5. Loss of kidney function Impaired blood flow Acute tubular necrosis Urinary tract obstructions decrease GRF Glomeruli damage Failure to restore blood and oxygen

15. Accumulation of protein in the blood Renal failure declines Reduce renal reserve Renal insufficiency ESRD (CRF)

21. NEPHRECTOMY PERITONEAL DIALYSIS UREMIA

22. UREMIA INTRODUCTION Uremia is a clinical syndrome associated with fluid, electrolyte, and hormone imbalances and metabolic abnormalities, which develop in parallel with deterioration of renal function. CONTINUE

23. ETIOLOGY Uremia may also be caused by specific lifestyle choices and certain types of trauma. A high protein diet or drug use, for example, can cause uremia. In addition, an increase in protein breakdown may occur from an infection, surgery, cancer , or trauma. This can also lead to uremia, as can gastrointestinal bleeding. Each of these potential causes of uremia makes the liver produce excessive amounts of urea, which may present in the blood stream. Uremia can also develop because urea is not eliminated from the body quickly enough. This can be caused by a blockage preventing urine from exiting the body. It may also be the result of decreased blood flow in the kidneys, which may be brought on by cardiac failure or hypotension . CONTINUE

24. Normally, the kidney is the site of hormone production and secretion, acid-base homeostasis, fluid and electrolyte regulation, and waste-product elimination. In the presence of renal failure, these functions are not performed adequately and metabolic abnormalities, such as anemia, acidemia, hyperkalemia, hyperparathyroidism, malnutrition, and hypertension, can occur. Uremia usually develops only after the creatinine clearance falls to less than 10 mL/min, although some patients may be symptomatic at higher clearance levels, especially if renal failure acutely develops. The syndrome may be heralded by the clinical onset of nausea, vomiting, fatigue, anorexia, weight loss, muscle cramps, pruritus, and change in mental status. PATHOPHYSIOLOGY CONTINUE

25. ASSESSMENT SKIN The classic skin finding in persons with uremia is uremic frost. The skin may have a velvety appearance and feel, particularly in patients who are pigmented. Patients who are uremic also may have a sallow coloration of the skin. Patients may become hyperpigmented as uremia worsens (melanosis). Neurologic system: Uremic encephalopathy symptoms include fatigue, muscle weakness, malaise, headache, restless legs, asterixis, polyneuritis, mental status changes, muscle cramps, seizures, stupor, and coma. Amyloid deposits may result in medial nerve neuropathy, carpal tunnel syndrome, or other nerve entrapment syndromes. CONTINUE

26. Head, ears, eyes, nose, and throat: Sclera may become slightly icteric. The oral pharynx may be dry. Stomatitis may be present. Calcium deposition in the sclera can cause "red eye." Cardiovascular system: Uremic pericarditis can be associated with a pericardial rub or a pericardial effusion. Increased fluid retention may result in pulmonary edema, peripheral edema, and severe hypertension. CONTI N UE

34. PERITONEAL DIALYSIS Introduction Peritoneal dialysis (PD) is based on the same filtering process as hemodialysis. But instead of using an artificial kidney as the filter, the peritoneal membrane is used. The peritoneal membrane — also called the peritoneum — is a thin membrane that lines the abdominal cavity. A catheter, or flexible hollow tube, is surgically placed in the lower abdomen. It’s about a foot long, but only four or five inches of it lies outside the body. Catheter insertion is done in an operating room, often with local anesthesia. CONTINUE

46. Intraoperative complications include injury to any gastrointestinal organs (eg, liver, spleen, pancreas) or to any major blood vessels (eg, aorta, inferior vena cava). Pleural injuries can result in pneumothorax. Postoperative complications include secondary hemorrhage from the renal pedicle or any unrecognized injury, atelectasis, ileus, both superficial and deep wound infections, temporary or permanent renal failure, and incisional hernia. Systemic complications include myocardial infarction, congestive heart failure, pulmonary embolism, cerebrovascular accident, pneumonia, and thrombophlebitis. Complication CONTINUE

51. Is a bladder dysfunction that results from a lesion of the nervous system. It may be caused by spinal cord injury, spinal tumor, herniated vertebral disc, multiple sclerosis, congenital anomalies (spinal bifida or myelomenignocele ) infection or diabetes mellitus. Neurogenic Bladder

55. Pathophysiology Lesions at the lower motor neuron level of the spinal cord often directly interfere with the reflex arc leading to inappropriate interpretation of efferent and afferent impulses. When the bladder fills, the message is transmitted through afferent fibers to the brain cortex. The injury keeps these impulses from being correctly interpreted, leading to the loss of the micturition reflex. A flaccid bladder with urinary retention is the result. With upper motor neuron lesions, impulses are not transmitted to or from the lower spinal areas to the cortex. When the bladder distends, no sensation is transmitted. Because the lower cord is intact, activity of the reflex arc can occur. The client would have reflex incontinence in result. When the damage is to the cortical area itself, as with a stroke or trauma, the client cannot correctly interpret the impulses that are being transmitted. Unless the client is evaluated and treated appropriately, serious UTIs, skin breakdown associated with incontinence, and even renal failure due to chronic overdistention of the bladder are more likely to develop.