Urinary System

• Consist of:

– Kidneys

– Ureters

– Bladder

– Urethra

General

Function:

• Excretory

• Regulatory

• Secretory

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

Kidney

• Bean-shaped, brownish-red structures.

• Retroperitoneal, posterior wall of abdomen, 12th thoracic vertebra.

• Filter any products from the blood which has no use in the body.

A. Regions

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

B. Nephrons
- Functional units of kidney:

a) Glomerulus

b) Bowman’s capsule

c) Proximal tubule

d) Distal tubule

e) Loop of Henle

f) Collecting ducts

C. Calyx

• Minor calyx- 4-13 minor calices

• Major calyx- 2-3 major calices

• 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 layer

2. Detrusor- beneath the adventitia

3. Lamina Propria- interface between detrusor and urethelium.

4. Urothelium- innermost layer

Urethra
• Extends from the bladder to the urinary meatus

• Exit passageway for urine

• Lined with mucous membrane

• In male, it serves as a passageway for both semen and urine

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 (HCO 3 - ) in the

proximal tubule

 Acids

 release hydrogen ions (H + ) in solutions

 Ex. Hydrochloric acid (HCl)- strong acid

Carbonic acid (H 2 CO 3 )- weak acid

 Bases or alkalis

 decrease hydrogen ion (H + ) concentration

 accept H + in solutions

 Ex: Sodium Hydroxide (NaOH) – strong base

Bicarbonate (HCO 3 )

weak baseRegulation 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-

C. 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. Manifestations

A. 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 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

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 U- waves seen in ECG)

F. 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.

3. 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

- 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

b. 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)

D. 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

E. 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

F. 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

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

Complications

• kidney infection (pyelonephritis)

• urinary tract infection

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

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

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

Complications

• Damage and scarring of the urinary tract lining

• Pyelonephritis

• Chronic Renal Failure due to extensive kidney damage

• Sepsis

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

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

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

Complications

• Metabolic acidosis

• Pulmonary edema

• Pericarditis

• Uremic encephalopathy

• Uremic gastrointestinal bleeding

• Uremic neuropathy

• Severe anemia and hypocalcemia

• Hyperkalemia