Disorders of the Genitourinary System and

Nursing Responsibilities

July-2022

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 Anatomy and Physiology of
Genitourinary System Overview
1. Kidneys (2)
2. Ureters (2)
3. Urinary bladder (1)
4. Urethra (1)

2
 Location of the Kidneys
 Dimensions
 Reddish-brown, bean shaped
 12cm long, 6cm wide, 3cm thick
 High on posterior abdominal wall
 at the level of T12 to L3- superior lumbar region
 Retroperitoneal & against the dorsal body wall
 The right kidney is slightly lower than the left ,convex laterally
 Attached to ureters, renal blood vessels, and nerves at renal
hilus (medial indention)
 A top each kidney is an adrenal gland

3
 Physiology of the Kidneys
• Urine formation

• Excretion of waste products

• Regulation of electrolytes

• Regulation of acid–base balance

• Control of water balance

• Control of blood pressure

• Synthesis of vitamin D to active form

• Regulates calcium and phosphorus balance

4
 Physiology of the Urinary System
 Elimination of waste products
 filtering gallons of fluid from the bloodstream every day
creating “filtrate”
 “filtrate” includes: metabolic wastes, ionic salts, toxins, drugs
 Maintenance of blood
 Red blood cell production- by producing hormone
erythropoietin to stimulate RBC production in bone
marrow
 Blood pressure (vessel size)- by producing renin which
causes vasoconstriction
 Blood volume (water balance)- ADH released from
Anterior Pituitary targets the kidney to limit water loss
when blood pressure decreases or changes in blood
composition
 Blood composition (electrolyte balance)- water follows
salt; aldosterone reclaims sodium to the blood
 Blood pH- regulates H+ ions and HCO3- ions 5
7
 Nephrons
 The structural and functional units of the kidneys
 Over 1 million
 Responsible for forming urine
 Consist of renal corpuscle and renal tubule
 Renal corpuscle composed of a knot of capillaries
called the Glomerulus (a.k.a. Bowman’s Capsule)
 Renal tubule- enlarged, closed, cup-shaped end
giving rise to the PCT, dLOH, aLOH, DCT, and CD.

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 Urine Formation Processes
 Filtration- Water & solutes smaller than
proteins are forced through the capillary
walls and pores (of the glomerulus) into
the renal tubule.
 Reabsorption- Water, glucose, amino
acids & needed ions are transported out
of the filtrate into the peritubular
capillary cells and then enter the
capillary blood.
 Secretion- Hydrogen ions, Potassium
ions, creatinine & drugs are removed
from the peritubular capillaries (blood)
and secreted by the peritubular capillary
cells into the filtrate.
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 ASSESSEMEN OF URINARY SYSTEM
 Symptoms of genitourinary diseases

 Ureteric pain-

 Hematuria

 Anuria-Is total urine output less than 50 mL in 24 hours.

 Polyuria- urine output of more than 3L per 24 hours

 Urinary frequency-voiding more frequently than every 3

hours
 Nocturia: Implies the need to rise during hours of sleep to empty the
bladder 10
 Dysuria-painful or difficult urination

 Urgency-Is the loss of the normal ability to postpone

micturation beyond the time when the desire to pass urine is
initially perceived.
 Incontinence: Refers to an involuntary loss of urine that
has become a social or hygienic problem
 Hesitancy: Is difficulty initiating the process of micturation

 Terminal dribbling: is difficulty of completing micturation

in a clean stop fashion
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 Dysmenorrhea- is pain with menstruation

 Dyspareunia: Is pain on sexual intercourse.

 Vaginismus- refers to an involuntary spasm of the muscles
surrounding the vaginal orifice that makes penetration
during intercourse painful or impossible.

12
 Physical examination
 Kidneys

• Assess each kidney for tenderness.

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 DIAGNOSTIC STUDIES OF URINARY SYSTEM
1. URINANALSIS
• Findings are: Color, Smell, protein, glucose, ketones,
specific gravity, osmolality, PH, WBC, RBC, casts,
culture for organisms, etc...

2. Blood Chemistry
 BUN ( Blood urea nitrogen ) NR 10-30 mg/dl)

 serum creatinine (NR 0.5 - 1.5 mg/dl )

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 Fluid imbalances
Fluid Volume Deficits(FVD)

 Causes

 Inadequate fluid intake

• Unconsciousness/coma or inability to express thirst

• Oral trauma or inability to swallow

• Impaired thirst mechanism

• Withholding of fluid for therapeutic reason

17
 Excessive fluid losses
• GI losses
-vomiting
-diarrhea
-GI suctioning
-fistula drainage
• Urine losses
-diuretics therapy
-osmotic diuresis(hyperglycemia)
-salt wasting renal diseases

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• Skin losses

-Exposure to hot environment

-Fever

-Burns and wounds that remove skin

 Other risk factors

• hemorrhage

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C/M
• Acute weight loss(% body weight)

• Mild FVD: 2% loss

• Moderate: 2-5% loss

• Sever: 6% or more loss

• thirst, nausea

• decrease urine out put(oliguria)

• Increase urine osmolality

• Increase specific gravity

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• Increase hematocrit

• Increase BUN

-decrease vascular volume

• Tachycardia, weak thready pulse

• Postural hypotention

• Vein filling & vein refilling time

• Hypotension & shock

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• Sunken eyes & soft eyeballs

• Dry skin (skin turgor) & mucous membrane

• Cracked & fissured tongue

• Decrease salivation & lacrimation

• Neuromascular weakness & cramps

• Fatigue

-increased body temperature

• Cool calmy skin related to peripheral vasoconstriction

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Diagnosis
• Hx

• Physical exam

• Increased BUN

• Increased HCT

• Electrolyte changes may ocure

• Urine osmolality increased as kidney attempt to

conserve water

24
 Management
• Identify & treat the cause

• Isotonic fluid replacement ex 0.9%Nacl solution, ringers

lactate
• Correct with oral fluid replacement

• Monitoring intake & out put at least every 8 hr &

sometimes every hr.
• Monitoring daily body weight at the same time of day

25
 Mgt……
• Monitoring vital signs

• Monitoring skin & tongue turgor

• Do not allow the patient to sit or stand up quickly as long as

circulation is compromised to avoid orthostatic hypotension
or possible syncope.

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 Fluid volume excess(FVE)
• FVE refers to an isotonic expansion of the ECF caused by
the abnormal retention of water & sodium in
approximately the same proportion in which they exist in
the total body fluid.
cause
• Excessive sodium & water intake
-dietary intake
-ingestion of medications or home remedies containing
sodium

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• Inadequate renal losses -renal disease(renal failure)

• CHF

• Cirrhosis of liver

C/M
• Acute wt gain (in excess of 5%)

• Pitting edema of extermities

• Puffy eyelid

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• Pulmonary edema
-SOB
-wheezing
-dyspnea
-cough
• Tachycardia, full & bounding pulse
• Increased BP & pulse pressure
• Distended neck vein
• Increased urinary out put

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distended neck veins
Diagnosis
• Hx
• Physical exam
• Decreased BUN
• HCT may be decreased
• Decreased serum osmolarity
• Chest x-ray reveals pulmonary congestion

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 Management
• Mgt is directed towards the cause

-if related to excessive administration, discontinuing the

infusion

-diuretics(thiazides)

-restricting fluid and sodium intake

- Encourage rest to relieve dyspnea& fatigue

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 Mgt….

 Monitoring

-daily input & output

-daily body wt

-degree of edema in most dependent body parts

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 Assignment- Read
 Sodium imbalance
 Potassium imbalance
 Calcium imbalance
 Magnesium imbalance
 Chloride imbalance
 phosphate imbalance
 Male Reproductive System Disorders

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 ACID BASE BALANCE

• Normal Acid Base Balance=

Normal PH 7.35-7.45

Narrow normal range

Compatible with life ( if PH= 6.8-8.0)

• PH = 6.8-7.2 is a severe life threatening acidosis

• PH = 7.7-7.9 is a severe life threatening alkalosis

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 I/ Intracellular electrolytes
Potassium, controls cellular osmotic pressure,
influences skeletal and cardiac muscle activity, and
is dramatically affected by acid–base imbalance
Magnesium ,contained mostly in bone; it activates
intracellular enzymes, contributes to carbohydrate
and protein metabolism, and acts to dilate
b/vessels, decrease blood pressure; imbalances can
trigger ventricular arrhythmias and cardiac arrest
Phosphate, it’s essential for muscle, red blood cell
(RBC), and nervous system functioning, and it plays
a role in carbohydrate, protein, and fat metabolism
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 II/Extracellular electrolytes
Sodium is responsible for the osmotic pressure of ECF,
and it doesn’t readily cross the cell membrane
Calcium is concentrated in the skeletal system; it acts
as cell cement, has a sedative effect on nerve cells,
regulates muscle contraction and relaxation
(including heartbeat), activates enzymes and plays a
role in blood coagulation
Bicarbonate plays a role in acid–base balance; it serves
as a buffer to keep serum pH within normal limits
and is regulated primarily by the kidneys
◗ Chloride helps maintain acid-base balance and works
with sodium to help maintain osmotic pressure 38
• The normal pH in arterial blood= 7.35-7.45
• Acid base balance is regulated by three
mechanisms:
(1) Buffers
(2) Respiratory system (lung)
(3) Renal system (kidney)

39
 Buffers
• Are chemicals that help control the pH
• Weak acids which
– Release H+ when fluid is alkaline
– Take up H+ when fluid is acidic
• Bicarbonate (HCO3-) is the chief buffer of the
ECF
• HCO3- + H+ H2CO3 CO2 + H20
• At normal pH- HCO3-:H2CO3 = 20:1
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 Buffering
• Buffering is a normal body mechanism that occurs
rapidly in response to acid-base disturbances in
order to prevent changes in H+
Two major systems of buffering
Chemical buffer systems
• Bicarbonate buffer system (ECF)
• Phosphate buffer system (Kidney)
• Protein buffer systems (ICF)
Physiological buffer systems
• Respiratory mechanisms
• Renal mechanisms 41
42
 Chemical buffer systems
1. Bicarbonate buffer systems- react less than a second
- For ECF (blood & tissue fluid)
Carbonic acid(H2Co3= weak acid ) & NaHCo3= weak base
EX1. HCl + NaHCo3 NaCl + H2Co3
EX2. NaOH + H2Co3 H2O + NaHCo3
2. Phosphate buffer system ( by the Kidney) reacts slowly
 Sodium dihydrogen phosphate = Weak acid =NaH2Po4
 Sodium monoydrogen phosphate = Weak
base = Na2HPo4
Ex1. NaOH + NaH2Po4 H2O + Na2HPo4
Ex2. HCl + Na2HPo4 NaCl + NaH2Po4 43
 Chemical buffer systems
Protein buffer systems
- Most important for intracellular fluid(ICF)
- A. Acids have Carboxyl (CooH) & Amine(NH2) group
- COOH act as acid b/se it donates H+
H H
EX. NH2- C-COOH NH2-C- Coo- + H+
H R
H H
Ex. COOH- C-NH2 COOH- C-NH3
R R
__________________________________________ 44
 Physiogical buffer systems
I) Respiratory mechanism (CO2 excretion by the lungs)- Acts
within sec to mins
• CO2 + H2O---- H2CO3 ------------ H+ + HCO3- 
Hgb is a buffer
NB. 12,000-20,000 meq of CO2 excreted by lungs
II) Renal mechanism (H+ excretion by the kidney)- Acts within
Hrs to days
NB. The kidney excretes 70 meq of acids daily
Ex1. NH3 + H+ ----- NH4 (excreted)
Ex2. H2CO3 ------------ H+(excreted) + HCO3-(reabsorbed in the blood)
During acidosis: Kidney excretes more H+ & conserves HCO3-
During alkalosis : Kidney excretes more HCO3- & conserves H+
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 Blood gas analysis
Arterial sample Venous sample
• PH = 7.35 – 7.45 • PH = 7.33 – 7.41
• Pa Co2 = 35 - 45 mmHg • Pa Co2 = 41- 51 mmHg
• HCO3- = 22-26 meq/l • HCO3- = 22-29 meq/l
• Pao2 = 80-100 mmHg • Pao2 = 30- 40 mmHg

• O2 saturation = 95- 99 % • O2 saturation = 60-85%

• Anion gap = 8-16 meq/l • Na+ = 136- 142 meq/l

Major cations – major • Cl- = 95-103 meq/l

anion • O2 consumption =
3- 4ml/kg/min 46
47
 ABG
• PH: 7.35 – 7.45 HCO3-: 22 – 26 mEq/L
• PaCO2: 35 – 45 mmHg PaO2: 80 – 100 mmHg
• SaO2: 95- 99 % (pulse oximetry)
Acid Base
PH= 7.35- 7.45
Paco2 = 45-35 mmHg (Respiratory indicator)
HCO3-= 22-26 mEq/L (Metabolic indicator)

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 ABG
Acid Base
• PH = 7.35- 7.45
• PCO2 = 45-35mmhg(respiratory indicator)
• HCO3 = 22-26 meq/l( metabolic indicator)

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 Respiratory System
• Cells are continually producing CO2
• CO2 + H2O → H2CO3 (carbonic acid)
• The lung excretes CO2 during respiration
• Rate and depth of respiration depends on the
PaCO2 and pH of the blood
• ↑carbonic acid → ↑ depth and rate of resp
• ↓carbonic acid → ↓ depth and rate of resp
• Lung excretes only the volatile acid
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 Renal System
• Kidney can excrete every acid in the body except
H2CO3
• The kidney excretes non volatile (metabolic)
acids which are produced by metabolism
• For each H+ excreted one HCO3- is returned to
the blood
• [HCO3-] in plasma is the measure of the
effectiveness of renal regulation of metabolic
acids
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 PH(Potential Hydrogen) is a measure of the activity of
H+ in a solution.
 Maintenance of balance by:-

Buffering system

Lungs

kidneys
 Bicarbonate – carbonic acid buffer

active in ECF and ICF

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 Bicarbonate – carbonic acid= body’s major buffer. The
ratio is = 20:1

.This value is not absolute.

 Regulations

Acid = substance that contain H+ ions .

Base = substance that can accept H+ ions

• As Co2 increases carbonic acid increase, H+ ion increase
and PH drops ( ≤ 7.35).
• As Hco3 increase , H+ decreases and PH rises (≥7.45).

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1. Respiratory regulations = it is rapid mechanism of control
include.
 Hyperventilation – blowing off Co2
 Hypoventilation --- retain of Co2
 Measured by paCo2 =35-45mmHg (normal).
2. Renal regulation= it is slow ( hours to days to take change
PH).
Mechanisms include like ;
 Excretion and retention of H+ & Hco3
 Normal serum level is = 22-26mEq/L

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 Acid- Base Imbalance
Ratio of 20 to 1 is out of balance.

It may be:-
 Acidosis: = An increase in blood H2Co3 & a decrease in HCo3-

• Acidosis = PH falls below 7.35

 Alkalosis: = An increase in HCo3-& a decrease in H+

 Alkalosis = PH greater than 7.45
.↑ Hco3 or
. ↓ H2co3

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 Causes
 Metabolic = change brought by systemic alterations or
cellular level.
 Respiratory = change brought by respiratory
alteration.
Compensation
• It means corrective response of lungs & kidneys
• Compensated =if restoration of PH & 20:1 ratio
• Un compensated = inability to adjust PH
or 20:1 ratio.

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 Normal Values of ABGS

• PH - 7.35-7.45

• Paco2 - 35-45mmHg (Respiratory indicator)

• Hco3 - 22-26mE/L (Metabolic indicator)

• Pao2 - 80-100mmHg

• 02 saturation - 95-100% (pulse oximetry)

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 Acid-Base Imbalance
• The four primary Acid-Base disorders
1. Metabolic acidosis
2. Respiratory acidosis
3. Metabolic alkalosis
4. Respiratory alkalosis

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Interpreting ABGS
1. Start with PH .Normal ?
.Acidosis ?
. Alkalosis ?
2. Assess paco2 ( respiratory)
. Normal ?
. respiratory acidosis ?
. respiratory alkalosis. ?
3. Assess bicarbonate (Hco3)
. Normal ?
. Metabolic acidosis . ?
. Metabolic alkalosis. ?

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4. Determine amount of hypoxemia present.
normal pao2 .<70 yrs =80-100mmHG
70-79 yrs= 70-100mmHg
Drop each 10 mmHg for each decade.
IF it is hypoxemia= < 70mmHg for adult <70 yrs
.mild = 60-80mmHg
. Moderate = 40-60mmHg
. Sever = <40mmHg
• Oxygen saturation (pulse oximetry).
• 95-100%
• <91% =confusion
• <70% = life threatening

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 1.Respiratory Acidosis

• Etiology – Excess carbonic acid (CO2) caused

by factors which impair respiratory excretion
– Impaired gas exchange
– Impaired neuromuscular function
– Impaired brain stem function (resp center)
• Arterial blood gas – increased PaCO2
• Compensatory response increased renal
excretion of H+ causing increase [HCO3-]

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 Respiratory Acidosis Causes
• Impaired Gas Exchange
– Chronic Obstructive Pulmonary Disease
– Pneumonia
– Severe Asthma
– Pulmonary edema
– ARDS
– Obstructive sleep apnea

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 Respiratory Acidosis Causes
• Impaired nueromuscular function
– Guillain-Barre syndrome
– Chest injury or surgery
– Hypokalemia
– Kyphoscoleosis
– Resp mm fatigue
• Brain stem dysfunction
– Barbiturates, narcotics
– Central sleep apnea
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 S/S - Respiratory acidosis
 Tachycardia
 ↓RR
 Disorientation  fatigue
 Shallow breathing  Headeache
 restless
 weakness
 Dyspnea
 agitation  Decreased responsive

 seizure
 Diminished reflexes

 Nausea & vomiting

64
 2.Respiratory Alkalosis
• Etiology – carbonic acid deficit – blood is
alkaline
– Hyperventilation
• PaCO2 is low because of the primary defect
• Compensatory response causes the kidney to
decrease excretion of metabolic acids
resulting in decreased HCO3-

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 Respiratory Alkalosis - Causes
• Anxiety, psychological distress
• Prolonged sobbing
• Hypoxemia
• Alcohol withdrawal
• Stimulation of the brainstem (salicilate
overdose, meningitis, head injury)

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 S/S- Respiratory alkalosis
• Hyper ventilation • Syncope
• ↓ psychomotor • tetany
• Breathlessnes • Vertigo
• Hyperreflexia • seizure
• Cardiac dysrhythmias • Anxiety
• Muscle cramp • Nervousness
• Hypotension • Confusion
• Decreased level of
• twitching consciousness
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 3. Metabolic Acidosis
• Etiology – excess of any acid except H2CO3
– Increased acid – starvation ketosis, DKA
– Decreased base - diarrhea
– Combination of the above
• Whatever the cause blood becomes acidic and
HCO3- is used up to buffer the excess acid
• Decreased [HCO3-]
• Compensatory response – hyperventilation to
remove more H2CO3 results in decreased
PaCO2
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 Metabolic Acidosis - Causes
• Increased Acid
– Ketoacidosis (diabetes, starvation)
– Hyperthyroidism
– Severe infection
– Burns
– Shock
– Tissue Anoxia
– Renal failure
– Intake of acids and acid precursors
• Decrease in Base
– Diarrhea, GI fistula, Intestinal decompression 69
 S/S of Metabolic acidosis
 Apathy
 Tachypnea  Poor perfusion
 Fatigue
 Kussmal breathing  seizure
 Drowsiness  Un resposiveness
 Dysrhythmias
 confusion  N&V
 Decrease pulse
 Hypotension
 Distension & pain
 Decreased urine out put

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 4. Metabolic Alkalosis
• Etiology – relative deficit of any acid except
H2CO3
– Increased alkali intake ( antiacid containing HCO3-)
– Decrease in acid (vomiting, GI suction)
– Combination
• Raised [HCO3-] - primary abnormality
• Compensatory response – hypoventilation to
retain carbonic acid (CO2) results in increased
PaCO2

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 Metabolic Alkalosis - Causes
• Increase in base
– Intake of bicarbonate or its precursors
– Massive transfusion with citrated blood
– ECF volume depletion
• Decrease in Acid
– Emesis
– Gastric suction
– Hyperaldosteronism
– hypokalemia

72
 S/S- Metabolic Alkalosis.
 Hypoventilation  Hypotension

 Hyper reflexia  N&V

 Confusion
 Dysrhythemia
 diarrhea
 Tetany
 Lethargy
 Decreased perfusion  Unresponsiveness
 Muscle cramp
 seizure  twitching

73
 Mixed Acid-Base Imbalances
• Two primary imbalances
• Example-
– Bacterial pneumonia plus severe diarrhea (resp
acidosis plus metabolic acidosis)
– Head injury, ARF – resp alkalosis +metabolic
acidosis

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 Summary – Acid-Base Imbalances

 Acidosis – relative excess of acid

 Alkalosis – relative excess of base
• Metabolic acidosis - ↓ pH,↓ [HCO3-],↓PaCO2
• Metabolic Alkalosis - ↑ pH,↑[HCO3-],↑PaCO2
• Respiratory acidosis - ↓pH,↑ PaCO2 ,↑[HCO3],
• Respiratory alkalosis - ↑pH,↓PaCO2,↓[HCO3-],

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 Disorder of Urinary Tract
Infection of urinary tract
• It is classified as
1. Upper UTI: pyelonephritse
2. Lower UTI: cystitis ,prostatitis & urethritis
Risk factor
 Failure to empty bladder
 Obstructed urine flow
 Low host defense
 Instrumentation
 Gender
 Sexual activity
76
 Lower UTIs
• most UTIs result from fecal organisms.
Causes
• Gram negative bacteria
• Staphylococcus
• Klebsiella
• Enterobacter
Route of infection
 Up the urethra
 Hematogenous
 Direct extension

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1. Cystitis
An inflammation of the urinary bladder.
Causes:
 Bacteria
 Toilet hygiene
 Catheterization
 BPH
 Pregnancy
 Honey moon cystitis(increased frequency of sexual
activity)
 STIs
 Parasities

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 C /m
• Dysurea
• Frequency
• Cloudy or foul smelling urine
• Supra pubic pain
• Urgency ,nocturia , incontinency
• Hematuria & back pain
• fever

79
2. Urethritis
• inflammation of urethra is usually caused by
infections.
C/M
• Burning sensation or pain on urination
• Frequency
• N/V
• Hematuria
• lower back pain
• Fever &chills

80
Medical management for lower UTIs
• If uncomplicated -amoxaccilin ,ciprofloxaccilin, cotrimoxazole

 If complicated- cephalosporine, ampiccilin/ aminoglyscoide

combinations.
Nursing management
• Analgesics & applying heat to the pernium
• Encourage the patient to take enough amount of H2o.
• Avoiding urinary tract irritants.
• Frequent voiding
• During urination empty the bladder completely.

81
Upper Urinary Tract Infection

Pyelonephritis

• Bacterial infections of renal pelvis, tubule and

interstitial tissue.

Two types.

1. Acute pylonephriitse - sudden inflammation by

bacteria ,primarily renal pelvis & interstitial
• most common renal disease

• Known as acute infective tubulointerstitial nephritis.

82
• Causea : bacteria like:_
o E. coli
o Proteus
o Pseudo moniasis
o Staphylococcus aureus
o Streptococcus
o Inability to empty the bladder
o Urinary obstructions.
More common in women’s. B/c of
 Shorter urethra
 Proximity of the urinary meatus to the vagina

83
 Risk factors :
• Sexually active women
• Pregnant women
• Diabetics
• People with other renal disease.
Sign and symptoms
 Urgency ,frequency .anorexia
 Dysuria ,nocturia . CVA tenderness
 Cloudy urea . Hematurea
 Pyrexia
 Shaking chills
 Flank pain

84
• Dx = requires urinalysis and culture
 Pyuria
 Bacteriuria
 low specific gravity
 alkaline pH
 X-rays
 ultrasound or CT scan
 Management
 For out patient a 2 weeks course of antibiotics
e.g = Sulfa drugs like Amoxacillin,
cephalosporine ,levofloxacillin and ciprofloxacillin.

85
2. Chronic pyelonephritis
• It is persistent kidney inflammation that can
scar the kidneys and may lead to chronic renal
failure.
Cause
Perisistent acute pyelonephritis (result from)
. Urinary tract anomally
. Urinary obstruction
. Vesicoureteral reflux

86
 C/M DX.
• Fatigue . HX & P/E
• headache . Creatinine Clearance

• poor appetite . BUN

• polyuria . Bacteriuria
• exccesive thirst
• weight loss
 Complication
Hpertension
Kidney disease

87
Medical Mgt:
o Antimicrobial agent based on identified pathogen
o Increased fluid intake.
Nursing management
1. Monitor intake & out put
2. Assess temperature every 4 hours and administer
antipyretics & antibiotics as prescribed.
3. Patient education on prevention of UTIS through
 adequate fluid intake.
 Empty the bladder regularly
 Perineal hygiene -Wiping from front to back
 Cleaning after sexual intercourse
88
 Immunologic Renal Disorders
Primary glomerular disease
 acute and chronic glomerulonephritis and
 nephrotic syndrome.
• The glomerular capillaries are primarily involved & their
glomerular effect are caused by injury to be glomeruli.
• Injury to the glomeruli is because of the two immune
mechanisms:
 Injury resulting from circulating antigem antibody
complex.
 Injury resulting from antiglomerular antibodies reacting
with glomerular antigen.
89
1. Acute Glomerulonephritis(AGN).
 Acute glomerulonephritis is an inflammation of the
glomeruli that occurs when Ag-Ab complexes become
trapped in the glomerular capillary membranes.
Risk factors
• Immunological reactions
• Primary infection with group A beta-hemolytic
streptococcal infection (most common)
• Vascular injury (hypertension)
• Metabolic disease (diabetes mellitus)
• Nephrotoxic drugs
• Excessively high protein and high sodium diets
90
 Pathological events in glomerulonephritis

1/ Immune response with antibody production

2/ Glomerular capillary damage

3/ Hematuria & proteinuria

4/ Salt & water retention

5/ Edema

91
• C/M:
 Hematurea b/c erythrocytes

 Proteinurea ,Oliguria

 BUN & serum creatinine may rise

 Edema in periorbital or generalized & dependant area, wt gain

 CVA tenderness (Costo-vertebral angle)

 Hypertension (in more than 50% of pts)

 Headache ,malaise , flank pain in sever case.

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• DX .
 Serum BUN (elevated: 100 to 200 mg/dL)
 Creatinine (elevated: greater than 6 mg/dL)
 Creatinine clearance (decreased: 50 mL/min; normal
80 to 140 mL/min)
 Urinalysis: Proteinuria, hematuria, cell debris (red
cells and casts), increased urine specific gravity
 Electrolytes: Hyperkalemia,hypermagnesemia,
dilutional hyponatremia if urine output is decreased
 Antistreptolysin-O (ASO) titer (positive indicating the
presence of strep antibodies)

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 Complication
• Renal Failure
• Uremia
• Pulmonary Edema
• Congestive Heart Failure
• Anemia
Medical mgt
• Antibiotics ( Benzathine penicilin)
• Diuretics(Furosemide)
• Na & water restriction
• cortico steroids
• dietary protein restriction (azotemia)
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Nursing management
 Carbohydrate are given to provide energy &

to reduce catabolism of protein.

 Input and out put measurement.

 Basic infection control principles.

 Follow up evaluation of BP, U/A for

proteinuria ,serum BUN & creatinine level.

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 2. Chronic glomerulo nephritis
• It is advanced stage of a group of kidney
diorders ,resulting in inflammation and
gradual ,progressive destruction of the glomeruli.
Cause
 Repeated attack of AGN
C/M
 Elevated BUN
 Sudden , sever nose bleeding
 Feet slightly swollen at night
 Chroni renal failure may be developed.

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• DX.

 Hx &P/E

 U/A

 Protein urea

 RBC casts

 Serum -increase creatinine level & increased BUN

 X-ray - may show cardiac enlargement and pulmonary

edema.

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 Management
• depend on symptom guide
 If the patient has hypertension
-sodium & H2o restriction
-antihypertensive agent.
 Monitor daily weight
 Diuretics for fluid over load
 Providing proteins of high biologic value dairy products
like eggs , meat).
 Dialysis or transplantation to prevent death.
 Emotional supports.
 Observing the patient for changes in fluid and
electrolytes status of determination of renal function.

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 Nephrotic Syndrome.
• Is not specific glomerular disease but a constellation
of clinical finding result from increased permeability
to the plasma protein.
• Nephrotic syndrome is a group of symptoms, not a
disease
• It is characterized by :
 Massive protein urea( >3.5g/dl).
 Hypoalbunemia (<3g/dl).
 Edema
 Hyperlipidemia(300mg/dl)

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• Can be congenital, primary (idiopathic), & secondary

 Secondary

 Chronic glomerulo nephritis,

 DM with intracapillary glomerulosclerosis

 Malignancy

 Renal vein thrombosis

 Damaged of glomerular capillary membrane leads to

↑permeability of glomerular capillaries to protein.

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C/M
• Hypoalbuminemia
• Hyperlipidemia
• Decreased urine output
• Irritability, fatique, anorexia, N/V
• Profound Wt gain
• Proteinuria, Hematuria
• Edema (Periorbital and dependent)
• Hypertension
• Anemia (hemoglobin < 12 g/dL)
• Azotemia: Elevated serum BUN and serum creatinine
• Uremia (symptoms of renal failure)

DX
HX & P/E
U/A
Needle biopsy of the kidney

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Complication
.renal failure
Management:
• Treat causative glomerular disease
• Rest with activity
• Loop diruetics and low sodium
• Corticosteroid drugs
• a major nursing intervention for patient’s with
nephrotic syndrome is edema

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 Renal Failure
• Renal failure = sever impairment or total lack of kidney
functions(inability to remove waste metabolic end
products).
• It can be Acute & chronic .
A. Acute renal failure
• It is sudden & almost loss of kidney function (↓GFR),with
progressive azotemia(retention of metabolic wastes).
Causes
1. Prerenal :- 50-70 %
Factors out side the kidneys that impair renal blood flow.

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• These may include
o Hypovolemia
o Hemmorhage
o Burns
o dehydration
o GI loss
o Vasodilation
 sepsis
 Vasodilators
 Anphylaxis .
o ↓cardiac out put
 MI
 Dysrhythmias
 HF
 Cardiac shock

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2. Intrarenal causes. 20-30%
• It leads to actual damage to the renal tissues
(parenchymia)resulting in malfunctioning of
nephrons.
• It may include nephrotoxic injury caused by
 Drugs (like aminoglycoside, NSAD&ACEI)
 Heavy metals
 Hemolytic blood transfusion reaction
 Primary renal disorders(APN,AGN)
 Toxemia of pregnancy /eclampsia
 Malignant hypertension

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3. Post renal causes (1-10%) involve mechanical
obstruction of urinary out flow some where distal
to the kidney.
• Prostate cancer
• Trauma
• BPH
• Tumors
• Calculi

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 Clinical course of ARF
• It may progress through the phases of
initiation ,olguria, diuretics and recovery.
1. Initiation phase =begins with the initial insult and
ends when oligurea develops.
2. Oliguric phase:
• Urinary volume less than 400 ml/day
• Is the most cardinal symptom
• Azotemia (abnormal collection of nitrogenous
wastes)- rise in BUN and creatinine
• Circulatory congestion
• Hyperkalemia, hyperphosphatemia, hyper uricemia
(an excess of urea & other nitrogenous wastes in the
blood)
• Metabolic acidosis
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• Anemia due to depressed erythropoisis, uremic GI
lesion and  RBC lifespan.
3.Diuretic phase
• The pt experiences gradually increasing urinary
output, which signals that glomerular filtration has
started to recover.
• Although urinary output may reach normal, renal
function may be markedly abnormal.
• Urinary output doubles from oliguric phase
• Hypokalemia is danger in this phase.

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 4. Recovery phase
• Signals improvement of renal function
• Marked by fall in BUN and creatinine
C/M
• Lethargic
• Nausea ,vomitting and diarrhea
• Dry skin and mucous membrane
• odor of urine of breath
• CNS manifestation like drowsiness ,headache, convulsion.
• Acidosis
• Hyperkalemia ,dysrhthemia &cardiac arrest
• Anemia

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 Management of ARF
• Depends on the causes

• Sodium and water balance

• Measure body wt.

• Increase carbohydrates to spare catabolism of protein(oliquric

phase).
• Restrict food & fluids containing potassium and phospherous
during oliquric phase

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• After diuretic phase, the pt is placed on a high protein,
high calori diet.
• IV glucose & insulin as an emergency and temporary
measure to treat hyperkalmia that is released due to
break down of proteins.
• Na HCo3 to treat acidosis
• Dialysis if there is excess serum urea, creatinine,
hyper kalemia, pericarditis, neuropathy,
encephalopathy.
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• Measure daily urine output & calculate daily
requirements of fluid by adding insensitive loss of
350ml/m2 to the urine output
• No electrolyte is permissible in oliguric phase but
during diuresis phase
• Treat HPN, if any

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 Nursing Intervention
• Assess fluid and electrolyte status

– Daily weight changes

– precise intake and output balance

– skin turgor & presence of edema

– Distension of neck veins

– Bp, PR, RR

– Identify potential sources of fluids

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• Explain to patient and family rationale for restriction
of certain foods and fluids.
• Assess nutritional status

• Weight change

• Encourage high calori, low protein (the protein given

should be of having high biological value i.e animal
origin), low sodium and low potassium.

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B-Chronic Renal Failure (End-stage renal
disease)
• It is a progressive, irreversible deterioration in renal
function in which the body's ability to maintain
metabolic and fluid and electrolyte balance fails,
resulting in uremia.
Cause
• Glomerulonephritis . diabets
• Pyelonephritis .obstruction of UTI
• Hypertension .vascular disorder
• Drugs .cystic kidney disease

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• Although there are no distinct stages in CRF the
disease progression may be divided in to three
stages.
1.Diminished renal reserve= characterized by 40-
75% loss of nephrons’ functions.
• normal BUN & serum creatine level
• no symptoms
2. Renal insufficency =75-90% loss of nephron’s
functions
• polyuria & nocturia
• ↑BUN & creatine
• Anemia

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3. End stage renal disease
.<10% of nephron’s are functional
. GFR<5%to10%
.Elevated creatinine , BUN electrolyte imbalance
.Impaired kidney functions
C/M
• 35 to 50% reduction in renal function is tolerated and
pts are symptom free
• When GFR falls to 20-35% of normal, azotemia
appears
• GFR of 10-20% of normal, azotemia is pronounced
and there is overt renal failure.

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• Electrolyte disturbance

• Endocrine disturbances

• Decrease libido, impotence, amenorrhea

• Metabolic disturbances

• Neuromuscular disturbances

• CVs disturbance

• Dermatological disturbances

• Gastro intestinal disturbances

• Haematologic disturbances
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 Management
•  Reduced protein intake why?
• Salt restriction

• Restrict potassium containing foods

• Calcium supplement along with synthetic vit.D to minimize

symptoms of renal osteodystrophy.
• Antihypertensive

• Dialysis

• Renal transplantation
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120
 Urolithiasis
• Urolithiasisis the presence of calculi (stones) in the urinary
tract.
• The cause of urolithiasisis unknown but it may be related to
changes in urine pH, volume depletion, or use of diuretics or
other drugs
• The majority of stones (80 -90 %) are composed of calcium
oxalate /calcium phosphate but may contain other substances
such as uric acid (5-10%), struvite (Staghorn,1-4 %), or
cystine (1-4 %)
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• High urine acidity or alkalinity contributes to
stone formation
• Urinary stasis, urinary retention, infection,
sedentary lifestyle/immobility/, persistently
low urine output and dehydration contribute to
an environment favorable for stone formation

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 Nephrolithiasis
• Nephrolithiasis refers to the presence of stones, or
calculi in the renal pelivis
• Men are affected more frequently than women, &
recurrences are possible
Clinical manifestations
• Pain pattern (referred to as colic) depends on site of
obstruction
• Chills, fever, dysuria, frequency & hematuria –
secondary to infection
• N/V ,diarrhea & general abdominal discomfort
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 Diagnostic evaluation
• X-ray of KUB

• Ultrasonography

• Urinalysis --- Hematuria, pyuria

• Serum RFT

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 Management
I/ Non-surgical management
• Extracorporeal Shock Wave Lithotripsy (ESWL)
• ESWL is the most commonly used procedure to treat
urinary calculi
- Uses sound, laser or shock-wave energies to break the
stone into fragments
- In this procedure, ultrasonic shock waves pulverize
the calculi into many small fragments that pass
through the urinary tract over several months

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II. Surgical management

Open surgery
 Used for large or impacted stones (such as staghorn
calculi),or
 Used for stones not removed by other approaches

 Ureterolithotomy (into the ureter)

 Nephrolithotomy (into the kidney)

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 Nursing management
• High fluid intake

 active in sports

 living in dry climate

 having family history of renal calculi.

• Pain management and pt comfort

• Teaching ways to prevent recurrence.

 Increase fluid intake to maintain urine out put at 2-3

liters/day.
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Male Reproductive System Disorders -
Assignment

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