Question

Louis, a 60-year-old man, has not been feeling himself lately. He has been drowsy and fatigued. He becomes short of breath walking from one room to the next. On a recent visit, his daughter noticed that he seemed to be scratching a lot. His legs, ankles, and feet were extremely swollen, and his shortness of breath was becoming worse. He began to complain of chest pain and was immediately taken to the emergency room. A review of Louis’ medical history revealed that he was currently being treated for a urinary tract infection. His infection was resistant to the antibiotics with which he was initially treated. He began treatment with gentamicin 5 days ago. Physical examination confirms the observations of Louis’ daughter. A urinary catheter was placed in Louis’ bladder to determine urine output. A sample was sent to the laboratory for analysis. His urine analysis showed cloudy, dark urine. Casts were seen. A diagnosis of acute renal failure caused by nephrotoxic acute tubular necrosis (ATN) was made.

1. What is the pathophysiology associated with nephrotoxic ATN?

2. What is the most likely cause of Louis’ condition?

3. What are the clinical manifestations of pain that Louis demonstrates?

4. How can Louis be diagnosed?

5. What is the treatment for Louis?

6. What is Louis’s prognosis?

PLEASE BE AS Specific as possible

Answer 1

1.The tubule cell damage and cell death that characterise acute tubular necrosis usually result from an acute is chemical or toxic event.Nephrotoxic mechanisms of acute tubular necrosis include direct drug toxicity, intra renal vasoconstriction and intra tubular obstruction.

2.pre renal

Hypovolemia

Decreased cardiac output

Decreased peripheral vascular resistance

Decreased renovascular blood flow

INTRARENAL

Prolonged prerenal ischemia

Nephrotoxic injury

Interstitial nephritis

Acute glomerulonephritis

Thrombotic disorder

Toxemia of pregnancy

Malignant hypertension

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PoSTRENAL

Benign prostatic hyperplasia

Bladder cancer

Calculi formation

Neuromuscular disorder

Prostate cancer

Spinal cord diseases

Stricturesults

Trauma

3.decreases urinary output

Proteinuria

Casts

Decrease specific gravity

Decrease osmolality

Decrease urinary sodium

Heart failure

Hypotension

Pericarditis

Dysrhythmical

Pulmonary edema

Pleural effusion

Nausea

Vomiting

Anorexia

Stomatitis

Bleeding

Diarrhea

Constipation

Anemia

Leukocytosis

Lethargy

Seizure

Increase BUN

Increase creatinine

Decrease sodium

Increase potassium

Decrease PH

Decrease bicarbonate

Decrease calcium

Increase phosphate

4.history and physical examination

Identif I cation of precipitating causes

Serum creatinine and BUN levels

Serum electrolyte

Urinalysis

Renal ultra sound

Renal scan

CT scan or MRI

Retrograde pyelogram

5.treatment of precipitating cause

Fluid restriction

Nutritional therapy

Adequate protein intake (0.6_2g/kg/day)depending on degree of catabolism

Potassium restrictions

Phosphate restrictions

Sodium restrictions

Measure to lower potassium

Calcium supplement or phosphate binding agents

Parenteral nutrition

Enteral nutrition

Initiation of dialysis

Renal replacement therapy

6.acute renal failure died from severe electrolyte imbalance (hyperkalemia,acidosis )or from the ure Microsoft toxins themselves. Patient from ARF are at risk for numerous complications that may lead to death such as seizure, bleeding, coma.oliguria ARF patient continue to have a high mortality rate .patient withe non oliguric ARF tend to have a more favour able prognosis and are often easier to treat.

ARF usuallydevelops over hours or days with progressive elevation ofBUN,creatinine, and potassium with or without oliguria. Most commonly ARF follows severe prolonged hypotension or hypovolemia or exposure to a nephrotoxic agent.five percent to 7%of all hospitalized patients are affected.

Adequate protein intake (0.6_2

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