Advanced Concept of Nursing- IIUNIT-VI

Advance Nursing Managementof Genitourinary (GU) Diseases.

In The Name of God

(A PROJECT OF NEW LIFE COLLEGE OF NURSING KARACHI)

UNIT-VIAdvance Nursing Managementof Genitourinary (GU) Diseases.

Shahzad BashirRN, BScN, DCHN,MScN (Std.DUHS)

InstructorNew 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. Acute renal failure (ARF)2. Chronic renal failure (CRF)3. Polycystic kidney disease (PKD)4. Nephritic Syndrome (NS)

2. Integrate pathophysiology and pharmacology concepts ofGenitourinary disease

3. Apply nursing process with support on Evidence-BasedNursing (EBN) to provide to the clients with Genitourinarydisorders

4. Discuss the holistic approach for nursing management of thepatient with Genitourinary diseases

5. Develop a teaching plan for a client experiencing disordersof the Genitourinary disorders.

• 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. Acute renal failure (ARF)2. Chronic renal failure (CRF)3. Polycystic kidney disease (PKD)4. Nephritic Syndrome (NS)

2. Integrate pathophysiology and pharmacology concepts ofGenitourinary disease

3. Apply nursing process with support on Evidence-BasedNursing (EBN) to provide to the clients with Genitourinarydisorders

4. Discuss the holistic approach for nursing management of thepatient with Genitourinary diseases

5. Develop a teaching plan for a client experiencing disordersof the Genitourinary disorders.

8/22/2016 2Shahzad Bashir, Lecturer NLCON

Terms• Azotemia– 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 flowbelow 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 renaldamage.

– Renal failure with clinical signs and symptoms

• Azotemia– 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 flowbelow 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 renaldamage.

– 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 wastesaccumulating 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 diseaseof 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)

• Definitions• Acute renal failure is a sudden reduction in

kidney function that results in nitrogenous wastesaccumulating 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 diseaseof 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 inflammation of the kidney, typically causedby 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 complexwhich becomes entrapped in between theendothelium and basement membrane or theepithelium and the basement membrane– Antibodies against the endothelial basement

membrane or the glomerular tissue bind to theirtarget antigen and can block filtration or causetissue injury in the long term (complement orphagocyte activation)

• Pathology–As antibodies build up, they bind antigen

resulting in an insoluble immune complexwhich becomes entrapped in between theendothelium and basement membrane or theepithelium and the basement membrane– Antibodies against the endothelial basement

membrane or the glomerular tissue bind to theirtarget antigen and can block filtration or causetissue injury in the long term (complement orphagocyte 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 tubulesof the kidneys. Common causes of ATN includelow 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)

• ATN is a medical condition involving the deathof tubular epithelial cells that form the renal tubulesof the kidneys. Common causes of ATN includelow 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 ofcasts leads to obstruction and increased intraluminal pressure, which reduces glomerularfiltration. Afferent arteriolar vasoconstriction, caused in part by tubuloglomerular feedback,results in decreased glomerular capillary filtration pressure. Tubular injury and increasedintraluminal 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 causethem to slough away from their basementmembrane and plug up the tubules (casts).–If the basement membrane remains intact a new

epithelium can grow repairing damage in 1-20days.

• Pathology• Each of these causes results in the death of

the renal tubular epithelium, which causethem to slough away from their basementmembrane and plug up the tubules (casts).–If the basement membrane remains intact a new

epithelium can grow repairing damage in 1-20days.

Classification of ATNIschemic ATN– Occlusion of tubular

lumens by casts of celldebris.

– Especially vulnerable arethe proximal tubule andthe thick ascending limb.

ATN due to poisoning• Most obviously effects the

proximal tubule– Necrosis and occlusions.

– Occlusion of tubularlumens by casts of celldebris.

– Especially vulnerable arethe proximal tubule andthe thick ascending limb.

AKI Phases• Initiation phase• Oliguric Phase:– 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

• Initiation phase• Oliguric Phase:– 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 overmonths to years; symptoms and signs occurwhen 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,

• Progressive irreversible azotemia develops overmonths to years; symptoms and signs occurwhen 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.

• 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.

–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 loopsin the glomeruli.

• Onset–Slowly progressive.–Unlike acute glomerulonephritis not due to

streptococcal infection.

• Inflammation and damage to the capillary loopsin 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 plasmaprotein permeability in the glomeruli resulting inexcretion of protein in the urine).

• 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 plasmaprotein permeability in the glomeruli resulting inexcretion 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

• Injury to the renal interstitial tissue due to a bacterialinfection (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. coliinfection originatingfrom fecalcontamination of theurinary tract.

•Onset–Most commonly

caused by E. coliinfection originatingfrom fecalcontamination of theurinary 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.

• 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

• 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 congenitalhepatic fibrosis2. Autosomal dominant (ADPKD)

– Simple renal cysts (adult)– Acquired renal cystic disease

• Polycystic kidney diseases:1. Autosomal recessive (ARPKD)

Classic infantile polycystic disease with congenitalhepatic fibrosis2. Autosomal dominant (ADPKD)

– Simple renal cysts (adult)– Acquired renal cystic disease

Autosomal Recessive Polycystic KidneyDisease ( ARPKD )

• Autosomal-recessive (childhood) polycystic kidneydisease (ARPKD) is genetically distinct from adultpolycystic 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

• Autosomal-recessive (childhood) polycystic kidneydisease (ARPKD) is genetically distinct from adultpolycystic 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

• 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 juvenileforms) may develop a peculiar type of hepatic fibrosischaracterized by bland periportal fibrosis and theproliferation of welldifferentiated biliary ductules, acondition now termed congenital hepatic fibrosis. Inolder children the hepatic disease is the predominantclinical concern. Such patients may develop portalhypertension with splenomegaly. Curiously, congenitalhepatic fibrosis sometimes occurs in the absence ofpolycystic kidneys and has been reported occasionallyin the presence of adult polycystic kidney disease.

• Patients who survive infancy (infantile and juvenileforms) may develop a peculiar type of hepatic fibrosischaracterized by bland periportal fibrosis and theproliferation of welldifferentiated biliary ductules, acondition now termed congenital hepatic fibrosis. Inolder children the hepatic disease is the predominantclinical concern. Such patients may develop portalhypertension with splenomegaly. Curiously, congenitalhepatic fibrosis sometimes occurs in the absence ofpolycystic kidneys and has been reported occasionallyin 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.

• Porter, P. A & Perry, A. G. (2003). BasicNursing: 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 30Shahzad Bashir, Lecturer NLCON

THANKSTHANKS THANKS

8/22/2016 31Shahzad Bashir, Lecturer NLCON