Medical treatments o Potential complications o Nursing assessments and interventions

Acute Kidney Injury: Acute kidney injury (AKI) is a rapid loss of renal function due to damage to the kidneys. Depending on the duration and severity of AKI, a wide range of potentially life-threatening metabolic complications can occur, including metabolic acidosis as well as fluid and electrolyte imbalances. Treatment is aimed at replacing renal function temporarily to minimize potentially lethal complications and reduce potential causes of increased kidney injury with the goal of minimizing long-term loss of renal function. AKI is a problem seen in patients who are hospitalized and those in outpatient settings. A widely accepted criterion for AKI is a 50% or greater increase in serum creatinine above baseline (normal creatinine is less than 1 mg/dL). Urine volume may be normal, or changes may occur. Possible changes include nonoliguria (greater than 800 mL/day), oliguria (less than 0.5 mL/kg/hr), or anuria (less than 50 mL/day Pathophysiology: Although the pathogenesis of AKI and oliguria is not always known, many times there is a specific underlying cause. Some of the factors may be reversible if identified and treated promptly, before kidney function is impaired. This is true of the following conditions that reduce blood flow to the kidney and impair kidney function: (1) hypovolemia; (2) hypotension; (3) reduced cardiac output and heart failure; (4) obstruction of the kidney or lower urinary tract by tumor, blood clot, or kidney stone; and (5) bilateral obstruction of the renal arteries or veins. If these conditions are treated and corrected before the kidneys are permanently damaged, the increased BUN and creatinine levels, oliguria, and other signs may be reversed. Although renal stones are not a common cause of AKI, some types may increase the risk of AKI. Some hereditary stone diseases, primary struvite stones, and infection-related urolithiasis associated with anatomic and functional urinary tract anomalies and spinal cord injury may cause recurrent bouts of obstruction as well as crystal-specific damage to tubular epithelial cells and interstitial renal cells. Clinical manifestations: Almost every system of the body is affected with failure of the normal renal regulatory mechanisms. The patient may appear critically ill and lethargic. The skin and mucous membranes are dry from dehydration. Central nervous system signs and symptoms include drowsiness, headache, muscle twitching, and seizures. Table 54-3 summarizes common clinical characteristics in all three categories of AKI. Medical treatments: The kidneys have a remarkable ability to recover from insult. The objectives of treatment for AKI are to restore normal chemical balance and prevent complications until repair of renal tissue and restoration of renal function can occur. Management includes eliminating the underlying cause; maintaining fluid balance; avoiding fluid excesses; and, when indicated, providing renal replacement therapy. Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Intrarenal azotemia is treated with supportive therapy, with removal of causative agents, aggressive management of prerenal and postrenal failure, and avoidance of associated risk factors. Shock and infection, if present, are treated promptly. The presence of myoglobin in the urine (i.e., myoglobinuria) in the patient who has had a crush injury, compartment syndrome, or heat-induced illness is treated for rhabdomyolysis. Maintenance of fluid balance is based on daily body weight, serial measurements of central venous pressure, serum and urine concentrations, fluid losses, blood pressure, and the clinical status of the patient. The parenteral and oral intake and the output of urine, gastric drainage, stools, wound drainage, and perspiration are calculated and are used as the basis for fluid replacement. The insensible fluid produced through the normal metabolic processes and lost through the skin and lungs is also considered in fluid management. Fluid excesses can be detected by the clinical findings of dyspnea, tachycardia, and distended neck veins. The patient's lungs are auscultated for moist crackles. Because pulmonary edema may be caused by excessive administration of parenteral fluids, extreme caution must be used to prevent fluid overload. The development of generalized edema is assessed by examining the presacral and pretibial areas several times daily. Mannitol (Osmitrol), furosemide (Lasix), or ethacrynic acid (Edecrin) may be prescribed to initiate diuresis. Adequate renal blood flow in patients with prerenal causes of AKI may be restored by IV fluids or transfusions of blood products. If AKI is caused by hypovolemia secondary to hypoproteinemia, an infusion of albumin may be prescribed. Dialysis may be initiated to prevent complications of AKI, such as hyperkalemia, metabolic acidosis, pericarditis, and pulmonary edema. Dialysis corrects many biochemical abnormalities; allows for liberalization of fluid, protein, and sodium intake; diminishes bleeding tendencies; and promotes wound healing. Hemodialysis (a procedure that circulates the patient's blood through an artificial kidney [dialyzer] to remove waste products and excess fluid), peritoneal dialysis (PD; a procedure that uses the patient's peritoneal membrane [the lining of the peritoneal cavity] as the semipermeable membrane to exchange fluid and solutes), or a variety of continuous renal replacement therapies (CRRTs) (methods used to replace normal kidney function by circulating the patient's blood through a hemofilter) may be performed. These and other treatment modalities for patients with renal dysfunction are discussed later in this chapter. Pharmacologic Therapy Hyperkalemia is the most life threatening of the fluid and electrolyte changes that occur in patients with kidney disorders. Therefore, the patient is monitored for hyperkalemia through serial serum electrolyte levels (potassium value greater than 5.0 mEq/L [5 mmol/L]), ECG changes (tall, tented, or peaked T waves), and changes in clinical status (see Chapter 13). Other symptoms of hyperkalemia include irritability, abdominal cramping, diarrhea, paresthesia, and generalized muscle weakness. Muscle weakness may present as slurred speech, difficulty breathing, paresthesia, and paralysis. As the potassium level increases, both cardiac and other muscular function declines, making this a medical emergency. The elevated potassium levels may be reduced by administering cation-exchange resins (sodium polystyrene sulfonate [Kayexalate]) orally or by retention enema. Kayexalate works by exchanging sodium ions for potassium ions in the intestinal tract. Sorbitol may be given in combination with Kayexalate to induce a diarrhea-type effect (it induces water loss in the GI tract). If a Kayexalate retention enema is given (the colon is the major site of potassium exchange), a rectal catheter with a balloon may be used to facilitate retention if necessary. The patient should retain the Kayexalate for at least 30 to 60 minutes (preferable 6 to 10 hours) to promote potassium removal. Afterward, a cleansing enema may be prescribed to remove remaining medication as a precaution against fecal impaction. If the patient is hemodynamically unstable (low blood pressure, changes in mental status, dysrhythmia), IV dextrose 50%, insulin, and calcium replacement may be given to shift potassium back into the cells. The shift of potassium into the intracellular space is temporary, so arrangements for dialysis need to be made on an emergent basis. Many medications are eliminated through the kidneys; therefore, dosages must be reduced when a patient has AKI. Examples of commonly used agents that require adjustment are antibiotic medications (especially aminoglycosides), digoxin (Lanoxin), phenytoin (Dilantin), ACE inhibitors, and magnesium-containing agents. In addition, many medications have been used in patients with AKI in an attempt to improve patient outcomes. Diuretic agents are often used to control fluid volume, but they have not been shown to improve recovery from AKI. In patients with severe acidosis, the arterial blood gases and serum bicarbonate levels (CO2) must be monitored because the patient may require sodium bicarbonate therapy or dialysis. If respiratory problems develop, appropriate ventilatory measures must be instituted. The elevated serum phosphate level may be controlled with phosphate-binding agents (e.g., calcium or lanthanum carbonate) that help prevent a continuing rise in serum phosphate levels by decreasing the absorption of phosphate from the intestinal tract. Nutritional Therapy AKI causes severe nutritional imbalances (because nausea and vomiting contribute to inadequate dietary intake), impaired glucose use and protein synthesis, and increased tissue catabolism. The patient is weighed daily and loses 0.2 to 0.5 kg (0.5 to 1 lb) daily if the nitrogen balance is negative (i.e., caloric intake falls below caloric requirements). If the patient gains or does not lose weight or develops hypertension, fluid retention should be suspected. Nutritional support is based on the underlying cause of AKI, the catabolic response, the type and frequency of renal replacement therapy, comorbidities, and nutritional status. Replacement of dietary proteins is individualized to provide the maximum benefit and minimize uremic symptoms. Caloric requirements are met with high-carbohydrate meals, because carbohydrates have a protein-sparing effect (i.e., in a high-carbohydrate diet, protein is not used for meeting energy requirements but is "spared" for growth and tissue healing). Foods and fluids containing potassium or phosphorus (e.g., bananas, citrus fruits and juices, coffee) are restricted. The oliguric phase of AKI may last 10 to 14 days and is followed by the diuretic phase, at which time urine output begins to increase, signaling the patient is in the recovery phase (Prentice, 2013). Results of blood chemistry tests are used to determine the amounts of sodium, potassium, and water needed for replacement, along with assessment for over- or underhydration. Following the diuretic phase, the patient is placed on a high-protein, high-calorie diet and is encouraged to resume activities gradually. Nursing assessments and interventions: ** Hyperkalemia is the most immediate life-threatening imbalance seen in AKI. Parenteral fluids, all oral intake, and all medications are screened carefully to ensure that sources of potassium are not inadvertently given or consumed.** The nurse has an important role in caring for the patient with AKI. The nurse monitors for complications, participates in emergency treatment of fluid and electrolyte imbalances, assesses the patient's progress and response to treatment, and provides physical and emotional support. In addition, the nurse keeps family members informed about the patient's condition, helps them understand the treatments, and provides psychological support. Although the development of AKI may be the most serious problem, the nurse continues to provide nursing care indicated for the primary disorder (e.g., burns, shock, trauma, obstruction of the urinary tract). Monitoring Fluid and Electrolyte Balance Because of the serious fluid and electrolyte imbalances that can occur with AKI, the nurse monitors the patient's serum electrolyte levels and physical indicators of these complications during all phases of the disorder. IV solutions must be carefully selected based on the patient's fluid and electrolyte status. The patient's cardiac function and musculoskeletal status are monitored closely for signs of hyperkalemia. The nurse monitors fluid status by paying careful attention to fluid intake (IV medications should be given in the smallest volume possible), urine output, apparent edema, distention of the jugular veins, alterations in heart sounds and breath sounds, and increasing difficulty in breathing. Accurate daily weights, as well as I&O records, are essential. Indicators of deteriorating fluid and electrolyte status are reported immediately to the primary provider, and preparation is made for emergency treatment. Severe fluid and electrolyte disturbances may be treated with hemodialysis, PD, or CRRT. Reducing Metabolic Rate The nurse takes steps to reduce the patient's metabolic rate. Bed rest may be indicated to reduce exertion and the metabolic rate during the most acute stage of the disorder. Fever and infection, both of which increase the metabolic rate and catabolism, are prevented or treated promptly. Promoting Pulmonary Function Attention is given to pulmonary function, and the patient is assisted to turn, cough, and take deep breaths frequently to prevent atelectasis and respiratory tract infection. Drowsiness and lethargy may prevent the patient from moving and turning without encouragement and assistance. Preventing Infection Asepsis is essential with invasive lines and catheters to minimize the risk of infection and increased metabolism. An indwelling urinary catheter is avoided whenever possible due to the high risk of UTI associated with its use but may be required to provide ongoing data required to accurately monitor fluid I&O. Providing Skin Care The skin may be dry or susceptible to breakdown as a result of edema; therefore, meticulous skin care is important. In addition, excoriation and itching of the skin may result from the deposit of irritating toxins in the patient's tissues. Bathing the patient with cool water, frequent turning, and keeping the skin clean and well moisturized and the fingernails trimmed to avoid excoriation are often comforting and prevent skin breakdown. Providing Psychosocial Support The patient with AKI may require treatment with hemodialysis, PD, or CRRT. The length of time that these treatments are necessary varies with the cause and extent of damage to the kidneys. The patient and family need assistance, explanation, and support during this period. The purpose of the treatment is explained to the patient and family by the primary provider. However, high levels of anxiety and fear may necessitate repeated explanation and clarification by the nurse. The family members may initially be afraid to touch and talk to the patient during these procedures but should be encouraged and assisted to do so. In an intensive care setting, many of the nurse's functions are devoted to the technical aspects of patient care; however, it is essential that the psychological needs and other concerns of the patient and family be addressed. Continued assessment of the patient for complications of AKI and precipitating causes is essential.

Define: Acquired Immunity

Acquired Immunity (specific against foreign antigen) Acquired (adaptive) immunity usually develops as a result of prior exposure to an antigen through immunization (vaccination) or by contracting a disease, both of which generate a protective immune response. Weeks or months after exposure to the disease or vaccine, the body produces an immune response that is sufficient to defend against the disease on re-exposure. In contrast to the rapid but nonspecific natural immune response, this form of immunity relies on the recognition of specific foreign antigens. The acquired immune response is broadly divided into two mechanisms: (1) the cell-mediated response, involving T-cell activation, and (2) effector mechanisms, involving B-cell maturation and production of antibodies. The two types of acquired immunity are known as active and passive and are interrelated. Active acquired immunity refers to immunologic defenses developed by the person's own body. This immunity typically lasts many years or even a lifetime. Passive acquired immunity is temporary immunity transmitted from a source outside the body that has developed immunity through previous disease or immunization. Examples include immunity resulting from the transfer of antibodies from the mother to an infant in utero or through breast-feeding or receiving injections of immune globulin. Active and passive acquired immunity involve humoral and cellular (cell-mediated) immunologic responses (described later).

Identify those at risk for compromised immunity

Age and Gender, females are more likely than males to have autoimmune diseases, older adults have a declining immune systems and cellular changes. Lifestyle factors such as smoking or drinking. Poor nutrition can reduce antibody and cellular responses. Those that do not have their immunization. Those with allergies. Those with condition or disorders, such as autoimmune disorders, cancer, chronic illness, surgery or trauma. Medications and transfusions can weaken the immune system, i.e. antibiotics and corticosteroids can weaken/suppress immune system. Psychoneuroimmunologic factors.

Identify alterations in immunity based on: o Age o Nutrition

Age: (See TABLE 35-4 Screenshot) Age-related changes in many body systems also contribute to impaired immunity. For example, postmenopausal females are at a greater risk for urinary tract infections due to residual urine, urinary incontinence, and estrogen deficiency. Secondary changes, including malnutrition and poor circulation, as well as the breakdown of natural mechanical barriers such as the skin, place the aging immune system at even greater disadvantage against infection. The effects of the aging process and psychological stress interact, with the potential to negatively influence immune integrity. Consequently, continual assessment of the physical and emotional status of older adults is imperative, because early recognition and management of factors influencing immune response may prevent or mitigate the high morbidity and mortality seen with illness in the older adult population. Gerontologic Considerations Immunosenescence is a complex route in which the aging process stimulates changes in the immune system. Some of the changes that occur in immunosenescence include, but are not limited to, bone marrow defects, dysfunction of the thymus gland, and impaired lymphocytes. Cellular changes occur as the result of aging and include impaired neutrophil function, decreased amount of circulating macrophages, impaired dendritic cell function, and reduced T-cell activation. As the immune system undergoes age-associated alterations, its response to infections progressively deteriorates. The capacity for self-renewal of hematopoietic stem cells diminishes. There is a notable decline in the total number of phagocytes, coupled with an intrinsic reduction in their activity. The cytotoxicity of NK cells decreases, contributing to a decline in humoral immunity. Acquired immunity may be negatively affected; the efficacy of vaccines is frequently decreased in older adults. Inflammatory cytokines tend to increase with age. Older adults have increased the incidence of infections, autoimmune diseases, metabolic diseases, osteoporosis, and neurologic disorders. The increased incidence of autoimmune diseases may be from a decreased ability of antibodies to differentiate between self and non-self. Failure of the surveillance system to recognize mutant or abnormal cells also may be responsible, in part, for the high incidence of cancer associated with increasing age. Nutrition: The relationship of infection to nutritional status is a key determinant of health. Traditionally, this relationship focused on the effect of nutrients on host defenses and the effect of infection on nutritional needs. This has expanded in scope to encompass the role of specific nutrients in acquired immune function—the modulation of inflammatory processes and the virulence of the infectious agent itself. Iron and the immune system are linked in homeostasis and pathology, thus making it essential for maximum function. The list of nutrients affecting infection, immunity, inflammation, and cell injury has expanded from traditional proteins to several vitamins, multiple minerals, and, more recently, specific lipid components of the diet. One review looked at the role of Vitamins A, C, D, E, and K in treatment of pancreatic cancer but concluded that not enough evidence based on clinical trials is available to fully support the use of these vitamins as an intervention. The role of micronutrients and fatty acids on the response of cells and tissues to hypoxic and toxic damage has been recognized, suggesting that there is another dimension to the relationship. Deficiencies in micronutrients have been connected to impairment in various body functions, including immunity. Zinc deficiency in particular has been linked to the development of a number of diseases. Zinc plays an important role in homeostasis, immune function, and apoptosis, among other functions. The effects exerted by polyunsaturated fatty acids on immune system functions are under investigation. Studies suggest that these elements play a role in diminishing the incidence and severity of inflammatory disorders. Recent studies suggest that diets high in olive oil are not as immunosuppressive as diets rich in fish oil. The contribution of immune modulation by lipids to the high risk of infectious complications associated with the use of parenteral nutrition is unclear; however, a recent meta-analysis revealed that the use of glutamine-supplemented parenteral nutrition decreased the incidence of infections postoperatively. Depletion of protein reserves results in atrophy of lymphoid tissues, depression of antibody response, reduction in the number of circulating T cells, and impaired phagocytic function. As a result, susceptibility to infection is greatly increased. During periods of infection or serious illness, nutritional requirements may be further altered, potentially contributing to depletion of protein, fatty acid, vitamin, and trace elements and causing even greater risk of impaired immune response and sepsis. Nutritional intake that supports a competent immune response plays an important role in reducing the incidence of infections; patients whose nutritional status is compromised have a delayed postoperative recovery and often experience more severe infections and delayed wound healing. The nurse must assess the patient's nutritional status, caloric intake, and quality of foods ingested. There is evidence that nutrition plays a role in the development of cancer and that diet and lifestyle can alter the risk of cancer development as well as other chronic diseases. The nurse must assume a proactive role in ensuring the best possible nutritional intake for all patients as a vital step in preventing disease and poor outcomes.

Identify the proponents of a nursing assessment focusing on the immune system

An assessment of immune function begins during the health history and physical examination. Areas to be assessed include nutritional status; infections and immunizations; allergies; disorders and disease states, such as autoimmune disorders, cancer, and chronic illnesses; surgeries; medications; and blood transfusions. In addition to inspection of general characteristics, palpation of the lymph nodes and examinations of the skin, mucous membranes, and respiratory, gastrointestinal, musculoskeletal, genitourinary, cardiovascular, and neurosensory systems are performed. During the physical examination, the skin and mucous membranes are assessed for lesions, dermatitis, purpura (subcutaneous bleeding), urticaria, inflammation, or any discharge. Any signs of infection are noted. The patient's temperature is recorded, and the patient is observed for chills and sweating. The anterior and posterior cervical, supraclavicular, axillary, and inguinal lymph nodes are palpated for enlargement; if palpable nodes are detected, their location, size, consistency, and reports of tenderness on palpation are noted. Joints are assessed for tenderness, swelling, increased warmth, and limited range of motion. The patient's respiratory, cardiovascular, genitourinary, gastrointestinal, and neurosensory systems are evaluated for signs and symptoms indicative of immune dysfunction. Any functional limitations or disabilities the patient may have are also assessed.

Identify patient education regarding s/sx potential allergic reactions and when to contact the provider

Anytime breathing is compromised, or you have swelling in your face or tongue you should contact provider right away. If patient uses Epi-pen they still need to seek treatment because they can have a rebound reaction a few hours later.

Define: Autoimmune disorder

Body sees own cells/tissues as foreign Autoimmune disorders affect people of both genders of all ages, ethnicities, and social classes. Autoimmune disorders are a group of disorders that can affect almost any cell or tissue in the body. As mentioned previously, they tend to be more common in women because estrogen tends to enhance immunity. Androgen, on the other hand, tends to be immunosuppressive. Autoimmune diseases are a leading cause of death by disease in females of reproductive age. The patient is asked about any autoimmune disorders, such as lupus erythematosus, rheumatoid arthritis, multiple sclerosis, or psoriasis. The onset, severity, remissions and exacerbations, functional limitations, treatments that the patient has received or is currently receiving, and effectiveness of the treatments are described. The occurrence of different autoimmune diseases within a family strongly suggests a genetic predisposition to more than one autoimmune disease.

Identify the causes and treatment modalities for the following: o Allergic rhinitis

Causes: Allergic rhinitis (hay fever, seasonal allergic rhinitis) is the most common form of respiratory allergy, which is presumed to be mediated by an immediate (type I hypersensitivity) immunologic reaction. It is among the top 11% of all primary care visits and affects about 12% (1 in 8 adults) in the United States. Symptoms are similar to those of viral rhinitis (see Chapter 22) but are usually more persistent and demonstrate seasonal variation; rhinitis is considered to be the allergic form if the symptoms are caused by an allergen-specific IgE-mediated immunologic response. However, approximately one third of patients with rhinitis have associated conjunctivitis, sinusitis, and asthma. The proportion of patients with the allergic form of rhinitis increases with age. It often occurs with other conditions, such as asthma, and cystic fibrosis. If symptoms are severe, allergic rhinitis may interfere with sleep, leisure, school, and overall quality of life. Chronic rhinitis accounts for an average of 1 to 2 missed work days per patient per year. These patients experience a 36% reduction in on-the-job effectiveness and 38% loss of productivity. Early diagnosis and adequate treatment are essential to reduce complications and relieve symptoms. Because allergic rhinitis is induced by airborne pollens or molds, it is characterized by the following seasonal occurrences: Early spring—tree pollen (oak, elm, poplar) Early summer—grass pollen (Timothy, Redtop) Early fall—weed pollen (ragweed) Symptoms: The four major signs and symptoms of allergic rhinitis include copious amounts of serous nasal discharge, nasal congestion, sneezing, as well as nose and throat itching. Patients may experience post-nasal drip, itching, watery eyes, headache, and hyposomnia. Bronchial asthma is more persistent in patients with chronic rhinitis than in those with allergic rhinitis. The symptoms of this chronic condition depend on environmental exposure and intrinsic host responsiveness. Allergic rhinitis can affect quality of life by also producing sleep disturbance, impairment of daily activities, and missed school and work Treatment modalities: Diagnosis of seasonal allergic rhinitis is based on history, physical examination, and diagnostic test results. Diagnostic tests include nasal smears, peripheral blood counts, total serum IgE, epicutaneous and intradermal testing, serum-specific IgE, and nasal provocation tests. Results indicative of allergy as the cause of rhinitis include increased IgE and eosinophil levels and positive reactions on allergen testing. False-positive and false-negative responses to these tests, particularly skin testing, may occur. The goal of therapy is to provide relief from symptoms. Therapy may include one or all of the following interventions: avoidance therapy, pharmacologic therapy, and immunotherapy. Verbal instructions must be reinforced by written information. Knowledge of general concepts regarding assessment and therapy in allergic diseases is important so that the patient can learn to manage certain conditions as well as prevent severe reactions and illnesses. (See Table 37-2 for Antihistamine Chart) **Read Pages 1067-1071 for more info on treatment modalities.

Identify the causes and treatment modalities for the following: o Contact dermatitis

Causes: a type IV delayed hypersensitivity reaction, is an acute or chronic skin condition caused by contact with an exogenous substance that elicits an allergic response. There are four basic types: allergic, irritant, phototoxic, and photo allergic (see Table 37-4). Eighty percent of cases are caused by excessive exposure to or additive effects of irritants (e.g., soaps, detergents, organic solvents). Skin sensitivity may develop after brief or prolonged periods of exposure, and the clinical picture may appear hours or weeks after the sensitized skin has been exposed. Symptoms include itching, burning, erythema, skin lesions (vesicles and papules), and edema, followed by skin thickening, hardening, and scaling. In severe responses, hemorrhagic bullae may develop. Repeated reactions may be accompanied by thickening of the skin and pigmentary changes. Secondary invasion by bacteria may develop in skin that is abraded by rubbing or scratching. Usually, there are no systemic symptoms unless the eruption is widespread. Treatment modalities: Determining allergens responsible requires a history, physical examination, and patch testing. Assessment should include the date of onset, and any identifiable relationship to work environment and skin care products. The location of the lesions, distribution of the dermatitis, absence of other etiologies, and the history of exposure aid in determining the condition. Patch testing and environmental history of exposure to contact allergens are required to verify the diagnosis. Patch testing is indicated in cases in which inflammation persists despite avoidance therapy. The patch test most commonly used is the Thin-layer Rapid Use Epicutaneous (T.R.U.E.) test. The treatment is to avoid offending material, aluminum acetate or cool water compress, systemic corticosteroids, topical corticosteroids (for mild cases), or oral antihistamines. Antibiotics can be used for infection.

Identify the causes and treatment modalities for the following: o Allergy-induced asthma

Causes: dust mites, cockroaches, pollen, molds, animal allergens, rodents etc.. The same substances that trigger hay fever (allergic rhinitis) symptoms, such as pollen, dust mites and pet dander, may also cause asthma signs and symptoms. In some people, skin or food allergies can cause asthma symptoms. This is called allergic asthma or allergy-induced asthma. Treatment modalities: Most treatments are designed to treat either asthma or allergic rhinitis. But a few treatments help with both conditions. Some examples: Leukotriene modifier. This type of medication can ease both allergic rhinitis and asthma symptoms. Called a leukotriene modifier, this daily pill helps control immune system chemicals released during an allergic reaction. Montelukast (Singulair) is the leukotriene modifier that can treat both asthma and allergic rhinitis. Allergy shots (immunotherapy). Allergy shots can help treat asthma by gradually reducing your immune-system response to certain allergy triggers. Immunotherapy involves getting regular injections of a tiny amount of the allergens that trigger your symptoms. Your immune system builds up a tolerance to the allergens over time, and your allergic reactions diminish. In turn, asthma symptoms decrease as well. This treatment generally requires regular injections over a period of time. Anti-immunoglobulin E (IgE) therapy. When you have an allergy, your immune system mistakenly identifies a specific substance as something harmful and releases antibodies, known as IgE, against the culprit allergen. The next time you encounter that allergen, the IgE antibodies sense it and signal your immune system to release a chemical called histamine, as well as other chemicals, into your bloodstream. The medication omalizumab (Xolair) interferes with IgE in the body and helps prevent the allergic reaction that triggers asthma symptoms. This treatment is used for more severe allergic asthma, but it might also help allergic rhinitis.

List the chemical barriers within the body that help with immunity

Chemical barriers, such as mucus, acidic gastric secretions, enzymes in tears and saliva, and substances in sebaceous and sweat secretions, act in a nonspecific way to destroy invading bacteria and fungi.

Identify the function of the complement system

Circulating plasma proteins, known as complement, are made in the liver and activated when an antibody connects with its antigen. Complement plays an important role in the defense against microbes. Destruction of an invading or attacking organism or toxin is not achieved merely by the binding of the antibody and antigens; it also requires activation of complement, the arrival of killer T cells, or the attraction of macrophages. Complement has three major physiologic functions: defending the body against bacterial infection, bridging natural and acquired immunity, and disposing of immune complexes and the by-products associated with inflammation. The proteins that comprise complement interact sequentially with one another in a cascading effect. The complement cascade is important to modifying the effector arm of the immune system. Activation of complement allows important events, such as removal of infectious agents and initiation of the inflammatory response, to take place. These events involve active parts of the pathway that enhance chemotaxis of macrophages and granulocytes, alter blood vessel permeability, change blood vessel diameters, cause cells to lyse, alter blood clotting, and cause other points of modification. These macrophages and granulocytes continue the body's defense by devouring the antibody-coated microbes and by releasing bacterial products. The complement cascade may be activated by any of three pathways: classic, lectin, and alternative. The classic pathway is triggered after antibodies bind to microbes or other antigens and is part of the humoral type of adaptive immunity. The lectin pathway is activated when a plasma protein (mannose-binding lectin) binds to terminal mannose residue on the surface glycoproteins of microbes. The alternative pathway is triggered when complement proteins are activated on microbial surfaces. This pathway is part of natural immunity. Complement components, prostaglandins, leukotrienes, and other inflammatory mediators all contribute to the recruitment of inflammatory cells, as do chemokines, a group of cytokines. The activated neutrophils pass through the vessel walls to accumulate at the site of infection, where they phagocytize complement-coated microbes. This response is usually therapeutic and can be lifesaving if the cell attacked by the complement system is a true foreign invader. However, if that cell is part of the human organism, the result can be devastating disease and even death. Many autoimmune diseases and disorders characterized by chronic infection are thought to be caused in part by continued or chronic activation of complement, which in turn results in chronic inflammation. The RBCs and platelets have complement receptors and, as a result, play an important role in the clearance of immune complexes that consist of antigen, antibody, and components of the complement system.

End-Stage Kidney Disease (ESKD) o Risk factors

End Stage Renal Disease: When a patient has sustained enough kidney damage to require renal replacement therapy on a permanent basis, the patient has moved into the fifth or final stage of CKD, also referred to as ESKD. As renal function declines, the end products of protein metabolism (normally excreted in urine) accumulate in the blood. Uremia develops and adversely affects every system in the body. The greater the buildup of waste products, the more pronounced the symptoms. The rate of decline in renal function and progression of ESKD is related to the underlying disorder, the urinary excretion of protein, and the presence of hypertension. The disease tends to progress more rapidly in patients who excrete significant amounts of protein or have elevated blood pressure than in those without these conditions. Risk Factors: Diabetes, hypertension, chronic glomerulonephritis, interstitial nephritis, and urinary tract obstruction are among the causes for ESKD in older adults. The signs and symptoms of kidney disease in older adults are often nonspecific. The occurrence of symptoms of other disorders (heart failure, dementia) can mask the symptoms of kidney disease and delay or prevent diagnosis and treatment. Hemodialysis and PD are used effectively in treating older patients with ESKD. Initiation of dialysis among older patients has dramatically increased in the past decade. Implementation of palliative care has also increased among patients who choose not to start dialysis or who decide to stop dialysis.

Glomerulonephritis o Pathophysiology o Clinical manifestation

Glomerulonephritis: Diseases that destroy the glomerulus of the kidney are the third most common cause of stage 5 CKD. In these disorders, the glomerular capillaries are primarily involved. Antigen-antibody complexes form in the blood and become trapped in the glomerular capillaries (the filtering portion of the kidney), inducing an inflammatory response. Immunoglobulin G (IgG)—the major immunoglobulin (antibody) found in the blood—can be detected in the glomerular capillary walls. The major clinical manifestations of glomerular injury include proteinuria, hematuria, decreased GFR, decreased excretion of sodium, edema, and hypertension (see Chart 54-2). Pathophysiology: Primary glomerular diseases include postinfectious glomerulonephritis, rapidly progressive glomerulonephritis, membrane proliferative glomerulonephritis, and membranous glomerulonephritis. Postinfectious causes are group A beta-hemolytic streptococcal infection of the throat that precedes the onset of glomerulonephritis by 2 to 3 weeks (see Fig. 54-1). It may also follow impetigo (infection of the skin) and acute viral infections (upper respiratory tract infections, mumps, varicella zoster virus, Epstein-Barr virus, hepatitis B, and human immune deficiency virus [HIV] infection). In some patients, antigens outside the body (e.g., medications, foreign serum) initiate the process, resulting in antigen-antibody complexes being deposited in the glomeruli. In other patients, the kidney tissue itself serves as the inciting antigen. Clinical manifestation: The primary presenting features of an acute glomerular inflammation are hematuria, edema, azotemia (an abnormal concentration of nitrogenous wastes in the blood), and proteinuria (excess protein in the urine). The hematuria may be microscopic (identifiable only through microscopic examination) or macroscopic (visible to the eye). The urine may appear cola colored because of red blood cells (RBCs) and protein plugs or casts; RBC casts indicate glomerular injury. Glomerulonephritis may be mild and the hematuria discovered incidentally through a routine urinalysis, or the disease may be severe, with AKI and oliguria. Some degree of edema and hypertension is present in most patients. Marked proteinuria due to the increased permeability of the glomerular membrane may also occur, with associated pitting edema, hypoalbuminemia, hyperlipidemia, and fatty casts in the urine. Blood urea nitrogen (BUN) and serum creatinine levels may increase as urine output decreases. In addition, anemia may be present. In the more severe form of the disease, patients also complain of headache, malaise, and flank pain. Older patients may experience circulatory overload with dyspnea, engorged neck veins, cardiomegaly, and pulmonary edema. Atypical symptoms include confusion, somnolence, and seizures, which are often confused with the symptoms of a primary neurologic disorder.

Identify the most common food allergies

IgE-mediated food allergy, a type I hypersensitivity reaction, occurs in about 2% of the adult population; it is thought to occur in people who have a genetic predisposition combined with exposure to allergens early in life through the gastrointestinal or respiratory tract or nasal mucosa. More than 170 foods have been reported to cause IgE-mediated reactions. Almost any food can cause allergic symptoms. Any food can contain an allergen that results in anaphylaxis. The most common offenders are seafood (lobster, shrimp, crab, clams, fish), peanuts, tree nuts, berries, eggs, wheat, milk, and chocolate. Peanut and tree nut (e.g., cashew, walnut) allergies are responsible for the most severe food allergy reactions. There is insufficient evidence that maternal diet during pregnancy or lactation affects the development of food allergies later in life. One of the dangers of food allergens is that they may be hidden in other foods and not apparent to people who are susceptible to the allergen. For example, peanuts and peanut butter are often used in salad dressings and Asian, African, and Mexican cooking and may result in severe allergic reactions, including anaphylaxis. Previous contamination of equipment with allergens (e.g., peanuts) during preparation of another food product (e.g., chocolate cake) is enough to produce anaphylaxis in people with severe allergy. Medical Management Therapy for food hypersensitivity includes elimination of the food responsible for the hypersensitivity. Pharmacologic therapy is necessary for patients who cannot avoid exposure to offending foods and for patients with multiple food sensitivities not responsive to avoidance measures. Medication therapy involves the use of H1 blockers, antihistamines, adrenergic agents, corticosteroids, and cromolyn sodium. All patients with food allergies, especially seafood and nuts, should have an auto-injectable epinephrine (e.g., EpiPen or Auvi-Q) device prescribed. Another essential aspect of management is educating patients and family members about how to recognize and manage the early stages of an acute anaphylactic reaction. Many food allergies disappear with time, particularly in children. Nursing Management In addition to participating in management of the allergic reaction, the nurse focuses on preventing future exposure of the patient to the food allergen. If a severe allergic or anaphylactic reaction to food allergens has occurred, the nurse must instruct the patient and family about strategies to prevent its recurrence. Patients' food allergies should be noted on their medical records, because there may be risk of allergic reactions not only to food but also to some medications containing similar substance.

Define: Immunodeficiency

Inability of immune response to develop and clear antigen sufficiently

Indwelling catheters o Purpose o Post-removal care to promote baseline voiding routine

Indwelling catheters: When an indwelling catheter cannot be avoided, a closed drainage system is essential. This drainage system is designed to prevent any disconnections, thereby reducing the risk of contamination. Triple-lumen catheters are commonly used after transurethral prostate surgery (see Chapter 59). This system has a triple-lumen indwelling urethral catheter attached to a closed sterile drainage system. With the triple-lumen catheter, urinary drainage occurs through one channel. The retention balloon of the catheter is inflated with water or air through the second channel, and the bladder is continuously irrigated with sterile irrigating solution through the third channel. The spout (or drainage port) of any urinary drainage bag can become contaminated when opened to drain the bag. Bacteria enter the urinary drainage bag, multiply rapidly, and then migrate to the drainage tubing, catheter, and bladder. By keeping the drainage bag lower than the patient's bladder and not allowing urine to flow back into the bladder, this risk is reduced. Purpose: In patients with a urologic disorder or with marginal kidney function, care must be taken to ensure that urinary drainage is adequate and that kidney function is preserved. When urine cannot be eliminated naturally and must be drained artificially, catheters may be inserted directly into the bladder, the ureter, or the renal pelvis. Catheters vary in size, shape, length, material, and configuration. The type of catheter used depends on its purpose. Catheterization is performed to achieve the following: Relieve urinary tract obstruction Assist with postoperative drainage in urologic and other surgeries Provide a means to monitor accurate urine output in patients who are critically ill Promote urinary drainage in patients with neurogenic bladder dysfunction or urine retention Prevent urinary leakage in patients with stage III to IV pressure ulcers (see Chapter 10) A patient should be catheterized only if necessary, because catheterization commonly leads to UTI. Catheters impede most of the natural defenses of the lower urinary tract by obstructing the periurethral ducts, irritating the bladder mucosa, and providing an artificial route for organisms to enter the bladder. Organisms may be introduced from the urethra into the bladder during catheterization, or they may migrate along the epithelial surface of the urethra or external surface of the catheter. In addition, urinary catheters have been associated with other complications, such as bladder spasms, urethral strictures, and pressure necrosis Post-removal care to promote baseline voiding routine: Retraining the Bladder, when an indwelling urinary catheter is in place, the detrusor muscle does not actively contract the bladder wall to stimulate emptying because urine is continuously draining from the bladder. As a result, the detrusor may not immediately respond to bladder filling when the catheter is removed, resulting in either urine retention or urinary incontinence. This condition, known as postcatheterization detrusor instability, can be managed with bladder retraining (see Chart 55-11). Immediately after the indwelling catheter is removed, the patient is placed on a timed voiding schedule, usually every 2 to 3 hours. At the given time interval, the patient is instructed to void. The bladder is then scanned using a portable ultrasonic bladder scanner, and if the bladder has not emptied completely, straight catheterization may be performed. After a few days, as the nerve endings in the bladder wall become resensitized to the bladder filling and emptying, bladder function usually returns to normal. If the patient has had an indwelling catheter in place for an extended period (e.g., greater than 1 month), bladder retraining will take longer; in some cases, function may never return to normal, and long-term intermittent catheterization may become necessary. Instruct the patient to drink a measured amount of fluid from 8 am to 10 pm to avoid bladder overdistention. Offer no fluids (except sips) after 10 pm. At specific times, ask the patient to void by applying pressure over the bladder, tapping the abdomen, or running water to trigger the bladder. Immediately after the voiding attempt, perform a bladder scan to determine the amount of residual urine. Measure the volumes of urine voided. Palpate the bladder at repeated intervals to assess for distention. Instruct the patient who has no voiding sensation to be alert to any signs that indicate a full bladder, such as perspiration, cold hands or feet, or feelings of anxiety. Perform straight catheterization, as prescribed, usually for residual urine of >300 mL. Lengthen the intervals between catheterizations as the volume of residual urine decreases. Catheterization is usually discontinued when the volume of residual urine is <100 mL.

Define: Natural Immunity

Natural Immunity (nonspecific response) Natural immunity, which is nonspecific, provides a broad spectrum of defense against and resistance to infection. It is considered the first line of host defense following antigen exposure, because it protects the host without remembering prior contact with an infectious agent. Responses to a foreign invader are very similar from one encounter to the next, regardless of the number of times the invader is encountered. Natural (innate) immunity co-coordinates the initial response to pathogens through the production of cytokines and other effector molecules, which either activate cells for control of the pathogen (by elimination) or promote the development of the acquired immune response. The cells involved in this response are monocytes, macrophages, dendritic cells, natural killer (NK) cells, basophils, eosinophils, and granulocytes. The early events in this process are critical in determining the nature of the adaptive immune response. Natural immune mechanisms can be divided into two stages: immediate (generally occurring within minutes) and delayed (occurring within several days after exposure). White Blood Cell Action The cellular response is the key to the effective initiation of the immune response. WBCs, or leukocytes, participate in both the natural and the acquired immune responses. Granular leukocytes, or granulocytes (so called because of granules in their cytoplasm), fight invasion by foreign bodies or toxins by releasing cell mediators, such as histamine, bradykinin, and prostaglandins, and by engulfing the foreign bodies or toxins. Granulocytes include neutrophils, eosinophils, and basophils. Neutrophils (polymorphonuclear leukocytes) are the first cells to arrive at the site where inflammation occurs. Eosinophils and basophils, other types of granulocytes, increase in number during allergic reactions and stress responses. Nongranular leukocytes include monocytes or macrophages (referred to as histiocytes when they enter tissue spaces) and lymphocytes. Monocytes are the first to arrive on the scene and function as phagocytic cells, engulfing, ingesting, and destroying greater numbers and quantities of foreign bodies or toxins than granulocytes do. Lymphocytes, consisting of B cells and T cells, play major roles in humoral and cell-mediated immune responses. About 70% to 80% of lymphocytes in the blood are T cells, and about 10% to 15% are B cells. Inflammatory Response The inflammatory response is a major function of the natural immune system that is elicited in response to tissue injury or invading organisms. Chemical mediators assist this response by minimizing blood loss, walling off the invading organism, activating phagocytes, and promoting formation of fibrous scar tissue and regeneration of injured tissue. The inflammatory response is facilitated by physical and chemical barriers that are part of the human organism. Physical and Chemical Barriers Activation of the natural immunity response is enhanced by processes inherent in physical and chemical barriers. Physical surface barriers include intact skin, mucous membranes, and cilia of the respiratory tract, which prevent pathogens from gaining access to the body. The cilia of the respiratory tract, along with coughing and sneezing responses, filter and clear pathogens from the upper respiratory tract before they can invade the body further. Chemical barriers, such as mucus, acidic gastric secretions, enzymes in tears and saliva, and substances in sebaceous and sweat secretions, act in a nonspecific way to destroy invading bacteria and fungi. Viruses are countered by other means, such as interferon. Immune Regulation Regulation of the immune response involves balance and counterbalance. Dysfunction of the natural immune system can occur when the immune components are inactivated or when they remain active long after their effects are beneficial. A successful immune response eliminates the responsible antigen. If an immune response fails to develop and clear an antigen sufficiently, the host is considered to be immunocompromised or immunodeficient. If the response is overly robust or misdirected, allergies, asthma, or autoimmune disease results. The immune system's recognition of one's own cells or tissues as "foreign" rather than as self is the basis of many autoimmune disorders. Despite the fact that the immune response is critical to the prevention of disease, it must be well controlled to curtail immunopathology. Most microbial infections induce an inflammatory response mediated by T cells and cytokines, which, in excess, can cause tissue damage. Therefore, regulatory mechanisms must be in place to suppress or halt the immune response. This is mainly achieved by the production of cytokines and transformation of growth factor that inhibit macrophage activation. In some cases, T-cell activation is so acute that these mechanisms fail, and pathology develops. Ongoing research on immunoregulation holds the promise of preventing graft rejection and aiding the body in eliminating cancerous or infected cells. Although natural immunity can often effectively combat infections, many pathogenic microbes have evolved that resist natural immunity. Acquired immunity is necessary to defend against these resistant agents.

Peritoneal dialysis (know difference between peritoneal and hemodialysis) o Potential complications for each

Peritoneal dialysis: The goals of PD are to remove toxic substances and metabolic wastes and to reestablish normal fluid and electrolyte balance. PD may be the treatment of choice for patients with kidney disease who are unable or unwilling to undergo hemodialysis or kidney transplantation. Patients who are susceptible to the rapid fluid, electrolyte, and metabolic changes that occur during hemodialysis experience fewer of these problems with the slower rate of PD. Therefore, patients with diabetes or cardiovascular disease, many older patients, and those who may be at risk for adverse effects of systemic heparin are likely candidates for PD. In addition, severe hypertension, heart failure, and pulmonary edema not responsive to usual treatment regimens have been successfully treated with PD. Fewer than 8% of patients with ESKD receive PD as their treatment modality. In PD, the peritoneal membrane that covers the abdominal organs and lines the abdominal wall serves as the semipermeable membrane. A sterile dextrose dialysate fluid is introduced into the peritoneal cavity through an abdominal catheter at established intervals (see Fig. 54-7). Once the sterile solution is in the peritoneal cavity, uremic toxins such as urea and creatinine begin to be cleared from the blood. Diffusion and osmosis occur as waste products move from an area of higher concentration (the bloodstream) to an area of lesser concentration (the dialysate fluid) through a semipermeable membrane (the peritoneum). This movement of solute from the blood into the dialysate fluid is called clearance. Because substances cross the peritoneal membrane at different rates, adjustments in solution dwell time in the peritoneal cavity and amount of fluid used are made to facilitate the process. Ultrafiltration (water removal) occurs in PD through an osmotic gradient created by using a dialysate fluid with a higher glucose concentration than the blood. Complications: Most complications of PD are often minor; however, several, if unattended, can have serious consequences. Acute Complications Peritonitis is the most common and serious complication of PD. The first sign of peritonitis is cloudy dialysate drainage fluid. Diffuse abdominal pain and rebound tenderness occur much later. Hypotension and other signs of shock may also occur with advancing infection. The patient with peritonitis may be treated as an inpatient or outpatient (most common), depending on the severity of the infection and the patient's clinical status. Drainage fluid is examined for cell count; Gram stain and culture are used to identify the organism and guide treatment. Antibiotic agents (aminoglycosides or cephalosporins) are usually added to subsequent exchanges until Gram stain or culture results are available for appropriate antibiotic determination. Intraperitoneal administration of antibiotic agents is as effective as IV administration and therefore most often used. Antibiotic therapy continues for 10 to 14 days. Careful selection and calculation of the antibiotic dosage are needed to prevent nephrotoxicity and further compromise of residual renal function. Regardless of the organism causing peritonitis, the patient loses large amounts of protein through the peritoneum. Acute malnutrition and delayed healing may result. Therefore, attention must be given to detecting and promptly treating peritonitis. Leakage Leakage of dialysate through the catheter site may occur immediately after the catheter is inserted. Usually, the leak stops spontaneously if dialysis is withheld for several days, giving the tissue surrounding the cuffs located on the abdominal catheter a chance to infiltrate the Dacron and seal the insertion tunnel. It also allows the exit site time to heal. During this time, it is important to reduce factors that might delay healing, such as undue abdominal muscle activity and straining during bowel movement. In many cases, leakage can be avoided by using small volumes (500 mL) of dialysate, gradually increasing the volume up to 2000 to 3000 mL. Bleeding A bloody effluent (drainage) may be observed occasionally, especially in young, menstruating women. (The hypertonic fluid pulls blood from the uterus, through the opening in the fallopian tubes, and into the peritoneal cavity.) Bleeding is also common during the first few exchanges after a new catheter insertion because some blood enters the abdominal cavity following insertion. In many cases, no cause can be found for the bleeding, although catheter displacement from the pelvis has occasionally been associated with bleeding. Some patients have had bloody effluent after an enema or from minor trauma. Most often, bleeding stops in 1 to 2 days and requires no specific intervention. More frequent exchanges and the addition of heparin to the dialysate during this time may be necessary to prevent blood clots from obstructing the catheter. Long-Term Complications Hypertriglyceridemia is common in patients undergoing long-term PD, suggesting that the therapy may accelerate atherogenesis. Cardiovascular disease is the leading cause of morbidity and mortality in patients with kidney failure, and many patients have suboptimal blood pressure control. Beta-blockers and ACE inhibitors should be used to control hypertension or protect the heart, and the use of aspirin and statins should be considered (James, Oparil, Carter, et al., 2014). Other complications that may occur with long-term PD include abdominal hernias (incisional, inguinal, diaphragmatic, and umbilical), probably resulting from continuously increased intra-abdominal pressure. The persistently elevated intra-abdominal pressure also aggravates symptoms of hiatal hernia and hemorrhoids. Low back pain and anorexia from fluid in the abdomen and a constant sweet taste related to glucose absorption may also occur. Mechanical problems occasionally occur and may interfere with instillation or drainage of the dialysate. Formation of clots in the peritoneal catheter and constipation are factors that may contribute to these problems.

Define: Rheumatic Disorder

Rheumatic disease is an umbrella term that refers to arthritis and several other conditions that affect the joints, tendons, muscle, ligaments, bones, and muscles (arthritis refers to disorders that mainly affect the joints).

Define: Humoral Immunity

The humoral response is characterized by the production of antibodies by B lymphocytes in response to a specific antigen. Antibodies are the agents of humoral immunity. Antibodies occur in the blood, in gastric and mucus secretions, and in breast milk. Antibodies in these bodily fluids can bind pathogens and mark them for destruction by phagocytes before they are able to infect cells. The major difference between humoral and cell-mediated immunity is that humoral immunity produces antigen-specific antibodies, whereas cell-mediated immunity does not. T lymphocytes, on the other hand, kill infected cells by triggering apoptosis.

Fistula

What is a Fistula: The preferred method of permanent vascular access for dialysis is an arteriovenous fistula (AVF) that is created surgically (usually in the forearm) by joining (anastomosing) an artery to a vein, either side to side or end to side (see Fig. 54-5A). Needles are inserted into the vessel to obtain blood flow adequate to pass through the dialyzer. The arterial segment of the fistula is used for arterial flow to the dialyzer and the venous segment for reinfusion of the dialyzed blood. This access will need time (2 to 3 months) to "mature" before it can be used. As the AVF matures, the venous segment dilates due to the increased blood flow coming directly from the artery. Once sufficiently dilated, it will then accommodate two large-bore (14-, 15-, or 16-gauge) needles that are inserted for each dialysis treatment. The patient is encouraged to perform hand exercises to increase the size of these vessels (i.e., squeezing a rubber ball for forearm fistulas) to accommodate the large-bore needles. Once established, this access has the longest useful life and thus is the best option for vascular access for the patient requiring ongoing hemodialysis. Patient education and precautions for a Fistula: If you have a fistula, please begin fistula exercises one week after your dialysis access surgery. Fistula exercises will help your fistula enlarge and mature. Your access site will need some long-term attention to make sure it continues to function well. Please note the following precautions, which you must follow for as long as you have this access: Do not let anyone draw blood or put an IV in your access arm. Ask your doctor or nurse about how to order a bracelet that will alert healthcare providers that you have dialysis access. Do not have your blood pressure taken in your access arm. Do not wear a tight sleeve, a watch, or other constricting jewelry on your access arm. Do not carry a handbag or briefcase on your access arm. Try not to sleep on your access arm. Keep fistula clean and monitor for signs of infection. Check on fistula blood flow daily. This is done by touch and sound. When you place your fingers over your fistula, you should be able to feel the motion of the blood flowing through it. This sensation is the "thrill." Let your doctor know if the thrill ever feels different. To listen for your blood flow, use a stethoscope and place the bell flat on your fistula. The sound you hear is called the "bruit" (pronounced broo-ee). Any change in the pitch may indicate a clot (thrombolysis) or a narrowing (stenosis) of the fistula. This sound may change from a whooshing noise to a whistle-like sound.