Sie sind auf Seite 1von 14

A bladder stone (also called a vesical calculus or cystolith) is a solid concretion or crystal aggregation found in the urinary bladder.

The term cystolithiasis refers to the presence of stones in the bladder. Signs and symptoms Bladder stones are small particles that can form in the bladder. In most cases bladder stones develop when the urine becomes very concentrated or when one is dehydrated. This allows for the minerals like calcium or magnesium to crystallize and form stones. Bladder stones vary in number size and consistency. In some cases bladder stones do not cause any symptoms of signs and are discovered as an incidental finding on a plain radiograph. However, when symptoms do occur these may include severe lower abdominal and back pain, difficult urination, frequent urination at night, fever, painful urination and blood in the urine. The majority of individuals who are symptomatic will complain of pain which comes in waves. The pain may also be associated with nausea, vomiting and chills.[2] Bladder stones vary in their size, shape and texture- some are small, hard and smooth whereas others are huge, spiked and very soft. One can have one or multiple stones. Bladder stones are somewhat more common in men who have prostate enlargement. The large prostate presses on the urethra and makes it difficult to pass urine. Over time stagnant urine collects in the bladder and minerals like calcium start to precipitate. Other individuals who develop bladder stones include those who have had spinal cord injury, paralysis or some type of nerve damage. When nerves to the back are damaged, the bladder cannot empty and stagnant urine results.[3] [edit]Causes Bladder stones may occur whenever the kidneys, bladder, or ureters become inflamed. The use of urinary catheters may cause a bladder stone. Individuals who are paralyzed or are unable to adequately pass urine may require the use of small plastic tubes (catheters) placed into the bladder. The use of these tubes may lead to an infection, which irritates the bladder, resulting in stone formation. Finally, a kidney stone may travel down the ureter into the bladder and become a bladder stone. There is some evidence indicating that chronic irritation of the bladder by retained stones may increase the chance of bladder cancer. Urinaryschistosomiasis, a disease caused by the digenean trematode Schistosoma haematobium, has been implicated in the development of vesical calculi.[4][5] However, evidence accumulated thus far has not supported this hypothesis.[6][7] [edit]Diagnosis The diagnosis of bladder stone includes urinalysis, ultrasonography, x rays or cystoscopy (inserting a small thin camera into the urethra and viewing the bladder). The intravenous pyelogram can also be used to assess the presence of kidney stones. This test involves injecting a radiocontrast agent which is passed into the urinary system. X-ray images are then obtained every few minutes to determine if there is any obstruction to the contrast as it is excreted into the bladder. Today, intravenous pyelogram has been replaced at many health centers by CT scans. CT scans are more sensitive and can identify very small stones not seen by other tests.[8] [edit]Prevention The best way to prevent bladder stones is to drink plenty of liquids. Juices containing citrates are thought to reduce the risk of stone formation. A study published in the Clinical Journal of the American Society of Nephrology indicate orange juice is more effective at preventing stone formation than other citrus juices.[9] Men who have difficulty with urination due to prostatic hypertrophy should seek treatment.[10] [edit]Management Increasing fluid intake can facilitate the passage of small bladder stones. However, larger stones may require other methods of treatment.[11] Fragmentation of bladder stones can be achieved by use of acystoscope which is inserted into the bladder. The urologist visualizes the stone and uses ultrasonic energy or laser lithotripsy to to cause fragmentation of the stones into small pieces which are then flushed out of the bladder. This procedure requires anesthesia and may require admission to a hospital. Complications of this treatment include infection and damage to the bladder.[12] Some stones are too large even for cystoscopic treatment and may require open cystotomy, in which an incision is made in the bladder and the stones are removed manually. [edit]History Lithoclastic cystotomy is attributed to Ammonius Lithotomos (stone-cutter) of Alexandria, Egypt. The term "lithotomy" is derived from the same words ( (lithotomia) - stone-cutting). Aulus Cornelius Celsuswrote that Lithotomos developed instruments to break up and extract bladder stones.[13] Celsus gave the first description of lithotomy as performed before and during his time, and the operation has ever since borne his name the Celsian method.[14]

Generic Name: Hyoscine ButylBromide Brand Name: Buscopan Classification: Belladona alkaloid, antimuscarinic Indication & Dosages: Spastic states Adults: 0.4 to 0.8 mg P.O. Delirium, preanesthetic sedation and obstetric amnesia with analgesics Adults: 0.3 to 0.65 mg I.V., I.M., or subcutaneously. Dilute solution with sterile water for injection before giving I.V. Children: 0.006mg/kg I.V., I.M., or subcutaneously. Maximum dose, 0.3 mg. Dilute solution with sterile water for solution before giving I.V. To prevent nausea and vomiting from motion sickness Adults: One Transderm-Scop, formulated to deliver 1mg scopolamine over 3 days, applied to the skin behing the ear at least 4 hours before antiemetic is needed. Or, 0.3 to 0.65 mg hydrobromide I.V., I.M. or subcutaneously. Or, 0.25 to 0.8 mg P.O. 1 hour before exposure to motion. Further doses of 0.25 to 0.8 mg may be given t.i.d., p.r.n. Children: 6 mcg/k or 200 mcg hydrobromide I.V., I.m., or subcutaneously Mode of Action: Inhibits muscarinic actions of acetylcholine on autonomic effectors innervated by postganglionic cholinergic neurons. May effect neural pathways originating in the inner ear to inhibit nausea and vomiting. Contraindication: Contraindicated in patients with angleclosure glaucoma, obstructive uropathy, obstructive disease of the GI tract, asthma, chronic pulmonary disease, myasthenia gravis, paralytic ileus, intestinal atony, unstable CV status in acute hemorrhage, tachycardia from cardiac insufficiency, or toxic megacolon. Contraindicated in patients with hypersensitive to belladonna or barbiturates. Use cautiously in patients with autonomicneuropathy, hyperthyroidism, coronary artery disease, arrhythmias, heart failure, hypertension, hiatal hernia with ferlux esophagitis, hepatc or renal disease, known as suspected GI infection, or ulcerative colitis. Use cautiously in children. Use cautiously in patients in hot or humid environments; drug can cause heat stroke. Side Effects: Frequent: Dry mouth (sometimes severe), decreased sweating, constipation. Occasional: Blurred vision; bloated feeling; urinary hesitancy; somnolence (with high dosage); headache; intolerance to light; loss of taste; nervousness; flushing; insomnia; impotence; mental confusion or excitement (particularly in the elderly and children); temporary lightheadedness (parenteral form); local irritation(with parenteral form). Adverse Reaction: Overdose may produce temporary paralysis of ciliary muscle; papillary dilation; tachycardia; palpitations; hot, dry, or flushed skin; absence of bowel sounds; hyperthermia; increased respiratory rate; EKG abnormalities; nausea; vomiting; rash over face or upper trunk; CNSstimulations; and psychosis (marked by agitation, restlessness, rambling speech, visual hallucinations, paranoid behavior, and delusions, followed by depression). Nursing Responsibilities:

Advise patient to apply patch the night before a planned trip. Transdermal method releases a controlled therapeutic amount of drug. Transderm-Scop is effective if applied 2 or 3 hours before experiencing motion but is more effective if applied 12 hours before. Instruct patient to remove one patch before applying another Instruct patient to wash and dry hands thoroughly before and after applying the transdermal patch (on dry skin behind the ear) and before touching the eye because pupil may dilate. Tell patient to discard patch after removing it and to wash application site thoroughly. Tell patient that if patch becomes displaced, he should remove it and apply another patch on a fresh skin site behind the ear. Alert patient to possible withdrawal signs or symptoms (nausea, vomiting, headache, dizziness) when transdermal system is used for longer than 72 hours. Advice patient that eyes may be ore sensitive to light while wearing patch. Advice patient to wear sunglasses for comfort Urge patient to report urinary hesitancy or urine retention.

Brand Name:Vastarel MR Generic Name: Trimetazidine Indication: Long treatment of coronary insufficiency, angina pectoris. Drug Classification: Anti-Anginal Drugs Mechanism of Action: acts by directly counteracting all the major metabolic disorders occurring within the ischemic cell. The actions of trimetazidineincludelimitationofintracellularacidosis, correction of disturbances of transmembrane ion exchanges, and prevention ofexcessive production of free radicals.decrease myocardial oxygen requirement bydecreasing the heart rate, ventricular volume, blood pressure and contractility. In some cases, myocardial oxygen delivery is increased thru reversing coronary arterial spasm. Dosage: 1 tab morning and evening Special Precaution: Pregnancy and Lactation Pregnancy Risk Category: Adverse Reaction: Rare cases of GI disorders. Contraindications: MAOI s (monoamine oxidase inhibitors) Form: 35 mg tablets Nursing Responsibility:  use cautiously in patients with heart failure or hypertension and in elderly

patients.

Trimetazidine is a drug for angina pectoris, sometimes referred to by the brand name Vastarel MR. Each tablet contains 35 mg of trimetazidine. Trimetazidine is an anti-ischemic (anti-anginal) metabolic agent, which improves myocardial glucose utilization through inhibition of fatty acid metabolism. By preserving the energy metabolism in cells exposed to hypoxia or ischemia, trimetazidine prevents a decrease in intracellular adenosine triphosphate levels, thereby ensuring the proper functioning of ionic pumps and transmembranous sodium-potassium flow whilst maintaining cellular homeostasis. It also inhibits oxidation of fatty acid in blood vessels. Controlled studies in angina patients have shown that trimetazidine increases coronary flow reserve, thereby delaying the onset of ischemia associated with exercise, limits rapid swings in blood pressure without any significant variations in heart rate, significantly decreases the frequency of angina attacks, and leads to a significant decrease in the use of nitrates.

It improves left ventricular function in diabetic patients with coronary heart disease. Recently, it has been shown to be effective in patients with heart failure of different etiologies (5-6). Trimetazidine is described as the first cytoprotective anti-ischemic agent developed and marketed by Les Laboratoires Servier (France). It acts by directly counteracting all the major metabolic disorders occurring within the ischemic cell. The actions of trimetazidine include limitation of intracellular acidosis, correction of disturbances of transmembrane ion exchanges, and prevention of excessive production of free radicals. Trimetazidine is usually prescribed as a long-term treatment of angina pectoris, and in some countries (including France) for tinnitus and dizziness. It is taken twice a day. Trimetazidine has high safety and tolerability profile. It has no known drug interactions. PRINOL

Generic : PPD Drug Class: Needs a Prescription: Indications:

Allopurinol Analgesics/ Uricosurics Yes (please see your doctor for proper supervision) Prophylaxis of gout and of uric acid and calcium oxalate renal stones. Prophylaxis of hyperuricemia associated with cancer chemotherapy. For dosage information of prescription medicine, please consult with your doctor. Acute attack of gout. Renal and hepatic impairment. Lactation. Aspirin and salicylates. ACE inhibitors or thiazide diuretics. Azathioprine, mercaptopurine, ciclosporin, sulfonylurea antidiabetics, theophylline and vidarabine. Skin rash (withdraw immediately), fever and chills, lymphadenopathy, leucopenia and leucocytosis, eosinophilia, arthralgia and vasculitis. Hepatotoxicity and altered liver function. Increase in acute attacks on start of treatment. Cap 300 mg , 100 mg .

Recommended Dosage: Contraindication: Precaution: Drug Interaction:

Side Effect:

Available Forms:

DIBENCOZIDE HERACLENE

FORMULATION: Each capsule contains dibencozide ...............1mg ACTIONS: Dibencozide increases the protein "efficiency coefficient", i.e., the percentage of "bound nitrogen" for protein build up in the body compared to "ingested nitrogen" with food intake. The initial sign of effectiveness is manifested by a marked increased in appetite.

Thus, dibencozide: facilitates optimum utilization of dietary protein intake contributes to the formation and repair of body tissues stimulates appetite INDICATIONS: Premature babies, low birth weight, retarded growth, poor appetite in infants, children and adults, adjuvant to treatment of tuberculosis and other chronic ailments, convalescence from acute infection or surgery, faulty nutrition in older people. DOSAGE: Premature babies and infants: 1 capsule daily (The capsule may be opened and the odorless, tasteless powder mixed with milk or juice). Children and adolescents: 2 to 3 capsules daily Adults: 3 capsules daily or as prescribed by the physician CAUTION: Food, Drugs, Devices and Cosmetics Act prohibits dispensing without prescription. AVAILABILITY: Box of 100 capsules Brand name: Moriamin Forte Generic name: Calcium pantothenic Indication: malnutrition, protein and vitamin deficiencies, anemia, convalescence, restoration and maintenance of body resistance, pregnancy and lactation, adjuvant in the therapy of peptic ulcer and TB. Drug classification: multivitamins and minerals Mechanism of action: Dosage: adult 1-2 cap/day; children 1 cap/day Special precaution: may color urine yellow Pregnancy risk category Adverse reactions: hypervitaminosis (large doses) Contraindications: contraindicated for patient s with malabsorption syndrome Form: cap 100 s Nursing responsibilities:  Assess patient for signs of vitamin deficiency before and periodically throughout

therapy. Assess nutritional status through 24 h diet recall. Determine frequency of consumption of vit rich foods

Sambong for treatment of kidney stone Written by Philippine Star Monday, 25 January 2010 11:22 Normal 0 false false false MicrosoftInternetExplorer4 st1\:*{behavior:url(#ieooui) } /* Style Definitions */ table.MsoNormalTable {msostyle-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-parent:""; msopadding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:10.0pt;

font-family:"Times New Roman"; mso-ansi-language:#0400; mso-fareast-language:#0400; mso-bidi-language:#0400;} Abdominal pain, blood in the urine, recurrent urinary infection (UTI). These are the most common complaints of Dr. Frederick Mendiola s patients suffering from kidney stones. Kidney stones are considered as one of the most common illnesses or disease affecting mostly middleaged Filipinos today. According to Mendiola, an invasive urologic surgeon at St. Luke s Medical Center Global City, about 50 to 60 percent of his patients are inflicted with kidney stones. Kidney problems are usually detected when a patients experiences abdominal pains and hematuria or blood in the urine, he says. However, there are also instances when a patient does not experience any of these. Instead, the most common symptom is a recurrent case of UTI. Therefore, it is highly recommended that patients visit a doctor regularly to prevent the illness. If left untreated, Mendiola says a patient may develop severe infection that will later affect the blood, leading to death. It may also lead to chronic renal failure, destroying the kidney and its function, which will result in lifetime dialysis or a kidney transplant, he adds. Although this illness is more common to occur in males, it is imperative for women to have themselves checked up once they feel any of the above-mentioned symptoms. To prevent kidney stones, Mendiola advises patients to avoid diets which are high in sodium and uric acid. Some examples of these diets include dairy products, beans, nuts and shellfishes. Aside from diet, patient with kidney stones also need something that will induce urine formation. He suggests drinking three to four liter of liquid a dat to prevent stone formation. When it comes to medications, Mendiola says potassium citrate and sodium bicarbonate are effective in treating this condition if combined with Sambong. Potasium citrate and sodium bicarbonate can be obtained from certain prescription drugs. On the other hand, an optimum amount of Sambong ca be obtained from Re-Leaf Forte, made of processed organic Sambong (Blumea balsamifera), a two-in-one medication that is not only anti-urolithiasis but a diuretic as well. Studies show that Sambong is effective in preventing calcium and uric acid kidney stone formation as well as in helping stones from lower urinary tract to pass spontaneously.

GENERIC NAME: Potassium Citrate BRAND NAME: Acalka CLASSIFICATION: Antiurolithic DOSAGE: 10 mEq MECHANISM OF ACTION: The aim of the treatment is to restore the level of the urinary citrate and to increase the pH of urine to 6-7, and to this end, the dosage pattern are: - In patients with slight hypocitraturia start the treatment with a dose of 30mEq (3 tabs/day, divided into 3 takings daily. It is recommended to take the tablets 30 minutes after meals. Approx 24 hrs after having started the treatment, make a determination of urinary citrate and pH, and adjust the dose in accordance with the needs of the patient. If necessary, the dose can be increased, though it is not advisable to exceed the dose of 100 mEq (10 tablets)/day. INDICATION: -Treatment of patients with renal lithiasis and hypocitraturia, chronic formers of calcium oxalate, phospate calculia. - Uric acid lithiasis alone or accompanied by calcium lithiasis CONTRAINDICATIONS: - Renal insufficiency Persistent alkaline urinary infections - Obstruction of the urinary tract - HyperpotassemiaAdrenal insufficiency

- Respiratory or metabolic alkalosis - Active peptic ulcer - Intestinal obstruction - Patients submitted to anticholinergic therapy - Patients with slow gastric emptying. SIDE EFFECTS/ ADVERSE EFFECTS: - Slight gastrointestinal disorders may appear which can be palliated by means of the joint administration of food. NURSING IMPLICATIONS/RESPONSIBILITIES: - The tablets must not be masticated or diluted. The active component of Acalka is contained with a porous wax matrix. As this was matrix is insoluble, it can be eliminated in visible form in the feces. The active component, however, has been released in the gastrointestinal tract. - Must not be administered to patients receiving potassium-sparing diuretics (traimterene, spirolactone, or amyloride). - It is advisable to carry out an evaluation of electrolytes (Na-K-Cl) and CO2, creatinine and hemogram every 4 hrs. - It is recommended that the patients in treatment with Acalka follow a diet w/o salt and increase the intake of fluids. - The recommended treatment in case of hyperpotassemia is: IV administratioin f 10% dextrose solution, containing 10-12 units of insulin/1000ml. Correction of the possible acidosis with IV sodium bicarboate and hemodialysis or peritoneal dialysis. GENERIC NAME FOR LANOXIN Digoxin 0.125mg, 0.25mg; scored tabs. LEGAL CLASSIFICATION: Rx PHARMACOLOGICAL CLASS FOR LANOXIN Cardiac glycoside. MANUFACTURER OF LANOXIN GlaxoSmithKline Pharmaceuticals INDICATIONS FOR LANOXIN Mild-to-moderate heart failure (with a diuretic and an ACE inhibitor when possible). Control of ventricular response rate in chronic atrial fibrillation. ADULTS AND CHILDREN: Individualize: see literature. Reduce dose in premature and immature infants. Children usually need proportionally larger doses (based on body weight or surface area) than adults. Use divided doses for children <10 yrs. Retitrate when changing formulations (esp. oral tabs to or from other dose forms). Lanoxicaps: if dose is 0.3mg/day, or if history of or predisposition to digoxin toxicity, or if compliance is not a problem, use divided doses. ALSO: LANOXICAPS LANOXIN INJECTION LANOXIN INJECTION PEDIATRIC CONTRAINDICATIONS FOR LANOXIN Ventricular fibrillation. WARNINGS/PRECAUTIONS FOR LANOXIN Renal dysfunction: reduce dose. Sinus node disease. Incomplete AV block. Accessory AV pathway (Wolff-Parkinson-White syndrome). Heart failure with preserved LV ejection fraction (eg, restrictive cardiomyopathy, constrictive pericarditis, amyloid heart disease, acute cor pulmonale, idiopathic hypertrophic subaortic stenosis). Electrical cardioversion. Acute MI. Toxicity risk increased by hypokalemia,

hypomagnesemia, hypercalcemia. Hypocalcemia may nullify effects. Thyroid disease. Hypermetabolic states. Monitor digoxin levels, electrolytes, renal function. Premature infants. Neonates. Pregnancy (Cat.C). Nursing mothers. INTERACTIONS FOR LANOXIN Toxicity risk increased by potassium-depleting drugs (eg, diuretics, amphotericin B, corticosteroids). Digoxin levels increased by antibiotics (eg, macrolides, tetracyclines), amiodarone, propafenone, quinidine, verapamil, indomethacin, itraconazole, alprazolam, spironolactone, drugs that reduce GI motility (eg, propantheline, diphenoxylate), thyroid antagonists, drugs that reduce renal function. Digoxin levels decreased by thyroid hormones, antacids, kaolin-pectin, cholestyramine, rifampin, sulfasalazine, neomycin, drugs that increase GI motility (eg, metoclopramide), some antineoplastics. Digoxin levels possibly affected by quinine, penicillamine, felodipine, others. Arrhythmias with sympathomimetics, succinylcholine, or rapid calcium infusion. Heart block with drugs that affect cardiac conduction (eg, calcium channel blockers, -blockers). ADVERSE REACTIONS FOR LANOXIN GI upset, anorexia, CNS effects (eg, blurred or yellow vision, or mental disturbances, confusion, headache, weakness, dizziness, apathy), gynecomastia, rash, heart block, arrhythmias (esp. children). HOW IS LANOXIN SUPPLIED? Tabs 100, 1000; Inj 0.25mg/mL (2mL amps) 10, 50; Inj Pediatric (1mL amp) 10; Lanoxicaps 100

RELATED DISEASE: CHF and arrhythmias {CHF and arrhythmias} Pathophysiology due to causes like dehydration,hypovolemic shock, urinaryobstruction, urea spliting organisms. decreased circulatory fluid volume increased concentration of urine formation of sedimentsin theurinary tract irritation and injury to the urinarytract inflammation and hematuria further increased concentration of urine and formation of stones in theureter accumulation of urine in theureter hydroureter formation of fish hooking of ureterbecause of accumulated water lodging of stonesin the ureter andkidney further injury to the nephones(nephritis) backflow of urine from ureter tokidneys. accumulation of water intokidney.( hydronphrosis) acute renalfailure Introduction Urolithiasis. The process of forming stones in the kidney, bladder,and/or urethra (urinary tract). Kidney stones are a common cause ofblood in the urine and pain in the abdomen, flank, or groin. Kidneystones occur in 1 in 20 people at some time in their life.

The pain with kidney stones is usually of sudden onset, verysevere and colicky (intermittent), not improved by changes in position,radiating from the back, down the flank, and into the groin. Nauseaand vomiting are common. Factors predisposing to kidney stonesinclude recent reduction in fluid intake, increased exercise withdehydration, medications that cause hyperuricemia (high uric acid)and a history of gout. Treatment includes relief of pain, hydration and, if there isconcurrent urinary infection, antibiotics. The majority of stones passspontaneously within 48 hours. However, some stones may not. Thereare several factors which influence the ability to pass a stone. Theseinclude the size of the person, prior stone passage, prostateenlargement, pregnancy, and the size of the stone. A 4 mm stone hasan 80% chance of passage while a 5 mm stone has a 20% chance. If astone does not pass, certain procedures (usually by a urology specialistdoctor) may be needed. The process of stone formation, urolithiasis, is also callednephrolithiasis. "Nephrolithiasis" is derived from the Greek nephros-(kidney) lithos (stone) = kidney stone "Urolithiasis" is from the Frenchword "urine" which, in turn, stems from the Latin "urina" and the Greek"ouron" meaning urine = urine stone. The stones themselves are also

called renal caluli. The word "calculus" (plural: calculi) is the Latin word for pebble. Medical Therapy and New Approaches to Urolithiasis Extracorporeal Shockwave lithotripsy, this technology hasreduced considerably the morbidity of stone disease, by allowingrelatively noninvasive removal of stones.Unfortunately, the facilitatedremoval of stones by ESWL has led some urologists to abandon ordisparage the medical approach to stone management. The propensityfor stone recurrence is not altered by removal of stones with ESWL.Ample evidence has accumulated, however, showing that a variety ofmedical treatments can prevent recurrence of stones. There have been notable advances in the medical managementof urolithiasis. A graphic display of stone risk factors is now availablecommercially. A step-by-step approach to diagnosis and treatment ofdifferent causes of urolithiasis was described in 1996. Step 1.History and minimum diagnostic tests Step 2. 24-hour urinary stone risk profile(cstomary diet) Identification of abnormal dietary risk factors Short-term dietary modification Step 3. Repeat stone risk profile after dietary modification Step 4. Elucidation of causes and construction of treatment options for abnormal risk factors A full 24-hour stone risk profile is measured on a random dietand fluid intake. Another stone risk profile is obtained after a short-term dietary modification. Anatomy and Physiology The urinary system which is also calledexcretory system or thegenitourinary system(GUS) is the organ systemthat produces, stores, andeliminates urine. Inhumans it includes twokidneys, two ureters, thebladder, and the urethra. The kidneys

are bean-shaped organs, which lie in the abdomen, rump or retroperitoneal to the organs of digestion, around or just belowthe ribcage and close to the lumbar spine. The organ is about the sizeof a human fist and is surrounded by what is called peri-nephric fat,and situated on the superior pole of each kidney is an adrenal gland.The kidneys receive their blood supply of 1.25 L/min (25% of thecardiac output) from the renal arteries which are fed by the abdominalaorta. This is important because the kidneys' main role is to filter watersoluble waste products from the blood. The other attachments of thekidneys are at their functional endpoints the ureters, which lies moremedial and runs down to the trigone of the bladder. Functionally the kidney performs a number of tasks. In its role inthe urinary system it concentrates urine, plays a crucial role inregulating electrolytes, and maintains acid-base homeostasis. The

kidney excretes and re-absorbs electrolytes (e.g. sodium, potassiumand calcium) under the influence of local and systemic hormones. pHbalance is regulated by the excretion of bound acids and ammoniumions. In addition, they remove urea, a nitrogenous waste product fromthe metabolism of proteins from amino acids. The end point is ahyperosmolar solution carrying waste for storage in the bladder prior tourination. Humans produce about 1.5 liters of urine over 24 hours, although thisamount may vary according to circumstances. Because the rate offiltration at the kidney is proportional to the glomerular filtration rate,which is in turn related to the blood flow through the kidney, changesin body fluid status can affect kidney function. Hormones exogenousand endogenous to the kidney alter the amount of blood flowingthrough the glomerulus. Some medications interfere directly orindirectly with urine production. Diuretics achieve this by altering theamount of absorbed or excreted electrolytes or osmalites, whichcauses a diuresis. In humans and other related organisms, the urinary bladder is ahollow muscular organ shaped like a balloon, located in the anteriorpelvis. The bladder stores urine. The maximum that it can hold is oneliter. It swells into a round shape when it is full and gets smaller whenempty. In the absence of bladder disease, it can hold up to 300 ml ofurine comfortably for two to five hours. The epithelial tissue associatedwith the bladder is called transitional epithelium. Normally the bladderis sterile. Sphincters (circular muscles) regulate the flow of urine from thebladder. The bladder itself has a muscular layer (detrusor muscle) that,when contracted, increases pressure on the bladder and createsurinary flow.

Urination is a conscious process, generally initiated by stretchreceptors in the bladder wall which signal to the brain that the bladderis full. This is felt as an urge to urinate. When urination is initiated, thesphincter relaxes and the detrusor muscle contracts, producing urinaryflow. The endpoint of the urinary system is the urethra. Typically the urethrain humans is colonized by commensal bacteria below the externalurethral sphincter. The urethra emerges from the end of the penis inmales and between the clitoris and the vagina in females. Synthesis of the Disease Urinary Calculi (Urolithiasis) are calcifications in the urinarysystem. Commonly called stones, calculi form primarily in the kidney(nephrolithiasis), but they can form in or migrate to the lower urinarysystem. They are typically asymptomatic until they pass into the lowerurinary tract. Stones are usually managed by an urologist. Primarilybladder calculi are rare and usually develop from a history of urinarystasis from obstruction or chronic infection. Up to 4% of the populations in the United States haveurolithiasis. About 12% of the male populations have a renal stones byage of 70 years. More than 200,000 Americans can requirehospitalization for treatment of stones each year. Many more peoplepass stones spontaneously with only minor manifestations that requireno treatment, whereas others are treated in an ambulatory setting. Therecurrence rate for calcium oxalate stones is about 5% within 5 years. The two primary causative factors are (1) urinary stasis and (2)supersaturation of urine with poorly soluble crystalloids. Increasedsolute concentration occurs because of fluid depletion or an increasedsolute load. This increased concentration leads to the precipitation of

crystals, such as calcium, uric acid, and phosphate. Urinary pHinfluences the solubility of certain crystals, with some crystal typesprecipitating readily on acid urine and some in alkaline urine. Inhibitor substances, such as citrate and magnesium, appear tokeep particles form aggregating and forming crystals; a lack ofinhibitors increases risk of stones development. Not only doesdeficiency of inhibitors but there are maybe anti inhibitors in theurine, such as aluminum, iron and silicone. Medication such asacetozolamide, absorbable alkalis (calcium carbonate and sodiumbicarbonate), and aluminum hydroxide. Massive doses of vitamin Cincreases urinary oxalate levels. Types of Calculi 1.Calcium most common substance and it is found in up to 90% ofstones. Calcium stones are usually composed of calciumphosphate or calcium oxalate. Peak onset is during a person s20s, and these stones affect primarily males. Hypercalciuria, is caused by four main components:

High rate of bone reabsorption, Paget s Disease,Hyperthyroidism, Cushing Disease, immobility, andosteolysis caused by malignant tumors.

Milk alkali syndrome, sarcoidosis and excessive intake of vitamin D

Impaired renal tubular absorption of filteres calcium, as in renal tubular acidosis

Structural abnormalities 35% of all clients do not have high serum levels of calcium

Increased intestinal absorption

Renal Leak of calcium, the other abnormality is causedby tubular defect. Hypocalcemia would increase PTHproduction thus increase intestinal absorption of calciumleading to increase calcium solute often called as CalciumWasters 2.Oxalate second major cause, most common in areas wherecereals are major dietary component and low dairy farmingregions.

Hyperabsorption of oxalate with inflammatory bowel disease and high intake of soy based products.

Postileal resection or small bowel bypass surgery

Overdose Vitamin C which metabolizes into oxalate

Familial oxaluria

Fat malabsoption which may cause Ca binding, thus freeing oxalate for absorption. 3.Struvite triple phosphate composed of carbonate andmagnesium ammonium phosphate. These are cause by certainbacteria, usually Proteus which contain enzymes urease. Thisenzyme split urea into to two ammonia molecules whichincreases the urine pH. Stones formed in this manner arestaghorn calculi 4.Uric Acid uric acid stones are caused by increased urateexcretion, fluid depletion, and low urinary pH. Hyperuricuria isthe result of either increased in uric acid production oradministration of uricosuric agents. 5. Cystine is the result of congenital metabolic error inherited asan autosomal recessive disorder. Cystine stones typically appearduring childhood and adolescence; development in adults is veryrare. 6.Xnathine stones occur as a result of a rare hereditary conditionin which there is a xanthine oxidase deficiency. This crystalprescipitates readily in an acid urine. Sign and symptoms

Pain- pain is the key symptom of the disease, which is usuallyresulted from an obstruction of a large rough calculi that occludethe opening to the ureters and increase the frequency and forceof peristaltic contractions. This is usually felt on thecostovertebral angle to the flank, to the suprapubic area going tothe external genitalia.

Nausea and Vomiting- usually accompanied by severe pain.

Fever- as a result of inflammatory processes

Hematuria- in the event that the stones abrade a ureters

Pyuria- resulted from pus formation due to tissue necrosis

Anuria- rarely happens but due to total occlusion of the passage to the ureters Medical Management Medications Absorptive Hypercalciuria Type I Thiazides are commonly used for the management of absorptivehypercalciuria Type I as these medications stimulate calciumreabsorption in the distal nephron, preventing formation of kidneystones by reducing the amount of calcium in the urine. Side effectsinclude decreased level of potassium, frequent urination, sexualdysfunction, and increased triglycerides. Orthophosphate and sodium cellulose phosphate reduce the absorptionof calcium from the intestines thereby reducing calcium in the urine.Neither sodium cellulose phosphate nor thiazide corrects the basic,underlying physiological defect in absorptive hypercalciuria.

Sodiumcellulose phosphate should be used in patients with severe absorptivehypercalciuria Type I (urinary calcium > 350 mg/day) or in thoseresistant to or intolerant of thiazide therapy. Side effects includeabdominal discomfort, nausea, and vomiting. Absorptive Hypercalciuria Type II Many patients show disdain for drinking fluids and excretingconcentrated urine. Normal urine calcium excretion would be restoredby dietary calcium restriction alone, and the increase in urine volumewould help reduce urinary saturation of calcium oxalate. Renal Hypercalciuria Thiazides are indicated for the treatment of renal hypercalciuria. Hyperoxaluria A high fluid intake is recommended to assure adequate urine volume inpatients with enteric hyperoxaluria. Calcium citrate may theoreticallyhave a role in the management of enteric hyperoxaluria. Thistreatment may lower urinary oxalate by binding oxalate in theintestinal tract. Calcium citrate may also raise the urinary citrate leveland pH. Side effects are constipation, gas, and increased calcium leak.Cholestyramine is also another method used to treat calcium oxalatestones. Side effects are rash, diarrhea, and increased liver enzymes. Use of potassium citrate in hyperuricosuric calcium oxalatenephrolithiasis is warranted since citrate has an inhibitory activity withrespect to calcium oxalate (and calcium phosphate) crystallization,aggregation, and agglomeration. Potassium citrate (30 to 60 mEq/dayin divided doses) may reduce the urinary saturation of calcium oxalate. Hypocitraturia For patients with hypocitraturic calcium oxalate nephrolithiasis,treatment with potassium citrate can restore normal urinary citrate,thus lowering urinary saturation of calcium and inhibitingcrystallization of calcium salts. Distal Renal Tubular Acidosis Potassium citrate therapy is able to correct metabolic acidosis andhypokalemia found in patients with distal RTA. Since urinary pH isgenerally elevated in patients with RTA, the overall rise in urinary pH issmall. Citrate is a significant urinary calcium stone inhibitor thatretards crystallization of calcium oxalate and calcium phosphate.Potassium citrate binds to calcium in the urine, preventing formation ofcrystals and raising the urinary citrate level and pH. Urinary pH shouldbe monitored periodically during citrate therapy because of excessive alkalinization. Side effects are mucous loose stools and minor GIcomplaints. Sodium citrate and citric acids are other alkalizing agentsused to prevent kidney stones by inhibiting stone formation throughalkalization. Potassium citrate therapy can significantly reduce the stone formationrate in these patients. The dose of potassium citrate is dependent onthe severity of hypocitraturia in these patients. Cystinuria The initial treatment program includes a high fluid intake and oraladministration of soluble alkali (potassium citrate) at a dose sufficientto maintain the urinary pH at 6.5 to 7.0. Potassium citrate is absorbedto prevent uric acid stones as it binds to calcium in urine, preventingformation of crystals. Sodium bicarbonate makes the urine less acidic,which makes uric acid or cystine kidney stone formation less likely.Possible side effects include increased formation of calcium-typestones, fluid retention, and sodium in blood. Urinary pH should bemonitored periodically during citrate therapy because excessivealkalinization may occur, which can increase the risk of calciumphosphate precipitation and stones. Sodium citrate and citric acid areother alkalizing agents used to prevent kidney stones by inhibitingstone formation through alkalization. Struvite (Infection) Lithiasis Acetohydroxamic acid (AHA) is a urease inhibitor that retards stone formation by reducing the urinary saturation of struvite. Drug-Induced Nephrolithiasis Ephedrine Calculi. There are no limited studies that address the management of these calculi. As with other calculi, a urine output of at

least two liters/day is recommended. Guaifenesin Calculi. As with ephedrine calculi, there are no limited studies regarding pharmacologic management of these calculi. Indinavir Calculi. Initial measures in the management of these calculi should focus on hydration and analgesia as well as drug discontinuation and substitution with another protease inhibitor. Xanthine Calculi. The medical management of xanthine calculi is limited because the solubility of these calculi is essentially invariablewithin physiologic pH ranges. Currently the recommendation includes afluid intake of at least three liters/day. If significant quantities of otherpurines are present in the urine, then urinary alkalization withpotassium citrate in the range of 6.0 to 6.5 is indicated to preventhypoxanthine or uric acid calculi. Nursing Care Management Encourage client to increase fluid intake Encourage client to schedule micturation Monitor intake of fluid amount and urinary output. Medicate for pain as prescribed. Continue antibiotic therapy as prescribed. Correct diet to include reduced protein and calcium content.

Das könnte Ihnen auch gefallen