Disorder of the Genitourinary

System

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 Learning objectives
• At the end of the course the students will be able
to: -
1. Revise the anatomy and physiology of GUT
2. Review the approach in pts. with GUT disorders
3. Describe and identify the common GUT
disorders.
4. Develop a nursing care for a patient with a GUT
problems

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 Introduction
The term "genitourinary" actually refers to two different
systems.
 Urinary system -responsible for removal of
 Nitrogenous waste products of metabolism from
the bloodstream,
 Disposal of concentrated wastes (urine).
 Genito - the genital organs and the reproductive
system, which is responsible for production of
succeeding generations for perpetuation of the
species.

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Anatomy and physiology review of GUT

The renal and urinary

systems include:
kidneys
Ureters
Bladder
Urethra

4
 Kidneys
 Are a pair of bean-shaped, brownish-red structures
located retroperitoneally(behind and outside the
peritoneal cavity).
 Each kidney has about 1 million nephrons.
 The kidneys receive 20% to 25% of the total cardiac
output.

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 Functions of the Kidney
Urine formation
Excretion of waste products
Regulation of electrolytes
Regulation of acid–base balance
Control of water balance
Control of blood pressure
Renal clearance
Regulation of red blood cell production
Synthesis of vitamin D to active form
Secretion of prostaglandins
Regulates calcium and phosphorus balance 6
 Ureters
 Are long fibromuscular tubes that connect each
kidney to the bladder
 Each tube is about 24 to 30 cm long
 For passage of urine from each renal pelvis into the
bladder
Urinary bladder
 Is a muscular, hollow sac located just behind the
pubic bone.
 It is the reservoir for urine
 The capacity of the adult bladder is 400 to 500ml
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 Urethra
 Arises from the base of the bladder
 In male
 it passes through the penis and transports
semen and urine from the body.
 In women
it opens just anterior to the vagina and used to
carry urine from the body.

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APPROACH TO THE PHYSICAL
DIAGNOSIS OF THE
GENITOURINARY SYSTEM
(GUS)

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 Common symptoms
1. Urinary Tract
. Renal pain:
 This is pain arising from the kidneys
 Is usually felt at or below the costal margin posteriorly
 May radiate Anteriorly towards the umbilicus
 . Ureteric pain:
 Results from sudden distention of the ureter and possibly the
renal pelvis.
 It is severe colicky pain which originates in the
costovertebral angle.
 It may radiate into the lower quadrant of the abdomen and
possibly to the upper thigh and testicle or labium 10
 Renal vs. uretral pain
Kidney pain occurs in acute pyelonephritis.
 Ureteral colic is caused by sudden obstruction of a
ureter, as by urinary stones or blood clots.

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Hematuria:
 Is the presence of red blood cells in the urine.
Oliguria:
 Denotes the passage of less than 400 ml of urine per
day.
Anuria:
 Is the complete absence of urine output
Polyuria:
 Implies a high urine output.
 Usually urine output of more than 3L per day.

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Urinary frequency:
 Is an abnormally frequent voiding.
 Occurred in bladder irritation or inflammation
Dysuria:
 Is a specific form of discomfort arising from the
urinary tract in which there is pain immediately
before, during or immediately after micturation
Urgency:
 Is the loss of the normal ability to postpone
micturation beyond the time when the desire to pass
urine is initially perceived.
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Incontinence:

 Refers to an involuntary loss of urine.

Hesitancy:

 Is difficulty initiating the process of micturition.

Terminal dribbling

 is difficulty of completing micturation in a clean

stop fashion.

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 THE MALE GENITAL TRACT

URETHRAL DISCHARGE:
 The color, amount and duration of the discharge
have to be ascertained.
 Commonest causes are sexually transmitted
infections.
Genital ulcer:
 single or multiple, painful or painless.

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 THE FEMALE GENITAL TRACT
VAGINAL DISCHARGE
 Can be associated with itching.
 The color, odor and amount should be characterized.
Menstrual History:
 This part of history should be included to know
mainly the extent of bleeding, regularity ,age at
menarche, Last menstrual period, length of time
between periods, How heavy is the flow ,Bleeding
between periods.
Dyspareunia: Is pain on sexual intercourse
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 Physical
Examination
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 THE KIDNEYS
Palpation of the Left Kidney.
 Place your left hand behind the patient just below
and parallel to the 12th rib.
 Place your right hand gently in the right upper
quadrant
 Ask the patient to take a deep breath.
 At the peak of inspiration, press your right hand
firmly and deeply , just below the costal margin, and
try to “capture” the kidney between your two hands.
 If it is palpable, describe its size, shape, and any
tenderness. 18
Palpating the left kidney

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 Percussion
 Assessing Kidney Tenderness.
 The costovertebral angle—the angle formed by the
lower border of the 12th rib and the transverse
processes of the upper lumbar vertebrae—defines the
region to assess for kidney tenderness.
 Place the ball of one hand in the costovertebral angle
and strike it with the ulnar surface of your fist.
 Direct percussion with the fist over the CVA is also
acceptable.
 Pain with pressure or fist percussion suggest
pyelonephritis, but may also have a musculoskeletal
cause. 20
costovertebral angle

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BLADDER
 palpate for enlarged bladder.
 Palpate for tenderness, distention.
GENITAL EXAMINATION
MALE
THE PENIS
 Check the external meatus of the urethra for any
discharge.
 Inspect for abnormal meatal opening.
 Palpate the ventral and dorsal aspect of the shaft for
tenderness or lesions.
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Diagnostic Procedures

Nursing responsibilities

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 Common procedures

 Urinalysis and urine culture

 Renal function tests

 X-ray and other imaging modalities

 Endo urological procedures

 Biopsy

 Uro dynamic Tests

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 Diagnostic tests
Laboratory Tests
 Urine Tests
Urinalysis- give information regarding
kidney function and helps to diagnose
other diseases.
Urine culture- determines whether
bacteria are present in the urine, as well
as their strains and concentration.
 Also used to identify the antimicrobial therapy
that is best suited for the particular strains.
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 Urinalysis and urine culture

 Clean catch/mid stream urine

 24 hrs urine collection

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 Renal Function Tests:
 Renal concentration tests
 Specific gravity
 Purpose:
 Evaluate ability of kidneys to concentrate
solutes in urine
 NV: 1.010-1.025

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 Urinary osmolality
 Concentrating ability is lost early in
kidney diseases, hence these test findings
may disclose early defects in renal
function
 NV: 300-900mmol/Kg/24hrs, 50-1200
mmol/Kg -Random sample

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 Blood urea nitrogen (BUN)
 Urea forms in the liver, constitutes the final product of
protein metabolism.
 Amount of excreted urea varies directly with dietary protein
intake.
 The test for BUN which measures the nitrogen portion of
urea is used as an index of glomeruli function in excretion
of urea.
 Thus, serves as an index of renal functioning
 A marked increase in BUN = severe impaired renal function

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 BUN
 Serve as index of renal function
 Urea is nitrogenous end product of protein
metabolism
 Test values are affected by protein intake,
tissue breakdown, and fluid volume
changes
 NV:
 Adult: 7-18 mg/dl
 Elderly 8-20 mg/dl

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 Urine Creatinine
 Amino acid waste product derived from muscle creatine (a
product of protein metabolism)

 All creatinine filtered by kidneys in a certain timeframe goes

into the urine, creatinine levels thus are equal to the glomeruli
filtration rate.

 Disorders of kidney interfere with normal secretion of

creatinine

 Thus creatinine measures effectiveness of renal functioning

(serum creatinine)

(Volume of urine [mL/min] urine creatinine [mg/dL])

Serum creatinine (mg/dL)

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 The adult GFR can vary from a normal of
approximately 125 mL/min (1.67 to 2.0 mL/sec)
to a high of 200 mL/min
 Keep in mind that rate normally decreases as
we age
• Urine creatinine men 0.8 -1.8 g/24h
• Urine creatinine women 0.6 - 1.6 g/24h
• Serum creatinine: 0.4-1.5 mg/dl
• Sensitive indicator of renal disease used
to follow progression of renal disease

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 BUN to Creatinine Ratio

 Evaluates hydration status of pts

 An elevated ratio is seen in hypovolemia
 A normal ratio with an elevated BUN and
creatinine is seen in intrinsic renal diseases
 NV: about 10:1

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 Creatinine Clearance
 Decreased
– Impaired kidney function
– Kidney Disease
– Shock & dehydration
– CHF
 Increased
– State of high cardiac output
– Pregnancy
– Burns

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 Dx cont
 KUB X-ray
– An abdominal plain X-ray film that include the
kidneys, ureters, and the bladder
– Is an AP (anteroposterior) abdominal x ray.
 Purpose to:
– Detect kidney stones,
– As a preliminary film for an IVP
– As a follow-up x ray after ureteral stents

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 Dx cont
 Precautions
 Pregnant women
 Is a screening test for kidney stones/should be
followed by a other diagnostic tests [US/IVP/CT
 Description
 A KUB is typically a single x-ray procedure.
 Preparation
 No special preparation
 Aftercare
 No special aftercare required

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 Intravenous Pyelogram (IVP)
 Is an X-ray examination of the KUB using contrast
medium.

 The contrast injected travels through the blood

stream and collects in the kidneys and urinary tract,
turning these areas bright white.

 Allows to see and assess the anatomy and function of

the KUB

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 IVP- Indications To:

 Assess abnormalities in the urinary system

 kidney stones
 Enlarged prostate
 Tumors in the kidney, ureters or urinary
bladder
 Diagnose symptoms such as blood in the
urine or flank pain or lower back.

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 Pt preparation
 NPO after midnight on the night before your exam

 Mild laxative the evening before the procedure.

 Assess for history of allergies

 Remove jewelry, eye glasses and any metal objects or

clothing that might interfere with the x-ray images.

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 Is relatively comfortable procedure.
 Pt may feel a minor sting as the contrast
material is injected
 Some patients experience a flush of
warmth, a mild itching sensation and a
metallic taste
 Usually disappear within a minute or two
and are harmless.
 Assess for allergic reaction

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 During the imaging pt may be asked to turn
from side to side/different positions to
capture views from several angles.

 Pt may be asked to empty his bladder so

that an additional x-ray can be taken after it
empties.

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 Benefits
– Minimally invasive imaging procedure.
– Provides valuable, detailed information
to diagnose and treating urinary tract
conditions: kidney stones/cancer.
– provide information on obstructions to
direct treatment

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 Limitations of IVP studies
– Doesn’t shows mainly details of structural
problems of the tract; kidneys, ureters
and bladder
– CT/MRI more valuable functioning tissue
of the kidneys and surrounding
structures

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 Endourological Diagnosis and Treatment
Procedures
 Visualization of urinary tract with endoscope.
 Endo urological procedures include:
 Cystoscopy (cysto)
 Ureterorenoscopy
Cystoscopy
 Is the procedure to visualize the urethra and urinary
bladder with the help of a Cystoscopy.
 It has a self-contained optical lens system that
provides a magnified, illuminated view of the bladder.

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 Indications
 Obstruction in the urethra
– Stone
– Tumors
– Stricture
 Enlargement of the prostate
– BPH
– Prostatitis
– Cancer

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 Bladder changes
– Stones
– Tumors
– Inflammation
– Neurogenic bladder
– Congenital

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 Cystoscopy
used to find the cause of :
 Frequent urinary tract infections
 Hematuria
 Frequency and urgency
 Unusual cells found in a urine sample
 Dysuria, chronic pelvic pain, or cystitis

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 Procedure/nursing responsibilities
 Consent
 Position—dorsal/lithotomy
 Sedative may be administered
 A local topical anesthetic is instilled into the
urethra by the urologist before the Cystoscopy
is inserted.
 IV diazepam (valium) in combination with
topical urethral anesthesia may be administered.

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 Alternative spinal (regional) or general
anesthesia may be used.
 Assemble instrument
 Connect light to the source
 Connect to the irrigating can (distilled
water)
 Lubricate the scope- KY jelly/Lidocaine

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Rigid cystoscope (left) and semirigid uretero scope (right).

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 Ureterorenoscopy

 Procedure carried out on any part of the

ureter.
 Indications:
– Stones
– Stricture
– Tumors

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 Procedure:
– Cystoscope is done 1st
– Then guide wire is passed to the ureter
 Stone
– Removed intact if small
– Fragmented by litho if large
 Tumor
– Bxed, fulgurated or resected as indicated

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 Stricture
– Dilated/divided
 Stenting- based on the ureter
circumstance
 Empty bladder by catheter

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 Complications of Ureterorenoscopy
 False placing
 Perforation
 Bleeding
 evulsions

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 Aftercare
 Observe for complications
 Bleeding
 False spacing
 Injury to the surrounding
 Extravasations of fluid/urine into penis
 Can occur if the division was forceful and
in the wrong plane
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 Renal biopsy
 Is a tissue of living kidney taken for
pathological or immunological purpose.
 Indications
– Nephrotic syndrome
– Acutely progressing pyelonephritis
– Systemic vacuities
– Goodpature’s syndrome progressive
glomerulopnephritis, hemoptysis.
– Diabetic nephropathy
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 Nursing responsibilities before Procedure

 Bleeding time
 Platelet count (< 100,000/cmm)
thrombocytopenia
 Low Hgb.
 Anemia
 Drugs- what drugs pt is on (antiplatelet.
Anticoagulant).

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 Nursing cont.
 Explain the procedure to the pt.
 Obtain the consent.
 Premedicate the pt.
 Always done US guided, CT scan guided
 Done by nephrologists/radiologist

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 Nursing cont
 Pillow under the other side flank
 Local injection- lidocaine
 Right kidney is preferred for convenience
 Long kidney biopsy needle.
 Small skin cut and introduce the Bx needle
 Needle is put into the kidney while pt is
allowed to take deep breath.
 Immediately deliver the Bx to the lab.
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 Post procedural Nursing care
 Keep the pt on the same position for 24hrs.
 Close observation-BP, pulse q 15minutes for
1hour
 Complete bed rest for 6hrs and 3 consecutive
urine sample for hematuria
 If hematuria is increasing report.

60
 Complications

 Hemorrhage- because kidney is highly

vascularized organ
 Discharge pt after 24 hrs if no
complications.
 Instruct pt not to do any exercise for 2-3
days.

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 Fluid and electrolyte disturbance
• Approximately 60% of lean body weight is
water,
- 2/3 is intracellular and
- 1/3 is extracellular compartments,
mostly as interstitial fluid
• Only 5% of total body water is in blood
plasma.

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 Fluid and electrolyte imbalance
Fluid volume deficit (hypovolemia)
Lose of ECF exceeds the intake of fluid.
Contributing factors
Loss of water and electrolytes,
as in vomiting,
diarrhea,
fistulas, fever,
excess sweating,
burns, blood loss,
gastrointestinal suction, and third-space fluid shifts (from the vascular
system to other body spaces).
Decreased intake, as in anorexia, nausea, and inability to
gain access to fluid.
Diabetes insipidus and uncontrolled diabetes mellitus also
contribute to a depletion of extracellular fluid volume.
63
 Clinical presentations

Acute weight loss

Decreased skin turgor
Oliguria, concentrated urine
Postural hypotension, weak rapid pulse, capillary
filling time prolonged, low central venous
pressure , ↓ blood pressure
Dizziness, weakness, thirst and confusion,
↑ pulse
Muscle cramps.

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Labs indicate:
↑ hemoglobin and hematocrit
↑ serum and urine osmolality and specific
gravity,
↓ urine sodium,↑ BUN and creatinine

65
 Management
 If the deficit is not severe, the oral route is preferred,
provided the patient can drink.
 If fluid losses are acute or severe, the IV route is
required
 Isotonic electrolyte solutions (e.g. lactated Ringer’s
solution, 0.9%Nacl) are frequently used
 As the patient becomes normotensive, a hypotonic
electrolyte solution (e.g 0.45% Nacl)
 Avoid fluid overload

66
 Fluid volume excess (hypervolemia)
 Contributing factors:
Compromised regulatory mechanisms, such as renal
failure, heart failure, and cirrhosis.
Consumption of excessive amounts of table or other
sodium salts.
Overzealous administration of sodium-containing
fluids.
Prolonged corticosteroid therapy, severe stress, and
hyperaldosteronism

67
 Clinical Manifestations
• Acute weight gain,
• Peripheral edema and
• Ascites, distended jugular veins,
• Crackles, shortness of breath and wheezing,
• Increased BP, and cough.
Labs indicate:
↓Hemoglobin and Hematocrit
↓Serum and urine osmolality
↓Urine sodium and specific gravity
Chest x-ray may reveal pulmonary congestion
68
 Management
 Management is directed at the causes
 Dietary restriction of sodium
 Symptomatic treatment consists of administering
diuretics and restricting fluids and sodium.
 Potassium supplements can be prescribed
 If renal function is so severely impaired hemodialysis
or peritoneal dialysis may be used to remove
nitrogenous wastes and control potassium and acid-
base balance, and to remove sodium and fluid.

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 Electrolyte Imbalances
Hyponatremia
Refers to a serum sodium level that is < 135 mEq/L
Can be due to:
Loss of sodium, as in use of diuretics, loss of GI fluids,
renal disease, and adrenal insufficiency.
Gain of water, as in excessive administration of D5W.
Disease states associated with syndrome of
inappropriate secretion of ADH(SIADH) such as head
trauma.
Medications associated with water retention (oxytocin
and certain tranquilizers)
Hyperglycemia and heart failure cause a loss of Na. 70
 Clinical manifestations
 Anorexia, nausea and vomiting
 Dry skin, increase pulse, decrease BP, weight
gain, edema.
 Headache, lethargy, dizziness, confusion
 Muscle cramps and weakness, muscular
twitching, seizures, papilledema

71
 Management
• Administration of sodium by mouth, nasogastric
tube, or a parenteral route
• lactated Ringer’s solution or isotonic saline (0.9%
sodium chloride) solution may be used.
• In a patient with normal or excess fluid volume,
hyponatremia is treated by restricting fluid.

72
 Hypernatremia
Is a serum sodium level higher than 145 mEq/L
Can be caused by:
Water deprivation in patients unable to drink is a
common cause.
Hypertonic tube feedings without adequate water
supplements
Excess sodium bicarbonate, and sodium chloride
administration.
Salt water near-drowning victims.

73
 Clinical manifestations
• Thirst
• Elevated body temperature
• Swollen dry tongue and sticky mucous membranes
• Hallucinations, lethargy, restlessness, irritability,
seizures
• Pulmonary edema
• Hyperreflexia , twitching
• Nausea, vomiting, anorexia
• Increased pulse and BP

74
 Management
Gradual lowering of the serum sodium level by the
infusion of a hypotonic electrolyte solution ( 0.3%
sodium chloride) or an isotonic solution (D5W).
The serum sodium level is reduced at a rate no
faster than 0.5 to 1 mEq/L/h
Too-rapid reduction in the serum sodium level
renders the plasma temporarily hypo osmotic to the
fluid in the brain tissue, causing movement of fluid
into brain cells and dangerous cerebral edema.

75
 Potassium deficit (hypokalemia)
Is when serum potassium <3.5 mEq/L.
Contributing factors:
Medications like thiazides and loop diuretics,
corticosteroids, and amphotericin B.
GI loss of potassium- diarrhea, vomiting and
gastric suction.
Metabolic alkalosis that promotes the
transcellular shift of potassium : hydrogen ions
move out of the cells in alkalotic states to help
correct the high pH, and potassium ions move in
to maintain an electrically neutral state.
76
 …cont’d
 Hyperaldosteronism increases renal potassium
wasting.
 Patients with persistent insulin hypersecretion
(insulin promotes the entry of potassium into
skeletal muscle and hepatic cells)
 Magnesium depletion causes renal potassium loss.

77
 Clinical Manifestations
Fatigue, anorexia, nausea, vomiting, muscle
weakness, leg cramps, decreased bowel motility,
paresthesias and dysrhythmias.
If prolonged, inability of the kidneys to concentrate
urine (resulting in polyuria, nocturia) and excessive
thirst.
Potassium depletion suppresses the release of
insulin and results in glucose intolerance.
Decreased muscle strength can be found on physical
assessment.
Severe hypokalemia can cause death through
cardiac or respiratory arrest.
78
 Management
Increased intake in the daily diet or by oral
potassium supplements
Foods high in potassium include most fruits and
vegetables, legumes, whole grains, milk, and meat.
Cautiously IV replacement for patients with severe
hypokalemia (e.g. serum level of 2mEq/L)
Monitor for sign of hyperkalemia; smooth muscle
hyperactivity can lead to hyperactive bowel sounds.

79
 Potassium excess (hyperkalemia)
Is when serum potassium >5.0 mEq/L
It is less common than hypokalemia, but is usually
more dangerous, because cardiac arrest is more
frequently associated with high serum potassium
levels.
Three major causes are:
Decreased renal excretion of potassium
Rapid administration of potassium and
Movement of potassium from the ICF
compartment to the ECF compartment.

80
 …cont’d
 Medications commonly implicated are potassium
chloride, heparin, ACE inhibitors, NSAIDs, beta-
blockers, and potassium sparing diuretics.
 In acidosis, as hydrogen ions enter the cells to buffer
the pH of the ECF.

81
 Clinical Manifestations

Muscle weakness, tachycardia, dysrhythmias and

cardiac arrest.
Flaccid paralysis, paresthesia
Nausea, Intestinal colic, cramps, abdominal
distention, and diarrhea.
Irritability, anxiety

82
 Management
In nonacute situations, restriction of dietary
potassium and potassium-containing medications
may correct the imbalance.
If serum potassium levels are dangerously elevated,
administer IV calcium gluconate (calcium
antagonizes the action of hyperkalemia on the heart,
but it does not reduce the serum potassium
concentration)
Monitor the BP hence hypotension may result from
the rapid IV administration of calcium gluconate

83
 …magt cont’d
IV administration of sodium bicarbonate, regular
insulin and a hypertonic dextrose solution may be
necessary to alkalinize the plasma, cause a temporary
shift of potassium into the cells.
Loop diuretics increase excretion of potassium
Beta-2 agonists, such as albuterol are highly effective
in decreasing potassium (move potassium into the
cells)

84
 Calcium deficit (hypocalcemia)
Occur when serum calcium level is lower than 8.6
mg/dl.
Contributing factors:
 Hypoparathyroidism (primary or post
surgical(thyroidectomy or Parathyroidectomy)
 After radical neck dissection
 Excessive secretion of glucagon from the inflamed
pancreas, which results in increased secretion of
calcitonin.

85
 …cont’d
 Patients with renal failure, because these patients
frequently have elevated serum phosphate levels
which causes a drop in the serum calcium level.
 Inadequate vitamin D consumption
 Medications like aluminum-containing antacids,
aminoglycosides, caffeine, and corticosteroids.

86
 Clinical Manifestations
Tetany; a general muscle hypertonia with:
Numbness and tingling in extremities
Stiffness of hands and feet
Bronchospasm, laryngeal spasm, carpopedal
spasm,
Photophobia, cardiac dysrhythmias and
seizures.
Hyperactive deep tendon reflexes.
Impaired clotting time, dry and brittle hair, diarrhea.

87
 …c/f cont’d
Positive:
Trousseau’s sign- carpopedal spasm is induced by
occluding the blood flow to the arm for 3
minutes with a blood pressure cuff.
Chvostek’s sign-when a sharp tapping over the
facial nerve just in front of the parotid gland and
anterior to the ear causes spasm or twitching of
the mouth, nose, and eye.
Osteoporosis

88
 Management
Acute symptomatic hypocalcemia is life-threatening
and requires prompt treatment with IV
administration of a calcium salt (calcium gluconate,
calcium chloride, and calcium gluceptate).
Calcium should be diluted in D5W and administered
as a slow IV bolus or a slow IV infusion.
0.9% sodium chloride solution should not be used
with calcium because it increases renal calcium loss.

89
 …magt cont’d
The patient is kept in bed during IV infusion, and
blood pressure should be monitored.
Vitamin D therapy can increase calcium absorption
from the GI tract.
Aluminum hydroxide, calcium acetate, or calcium
carbonate antacids may be prescribed to decrease
elevated phosphorus levels.
Increasing the dietary intake of calcium to at least
1000 to 1500 mg/day in the adult is recommended.

90
 Calcium excess (hypercalcemia)
Occurs when serum calcium level is greater than
10.2 mg/dl.
Reduces neuromuscular excitability because it
suppresses activity at the myoneural junction.
The most common causes are malignancies and
hyperparathyroidism.

91
Other factors include:
Immobilization after severe or multiple
fractures or spinal cord injury
Thiazide diuretics reducing urinary calcium
excretion
Prolonged period with milk and alkaline
antacids.
Vitamin A and D intoxication

92
 Clinical manifestations
Decreased tone in smooth and striated muscle may
cause symptoms such as muscle weakness,
incoordination, anorexia, nausea, vomiting,
constipation and dehydration.
Patients with chronic hypercalcemia may develop
symptoms similar to those of peptic ulcer disease
because hypercalcemia increases the secretion of
acid and pepsin by the stomach.

93
 …s/s cont’d
Confusion, impaired memory, slurred speech,
lethargy, acute psychotic behavior, or coma may
occur.
Hypercalcemic crisis refers to an acute rise in the
serum calcium level to 17 mg/dl or higher.
 Severe thirst and polyuria are characteristically
present.
 Can result in life-threatening neurologic,
cardiovascular and renal symptoms.

94
 Management
Treating the underlying cause (e.g.chemotherapy for a
malignancy or partial parathyroidectomy for
hyperparathyroidism)
Administering fluids to dilute serum calcium and
promote its excretion by the kidneys.
Phosphate therapy to promote calcium deposition in
bone and reducing GI absorption of calcium.
Loop diuretics promote renal excretion of calcium.
Calcitonin IM increases the deposit of calcium and in the
bones, and increases urinary excretion of calcium.
Mobilizing the patient to promote bone retention of
calcium.
Restricting dietary calcium intake. 95
 Acid-base imbalance
 Results If either bicarbonate or carbonic acid is
increased or decreased so that the 20:1 ratio is no
longer maintained.

96
 Metabolic acidosis
(base bicarbonate deficit)
• Is characterized by a low pH (increased H+ concentration)
and a low plasma bicarbonate concentration.
Results from:
Direct loss of bicarbonate, as in diarrhea, lower intestinal
fistulas, and use of diuretics.
Administration of parenteral nutrition without
bicarbonate or bicarbonate-producing solutes (e.g.
lactate).
Excessive administration of chloride
Excessive accumulation of fixed acid occurs in
ketoacidosis, lactic acidosis, and the late phase of salicylate
poisoning.
97
 Clinical Manifestations
Signs and symptoms vary with the severity of the
acidosis.
Headache, confusion, drowsiness, increased
respiratory rate and depth.
Nausea and vomiting
Peripheral vasodilation and decreased cardiac output
occur when the pH falls below 7.
Decreased BP, cold and clammy skin, dysrhythmias,
and shock .
The cardinal feature is a decrease in the serum
bicarbonate level(less than 22 mEq/L).
Low pH(less than 7.35). 98
 Management
 Treatment is directed at correcting the metabolic
defect.
 e.g. If the problem results from excessive intake of
chloride, eliminating the source.
 Bicarbonate is administered if the pH is less than 7.1
and the bicarbonate level is less than 10 mEq/L.
 In chronic metabolic acidosis, hemodialysis or
peritoneal dialysis may also be included.
 Although hyperkalemia occurs with acidosis,
hypokalemia may occur with reversal of the acidosis
and subsequent movement of potassium back into
the cells. Therefore, the serum potassium level is
monitored closely. 99
 Metabolic alkalosis
(base bicarbonate excess)
Characterized by a high pH (decreased H+
concentration) and a high plasma bicarbonate
concentration.
The most common cause is vomiting or gastric
suction with loss of hydrogen and chloride ions (loss
of this highly acidic fluid increases the alkalinity of
body fluids).
Hypokalemia :
The kidneys conserve potassium, and thus H+
excretion increases; and

100
 …cont’d
 Cellular potassium moves out of the cells into the
ECF in an attempt to maintain near-normal
serum levels thus, H+ must enter to maintain
electroneutrality.
Excessive alkali ingestion from antacids containing
bicarbonate.
Chronic ingestion of milk
Long-term diuretic therapy

101
 Clinical Manifestations
Tingling of the fingers and toes, dizziness, and
hypertonic muscles.
Atrial tachycardia, respirations are depressed as a
compensatory action by the lungs.
As the pH increases >7.6 and hypokalemia
develops, ventricular disturbances may occur.
Evaluation of arterial blood gases reveals a PH
greater than 7.45 and a serum bicarbonate
concentration greater than 26 mEq/L.

102
 Management
Treatment is aimed at reversing the underlying
disorder.
Chloride supplementation for the kidney allows
excretion of excess bicarbonate.
Restoring normal fluid volume by administering
sodium chloride fluids.
Potassium is administered as KCl to replace both K+
and Cl− losses
Monitor patient’s fluid intake and output

103
 Respiratory acidosis
(Carbonic acid excess)
Is a condition in which the pH is <7.35 and the PaCO2
is >42 mm Hg.
Is always due to inadequate excretion of CO2 with
inadequate ventilation, resulting in elevated plasma
CO2 levels and thus elevated carbonic acid (H2CO3)
levels and a decrease in PaO2
It can also occur in diseases that impair respiratory
muscles, such as muscular dystrophy, myasthenia
gravis, and Guillain-Barre syndrome.
Chronic respiratory acidosis occurs with pulmonary
diseases such as chronic emphysema and bronchitis,
obstructive sleep apnea, and obesity. 104
 Clinical Manifestations
Increased PR, RR and BP
Mental cloudiness, and feeling of fullness in the
head.
Cerebrovascular vasodilation and increased cerebral
blood flow.
In severe form ,sign of increased ICP (papilledema
and dilated conjunctival blood vessels)
Cyanosis and tachypnea
Hyperkalemia(shift of potassium out of the cell).

105
 Management
Treatment is directed at improving ventilation
Bronchodilators to reduce bronchial spasm
Antibiotics for respiratory infections
Anticoagulants for pulmonary emboli
Pulmonary hygiene measures, to clear the
respiratory tract of mucus and purulent drainage.
Hydration (2–3 L/day) to keep the mucous
membranes moist and thereby facilitate the
removal of secretions.

106
 …magt cont’d
Supplemental oxygen
Mechanical ventilation
Placing the patient in a semi-Fowler’s position
facilitates expansion of the chest wall.

107
 Respiratory alkalosis
(Carbonic acid deficit)
 A condition in which the arterial pH is >7.45 and the
PaCO2 is less than 38 mm Hg.
 Is always due to hyperventilation, which causes
excessive “blowing off” of CO2 and, hence, a
decrease in the plasma carbonic acid concentration
 Causes can include extreme anxiety, hypoxemia, the
early phase of salicylate intoxication, gram-negative
bacteremia, and inappropriate ventilator settings.

108
 Clinical Manifestations
Lightheadedness due to vasoconstriction and
decreased cerebral blood flow.
Numbness and tingling from decreased calcium
ionization.
Tinnitus, Inability to concentrate, at times loss of
consciousness.
Tachycardia and ventricular and atrial dysrhythmias.

109
 Management
Treatment is directed at correcting the underlying
problem.
If the cause is anxiety, the patient is instructed to
breathe more slowly to allow CO2 to accumulate or
to breathe into a closed system (such as a paper
bag).
A sedative may be required to relieve
hyperventilation in very anxious patients.

110
 Reading assignment

Magnesium imbalance
Phosphorus imbalance
Chloride imbalance

111
URINARY TRACT
IFECTIONS

112
 Terminologies
Frequency-frequent voiding(more than every 3 hrs).
Urgency-Strong desire to void.
Dysuria-Painful or difficult voiding.
Hesitancy-Delay, difficulty in initiating voiding.
Nocturia-Excessive urination at night.
Incontinence-Involuntary loss of urine.
Enuresis- Involuntary voiding during sleep.
Polyuria- Increased volume of urine voided
Oliguria- Urine output less than 500mL/day
Anuria-Urine output less than 50 mL/day
Hematuria-Red blood cells in the urine
Pyuria: white blood cells in the urine 113
 …terms cont’d
Proteinuria- Abnormal amounts of protein in the urine.
Uremia: an excess of urea and other nitrogenous wastes
in the blood
Bacteriuria: more than 105colonies of bacteria/ ml of
urine
Cystitis: inflammation of the urinary bladder
Prostatitis: inflammation of the prostate gland
Pyelonephritis: inflammation of the renal pelvis
Urethritis : inflammation of the urethra
Pyonephrosis: pus accumulation around the kidney
Urinary casts: microscopic particles formed in the
kidney from abnormal constituents in the urine such as
WBCs, RBCs, or pus. 114
 Introduction
Urinary tract infection(UTI) is a general term that
refers to invasion of the urinary tract by bacteria;
commonly Escherichia coli which found in stool.
classification
Lower UTIs include:
bacterial cystitis
bacterial prostatitis
bacterial urethritis
Upper UTIs-much less common and they includes:
Pyelonephritis
Interstitial nephritis
renal abscesses. 115
 Predisposing Factors for UTIs
Stasis of urine in the bladder serves as a culture
medium for bacterial growth.
Contamination in the perineal and urethral areas.
Instrumentation, the most common cause is urinary
catheterization.
Reflux of urine from the urethra to the bladder or the
bladder to the ureter because of faulty valves to
maintain one-way flow. (congenital, or result of
previous infections).
Previous history of UTIs.
Decreased natural host defenses or
immunosuppression. 116
 Urethritis

• Is inflammation of the urethra that may be due to:

A chemical irritant (detergents or lotions,
spermicidal agents) or
Infectious causes (typically sexually
transmitted)
Gonococcal urethritis (GCU) - Neisseria
gonorrhea
Nongonococcal urethritis (NGU) -
Chlamydia trachomatis, or Trichomonas
vaginalis.

117
 Clinical features
Urinary frequency, urgency, and dysuria.
In male, purulent discharge(GCU) and clear
discharge(NGU) from the penis.
It is difficult to diagnose in women (discharge
may not be present).

118
 Diagnosis
Urinalysis- 5 or more granulocytes per High
Power Field
Urine culture
inspect the prostate gland for swelling or
infection.
Tests to check for sexually transmitted diseases

119
 Management
Removal of the cause if it is caused by a chemical
irritant.
If bacteria, an antibiotic is prescribed based on the
results of a culture.
Analgesics
Sex partners should be referred for appropriate
evaluation and treatment.
Proper perineal hygiene should be stressed.

120
 Cystitis
Is inflammation of the bladder, usually caused by a
bladder infection (commonly by escherichia coli).
Other causes include radiotherapy and certain
chemicals.
It may also occur as a complication of another
illness.
Cystitis can be simple or complicated type.

121
Uncomplicated (Simple) cystitis
– In healthy adult woman
– Non-pregnant
– No signs of systemic disease(fever, nausea,
vomiting, flank pain)
Complicated cystitis
– Females with comorbid medical conditions
– All male patients
– Indwelling foley catheters
– Urosepsis/hospitalization
– Repeated infection

122
 Signs and Symptoms
Burning or pain when passing urine
Needing to pass urine a lot
A constant, dull ache in the lower abdomen
Urine that smells, or contains blood or is
cloudy.

123
 Diagnosis
Clinical presentations
Urinalysis-for uncomplicated
cloudy urine and the presence of WBCs,
bacteria, RBCs
Urine culture and sensitivity-For the complicated
UTI.

124
 Management
Uncomplicated cystitis sulfamethoxazole and
trimethoprim (Bactrim). about 80% of cases are
cured after 3 days of treatment.
Complicated cystitis is often treated with
ciprofloxacin or other broad spectrum antibiotic.
Other antibiotics may be prescribed depending on
the results of the urine culture and sensitivity.
Cephalosporins and penicillins are recommended
in pregnancy.

125
 Pyelonephritis
 Is an inflammation of the renal parenchyma,
calyces, and pelvis.
 It is commonly caused by bacterial infection that
has spread up the urinary tract or travelled through
the bloodstream to the kidneys.
 Almost always caused by Bacteria found in stool
(such as E. coli or klebsiella)
 Maybe acute or chronic

126
 Acute pyelonephritis
Results from bacterial invasion of the renal
parenchyma.
Patients with acute pyelonephritis usually have
enlarged kidneys with interstitial infiltrations of
inflammatory cells.

127
 Sign and symptoms
Patient will become acutely ill,
Chills , fever, malaise, and flank pain.
Dysuria and frequency
CVA tenderness to percussion is a common
finding

128
 Diagnosis
Hx ad P/E
Urine test to check for bacteria.
The urine will also be checked for concentration,
blood, pus, and casts
Urine culture and sensitivity
X-rays or an ultrasound to look for cysts or tumors
in the urinary tract.

129
 Management
Pt with mild signs and symptoms may be treated on
an outpatient basis with antibiotics for 14 to 21 days.
Other patients, including all pregnant women, may
be hospitalized for at least 2 or 3 days of parenteral
antibiotic therapy.
Antibiotics are selected according to results of
urinalysis, culture and sensitivity and may include
broad-spectrum medications.
A follow-up urine culture is done 2 weeks after
completion of antibiotic therapy to document
clearing of the infection.

130
 Chronic Pyelonephritis
Implies recurrent kidney infections, and can result
in scarring of the renal parenchyma and impaired
function.
The kidneys become scarred, contracted, and
nonfunctioning.
It may develop in association with other renal
disease unrelated to infection processes.

131
 Clinical Manifestations
Patient usually has no symptoms of infection unless
an acute exacerbation occurs.
Noticeable signs and symptoms may include
fatigue, headache, poor appetite, polyuria, excessive
thirst, and weight loss.
A perinephric abscess and/or pyonephrosis may
develop in severe cases.
Persistent and recurring infection may produce
progressive scarring of the kidney, which may result
in renal failure(ESRD).

132
 Diagnosis

 Intravenous urogram
 measurements of creatinine clearance
 BUN and serum creatinine levels.

133
 Management
Antibiotic therapy for acute infections
Antibiotic prophylaxis for prevention of recurrent
infections
Close monitoring of patients
Investigation and management as appropriate for
underlying structural abnormalities
Management of renal impairment as indicated by the
degree of impairment

134
Obstruction of Urinary
system

135
 Urethral Strictures
Is a narrowing of the lumen of the urethra caused by
scar tissue.
A common cause of stricture is:
Urethral injury resulting from insertion of
catheters or surgical instruments.
Direct application of force to the perineal area
Sexually transmitted infections (untreated
gonorrhea)
Congenital abnormalities.

136
 Signs and symptoms
Diminished force and volume of the urinary stream
Inability to fully empty the bladder
Symptoms of urinary infection and retention occur
Hydronephrosis (distension and dilation of
the renal pelvis and calyces)

137
 Treatment
Urethral dilatation and drainage of the urinary
bladder with metal sounds(bougies) or surgery
(internal urethrotomy)
Insertion of a suprapubic catheter.
After dilation
Hot sitz baths and nonopioid analgesic agents to
control pain.
Antibiotic for several days
Surgery (urethroplasty) -the repair of an injury or
defect within the walls of the urethra.

138
 Urolithiasis
Refers to stones (calculi)any were in the urinary
tract.
Are formed when there is a high concentrations of
mineral(s);i.e. calcium (hypercalciuria), oxalate
(hyperoxaluria), or uric acid (hyperuricosuria) in
the urine.
They may vary in size from minute granular
deposits, called sand or gravel, to bladder stones as
large as an orange.

139
 ...cont’d

Calcium oxalate is a major constituent of most

urinary stones.
Stones can be classified by their location or by
their chemical composition
80% of those with kidney stones are men,
commonly b/n 20-30 years of age.

140
 Risk factors
Early onset of urolithiasis
Familial stone formation
Genetic predisposition
Fluid intake pattern
Dehydration
High doses of vitamin C-result in high levels of
oxalate in the urine
A low level of citrate
Gout (excessive uric acid in the blood)
Infection-provide nucleus for stone formation
Only one functioning kidney

141
 …risk factors cont’d
Disease associated with stone formation: 
e.g. - hyperparathyroidism 
- renal tubular acidosis 
  - malabsorptive conditions 
Medication associated with stone formation: 
e.g. - calcium supplements 
- vitamin D supplements 
- acetazolamide
Anatomical abnormalities associated with stone
formation:
  e.g 
- ureteral stricture 
- vesico-ureteral reflux 
142
 Location of stones
Nephrolithiasis (renal calculus) -stones in
the kidney
Ureterolithiasis-stones in the ureter.
Cystolithiasis-refers to stones which form or have
passed into the urinary bladder.

143
 Pathophysiology
For precipitation of crystals in urine to occur, the
urine must be "supersaturated“.
Urine normally contains chemicals citrate,
magnesium, and pyrophosphate that prevent the
formation of crystals.
Low levels of these inhibitors can contribute to the
formation of kidney stones.
Citrate is thought to be the most important.
Insufficient water in the kidneys to dissolve waste
products is also an other contributing factor.

144
 ….cont’d

The chemical composition of stones depends on

the chemical imbalance in the urine.
The four most common types of stones are
comprised of calcium, uric acid, struvite, and
cystine.

145
 Calcium Stones
Approximately 85% of stones are composed
predominantly of calcium compounds.
The most common cause of calcium stone
production is excess calcium in the urine
(hypercalciuria).
Excess calcium builds up in the kidneys and urine,
where it combines with other waste products to
form stones.
Low levels of citrate, high levels of oxalate and
inadequate urinary volume may also contribute.
Calcium stones are composed of calcium oxalate or
calcium phosphate.

146
 …cont’d
These stones come in 2 different types -
monohydrate and dihydrate.
Calcium oxalate dihydrate stones usually break
easily with lithotripsy.
Monohydrate stones are among the most difficult
stones to fragment.

147
 Uric Acid Stones
 Approximately 10% of patients with kidney stone disease
develop this type of stone.
 Digestion produces uric acid.
 If the acid level in the urine is high or too much acid is
excreted, the uric acid may not dissolve and uric acid
stones may form.
 Patients with gout often develop these stones.
 Genetics may play a role in the development of uric acid
stones, which are more common in men.
 They are not visible on X-rays.
 Uric acid stones form in acidic urine and often dissolve
when the urine is alkalinized.
148
 Struvite Stones
Also called an infection stone
Develops when a urinary tract infection affects the
chemical balance of the urine.
Bacteria in the urinary tract release chemicals that
neutralize acid in the urine, which enables bacteria
to grow more quickly.
They are capable of splitting urea into ammonia,
decreasing the acidity of the urine and resulting in
favorable conditions for the formation of struvite
stones.
Struvite stones are more common in women.
Accounts about 15% of urinary calculi
149
 Cystine Stones
Some people inherit a rare, congenital condition
that results in large amounts of cystine in the
urine. This condition (called cystinuria) causes
cystine stones.
They are difficult to treat and requires life-long
therapy.
1% to 2% of all stones.

150
 Clinical Manifestations
Manifestations depend on obstruction, infection,
and edema.
Stones in the renal pelvis may be associated with:
Intense, deep ache in the CVA region that
radiates anteriorly and downward to the
bladder in female and testis in male
Hematuria, pyuria
Nausea and vomiting
Diarrhea and abdominal discomfort may also
occur.

151
 …s/s cont’d
Stones lodged in the ureter cause :
Acute, colicky, wavelike pain, radiating down the
thigh and genitalia.
Desire to void, but little urine is passed, and it
usually contains blood because of the abrasive
action of the stone. This group of symptoms is
called ureteral colic.

152
 …s/s cont’d
Stones lodged in the bladder usually produce
symptoms of irritation and may be associated with
UTI and hematuria.
If the stone obstructs the bladder neck, urinary
retention occurs.
If infection is associated with a stone, the condition
is far more serious, with sepsis threatening the
patient’s life.

153
 Diagnosis
Diagnosis of is often made on the basis of clinical
symptoms alone, although confirmatory tests are
usually performed.
Hx including assessing risk factors
Physical findings
Laboratory tests
Microscopic urinalysis
Serum creatinine level
Serum electrolyte level
Serum and urinary pH level
154
Radiology
X-ray studies-most stones are radiopaque.
Ultrasonography

155
 Management
Patients can urinate stones if they are 5 mm or smaller;
larger stones do not pass.
IV hydration
Po/IV narcotic analgesics (e.g, codeine, morphine
sulfate)
NSAIDS- in addition to relieving pain, inhibit the
synthesis of prostaglandin E, reducing swelling and
facilitating passage of the stone.
Hot baths or moist heat to the flank areas
Encouraged fluids -to keep the urine dilute
Antiemetics (e.g. metoclopramide)
Antibiotics (e.g. ampicillin, gentamicin, ciprofloxacin)
156
 …mag’t cont’d

Uricosuric agents (eg, allopurinol)

Alkalinizing agents (eg, potassium citrate, sodium
bicarbonate): for uric acid and cystine calculi.
Nutritional Therapy
E.g for uric acid stones, the patient is placed on a
low-purine diet to reduce the excretion of uric
acid in the urine.
Lithotripsy-is used to break the stones into smaller
parts that can then be removed or urinated out.
Surgery-if the stone does not respond to other forms
of treatment
157
 Surgical procedures
 Nephrolithotomy -incision into the kidney with
removal of the stone .
 Nephrectomy- if the kidney is nonfunctional
secondary to infection or hydronephrosis.
 Stones in the kidney pelvis are removed by a
pyelolithotomy, those in the ureter by
ureterolithotomy, and those in the bladder by
cystotomy.

158
Lithotripsy

159
Percutanous nephrolithotomy

160
Extracorporal shock wave lithotripsy(ESWL)

161
Endourological removal (cystoscopy)

162
 Preventing Kidney Stones
Restriction of protein intake
Reducing sodium intake hence, sodium competes
with calcium for reabsorption in the kidneys.
Low-calcium diets are not generally recommended,
except for true absorptive hypercalciuria. limiting
calcium, especially in women, can lead to
osteoporosis and does not prevent renal stones.
Avoiding intake of oxalate-containing foods.
During the day, drink fluids (ideally water) every 1 to
2 hours.

163
 …prev. cont’d
Drink two glasses of water at bedtime and an
additional glass at each nighttime.
Avoid activities leading to sudden increases in
environmental temperatures that may cause
excessive sweating and dehydration.
Contact your primary health care provider at the first
sign of a urinary tract infection.

164
BENIGN PROSTATIC HYPERPLASIA (BPH)

BPH is a progressive adenomatous enlargement

of the prostate gland that occurs with aging.
It is also called benign enlargement of the
prostate (BEP), adenofibromyomatous
hyperplasia and benign prostatic hypertrophy.
The gland enlarges, extending upward into the
bladder and obstructing the outflow of urine
Affects half of men over age 50 and 90% of men
over age 80.

165
166
 Causes of BPH
 The cause is not completely understood
 BPH is part of the natural aging process
 Dihydrotestosterone (DHT), a metabolite of
testosterone, is a critical mediator of prostatic
growth.
 DHT is synthesized in the prostate from circulating
testosterone by the action of the enzyme 5α-
reductase, type 2.
 This enzyme is localized principally in the stromal
cells; hence, those cells are the main site for the
synthesis of DHT.

167
 Facts about BPH
Castrated boys do not develop BPH when they are
aged.
BPH cannot be prevented.
BPH can be treated.
BPH does not predispose to the development of
prostate cancer.

168
Pathophysiology

169
 Clinical Manifestations
Symptoms are classified as storage or voiding.
Storage symptoms include urinary frequency,
urgency, incontinence, and nocturia.
Voiding symptoms include hesitancy,
intermittency, straining to void, and dribbling.
This symptoms can be evaluated using the IPSS
questionnaire
Frequent UTIs
Gradual dilation of the ureters (hydroureter) and
kidneys (hydronephrosis)

170
 Diagnostic tests
Medical history
Validated symptom questionnaire
Physical examination
Urinalysis
CBC –to monitor post op complications
Transrectal Ultrasound of Prostate
Biopsy

171
 Possible findings
 Symmetrical enlargement of the gland
 Marked protrusion into the rectal lumen
 Smooth with no nodularity
 Median sulcus may be indistinguishable
 Consistency is slightly elastic
 Non tender

172
 International prostate symptom score (IPSS)
 

questions More
Less Less
About than
than 1 than Almost Your
Not at all half the half
time half the always score
time the
in 5 time
time

INCOMPLETE EMPTYING 
OVER THE PAST MONTH, HOW OFTEN HAVE YOU HAD A
SENSATION OF NOT EMPTYING YOUR BLADDER
0 1 2 3 4 5  
COMPLETELY AFTER YOU FINISH URINATING?

FREQUENCY
OVER THE PAST MONTH, HOW OFTEN HAVE YOU HAD TO
URINATE AGAIN LESS THAN TWO HOURS AFTER YOU
0 1 2 3 4 5  
FINISHED URINATING?
 
 
INTERMITTENCY
OVER THE PAST MONTH, HOW OFTEN HAVE YOU FOUND
YOU STOPPED AND STARTED AGAIN SEVERAL TIMES WHEN
0 1 2 3 4 5  
YOU URINATED?

URGENCY
OVER THE LAST MONTH, HOW DIFFICULT HAVE YOU 0 1 2 3 4 5  
FOUND IT TO POSTPONE URINATION?

Weak stream
OVER THE PAST MONTH, HOW OFTEN HAVE YOU HAD A WEAK 0 1 2 3 4 5  
URINARY STREAM?
 
Straining
OVER THE PAST MONTH, HOW OFTEN HAVE YOU HAD TO PUSH OR 0 1 2 3 4 5  
STRAIN TO BEGIN URINATION?

Nocturia  None 1 time 2 times 3 times

4
times
5 times
or more
OVER THE PAST MONTH, MANY TIMES DID YOU MOST TYPICALLY
GET UP TO URINATE FROM THE TIME YOU WENT TO BED UNTIL THE
TIME YOU GOT UP IN THE MORNING?
Total score:
0-7 Mildly symptomatic;
8-19 moderately symptomatic;
20-35 severely symptomatic.

174
 Management

Mild symptoms managed with watchful

waiting.
Moderate to Severe symptoms needs:
Watchful waiting
Medical management and
Surgical treatment.

175
 Watchful Waiting and Behavioral Modification
Decrease caffeine, alcohol consumption.
Avoid taking large amounts of fluid over a short
period of time.
Void whenever the urge is present, every 2-3 hours
Maintain normal fluid intake, do not restrict fluid
Avoid bladder irritants.
Limit nighttime fluid consumption.
Patients will be examined yearly for the need of
additional treatment.

176
Medical Management
Foley’s catheter (stylet, metal catheters)
Drug therapy
alpha blockers – relax the smooth muscles along
urinary tract which improves urine flow
(doxazosin, terazosin, tamsulosin)
5-alpha reductase inhabitors - antiandrogen
agents; shrink the prostate gland (finasteride,
dutasteride)
narcotic analgesic – relieve post-op pain
(morphine, codeine)

177
Surgical treatment
Indicated for IPSS of >16
TURP(closed procedure)
Gold Standard” of care for BPH
Uses an electrical “knife” to surgically cut and
remove excess prostate tissue
Long lasting and effective in relieving symptoms
and restoring urine flow

178
 …surgery cont’d

Prostatectomy
Perineal prostectomy –incision between the
scrotum and anus(rare)
Suprapubic resection – lower abdomen – incision
through the bladder.
Retropubic –midline abd. incision– does not go
through the bladder.
Laparoscopic prostatectomy

179
 Complications of BPH
Urinary retention
UTI
Residual urine
Sepsis secondary to UTI
Calculi
Hematuria
Renal failure

180
 Care of prostate surgery
Relieving pain
Monitoring V/S, I&O
Continuous irrigation & maintain catheter
patency( three lumen system of catheterization)
Blood clots and hematuria are expected for the first 24-
36 hours.
After catheter is removed – check for urinary retention
and urinary stream.
Encourage Kegal exercise pelvic muscle floor technique
hourly.
Stool softeners to avoid straining
Sitting and walking for long periods should be avoided
181
 ….care cont’d
 Reduce anxiety
 Monitoring and managing potential complications
Bleeding
Infection
Clot formation
Erectile dysfunction(damage to the pudendal
nerves)
Retrograde ejaculation
Urinary incontinency or dribbling

182
Diseases of the
Kidney

183
 Acute glomerulonephritis
Glomerulonephritis is an inflammation of the
glomerular capillaries.
Acute glomerulonephritis is primarily a disease of
children older than 2 years of age, but it can occur at
nearly any age.
It occurs over days or weeks
It is not infection of the kidney but, rather untoward
side effects of the defense mechanism of the body.

184
 Causes
In most cases, a group A beta-hemolytic
streptococcal infection of the throat precedes the
onset of glomerulonephritis by 2 to 3 weeks.
It may also follow impetigo (infection of the skin)
and acute viral infections (URIs, mumps, HBV, HIV
infection).
In some patients, antigens outside the body (eg,
medications, foreign serum) initiate the process,
resulting in antigen-antibody complexes being
deposited in the glomeruli.
In other patients, the kidney tissue itself serves as
the inciting antigen.
185
Pathophysiology

186
 Clinical Manifestations
hematuria, which may be microscopic or
macroscopic
cola-colored Urine because of RBCs and protein
plugs or casts. (RBC casts indicate glomerular
injury.)
Proteinuria-due to the increased permeability of the
glomerular membrane.
hypoalbuminemia
BUN and serum creatinine levels may rise as urine
output drops.
The patient may be anemic.
Edema and hypertension in 75% of patients 187
 …c/f cont’d
In the more severe form:
The patient has ARF with oliguria
headache, malaise, and flank pain
circulatory overload
Confusion and seizures

188
 Diagnostic Findings
kidneys become large, edematous, and congested
Lab test
Urinalysis test-Look for protein, RBCs, WBCs,
casts
 Blood tests may show anemia, abnormal
albumin levels, abnormal BUN, and high
creatinine levels.

189
 Management
Most cases resolve spontaneously in about a week,
but some progress to renal failure.
Treatment is primarily symptomatic and treat
complications promptly.
Corticosteroids, managing hypertension
Sodium and fluid restrictions may be ordered along
with diuretics when the patient has hypertension,
edema, and heart failure.
If associated with a streptococcus infection,
antibiotics are given (penicillin is the agent of
choice).
190
 Complications
Majority of children recover completely.
Adults who develop glomerulonephritis may recover
renal function or progress to chronic
glomerulonephritis.
Hypertensive encephalopathy
Heart failure and
Pulmonary edema
Without treatment, ESRD develops in a matter of
weeks or months

191
 Chronic glomerulonephritis
Characterized by irreversible and progressive
glomerular and tubulointerstitial fibrosis,
ultimately leading to a reduction in the glomerular
filtration rate (GFR) and retention of uremic toxins.
Caused by slow, cumulative damage and scarring of
the tiny blood filters in the kidneys.
May lead to gradual loss of renal function, and
eventual renal failure.

192
 Causes
The specific cause of most cases of chronic
glomerulonephritis is unknown.
Viral infections, such as hepatitis B or C and AIDS.
Autoimmune disorders, such as systemic lupus
erythematosus, or other causes of vasculitis
May be due to repeated episodes of acute
glomerulonephritis.

193
 Clinical Manifestations
May develop silently (without symptoms) over
several years.
Early signs and symptoms may include:
Blood or protein in the urine (hematuria,
proteinuria)
High blood pressure
Swelling of ankles or face (edema)
Frequent nighttime urination
Very bubbly or foamy urine

194
 …c/f cont’d
As the disease progresses, signs and symptoms of
renal insufficiency and chronic renal failure may
develop
Loss of appetite, nausea and vomiting
Periorbital and peripheral (dependent) edema
Dry and itchy skin
Sign of anemia, heart failure
Peripheral neuropathy
Reversal in sleep pattern
Nighttime muscle cramps
Seizures, tremors
195
 Diagnostic Findings
History and physical examination
Laboratory studies-Blood and urine tests
Chest x-ray- to show fluid overload.
Ultrasound study of the kidneys may be performed
to evaluate the size of the kidneys.
kidneys are reduced to as little as one-fifth their
normal size (consisting largely of fibrous tissue).
A kidney biopsy may be performed.

196
 Management
Symptomatic management
If the patient has hypertension, the blood pressure
is reduced with sodium and water restriction,
antihypertensive agents, or both
Weight is monitored daily
Medications are prescribed to treat fluid overload
Treat UTIs to prevent further renal damage.
Initiation of dialysis is considered early in the
course of the disease to keep the patient in optimal
physical condition.

197
 Nephrotic syndrome
Is a 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
(hyperlipidemia)
It is characterized by an increase in permeability of the
capillary walls of the glomerulus.
It is most common in children but can affect all age
groups.
198
 Causes
• Most commonly, it is primary or idiopathic.
• Primary causes include:
Minimal-change nephropathy
Focal glomerulosclerosis
Membranous nephropathy
Hereditary nephropathies
• Secondary causes include 
Diabetes mellitus
Lupus erythematosus
Amyloidosis and paraproteinemia
Multiple myeloma
Viral infections (eg, hepatitis B, hepatitis C, HIV)
199
P
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y 200
 Clinical Manifestations
Soft and pitting edema that commonly occurs
around the eyes (periorbital), in dependent areas
(sacrum, ankles, and hands), and in the abdomen
(ascites).
Malaise, headache, irritability, and fatigue
Poor appetite
Unintentional weight gain
Foamy urine 

201
 Diagnostic Findings
Urinary protein measurement
Proteinuria exceeding 3 to 3.5 g/day is sufficient for
the diagnosis of nephrotic syndrome
Serum albumin
hypoalbuminemia: albumin levels of ≤2.5 g/dl
Renal function tests
Lipid profile- elevated LDL, VLDL
Renal ultrasonography
Renal biopsy

202
 Management
Treatment can be symptomatic or can directly
address the injuries caused to the kidney.
Diuretic agents may be prescribed for the patient
with severe edema.
The use of ACE inhibitors in combination with
diuretics often reduces the degree of proteinuria but
may take 4 to 6 weeks to be effective.
Antineoplastic agents or immunosuppressant
medications.
No data to show that lipid-lowering drugs improve
renal or patient outcomes.
Blood thinners may be needed to treat or prevent
blood clots. 203
 …magt cont’d
low-sodium, liberal-potassium diet to enhance the
sodium/potassium pump mechanism, thereby
assisting in elimination of sodium to reduce edema.
Protein intake should be about 0.8 g/kg/day, with
emphasis on high biologic proteins (dairy products,
eggs, meats), and the diet should be low in saturated
fats (not consume more than 1 g of protein/kg body
weight/ day).
Ongoing activity, rather than bed rest, will reduce
the risk of blood clots.

204
 Complications
Infection
Renal vein thrombosis
Atherosclerosis and related heart diseases
Acute renal failure
Chronic kidney disease
Fluid overload, CHF, pulmonary edema
Malnutrition

205
 Renal Failure
Also called kidney failure, is diagnosed when the
kidneys cannot remove the body’s metabolic wastes
or perform their regulatory functions.
Results in dysfunction in almost all other parts of
the body as a result of imbalances in fluid,
electrolytes, and calcium levels, as well as impaired
RBC formation and decreased elimination of waste
products.
It can be acute or chronic

206
 Acute renal failure (ARF)
• Is a rapid loss of renal function due to damage to the
kidneys.
• In ARF, rapid damage to the kidney causes waste
products to accumulate in the bloodstream,
resulting in the symptoms of renal failure.
• Has a high mortality rate that ranges from 25% to
90%.

207
 Causes
• Prerenal Failure (hypoperfusion of kidney)
• Occurs in 60% to 70% of cases
Volume depletion resulting from:
 Hemorrhage, Renal losses (diuretics, osmotic
diuresis),GI losses (vomiting, diarrhea, nasogastric
suction)
Impaired cardiac efficiency resulting from:
 MI, HF, dysrhythmias, cardiogenic shock
Vasodilation resulting from:
 Sepsis, anaphylaxis, medications like
antihypertensive or others
208
 …cause cont’d
• Intrarenal Failure (actual damage to kidney tissue)
Prolonged renal ischemia resulting from:
 Pigment nephropathy, myoglobinuria,
hemoglobinuria
Nephrotoxic agents such as:
 Certain antibiotics (aminoglycosides, tetracyclines),
NSAIDs, ACE inhibitors, contrast agents, Heavy
metals (lead, mercury), chemicals (carbon
tetrachloride, arsenic),
Infectious processes such as:
 acute pyelonephritis, acute glomerulonephritis
209
 …cause cont’d
• Postrenal Failure (obstruction to urine flow)
Urinary tract obstruction, including:
Calculi (stones)
Tumors
Benign prostatic hyperplasia
Strictures
Blood clots
 In this case the blood supply to the kidneys and
nephron function initially may be normal, but
resulting in impaired nephron function.

210
 Phases of Acute Renal Failure
• There are four phases of ARF:
Initiation
Oliguria
Diuresis and
Recovery

211
 …Phases cont’d
Initiation period begins with the initial insult and
ends when oliguria develops.
Oliguria period is accompanied by an increase in the
the serum concentration of substances excreted by
the kidneys .
In phase uremic symptoms first appear and life-
threatening conditions such as hyperkalemia develop.
Diuresis period is marked by a gradual increase in
urine output, which signals that glomerular filtration
has started to recover. Uremic symptoms may still be
present. The patient must be observed closely for
dehydration during this phase.
212
 …Phases cont’d
Recovery period signals the improvement of renal
function and may take 3 to 12 months.
Laboratory values return to the patient’s normal
level.
Although a permanent 1% to 3% reduction in the
GFR is common, it is not clinically significant.

213
 Clinical Manifestations
Almost every system of the body is affected with
failure of the normal renal regulatory mechanisms.
The patient may appear critically ill and lethargic.
The skin and mucous membranes are dry from
dehydration.
CNS symptoms; drowsiness, headache, muscle
twitching, and seizures.
Sign of metabolic acidosis and electrolyte
imbalance.

214
 Diagnostic Findings
Common laboratory finding
A widely accepted criterion for ARF is a 50% or
greater increase in serum creatinine above baseline
(normal is < 1.0 mg/dl)
Evaluation for changes in the urine
Urine volume may be normal, or changes may
occur. Oliguria (<500 mL/day), nonoliguria (>800
mL/day), or anuria(<50 mL/day)
Hematuria may be present, and the urine has a low
specific gravity.

215
 …dx cont’d
Serum electrolyte levels
Anemia
X-ray examination of the kidneys, ureters, and
bladder to diagnose causes of postrenal failure
Ultrasonography

216
 Management
The objectives of treatment are:
to restore normal chemical balance and
prevent complications
Management includes:
Eliminating the underlying cause
Maintaining fluid balance; and
Providing renal replacement therapy (when
indicated)

217
 …magt cont’d
 Prerenal azotemia is treated by optimizing renal
perfusion
 Intrarenal azotemia is treated with supportive
therapy
 Postrenal failure is treated by relieving the
obstruction.
 Adequate renal blood flow in patients with prerenal
causes of ARF may be restored by IV fluids or
transfusions of blood products.
 Dialysis may be initiated to prevent complications of
ARF, such as hyperkalemia, metabolic acidosis,
pericarditis, and pulmonary edema.
218
 Methods to replace normal kidney
• Continuous renal replacement therapies
(CRRTs)-function by circulating the patient’s blood
through a hemofilter.
• Hemodialysis- is a procedure that circulates the
patient’s blood through a dialyzer to remove waste
products and excess fluid
• Peritoneal dialysis- a procedure that uses the
patient’s peritoneal membrane as the
semipermeable membrane to exchange fluid and
solutes

219
 Prevention of ARF
Provide adequate hydration to patients at risk for
dehydration
Prevent and treat shock promptly with blood and
fluid replacement.
Monitor central venous and arterial pressures and
hourly urine output of critically ill patients to detect
the onset of renal failure as early as possible.
Continually assess renal function (urine output,
laboratory values) when appropriate.
Appropriately administer blood in order to avoid
severe transfusion reactions, which can precipitate
renal failure.
220
 …prev cont’d
Prevent and treat infections promptly.
Pay special attention to wounds, burns, and other
precursors of sepsis.
Give meticulous care to patients with indwelling
catheters. Remove catheters as soon as possible.
Closely monitor dosage, duration of use, and blood
levels of all medication metabolized or excreted by
the kidneys.

221
 Chronic Renal Failure or ESRD
It occurs with a gradual decrease in the function of
the kidneys over time.
This loss of function is not reversible.
The causes of chronic renal failure are numerous;
common ones include:
Diabetic nephropathy
Chronic hypertension causing nephrosclerosis
Glomerulonephritis, and
Autoimmune diseases

222
 Clinical Manifestations
Every body system is affected in ESRD, patients
exhibit a number of signs and symptoms.
Uremia develops and adversely affects every system
in the body.
In the early, or silent, stage the patient is usually
without symptoms, even though up to 50% of
nephron function may have been lost.
The renal insufficiency stage occurs when the patient
has lost 75 % of nephron function and some signs of
mild renal failure are present. Anemia and the
inability to concentrate urine may occur. The BUN
and creatinine levels are slightly elevated.
223
 ….s/s cont’d
ESRD occurs when 90% of the nephrons are lost.
Patients at this stage experience chronic and
persistent abnormal kidney function.
The BUN and creatinine levels are always elevated.
These patients may make urine but not filter out the
waste products, or urine production may cease.

224
 Diagnostic Findings
Decreased GFR
Sodium and Water Retention
Metabolic acidosis
Anemia
Serum electrolyte disturbance (see what happens)

225
 Management
Complications can be prevented or delayed by
administering prescribed phosphate-binding
agents, calcium supplements, antihypertensive and
cardiac medications, antiseizure medications, and
erythropoietin.
Dietary intervention-Protein is restricted. The
allowed protein must be of high biologic value.
Calories are supplied by carbohydrates and fat to
prevent wasting.
Vitamin supplementation is necessary because a
protein-restricted diet does not provide the
necessary complement of vitamins
226
 …magt cont’d
Hyperkalemia is usually prevented by ensuring
adequate dialysis treatments with potassium
removal and careful monitoring of diet,
medications, and fluids for their potassium content.
The patient with increasing symptoms of renal
failure is referred to a dialysis and transplantation
center early in the course of progressive renal
disease.

227
 Complications
Hyperkalemia
Acidosis
Pericarditis, pericardial effusion, and pericardial
tamponade
Hypertension
Anemia
Irritating during hemodialysis
Bone disease and metastatic and vascular
calcifications

228
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