Nursing homes and plans CLIENT KIDNEY FAILURE

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Nursing homes and plans CLIENT KIDNEY FAILURE

Nursing homes and plans CLIENT KIDNEY FAILURE

(Renal failure)
Renal failure or severe damage to total loss of kidney function. Kidney failure is the inability of the kidneys remove metabolic waste products and water, which then can cause dysfunction of all body systems. Kidney failure is classified into acute and chronic.
Acute renal failure usually occurs with acute renal failure cepat.Walaupun improved potential return, but the mortality rate due to renal failure is high enough and require further treatment.
Chronic renal failure and dangerous and should be done dialysis or transplantation in order to prolong life expectancy.
Acute Renal Failure (ARF)
Marked by a rapid decline of renal function with increasing azotemia (accumulation of nitrogen waste products such as BUN) and increased serum creatinine.
Uremia is a condition in which the occurrence of azotemia that is progress with accompanying symptoms. ARF is usually associated with decreased urine output of less than 400 ml / day, although the possibility of normal or increased urine output. There was no relationship between the number of products of urine and renal failure severity.
ARF usually occurs several hours or days with progressively increased BUN, increased creatinine, and potassium, with or without oliguria. More often ARF is more severe, long or hipovolumia hypertension or contact with agent neprotoxic.
Etiology and pathophysiology
The cause multiple and complex. Can be categorized into prerenal, intrarenal, and psotrenal.
Prerenal, ie factors beyond the kidney that reduce flow and increased renal adarah decreased glomerular perfusion and glomerular filtration. Hipovolumia can lead to decreased renal perfusion, as well as heart failure where the declining effectiveness of circulating blood volume. Treatment can be started including NSAID treatment sistesa where these drugs block prostaglandins, and angiotesinogen-converting enzyme (ACE) inhibitors, and block the synthesis of angiotensin II. Prerenal disease can lead to intrarenal disease (nekrotis tubules) if renal ischemic long experience. Prerenal is the most frequent causes of ARF, an average of 70% of all cases.
Intrarenal, which cause direct damage to the kidney tissue (parenchyma) which resulted in malfunction of the nephron. Intrarenal which is the cause averaging 25% of all cases of ARF. Primary kidney disease such as acute glomerulonephritis and acute pyelonepritis can lead to ARF. Lebi often is acute tubular nektorits (ATN = acute tubular necrosis) is a predisposisi.ATN can be caused by ischemia, nephrotoxin (eg antibiotics), hemoglobin that is released from erythrocyte hemolysis, or myoglobin released from muscle cells that nekrotis. Nephrotoxic chemicals and drugs can cause obstruction of intrarenal structure of the crystals or obvious damage to the epithelial cells of tubules. Many drugs that cause injury nephrotoxic aminoglycoside antibiotics and agents that radiocontras. Hemoglobin and myoglobin block the tubules and cause renal vasoconstriction.
Postrenal, including mechanical obstruction of urine flow. When experiencing blocking urine flow, urine back into the cup kidney, causing kidney failure. Which is mainly the cause of BPH, stones, trauma, prostate cancer, and other tumors. Due to this postrenal average amounts to less than 5% of all cases, and the highest incidence occurs in old age. This situation can usually be treated well if not a permanent kidney damage.
There are two main mechanisms that increase the incidence of ARF is renal ischemia and nephrotoxic injury. ARF caused by two things cause ATN. Severe renal ischemia results in impaired basement membrane and cause damage to epithelial tubules. Nephrotoxic agents mrenyebabkan necrosis of tubular epithelial cells, where the tubules become loose. ATN embran potentially reversible if the base is not undermined and if the necrosis of epithelial tubules have regenerated.
Pathological processes include:

Renal vasoconstriction. Hipovolumia and a decrease in renal blood flow stimulates the release of renin, which activates the angiotensin-aldosterone system that causes vasoconstriction of peripheral arteries and arterioles afferen kidney. With the decrease in renal blood flow, will reduce glomerular capillary pressure and GFR and tubular dysfunction mneyebabkan and oliguria occur.
Cellular edema. Ischemia causes anoksia, which will trigger the occurrence of endothelial cell edema. Edema cellular networks will increase pressure on capillary flow pressure so that blood flow through artriol impaired. Inadequate renal blood flow causes the depression of GFR.
Decrease in glomerular capillary permieabilitas. Ischemia would disrupt the glomerular epithelial cells and subsequent decline in glomerular capillary permeability and subsequently occurs enurunan GFR.
Intratubuler obstruction. When the tubule is damaged, there will be insterstitiel edema, and necrosis of epithelial cells accumulate in the tubules. Stacking is also the case of low GFR, by tubular obstruction and increased pressure intratubuler.
Leakage of glomerular filtration. Leakage of glomerular filtration will be back into the plasma through leakage from the tubular membrane damage, and then decreasing the flow of fluid intratubulus.

Incidence of clinic:
The clinic ARF became progressively through phase oliguria, diuresis, and recovery. In certain situations the patient can not recover from ARF, and will continue to be chronic renal failure.
Phase oliguria.
Manifestations that often occurs in ARF is oliguria caused by a decrease in GFR. Oliguria usually occurs within 1 to 7 days. If ischemia, oliguria occurs within 24 hours, but when nephrotoxic drugs then maybe start a little slow for several weeks. The existence of anuria (urine/24 output ≤ 400 ml h) and this rarely happens unless the trigger is a disorder that causes obstruction. (ARF nonoliguria may also occur. In these circumstances, the start can not clear with hipervolemia or abnormal increase in BUN occurred since the beginning). The duration of oliguria can berentang phase of several days to several weeks. In certain cases until a few months. The average length of 10-14 days, the prognosis is poor for the return of kidney function.
It is important to distinguish prerenal from oliguria oliguria of ARF. Prerenal oliguria no damage to the kidney tissue. Oliguria caused by a decrease in circulating blood volume (eg shock, burns, severe dehydration, decreased cardiac output) and is usually reversible. (Many cases failed to intrarenal also potentially reversible) with a decrease in the volume of blood circulation, autoregulation mechanisms such as increased angiotensin II, increased norpeineprin, ADH increased to meet the blood flow to the organs of the body. The occurrence of vasoconstriction with water and sodium retention. Prerenal oliguria characterized by elevated urine specific gravity and low salt concentrations.
In contrast, intrarenal oliguria characterized by normal urine specific gravity and high sodium concentration, indicated the existence of tubular injury that can no longer respond to the mechanism of autoregulation. Failed intrarenal oliguria caused by ATN in relation to ischemia or toxins are characterized by granules or inclusion of epithelial cells in the urine.
Manifestations of oliguria phase changes in urine output, fluid elektrolityang not normal, and occur uremia. Nurses should be cautious of signs of this phenomenon.
Changes in urination.
Decrease in urine output of less than 400 ml/24 hours. Urine visible blood mixed but usually not. Urine contains erythrocytes and leucocytes, urine enis weight of about 1010, and the urine osmolality at about 30 mOsm / kg (300 mmol / kg). These conditions indicate the existence of tubular damage with loss of the ability of concentration by the kidneys. Proteinuria can occur if the kidney failure associated with glomerular membrane dysfunction.
Fluid volume excess.
At the time of decreased urine output, fluid retention will occur in the body. Severity of symptoms depends on the spread of excess fluid. Appears to have distended neck veins, the pulse becomes more limited, and central and peripheral edema and hypertension occurs. Excess fluid can lead to congestive heart failure, pulmonary edema, and pleural effusions and pleural pericadium.
Metabolic acidosis
Kidney failure where the kidney can not synthesize ammonia, which is necessary in order meneksresi H, or issue a dimeabolsme acid. Serum bicarbonate levels decreased because bicarbonate is used to store Oin H. interruption occurs bicarbonate reabsorption and regeneration. The patient will experience respiratory kusmaul (fast, and in) to peningktan expenditure CO2.
Sodium balance.
Tubule damage can not store more sodium. So mengekresi urine sodium will increase, causing decreased serum sodium. Increased levels of sodium can be reduced presence hipervolemia (dilution hyponatremia). Excessive sodium intake should be avoided because it can increase the volume expansion, hypertension, and congestive heart failure.
Excessive potassium.
Potassium levels increase. Kidneys have the ability mengeksresi body potassium by 80 to 90%. In case of ARF due to massive tissue trauma, the damage will release additional cells into the extracellular potassium. Thus, patients with tissue injury will increase serum potassium levels. With acidosis may increase the movement of potassium from intracellular to extracellular fluid.
If potassium exceeding 6 mEq / L (6 mmol / L), immediate treatment to prevent the occurrence of cardiac arrhythmias. ECG appears to increase the T wave, QRS complex prolonged, ST depression. Otat jantun most tolerance when an increase in potassium suddenly.
Reduction of calcium and excess phosfat.
Low serum calcium levels as a result of decreased calcium absorption in the digestive system. Absorption of calcium from the gastrointestinal tract are activated by vitamin D. Only the kidneys to activate vitamin D yng so that the absorption of calcium from the gastrointestinal tract occurs. When calcium is released from bone by parathyroid hormone response, then phosfat also released. Increased serum caused a decrease ekresi phosfat by the kidneys. Normally found in plasma ionized calcium (physiologically active form) or a bond with the protein. In renal failure, hypocalcaemia occurred because acidosis mengskibatkan save a lot of calcium to form the ionization. Sometimes low levels of ionized calcium in serum causing tetany.
Accumulation of nitrogen products.
Kidney adalam Ogan main peembuangan urea, the end product of protein metabolism, creatinine, and metabolic end products of endogenous muscle. BUN and creatinine levels meningkatpada kidney failure. Increased BUN should be interpreted with due to dehydration and catabolism, caused by various factors such as infection, fever, severe injury, or gastrointestinal bleeding, which can increase BUN. Serum is the best indicator for kidney failure is not usually happen because creatinine interference by other factors as the BUN.
In fact, all body systems be affected in case of acute uremia syndrome.
Diuretic Phase
Diuretic phase begins gradually with increasing urine output per day from 1 to 3 liters / day, also to 3 to 5 L / day or lebih.Walaupun increased urine output, still not functioning nephrons penuh.Peningkatan urine volume caused by osmotic diuresis from high concentration of urea in the glomerular filtration and tubular inability to maintain concentration of urine. At this phase in which the kidneys recover their ability mengekresi trash but do not have the concentration of urine. In phase hypovolemia and hypotension may occur due to excessive fluid loss.
This stage uremia will occur are more severe, as evidenced by the presence of low creatinine clearance and increased serum creatinine and BUN. As a result of losing a lot of fluid and electrolytes, patients must be monitored the hyponatremia, hypokalemia, and dehydration. Phase diuretk more than 1 to 3 weeks. Near the end of this phase which the patient started normal acid-base balance, electrolytes, and waste products.
Phase recovery
Recovery phase begins when an increase in GFR which the BUN and creatinine levels began to stabilize and menurun.Walaupun even more elevated in the first 1 to 2 weeks of this phase, renal function will increase over 12 months after ARF.
Results from ARF affects the whole health of patients, severity of kidney failure, and the number and type of complications. The death rate due to ARF between 30 to 60%, depending on whether the patient megalami ATN and oliguria who have a risk of death by 50%. Deaths occurred as a result of infection. Infection occurs in 30% to 70% of individuals who experience ARF. The incidence of infection is increased in individuals who suffered injury from surgery or trauma that caused kidney failure.
Some patients do not recover and continues to be chronic renal failure. Old age is more ugly than the age of easy.
Diagnostic tests
Examination of urine is important for diagnostic tests, such as urine sediment with the content therein. Hematuria, pyuria, and the presence of crystals in urine may be associated with postrenal.
Ultrasound, renal scan, retrogradepyelogram, CT Scan and MRI can be considered for diagnostic tests.
Medical Treatment:
Therefore potentially reversible ARF, the main goal of treatment is to keep patients under normal conditions so that gainjal own improvement. Factors triggering the occurrence of ARF ditetntukan and repaired. Treatment is aimed at monitoring the symptoms and prevention of complications.
First step is to adequately maintain intravascular volume and cardiac output in order to ensure the inadequate perfusion of the kidney. Diuretic therapy is carried out throughout the volume expander to prevent excessive fluid. Diuretic therapy including furosemide (Lasix), edecrin, bumex, or osmotic diuresis (mannitol). Conservative therapy is required until renal function returned. Dialysis is generally done in order to memngurangi symptoms and prevent complications.
Caioran intake monitored closely during oliguria phase. Calculation of fluid returns by considering the expenditure within 24 hours (for example through the urine, diarrhea, vomiting, blood) plus 500 to 600 ml of IWL (eg through breathing, sweating). For example, if the patient's urine 300ml issued on Monday by without the loss of other fluids, the fluid returns on Tuesday by 800 to 900 ml.
Hyperkalaemia is one of the most dangerous complication in ARF can cause the occurrence of life threatening cardiac arrhythmias. Diberika therapy to reduce levels of potassium. Sodium polystyrene sulfonate (Kayexalate) can not be given to patients who experienced paralytic ileus.
Indications performed dialysis:
1. Excessive volume causing congestive heart failure and pulmonary edema.
2. Potassium levels above 6 mEq / L (6 mmol / L) in the presence of ECG changes.
3. Metabolic acidosis (serum bicarbonate levels less than 15 mEq / L (15 mmol / L)
4. BUN levels above 120 mg / dl (43 mmol / L)
5. The changes are significant mental sattus
6. Pericarditis, pericardium effusion, or cardiac tamponade.
7. Also required laboratory tests, and clinical assessment is needed as a guide to determine the need for dialysis.
Nutritional therapy
Furthermore, fluid restriction and nutritional therapy is determined by weight loss 0.25 to 0.5 kg / day of loss of tissue catabolism by the low protein diet. Patients who do not receive adequate nutrition, then katabiolisme protein the body will occur. This will increase the levels of urea, phosfat, and potassium. The main objective of nutrition therapy is to reduce body protein catabolism. Enough energy is obtained from the KH and fat source in order to prevent ketosis from fat-solving and gluconeogenesis from protein breakdown. Nonprotein calories provided each day (35 to 55 kkcl / kg body weight). Intake of protein is generally 1.0 to 1.5 g / kg. Provision of essential amino acids (eg Amin-Aid) can be given.
Potassium and sodium levels can be adjusted according to the plasma. Sodium restriction is needed to prevent edema, hypertension, and congestive heart failure. Patients received 30% to 40% of total calories from fat. When the gastrointestinal tract is not functioning, total parenteral nutrition (TPN) is more precise given to maintain adequate nutrition.
Nursing care
Assessment of nursing:
Includes a specific area. It is important to monitor blood pressure, pulse, frequency and pattern of breathing, and body temperature. Studied included general appearance of skin color, peripheral edema, distended neck veins, and the wound.
When done hemodialysis, examine blood vessels in the HD area for any possible signs of inflammation. The level of awareness needs to be studied. Oral mucosa is dry or inflamed. Lung must diauskultasi presence or ronchi Crackle. Heart sounds should be monitored for the existence of S3 sounds and murmurs. Results ECG possibility of arrhythmia. Including the volume of urine output, color uirne BD, the blood, glucose, and protein sediments.
Nursing Diagnosis:
1. Caian excessive volume associated with kidney failure and fluid retention
2. The risk of infection associated with invasive tinfdakan, urea poisoning and impaired immune response due to kidney failure.
3. Nutritional deficiencies; Less than needs associated with metabolic disorders and dietary restrictions.
4. Impaired sensory perception associated with urea poisoning and impaired fluid balance, electrolyte and acid-base balance.
5. Impaired thinking process related to the poisoning effect of urea on central nervous system.
6. Itegritas skin damage associated with HD installation location or peritonial dialysis and kidney failure.
7. Fatigue associated with anemia and urea poisoning.
8. Anxiety associated with the disease process, the action procedure.
9. The risk of complications: hyperkalemia associated decline in spending of potassium from the kidneys.
10. The risk of complications: arrhythmias associated with electrolyte imbalance.
Planning
The main purpose of the patient:
1. Recover completely without any disturbance of kidney function.
2. Maintaining fluid and electrolyte balance.
3. Lowering anxiety
4. obedient and aware of the need for further treatment.
Nursing action
Improved health.
Prevention of ARF is very important since the high mortality rate, therefore prevention efforts aimed at identifying and memitoring high-risk population, control the chemical industry and the drugs that are nephrotoxic, and prevention of prolonged hypotension and hypovolemia. At the hospital in patients who experience ARF berisikotinggi in patients who experienced massive trauma, major surgery, extensive burns, heart failure, sepsis, individuals who experienced renal insufficiency due to chronic diseases such as hypertension, diabetes mellitus, or systemic lupus erythematosus. Patients should be monitored carefully to the intake and output, fluid and electrolyte balance, and the possibility of blood transfusion reactions. Ekstrarenal the fluid loss from vomiting, diarrhea, bleeding, and increased IWL. Giving fluids immediately to prevent ischemia dasn tubular damage that relating to trauma, burns, and surgery. Recording intake and output were recorded and weighed and this weight as an indicator of body fluid volume state. Giving diuretics in patients who have excess body fluids need to be monitored because it can cause interference with the renal vein yag perfusion is inadequate.
Stretokokus infection are identified and given antibiotic treatment. Complications of streptococcal infections are acute glomerulonephritis and rheumatic heart disease.
In adult individuals with diabetes performed various diagnostic tests necessary precautions to avoid kidney failure. Industrial and agricultural chemicals and other products (organic solvent, insecticide, cleaning materials) should be monitored regularly in order to protect workers and residents in general. Individuals who frequently consume drugs at risk of nephrotoxic and should be monitored serum creatinine and BUN. Treatments that are nephrotoxic provided only with an effective dose and in a short period. The patient is prevented from excessive use of analgesics (mainly NSAID) as this could lead to kidney failure.
Immediate intervention.
Patients with ARF is a critical illness and suffered not only due to kidney disease but also nonrenal diseases (such as trauma, heart disease) that can mengkonstribusi renal failure. Nursing staff should give attention to patients with urine output did not forget the physical and emotional needs of patients. Patients and their families need help to understand the functions of the entire body that can cause kidney failure.
Nursing care helps maintain fluid and electrolyte balance, especially during the phase and phase olighuria diuretics. Observe and record the accuracy of fluid intake and output. Weigh the body weight every day is important to evaluate and detect an increase in weight or fluid loss (1 kg equal to 1000 ml of liquid). Nurses have pengetahuian enough about the signs and symptoms that lead to hipervolemia (in phase diuretics) or hypovolemia (in phase diuretics), hypernatremia or hyponatremia, hyperkalemia or hypokalemia and other electrolyte imbalances that can occur in ARF. Hyperkalemia is manifested by the existence of neuromuscular dysfunction, abdominal cramp, paralysis, and loss of tendon reflexes are signs of neuromuscular disorders. Cardiac conduction abnormalities that are known through the PR interval prolonged, QRS interval elongated, peaked T waves and ST segment depression.
Because infection is the leading cause of death in ARF, then action is required in every act of aseptic invasive. Nurses to be careful on local manifestation derngan infection (eg swelling, redness, pain) and systemic manifestations (eg, anorexia, malaise, lekositosis) because of increased temperatures may not occur in patients with renal failure. (Patients with renal failure often experience hypothermia). If antibiotics are used in the treatment of infection, be careful with the type and dose because of renal role mengeksresi various antibiotics.
Respiratory complications, particularly pneumonia, can be prevented. Humidified oxygen, intermittent positive-pressure-breathing, lying position changes, deep breathing, and ambulation should be considered in order to help maintain adequate respiratory ventilation.
Nurses and the prevention of decubitus skin needs to be done especially pdapasien who already have edema, and decreased muscle tone. Oral care necessary to prevent stomatiti, with the formation of ammonia (produced by bacteria from the breakdown of urea) in the saliva will irritate the mucous membrane of the mouth.
Ambulation and nurses at home.
Recovery from ARF depends of the condition of the patient's illness. The general condition and age of patient, duration of experienced oliguria phase, and help determine patient treatment pemulihan.Nutrisi good condition, resting, and restrictions aktiiftas needed to restore the patient's condition to the functional level. Diets high in calories, protein and potassium need to be regulated because they relate to kidney function. Patients should be informed of signs and symptoms of kidney disease recurrence, particularly manifestations of fluid and electrolyte imbalance. Recovery from diseases that take a long time is 3 to 12 months, causing financial and social constraints of family, therefore it needs to be consulted on a particular institution. Apibila ARF can not be solved then the patient will arrive in chronic renal failure.
Evaluation
Results are expected in ARF patients, patients will
1. restore and maintain fluid and electrolyte balance.
2. Following treatment progrm.
3. No complications of infection
4. have perfect recovery.
Chronic renal failure (chronic renal failure).
Nephron in chronic renal failure is damage to both kidneys that are progressive and irreversible. In which the body fails to maintain metabolism and fluid and electrolyte balance, leading to uremia (retention of urea and other nitrogen wastes in the blood). This can be caused by diseases such as diabetes sistemk melius, chronic glomerulonephritis, pyelonephritis, uncontrolled hypertension, urinary tract obstruction, hereditary lesions, infections, drugs or other toxic materials. Environmental and hazardous agents are emmpengaruhi chronic renal failure include lead, mercury, and chromium.
More than 80% of GFR (aimed at the measurement of creatinine clearance) which may be reduced but only little changes in body function. A person born with 2 million nephron and can sustain life with 20,000 nephron. Many cases where individuals are experiencing the early stages of chronic renal failure without knowing the condition of the disease experience of compensation where nephro nephron hypertrophy. At creatinine clearance below 10 ml / min (NORML 85 to 135 ml / min on average in adults), then dialysis or kidney transplantation is required for survival of patients.
Although it is not clear stages in chronic renal failure, progressive disease that can be divided into 2 stages
1. Diminished renal reserve. This stage is characterized him kreatini BUN and serum in the normal range, and did not show any symptoms.
2. Renal insufficiency. This stage occurs when the GFR of approximately 25% of normal. Levels of BUN and serum kreatini will increase. Easily feels tired and weak a symptom that is often perceived. Progressive renal failure, headache, nausea, and pruritus will occur as a result of loss of ability of the kidneys to concentrate urine.
3. End-stage renal disease (ESRD) or uremia. The final stage happens when the GFR is less than 5% to 10% of normal or creatinine clearance less darti 5 to 10 ml / min. At this stage, many patients who have difficulty in ADLnya because the influence of accumulation and development of symptoms.
Incident
In the United States over 290,000 individuals who have ESRD undergoing dialysis or transplant. This number doubled after 7 years. Every year 30,000 die of kidney disease. More adult patients experiencing ESRD. Prior to 1970, the most common cause of chronic renal failure are glomerulonephritis and interstitial nephritis. Similarly, diabetes mellitus and hypertension the most common cause leading to chronic renal failure in the U.S.. In Canada ESRD caused mainly by diabetes mellitus and glomerulonephritis ..
Manifestation klnik
As a result of impaired renal function, all organ function also disrupted. Clinical manifestations occur as a result of various substances, including urea, creatinine, phenols, hormones, electrolytes, water, and various other substances. Uremia is a syndrome that affects many body systems in patients with chronic renal failure.
Urinal system. At this stage of renal insufficiency, showed signs of polyuria which is caused by the inability of the kidneys concentrate the urine. Patients often wake up the night to urinate (nocturia). Therefore, a decrease in the ability of the kidneys in urine concentrate then found the BD urine gradually to around 1010. When kidney failure continues, which is found is the occurrence of oliguria, and subsequent anuria. If the patient is still producing urine, will be found of pyuria, and hematuria.
Metabolic disorders. Stacking the production of waste disposal. When the GFR decreases, there will be elevated levels of BUN and creatinine. BUN not only affect renal failure but also protein intake, fever, katabolisma rate. Kreatini serum and creatinine clearance as a consideration very accurate indicator of renal function than BUN. Increased BUN, nausea, vomiting, lethargi, fatigue, impaired thinking process, and head pain is a common complaint.
The decrease in muscle mass and decreased muscle aktiiftas therefore kreatini often found as final products in muscle metabolism.
Carbohydrate metabolism disorders. Ganggaun KH metabolism caused by impaired glucose utilization due to the insensitivity of cells in normal activity of insulin. Mild hyperglycemia, hyperinsulinemia, and glucose tolerance test will often encounter. Insulin and glucose metabolism can be increased (but not in normal values) after dialysis.
Individuals who have diabetes mellitus and uremia may have received less insulin than before the start of chronic renal failure. By insulin krena endogenik eksgenik and will circulate longer in the kidney who experienced kidney failure. Therefore, patients with diabetes need to be monitored carefully.
Increased triglycerides. Hyperinsulinemia stimulates prosduksi triglycerides in the liver, and assimilation reduced triglycerides by peripheral tissues. Many patients with uremia also had hyperlipidemia. Fat metabolism disorders associated with decreased lipoptritein enzyme lipase, which is an important enzyme to break down lipoproteins. Serum triglycerides usually do not decrease after dialysis began.
Electrolyte imbalance and acid-base balance.
Potassium, hyperkalaemia electrolyte of the most serious problem associated with kidney failure. Fatal arrhythmia which can occur when the serum potassium to be 7 to 8 mEq / L (7 to 8 mmol / L) hyperkalaemia occurs because removing kidney failure, cell protein breakdown and subsequent release of potassium, and acidosis which encourages the movement of potassium from intracellular to extra cells. Potassium is obtained from the diet, providing potassium, treatment, and infusion.
Calcium and phosphate. See explanation in ARF.
Sodium. Hypernatremia is likely to occur due to stuck in the water. Sodium can cause edema, hypertension, and congestive heart failure. Generally conducted dietary sodium restriction.
Metabolic acidosis.
Occurred because of the inability of the kidneys mengeksresi acid load (mainly ammonia) and the presence of disturbance and regeneration of bicarbonate reabsorption. The average adult produces 80 to 90 mEq of acid per day. Plasma bicarbonate biuasanya stable around 16 to 20 mEq / L (16 to 20 mmol / L). Generally not until below that level because of hydrogen ions produced is usually balanced by a buffer of demineralization of bone (phosphate buffer system). Respiratory kusmaul less prominent in chronic renal failure than in ARF, decreased breathing pattern in case of severe acidosis due to increased excretion of CO2.
Hematological System
Anemia, which is associated with chronic renal failure in the form normositik dilasifikasikan, and normochromic. The main cause of anemia adalahj declining production of the hormone erythropoietin by the kidneys, causing a decline erythropoiesis by bone marrow. Erythropoietin mensatimulasi memprosuksi bone marrow erythrocytes. Another factor that can cause anemia is a nutritional deficiency, increased erythrocyte hemolysis, frequent blood sampling for examination, and gastrointestinal bleeding. Many patients with renal failure have iron deficiency, in patients who are still being done HD, blood loss through dialysis can lead to anemia. Perningkatan parathyroid hormone levels (produced as a compensation for low serum calcium) may inhibit erythropoiesis, so that a short life span of erythrocytes.
Bleeding tendency, often bleeding in patients with uremia due to platelet disorders. Impaired platelet function led to the possibility of bleeding. Disorders of coagulation with increased concentrations of factor VIII and fibrinogen are found in the serum of patients.
Infection, a complication that caused changes in leukocyte function and impaired immune response. Menurunnnya response to the inflammatory response due to interference kemotaksis namely neutrophils and monocytes. Resopon cellular and humoral immune depressed also characterized by the presence limfopenia, atrophy of lymphoid (particularly thimus gland), decreased antibody production and hypersensitivity response suppression late. Other factors that could cause infection is protein malnutrition, hyperglycemia, and external trauma (eg, catheter placement, injection).
Cardiovascular system
In general due to hypertension, which is usually caused by sodium retention and increase in intracellular fluid volume. In some individuals, increased production of renin will help spur the interference with the heart. Hypertension that accelerate atherosclerotic vascular disease, causing intrarenal artery spasm, and even increases the occurrence of left ventricular hypertrophy and congestive heart disease. Hypertension also cause retinophaty and encephalopahty.
Congestive heart disease and left ventricular hypertrophy can cause pulmonary edema. Peripheral edema is also usually the case. Cardiac arrhythmia caused by hyperkalemia, hypokalemia, and decreased coronary artery perfusion.
Uremic pericarditis that occurred which developed into the pericardium effusion and cardiac tamponade. Pericarditis manifested the sound of friction (friction rub), chest pain, and fever.
Perubaan blood vessels due to hypertension of the old and the incidence of atherosclerosis due to elevated triglyceride levels that are many causes of heart complications (eg myocardial infarction, stroke).
Respiratory system,
The occurrence of respiratory Kusmaul, dyspnea due to congestive heart failure, pulmonary edema, uremic pleuritis, pleural effusion, and other respiratory infections. It appears thick sputum, and the cough reflex suppression. Uremic lung are often found in chronic renal failure and edema appear intestitial on chest x-ray.
Gastrointestinal System
Every part of the digestive system is affected due to inflammation of the intestinal mucosa due to excessive urea. Mucosal ulceration found in the gastrointestinal tract caused by the increase of ammonia by bacteria that break diprodsuksi urea. Often found any stomatitis, metallic taste in mouth feel, the smell of urea. Anorexia, nausea, and vomiting caused by irritation of the gastrointestinal tract by production of waste disposal in losing weight. Diarrhea disebbkan by hyperkalemia and calcium metabolism disorders.
Neurological system. Occur due to excessive waste waste products, electrolyte imbalance, and atrophy of axons and demyelination of nerve fibers. Increased levels of urea affect axon damage.
Central nervous system depression caused lethargi, apais, decreased ability to concentrate, fatigue, and gangguna mental abilities. Seizures and coma occur rapidly due to increased BUN and hypertension encephalophaty.
Musculoskeletal system
Renal osteodystrophy in which as a result of disturbances of calcium and phosphate metabolism. When GFR decreases the phosphate is not excreted from the kidneys resulting in increased serum phosphate.
In normal kidneys metabolize vitamin D into the active form. Active form of vitamin D needed for calcium absorption from the gastrointestinal tract. In failing gnjal where renal failure activates vitamin D and absorption was down, so the serum calcium neurun. The low serum calcium stimulating hormone parairoid, causing reabsorption of calcium and phosphate from bone.
Changes due to increased retention of phosphate, calcium reabsorption from bone, absorption of calcium is inadequate, and increased parathyroid hormone, leads to:
1. Osteomalacia, suatukondisi reduced mineralization of bone formation. And can result in hypocalcaemia. It can also cause the accumulation of aluminum. The main source of aliminum is aliminum-alkaline phosphate bond. Decrease the use of bonding aluminum phosphate-base and will happen osteomalacia.
2. Osteitis fibrosa. Kalisum result of bone reabsorption and formation of fibrotic tissue. The occurrence of osteitis fibrosa due to elevated levels of parathyroid resulting homrmon tualng reabsorption.
3. Metastatic calcification. Caused by calcium-phosphate deposits in soft tissues of the body, namely the blood vessels, joints, muscles, heart muscle, and eye. Uremic-red-eye is caused by irritation due to calcium-phosphate deposits in the eye. Metastatic calcification in arteries fingers and toes can lead to gangrene. May inhibit calcification intrakardial mneyebabkan conduction system and cardiac arrest.
Integumentary System.
Yellowish skin as a result of changes in absorption and retention of urinary chromogen that normally gives color to the urine. The skin appears pale due to anemia, dry and berisisk because menurunnnya akitifitas oil and sweat glands.
Pruritus due to a combination of dry skin, calcium-phosphate deposits in the skin, and sensory neuropathy. Skin infections due to scratching because of perceived skin itching. Hair becomes dry and fall off easily. The existence of petechiae and ekimosis occur because of interference permbekuan.
Reproductive System
Characterized by infertility and decreased libido. Women have decreased levels of estrogen, progesteon, and lutein hormone, causing mestruasi anovulation and amenorrhea occurred. In men megalami decrease in testosterone, and low sperm count. The presence of sexual dysfunction in both sexes due to the anemia which causes fatigue and decreased libido. Peripheral neuropathy can cause impotence in men and anorgasme in women. Other factors that affect the libido are psychological factors (eg anxiety, depression), physical stress, and the effect of treatment.
Endocrine System
Hypothyroidism occurs where decreasing levels of T3 and T4 .. not clearly known why this occurs.
Psychological changes
Changes in personality and behavior, emotional instability, withdrawal, and depression usually occur. Changes in self image due to edema, disruption of integument, and installation of equipment (eg fistula, a catheter) will cause anxiety and depression. Decrease in concentration and the decreased ability to make the patient's mental akitiftas ampak silent, and less attention to their environment. Aadanya changes in lifestyle, occupation, family responsibilities, and financial status. Patients experiencing dependence on medication, diet restriction, dialysis, and possible kidney transplant. Patients will feel the loss of kidney function. In some patients it megalami this condition for a long time.
Medical Treatment
Conservative treatment is not for the treatment of disease but to prevent the development of disease. There are 5 goals in patients with chronic renal failure of medical menanganan:
1. Maintaining kidney function.
2. Avoid / postpone dialysis or a transplant done done sejauhmemungkinkan.
3. Maintaining a body chemical
4. Manangani various symptoms
5. provide optimal quality of life in patients and their families.
Treatment of pruritus with salf, lotion, antihistamines, ultraviolet irradiation. Subtotal parathyroidectomy, and dialysis measures to reduce the symptoms very effectively done oada many patients.
Neurological manifestations conducted security to prevent the patient from an accident. Giving sedativa anticonvulsants and can be used.
Provision of water-soluble vitamins are usually given. Sulphate of iron and vitamin C is used only if anemia occurs.
Settings fluid and sodium is important in patients with congestive heart failure.
Antihypertensive drug treatment, performed pericardial drainage in patients with cardiac tamponade (fluid in the pericardium).
Rendak dietary protein, nonprotein calories given to prevent or reduce catabolism. Diets low in salt and potassium. Adequate calcium intake if low levels of calcium, providing calcium carbonate, calcium lactate, or calcium gluconate.
Dialysis, there are two kinds of dialysis and hemodialysis peritonial. On an ongoing disease, dialisisi be performed continuously in order to control uremia.
The purpose of dialysis therapy:
1. Pengeluarkan peroduk end of protein metabolism, such as urea and creatinine from the blood.
2. maintain a safe concentration of serum electrolytes.
3. Improving acidosis and increased blood bicarbonate buffer system.
4. Removing the excess fluid from the blood.
Nursing care
Assessment
If the patient has chronic renal failure, the nurse should obtain complete information, and give attention to the presence of risk factors. Iformasi about the treatment of past and present, diet, and a change in body weight, energy level and pattern of urinary elimination.
Nurses assess patients with chronic renal failure influences on the cardiovascular system of the body such as tau respiratory, neurological changes, gastrointestinal problems, and skin changes.
Nurses need to assess the patient's understanding of pernyakitnya, diagnostic tests conducted. What is the level of anxiety and ability to adjust to chronic illness and its treatment.
When a client is set to dialysis, the nurse examines pemahamannnya about treatment programs that will be undertaken. If done hemodialysis, studies conducted on the location of the stabbing the possibility of blockage or infection.
If the client receives a kidney transplant, is necessary to study the level of understanding related to procedure and folow-up.
Nursing Diagnosis
1. Excess fluid volume associated with the inability of the kidneys remove fluid, inadequate dialysis, excess fluid intake characterized by edema, hypertension, weight gain, shortness of breath, pulmonary edema.
Goal: Patient will maintain adequate fluid balance remains marked by tiudak of the edema, no dyspnea, body weight within the ideal blood pressure within normal limits.
Action:
· Monitor increase in blood pressure, periorbital and peripheral edema, dyspnea and a pericardial friction rub (as an indicator of excess fluid).
· Auscultation lung there may Crackle (identify the fluid in the lungs)
· Teach the patient how to maintain a low-salt diet (helps control edema and hypertension)
· Teach the patient to control the fluid and the importance pemimbangan body weight daily (to help monitor and control the excess fluid and is associated with hypertension).
· Teach the patient on hemodialysis or peritoneal dialysis and how to weight the expected (to help maintain a good fluid balance).
· Provide skin care, especially diarea edema (in the area at risk of skin damage).
2. Less than the needs of nutritional deficiencies associated with membatasan certain nutrients (especially proteins), nausea, vomiting, anorexia, stomatitis, and nutritional metabolic disorders characterized by decreased appetite, weight loss, electrolyte balance disorders.
Goal: Patient will demonstrate adequate nutrition remains characterized by ideal body weight were maintained, and albumin and total protein levels within acceptable limits.
Action:
· Monitor weight, BUN, serum creatinine, albumin, total protein, serum electrolytes (indicator of the effectiveness of dialysis, nutritional status, and response to treatment).
· Give oral care on a regular basis (preventing stomatitis, prevent bad breath, improve patient comfort.)
· Leave ate a little, but often (eat in poersi bit will prevent the occurrence of nausea and vomiting).
· Leave a chance for patients to specify the type of food and fluid intake as instructed (improving self-control patients).
· 2000-2500 Give pic / day with a high carbohydrate (to minimize protein catabolism and maintain body weight).
E. Avoid protein and phosphate according to the instructions (reducing merabolisme and product urea, potassium, phosphate, and hydrogen ions).
3. Activity intolerance related to uremia and anemia due to blood loss during dialysis is characterized by fatigue, shortness of breath, pale, dyspnea, tachycardia.
Objective: Patients will participate in a treatment program / treatment, with the criteria of hematocrit within normal limits, able to perform ADL without any complaint tired.
Action:
· Monitor hematocrit and hemoglobin (an indicator of oxygen transport kapasiatas)
· Give iron between meals and also eritpropoietin accordance with the instructions (to maintain normal erythropoiesis and stimulates production of erythrocytes).
· Give vitamin C before and during undergo hemodialysis (Vitamin will come out during dialysis).
· Provide adequate rest (energy required to ADL)
· Prevent blood loss during dialysis and note the possibility of bleeding diarea puncture (haemorrhage will decrease eristrosit and reduces the body's oxygen demand)
· Teach in planned activities (in order to avoid fatigue)
· Assess the patient's response activities (necessary to restructure the program the next activity.)
4. Damage to the integrity of the skin associated with decreased aktiiftas oil glands and sweat glands, accumulation of calcium-phosphate, excess fluid, and neuropathy is characterized by complaints of itching, sores, dry skin, edema and ekskoreasi.
Objectives:
Clients maintain the integrity of the skin remains intact, with the criteria is not itchy, keep skin moist, clean skin.
Action:
· Kaji examine the possibility of a change in skin color, texture, turgor, and vascularization (memberika instructions for proper care.)
· Examine the possibility of injury Ananya, purpura, and signs of infection (early detection of signs of problems)
· Give your skin care with a compress with water, or lotion (to reduce itching, and skin stays moist)
· Give antihistamines and antipruritis (reduce itching)
· Nails cut short and kept clean (reduces skin damage from scratching and prevent infection)
· Monitor serum calcium and phosphate (elevated calcium-phosphate as the originator of disorders of the skin).
READING MATERIAL

Lemone & Burke (1996), Medical-surgical nursing: Critical thinking in client care, Menlo Park: Addison-Wesley
Lewis, Hettkemper & Dirksen (2000), Medical-surgical nursing: Assessment and Management, od clinical problems (6th.ed), St.Louis: Mosby.
Polaski & Tatro (1996), Core Principles and Practice of Medical-Surgical Nursing, Philadelphia: WbSaunders Company.

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