Question

Disease teaching

TOPIC:           Acute kidney injury

Write the following summary of the disease, making sure to include all of the points below. Your lesson should include:

• Pathophysiology of the disease: In your own words, write the pathophysiology of the disorder and relate the clinical manifestations of each back to the pathophysiology based on the information you taught your peer.

• Clinical manifestations of the disease (at least two assessment findings)

• Two nursing diagnoses: Discuss 2 nursing diagnoses common to patients and the interventions you chose for each diagnosis.

• Treatment plan (at least two interventions: intraprofesional and nursing care) and the rationale for interventions

• Four patient teaching points for this disease: Include the disease, the treatment plan, and the evaluation of the effectiveness of your teaching.

Answer 1

ANSWER:-

PATHOPHYSIOLOGY:-

The driving force for glomerular filtration is the pressure gradient from the glomerulus to the Bowman space. Glomerular pressure depends primarily on renal blood flow (RBF) and is controlled by the combined resistances of renal afferent and efferent arterioles. Regardless of the cause of AKI, reductions in RBF represent a common pathologic pathway for decreasing glomerular filtration rate (GFR). The etiology of AKI consists of 3 main mechanisms: prerenal, intrinsic, and obstructive.

In prerenal failure, GFR is depressed by compromised renal perfusion. Tubular and glomerular function remain normal.

Intrinsic renal failure includes diseases of the kidney itself, predominantly affecting the glomerulus or tubule, which are associated with the release of renal afferent vasoconstrictors. Ischemic renal injury is the most common cause of intrinsic renal failure. Patients with chronic kidney disease may also present with superimposed AKI from prerenal failure and obstruction, as well as intrinsic renal disease.

Obstruction of the urinary tract initially causes an increase in tubular pressure, which decreases the filtration driving force. This pressure gradient soon equalizes, and maintenance of a depressed GFR then depends on renal efferent vasoconstriction.

CLINICAL MANIFESTATIONS:-

Skin

Skin examination may reveal the following in patients with AKI:

• Livedo reticularis, digital ischemia, butterfly rash

• Palpable purpura: systemic vasculitis

• Maculopapular rash: Allergic interstitial nephritis

• Track marks (ie, intravenous drug abuse): Endocarditis

Eyes

Eye examination may reveal the following:

• Keratitis, iritis, uveitis, dry conjunctivae: Autoimmune vasculitis

• Jaundice: Liver diseases

• Band keratopathy (ie, hypercalcemia): Multiple myeloma

• Signs of diabetes mellitus

• Signs of hypertension

• Atheroemboli: Retinopathy (ie, Hollenhorst plaque in cholesterol microembolism)

Ears

Examination of the patient’s ears may reveal the following signs:

• Hearing loss: Alport disease and aminoglycoside toxicity

• Mucosal or cartilaginous ulcerations: granulomatosis with polyangiitis (Wegener granulomatosis)

Cardiovascular system

Cardiovascular examination may reveal the following:

• Irregular rhythms (ie, atrial fibrillation): Thromboemboli

• Murmurs: Endocarditis

• Pericardial friction rub: Uremic pericarditis

• Increased jugulovenous distention, rales, S₃: Heart failure

Abdomen

The following signs of AKI may be discovered during an abdominal examination:

• Pulsatile mass or bruit: Atheroemboli

• Abdominal or costovertebral angle tenderness: Nephrolithiasis, papillary necrosis, renal artery thrombosis, renal vein thrombosis

• Pelvic, rectal masses; prostatic hypertrophy; distended bladder: Urinary obstruction

• Limb ischemia, edema: Rhabdomyolysis

Pulmonary system

Pulmonary examination may reveal the following:

• Rales: pulmonary edema, infectious pulmonary process

• Hemoptysis: ANCA vasculitis, anti–glomerular basement membrane (anti-GBM, Goodpasture) syndrome

NURSING DIAGNOSIS :- 1. risk of ineffective gastrointestinal perfusion

                                       2. risk of ineffective kidney perfusion

TREATMENT PLAN :-

Risk of infection				Promotion against infection
				Control of infection
				Maintenance of dialysis access
Risk of inefficient gastrointestinal perfusion				Hydroetrolitic control
				Urinary elimination control
Inefficient risk of renal perfusion				Acid-base control
				Hemofiltration therapy
				Hemodialysis therapy
				Urinary elimination control
				Eletrolyte control
				Hidroeletrolyte control
Excessive fluid volume				Hypervolemia control
				Hydric control
				Hydric monitoring
Risk of electrolytic imbalance				Acid-base control
				Eletrolyte control
Risk for imbalanced fluid volume				Hydric control
				Hypervolemia control
Impaired gas exchange				Breathing physiotherapy
				Breathing monitoring
Risk of bleeding				Bleeding reduction
				Precaution against bleeding
				Blood products Administration
Impaired skin integrity				Positioning
				Injuries care
				Pressure ulcer prevention
				Skin supervision