General notes GENITO-URINARY DISORDERS.pptx

JohnHawkins862343 34 views 132 slides Aug 20, 2024
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About This Presentation

Detailed notes on gento urinary disorders


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GENITO-URINARY DISORDERS MISS WANYONYI

COURSE OUTLINE introduction course objectives review anatomy and physiology  

RENAL CONDITIONS Pyelonephritis Renal failure Haemodailysis Peritoneal diaysis Tuberculosis of kidney Renal calculi Renal trauma Renal tumours Hydronephrosis

COURSE OUTLINE URINARY CONDITONS Fistulae Neurologic bladder Diverticuli Tumours Benign prostate hypertrophy Carcinoma of prostate Hypospadias,epispadias urethral strictures

Course objectives Describe the anatomy and physiology of the upper and lower urinary tracts. 2. Identify the assessment parameters used for determining the status of upper and lower urinary tract function. 3. Describe the diagnostic studies used to determine upper and lower urinary tract function. 4.State genitourinary conditions, causes, signs and symptoms and management

Review of anatomy and physiology The urinary system comprises the kidneys, ureters, bladder, and urethra. Kidneys The kidneys are a paired organs located retro-peritoneally from the T12 to the L3 in the adult. They are surrounded by a fibrous capsule .It consists of distinct regions, the renal paren- chyma and the renal pelvis . The renal parenchyma is divided into the cortex and the medulla . The cortex contains the glomerul i, proximal and distal tubules , and cortical collecting ducts and their adjacent peritubular capillaries .

ANATOMY &PHYSIOLOGY The medulla resembles conical pyramids. 2 to 3 major calices that open directly into the renal pelvis. The hilum , or pelvis, is the concave portion of the kidney through which the renal artery enters and the renal vein exits Blood supply is from the renal artery, a branch of the abdominal aorta. Kidneys are drained by the renal vein into the inferior vena cava. The basic functional unit of the kidney is the nephron. There are approximately one million in each kidney.

The nephron consists of a glomerulus which has tufts of capillaries supplied with blood by the afferent arteriole and drained by the efferent arteriole . The glomerulus at the base forms a tubule that is divided into 3 parts- proximal tubule, loop of henle and distal tubule . The distal tubules join to form collecting ducts approx. 20mm long. The ducts connect to the renal pyramids(8-18 pyramids), the pyramids drain into minor calyces(4-13) which drain into(2-3) major calices that open into the renal pelvis. Each renal pelvis gives rise to a ureter which is approx 25 cm. it connects each kidney to the bladder.

FUNCTIONS OF KIDNEY Urine Formation- Urine is formed in the nephrons through a complex three-step process: glomerular filtration, tubular reabsorption, and tubular secretion. Excretion of waste products -The major waste product of protein metabolism is urea, All of it must be excreted in the urine; otherwise it will accumulate in body tissues. Others are creatinine, phosphates, and sulfates . Uric acid, formed as a waste product of purine metabolism, is also eliminated in the urine.

ct Regulation of Electrolyte Excretion includes sodium and potassium. Regulation of Water Excretion - by osmolarity, specific gravity and ADH. Vitamin D Synthesis -The kidneys are responsible for the final conversion of in- active vitamin D to its active form Secretion of Prostaglandins- which have a vasodilatory effect and are important in maintaining renal blood flow.

Regulation of Acid Excretion phosphoric and sulfuric acids . Their accumulation in the blood make it more acidic and inhibit cell function, they must be excreted in the urine. They are bound to chemical buffers so they can be excreted in the urine. Two important chemical buffers are phosphate ions and ammonia (NH3).

Autoregulation of Blood Pressure Specialized vessels of the kidney called the vasa recta constantly monitor blood pressure as blood begins its passage into the kidney. When the vasa recta detect a decrease in blood pressure, specialized juxtaglomerular cells secrete the hormone renin. Renin converts angiotensinogen to angiotensin I, which is then converted to an- giotensin II, the most powerful vasoconstrictor known. The vaso- constriction causes the blood pressure to increase. The adrenal cortex secretes aldosterone in response to stimulation by the pi- tuitary gland, which in turn is in response to poor perfusion or increasing serum osmolality. result is an increase in Bp

ct Renal Clearance- Renalclearancerefers to the ability of the kidneys to clear solutes from the plasma Regulation of Red Blood Cell Production . Erythropoietin stimulates the bone marrow to produce red blood cells.

ASSESSMENT OF THE RENAL SYSTEM Major history Pain- usually in the lumbar region Voiding patterns- frequency, amount, color,dysuria ,nocturia history of diabetes, hypertension, gout,. History of STI or UTI and treatment. History of manipulation of the urinary tract through diagnostic means e.g. catheterization. Family history of kidney disease Unexplained anaemia

Physical exam Inspection head to toe to detect any changes Face- assess for any puffiness Skin yellowishness due accumulation of nitrogenous wastes Skin excoriation due to uremic acid Unexplained anaemia

Assess the breath odour- uremic fetor Assess for changes in body weight? Increased body weight due to edema. AUSCULTATE: Lung sounds to rule out pulmonary edema secondary to fluid retention. Renal artery bruits-above and to the left of the umbilicus. PERCUSS: Bladder for fullness. Empty bladder is tympanic while full bladder gives off a dull sound. percuss abdomen to rule out ascites.

PALPATE: The flanks for any palpable mass. The kidneys are not normally palpable, though the smooth, round lower pole of the kidney especially the right may be palpated. Inguinal lymph nodes

DIAGNOSTIC EVALUATION URINALYSIS &URINE CULTURE: Urine culture determines whether bacteria are present in urine, their strains and concentration. Urine culture &sensitivity also identifies the antimicrobial best suited. Urine is examined for:- colour and clarity Odour Ph Specific gravity-measures the density of a solution compared to that of water. Normal is 1.003-1.030. urine is most concentrated in the morning hours and becomes less concentrated with fluid intake .

Urine color , Urine clarity and odor ,Urine pH and specific gravity, protein, glucose, and ketone bodies in the urine Microscopic examination of the urine sediment after centrifuging to detect RBCs (hematuria), white blood cells, casts (cylindruria), crystals (crystalluria), pus (pyuria), and bacteria (bacteriuria)

RENAL FUNCTION TESTS: Evaluate the severity of kidney disease and assess the status of the patients kidney function. They include:- Serum Urea Nitrogen/Blood Urea Nitrogen(BUN), creatinine clearance in 24hours. LAB STUDIES ON BLOOD TO DETECT KIDNEY DISORDERS; Serum creatinine levels- elevated in disease. Serum osmolality - potassium levels will be high Calcium levels- low in kidney disease as kidneys help in conversion of Vit D to its active form. Phosphorus levels- elevates as phosphorus is retained in the body due to low calcium levels. Magnesium levels-Mg is an antagonist of Ca thus levels are elevated Albumin levels( oncotic pressure) albumin is filtered if kidneys are damaged thus levels are low.

TISSUE STUDIES: Renal biopsy-an invasive procedure used to determine histological diagnosis and severity of disease process. It can be done using needle puncture or surgical incision. RADIOLOGICAL STUDIES: KUB(kidney, ureter, bladder studies)- x-ray to show size, shape, position of kidneys. Renal ultrasonography CT Scan and MRI Retrograde pyelogram -catheters are advanced through the ureters into the renal pelvis by cystoscop. A contrast agent is then injected. Cystography - a catheter is inserted into the bladder and contrast agent is injected. It evaluates vesicoureteral reflux(backflow of urine into ureters ).

Renal angiography/arteriography- provides an image of the renal arteries. The femoral vein is pierced with a needle and a catheter is advanced up through the femoral and illiac arteries into the aorta and then the renal artery. A contrast agent is then injected to opacify. Intravenous pyelography- intravenous injection of contrast media, then a series of radiological films are obtained.

RENAL FAILURE It is a condition that results when the kidneys cannot remove the body’s metabolic waste or perform their regulatory functions.resulting in accumulation of waste products in the body There are two type:- Acute renal failure Chronic renal failure ACUTE RENAL FAILURE: It is a reversible clinical syndrome where there is sudden and almost complete loss of kidney function over a period of hours or days.

Classification of Acute Renal Failure PRE RENAL It results from impaired blood flow to the kidney causing hypo perfusion of the kidney & reduced glomerular filtration rate. causes Volume depletion states; hemorrhage, gastrointestinal loses (vomiting, diarrhoea ), renal loses(diuretics). Impaired cardiac efficiency: myocardial infarction, heart failure, cardiogenic shock, dysrhythmias . Vasodilation : sepsis, anaphylaxis, antihypertensives or other drugs that cause vasodilation .

INTRA RENAL FAILURE: It is as a result of actual parenchymal damage to the glomeruli or kidney tubules. Causes Prolonged renal ischemia resulting from Pigment nephropathy (associated with the breakdown of blood cells containing pigments that in turn occlude kidney structures) Blood clots renal ,Cholesterol deposits trauma, crush injuries, burns) transfusion reaction, hemolytic anemia Glomerulonephritis,pyelonephritis

Nephrotoxic agents such as: Aminoglycoside antibiotics (gentamicin, tobramycin) Radiopaque contrast agents Heavy metals (lead, mercury) Solvents and chemicals (ethylene glycol, carbon tetrachloride, arsenic) Nonsteroidal anti-inflammatory drugs (NSAIDs) Medication i.e dyes used in imaging studies

POST RENAL FAILURE: It is the result of obstruction somewhere distal to the kidney. The obstruction leads to stasis of urine all the way to the renal pelvis, accumulation of urine in the renal pelvis Causes include:- Caliculi Tumors Benign prostatic hyperplasia Strictures Blood clots creates tension in the kidney.

PHASES OF ACUTE RENAL FAILURE; There are four clinical phases of ARF:- I) Initiation II) Oliguria III) Diuresis IV) Recovery

Initiation: Begins when kidney function is affected by the disease and precipitating event. 2. Oliguria There is reduced output of urine less than 400mls/day There is a rise in serum concentrations of substances usually excreted by the kidneys- urea, creatinine , uric acid, organic acids & intracellular cations ( Mg, K) uremic symptoms first appear & life threatening conditions such as hyperkalemia develop. Hypervolemia , hypocalemia , hyperphosphotemia .

3. Diuresis: It is marked by a gradual increase in urine output which signals that glomerular filtration has started to recover. Urine volume may be normal or elevated, however, renal function may still be markedly abnormal. Patient should be observed closely for signs of dehydration during this phase. If dehydration occurs, the uremic symptoms are likely to increase. 4. Recovery period: It signals the improvement of renal function and may take 3-12 months. Lab values return to normal.

PATHOPHYSIOLOGY: When there is reduced blood volume and redistribution of blood away from kidneys, renal blood flow is reduced. This reduces oxygen & nutrient supply to the kidney. This causes ischaemia leading to damage. Ischaemia leads to necrosis of cells of renal tubules. The cells slough off & block the renal tubules.

CLINICAL MANIFESTATIONS: Depends on the affected system:- Decreased urinary output Fluid retention leading oedema Anaemia due hemolysis and reduced erythropoetin production Increased BUN( azotemia )- i.e. there is increased protein catabolism which leads to increased urea, creatinine & uric acid levels in blood. This manifests as anorexia, nausea, vomiting, diarrhoea , hiccups, headache, drowsiness, muscle twitching & convulsions. Hyperkalemia due to decreased potassium excretion. Metabolic acidosis – due to inability to excrete hydrogen ions & loss of kidneys buffering mechanism Increased respiration in an attempt to correct metabolic acidosis, it removes excess carbon dioxide.

MEDICAL MANAGEMENT: The objective is to restore normal chemical balance , mantaining normal fluid balance& prevent complications until repair of renal tissue & restoration of renal functioning can occur. management The underlying cause is identified and treated Prerenal azotemia is treated by optimizing renal perfusion, whereas postrenal failure is treated by relieving the obstruction. Treatment of intrarenal azotemia is supportive, 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

Overall, medical management includes maintaining fluid balance, avoiding fluid excesses, or pos- sibly performing dialysis . Maintainance of fluid balance - is based on daily body weight, measurement of central venous pressure, serum & urine concentration, fluid losses, BP & clinical status of the patient. Monitor input and output

Fluid excesses can be detected by dyspnea , tachycardia, distended neck veins, crackles in the lungs & generalised edema. Restrict fluid intake Mannitol , furosemide or ethacrynic acid may be prescribed to initiate diuresis & prevent complications. Adequate blood flow to the kidney may be restored by IV fluids or transfusion of blood products. If ARF is due to hypovolemia secondary to hypoproteinemia , albumin infusion is given. Dialysis may be initiated to prevent serious complications

. PHAMACOLOGICAL THERAPY: Hyperkalemia - (is the most life threatening) monitor for potassium levels abnormal >5.5 & ECG changes. administer cation exchage resin s orally or retention enema . They exchange sodium ions for potassiun ions in the intestinal tract. IV 50% dextrose, insulin & calcium replacement which shifts K back into the cells In patients with severe acidosis, the arterial blood gases or serum bicarbonate levels (CO2-combining power) must be monitored because the patient may require sodium bicarbonate therapy or dialysis. The elevated serum phosphate level may be controlled with phosphate-binding agents (aluminum hydroxide)

NUTRITIONAL THERAPY: The patient is weighed daily, if the patient gains weight or develops hypertension, fluid retention should be suspected. Give low phosphorus and potassium diet 1.e apples, cabbages Avoid products with added salt Limit dietary proteins High carbohydrate meals are given to meet caloric needs and to give a protein sparing effect. Blood chemistry evaluations are made to determine the amounts of sodium, potassium, and water needed for replacement

Nursing interventions Monitoring fluid and electrolyte balance Reducing metabolic rate by ensuring bed rest Promoting pulmonary function by Assisting patient to turn, cough, take deep breaths frequently to prevent atelectasis & respiratory tract infection. Maintain asepsis with invasive lines & catheters to minimize the risk of infection.Avoid indwelling catheters whenever possible due to high risk of UTI. Frequent turning, keeping skin clean & well moisturised to prevent skin breakdown. Give patient & family psychological support

CHRONIC RENAL FAILURE ( END STAGE RENAL DISEASE) It is a progressive, irreversible deterioration in renal function in which the body’s ability to maintain metabolic & fluid – electrolyte balance fails resulting in uremia or azotemia . Causes: Systemic diseases: diabetes, hypertension, chronic glomerulonephritis, pyelonephritis, SLE. Obstruction of the urinary tract Hereditary lesions: polycystic kidney disease. Vascular disorders. Medications or nephrotoxic agents – leads, cadmium, mercury, chromium.

Pathophysiology: There is deterioration and destruction of nephrons due to ischaemia or infections or toxicity leading to progressive loss of renal function. GFR falls and serum urea nitrogen & creatinine levels increase. The remaining functional nephrons hypertrophy, due to larger amount of filtering required & consequently the kidneys lose their ability to concentrate urine resulting in polyuria .

Clinical manifestations: All body systems are affected by the uremia of chronic renal failure thus a variety of signs & symptoms. Cardiovascular system Hypertension Heart failure & pulmonary edema due to fluid overload Pericarditis - Edema, engorged neck veins, hyperkalemia, hyperlipidemia . Dermatological manifestations Severe pruritus (itching) Uremic frost – the deposition of urea crystals on the skin. Bruising.

Gastrointestinal manifestation: Anorexia, nausea, vomiting, hiccups. Patients breath may have odour of urine/ammonia(uremic fetor). Constipation. Neurological manifestations: Altered level of consciousness, inability to concentrate, muscle twitching, agitation, confusion and seizures. Peripheral neuropathy. Pulmonary manifestations: Pulmonary edema due to fluid overload Hyperventilation( Kussmaul breathing) due to metabolic acidosis.

Hematological manifestations: Anaemia due to lack of erythropoietin, hemolysis and GI losses. Clotting abnormalitites Lowered immunity Musculoskeletal manifestations: muscle cramps due to loss of calcium, loss of muscle strength, bone pain and fractures. Assignment- read on stages of chronic renal failure & diagnostic tests

MANAGEMENT The goal of management is to maintain kidney function & homeostasis for as long as possible. All factors that contribute to ESRD and are reversible are identified and treated.

a) Pharmacotherapy Antacids - are given to treat hyperphosphatemia & hypocalcemia . They bind dietary phosphorus in the intestinal tract Antihypertensives -. calcium channel blockers – nifedipine , amilodipine ACE inhibitors – enalapril , captopril vasodilators – hydralazine Heart failure and pulmonary edema may be treated with fluid restriction, low sodium diet, diuretics, inotropic agents e.g. digoxin & dobutamine & dialysis.

Antisezuire agents – give IV diazepam 10 – 20mg or phenytoin to control seizures. Anaemia is treated with recombinant erythropoietin . Calcium and vit D suppplements Ensure adequate iron stores, Vit B12 & folic acid. b) Nutritional therapy: Regulate sodium, potasium,Proteins and fluid intake High caloric diet from carbohydrates & fats to prevent muscle wasting Vitamin supplementation Promote intake of high biologic value protein foods C. other therapy- dialysis, kidney transplant

DIALYSIS It refers to the process of artificial removal of waste products & excess water in the body. There are three methods: Hemodialysis Peritoneal dialysis Continous Renal Replacement Therapy(CRRT)

The need for dialysis may be acute or chronic. Acute dialysis is indicated when there is high & increasing level of serum potassium, fluid overload, or impending pulmonary edema, increasing acidosis, pericarditis & severe confusion It is also used to remove certain meds or other toxins( poisoning, overdose) from the blood. chronic/ maintenance dialysis is indicated in ESRD (end stage renal failure . Patients with no renal function can be maintained on dialysis for years

HEMODIALYSIS Most commonly used method. The objectives of hemodialysis are to extract toxic nitrogenous substances from the blood and to remove excess water the blood, laden with toxins and nitrogenous wastes, is diverted from the patient to a machine, a dialyzer, in which the blood is cleansed and then returned to the patient.

Hemodialysis system. (A) Blood from an artery is pumped into (B) a dialyzer where it flows through the cellophane tubes, which act as the semipermeable membrane (inset). The dialysate, which has the same chemical composition as the blood except for urea and waste products, flows in around the tubules. The waste products in the blood diffuse through the semipermeable membrane into the dialysate.

components of hemodialysis Dialyser Clot & bubble trap Blood pump BP monitor Dialysate flow system Blood lines, Heparin pump

Principles of hemodialysis: Diffusion Toxins and wastes in the blood are removed by diffusion from an area of higher concentration in the blood to an area of lower concentration in the dialysate. Osmosis Movement of a solvent such as water across a semi permeable membrane from areas of higher solute(blood) to areas of low concentration (dialysate). Ultrafiltration Movement of a fluid across a semi permeable membrane from a high pressure area to a low pressure area. It is more efficient in removal of water than osmosis. is ac- complished by applying negative pressure or a suctioning force to the dialysis membrane

. Treatment usually occurs three times a week for 3 – 4 hours per treatment. The body’s buffer system is mainted using a dialysate bath made up of bicarbonate ( most common) or acetate which is metabolised to form bicarbonate. The cleaned blood is returned to the body after the removal of many waste products and the restoration of electrolyte balance. Basic diagram of a hemodialyser

Vascular access: Use of large veins: Used in immediate access to the patients circulation for acute hemodialysis & is achieved by inserting a double lumen catheter into the subclavian , internal jugular & femoral vein. Arteriovenous fistula: It is the preferred method of permanent access. It is created surgically usually in the forearm by anastomosing (joining) an artery to a vein, either side to side or end to side Arteriovenous graft: It is created subcutaneously using biologic or synthetic graft material interposing between an artery and a vein

Complications of hemodialysis: Disturbance of lipid metabolism – hypertryglyceridemia . Gastric ulcers Disturbed calcium metabolism Sleep disturbance Painful muscle cramping due to rapid fluid shift from the extravascular space. Hypotension if too much fluid is eliminated.

Blood loss if blood lines separate or dialysis needles dislodge. Air embolism- rare- but can occur if air enters the vascular system . Dysrythmias

PERITONEAL DIALYSIS The goal is to remove toxic substances, metabolic wastes & reestablishing normal fluid & electrolyte balance. Indications: Patients with renal failure unable or unwilling to undergo hemodialysis or renal transplant. Patients susceptible to rapid fluid & electrolyte, & metabolic changes that occur with hemodialysis. Patients at risk of adverse effects of systemic heparin. With peritoneal dialysis, it takes 36 – 48 hours to achieve what hemodialysis accomplishes in 6 – 8 hours.

Underlying Principles the peritoneum , serves as the semipermeable membrane.. Sterile dialysate fluid is introduced into the peritoneal cavity through an abdominal catheter at intervals. Urea and creatinine, metabolic end products are cleared from the blood by diffusion and osmosis as waste products,move from an area of higher concentration (the peritoneal blood supply ) to an area of lower concentration (the peritoneal cavity) across a semipermeable membrane (the peritoneal membrane)

Complications: Peritonitis commonly leakage of dialysate through the catheter site. Bleeding –. Long term abdominal hernias, Peritoneal perforations Increased intra abdominal pressure Hypoxemia Muscle cramps, nausea, and vomiting Check for contraindication and the types

Peritoneal dialysis

NURSING CARE OF A PATIENT UNDERGOING DIALYSIS Protecting vascular access sites from damage. Assess vascular access sites for patency and ensure the extermity with the vascular access is not used to measure BP, tight dressings, restraints or jewellery. keep accurate intake – output records Monitor for symptoms of uraemia Detect cardiac & respiratory complications – crackles.

NURSING CARE OF A PATIENT UNDERGOING HEMODIALYSIS BEFORE DIALYSIS Allow the client to void Document the clients weight Obtain vital signs as baseline Check medication history of the pateint i.e antihypertensives, vasodilators

During the hemodialysis Obtain vital signs periodically between 30 min Observe proper body alignment , allow frequent position changes Monitor for episodes of nausea and vomiting Monitor for signs of bleeding by taking clotting time an hour before client comes off the machine

AFTER DIALYSIS Check the client weight note any difference Assess for complications Check for signs of bleeding and status of the fistula

INFECTIONS OF THE URINARY TRACT PYELONEPHRITIS It is a bacteria infection of the renal pelvis, tubules and interstitial tissues of one or both kidneys. Bacteria reach the kidney from the bladder or spread from systemic sources reaching the kidney through the bloodstream. Mostly caused by Escherichia coli that ascends the urinary tract. Kleibsiella sp. & Proteus sp. It is more common in females than in males because:- The female urethra is short Close proximity of the urethral opening to the anus Pregnancy-due to kinking of ureters causing stasis and reflux of urine

Risk factors Obstructed urinary flow- tumors, stricture, benign prostatic hyperplasia, urinary stones. Decreased natural host defense mechanisms. Instrumentation of the urinary tract e.g. catheterization & cystoscopic procedures. Other conditions e.g. diabetes mellitus- glucose creates an infection prone environment in the urinary tract. Presence of a STI.

Acute pyelonephritis Is an active inflammation of the parenchyma and pelvis of the kidney. Signs & symptoms Chills & fever Flank pain General malaise Anorexia Frequency of micturation Dysuria Nausea and vomiting Foul smelling cloudy urine( bacteria & pus) Enlarged kidneys

Diagnosis Ultrasound or CT scan to rule out or locate obstruction. Midstream urine specimen for culture and sensitivity. MANAGEMENT If patient is not dehydrated and has no signs of sepsis, manage as an outpatient. Pregnant women may be hospitalized for 2-3 days of parenteral antibiotic therapy and changed to oral once there is improvement. In out patient, antibiotics are given for two weeks, mostly quinolones e.g. ciprofloxacin 100-500mg BD, nitrofurantoin 50-100mg QID, 3 rd generation cephalosporins e.g. ceftriaxone or penicillins e.g. ampicillin.

A follow up urine culture is obtained two weeks after completion of antibiotics. Give plenty of fluids to ‘flush’ the urinary tract. Analgesics for pain. Paracetamol 1 gm tds Apply heat to reducer feeling of pain and pressure.

CHRONIC PYELONEPHRITIS Occurs with repeated bouts of acute pyelonephritis. Signs and symptoms Usually has no signs unless an acute exacerbation occurs. Fatigue Headache Poor appetite Polyuria Excessive thirst Weight loss Persistent reccuring infection may produce progressive scarring of the kidney resulting in kidney failure.

Assessment & diagnostic findings Creatinine clearance and serum levels BUN Urine for culture and sensitivity IV urogram to assess extent of disease MANAGEMENT Antibiotics based on culture and sensitivity Nitrofurantoin is used to supress bacterial growth 50-100mg 1 week.

Interventions Give antibiotic medication and anti inflammatory drugs. Give a balanced diet, small frequent meals and monitor weight. Monitor urine output through a strict input- output chart. Give plenty of fluids(3-4 litres per day). Health education on drug compliance and hygiene( perineal), importance of plenty of fluids, regular bladder emptying.

KIDNEY STONES/ UROLITHIASIS refers to stones (calculi) in the urinary tract. Stones are formed in the urinary tract when urinary concentrations of substances such as calcium oxalate, calcium phosphate, and uric acid increase. Stones can also form when there is a deficiency of substances that normally prevent crystallization in the urine, such as citrate, magnesium The fluid volume status of the patient more often in dehydrated patients is another factor playing a key role in stone development. Predisposing factors: Lifestyle- sedentary lifestyle causes slowing of renal drainage. Being obese

Hypercalcemia- abnormally high concentrations of blood calcium compounds. Hypercalciuria- abnormally high amounts of calcium in urine. Infection and urinary stasis Hyperuricosuria- high levels of uric acid secretion in urine caused by a diet rich in purines and over production of uric acid e.g in presence of gout. Medication- antacids, acetazolamide, Vit D, laxatives, high doses of asprin. Digestive diseases and surgery- gastric bypass surgery,inflammatory bowel disease, chronic diarrhea

Family or personal history . Dehydration. Not drinking enough water each day can increase your risk of kidney stones. People who live in warm climates and those who sweat a lot may be at higher risk than others. Certain diets. Eating a diet that's high in protein, sodium (salt) and sugar may increase your risk of some types of kidney stones. This is especially true with a high-sodium diet. Too much salt in your diet increases the amount of calcium your kidneys must filter and significantly increases your risk of kidney stones.

CLINICAL MANIFESTATIONS Pain – depends on the size and location of the stone. Small stones may be asymptomatic. In the renal pelvis , pain is intense and deep in the costovertebral angle. renal area radiates anteriorly and downward towards the bladder in the female and towards the testes in the male. renal colic- If pain suddenly becomes acute, with tenderness over the costovertebral angle accompanied by nausea and vomiting. In the ureters, the pain is acute, excruciating, colicky, wavelike radiating down the thigh & genitalia.

Severe pain in the side and back, below the ribs Pain that radiates to the lower abdomen and groin Pain that comes in waves and fluctuates in intensity Pain on urination N/B- Pain caused by a kidney stone may change — for instance, shifting to a different location or increasing in intensity — as the stone moves through your urinary tract.

ct Hematuria - because of abrasive action of stones Diarrhoea & abdominal discomfort due to proximity of kidney and GIT. Cloudy foul smelling urine Pink,brown urine Persistent need to urinate Fever, chills if infection is present Urinating small amounts of urine

types Calcium stones. Struvite stones Uric acid stones Cystine stones

ASSESSMENT & DIAGNOSTIC FINDINGS: Radiology- x-ray of Kidney Ureters & bladder(KUB), ultrasound, IV urography , retrograde pyelography . to confirm diagnosis. 24 hour urine test for measurement of calcium, uric acid, creatinine, sodium, pH, total volume. Blood tesing - shows increased ca and uric acid Dietary & medication history. Family history of kidney stones.

Diagram: Renal colic location

Medical management The goals of management are to eradicate the stone, determine the stone type, prevent destruction of the nephron, control infection and relieve any obstruction present. Pain- Opiod analgesics and NSAID’s to relieve pain and reduce swelling, hot baths and moist heat Encourage drinking of water(3l/day)may help flush out urinary system. It also reduces concentration of urinary crystalloids Medication that helps to relax muscles of the ureter helping to pass kidney stone i.e alpha blocker

Nutritional management Calcium stones: liberal fluid intake Restriction of dietary protein. High protein diet increases urinary excretion of calcium & uric acid Restriction of dietary sodium. High sodium increases amount of calcium in urine. Thiazide diuretics- to reduce calcium excretion in urine. Uric acid stones; Low purine diet to decrease uric acid excretion in urine. Foods high in purines include organ meats, mushrooms, asparagus. Allopurinol to reduce serum uric acid levels & urinary excretion of uric acid.

Surgical management Mostly indicated in large stones Using sound waves to break the stones i.extracorporeal shock lithotripsy Surgery to remove very large stones in the kidney using a telescope- percutaneous nephrolithotomy Parathyroid gland surgery Ureteroscopy- involves visualising the stone, inserting a ureteroscope into the ureter then inserting a laser or ultrasound device to fragment the stone

Renal cancer It may arise from renal capsule, paranhcyma, connective tissue or fatty tissue. Most are Adenocarcinoma. Risk factors Tobacco use Polycystic kidney disease Exposure to industrial chemicals Obestiy, Family history estrogen therapy Advanced kidney disease or being on long term dialysis

Clinical manifestations: Classical triad of signs & symptoms: Hematuria - usually gross, intermittent Flank pain Palpable abdominal or flank mass Symptoms of metastasis- unexplained weight loss, increasing weakness, anaemia ,. NB: many renal tumors produce no symptoms & are discovered on routine physical exam as a palpable abdominal mass.

management: Surgery, artery embolisation, radiotherapy Nursing Management: Give emotional support because client may be anxious about surgery, post- op renal function & possible recurrence of disease. Post- op the patient usually has catheters and drains in place to maintain a patent urinary tract, to drain urine and to permit accurate measurement of urine output. Frequent assistance in turning, deep breathing & coughing are encouraged to prevent atelectasis and other pulmonary complications

Nursing management Administer prescribed analgesics as needed by the patient. Prepare for nephrectomy as indicated.. Watch the patient for signs and symptoms of pulmonary, neurologic, and liver dysfunction. Monitor laboratory test results for anemia, polycythemia, and abnormal blood chemistry Ensure bedrest

Hydronephrosis It is dilation of the renal pelvis and calyces of one or both kidneys due to an obstruction. Obstruction to the normal flow of urine causes the urine to back up, resulting in increased pressure in the kidney

causes renal stone. tumor pressing on the ureter odd angle of the ureter as it leaves the renal pelvis twist or kink at ureteropelvic junction . an enlarged prostate gland. acute unilateral obstructive uropathy. Hydronephrosis can also occur in pregnancy because of the enlarged uterus.

Signs and symptoms pain in the abdomen or flank nausea vomiting pain when urinating incomplete voiding a fever  Frequent micturation hematuria

Medical Management identify and correct the cause of the obstruction To relieve the obstruction, the urine may have to be diverted by nephrostomy tube or stent The infection is treated with antibiotic agents. The patient is prepared for surgical removal of obstructive lesions Nephrectomy if one of the kidney is severly damaged

TUBERCULOSIS OF THE URINARY TRACT Pathophysiology It is caused by the organism Mycobacterium tuberculosis. The organism usually travels from the lungs by means of the blood- stream to the kidneys. On arrival in the kidney, the microorganism may lie dormant for years. After the organism reaches the kidney, a low-grade inflammation and the characteristic tubercles are seen. If the organism continues to multiply, the tubercles enlarge to form cavities, with eventual destruction of parenchymal tissue

Clinical Manifestations slight afternoon fever, weight loss, night sweats, loss of appetite, and general malaise. Hematuria and pyuria may be present., dysuria, and urinary frequency, In bladder involvement Cavity formations and calcifications may be noted on an intravenous urogram.

Medical Management The goal of treatment is to eradicate the offending organism. Combinations of ethambutol, isoniazid, and rifampin are used to delay the emergence of resistant organisms. Shorter-course chemotherapy (4 months) has been effective in eradicating the organism and in penetrating renal tissue. Surgical intervention may be necessary to treat obstruction and to remove an extensively diseased kidney.

Nursing Management interventions focus on patient education to include. Drug compliance. nature of tuberculosis; its cause, spread, and treatment; and necessary follow-up care maintaining a healthy lifestyle with a well-balanced diet, adequate intake of fluids, and exercise. Follow-up care is essential to reinforce the importance of taking medications

URETHRAL STRICTURES This is the narrowing of the lumen of the urethra as a result of scar tissue & contraction caused by urethral injury which can be from: Surgical instruments e.g. transurethral surgery Indwelling catheters Untreated urethritis, gonorrheal urethritis Cystoscopy Congenital abnormality Automobile accidents .

CLINICAL FEATURES decreased force and volume of urine stream. Hyperdistended bladder Sudden frequent urges to urinate Pain or burning on urination Incontinence Pain in pelvic or low abdomen Urethral discharge Hematuria Inability to void

MANAGEMENT: Gradual dilation of the narrowed area using a dilator After dilation, a warm sitz bath and analgesics to relieve pain. Antibiotics are prescribed for 5 days. Open uretrhoplasty for longer and more severe strictures

CANCER OF THE BLADDER It affects the transitional mucosa of the bladder. It is common in 50- 70 year olds and is more prevalent in men than women. It is the most frequent neoplasm of the urinary tract. Risk factors: Cigarette smoking Exposure to carcinogens: dyes, asbestos, rubber, leather, ink, aromatic amines. Recurrent or chronic cystitis or UTI’s. Bladder stones. High urinary pH. Pelvic radiation therapy. Cancers from prostate, colon & rectum in males.

Clinical features: Gross (visible) painless hematuria Infection of urinary tract producing frequency, urgency & dysuria . Pelvic or back pain may occur with metastasis Obstruction in voiding Assessment: Cystoscopy - visualize tumor directly & obtain biopsy specimen. Ultrasound- bladder & surrounding structures for metastasis. CT scan Biopsies of the tumor Cytological examination of the patients urine.

Management: Treatment of bladder cancer depends on the grade of the tumor(degree of cellular differentiation), the stage of the tumor growth(degree of local invasion) & presence or absence of metastasis. The patients age, physical & mental status are considered. Surgical management: For superficial bladder cancers, the tumor is controlled by transurethral resection or cauterization. Biological therapy (immunotherapy)- signaling the body immune system to help fight cancer cells

Incase of invasive or multifocal tumor, a simple or radical cystectomy is performed. in men it involves removal of the bladder, prostate and seminal vesicles while in women it involves removal of the bladder, lower ureter, uterus, fallopian tubes, ovaries, anterior vagina & urethra. It may involve removal of pelvic lymph nodes. Removal of the bladder requires urinary diversions. Radiotherapy and chemotherapy

BENIGN PROSTATIC HYPERPLASIA (ENLARGED PROSTATE) It is the enlargment of the prostate gland extending upward into the bladder and obstructing the outflow of urine by encroaching on the vesical orifice. a normal part of the aging process in men, caused by changes in hormone balance and in cell growth

Clinical Manifestations prostate gland that is large, rubbery, and nontender. incomplete emptying of the bladder and urinary retention. Dribbling of urine increased frequency of urination a decrease in the volume and force of the urinary stream Dysuria An urge to urinate soon after urinating Urinary tract infections may result from urinary stasis Difficult in starting urine stream

Assessment and diagnostic findings A physical examination with direct rectal exam urinalysis and urine culture studies to assess urine flow. Renal function tests. Complete blood studies Prostate specific antigen to rule out ca prostate ultrasonography

management The treatment plan depends on the cause of BPH, the severity of the obstruction, and the patient’s condition. If the patient is admitted on an emergency basis because he cannot void, he is immediately catheterized. Pharmacologic treatment antiandrogen agents, such as finasteride Alpha-adrenergic receptor blockers - relax the smooth muscle of the bladder neck and prostate Anticholinergic agents

Minimally invasive treatment Transurethral incision of the prostate (TUIP) Laser treatment - Used to cut or destroy prostate tissue Transurethral needle ablation of the prostate (TUNA) Prostatic stents - Flexible devices that expand when put in place to improve the flow of urine past the prostate

Surgery Transurethral resection of the prostate (TURP) Open prostatectomy - Reserved for patients with very large prostates

CANCER OF THE PROSTATE RISK FACTORS Old age Race-black Family history Obesity A diet high in red meat and fat

Signs and symptoms difficulty and frequency of urination, urinary retention Decreased size and force of the urinary stream. Other symptoms may include some painful ejaculation. Hematuria. Symptoms related to metastases include backache, hip pain, perineal and rectal discomfort, anemia, weight loss, weakness, nausea, and oliguria (decreased urine output).

ASSESSMENT AND DIAGNOSTIC FINDINGS prostate-specific antigen test measured in a blood specimen, and levels in crease with prostate cancer. Normal 0.2-4ng/ml Transrectal ultrasound (TRUS ) Direct rectal examination -doctor inserts gloved ,lubricated finger into rectum to examine texture,colour and size of the gland histologic examination of tissue removed surgically by transurethral resection, open prostatectomy, or transrectal needle biopsy

MEDICAL MANAGEMENT Treatment is based on the stage of the disease and the patient’s age and symptoms. MEDICAL MANAGEMENT Radiation therapy Hormone therapy - to stop the body from producing testosterone that help prostate gland cells to grow. medications that stops the body from producing testerone: luetinizing hormone agonist surgery to remove testicles(orchiectomy) chemotherapy uses drugs to kill rapidly growing cells Biological therapy uses body immune cell to fight cancer cells

management SURGICAL MANAGEMENT A radical prostatectomy -removal of the prostate and seminal vesicles Management after prostatectomy Urethral catheter should be left in place for 7-10 days Irrrigation to prevent obstruction by clots Ensure fluid balance by monitoring urine output and fluid used for irrigation Ensure increased fluid intake

Ct management Relieve b pain by ; giving medications that relieve bladder spasms,ambulation,warm compress monitors the drainage tubing and irrigates the system as prescribed to relieve any obstruction to avoid obstruction -observes the lower abdomen to ensure that the catheter has not become blocked, The drainage bag, dressings, and incisional site are examined for bleeding. The color of the urine is noted and documented , Continuous irrigation

NEUROGENIC BLADDER It is a dysfunction that results from a lesion of the nervous system. It May be caused by spinal cord injury, spinal tumor, herniated vertebral disk, multiple sclerosis, congenital anomalies (spina bifida or myelomeningocele), infection, or diabetes mellitus.

pathophysiology Several muscles and nerves must work together for your bladder to hold urine until you are ready to empty it. nerve messages go back and forth between the brain and the muscles that control the bladder emptying. if this nerves are damaged by illness and injury the muscles may not be able to tighten or relax at the right time. In neurogenic bladder muscles and nerves don't work well as a result the bladder may not fill or empty well

Bladder muscles may be overactive and squeeze more often than normal and before the bladder is full with urine. sometimes the muscles are too loose and let urine pass before you are ready . Underactive bladder- it will not squeeze when it is filled with urine and wont empty fully or at all. The sphincter muscles in the urethra may not work in the right way. they remain tight during the emptying

Signs and symptoms of overactive bladder Feel of sudden urge to urinate that’s difficult to control urge incontinence- involuntary loss of urine immediately following an urgent need to urinate Frequent urination nocturia

causes Stroke Multiple sclerosis Acute urinary tract infections Bladder tumours s or stones Enlarged prostate Excess consumption of caffeine Declining cognitive function related to age

treatment Behavioral interventions; Pelvic floor muscles exercises(kegel) strengthen pelvic floor muscles and urinary sphincter hence may help to stop involuntary muscle contractions Scheduled toilet trips Intermittent catheterization to empty the bladder completely Bladder training by delaying to void when you feel an urge to urinate Weight loss and wearing absorbent pads

Medications Drugs that relax the bladder can be helpful to relieve overactive bladder i.e tolterodine,oxybutynin Nerve stimulation to regulate nerve impulses to the bladder Surgery to increase bladder capacity

Underactive bladder Causes Damage to peripheral nerves Diabetes Pelvic surgery can injure the bladder nerves leading to decreased contractions Increasing age leads to decreased elasiticity Obstruction of the bladder by enlarged prostate and vaginal prolapse UTI Spinal cord injury at L1

Signs and symptoms Withholding large amount of urine without sensation to void Hesitancy to start urine stream Poor or intermittent stream Sensation of incomplete emptying

treatment Fluid restriction Drug that stimulate the nerve of bladder i.e bethanechol Catheterisation Placement of stent around the neck of bladder

Pathophysiology Types spastic (or reflex) bladder- caused by any spinal cord lesion above the voiding reflex arc). The result is a loss of conscious sensation and cerebral motor control. A spastic bladder empties on reflex, with minimal or no controlling influence to regulate its activity. Flaccid bladder is caused by a lower motor neuron lesion, commonly resulting from trauma. More common DM patients. The bladder continues to fill and becomes greatly distended, and overflow incontinence occurs. The bladder muscle does not contract forcefully at any time.

Complications Infection ,Urolithiasis, resulting from urinary stasis and catheterization. Renal failure Hydronephrosis. Medical Mmanagement long-term objectives • Preventing overdistention of the bladder • Emptying the bladder regularly and completely • Maintaining urine sterility with no stone formation • Maintaining adequate bladder capacity with no reflux

continuous, intermittent, or self-catheterization a diet low in calcium (to prevent calculi), encouragement of mobility and ambulation. A liberal fluid intake is encouraged to reduce the urinary bacterial count, reduce stasis, decrease the concentration of calcium. “double voiding Use of timed, or habit, voiding is also considered.

ct Parasympathomimetic medications, such as bethanechol may help to increase the contraction of the detrusor muscle. SURGICAL MANAGEMENT carried out to correct bladder neck contractures or vesicoureteral reflux or to perform some type of urinary diversion procedure. CATHETERIZATION
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