The parenchyma (actual tissue) of the kidney can be visualized on a longitudinal section of the kidney (Fig. 45-2). The outer layer is the cortex, and the inner layer is the medulla. The medulla consists of a number of pyramids. The apices (tops) of these pyramids are called papillae, through which urine passes to enter the calyces. The minor calyces widen and merge to form major calyces, which form a funnel-shaped sac called the renal pelvis. The minor and major calyces transport urine to the renal pelvis, from which it drains through the ureter to the bladder. The renal pelvis can store a small volume of urine (3 to 5 mL).

FIG. 45-2 Longitudinal section of the kidney.

Microstructure.

The nephron is the functional unit of the kidney. Each kidney contains approximately 1 million nephrons. Each nephron is composed of the glomerulus, Bowman’s capsule, and a tubular system. The tubular system consists of the proximal convoluted tubule, loop of Henle, distal convoluted tubule, and collecting tubules (Fig. 45-3). The glomerulus, Bowman’s capsule, proximal tubule, and distal tubule are located in the cortex of the kidney. The loop of Henle and collecting tubules are located in the medulla. Several collecting tubules join to form a single collecting duct. The collecting ducts eventually merge into a pyramid that empties via the papilla into a minor calyx.

FIG. 45-3 The nephron is the basic functional unit of the kidney. This illustration of a single nephron unit also shows the surrounding blood vessels.

Blood Supply.

Blood flow to the kidneys, approximately 1200 mL/min, accounts for 20% to 25% of the cardiac output. Blood reaches the kidneys via the renal artery, which arises from the aorta and enters the kidney through the hilus. The renal artery divides into secondary branches and then into still smaller branches, each of which forms an afferent arteriole. The afferent arteriole divides into a capillary network, the glomerulus, which is a tuft of up to 50 capillaries (see Fig. 45-3). The capillaries of the glomerulus unite in the efferent arteriole. This efferent arteriole splits to form a capillary network, the peritubular capillaries, which surround the tubular system. All peritubular capillaries drain into the venous system; the renal vein empties into the inferior vena cava.

Physiology of Urine Formation.

Urine formation is the outcome of a complex, multistep process of filtration, reabsorption, secretion, and excretion of water, electrolytes, and metabolic waste products. Although urine formation is the result of this process, the primary functions of the kidneys are to filter the blood and maintain the body’s internal homeostasis.

Glomerular Function.

Urine formation begins at the glomerulus, where blood is filtered. The glomerulus is a semipermeable membrane that allows filtration (see Fig. 45-3). The hydrostatic pressure of the blood within the glomerular capillaries causes a portion of blood to be filtered across the semipermeable membrane into Bowman’s capsule, where the filtered portion of the blood (the glomerular filtrate) begins to pass down to the tubule. Filtration is more rapid in the glomerulus than in ordinary tissue capillaries because the glomerular membrane is porous. The ultrafiltrate is similar in composition to blood except that it lacks blood cells, platelets, and large plasma proteins. Under normal conditions, the capillary pores are too small to allow the loss of these large blood components. In many kidney diseases, capillary permeability is increased, which permits plasma proteins and blood cells to pass into the urine.

The amount of blood filtered each minute by the glomeruli is expressed as the glomerular filtration rate (GFR). The normal GFR is about 125 mL/min. The peritubular capillary network reabsorbs most of the glomerular filtrate before it reaches the end of the collecting duct. Therefore only 1 mL/min (on average) is excreted as urine.

Tubular Function.

Since the glomerular membrane is a selective filtration membrane that filters primarily by size, provision is made for the reabsorption of essential materials and the excretion of nonessential ones (Table 45-1). The tubules and collecting ducts carry out these functions by means of reabsorption and secretion. Reabsorption is the passage of a substance from the lumen of the tubules through the tubule cells and into the capillaries. This process involves both active and passive transport mechanisms. Tubular secretion is the passage of a substance from the capillaries through the tubular cells into the lumen of the tubule. Reabsorption and secretion cause numerous changes in the composition of the glomerular filtrate as it moves through the entire length of the tubule.

TABLE 45-1

FUNCTIONS OF NEPHRON SEGMENTS

Component	Function
Glomerulus	Selective filtration.
Proximal tubule	Reabsorption of 80% of electrolytes and water, glucose, amino acids, HCO₃⁻. Secretion of H⁺ and creatinine.
Loop of Henle	Reabsorption of Na⁺ and Cl⁻ in ascending limb and water in descending loop. Concentration of filtrate.
Distal tubule	Secretion of K⁺, H⁺, ammonia. Reabsorption of water (regulated by ADH) and HCO₃⁻. Regulation of Ca²⁺ and PO₄²⁻ by parathyroid hormone. Regulation of Na⁺ and K⁺ by aldosterone.
Collecting duct	Reabsorption of water (ADH required).

ADH, Antidiuretic hormone.

In the proximal convoluted tubule, about 80% of the electrolytes are reabsorbed. Normally, all the glucose, amino acids, and small proteins are reabsorbed. Although most reabsorption occurs by active transport, hydrogen ions (H⁺) and creatinine are secreted into the filtrate.

As reabsorption continues in the loop of Henle, water is conserved, which is important for concentrating the filtrate. The descending loop is permeable to water and moderately permeable to sodium, urea, and other solutes. In the ascending limb, chloride ions (Cl⁻) are actively reabsorbed, followed by passive reabsorption of sodium ions (Na⁺). About 25% of the filtered sodium is reabsorbed in the ascending limb.

Two important functions of the distal convoluted tubules are final regulation of water balance and acid-base balance. Antidiuretic hormone (ADH) is required for water reabsorption in the kidney and is important in water balance. ADH makes the distal convoluted tubules and the collecting ducts permeable to water. This allows water to be reabsorbed into the peritubular capillaries and eventually returned to the circulation.

Decreases in plasma osmolality are detected in the anterior hypothalamus by osmoreceptors. These osmoreceptors send neural input to superoptic nuclei cells in the hypothalamus. These superoptic nuclei cells have neuronal axons that terminate in the posterior pituitary gland and act to inhibit secretion of ADH. In the absence of ADH, the tubules are essentially impermeable to water. Thus any water in the tubules leaves the body as urine.

Aldosterone (released from the adrenal cortex) acts on the distal tubule to cause reabsorption of Na⁺ and water. In exchange for Na⁺, potassium ions (K⁺) are excreted. The secretion of aldosterone is influenced by both circulating blood volume and plasma concentrations of Na⁺ and K⁺.

Acid-base regulation involves reabsorbing and conserving most of the bicarbonate (HCO₃⁻) and secreting excess H⁺. The distal tubule has different ways to maintain the pH of ECF within a range of 7.35 to 7.45 (see Chapter 17).

Myocyte cells in the right atrium secrete a hormone, atrial natriuretic peptide (ANP), in response to atrial distention, which is a result of an increase in plasma volume. ANP acts on the kidneys to increase sodium excretion. At the same time ANP inhibits renin, ADH, and the action of angiotensin II on the adrenal glands, thereby suppressing aldosterone secretion. These combined effects of ANP result in the production of a large volume of dilute urine. Furthermore, secretion of ANP causes relaxation of the afferent arteriole, thus increasing the GFR.

The renal tubules are also involved in calcium balance. Parathyroid hormone (PTH) is released from the parathyroid gland in response to low serum calcium levels. PTH maintains serum calcium levels by causing increased tubular reabsorption of calcium ions (Ca²⁺) and decreased tubular reabsorption of phosphate ions (PO₄²⁻). In kidney disease the effects of PTH may have a major effect on bone metabolism.

Vitamin D is a hormone that can be obtained in the diet or synthesized by the action of ultraviolet radiation on cholesterol in the skin. These forms of vitamin D are inactive and require two more steps to become metabolically active. The first step in activation occurs in the liver; the second step occurs in the kidneys. Active vitamin D is essential for the absorption of calcium from the gastrointestinal (GI) tract. The patient with kidney failure (also called renal failure) has a deficiency of the active metabolite of vitamin D and manifests problems of altered calcium and phosphate balance (see Chapter 47).

In summary, the basic function of nephrons is to cleanse blood plasma of unnecessary substances. After the glomerulus has filtered the blood, the tubules select the unwanted from the wanted portions of tubular fluid. Essential constituents are returned to the blood, and dispensable substances pass into urine.

Other Functions of Kidneys.

The kidneys perform vital functions through participation in red blood cell (RBC) production and blood pressure regulation. Erythropoietin is a hormone produced in the kidneys and secreted in response to hypoxia and decreased renal blood flow. Erythropoietin stimulates RBC production in the bone marrow. A deficiency of erythropoietin occurs in kidney failure, leading to anemia.

Renin is important in the regulation of blood pressure. Renin is produced and secreted by the kidney’s juxtaglomerular cells (Fig. 45-4). Renin is released into the bloodstream in response to decreased renal perfusion, decreased arterial blood pressure, decreased ECF, decreased serum Na⁺ concentration, and increased urinary Na⁺ concentration. The plasma protein angiotensinogen (from the liver) is activated to angiotensin I by renin. Angiotensin I is subsequently converted to angiotensin II by angiotensin-converting enzyme (ACE). ACE is located on the inner surface of all blood vessels, with particularly high levels in the vessels of the lungs. Angiotensin II stimulates the release of aldosterone from the adrenal cortex, which causes Na⁺ and water retention, leading to increased ECF volume. Angiotensin II also causes increased peripheral vasoconstriction. Release of renin is inhibited by an elevation in blood pressure. Excessive renin production caused by impaired renal perfusion may be a contributing factor in the etiology of hypertension (see Chapters 33 and 47).

FIG. 45-4 Renin-angiotensin-aldosterone system.

Most body tissues synthesize prostaglandins (PGs) from the precursor, arachidonic acid, in response to appropriate stimuli. (See Chapter 12 and Fig. 12-2 for a more detailed discussion of PGs.) In the kidney, PG synthesis (primarily PGE₂ and PGI₂) occurs primarily in the medulla. These PGs have a vasodilating action, thus increasing renal blood flow, and promote Na⁺ excretion. They counteract the vasoconstrictor effect of substances such as angiotensin and norepinephrine. Renal PGs may have a systemic effect in lowering blood pressure by decreasing systemic vascular resistance. The significance of renal PGs is related to the kidneys’ role in causing hypertension. In renal failure with a loss of functioning tissue, these renal vasodilator factors are also lost, which may contribute to hypertension (see Chapter 47).

Ureters

The ureters are tubes that carry urine from the renal pelvis to the bladder (see Fig. 45-1). Arranged in a meshlike outer layer, circular and longitudinal smooth muscle fibers contract to promote the peristaltic, one-way flow of urine through the ureters. Distention, neurologic and endocrine influences, and drugs can affect these muscle contractions. Each ureter is approximately 10 to 12 in (25 to 30.5 cm) long and 0.08 to 0.3 in (0.2 to 0.8 cm) in diameter.

The narrow area where each ureter joins the renal pelvis is termed the ureteropelvic junction (UPJ). Subsequently, the ureters insert into either side of the bladder base at the ureterovesical junctions (UVJs). Ureteral lumens are narrowest at the UVJs. These junctions, the UPJ and UVJ, are often sites of obstruction. The narrow ureteral lumens can be easily obstructed internally (e.g., urinary calculi) or externally (e.g., tumors, adhesions, inflammation). Sympathetic and parasympathetic nerves, along with the vascular supply, surround the mucosal lining of the ureters. Stimulation of these nerves during passage of a stone or clot may cause acute, severe pain, termed renal colic.

Because the renal pelvis holds only 3 to 5 mL of urine, kidney damage can result from a backflow of more than that amount of urine. The UVJ relies on the ureter’s angle of bladder penetration and muscle fiber attachments with the bladder to prevent the backflow (reflux) of urine and ascending infection. The distal ureter enters the bladder laterally at its base, courses along obliquely through the bladder wall for about 1.5 cm, and intermingles with muscle fibers of the bladder base. Circular and longitudinal bladder muscle fibers adjacent to the imbedded ureter help secure it. When bladder pressure rises (e.g., during voiding or coughing), muscle fibers that the ureter shares with the bladder base contract first, promoting ureteral lumen closure. Next, the bladder contracts against its base, ensuring UVJ closure and prevention of urine reflux through the junction.

Bladder

The urinary bladder is a stretchable (able to fill at relatively low pressures) organ positioned behind the symphysis pubis and anterior to the vagina and rectum (Fig. 45-5). Its primary functions are to serve as a reservoir for urine and to eliminate waste products from the body. Normal adult urine output is approximately 1500 mL/day, which varies with food and fluid intake. The volume of urine produced at night is less than half of that formed during the day because of hormonal influences (e.g., ADH). This diurnal pattern of urination is normal. Typically, an individual will urinate five or six times during the day and occasionally at night.

The trigone is the triangular area formed by the two ureteral openings and the bladder neck at the base of the bladder. The trigone is affixed to the pelvis by many ligaments and does not change its shape during bladder filling or emptying. The bladder muscle (detrusor) is composed of layers of intertwined smooth muscle fibers capable of considerable distention during bladder filling and contraction during emptying. It is attached to the abdominal wall by an umbilical ligament, the urachus. As a result of this attachment, as the bladder fills, it rises toward the umbilicus. The dome and the anterior and lateral aspects of the bladder expand and contract.

On average, 200 to 250 mL of urine in the bladder cause moderate distention and the urge to urinate. When the quantity of urine reaches approximately 400 to 600 mL, the person feels uncomfortable. Bladder capacity varies with the individual, but generally ranges from 600 to 1000 mL. Evacuation of urine is termed urination, micturition, or voiding.

The bladder has the same mucosal lining as that of the renal pelvises, ureters, and bladder neck. The bladder is lined by transitional cell epithelium and is referred to as the urothelium. The urothelium is unique to the urinary tract. Transitional cell epithelium is resistant to absorption of urine. Therefore urinary wastes produced by the kidneys do not leak out of the urinary system after they leave the kidneys. Microscopically, transitional cell epithelium is several cells deep. However, as urine enters the bladder, these cells stretch out to only a few cells deep to accommodate filling. As the bladder empties, the urothelium resumes its multicellular layer formation.

Transitional cell tumors occurring in one section of the urinary tract can easily metastasize to other urinary tract areas given that the mucosal lining throughout the urinary tract is the same. Malignant cells may move down from upper urinary tract tumors and embed in the bladder, or large bladder tumors can invade the ureter. Tumor recurrence within the bladder is common.

Urethra

The urethra is a small tube that incorporates the smooth muscle of the bladder neck and extends to the striated muscle of the external meatus. The urethra’s primary function is to serve as a conduit for urine from the bladder to the outside the body during voiding and to control voiding.

The female urethra is 1 to 2 in (2.5 to 5 cm) long and lies behind the symphysis pubis but anterior to the vagina (see Fig. 45-1, C). The male urethra, which is about 8 to 10 in (20 to 25 cm) long, originates at the bladder neck and extends the length of the penis (see Fig. 45-1, B).

Urethrovesical Unit

Together, the bladder, urethra, and pelvic floor muscles form what is called the urethrovesical unit. Voluntary control of this unit is defined as continence. Stimulating and inhibiting impulses are sent from the brain through the thoracolumbar (T11 to L2) and sacral (S2 to S4) areas of the spinal cord to control voiding. Distention of the bladder stimulates stretch receptors within the bladder wall. Impulses are transmitted to the sacral spinal cord and then to the brain, causing a desire to urinate. If the time to void is not appropriate, inhibitor impulses in the brain are stimulated and transmitted back through the thoracolumbar and sacral nerves innervating the bladder. In a coordinated fashion, the detrusor muscle accommodates to the pressure (does not contract) while the sphincter and pelvic floor muscles tighten (contract) to resist bladder pressure. If voiding is appropriate, cerebral inhibition is voluntarily suppressed, and impulses are transmitted via the spinal cord for the bladder neck, sphincter, and pelvic floor muscles to relax and for the bladder to contract. The sphincter closes and the detrusor muscle relaxes when the bladder is empty.

Any disease or trauma that affects the function of the brain, spinal cord, or nerves that directly innervate the bladder, bladder neck, external sphincter, or pelvic floor can affect bladder function. These conditions include diabetes mellitus, multiple sclerosis, paraplegia, and tetraplegia (quadriplegia). Drugs affecting nerve transmission also can affect bladder function.

Gerontologic Considerations

Effects of Aging on Urinary System

Anatomic changes in the aging kidney include a 20% to 30% decrease in size and weight between ages 30 and 90 years. By the seventh decade of life, 30% to 50% of glomeruli have lost their function. Atherosclerosis accelerates the decrease of renal size with age. Despite these changes, older individuals maintain body fluid homeostasis unless they encounter diseases or other physiologic stressors.¹

Physiologic changes in the aging kidney include decreased renal blood flow, due in part to atherosclerosis, resulting in a decreased GFR. Alterations in hormone levels, including ADH, aldosterone, and ANP, result in decreased urinary concentrating ability and alterations in the excretion of water, sodium, potassium, and acid. Under normal conditions, the aging kidney is able to maintain homeostasis. However, after abrupt changes in blood volume, acid load, or other insults, the kidney may not be able to function effectively because much of its renal reserve has been lost.

Physiologic changes also occur in the aging urethra and bladder. The female urethra, bladder, vagina, and pelvic floor undergo a loss of elasticity and muscle support. Consequently, older women are more prone to bladder infections and incontinence.

The prostate surrounds the proximal urethra. As men age, the prostate enlarges and may affect urinary patterns, causing hesitancy, retention, slow stream, and bladder infections.²

Constipation, a complaint often expressed by older adults, can also affect urination. Partial urethral obstruction may occur because of the rectum’s close proximity to the urethra.

TABLE 45-2

GERONTOLOGIC ASSESSMENT DIFFERENCES
Urinary System

Gerontologic Changes	Differences in Assessment Findings
Kidney
• ↓ Amount of renal tissue	• Less palpable
• ↓ Number of nephrons and renal blood vessels; thickened basement membrane of Bowman’s capsule and glomeruli	• ↓ Creatinine clearance, ↑ BUN level, ↑ serum creatinine
• ↓ Function of loop of Henle and tubules	• Alterations in drug excretion, nocturia, loss of normal diurnal excretory pattern because of ↓ ability to concentrate urine; less concentrated urine
Ureter, Bladder, and Urethra
• ↓ Elasticity and muscle tone	• Palpable bladder after urination because of retention
• Weakening of urinary sphincter	• Stress incontinence (especially during Valsalva maneuver), dribbling of urine after urination
• ↓ Bladder capacity and sensory receptors	• Frequency, urgency, nocturia, overflow incontinence
• Estrogen deficiency leading to thin, dry vaginal tissue	• Stress or overactive bladder, dysuria
• ↑ Prevalence of unstable bladder contractions	• Overactive bladder
• Prostatic enlargement	• Hesitancy, frequency, urgency, nocturia, straining to urinate, retention, dribbling

Question the patient about the presence or history of diseases that are related to renal or other urologic problems. Some of these diseases are hypertension, diabetes mellitus, gout and other metabolic problems, connective tissue disorders (e.g., systemic lupus erythematosus, systemic sclerosis [scleroderma]), skin or upper respiratory tract infections of streptococcal origin, tuberculosis, viral hepatitis, congenital disorders, neurologic conditions (e.g., stroke, back injury), or trauma. Note specific urinary problems such as cancer, infections, benign prostatic hyperplasia, and calculi.

Case Study

Patient Introduction

iStockphoto/Thinkstock

A.K. is a 28-yr-old African American man who comes to the emergency department (ED) in acute distress with complaints of severe abdominal pain. The pain began about 6 hr ago after he finished a 10-mile run as part of his training for a marathon. He says that the pain has steadily increased, he is nauseated, and his urine is a dark, smoky color.

Critical Thinking

As you read through this assessment chapter, think about A.K.’s symptoms with the following questions in mind:

1. What are the possible causes of A.K.’s abdominal pain, nausea, and urine color?

2. What would be your priority assessment of A.K.?

3. What questions would you ask A.K.?

4. What should be included in the physical assessment? What would you be looking for?

5. What diagnostic studies might you expect to be ordered?

Medications.

An assessment of the patient’s current and past use of medications is important. This should include over-the-counter drugs, prescription medications, and herbs. Drugs affect the urinary tract in several ways. Many drugs are known to be nephrotoxic (Table 45-3). Certain drugs may alter the quantity and character of urine output (e.g., diuretics). A number of drugs such as phenazopyridine (Pyridium) and nitrofurantoin (Macrodantin) change the color of urine. Anticoagulants may cause hematuria. Many antidepressants, calcium channel blockers, antihistamines, and drugs used for neurologic and musculoskeletal disorders affect the ability of the bladder or sphincter to contract or relax normally.

TABLE 45-3

POTENTIALLY NEPHROTOXIC AGENTS

Antibiotics	Other Drugs	Other Agents
amikacin (Amikin) amphotericin B bacitracin cephalosporins gentamicin kanamycin neomycin polymyxin B streptomycin sulfonamides tobramycin (Nebcin) vancomycin	captopril (Capoten) cimetidine (Tagamet) cisplatin (Platinol) cocaine cyclosporine ethylene glycol heroin lithium methotrexate nitrosoureas (e.g., carmustine) Nonsteroidal antiinflammatory drugs (e.g., ibuprofen, indomethacin) phenacetin quinine rifampin Salicylates (large quantities)	Gold Heavy metals

Surgery or Other Treatments.

Ask the patient about previous hospitalizations related to renal or urologic diseases and all urinary problems during past pregnancies. Inquire about the duration, severity, and patient’s perception of any problem and its treatment. Document past surgeries, particularly pelvic surgeries, or urinary tract instrumentation (e.g., catheterization). Ask the patient about any radiation or chemotherapy treatment for cancer.

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Nov 17, 2016 | Posted by admin in NURSING | Comments Off

Painful urination	Y	N
Changes in color of urine (blood, cloudy)	Y	N
Change in characteristics of urination (diminished, excessive)	Y	N
Problems with frequent nighttime urination (nocturia)	Y	N

Blood urea nitrogen
Serum creatinine
Urinalysis
Urine culture and sensitivity

Structures and Functions of Urinary System

Kidneys

Macrostructure.

Microstructure.

Blood Supply.

Physiology of Urine Formation.

Glomerular Function.

Tubular Function.

Other Functions of Kidneys.

Ureters

Bladder

Urethra

Urethrovesical Unit

Gerontologic Considerations

Effects of Aging on Urinary System

Assessment of Urinary System

Subjective Data

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Important Health Information

Past Health History.

Medications.

Surgery or Other Treatments.

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Urinary meatus for inflammation or discharge

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