MEDICAL-SURGICAL

NURSING

Arni A. Magdamo, MD, MHA, MBA, FPCP

University of the Philippines
College of Medicine
 MANAGEMENT OF
PATIENTS WITH GUT
DYSFUNCTION
 MANAGEMENT OF
PATIENTS WITH GUT
DYSFUNCTION

REVIEW OF THE
GENITOURINARY SYSTEM
THE URINARY SYSTEM
 The urinary system consists of the kidneys,
ureters, urinary bladder and urethra.
 The urinary system eliminates wastes,
controls blood volume regulates blood ion
concentration and pH, and regulates blood
cell production.
THE KIDNEYS
 Each kidney is behind the peritoneum, and
surrounded by a renal capsule and a renal
fat pad.
 The ureter expands to form the renal pelvis
within the renal sinus, and the renal pelvis
has flower-like extensions called renal
calyces.
 The kidney is divided into an outer cortex
and an inner medulla. Each renal pyramid
in the medulla has a base that extends into
the cortex. The apex of each renal
pyramid projects to a calyx.
The Kidneys and the Nephron
THE NEPHRON
 The functional unit of the kidney is the
nephron.
 The parts of the nephron are the renal
corpuscle, the proximal convoluted tubule,
the loop of Henle, and the distal convoluted
tubule.
 The filtration membrane is formed by the
glomerular capillaries, the basement
membrane and the podocytes of Bowman’s
capsule.
The Kidneys and the Nephron
Ureters, Urinary Bladder and
Urethra
 Ureters carry urine from the renal pelvis to
the urinary bladder.
 The urethra carries urine from the urinary
bladder to the outside of the body.
 The ureters and the urinary bladder are
lined with transitional epithelium and have
smooth muscle in their walls.
 The internal and external urinary sphincter
muscles regulate the flow of urine through
the urethra.
Ureters, Urinary Bladder and
Urethra
Regulation: Hormonal
 Antidiuretic hormone (ADH), otherwise
known as vasopressin, is secreted when
the osmolality of blood increases or when
blood pressure decreases. It increases the
permeability to water of the distal
convoluted tubule and collecting duct and
increases water reabsorption by the
kidney.
 Aldosterone increases the rate of sodium
chloride reabsorption, potassium secretion,
and hydrogen ion secretion.
Regulation: Hormonal
 Atrial natriuretic factor, secreted from the
right atrium in response to increases in
blood pressure, acts on the kidney to
increase sodium and water loss in the
urine.
Regulation: Neural
 Increased sympathetic activity decreases
blood flow to the kidney, decreases
filtration pressure, and decreases filtrate
and urine formation.
 Increased volume in the urinary bladder
stretches its wall and activates the
micturition reflex.
Regulation: Neural
 Parasympathetic impulses cause
contraction of the urinary bladder and
relaxation of the internal and external
urinary sphincters.
 Higher brain centers control the micturition
reflex.
Body Fluid Compartments
 Water and the electrolytes are distributed
in two major compartments. Sixty percent
of the total body weight is due to water.
 Of the sixty percent, roughly 60% is found
in the intracellular compartment, while 40%
is found in the extracellular compartment.
In the extracellular compartment, 1/3 is
found in plasma.
 The main intracellular ions are potassium,
phosphate, magnesium, and sulfate ions,
and there are more protein molecules
intracellularly than extracellularly.
Body Fluid Compartments
 Extracellular fluid contains more sodium,
chloride, and bicarbonate ions than in the
intracellular fluid.
 Water moves between compartments
continually in response to pressure
differences and osmotic differences
between the compartments.
Sodium Regulation
Increased ADH secretion, Decreased
urine volume and increased plasma DECREASED
INCREASED
volume SODIUM
SODIUM

Decreased aldosterone secretion,

decreased sodium reabsorption

NORMAL Na+

Decreased ADH secretion, Increased

urine volume and decreased plasma
volume INCREASED
DECREASED
SODIUM SODIUM

Increased aldosterone secretion,

increased sodium reabsorption
Potassium Regulation
Increased aldosterone secretion with
increased potassium secretion by the DECREASED
INCREASED
kidneys and increased potassium in POTASSIUM
POTASSIUM
urine

NORMAL K+

DECREASED Decreased aldosterone secretion with INCREASED

POTASSIUM decreased potassium secretion by the POTASSIUM
kidney and decreased potassium in
the urine
Calcium Regulation
Increased Calcitonin secretion with
decreased bone resorption

INCREASED DECREASED
CALCIUM Decreased parathyroid hormone CALCIUM
secretion with decreased bone
resorption, decreased intestinal
calcium absorption, and decreased
kidney calcium reabsorption

NORMAL Ca++

DECREASED INCREASED
CALCIUM Increased parathyroid hormone CALCIUM
secretion with increased bone
resorption, increased intestinal
calcium absorption, and increased
renal calcium reabsorption
Acid-Base Balance
 The respiratory system functions to
regulate pH. It responds rapidly.
 An increased respiratory rate raises the pH
because the rate of carbon dioxide
elimination is increased, and a reduced
respiratory rate reduces the pH because
the rate of carbon dioxide elimination is
reduced.
 The kidneys excrete hydrogen ions in
response to a decreasing blood pH, and
they reabsorb hydrogen ions in response
to an increasing blood pH.
Acid-Base Balance
 Acidosis is a decrease in pH below the
normal level, and alkalosis is an increase in
pH above the normal level.
 Acidosis occurs when the pH of blood falls
below 7.35. The two major types are
respiratory acidosis and metabolic
acidosis.
 Alkalosis occurs when the pH of blood
increases above 7.45. The two major
types are respiratory alkalosis and
metabolic alkalosis.
Acid-Base Regulation
Decreased respiratory rate with
increased hydrogen generated by
carbon dioxide retention DECREASED
INCREASED
BLOOD pH
BLOOD pH
Decreased rate of carbon dioxide
elimination with increased carbon
dioxide in extracellular fluid

NORMAL BLOOD pH

Increased respiratory rate with

increased carbon dioxide elimiantion
and consumption of hydrogen
DECREASED INCREASED
BLOOD pH BLOOD pH
Hydrogen secretion in the kidney
which lower blood hydrogen
concentration
 MANAGEMENT OF
PATIENTS WITH GUT
DYSFUNCTION

ASSESSMENT OF RENAL AND

URINARY TRACT FUNCTION
HEALTH HISTORY
 Urinary symptoms:
 Dysuria
 Hesitancy or straining
 Intermittency
 Terminal Dysuria
 Urgency
 Strangury
HEALTH HISTORY
 Urinary volume and frequency:
 Frequency
 Polyuria
 Nocturia
 Oliguria (< 400 cc/day)
 Anuria (<50 cc/day)
HEALTH HISTORY
 Urinary appearance / sediments:
 Hematuria (gross and microscopic)
 Pyuria (gross and microscopic)
 Lithuria
HEALTH HISTORY
 Inquire about the following:
Presence or history of genital lesions
Habits: use of tobacco, alcohol or recreational
drugs
Any prescription and over-the-counter
medications (including those prescribed for renal or
urinary problems)
HEALTH HISTORY
RISK FACTORS FOR SELECTED RENAL OR UROLOGIC DISORDERS
RISK FACTOR
Childhood disease: “strep throat,”
impetigo, nephrotic syndrome
Advanced age
Instrumentation of urinary tract,
cystoscopy, catheterization
Immobilization
Occupational, recreational, or
environmental exposure to chemicals
(plastics, pitch, tar, rubber)
Diabetes mellitus
POSSIBLE RENAL OR UROLOGIC
DISORDER
Chronic renal failure
Incomplete emptying of the bladder
leading to urinary tract infection
Urinary tract infection, incontinence
Kidney stone formation
Acute renal failure
Chronic renal failure, neurogenic
bladder
HEALTH HISTORY
RISK FACTORS FOR SELECTED RENAL OR UROLOGIC DISORDERS
RISK FACTOR
Hypertension
Systemic lupus erythematosus
Gout, hyperparathyroidism, Crohn’s
disease
Sickle cell disease, Multiple myeloma
Benign prostatic hypertrophy
Radiation therapy to the pelvis
Recent pelvic surgery
Spinal cord injury
POSSIBLE RENAL OR UROLOGIC
DISORDER
Renal insufficiency, chronic renal failure
Nephritis, chronic renal failure
Kidney stone formation
Chronic renal failure
Obstruction to urine flow, leading to
frequency, oliguria, anuria, obstructive
uropathy and chronic renal failure
Cystitis, fibrosis, fistula
Inadvertent trauma to the ureters or
bladder
Neurogenic bladder, UTI, incontinence
PHYSICAL EXAMINATION
 Head-to-toe assessment with special
emphasis on the abdomen, suprapubic
region, genitalia and lower back, and lower
extremities
 Direct palpation of the kidneys
 Rectal examination (men)
 Vulva, urethral meatus and vagina (women)
 Valsalva maneuver (men and women)
DIAGNOSTIC EVALUATION:
Urinalysis and Urine Culture
 Urine color
 Urine clarity and odor
 Urine pH and specific gravity
 Tests to detect protein, glucose and ketone
bodies
 Microscopic examination of urine sediments
after centrifuging to detect RBCs, WBCs,
casts, crystals, and bacteria
DIAGNOSTIC EVALUATION:
Renal Function Tests
 Used to evaluate the severity of kidney
disease and to assess the patient’s clinical
progress.
 Provide information on the effectiveness of
the kidney in carrying out its excretory
function.
 Renal concentration tests, creatinine
clearance, serum creatinine and blood urea
nitrogen levels
DIAGNOSTIC EVALUATION:
Renal Function Tests
TEST PURPOSE NORMAL VALUES
Renal Concentration Tests
Specific gravity Evaluates the ability of kidneys to 1.010 – 1.025
concentrate solutes in urine
Urine osmolality Concentrating ability is lost early in 300 – 900 mOsm/kg/24hr;
kidney disease; hence these test 50 – 1,200 mOsm/kg
findings may disclose early defects random sample
in renal function
24-Hour Urine Test
Creatinine Detects and evaluates progression Age Male Female
clearance of renal disease. Test measures < 30 88-146 81-134
volume of blood cleared in 1 30-40 82-140 75-128
minute which provides an
approximation of the glomerular 40-50 75-133 69-122
filtration rate. Sensitive indicator of 50-60 68-126 64-116
renal disease used to follow 60-70 61-120 58-110
progression of renal disease. 70-80 55-113 52-105
DIAGNOSTIC EVALUATION:
Renal Function Tests
TEST PURPOSE NORMAL VALUES
Serum Tests
Creatinine level Measures effectiveness of renal 0.6 – 1.2 mg/dL (50 – 110
function. Creatinine is end product μmol/L)
of muscle energy metabolism. In
normal function, level of creatinine,
which is regulated and excreted by
the kidneys, remains fairly constant
in the body.
BUN Serves as index of renal function. 7 – 18 mg/dL
Urea is nitrogenous end product of Patients over age 60:
protein metabolism. Test values 8 – 20 mg/dL
are affected by protein intake,
tissue breakdown, and fluid
volume changes.
BUN:Creat Evaluates hydration status. About 10:1
Elevated ratio seen in hypovolemia
IMAGING MODALITIES:
X-ray Films
 An x-ray study of the abdomen or kidney,
ureters and bladder (KUB plain) may be
performed to delineate the size, shape and
position of they kidneys.
 They reveal any abnormalities such as
calculi, hydronephrosis, cysts, tumors, or
kidney displacement by surrounding tissue
abnormalities.
IMAGING MODALITIES:
Ultrasonography
 Non-invasive procedure to detect
abnormalities such as fluid accumulation,
masses, congenital malformations, changes
in kidney size, or obstructions.
 Lower abdomen or genitalia may need to be
exposed.
 Requires a full bladder, fluid intake should be
encouraged before the procedure.
IMAGING MODALITIES:
CT and MRI
 Non-invasive techniques that provide
excellent cross-sectional views of the kidney
and urinary tract.
 Used in evaluating GUT masses, lithiases,
chronic renal infections, renal or urinary tract
trauma, metastatic disease and soft tissue
abnormalities.
 Claustrophobia is often a problem especially
with the MRI.
IMAGING MODALITIES:
CT and MRI
 Patient preparation includes removal of
metallic objects such as jewelry and clothing
with metallic clasps.
 MRI is contraindicated in patients with
pacemakers, surgical clips, or any metallic
objects anywhere in the body.
 Oral or intravenous radiocontrast agent may
be used to enhance visualization
Computed Tomography
Magnetic Resonance Imaging
IMAGING MODALITIES:
Intravenous Urography
 Includes excretory urography, IVP and
infusion drip pyelography.
 An intravenous dye is administered and, via
x-ray imaging, the dye is observed as it
moves through the upper and lower urinary
system.
 Visualizes the collecting system of the
kidneys and the length of the ureters, the
appearance of the bladder lumen and the
urethra.
IMAGING MODALITIES:
Retrograde Pyelography
 Catheters are advanced through the urethra,
bladder, ureters and into the renal pelvis by
means of cystoscopy, and a contrast agent is
then injected.
 X-ray films are taken to visualize the
collecting system of the kidneys to assess
kidney structure in patients who are allergic to
intravenous contrast agents.
UROLOGIC ENDOSCOPE
 Can be performed in two ways: through a
cystoscope inserted into the urethra, or
percutaneously through a small incision.
 Used to directly visualize the urethra and
bladder.
 The nurse describes the examination to the
patient and family to prepare them and to
allay their fears.
 If an upper cystoscopy is to be performed, the
patient is usually kept on NPO for several
hours beforehand.
UROLOGIC ENDOSCOPE
 Post-procedural management directed at
relieving any discomfort resulting from the
examination
 Moist heat to the lower abdomen and warm
sitz baths are helpful in relieving pain and
relaxing the muscles.
 Monitor for urine retention
 Monitor for signs and symptoms of UTI
KIDNEY BIOPSY
 Used in diagnosing and evaluating the extent
of kidney disease.
 Indications:
Unexplained renal failure
Persistent proteinuria or hematuria
Transplant rejection
Glomerulopathies
 Contraindications:
Bleeding tendencies
Uncontrolled hypertension
Solitary kidney
KIDNEY BIOPSY
 Patient is placed on NPO 6 to 8 hours before
the test and an IV line is established.
 Urine specimen is obtained and saved for
comparison with the post-biopsy specimen.
 Usually performed under sonographic
guidance.
 After the biopsy, pressure is applied to the
site and the patient is placed flat on bed for 6
to 8 hours to minimize bleeding.
 Vital signs monitoring every 15 minutes for 4
hours or until stable.
KIDNEY BIOPSY
 Collect all voided urine, one bottle per
voiding, for comparison.
 Patient instruction: avoid strenuous activities,
sports, heavy lifting for at least 2 weeks.
 MANAGEMENT OF
PATIENTS WITH GUT
DYSFUNCTION

DYSFUNCTIONAL VOIDING
PATTERNS
ADULT VOIDING
DYSFUNCTION
 Both neurogenic and non-neurogenic
disorders
 The micturition process involves several
highly coordinated neurologic responses that
mediate bladder function.
 A functional urinary system allows for
appropriate bladder filling and complete
bladder emptying.
 Usually involves the lower urinary system in
adults, but may progress to involve the upper
urinary system if not treated promptly.
URINARY INCONTINENCE
 Risk factors:
Pregnancy: vaginal delivery, episiotomy
Menopause
Genitourinary surgery
Pelvic muscle weakness
Incompetent urethra due to trauma
Immobility
High-impact exercise
Diabetes mellitus
Stroke
URINARY INCONTINENCE
 Risk factors:
Age-related changes in the urinary tract
Morbid obesity
Cognitive disturbances: dementia, Parkinson’s
disease
Medications: diuretics, sedatives, hypnotics,
opioids
Caregiver or toilet unavailable
URINARY INCONTINENCE:
Clinical Types
 Stress incontinence
 Urge incontinence
 Reflex incontinence
 Overflow incontinence
URINARY INCONTINENCE:
Assessment and Diagnosis
 Detailed description of the problem and a
history of medication use
 Voiding history and diary of fluid intake and
output
 Urodynamic tests (cystometrogram)
 Urinalysis and urine culture
URINARY INCONTINENCE:
Medical Management
 Depends on the underlying cause
 Behavioral therapy are always the first choice
to decrease or eliminate incontinence
Timed voiding
Prompted voiding
Habit retraining
Bladder retraining or “bladder drill”
Pelvic muscle exercises or Kegel exercises
Vaginal cone retention exercises
URINARY INCONTINENCE:
Medical Management
 Pharmacologic therapy
Anticholinergics (oxybutynin, dicyclomine)
Tricyclic antidepressants (imipramine, doxepin)
Pseudoephedrine (Sudafed)
Estrogen
URINARY INCONTINENCE:
Surgical Management
 Indicated in patients who have not achieved
continence using behavioral and
pharmacologic therapy.
 Options vary according to the underlying
anatomic and physiologic problem
URINARY INCONTINENCE:
Nursing Management
 Based on the premise that incontinence is not
inevitable with illness or aging and that it is
often reversible and treatable.
 Provide support and encouragement during
behavioral therapy
 Explain purpose of pharmacologic therapy
 Patient education
URINARY RETENTION
 Inability to empty the bladder completely
during attempts to void.
 Chronic urine retention often leads to
overflow incontinence.
 Residual urine is urine that remains in the
bladder after voiding (Normal: complete
bladder emptying in healthy adults younger
than 60; if > 60: 50 to 100 ml).
URINARY RETENTION
 Can occur postoperatively in any patient
particularly if the surgery affected the perineal
or anal regions.
 General anesthesia reduces bladder muscle
innervation and suppresses the urge to void,
impeding bladder emptying.
URINARY RETENTION:
Pathophysiology
 Urinary retention may result from diabetes,
prostatic enlargement, urethral pathology,
trauma, pregnancy, or neurologic disorders
such as cerebrovascular accident, spinal cord
injury, multiple sclerosis, or Parkinson’s
disease.
 May also be caused by medications
URINARY RETENTION:
Complications
 Chronic infections
 Calculi
 Pyelonephritis and sepsis
 Hydronephrosis and obstructive form of
uropathy and chronic renal failure
 Urine leakage with perineal skin breakdown
and irritation
URINARY RETENTION:
Nursing Management
 Prevent overdistention of the bladder
 Treat infection
 Correct obstruction
 Promote normal urinary elimination
 Providing privacy
 Ensuring an environment and a position conducive
to voiding
 Assisting the patient with the use of the bathroom
or commode
 Applying warmth to relax the sphincters
URINARY RETENTION:
Nursing Management
 Promote normal urinary elimination
 Giving patient hot tea
 Offering encouragement and reassurance
 Simple trigger techniques (turning on the water
faucet while the patient is trying to void, stroking
the inner thighs or abdomen, tapping above the
pubic area, dipping the patient’s hands in warm
water)
 Administering analgesics post-surgery
URINARY RETENTION:
Nursing Management
 Promote urinary elimination
 Transurethral catheterization
 Suprapubic catheterization
 Promoting home care
CATHETERIZATION
 Relieve urinary retention
 Assist with postoperative drainage in urologic
and other surgeries
 Provide means to monitor accurate urine
output in critically ill patients
 Promote urinary drainage in patients with
neurogenic bladder dysfunction or urine
retention
 Prevent urinary leakage in patients with stage
III to IV pressure ulcers
CATHETERIZATION:
Indwelling Devices
 A closed drainage system is essential
 Has to be changed at least every two weeks
using aseptic techniques
 Change drainage bags every three days
using aseptic techniques
CATHETERIZATION:
Nursing Management
 Assessing the patient and the system
 Minimizing trauma
 Use an appropriate-sized catheter.
 Lubricate the catheter adequately with a
water-soluble lubricant during insertion.
 Insert the catheter far enough into the
bladder to prevent trauma to the urethral
tissues when the retention balloon is
inflated.
 Secure catheter properly.
CATHETERIZATION:
Nursing Management
 Retraining the bladder.
 Preventing complications.
 MANAGEMENT OF
PATIENTS WITH GUT
DYSFUNCTION

URINARY DISORDERS
UTI
 Caused by pathogenic microorganisms in the
urinary tract and classified as either upper or
lower urinary tract infections
 Lower UTI:
 Cystitis (inflammation of the urinary bladder)
 Prostatitis (inflammation of the prostate gland)
 Urethritis (inflammation of the urethra
 Upper UTI:
 Acute and chronic pyelonephritis (inflammation of
the renal pelvis)
 Interstitial nephritis (inflammation of the kidney)
UTI
 One of the most common reasons patients
seek health care.
 Most cases occur in women, with one of
every five women in the US developing a UTI
sometime during her life (higher incidence in
developing countries).
 Urinary tract is also the most common site of
nosocomial infection.
UTI
 Risk factors:
 Inability or failure to empty the bladder completely
 Obstructed urinary flow
 Decreased natural host defenses or
immunosuppression
 Instrumentation of the urinary tract
 Inflammation or abrasion of the urethral mucosa
 Contributing conditions:
 Diabetes mellitus
 Pregnancy
 Neurologic disorders
 Gout
LOWER UTI
 Mechanisms which maintain the sterility of the
bladder:
 Physical barrier of the urethra
 Urine flow
 Ureterovesical junction competence
 Various antibacterial enzymes and antibodies
 Antiadherent effects mediated by the mucosal
cells of the bladder
LOWER UTI:
Pathophysiology
 Bacteria gains access to the bladder, attach
to and colonize the epithelium of the urinary
tract to avoid being washed out during
voiding.
 Pathogens evade host defense mechanisms.
 Inflammation is initiated.
 Most UTIs result from fecal organisms that
ascend from the perineum to the urethra and
the bladder and then adhere to the mucosal
surfaces.
LOWER UTI:
Pathophysiology
 Routes of infection:
 Ascending infection (up the urethra)
 Hematogenous (through the bloodstream)
 Direct extension (fistulous tract from the intestines)
LOWER UTI:
Clinical Manifestations
 Asymptomatic (50%)
 Frequent pain and burning on urination
 Frequency, urgency, nocturia, incontinence
 Suprapubic or pelvic pain and tenderness
 Back pain and hematuria
LOWER UTI: Assessment and
Diagnostic Findings
 UTI is diagnosed by bacteria in the urine:
colony count of 105 colony-forming units per
mL of urine on a clean-catch midstream or
catheterized specimen (major criterion).
 UTI have subsequent sepsis have occurred
with lower bacterial colony counts, however.
 Cellular studies:
 Microscopic hematuria (>4 RBCs/hpf)
 Pyuria (>4 WBCs/hpf)
LOWER UTI: Assessment and
Diagnostic Findings
 Urine cultures remain the gold standard in
documenting a UTI and can identify the
specific organisms present.
 The following groups of patients should have
urine cultures obtained when bacteriuria is
present:
 All men
 All children
 Women with a history of compromised immune
function or renal problems
 Diabetic patients
LOWER UTI: Assessment and
Diagnostic Findings
 The following groups of patients should have
urine cultures obtained when bacteriuria is
present (cont’d):
 Patients who have undergone recent
instrumentation (including catheterization) of the
urinary tract
 Patients who were hospitalized recently
 Patients with prolonged or persistent symptoms
 Patients with 3 or more UTIs in the past year
 Pregnant women
 Postmenopausal women
 Sexually-active women or with new partners
LOWER UTI:
Medical Management
 Management typically involves pharmacologic
therapy and patient education.
 Acute pharmacologic therapy:
 Uncomplicated in women: single-dose, short-
course (3 to 4 days), or 7- to 10-day therapeutic
courses
 Complicated UTI: cephalosporin or
ampicillin/aminoglycoside combination for 7 to 10
days; TMP-SMZ; quinolones
 Emphasize completion of regimen even if
symptoms subside
LOWER UTI:
Medical Management
 Long-term pharmacologic therapy
 Reinfection in women after completion of
antimicrobial therapy: another short course of full-
dose antimicrobial agent may be prescribed; if
there is no recurrence, medication is taken every
other night for 6 to 7 months.
 Other options: a dose of antimicrobial agent after
sexual intercourse, a dose at bedtime, or a dose
every other night, or three time per week
 Cranberry juice?
UPPER UTI:
Acute Pyelonephritis
 Bacterial infection of the renal pelvis, tubules,
and interstitial tissue of one or both kidneys.
 Frequently secondary to ureterovesical reflux;
other causes include urinary tract obstruction,
bladder tumors, strictures, BPH, urinary
stones
 Kidneys are often enlarged with interstitial
infiltration of inflammatory cells.
 Abscesses may be noted on the renal
capsule.
ACUTE PYELONEPHRITIS:
Assessment and Diagnosis
 An ultrasound or a CT scan may be
performed to locate any obstruction in the
urinary tract.
 IVP is rarely indicated during acute
pyelonephritis (normal findings in 75% of
patients)
 Urine culture and sensitivity tests are
performed to determine the causative
organism so that appropriate antimicrobial
agents can be prescribed.
ACUTE PYELONEPHRITIS:
Medical Management
 Uncomplicated: treated as outpatients
 Other patients, including pregnant women,
may be hospitalized for at least 2 to 3 days of
parenteral therapy. Once afebrile, oral
agents may be substituted.
 Pharmacologic therapy:
 2-week course of TMP-SMZ, ciprofloxacin,
gentamicin with or without ampicillin, or a third-
generation cephalosporin
 Analgesics to relieve pain
 Antipyretics to lyse the fever
CHRONIC
PYELONEPHRITIS
 Usually results from repeated bouts of acute
pyelonephritis
 May cause end-stage renal disease
 Usually no symptoms of infection unless an
acute exacerbation occurs
 Fatigue, headache, poor appetite, polyuria,
excessive thirst, weight loss
 Tests to determine the extent of the disease:
intravenous urogram, measurement of
creatinine clearance, BUN and creatinine
levels.
CHRONIC
PYELONEPHRITIS
 Complications:
 End-stage renal disease
 Hypertension
 Nephrolithiasis

 Medical management:
 Nitrofurantoin or TMP-SMZ to suppress bacterial
growth
 Careful monitoring of renal function with proper
adjustment of dosages depending on renal
clearance
CHRONIC
PYELONEPHRITIS
 Nursing management:
 Monitoring of fluid intake and output
 Unless contraindicated, liberal fluid intake up to 3
to 4 li/day
 Monitor TPR every 4 hours and administer
antipyretic drugs and antibiotics as prescribed
 Patient education on the prevention of UTI:
adequate fluid consumption, regular bladder
emptying and proper perineal hygiene
UPPER URINARY TRACT
INFECTIONS
ACUTE PN CHRONIC PN

Cause Poorly, untreated or Recurrent APN

complicated LUTI
Onset Fast, sudden Slow, imperceptible

Duration Short, reversible Chronic, irreversible

Course Dramatic, “toxic” Early: Insidious

Late: “toxic”
Symptoms More severe than Quiet at onset, with
LUTI CRF symptoms later
UPPER URINARY TRACT
INFECTIONS
ACUTE PN CHRONIC PN

Signs (+) Goldflam sign on Evidence of CRF in

PE later stages
Labs KUB-UTZ: enlarged, KUB-UTZ: small,
inflamed kidney scarred kidney
Treatment Aggressive antibx for Symptomatic,
> days dialysis in CRF
Outcomes Acute renal failure Chronic renal failure
Sepsis, septic shock ESRD
Recover or death Death
PRIMARY GLOMERULAR
DISEASES
 Includes acute and chronic
glomerulonephritis, rapidly progressive
glomerulonephritis, and nephrotic syndrome.
 The glomerular capillaries are primarily
involved: antigen-antibody complexes form in
the blood and become trapped in the
glomerular capillaries, inducing an
inflammatory response.
 IgG can be detected in the glomerular
capillary walls.
PRIMARY GLOMERULAR
DISEASES
PRIMARY GLOMERULAR
DISEASES
 Major clinical manifestations of glomerular
injury:
 Proteinuria
 Hematuria
 Decreased glomerular filtration rate
 Alterations in excretion of sodium
 Edema
 Hypertension
ACUTE
GLOMERULONEPHRITIS
 Glomerulonephritis is an inflammation of the
glomerular capillaries.
 AGN is a disease of children older than 2
years of age but can occur at any age group.
AGN: Pathophysiology
 In most cases, a group A β-hemolytic
streptococcal infection of the throat precedes
the onset of glomerulonephritis (Post-
streptococcal GN) by 2 to 3 weeks.
 May also follow impetigo and acute viral
infections (Post-infectious GN)
 In some patients, antigens outside the body
(medications, foreign serum) initiate the
process, resulting in antigen-antibody
complexes being deposited in the glomeruli.
AGN: Pathophysiology
ANTIGEN (GROUP A BETA-HEMOLYTIC STREPTOCOCCI)

ANTIGEN-ANTIBODY PRODUCT

DEPOSITION OF ANTIGEN-ANTIBODY COMPLEX IN GLOMERULUS

INCREASED PRODUCTION OF EPITHELIAL CELLS LINING THE GLOMERULUS

LEUKOCYTES INFILTRATE THE GLOMERULUS

AGN: Pathophysiology
LEUKOCYTES INFILTRATE THE GLOMERULUS

THICKENING OF THE GLOMERULAR FILTRATION MEMBRANE

SCARRING AND LOSS OF GLOMERULAR FILTRATION MEMBRANE

DECREASED GLOMERULAR FILTRATION RATE

RENAL FAILURE
AGN: Clinical Manifestations
 Hematuria (primary presenting feature)
 Proteinuria (primarily albumin)
 Azotemia (elevated BUN and serum
creatinine levels)
 Oliguria/anuria
 Anemia
 Edema and hypertension (75% of patients)
 Headache, malaise, flank pain
 CVA tenderness
AGN: Clinical Manifestations
 Circulatory overload with dyspnea, engorged
neck veins
 Cardiomegaly and pulmonary edema
 Confusion, somnolence and seizures (uremic
encephalopathy)
AGN: Assessment and
Diagnostic Findings
 Ultrasonography of the kidneys: large,
swollen and congested kidneys
 Electron microscopy and immunofluorescent
analysis if kidney biopsy samples:
demonstration of immunoglobulins and typical
glomerular changes
 Serologic tests: increased serum complement
levels (within 2 to 8 weeks)
 Urinalysis showing RBC casts and other
sediments
AGN: Complications
 Hypertensive encephalopathy
 Heart failure
 Pulmonary edema
 Uremia
AGN: Medical Management
 Treating symptoms
 Preserve kidney function
 Treat complications
 Pharmacologic therapy:
 Penicillin (if with residual streptococcal infection)
 Corticosteroids and immunosuppresants
 Loop diuretics and antihypertensive medications

 Dietary protein restriction when renal

insufficiency develops
 Sodium restriction
AGN: Nursing Management
 Carbohydrates are given liberally to provide
energy and reduce the catabolism of proteins.
 Fluid intake and output are carefully
measured and recorded. Fluids are given
according to patient’s fluid losses and daily
body weight.
 Bed rest during acute phase / discourage
ambulation.
 Patient education.
CHRONIC
GLOMERULONEPHRITIS
 May be due to repeated episodes of acute
glomerulonephritis, hypertensive
nephrosclerosis, hyperlipidemia, chronic
tubulointerstitial injury, or hemodynamically-
mediated glomerular injury and sclerosis.
 Kidneys are reduced to as little as one-fifth
their normal size consisting largely of scar or
fibrous tissue.
 The renal cortex decreases in thickness.
 Glomeruli become scarred and branches of
the renal artery become thickened.
CGN: Clinical Manifestations
 Hypertension
 Azotemia
 Edema
 Uremia
 Nutritional derangements
 Skin appears yellowish gray
 Anemia
 Cardiomegaly and pulmonary edema
 Peripheral neuropathy
CGN: Assessment and
Diagnostic Findings
 Urinalysis reveals fixed specific gravity of
about 1.010, variable proteinuria, and urinary
casts
 Hyperkalemia
 Metabolic acidosis
 Anemia
 Hypoalbuminemia
 Hyperphosphatemia
 Hypocalcemia
 Impaired nerve conduction
CGN: Assessment and
Diagnostic Findings
 Cardiac enlargement and pulmonary edema
on radiography
 ECG: left ventricular enlargement, evidence
of electrolyte abnormalities
CGN: Medical Management
 Symptoms guide the course of management
 Diet modification
 Control of hypertension:
 ACE-inhibitors and Angiotensin II receptor
blockers
 Calcium-channel blockers
 Beta-adrenergic blockers
 Central-acting drugs
 Diuretics
CGN: Medical Management
 Hemodialysis
 Kidney transplantation
CGN: Nursing Management
 Observe the patient for changes in fluid and
electrolyte status and for signs and symptoms
of deterioration of renal function.
 Report changes promptly to physician
 Give emotional support by providing
opportunities for the patient and family to
verbalize their concerns, have their questions
answered and explore their options
 Patient education in preparation for home and
community-based care.
NEPHROTIC SYNDROME
 Apparent in any condition that seriously
damages the glomerular capillary membrane
and results in increased permeability
 Primary glomerular disease characterized by:
 Marked increase in protein in the urine
(proteinuria)
 Decrease in albumin in the blood
(hypoalbuminemia)
 Edema
 High serum cholesterol and low-density
lipoproteins
NEPHROTIC SYNDROME:
Pathophysiology
 Can occur with almost any intrinsic renal
disease or systemic disease that affects the
glomerulus
 Generally considered a disease of childhood
but it does occur in adults, including the
elderly.
 Causes:
 Chronic glomerulonephritis
 Diabetes mellitus
 Amyloidosis and systemic lupus erythematosus
 Multiple myeloma
NEPHROTIC SYNDROME:
Pathophysiology DAMAGED GLOMERULAR CAPILLARY MEMBRANE

LOSS OF PLASMA PROTEIN (ALBUMIN)

STIMULATES SYNTHESIS OF LIPOPROTEINS HYPOALBUMINEMIA

HYPERLIPIDEMIA DECREASED ONCOTIC PRESSURE

GENERALIZED EDEMA
(FLUID MOVES FROM VASCULAR SPACE TO EXTRACELLULAR SPACE

ACTIVATION OF RENIN-ANGIOTENSIN SYSTEM

SODIUM RETENTION

EDEMA
NEPHROTIC SYNDROME:
Clinical Manifestations
 Edema (major manifestation)
 Malaise, headache, irritability and fatigue
 Hypertension usually not a manifestation
NEPHROTIC SYNDROME:
Assessment and Diagnosis
 Proteinuria exceeding 3 to 3.5 g/day is
sufficient for the diagnosis of nephrotic
syndrome.
 Pyuria and granular and epithelial casts on
urinalysis
 Needle biopsy of the kidney may be
performed for histologic diagnosis of the
etiology
 Serum markers (anti-C1q antibodies is the
most reliable for assessing disease activity in
lupus nephritis)
NEPHROTIC SYNDROME:
Complications
 Infection (deficient immune response)
 Thromboembolism
 Pulmonary emboli
 Acute renal failure
 Accelerated atherosclerosis
NEPHROTIC SYNDROME:
Medical Management
 Objective is to preserve renal function
 Diuretic agents for severe edema
 ACE-inhibitors in combination
 Cyclophosphamide and azathioprine
 Corticosteroids
 Low-sodium, liberal-potassium diet
 Protein intake should be about 0.8 g/kg/day
with emphasis on high biologic value proteins
(dairy products, eggs, meats)
 Diet should be low in saturated fats
NEPHROTIC SYNDROME:
Nursing Management
 Similar to that of acute glomerulonephritis
during the early phase of the disease
 As the disease worsens, management is
similar to that of chronic glomerulonephritis
 Patient education
 Monitoring and regulation of fluid intake and
output
 Monitoring for onset of acute infections
 Vigilance against possible thromboembolic
phenomena
RENAL FAILURE
 Transient or permanent inability of the
kidneys to perform their normal function
of urine formation (filtration, secretion
and reabsorption.
 Two types:
 Acuterenal failure – reversible, transient
 Chronic renal failure – irreversible,
permanent
ACUTE RENAL FAILURE
 Stages:
 Oliguric/anuricphase – azotemia
 Diuretic phase – increased urine output
 Recovery phase – full recovery of renal
function
 Types:
 Pre-renal ARF
 Intrinsic renal ARF
 Post-renal ARF
CHRONIC RENAL FAILURE
 Stages:
 Stage I: 80-125 ml/min (normal renal
function)
 Stage II: 50-80 ml/min (diminished renal
reserve; chronic renal impairment)
 Stage III: 20-50 ml/min (chronic renal
impairment)
 Stage IV: 5-20 ml/min (chronic renal
insufficiency
 Stage V: < 5 ml/min (ESRD)
MANIFESTATIONS
 Azotemia / Uremia
 Uremic frost
 Uremic fetor
 Uremic encephalopathy
 Uremic cardiomyopathy / pericarditis
 Uremic gastropathy
MANIFESTATIONS
 Edema
 Multiple electrolyte imbalance
 Hypernatremia
 Hyperkalemia
 Hypermagnesemia
 Hyperphosphatemia
 Hypocalcemia
MANIFESTATIONS
 Metabolic acidosis
 Anemia
 Hypertension
MANAGEMENT
 Aggressive Management
 Supportive Management
UROLITHIASIS
 Refers to stones (calculi) in the urinary tract.
 Formed when urinary concentrations of
calcium oxalate, calcium phosphate and uric
acid increase (supersaturation) and
dependent on the amounts of the substance,
ionic strength, and pH of the urine
UROLITHIASIS:
Pathophysiology
 Supersaturation of calcium oxalate, calcium
phosphate, uric acid
 Deficiency of substances that normally
prevent crystallization in the urine (citrate,
magnesium, nephrocalcin, uropontin)
 Stones often occur in dehydrated patients
 They may deposit in many areas of the
urinary tract, including the renal pelvis,
ureters, ureterovesical junction and urinary
bladder.
UROLITHIASIS:
Pathophysiology
 Factors that favor the formation of stones:
 Infection
 Urinary stasis
 Immobility
 Hypercalcemia
 Hyperuricemia

 75% of renal stones are calcium based, 5 to

10% are made up of uric acid, and 10 to 15%
are cystine or struvite stones which are
closely associated with infections.
UROLITHIASIS:
Clinical Manifestations
 Depend on the location of the stone and the
presence of attendant urinary tract infection
 Intense, deep ache in the costovertebral and
flank regions
 Acute pain + tenderness + nausea + vomiting
(renal colic)
 Hematuria
 Oligoanuria
 Fever and chills
UROLITHIASIS:
Assessment and Diagnosis
 Diagnosis is confirmed by x-ray films of the
kidneys, ureters and bladder (KUB) especially
if the stone is calcium-based
 Serum chemistries for uric acid, BUN
creatinine and calcium
 Chemical analysis of voided stones
UROLITHIASIS:
Medical Management
 Basic goals: eradicate the stone, determine
the stone type, prevent nephron destruction,
prevent recurrent stone formation
 Immediate goal: relieve the pain
 Nutritional therapy to prevent renal stones
 Liberal fluid intake, at least 8 8-oz glasses of
water daily to keep the urine dilute
 Keep urine output of at least 2 li/day
UROLITHIASIS:
Medical Management
 Dietary recommendations:
 Restricting protein to 60 g/day to decrease urinary
excretion of calcium and uric acid.
 A sodium restriction of 3-4 g/day. Table salt and
high-sodium foods should be reduced because
sodium competes with calcium for reabsorption in
the kidneys.
 Low-calcium diets are not generally
recommended, except for true absorptive
hypercalciuria.
 Oxalate-containing foods (spinach, strawberries,
rhubarb, tea, peanuts, wheat bran) may be
restricted.
UROLITHIASIS:
Surgical Management
 Done if stone is not passed spontaneously or
if complications occur.
 Ureteroscopy
 Extracorporeal shockwave lithotripsy (ESWL)
 Laser lithotripsy (new technology, not yet
widely performed)
 Percutaneous removal
UROLITHIASIS:
Nursing Management
 Assess for pain and discomfort as well as
associated symptoms such as nausea,
vomiting, diarrhea and abdominal distention
 Observe for signs and symptoms of UTI
 Elicit from the history risk factors for the
development of urinary calculi
 Pain relief
 Monitoring and managing potential
complications
 Patient education for avoiding recurrent
kidney stones
HEMODIALYSIS
 The objectives are to extract nitrogenous
waste substances from the body and to
remove excess water.
 Diffusion, osmosis and ultrafiltration are
the principles on which hemodialysis is
based.
HEMODIALYSIS:
Vascular Access
 Subclavian, internal, jugular, and femoral
catheters
 Fistula
 Graft
HEMODIALYSIS:
Complications
 Hypotension during treatment (nausea,
vomiting, diaphoresis, tachycardia and
dizziness)
 Painful muscle cramping
 Exsanguination
 Dysrhythmias
 Air embolism
 Chest pain
 Dialysis dysequilibrium
HEMODIALYSIS:
Long-Term Management
 The patient, the dialyzer and the dialysate
bath require constant monitoring because
numerous complications are possible.
 The nurse has an important role in
monitoring, supporting, assessing and
educating the patient.
 Nutritional and fluid therapy
 Meeting psychosocial needs
 Patient education
PERITONEAL DIALYSIS
 Goals: remove toxic substances and
metabolic wastes and to reestablish normal
fluid and electrolyte balance.
 Treatment option for patients who are unable
or unwilling to undergo hemodialysis or renal
transplantation.
 The peritoneum serves as the
semipermeable membrane that performs the
actions of diffusion, osmosis and
ultrafiltration, instead of an external dialyzer.
PERITONEAL DIALYSIS:
Procedure
 Preparing the patient
 Preparing the equipment
 Inserting the catheter
 Performing the exchange
PERITONEAL DIALYSIS:
Complications
 Peritonitis
 Leakage
 Bleeding
 Long-term complications:
 Hypertriglyceridemia
 Abdominal hernias
 Hemorrhoids
 Anorexia and low back pain
KIDNEY
TRANSPLANTATION
 Kidney transplantation has become the
treatment of choice for most patients with
ESRD.
 Involves transplanting a kidney from a living
donor or human cadaver to a patient.
 Transplants from well-matched living donors
who are related to the patient are slightly
more successful than those from cadaver
donors.
 Success rate increases if transplantation is
done before dialysis becomes necessary.
KIDNEY
TRANSPLANTATION
 PREOPERATIVE MANAGEMENT:
 Donor screening
 Patient and donor laboratory tests
 Psychological evaluation and counselling
 Continuation of renal replacement therapy while
awaiting transplantation
 INTRAOPERATIVE MANAGEMENT:
 Maintaining stable hemodynamic status for both
donor and patient
 Monitoring for potential intraoperative
complications
KIDNEY
TRANSPLANTATION
 POSTOPERATIVE MANAGEMENT
 Immediate postoperative monitoring for
complications
 Monitoring for success of transplantation
 Immunosuppressive therapy
 Preventing infection
 Addressing psychological concerns
 Promoting home and community-based care