Urinary system

Urinary System

Consist of: Kidneys Ureters Bladder Urethra

General

Function:

ExcretoryRegulatorySecretory

Specific Function:

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

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

Hilus On concave surface Vessels and nerves enter and exit

Renal capsule surrounds the kidney

A. Regions1. 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

B. Nephrons- Functional units of kidney:a) Glomerulusb) Bowman’s capsulec) Proximal tubuled) Distal tubulee) Loop of Henlef) Collecting ducts

C. Calyx• Minor calyx- 4-13 minor calices• Major calyx- 2-3 major calices

D. Glomerulus

3 filtering layers:1. Capillary endothelium

2. Basement membrane

3. Epithelium

Ureters Fibromuscular tube that connect each

kidney to the bladder Narrow, muscular tubes, 24-30 cm long

3 narrowed areas: 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

4 layers of the urinary bladder:1. Adventitia- outermost layer2. Detrusor- beneath the adventitia3. Lamina Propria- interface between detrusor and

urethelium.4. 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

Acid- Base Regulation Acid Base Balance

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

Acids release hydrogen ions (H+) in solutions

Ex. Hydrochloric acid (HCl)- strong acid

Carbonic acid (H2CO3)- weak acid

Bases or alkalis decrease hydrogen ion (H+) concentration accept H+ in solutions• Ex: Sodium Hydroxide (NaOH) – strong base

Bicarbonate (HCO3) – weak base

Regulation System1. 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 Imbalances1. 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 acidosis2. 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. ManifestationsA. Acute

- headache - drowsiness- nausea and vomiting - confusion- increased RR and depth - shock- peripheral vasodilation - dysrhythmia- cold and clammy skin - decreased BP

B. Chronic-asymptomatic

F. Medical and Nursing Management1. Correct metabolic defect2. 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 level5. Correct hypokalemia6. Give alkalizing agents, if serum bicarbonate level < 12meq/L7. Hemodialysis8. 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

-excessive diarrheaexcessive diarrhea

-hyperaldosteronism-hyperaldosteronism

- Cushing’s syndrome- Cushing’s syndrome

- villous adenoma- villous adenoma

- cystic fibrosis- cystic fibrosis

- hypokalemia- hypokalemia

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

E. Manifestationsa. 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 U-

waves 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. Manifestationsa. 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 Management1. Improve ventilation2. Bronchodilators3. Antibiotics4. Thrombolytics5. Pulmonary hygiene measures

6. Adequate hydration7. Supplemental oxygen PRN8. Mechanical ventilation, use appropriately9. 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

Manifestationsa. 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 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

DISTENTION OF THE KIDNEYSIRREVERSIBLE NEPHRON DESTRUCTION

SUSTAINED/INTERMITTENT INCREASE PRESSURE

PRESSURE IN THE KIDNEY WALLS

AssessmentAcute

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

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: Ultrasonography

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 kidney infection (pyelonephritis) urinary tract infection

Nursing Diagnosis 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

SURGICALPyeloplasty

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 Is a set of clinical

manifestations caused by protein wasting secondary to diffuse glomerular damage.

ETIOLOGY Nephrotic syndrome is a protein wasting disease

Caused by: glomerulonephritis diabetes mellitus Lupus erythematosus Amylodidosis Carcinoma

Membranous glomerulonephritis

Glomerular basement membrane damage

Glomerular permeability to plasma protein

Albumin depletion in the blood

Alteration in osmotic pressure in the vessels

Fluid moves to interstitial spacesIncrease synthesis of LDL, HDL in the liver with decrease lipid catabolism

Decreased plasma volume

Stimulates aldosterone secretion

Sodium & water retention

Decreased glomerular filtration rate

edema

edema

Hyperlipidemia

lipiduria

proteinuria

hypoalbuminemia

Assessment 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: Complete medical history and physical

examination Urinalysis Blood analysis Kidney biopsy

Complications 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 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 Inflammation of

the bladder or the urethra caused by gram-negative bacteria, with Escherichia coli causing most cases.

Etiology Caused by gram-negative bacteria

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

Upper Urinary Tract Infection (Pyelonephritis)

- Fever

- Chills

- Flank or Low Back Pain

- Nausea and Vomiting

- Headache

- Malaise

- Painful Urination

Diagnostics: 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 Damage and scarring of the urinary tract

lining Pyelonephritis Chronic Renal Failure due to extensive

kidney damage Sepsis

Nursing Diagnosis 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 Promotive

Eat well-balanced diet. Good hygiene practice.

Preventive Do not delay urination. Empty bladder regularly. Clean the urethral meatus after intercourse. Increase fluid intake. Careful sexual practice. Intake of grape juice.

Curative Medications given:

cholinergics to relieve urinary retentionanti-cholinergics to decrease bladder muscle spasmantibiotics: Ciprofloxacinphenazopyridine for pain

Revision of abnormalities in urinary tract. Rehabilitative

Education about importance of completing medication cycle. Evaluation and instruction about voiding patterns, sexual practices, and

hygiene practices.

ACUTE GLOMERULONEPHRITIS 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 Beta-hemolytic Streptococcal infection Viral or parasitic infection

A ntigen (group a beta-hemolytic streptococcus

Antigen- antibody product

Deposition of antigen-antibody complex in glomerulus

Increased production of epithelial cells lining the

glomerulus

Leukocytes infiltrate the glomerulus

Scarring and loss of glomerular filtration

membrane

Decreased glomerular filtration rate

Assessment Hematuria Oliguria Edema (peripheral or periorbital) Headache flank pain Shortness of breath or Dyspnea Hypertension Skin rashes Arthritis Pharyngitis Impetigo

Respiratory infection Pulmonary hemorrhage Heart murmur may

indicate endocarditis Scarlet fever Weight gain Abdominal pain Anorexia Skin pallor Palpable purpura in

patients with Henoch-Schönlein purpura

Oral ulcers

Diagnostics: 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 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 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 Promotive

eat balanced diet teach client to live healthfully

Preventive prompt treatment of URTI or sore throat culture and sensitivity test; antibiotics as indicated

Curative 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 maintain follow-up healthcare report any exacerbation in signs and symptoms

CHRONIC GLOMERULONEPHRITIS

Is the advanced stage of a group of kidney disorders, resulting in inflammation and slowly worsening destruction of glomeruli.

Etiology Acute glomerulonephritis Immunologic reactions in the body

AssessmentSigns: Hypertension Edema Nocturia Weight loss Hematuria Proteinuria Casts and blood in

the urine

Symptoms:HeadacheDyspneaBlurring of visionLassitudeWeakness or fatigue

DIAGNOSTICS: Serum chemistry CBC Urinalysis Renal ultrasonogram Biopsy Kidney

Urine analysisURINE ROUTINE EXAMINATION TEST OBSERVATION NORMAL GENERAL EXAMINATION Volume ml Colour Pale yellow Appearance Clear Deposits absent Reaction(pH) 4.5-8.0 Specific gravity 1.01- 1.03CHEMICAL EXAMINATION Urine Protein Absent Urine Sugar Absent Urine Ketones Absent Occult blood Negative Bile pigment Absent Bile salts Absent Urobilinogen Normal Nitrite NegativeMICROSCOPIC EXAMINATION Red blood cells Absent Pus cells Absent Epithelial cells Absent Crystals Absent Cast Absent Amorphous deposits Absent Bacteria Absent Trichomonas Vaginalis Absent Yeast cells Absent Pregnancy test

Complications• Metabolic acidosis • Pulmonary edema • Pericarditis • Uremic encephalopathy • Uremic gastrointestinal bleeding • Uremic neuropathy • Severe anemia and hypocalcemia • Hyperkalemia

Nursing Diagnosis 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 Promotive

eat balanced diet teach client to live healthfully

Preventive avoid infections, especially respiratory and urinary tract

infection Curative

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 maintain follow-up healthcare report any exacerbation in signs and symptoms