Chapter 70: Care Of Patients With Renal Disorders Flashcards
Etiology and risk of PKD
Those with the recessive form usually die in early childhood. 5 to 10% show no family history.
There is no way to prevent it, early detection can help slow the progression. Genetic counseling is needed.
More common in white people.
Pathophysiology of polycystic kidney disease
Fluid filled cysts develop in the nephrons.
In the inherited dominant form only a few nephrons have cysts until the person reaches the 30s. In the recessive form nearly 100% of nephrons have cysts from birth. The cysts become larger and more widely distributed. They damage the glomerular and tubular membranes. They are filled with fluid and enlarge and the kidney function deteriorates. The kidneys become very large, 2 to 3 times the normal size. The abdominal organs are displaced the patient has pain. The cysts are at risk for infection, rupture, and bleeding. Most patients have high blood pressure. The Renin/angiotensin system leads to hypertension also. Cysts can also occur in the liver and reduce liver function. Cerebral aneurysms are higher in these patients. Heart valve problems, left ventricular hypertrophy, colonic diverticula are common.
Manifestations of PKD
Abdominal or flank pain. Hypertension. Nocturia. Increased abdominal girth. Constipation. Bloody or cloudy urine. Kidney stones
Gently palpate the kidneys which are usually easily felt. Dull aching pain is caused by increased kidney size with distention or by infection within the cyst. Sharp intermittent pain occurs when cyst ruptures or a stone is present. When a cyst ruptures, the patient may have bright red or cola colored urine. If it is cloudy or foul-smelling infection is suspected. Nocturia is an early manifestation because of decreased concentrating ability.
As renal function further declines the patient has increasing hypertension, edema, anorexia, nausea and vomiting, pruritus, and fatigue. Berry aneurysms can occur and may cause a severe headache with or without neurologic or vision changes.
Diagnostic tests for PKD
Urinalysis shows the protein urea, hematuria, possibly bacteria.
Creatinine and BUN rises.
Creatinine clearances decrease.
Sodium up or down
Renal sonography, CT, MRI.
Treatment of polycystic kidney disease
Pain management however NSAID’s are used cautiously. Aspirin is avoided to avoid bleeding.
Antibiotics such as Cipro or Bactrim. Monitor creatinine levels because of nephrotoxicity. Dry heat promote comfort. Needle aspiration and drainage of a cyst.
Constipation: increase fluids, increase fiber, exercise. Use the stool softeners and a careful use of a laxative.
Control blood pressure. Drink at least 2 L to prevent dehydration. Restrict sodium. Antihypertensive agents and diuretics may be used.
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Patient teaching for PKD
Teach patient to measure blood pressure, monitor weight daily, self administer medications. Protein intake may be limited
Take your temperature. Limit intake of salt. Notify your doctor if your urine is foul-smelling or if there is blood. Notify if you have a headache that does not go away or if you have visual disturbances. Monitor bowel movements to prevent constipation
Hydronephrosis
The kidney enlarges as urine collects in the pelvis and kidney tissue. The capacity is normally only 5 to 8 mL. Obstruction in the pelvis or at the point where the ureter joins the renal pelvis quickly distends. In only a matter of hours the blood vessels in renal tubule can be damaged
Hydroureter
Enlargement of the ureter with an obstruction lower in the urinary tract. This usually obstructed where the iliac vessels cross or where the ureter enters the bladder. Ureter dilation occurs and enlarges as urine collects.
Urethral stricture
The obstruction is very low in the urinary tract, causing bladder distention before hydroureter and hydronephrosis. It still needs prompt treatment.
Urinary obstruction
Pressure builds on the kidney and can cause failure. Nitrogen waste products such as urea, creatinine, and uric acid as well as electrolytes such as sodium, potassium, chloride, and phosphorus are retained. Acid-base is impaired. Causes can be tumors, stones, trauma, structural defects, and fibrosis, radiation, surgical treatment.
Creatinine and BUN increase with reduced GFR.
CT, IV urography, or sonography.
Treatment for urinary obstruction
Remove the stone. Cystoscope or retrograde urogram. Nephrostomy can be performed. A nephrostomy diverts urine externally to prevent kidney damage
Nephrostomy
NPO, clotting studies, and moderate sedation. Patient is placed prone, kidney located under ultrasound or fluoroscope, local anesthesia. A needle is placed into the kidney. A catheter is inserted into the renal pelvis and the external is connected to a drainage bag. It remains in place until the obstruction is resolved.
Post op monitor I and O. Some urine will still drain through a Foley catheter. Assess amount hourly for the first 24 hours. If the drainage decreases and the patient has back pain, the tube maybe clogged. Notify the doctor immediately. Monitor for leaking urine or blood and notify Dr. A red tinge in the urine may last for 12 to 24 hours.w
Pathophysiology of Pyelonephritis
Bacterial infection of the kidney and the renal pelvis/the upper urinary tract. Acute pyelonephritis is the active bacterial infection. Chronic pyelonephritis results from repeated or continued upper UTIs. Chronic is usually from a tract defect, obstruction, or most commonly when you’re in refluxes from the bladder into the ureters.
Reflux occurs at the vesicoureteral junctions where the ureter joins the bladder.
Abscesses may occur anywhere in the kidney. Inflammation and fibrosis lead to deformity of the renal pelvis and calyces. Repeated infection create scar tissue changing blood vessel. Glomerular, and tubular structure. Filtration, reabsorption, and secretion are impaired and renal function is reduced
Etiology and risk of pyelonephritis
Reflex as a child can cause scarring which then leads to chronic pyelonephritis. If they do not have reflux as a child it usually comes from a spinal cord injury, bladder tumor, prostate enlargement, or stones. At risk if you have had manipulation of the urinary tract, diabetes mellitus, chronic renal stones, overuse of analgesics. NSAIDS can lead to reflux
E. coli is the most common. If it is blood-borne which is rare the most common is Staphylococcus arias and Candida and salmonella
More common in women Until the age of 65 and then it is more common in men because of prostatitis
Manifestations of acute pyelonephritis
Fever, chills, tachycardia, tachypnea, flank back or groin pain, tender costal vertebral angle, abdominal discomfort, nausea and vomiting, general malaise or fatigue, burning urgency or frequency of urination, nocturia
Manifestations of chronic pyelonephritis
Hypertension, inability to conserve sodium, decreased urine concentrating ability/nocturia, tendency to develop hyperkalemia and acidosis. It is less dramatic. Ask about vague symptoms and history.
Diagnostic tests for pyelonephritis
Urinalysis shows positive leukocyte esterase and nitrate. Presence of white blood cells and bacteria. Culture and sensitivity is needed. Blood cultures may be obtained along with C reactive protein and ESR. X-rays of the KUB and IV urography can diagnose stones or obstructions. Cystourethrogram maybe indicated. Examining the urine for antibody coated bacteria may help.
assessment gallium scan to identify active pyelonephritis or abscesses, or tests to examine anti-body coated bacteria in urine, to identify patients who may need long term antibiotic therapy.
Treatment for pyelonephritis
Acute pain is treated with antibiotics and antiseptic drugs. Increase fluids 2 to 3 L per day and ensure adequate calories from all food groups. Surgical interventions to correct the problem. Conserve kidney function as long as possible. Teach to adhere to drug therapy. Control blood pressure. Possible protein restriction. Balance rest and activity
- Pyelolithotomy (stone removal from kidney)
- Nephrectomy (removal of the kidney) last resort
- Ureteroplasty ureteral diversion, or reimplantation of ureter to restore proper bladder drainage.
Hypertension and renal failure
ØBlood pressure is necessary to reduce cardiovascular complications and slow progression of kidney dysfunction. Educate to promote self management and understanding
ØUrge patient to drink 2 L of fluid per day to prevent dehydration, and decrease urine concentration with nocturia.
ØRestricting sodium intake to control blood pressure. Antihypertensives and diuretics, ACE inhibitors, calcium channel blockers, beta blockers, and vasodilators. ACE inhibitors may help control growth aspects of PKD
Immunologic renal disorders/ glomerular nephritis
Glomerulonephritis (GN) is the third leading cause of end-stage kidney disease (ESKD).
Whether the disease starts in the kidney or occurs as the result of other health problems, the glomeruli are usually injured.
For disease that starts in the kidney, a genetic basis and immune problem are common. In addition, systemic diseases and infections can have kidney effects and cause glomerular injury. Conditions that lead to glomerular disease include systemic lupus erythematosus and diabetic nephropathy.
Each type of disease or syndrome has a specific pathophysiology and clinical manifestations. Their glomerular effects are caused by injury to the glomeruli and result in proteinuria, hematuria, decreased glomerular filtration rate (GFR) edema, and hypertension.
Pathophysiology of acute glomerular nephritis
An infection (group A beta-hemolytic Streptococcus, staphylococcal or gram-negative bacteremia or sepsis, pneumococcal, syphilis, hepatatis B, measles, mumps, refer to table 70-3), often occurs before the kidney manifestations of acute glomerulonephritis (GN). The onset of symptoms is about 10 days from the time of infection. Usually, patients recover quickly and completely from acute GN. The incidence of acute GN is unknown, and GN after a systemic streptococcal infection is more common in men.
Manifestations of acute Glomerulonephritis
Patient assessment
ØConnection with sore throat? Skin or upper respiratory tract, recent travel or other exposures to viruses, bacteria, fungi, or parasite, recent illness or surgery, or systemic diseases. Recent incisions body piercing
Physical assessment/clinical manifestations: look for edema in face eyelids, hands, and othr area, assess for fluid overload and circulatory congestion (which may accompany the sodium and fluid retention), difficulty breathing or shortness of breath, assess for crackles in the lung, an S3 gallop rhythm and neck vein distention.
Changes in urination pattern and urine color smoky, reddish brown, rusty, or cola colored, dysuria, oliguria. Weigh to assess for fluid retention.
Baseline blood pressure. They usually have mild to moderate hypertension because of sodium and fluid retention. Fatigue, lack of energy, anorexia, nausea and vomiting if urea from kidney failure is present.
Test for acute glomerulonephritis
Laboratory assessment
ØUrinalysis shows RBCs (hematuria) and protein (proteinuria). Early morning specimen of urine is preferred for urinalysis because urine is most acidic and formed elements are more intact at that time.
ØSerum and urine creatinine measured by 24-hour urine test for creatinine clearance, BUN
ØSpecimens from the blood, skin, or throat are obtained for culture.
Other diagnostic tests
ØKidney biopsy
Treatment of acute glomerular nephritis
Interventions focus on managing infection, preventing complications, and providing appropriate patient education.
Management of infection begins with appropriate antibiotic therapy such as PCN, erythromycin, or azitromycin. To prevent spread of infection, antibiotics for people in immediate close contact with the patient also may be prescribed. Stress personal hygiene and basic IC principles such as handwashing, and complete entire course of antibiotics.
Prevention of complications
ØFluid overload, hypertension, and edema, diuretics and a sodium and water restriction are prescribed. Antihypertensive drugs to control hypertension. Fluid allowance is equal to the 24-hour urine output plus 500-600 mL.
ØOliguria may have increased serum levels of potassium and blood urea nitrogen (BUN). Potassium and protein intake may be restricted to prevent hyperkalemia and uremia as a result of the elevated BUN.
Dialysis is necessary if if uremic symptoms or fluid volume excess cannot be controlled.
Plasmapheresis is the removal and filtering of the plasma to eliminate antibodies.