Transcript Urinary system

Urinary system
Urinary System
 Consist
of:
 Kidneys
 Ureters
 Bladder
 Urethra
General
Function:
Specific Function:
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 Excretory
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 Regulatory
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 Secretory
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Urine formation
Excretion of waste products
Regulation of electrolyte excretion
Regulation of acid excretion
Regulation of water excretion
Auto regulation of blood pressure
Regulation of red blood cell
production
Renal clearance
Vitamin D synthesis
Secretions of prostaglandins
Urine storage
Bladder emptying
Location and External Anatomy of
Kidneys
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Located retroperitoneally
Lateral to T12–L3 vertebrae
Average kidney
12 cm tall, 6 cm wide, 3 cm
thick
-Bean-shaped, brownish-red
structures.right lower than left
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Hilus
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On concave surface
Vessels and nerves enter and exit
Renal capsule surrounds the kidney
Regions
A.
1.
Renal parenchyma
a.
Cortex
• Glomeruli, proximal and distal convoluted
tubules, cortical collecting ducts, and adjacent
peritubular capillaries.
b.
Medulla
• Pyramids
 8- 18 pyramids/ kidney
2. Renal Pelvis
- it is the concave portion of the kidney
through which the renal artery enters and
the renal vein exits
- composed of afferent arteriole and
efferent arteriole
Nephrons
B.
- Functional units of kidney:
a)
b)
c)
d)
e)
f)
Glomerulus
Bowman’s capsule
Proximal tubule
Distal tubule
Loop of Henle
Collecting ducts
Calyx
C.
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Minor calyx- 4-13 minor calices
Major calyx- 2-3 major calices
Glomerulus
3 filtering layers:
D.
1.
2.
3.
Capillary endothelium
Basement membrane
Epithelium
Ureters
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Fibromuscular tube that connect each
kidney to the bladder
Narrow, muscular tubes, 24-30 cm long
3 narrowed areas:
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Ureteropelvic junction
Ureteral segment
Ureterovesical junction
- prevents reflux of urine
Urinary Bladder
Muscular, hollow- sac located just behind
the pubic bone
 300- 600 ml of urine
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4 layers of the urinary bladder:
1.
2.
3.
4.
Adventitia- outermost layer
Detrusor- beneath the adventitia
Lamina Propria- interface between detrusor and
urethelium.
Urothelium- innermost layer
Urethra
Small tube leading
from the floor of
urinary bladder
 1.5 inch in length
in females & 8 inch
in male
 Function:
passageway for
urine
& semen
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Acid- Base Regulation
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Acid Base Balance
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Homeostasis of the body fluids at a normal arterial
blood pH ranging between 7.35- 7.45
Body fluids are slightly alkaline, metabolic
processes of the body generally produced excess
acid.
Maintained partially through the reabsorption of
bicarbonate (HCO3-) in the proximal tubule
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Acids
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release hydrogen ions (H+) in solutions
 Ex. Hydrochloric acid (HCl)- strong acid
Carbonic acid (H2CO3)- weak acid
Bases or alkalis
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decrease hydrogen ion (H+) concentration
accept H+ in solutions
Ex: Sodium Hydroxide (NaOH) – strong base
Bicarbonate (HCO3) – weak base
Regulation System
1.
Buffer Regulation System
- chemicals which neutralizes excess acids and bases
a. bicarbonate buffer system
- controls the pH in ECF of the body
b. phosphate buffer system
- important ICF buffer system
c. protein buffer system
- largest buffer system of the body; includes Hgb in
RBC, histone proteins and nucleic acids inside the
cells.
2.
Respiratory Regulation System
- excretes or retains CO2 in the lungs
3.
Renal Regulation System
- excretion or retention of Hydrogen ions
(H+) and bicarbonate ions (HCO3)
Acid Base Imbalances
1.
Metabolic Acidosis (Base Bicarbonate Deficit)
A.
Definition
- results because of high acid content of the blood,
which also causes loss of sodium bicarbonate
- characterized by low pH and low plasma bicarbonate
concentration
- 2 forms:
1. high anion gap acidosis
2. normal anion gap acidosis
B.
Compensatory Mechanism
- increased ventilation and renal retention of
bicarbonate
- lungs “blow off” CO2 to raise pH and conserve HCO3-
Laboratory Findings (ABG)
- low plasma pH (below 7.35) or a normal pH (if
compensated)
- normal PCO2 or low if compensated in an attempt by the
lungs to blow off more acid
- low plasma bicarbonate:
-below 21 mEq/L in adults
-below 20 mEq/L in children
- low urine pH (below 6)
D.
Causes
-DKA or Diabetic Ketoacidosis with starvation
-Salicylate overdose
-Lactic Acidosis 2o hypoperfusion
-Methanol and ethylene Glycol toxicity
-uremia
E.
F.
Manifestations
A. Acute
- headache
- nausea and vomiting
- increased RR and depth
- peripheral vasodilation
- cold and clammy skin
B. Chronic
-asymptomatic
- drowsiness
- confusion
- shock
- dysrhythmia
- decreased BP
Medical and Nursing Management
1. Correct metabolic defect
2. If resulted from excessive intake of Chloride, eliminate the
source of Chloride.
3. Administer bicarbonate if pH < 7.1 and bicarbonate level < 10.
4. Closely monitor serum potassium level
5. Correct hypokalemia
6. Give alkalizing agents, if serum bicarbonate level < 12meq/L
7. Hemodialysis
8. Peritoneal dialysis
2.
Metabolic Alkalosis (Base Bicarbonate Excess)
A.
Definition
- marked by the heavy loss of acid from the body or
by increased level of bicarbonate
- characterized by increased pH and increased
plasma bicarbonate.
B.
Compensatory Mechanism
- decreased ventilation to conserve CO2 and
increase the PaCO2
- lung retains CO2 to lower pH
- kidney conserves H+ to excrete HCO3
C.
Laboratory Findings (ABG)
- high plasma pH (above 7.45)
- normal or high PCO2 (above 45 mmHg)
as a compensatory elevation
- high plasma bicarbonate:
- above 28 mEq/L in adults
- above 25 mEq/L in children
- high urine pH (above 7)
D.
Causes
- overzealous administration of sodium
bicarbonate
- excessive or prolonged vomiting
- excessive diuresis
- gastric suction with loss of hydrogen
and chloride ions
- pyloric stenosis
-excessive diarrhea
-hyperaldosteronism
- Cushing’s syndrome
- villous adenoma
- cystic fibrosis
- hypokalemia
E. Manifestations
a. Acute
- tingling of fingers and toes
- slow, shallow respiration (compensatory)
- hypertonic muscles
- tetany
- mental dullness
- dizziness
- respiratory depression
- atrial tachycardia may occur
- ventricular disturbances
- decreased motility and paralytic ileus
b. Chronic
- same with acute metabolic alkalosis
- PVC (premature ventricular contractions or Uwaves seen in ECG)
Medical and Nursing Management:
1. Sufficient chloride must be supplied.
2. Restore normal fluid volume by administering sodium
chloride fluids.
3. In patient with hypokalemia, administer potassium as KCl.
4. Administer H2-receptor antagonist such as Cimetidine
(Tagamet) to reduce the production of gastric HCl, thereby
decreasing the metabolic alkalosis associated with gastric
suction.
5. Carbonic anhydrase inhibitors are useful in patients who
cannot tolerate rapid volume expansion.
6. Monitor fluid intake and output.
7. Correct the underlying acid-base disorder.
Respiratory Acidosis (Carbonic Acid Excess)
A. Definition
- marked by an increased arterial CO2 concentration
(PaCO2), increased carbonic acid, and increased
hydrogen ion concentration (low pH)
- may be acute or chronic
- due to inadequate excretion of CO2 with
inadequate ventilation
B. Compensatory Mechanism
- excess hydrogen is excreted in the urine in
exchange for bicarbonate ions
- kidney eliminate hydrogen ion and retain HCO3
- kidney will retain increased amounts of HCO3 to
increase pH
C. Laboratory Findings (ABG)
- low plasma pH (below 7.35) or a normal pH (if compensated)
- increased PCO2 (above 45 mmHg)
- normal or high plasma bicarbonate (HCO3) if compensated
- above 28 mEq/L in adults
- above 25 mEq/L in children
D. Causes
- narcotic coma
- respiratory depression (drugs, CNS, trauma)
- pulmonary diseases (COPD, asthma, pneumonia)
- hypoventilation
- cardiac arrest/respiratory arrest
- head and spinal cord injury
- acute pulmonary edema
- aspiration of a foreign object
- atelectasis
- ventricular fibrillation (in anesthesized person)
- increased ICP
- papilledema
- dilated conjunctival blood vessels
- hyperkalemia
E. Manifestations
a. Acute
- increased RR, PR and BP
- mental cloudiness
- feeling of fullness in head
- hypoventilation, shallow respiration
- poor exhalation
- mental alertness and disorientation
- cerebrovascular vasodilation
- increased cerebral blood flow
Chronic
- cerebral vasodilation will increase ICP
- cyanosis and tachypnea will develop
- pneumothorax
- overdose of sedatives
- sleep apnea syndrome
- ARDS
- muscular dystrophy
- myasthenia gravis
- Guillain-Barre Syndrome
F. Medical and Nursing Management
1. Improve ventilation
2. Bronchodilators
3. Antibiotics
4. Thrombolytics
5. Pulmonary hygiene measures
6. Adequate hydration
7. Supplemental oxygen PRN
8. Mechanical ventilation, use appropriately
9. Semi-Fowler’s position
4. Respiratory Alkalosis (Carbonic Acid Deficit)
A. Definition
- marked by decreased PaCO2 and
increased pH
- clinical condition in which the arterial pH
is greater than 7.45 and the PaCO2 is less
than 38 mmHg
- acute and chronic condition may occur
B. Compensatory Mechanism
- renal excretion of bicarbonate increase, and
hydrogen ion is retained
- kidneys will excrete increased amounts of HCO3 to
lower pH
- kidneys conserve H+ and excrete HCO3
C. Laboratory Findings (ABG)
- high plasma pH (above 7.45)
- decreased PCO2 (below 35 mmHg)
- decreased plasma bicarbonate as a compensatory
measure
- below 21 mEq/L in adults
- below 20 mEq/L in children
- high urine pH (above 7)
Causes
- extreme anxiety
- “panic” attack
- hypoxemia
- early phase of salicylate intoxication
- gram-negative bacteremia
- inappropriate ventilator setting
- chronic respiratory alkalosis results
from chronic hypercapnia
- low serum bicarbonate level
Manifestations
a. Acute
- lightheadedness
- inability to concentrate
- numbness and tingling from decreased
calcium ionization
- tinnitus
- loss of consciousness at times
- tachycardia
- ventricular and atrial dysrhythmias
- deep or rapid breathing
- paresthesias
- mental restlessness and agitation
progressing to hysteria
Medical and Nursing Management
1. Instruct patient to breathe more
slowly to allow CO2 to accumulate or
breathe into a close system (such as a
paper bag)
2. Sedative may be required
3. Correct underlying problems
HYDRONEPHROSIS
 Is
distention of
the renal pelvis
and calices
caused by an
obstruction of
normal urine
flow.
Etiology
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congenital or acquired
stricture from ulceration of the ureter, or may be
due to a calculus.
thickening of the bladder walls from cystitis
enlarged prostate
urethral stricture
Pressure from a pregnant or displaced uterus
ovarian tumors
PRESENCE OF CALCULUS,
TUMORS, SCAR TISSUE,
CONGENITAL DEFECTS,
KINK IN THE URETER
URINE FLOW OBSTRUCTION
URINE ACCUMULATION & STASIS
PRESSURE IN THE KIDNEY WALLS
IRREVERSIBLE
NEPHRON
DESTRUCTION
DISTENTION OF THE KIDNEYS
SUSTAINED/INTERMITTENT INCREASE
PRESSURE
Assessment
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Acute
Renal colic
Severe back pain
Chronic
Dull, aching discomfort in the flank on the affected
side
Painful hydronephrosis that occurs intermittently
General
 Vague intestinal symptoms such as:
 nausea
 vomiting
 abdominal pain
 Pain in the sides
 Abdominal mass
 Nausea and vomiting
 Very high Fever
 Dysuria (Painful urination)
 Increased urinary frequency
 Hematuria (blood in the urine)
 High number of white blood cells in the urine
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Feel fatigued
Appear pale
Diarrhea
Respiratory distress
Foam in the toilet water, which may be caused by
excess protein in your urine
Weight gain due to excess fluid retention
High blood pressure
Thromboembolism
• severe pain and swelling in arm or leg
• changes in color or temperature of arm or leg
Diagnostics:
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Ultrasonography
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Intravenous pyelogram (IVP)
Abdominal magnetic resonance imaging (MRI)
Urine tests
Blood Test
Endoscopy
Kidney (Renal) Scan
Bladder catheterization (insertion of a hollow,
flexible tube through the urethra
Complications
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kidney infection (pyelonephritis)
urinary tract infection
Nursing Diagnosis
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Excess Fluid Volume related to Sodium
Retention
Impaired Urinary Elimination related to
Inflammation
Risk for Infection
Pain related to infection
Deficient Knowledge related to Factors of
Development of the Disease
INTERVENTION
MEDICAL
 Pain relief
 Analgesics
 Antispasmodic
 Antibiotics administration
SURGICAL
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Pyeloplasty
Pre operative
ensure optimal renal function
encourage to recognize and express feelings of anxiety
Post operative
VS
permit oral fluids after passage of flatus
maintain sterility of nephrostomy tube
ensure unobstruction in the nephrostomy tube or catheter
never clamp nephrostomy tube
MIO
In case of ureteral stent
Monitor for bleeding
MIO
Assess for signs of UTI
monitor colicky pain & decrease urine output (stent displacement)
NEPHROTIC SYNDROME
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Is a set of clinical
manifestations
caused by protein
wasting
secondary to
diffuse glomerular
damage.
ETIOLOGY
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Nephrotic syndrome is a protein wasting disease
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Caused by:
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glomerulonephritis
diabetes mellitus
Lupus erythematosus
Amylodidosis
Carcinoma
Membranous glomerulonephritis
Glomerular basement membrane
damage
Glomerular permeability to plasma protein
proteinuria
Albumin depletion in the blood
hypoalbuminemia
Alteration in osmotic pressure in the vessels
Fluid moves to interstitial spaces
Increase synthesis of LDL, HDL in the liver
with decrease lipid catabolism
Decreased plasma volume
edema
Hyperlipidemia
Stimulates aldosterone secretion
lipiduria
Sodium & water retention
Decreased glomerular filtration rate
edema
Assessment
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Proteinuria
Hypoalbuminemia (low level of albumin in the blood)
Edema (swelling)
Hypercholesterolemia (high level of cholesterol in the
blood)
High blood pressure
Susceptibility to infections
Oliguria
Hematuria
Diagnostics:
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Complete medical history and physical
examination
Urinalysis
Blood analysis
Kidney biopsy
Complications
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kidney infection (pyelonephritis)
urinary tract infection
Blood clots
High blood cholesterol and elevated blood
triglycerides
Poor nutrition
High blood pressure
Acute kidney failure
Chronic kidney failure
Nursing Diagnosis
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Altered Nutrition: Less Than Body Requirements
related to Increased Metabolic Demands
Fluid Volume Excess related to Reduced Urine
Output
Potential Impairment of Skin Integrity related to
Edema
Fatigue related to Increased Metabolic Demands
Risk for Infection Related to Altered Immune
Response Secondary to Treatment
URINARY TRACT INFECTION
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Inflammation of
the bladder or the
urethra caused by
gram-negative
bacteria, with
Escherichia coli
causing most
cases.
Etiology
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Caused by gram-negative bacteria
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Escherichia coli
Kleibshiella
Proteus
Pseudomonas
Obstruction of the urine flow
Benign Prostatic Hyperplasia
Assessment
Lower Urinary Tract
Infection (Cystitis)
- pain on urination
- Frequent urination
- Nocturia
- Incontenence
- Suprapubic pain
- Hematuria
` - dysuria
- foul-smelling urine
- increased WBC, pus and
bacteria in urine
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Upper Urinary Tract
Infection (Pyelonephritis)
- Fever
- Chills
- Flank or Low Back Pain
- Nausea and Vomiting
- Headache
- Malaise
- Painful Urination
Diagnostics:
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Antibiogram
Urinalysis
Urine culture and Sensitivity
Nitrate testing
Intravenous pyelography
Computed tomography (CT Scan)
Ultrasonography (Ultrasound)
Retrograde Urethrogram (Infants)
X-ray and Intravenous Urography (X-rays of the urological
system following intravenous injection of iodinated contrast
material)
Complications
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Damage and scarring of the urinary tract
lining
Pyelonephritis
Chronic Renal Failure due to extensive
kidney damage
Sepsis
Nursing Diagnosis
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Acute Pain related to Inflammation and Infection of Urethra,
Bladder and Other Urinary Tract Structures
Altered Urinary Elimination related to Irritation and
Inflammation of the Bladder Mucosa
Altered Health Maintenance related to Prevention of
Recurrent Infections
Deficient Knowledge related to Factors Predisposing the
Patient to Infection and Recurrence, Detection and
Prevention of Recurrence and Pharmacologic Therapy
Risk for Fluid Volume deficit related to Fever, Nausea,
Vomiting and Possible Diarrhea
NURSING INTERVENTION
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Promotive
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Preventive
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Do not delay urination.
Empty bladder regularly.
Clean the urethral meatus after intercourse.
Increase fluid intake.
Careful sexual practice.
Intake of grape juice.
Curative
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Eat well-balanced diet.
Good hygiene practice.
Medications given:
cholinergics to relieve urinary retention
anti-cholinergics to decrease bladder muscle spasm
antibiotics: Ciprofloxacin
phenazopyridine for pain
Revision of abnormalities in urinary tract.
Rehabilitative
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Education about importance of completing medication cycle.
Evaluation and instruction about voiding patterns, sexual practices, and hygiene
practices.
ACUTE GLOMERULONEPHRITIS
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A specific set of renal
diseases in which an
immunologic mechanism
triggers inflammation and
proliferation of glomerular
tissue that can result in
damage to the basement
membrane, mesangium,
or capillary endothelium
Etiology
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Beta-hemolytic Streptococcal infection
Viral or parasitic infection
Assessment
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Hematuria
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Oliguria
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Edema (peripheral or periorbital)
Headache
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flank pain
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Shortness of breath or
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Dyspnea
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Hypertension
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Skin rashes
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Arthritis
Pharyngitis
Impetigo
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Respiratory infection
Pulmonary hemorrhage
Heart murmur may
indicate endocarditis
Scarlet fever
Weight gain
Abdominal pain
Anorexia
Skin pallor
Palpable purpura in
patients with HenochSchönlein purpura
Oral ulcers
Diagnostics:
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Complete blood cell count
Electrolytes, including BUN and creatinine (to estimate the
glomerular filtration rate [GFR]): The BUN and creatinine
levels will exhibit a degree of renal compromise.
Urinalysis
Streptozyme test: This test includes many streptococcal
antigens that are sensitive for screening but are not
quantitative.
Antistreptolysin O (ASO)
Erythrocyte sedimentation ratio (ESR) usually is increased.
Urine or plasma creatinine level greater than 40; decreased
renin level is noted.
Blood cultures
Ultrasonography
Abdominal radiographic imaging (ie, computed tomography)
Renal biopsy
Complications
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Sclerosis progressing toward renal failure
Other complications can develop in patients who
present with severe hypertension,
encephalopathy, and pulmonary edema. It
includes the following:
 Hypertensive retinopathy
 Hypertensive encephalopathy
 Rapidly progressive glomerulonephritis
 Chronic renal failure
Nephrotic syndrome
Nursing Diagnosis
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Alteration in Nutrition due to Compromised Renal
Function
Fluid Volume Excess due to Reduced Urine Output
Activity Intolerance due to Need to Rest the Kidney
Potential Impairment of Skin Integrity due to Edema
Potential for Infection due to Reduction in Natural
Defense Mechanisms
Nursing Interventions
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Promotive
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Preventive
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prompt treatment of URTI or sore throat
culture and sensitivity test; antibiotics as indicated
Curative
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eat balanced diet
teach client to live healthfully
bed rest
dietary sodium restrictions
low protein diet
sufficient carbohydrate to prevent muscle wasting and nitrogen
imbalance
antibiotic: Penicillin
anti-hypertensive drugs
diuretic therapy
Rehabilitative
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maintain follow-up healthcare
report any exacerbation in signs and symptoms
CHRONIC
GLOMERULONEPHRITIS
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Is the advanced
stage of a group of
kidney disorders,
resulting in
inflammation and
slowly worsening
destruction of
glomeruli.
Etiology
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Acute glomerulonephritis
Immunologic reactions in the body
Assessment
Signs:
 Hypertension
 Edema
 Nocturia
 Weight loss
 Hematuria
 Proteinuria
 Casts and blood in
the urine
Symptoms:
Headache
Dyspnea
Blurring of vision
Lassitude
Weakness or fatigue
DIAGNOSTICS:
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Serum chemistry
CBC
Urinalysis
Renal ultrasonogram
Biopsy
Kidney
Complications
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Metabolic acidosis
Pulmonary edema
Pericarditis
Uremic encephalopathy
Uremic gastrointestinal bleeding
Uremic neuropathy
Severe anemia and hypocalcemia
Hyperkalemia
Nursing Diagnosis
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Altered Nutrition: Less Than Body Requirements
related to Increased Metabolic Demands
Fluid Volume Excess related to Reduced Urine
Output
Fatigue related to Increased Metabolic Demands
Risk for Impaired Skin Integrity
Risk for Infection related to Altered Immune
Response Secondary to Treatment
Nursing Interventions
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Promotive
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Preventive
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avoid infections, especially respiratory and urinary tract
infection
Curative
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eat balanced diet
teach client to live healthfully
high calorie, low protein, sodium restricted diet
provide/assist in hygiene
monitor signs of pulmonary edema and congestive heart
failure
rest is essential
take prescribed medications appropriately
Rehabilitative
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maintain follow-up healthcare
report any exacerbation in signs and symptoms