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NSG 3850 Unit 6 Reflection Questions 1. Describe the different types of urinary incontinence and potential causes of each.  Stress-places pressure on area causing leakage.  Urgency-suddenly have to pee.  Overflow-really full and can’t hold it anymore or leakage around an obstruction (like a tumor)  Functional-walking slow (cognitive impairment) or unable to walk (functional impairment)  Transient- urine leakage that is caused by a temporary (transient) situation such as an infection or new medicine.  Could be reversible, could be caused by UTI/constipation/fecal impaction.  Neurogenic bladder-usually spinal cord injury, when pons sends signal to release urine, the signal does not make it. (Can result in serious illness)  Fix problem, fix incontinence  Mixed-a combination of two types of incontinence 2. How much damage occurs to the nephrons before renal function is compromised?  <10% kidney function is a problem. The kidneys can function without incidence until 90% kidney function loss. 3. What is the clinical manifestation of cystitis in older adults?  Symptoms of cystitis in older adults may be atypical and include confusion (delirium) and new onset incontinence. Antibiotic treatment for symptomatic cystitis in the elderly should be managed with close drug monitoring to avoid toxicity. Asymptomatic bacteriuria in the elderly should not be treated with antibiotics. 4. Describe educational topics for your patient who has been diagnosed with a bladder infection or UTI.  Maintaining adequate fluid intake, empty your bladder often, urinate after sexual activity, take showers instead of baths, minimize douching, sprays, or powders in the genital area, and teach girls when potty training to wipe front to back. 5. What are common risk factors and clinical manifestations of acute pyelonephritis?  Pyelonephritis is an infection of the renal pelvis and kidney tubules that is usually caused by an ascending urinary tract infection. Costovertebral angle tenderness is the classic symptom. It is frequently accompanied by fever, chills, nausea, vomiting, and anorexia. Urinalysis usually shows evidence of infection. The presence of WBC casts is specifically indicative of an upper UTI as opposed to a lower UTI. When managed promptly and effectively, acute pyelonephritis does not generally result in decreased renal function.  Pregnancy is a risk factor for acute pyelonephritis in women because of the physiologic alterations that occur in the urinary tract. In nonpregnant women, men, and children, the most common risk factors are diabetes mellitus, anatomic abnormalities of the urinary tract, and obstructions. 6. Describe the etiology, pathophysiology, and diagnostics of chronic pyelonephritis.  Chronic reflux of infected urine into the renal pelvis is the typical cause of pyelonephritis. The kidneys are usually smaller than normal with caliceal deformity, chronic inflammation, and parenchymal scarring. It is the cause of 2-3% of ESKD. Individuals at risk for developing have bacteriuria associated with obstruction like renal calculi, neurogenic bladder, vesicoureteral reflux, or underlying intrarenal diseases. Chronic or recurrent pyelonephritis is one potential cause of chronic kidney disease.

 Urinalysis results typically parallel the findings of acute pyelonephritis but may not be profound. Diagnostic testing includes ultrasound that shows one or both kidneys to be smaller than normal with distorted architecture and significant scarring. Renal tubules can be dilated or atrophied. Other tests can determine underlying pathologies such as vesicoureteral reflux or obstruction caused by kidney stones. 7. Describe the risk factors and clinical manifestations of interstitial cystitis.  Bladder pain syndrome or interstitial cystitis is a genitourinary pain syndrome in which suprapubic pain is experienced with bladder filling, along with other lower urinary tract symptoms such as frequency, accompanied by UTO or other painful conditions. Pelvic pain must be of at least 6 months duration and be accompanied by at least one other lower urinary tract symptom. Urgency, dysuria, and dyspareunia may accompany pain, which can worsen with the consumption of certain foods and drinks (alcohol, caffeine, citrus juices and fruits, and hot peppers. Pain is often relieved with voiding. Classic IC manifests with visible inflammatory lesions of the bladder mucosa and submucosa (Hunner’s Lesions), but not everyone will have these. Women are more likely to have BPS/IC (5:1 ratio). This condition has a serious impact on quality of life, interferes with work, daily activities, sleep, family life, and sexual activity. 8. Describe the pathophysiology process behind the development of kidney stones and how can we reduce the risk of development?  Crystallization or stone formation occur with several solutes found in urine and may be promoted or inhibited by a number of factors. Some factors are inherent to the urinary tract and the characteristics of urine, whereas others are unique to the individuals and the type of renal calculi formed.  Contributing factors: HYPERparathyroidism (  ), gout, certain medications, HTN, UTIs, Chronic Inflammatory Bowel Disease, Irritable Bowel Disease, Chronic Diarrhea, Excessive Dietary Meat, Medical Hx or Family Hx of Stones, Obesity, Insulin Resistance/DMT2, Dehydration, Prolonged Immobility, Congenital Kidney Defects/Anatomic Alterations, and Vesicoureteral Reflux.  The pathogenesis of nephrolithiasis begins with urine becoming supersaturated with a specific solute. Some solutes have a tendency to form crystals if the concentration within the urine becomes great enough. These crystals usually begin developing in the concentrating areas of the nephron and kidney pelvis. Crystallization is enhanced when a person is dehydrated (decreased solvent) or has higher than normal levels of the solute in the urine from excessive excretion (calcium, uric acid). Crystals are unable to aggregate into a calculus of sufficient size to obstruct the urinary tract if urine is freely moving, so adequate fluid intake inhibits stone formation. Stasis of urine flow because of obstruction, immobility and sedentary lifestyle facilitates calculus formation. 9. Describe the laboratory values that are associated with chronic kidney disease.  Increased  Serum Creatinine, Serum BUN, Serum K+, Serum Phosphate, Serum Magnesium, Urinary Glucose, Urinary Protein, Occult Blood, Increased WBCs (during infection), and Urinary Casts.  Serum Sodium, Serum Calcium, Serum Bicarb, Arterial blood pH, Arterial blood Bicarb, Arterial blood CO2 pressure, Serum Hgb, Serum Hct, Urinary Specific Gravity, Urinary Creatinine

10. Describe the pathophysiologic process behind acute glomerulonephritis and name the clinical manifestations of acute glomerulonephritis.  Acute glomerulonephritis encompasses a group of inflammatory glomerulopathies that are characterized by the abrupt onset of varying degrees of hematuria, azotemia, proteinuria, oliguria, edema, and hypertension.  Postinfectious acute glomerulonephritis is known to follow skin (impetigo) and throat infections (Strep throat) with specific strains of the Group A Beta-Strep. Viruses are also associated with Postinfectious Acute Glomerulonephritis. The infectious organism stimulates the production of antibodies that bind to microbial antigens, initiating formation of antibody-antigen complexes. The onset of glomerular inflammation varies. Damage to the glomerulus typically occurs 1-3 weeks post-infection from Strep.  Clinical manifestations include smoky or coffee colored urine, increased circulating volume which produces edema, hypertension, and oliguria with increased serum levels of creatinine and BUN (nitrogenous wastes). Decreased urinary creatinine and BUN. 11. What acts as a natural barrier in the bladder to prevent infections?  Bacteria are cleaned from the cladder by the flushing and dilutional effects of the voiding. The high urea concentration with the high osmolality and low pH of urine acts as natural barriers to invading pathogens. Additionally, the mucous layer lining the bladder, as well as the ability of urothelial cells to initiate an immune response serve as host defenses. 12. Describe the pathophysiologic process behind anemia in chronic kidney disease patients.  RBCs are produced by bone marrow dependent on numerous cofactors. Erythropoietin, which is produced by the kidneys is possibly the most important. Erythropoiesis requires approximately 5 days to occur. When the kidneys lack erythropoietin, fewer RBCs are produced, and anemia becomes a persistent problem. Malnutrition can further complicate the problem when deficient of iron, folate, and B12. Chronic inflammation and elevations of PTH levels suppress the bone marrow while uremia associated with CKD produce a toxic environment for RBCs, reducing the life expectancy to 120 days. 13. What is nephrotic syndrome and its clinical manifestations?  Glomerulopathy in which there is a urinary elimination of more than 3-3.5g of protein/day resulting in glomerular leakiness. Usually, patients will develop HYPOalbuminemia (  ), HYPERlipidemia (  ), generalized edema, and a propensity for clot formation. The pathophysiology is an increased permeability of the glomerular membrane that allows large quantities of protein to leave the bloodstream and exit the body in the urine. The low serum albumin then stimulates the liver to increase production of substances like lipoproteins, which produces hyperlipidemia. Lipid casts or fat droplets can occur in the urine. As serum albumin is lost osmotic pressure decreases in the blood vessels and excess fluid moves into the interstitial spaces causing edema. As the circulating volume decreases, the RAAS causes sodium and water to retain, causing additional edema. 14. Describe the pathologic process behind edema development in nephrotic syndrome.  As serum albumin is lost osmotic pressure decreases in the blood vessels and excess fluid moves into the interstitial spaces causing edema. As the circulating volume decreases, the RAAS causes sodium and water to retain, causing additional edema. 15. What other organs may be affected by polycystic kidney disease?  In Recessive, may accompany pulmonary hypoplasia, liver as well as kidneys are cystic.

 In Dominant, liver is affected. Additional sites are the spleen, pancreas, lung, seminal vesicles, Circle of Willis, skin, and heart. 16. What are educational topics for your patient with polycystic kidney disease?  Diagnosis is based on family history, genetic testing, and imaging techniques. Where there is no family history of ADPKD, a presumption of the disease is made if imaging wither identifies cysts and bilaterally enlarged kidneys or shows cysts in the liver and both kidneys. Genetic testing is then performed to substantiate the diagnosis. Once EDRD is reached, dialysis or kidney transplant is required. This is the only thing that fixes it. 17. What are the types of acute kidney injury?  Pre-renal kidney injury-conditions that diminish perfusion of the kidney.  Hemorrhage, dehydration, burns, distributive shock, third-spacing/edema, cardiogenic shock, dysrhythmias, cardiac tamponade, heart failure, myocardial infarction, occlusion or stenosis of renal artery, or drug induced impairment of renal autoregulation in susceptible persons.  Intrinsic/Intrarenal injury-primary dysfunction of the nephrons or kidneys themselves.  Prolonged prerenal failure, transfusion reactions, rhabdomyolysis, prolonged postrenal failure, certain microbials (antibiotics, antifungals, and antivirals), radiographic contrast, certain cytotoxic chemotherapy, recreational drugs (amphetamines, heroin), environmental agents (heavy metals, carbon tetrachloride, insecticides), snake and insect venom, acute glomerulonephritis, allergic interstitial nephritis, acute pyelonephritis, vasculitis, emboli, and nephrosclerosis (from primary HTN, HTN emergencies, and urgency).  Postrenal injury-obstruction of the normal outflow of urine from the kidneys.  BPH, kinked or obstructed catheters, intra-abdominal tumors, strictures, and calculi. 18. What are potential causes of each type of acute kidney injury?  Prerenal  Absolute decrease in circulating volume  Hemorrhage, dehydration, and burns  Relative decrease in circulating volume  Distributive shock (neurogenic, anaphylactic, septic), third spacing/edema, decreased cardiac output (cardiogenic shock, dysrhythmias, cardiac tamponade, heart failure, and myocardial infarction)  Primary renal hemodynamic abnormalities  Occlusion or stenosis of the renal artery, and drug-induced impairment of renal autoregulation in susceptible persons.  Intrarenal/Intrinsic  Tubular (acute tubular necrosis)  Ischemic (a) Prolonged prerenal failure, transfusion reactions, and rhabdomyolysis.  Nephrotoxic (a) Prolonged postrenal failure, certain antimicrobials (antibiotics, antifungals, and antivirals), radiographic contrast media, certain cytotoxic chemotherapy agents, recreational drugs (amphetamines and heroin), environmental agents (heavy metals, carbon tetrachloride, and insecticides), and snake and insect venoms.  Glomerular

 Acute glomerulonephritis  Interstitial  Acute allergic interstitial nephritis, acute pyelonephritis  Vascular  Vasculitis, emboli, and nephrosclerosis (resulting from primary HTN, hypertensive emergency, and urgency)  Postrenal  BPH, kinked or obstructed catheters, intra-abdominal tumors, strictures, or calculi. 19. How is an acute kidney injury diagnosed?  KDIGO defines AKI as increase in serum creatinine (  ) within 48 hours, increase in serum calcium (  ) 1.5x baseline prior 7 days, and urine volume decreased for 6 hours. 20. Who is at risk for development of chronic kidney disease?  Acute tubular necrosis, developmental or congenital conditions (renal agenesis, aplastic kidneys, renal hypoplasia, ectopic/displaced kidneys, fused kidneys), cystic disorders, neoplasms, infections (recurrent pyelonephritis, renal tuberculosis), glomerulonephritis, systemic conditions (diabetes, HTN, HYPERparathyroidism, liver failure/cirrhosis, gout, amyloidosis, scleroderma, Goodpasture syndrome, Lupus) and other causes (genetics, advanced age, black race, overweight/obese, dyslipidemia, family hx of CVD, and smoking). 21. What is the relationship between hyperlipidemia and nephrotic syndrome?  The pathophysiology of nephrotic syndrome is increased permeability of the glomerular membrane allows large quantities of protein to leave the bloodstream and exit the body in the urine. This produces HYPOalbuminemia and proteinuria. Low serum albumin concentration serves to stimulate the liver to increase production of substances like lipoprotein which produces hyperlipidemia. 22. What is the purpose of hemodialysis and describe the components of dialysis.  In hemodialysis, an artificial kidney serves as the dialyzing semipermeable membrane. The patient’s blood passes through a bundle of hollow capillary tubules, and dialyzing fluid bathes these tubules. Solute that are present in high concentration in the uremic blood (phosphate, urea, creatinine, potassium) diffuse across the dialyzing tubule membrane into the dialyzing fluid and are discarded. Excess water in the uremic blood is eliminated through osmosis across the membrane. Access for hemodialysis is established by creating an AV fistula (usually in the arm). Dialysis is usually 3 days a week for about 4 hours. 23. Your patient has missed dialysis treatments, what electrolyte and acid/base imbalances may be present? What will your patient look like?  Phosphate, urea, creatinine, magnesium, and potassium will be imbalanced. Patient will have uremia and cardiac arrhythmias. 24. Why are your end stage renal disease patients at risk for bone fractures?  The inability to excrete phosphorus results in elevated serum phosphorus and likewise decreased serum calcium. When the body’s calcium levels are low, PTH is activated which releases calcium from the bones. Vascular and soft tissue calcifications and osteoporosis are the end results of prolonged PTH activation. This results in bone pain, deformities, and fractures.

Acute Kidney Injury Chronic Kidney Disease Patho/Etiology Damaged nephrons cannot function remaining nephrons try compensati increasing their clearance capacity. normal until about 75-80% of nephr or nonfunctional. Pre-Renal Because of conditions that diminish perfusion of the kidney Intra Renal Because of a primary dysfunction of the nephrons and the kidney itself Post Renal Caused by obstruction of the normal outflow of urine from the kidneys Diagnostic Tests CBC & Urinalysis Increase in Serum Creatinine within 48 hours, increase in serum creatinine to 1.5x baselines within past 7 days, or urine volume less than 0.5mL/kg/hr for 6 hrs. Decreased kidney function or kidne or more based on blood tests, urina studies. GFR<60 for 3 mos, with or without i kidney. Clinical Manifestations Disruptions in fluid, electrolytes, acid-base balances, retention of nitrogenous waste products, increased serum creatinine, and decreased GFR Complications HTN, CVD, Uremic Syndrome, Meta Electrolyte Imbalances, Bone and M Malnutrition, Anemia, Pain, and Dep Dialysis Hemodialysis, Peritoneal Dialysis (co and continuous cycling), CRRT (reall

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