AH2_Study_guide

Module 7 Renal Ignatavicius & Workman 7th ch70 pg1518, ch71 pg1537 1. Polycystic Kidney Disease pg1518 A. Pathophysiology a. an inherited disorder in which fluid-filled cysts develop in the nephrons; Cysts develop anywhere in the nephron as a result of abnormal kidney cell division; Incidence of cerebral aneurysms (berry aneurysms) is higher in clients with PKD—screen early. Assess for headaches with our without visual disturbances; only definitive Tx dialysis & kidney transplant i. Dominant form, few nephrons have cyst until person reaches 30s ii. Recessive from, 100% of nephron have cyst from birth b. (saunders) Cyst formation and hypertrophy of the kidneys, which leads to cystic rupture, infection, formation of scar tissue, and damaged nephron i. The ultimate result of this disease is chronic kidney disease ii. 2 types: 1. Infantile polycystic disease: An inherited autosomal recessive trait that results in the death of the infant within a few months after birth 2. Adult polycystic disease: An autosomal dominant trait that manifests between 30 and 40 years of age and results in end-stage kidney disease B. Clinical Manifestations a. Pain is often the first manifestation (abdominal (distended common) or flank pain); Nocturia (the need to urinate excessively at night) is an early manifestation, , hypertension, increased abdominal girth, constipation, bloodier cloudy urine (rupture), kidney stones; pay attention to headaches b. (saunders) Often asymptomatic until the age of 30 to 40 years; Flank, lumbar, or abdominal pain that worsens with activity and is relieved when lying down; Fever and chills; Recurrent urinary tract infections; Hematuria (rupture), proteinuria, pyuria; Calculi; Hypertension; Palpable abdominal masses and enlarged kidneys; Increased abdominal girt C. Treatment a. include pain management and prevention of infection, constipation, hypertension, and chronic kidney disease b. pain: NSAIDs used cautiously cause reduce kidney blood flow; ASA avoided risk of bleed; antibiotics trimethoprim/sulfamethoxazole (Bactrim, Septra, Trimpex) or ciprofloxacin (Cipro) are prescribed; low Na diet i. Apply dry heat to the abdomen or flank to promote comfort when kidney cysts are infected; Teach the patient methods of relaxation and comfort using deep breathing, guided imagery, or other strategies. c. Constipation: Teach patient w/ adequate urine output to prevent constipation by maintaining adequate fluid intake, increasing dietary fiber when fluid intake is more than 2500mL/24hr, and exercising regularly. d. HTN: done FIRST urge the patient to drink at least 2L of fluid per day to prevent dehydration; Restricting sodium intake may help control blood pressure. i. Drugs: Antihypertensive agents include angiotensinconverting enzyme (ACE) inhibitors, calcium channel blockers, beta blockers, and vasodilators; diuretics 1. Teach the patient and family how to measure and record blood pressure. e. (saunders) Monitor for gross hematuria, which indicates cyst rupture; Increase Na and H2O intake because sodium loss rather than retention occurs; Provide bed rest if ruptured cysts and bleeding occur; Prepare the client for percutaneous cyst puncture for relief of obstruction or for draining an abscess; Administer antihypertensives PRN; Prevent and/or treat urinary tract infections; Prepare the client for dialysis or renal transplantation; Encourage genetic counseling 2. Kidney Disorders: Review A&P of Kidney A. Hydroureter, Hydronephrosis, Urethral Stricture 1) Pathophysiology a. Hydronephrosis: kidney enlarges due to kidney obstruction b. Hydroureter: ureter enlarges due to obstruction of ureter c. Urethral stricture: obstruction causes bladder distension 2) clinical manifestations a. Known kidney/urologic disorders; Hx UTI; ask about recent flank/abd pain; chills, fever, malaise, abd pain, bladder distension, 3) nursing considerations a. Assess amount of drainage in collection bag b. If urine expected to drain, assess amount of drain hrly for first 24hrs c. If pt has back pain and drainage amount decrease, tube may b clogged/dislodged d. Monitor site for leaking urine/blood e. Red ting first 12-24hrs after procedure and gradually clear up f. Notify dr if drainage stops/decreases, becomes cloudy/ foul smelling, nephrostomy site leaks blood/urine, pt has back pain B. Glomerulonephritis, Pyelonephritis 1) Pathophysiology a. Pyelonephritis is either the presence of active organisms in the kidney or the effects of kidney infections. Acute pyelonephritis is the active bacterial infection, whereas chronic pyelonephritis results from repeated or continued upper urinary tract infections or the effects of such infections. b. Glomerulonephritis: Acute symptoms is about 10 days from the time of infection. Usually, patients recover quickly and completely from acute GN. Chronic develops over 20 to 30 years or even longer. The exact onset of the disorder is rarely identified 2) clinical manifestations a. Pyelonephritis i. Acute: active bacterial infection 1. Fever; chills; tachy & tachypnea; flank, back, loin pain; tender costovertebral angle; abd, discomfort; N/V; burning, urgency, freq of urination; nocturia ii. Chronic: repeated infections causing progressive inflammation & scarring 1. HTN; inability to conserve Na; decrease urine concentration ability; tendency to develop hyperkalemia & acidosis b. Glomerulonephritis i. Acute: skin lesions, edema of face, eyelids, hands, fluid overload and circulatory congestion, shortness of breath, crackles, JV D, smoky reddish brown rusty or cola colored urine, dysuria, oliguria, mild to moderate hypertension, fatigue, anorexia, nausea/vomiting ii. chronic: systemic circulation overload, crackles, S3 heart sounds, edema of foot, ankle, Shin, sacrum, JV D, slurred speech, ataxia, tremors, asterixis (flapping tremor of the fingers or inability to maintain a fixed posture with arms extended and risk hyperextended), yellowish color, texture, bruises, rashes, eruptions 3) nursing considerations a. pyelo i. Meds 1. Opioid analgesics, morphine sulfate, & morphine: moderate-sever pain 2. Antibiotics a. Mild – mod pyelo tx at home for 14 days w/ antiinfective i. Trimethoprim, sulfamethoxazole/trimethoprim ii. Quinolone antibiotic: ciprofloxacin levofloxacin 1. Stress the importance of completing the drug therapy as directed. ii. Surgery 1. Pyelolithotomy: remove large stone from kidney 2. Nephrolithotomy: remove kidney when all else failed 3. Ureteroplasty: repair ureter or ureteral reimplantation (preserves kidney functions & eliminates infections b. Glomerulonephritis i. Acute: antibiotic therapy. Penicillin, erythromycin, or azithromycin is prescribed for GN caused by streptococcal infection 1. Check for allergies before giving; Stress personal hygiene and basic infection control principles (e.g., handwashing) to prevent spread of the organism 2. Teach completing entire course of the prescribed antibiotic 3. diuretics and a sodium and water restriction are prescribed; antiHTN ii. Chronic: Management consists of diet changes, fluid intake sufficient to prevent reduced blood flow volume to the kidneys, and drug therapy to control the problems from uremia. 1. Eventually requiring dialysis or transplantation C. Nephrotic Syndrome 1) Pathophysiology a. is a condition of increased glomerular permeability that allows larger molecules to pass through the membrane into the urine and then be excreted 2) clinical manifestations a. Main feature severe proteinuria (more than 3.5g of protein in 24hrs) b. Edema (anasarca) c. Increased risk of infection d. Hyperlipidemia e. Hypoalbuminemia (Low serum albumin levels) f. Reduced kidney function; increased coagulation 3) nursing considerations a. Assess hydration status (vascular dehydration is common) D. Degenerative disorders a. Nephrosclerosis i. Path: is a problem of thickening in the nephron blood vessels, resulting in narrowing of the vessel lumens. This decreases kidney blood flow & tissue is chronically hypoxic 1. occurs with all types of hypertension, atherosclerosis, and diabetes mellitus; rarely seen when blood pressure is consistently below 160/110mm Hg. ii. Intervention: Management focuses on controlling high blood pressure and reducing albuminuria to preserve kidney function 1. Angiotensin-converting enzyme (ACE) inhibitors; diuretics b. Renovascular Disease i. Path: Processes affecting the renal arteries may severely narrow the lumen and greatly reduce blood flow to the kidney tissues ii. s/s: sudden onset of hypertension (difficult to control); poorly controlled diabetes or sustain hyperglycemia; elevated serum creatinine; decrease creatinine clearance iii. interventions: Balloon angioplasty with or without stent placement; Renal artery bypass surgery is a major procedure and requires 2 or more months for recovery; Renal angioplasty with metal stent placement is one safe and effective method to repair RAS c. Diabetic Nephropathy (leading cause of ESKD in white ppl) i. Path: occurs with either type 1 or type 2 DM; Severity of diabetic kidney disease is related to the degree of hyperglycemia ii. Saunders: Progressive decrease in kidney function iii. s/s: first manifestation is persistent proteinuria/albuminuria (as shown by dipstick or a urinary albumin excretion rate above 0.3g/dL), without evidence of other kidney disease; kidney size slightly increase, GFR rates higher than normal iv. saunders: Microalbuminuria; Thirst; Fatigue; Anemia; Weight loss; Signs of malnutrition; Frequent urinary tract infections v. intervention: Explain that the kidneys metabolize and excrete insulin. When kidney function is reduced, the insulin is available for a longer time and thus less of it is needed; saunders: Early prevention measures include the control of hypertension and blood glucose levels; Assess VS; Monitor I/O; Monitor the blood urea nitrogen, creatinine and urine albumin levels; Restrict dietary protein, sodium, and potassium intake as prescribed; Avoid nephrotoxic medications; Prepare the client for dialysis procedures if planned; Prepare the client for kidney transplant if planned; Prepare the client for pancreas transplant if planned. d. Renal Cell Carcinoma i. Path: most common type of kidney cancer and is also known as adenocarcinoma of the kidney ii. s/s: flank pain (ask about the nature of the flank or abdominal i. discomfort), blood in urine (late sign), palpated kidney mass, inspect skin for pallor, darkening of the nipples, and, in men, breast enlargement (gynecomastia); other late signs: muscle; wasting, weakness, poor nutritional status, and weight loss. e. Kidney Trauma pg 1535 i. Path: 1. Minor injuries include contusions, small lacerations, & tearing of the parenchyma and the calyx (forniceal disruption) caused by falls, contact sports, and blows to the back of torso 2. Major injuries include lacerations to the cortex, medulla, or branches of the renal artery or vein= hemorrhage 3. Pedicle injuries are lacerations or breaks in the renal artery or renal vein= hemorrhage i. S/s: Critical information to know is a history of kidney or urologic disease, surgical intervention, or health problems such as diabetes mellitus or hypertension; diffuse abdominal pain, local collections of urine, and infection; hemoglobin or red blood cells from renal blood vessel rupture; Hemoglobin and hematocrit values decrease with blood loss; inflammation or infection is present, the white blood cell count is elevated ii. Intervention: drug therapy, fluid therapy: Crystalloid solutions (0.9% sodium chloride (normal saline solution [NSS]), 5% dextrose in 0.45% sodium chloride, and lactated Ringer’s solution) 3. Kidney Injury/Disease Acute Renal Failure A. Acute Kidney Injury (AKI) 1) Types: i. A rapid decrease in kidney function, leading to the collection of metabolic wastes in the body; Saunders : Acute kidney injury (AKI) is the rapid loss of kidney function from renal cell damage; Occurs abruptly and can be reversible; AKI leads to cell hypoperfusion, cell death, and decompensation of renal function; The prognosis depends on the cause and the condition of the client; Near-normal or normal kidney function may resume gradually; increased in diabetic pts, DM 2, and aging population ii. Prerenal: conditions that reduce blood flow to the kidneys 1. most common problems leading to AKI are hypovolemic shock and heart failure (most common); reversible w/ correcting blood volume, increasing blood pressure, and improving cardiac output 2. saunders: Outside the kidney; caused by intravascular volume depletion, dehydration, decreased cardiac output, decreased peripheral vascular resistance, decreased renovascular blood flow, and prerenal infection or obstruction iii. Intrarenal: damage to the glomeruli, interstitial tissue, or tubules 1. By Infections (bacteria, viral, fungal), drugs (especially aminoglycoside antibiotics [-mycin drugs] and NSAIDs), and invading tumors (e.g., lymphomas or leukemias); radiographic dyes 2. Saunders: Within the parenchyma of the kidney; caused by tubular necrosis (lack of O2), prolonged prerenal ischemia, intrarenal infection or obstruction, and nephrotoxicity iv. Postrenal: obstruction of urine flow 1. ureter, bladder, urethral cancer; kidney, ureter, bladder stones; prostate hyperplasia/cancer; cervical cancer 2. saunders: Between the kidney and urethral meatus, such as bladder neck obstruction, bladder cancer, calculi, and postrenal infection(glomerulonephrintis & beta hemolytic strp) 2) Phases: onset, oliguric, diuretic, recovery