In The Name of God (A PROJECT OF NEW LIFE COLLEGE OF NURSING KARACHI) Advanced Concept of Nursing- II UNIT-VI Advance Nursing Management of Genitourinary (GU) Diseases. Shahzad Bashir RN, BScN, DCHN,MScN (Std.DUHS) Instructor New Life College of Nursing July 27, 2015
Objectives At the end of the unit, students will be able to: 1. Utilize Functional health pattern to identify patients problems related to Genitourinary disorders including: 1. 2. 3. 4. Acute renal failure (ARF) Chronic renal failure (CRF) Polycystic kidney disease (PKD) Nephritic Syndrome (NS) 2. Integrate pathophysiology and pharmacology concepts of Genitourinary disease 3. Apply nursing process with support on Evidence-Based Nursing (EBN) to provide to the clients with Genitourinary disorders 4. Discuss the holistic approach for nursing management of the patient with Genitourinary diseases 5. Develop a teaching plan for a client experiencing disorders of the Genitourinary disorders. 8/22/2016 Shahzad Bashir, Lecturer NLCON 2
Azotemia Terms Elevation of blood urea nitrogen (BUN) and creatinine levels largely related to a decreased GFR Prerenal azotemia is encountered when there is hypoperfusion of the kidney, BUN: creatinine ratio > 15:1 Examples: dehydration (e.g., diarrhea, vomiting, diuretics), congestive heart failure, shock Renal azotemia (uremia): BUN:creatinine ratio < 15:1 Examples: acute tubular necrosis, chronic renal failure Postrenal azotemia is seen when there is obstruction of urine flow below the level of the kidney. BUN: creatinine ratio > 15:1 Example: prostatic hyperplasia with obstruction of urethra Renal failure detectable only by lab tests Uremia Azotemia characterized by failure of renal excretory function in addition to metabolic and endocrine alterations resulting from renal damage. Renal failure with clinical signs and symptoms
Acute renal failure Definitions Acute renal failure is a sudden reduction in kidney function that results in nitrogenous wastes accumulating in the blood. Rapid decline in renal function with an accumulation of BUN and Creatinine. Sudden interruption of kidney function resulting from obstruction, reduced circulation, or disease of the renal tissue The kidney abruptly stops working entirely. They can recover to normal function by medical treatment especially : Acute glomerulonephritis Acute tubular necrosis (ATN)
AKI - RIFLE Criteria The criteria fulfilled by changes in serum creatinine relative to baseline.
Causes of AKI
Conti..
Acute Glomerulonephritis Acute inflammation of the kidney, typically caused by an immune response. Caused by abnormal immune reaction that damages the glomeruli. Symptoms Hematuria (blood in urine). Oliguria (little urination). Mild hypertension. Proteinuria. Edema.
Acute Glomerulonephritis Pathology As antibodies build up, they bind antigen resulting in an insoluble immune complex which becomes entrapped in between the endothelium and basement membrane or the epithelium and the basement membrane Antibodies against the endothelial basement membrane or the glomerular tissue bind to their target antigen and can block filtration or cause tissue injury in the long term (complement or phagocyte activation)
Robbins Basic Pathology 14-3
Acute Tubular Necrosis (ATN) ATN is a medical condition involving the death of tubular epithelial cells that form the renal tubules of the kidneys. Common causes of ATN include low blood pressure and use of nephrotoxic drugs. Most common cause of acute renal failure. Destruction of the epithelial cells in the renal tubules. Ischemia: shock, sepsis, burns, transfusion, other. Poisoning/ Toxic: Toxins: drugs, metals, poisons, solvents Medications (tetracyclines)
Acute Tubular Necrosis Pathogenesis: sloughing and necrosis of epithelial cells results in cast formation. The presence of casts leads to obstruction and increased intraluminal pressure, which reduces glomerular filtration. Afferent arteriolar vasoconstriction, caused in part by tubuloglomerular feedback, results in decreased glomerular capillary filtration pressure. Tubular injury and increased intraluminal pressure cause fluid backleak from the lumen into the interstitium.
Conti. Pathology Each of these causes results in the death of the renal tubular epithelium, which cause them to slough away from their basement membrane and plug up the tubules (casts). If the basement membrane remains intact a new epithelium can grow repairing damage in 1-20 days.
Classification of ATN Ischemic ATN Occlusion of tubular lumens by casts of cell debris. Especially vulnerable are the proximal tubule and the thick ascending limb. ATN due to poisoning Most obviously effects the proximal tubule Necrosis and occlusions.
Initiation phase Oliguric Phase: AKI Phases Decreased GFR causing oliguria (less than 400 ml per 24 hours) or anuria Elevated BUN and Creatinine Diuretic phase: Begins with gradual increase in UO; may last 1-3 weeks 1-3 liters/day--up to 3-5 L/day Kidneys have recovered ability to excrete waste but not to concentrate urine Uremia may still be severe Recovery phase: Begins when GFR increase so that BUN and Creatinine stabilize, then decrease Renal function can improve over 12 months Some progress to CRF
Chronic Renal Failure Progressive irreversible azotemia develops over months to years; symptoms and signs occur when GFR is less than 10-15 ml/min. Progressive loss of nephrons that gradually leads to kidney failure. Causes : Chronic Glomerulonephritis Chronic obstructive pyelonephritis Diabetic Mellitus, Hypertension,
Conti.
Chronic Renal Failure Four stage process Diminished renal reserve GFR is ~50% of normal Patients are asymptumatic. Renal insufficiency GFR is 20-50% of normal. Symptoms include anemia, polyuria, and nocturia.
Conti. Renal failure GFR <20-25% of normal. Kidneys can not regulate volume or solute concentration. As a result patients develop edema, acidosis, and hypocalcemia. Overt uremia (accumulation of urea, uric acid, and creatinine). End-stage renal disease. GFR is <5% of normal. Loss of kidney function to the point at which the person must have a kidney transplant or dialysis treatment.
Chronic Glomerulonephritis Inflammation and damage to the capillary loops in the glomeruli. Onset Slowly progressive. Unlike acute glomerulonephritis not due to streptococcal infection.
Chronic Glomerulonephritis Pathology Begins with a precipitation of antigen-antibody complexes. Result in inflammation and thickening of the membranes. Ultimately leading to fibrosis of the glomeruli. In the late stages the glomerular capillary filtration coefficient. Decreased number of filtering capillaries. Thickening of the membrane. Can lead to nephrotic syndrome (increased plasma protein permeability in the glomeruli resulting in excretion of protein in the urine).
Chronic Obstructive Pyelonephritis Injury to the renal interstitial tissue due to a bacterial infection (Acute pyelonephritis). Infection usually derived from bacteria that has traveled from the bladder.» Urinary Tract Infection Recurrent infections superimpose on one another. Obstruction predisposes kidney to additional infections. Symptoms Back pain Fever Pyuria Dysuria
Chronic Obstructive Pyelonephritis Onset Most commonly caused by E. coli infection originating from fecal contamination of the urinary tract.
Conti. Chronic tubulointerstitial inflammation with renal scarring. Important cause of end-stage renal disease. Two forms: reflux-associated: common, congenital vesicourtehral reflux or intrarenal reflux. obstructive: posterior urethral valves, ureteral calculi or abnormalities.
Polycystic kidney Fluid filled spaces within the kidney May involve cortex or medulla or both May be unilateral or bilateral May be unilocular or multilocular May be congenital or acquired May be sporadic or genetically determined Clinical significance may be trivial or grave
Classifications of Polycystic Kidney Polycystic kidney diseases: 1. Autosomal recessive (ARPKD) Classic infantile polycystic disease with congenital hepatic fibrosis 2. Autosomal dominant (ADPKD) Simple renal cysts (adult) Acquired renal cystic disease
Autosomal Recessive Polycystic Kidney Disease ( ARPKD ) Autosomal-recessive (childhood) polycystic kidney disease (ARPKD) is genetically distinct from adult polycystic kidney disease. Rare, 1:6-14000 live births Abnormal gene (PKHD1) located on chromosome 6p21 p23, PKHD1 gene encodes a large protein, fibrocystin. May be still born or neonatal death due to pulmonary insufficiency
ARPKD (Cont.) Enlarged but normally shaped pelvi-calyceal system Normal reniform shape complete with fetal lobation & normal sized (undilated) ureter Normal glomeruli and tubules Normal interstitium and no dysplasia Congenital hepatic fibrosis is almost always present Normal numbers of nephrons, no interstitial fibrosis and no dysplasia
Patients who survive infancy (infantile and juvenile forms) may develop a peculiar type of hepatic fibrosis characterized by bland periportal fibrosis and the proliferation of welldifferentiated biliary ductules, a condition now termed congenital hepatic fibrosis. In older children the hepatic disease is the predominant clinical concern. Such patients may develop portal hypertension with splenomegaly. Curiously, congenital hepatic fibrosis sometimes occurs in the absence of polycystic kidneys and has been reported occasionally in the presence of adult polycystic kidney disease.
References Porter, P. A & Perry, A. G. (2003). Basic Nursing: Essentials for practice (5th ed.) St. Louis: Mosby. Erb, G. K., (2000). Fundamentals of Nursing: Concept, process and practice (5th ed.). Addison: Wesley. Bruner, L.S., & Suddarth, D.S. (2001). Text book of Medical-Surgical Nursing (9th Ed.). Philadelphia: Lippincott. 8/22/2016 Shahzad Bashir, Lecturer NLCON 30
THANKS 8/22/2016 THANKS Shahzad Bashir, Lecturer NLCON 31