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Chapter 12
Urinary System
The Y-shaped urinary system consists of two kidneys,
two ureters, the urinary bladder, and the urethra
(Fig.
12.1). The bean-shaped kidneys lie behind the organs in the abdominal
cavity. The kidneys perform this system's main functions for homeostasis. In
doing so, they slowly produce urine, which passes through the ureters and into
the urinary bladder, where it is temporarily stored. When the bladder becomes
partially filled, it contracts, forcing the urine through the urethra and out
of the body.
Main Functions for Homeostasis
Several systems, including the circulatory, respiratory,
skeletal, and digestive systems, play major roles in maintaining chemical
homeostasis; the urinary system completes this list. Besides regulating
numerous chemicals, the urinary system assists other systems in regulating
blood pressure.
The urinary system makes seven contributions to homeostasis.
Each activity is adjusted to compensate for changing body conditions. Each
kidney function is regulated by the nervous system, the endocrine system, or
the characteristics of the blood flowing through the kidneys.
One function of the urinary system is removing wastes and
toxins (e.g., heavy metals, dyes) from the blood. Major waste materials removed
include urea, uric acid, and ammonia, which result primarily from the
metabolism of amino acids and proteins, and creatinine from
muscle cells. Although body concentrations of urea and creatinine can become
relatively high before causing significant harm, slight elevations in uric acid
cause the formation of irritating crystals (e.g., gout), and ammonia is highly
toxic at very low concentrations. Many drugs, which can reach toxic levels, are
also removed.
Osmotic pressure
is the total concentration of dissolved materials in a liquid. Since water and
many dissolved substances can pass through capillary walls, the osmotic
pressures of the blood and the fluid surrounding body cells (interstitial
fluid) are equal. The kidneys regulate the osmotic pressure of blood
and therefore that of interstitial fluid by adjusting the amounts of water and
dissolved materials that leave the body in urine.
If the osmotic pressure of the interstitial fluid is the
same as the osmotic pressure inside body cells, osmotic homeostasis exists and
the cells remain the same size. However, if the osmotic pressure surrounding
the cells rises, water will leave the cells by the process of osmosis, causing
them to shrink and their contents to become more concentrated. Conversely, if
the osmotic pressure surrounding the cells falls, water will diffuse into the
cells, causing them to swell and their contents to become dilute. In either
situation the cells malfunction because their structure and chemical
concentrations are disturbed. Swelling of brain cells is especially dangerous
because the excess pressure that develops inside the skull causes neuron injury
and malfunctioning.
Though all substances dissolved in the interstitial fluid
contribute to its osmotic pressure, the ratio between water and sodium is the
main determinant of its osmotic pressure. Therefore, the kidneys maintain
osmotic homeostasis primarily by adjusting the amounts of water and sodium that
remain in the blood and the amounts excreted in the urine. The kidneys must
frequently alter these amounts to compensate for factors that alter osmotic
pressure, including changes in intake (e.g., drinking fluids, eating salty
foods) and output (e.g., perspiring, having diarrhea).
Maintaining
Individual Concentrations
The urinary system maintains individual homeostatic
concentrations of specific minerals such as sodium, potassium, calcium,
magnesium, and phosphorus. Each mineral is important for specific cell
activities and must be available at the correct concentration for these
activities to occur properly. The kidneys adjust the retention and excretion of
each substance individually, compensating for changes in input (e.g., eating)
and output (e.g., perspiring, bleeding).
Maintaining acid/base balance (pH homeostasis) is important
because disturbances disrupt molecular structure and functioning (e.g., enzymes).
Many body activities tend to disturb acid/base balance because they produce
acids (e.g., carbonic acid, lactic acid, ketoacids). Acid/base balance can also
be disturbed by ingesting acidic substances such as vinegar and citrus fruits,
ingesting alkaline substances such as sodium bicarbonate and other antacids, or
changing CO2 levels through altered respiratory system functioning. The kidneys
help compensate for such disturbances and thus help maintain acid/base balance
by adjusting acid and buffer materials (e.g., sodium bicarbonate) in the blood.
The kidneys help regulate blood pressure by adjusting the
amount of water retained in the blood and thus help determine the volume of
blood in the vessels. Low blood pressure can be increased by retaining more
water, and high blood pressure can be reduced by allowing more water to leave
in the urine.
The kidneys also influence blood pressure by secreting an
enzyme (renin) when blood pressure in the kidneys is low. This enzyme causes
the formation of another substance in the blood (angiotensin II), which results
in increased production of the hormone aldosterone. Angiotensin II and
aldosterone increase blood pressure by causing small arteries to constrict and
causing the kidneys to retain more water. Conversely, when blood pressure
rises, less renin is produced. Then blood pressure can drop back to normal
because vessels can dilate and more water can leave in the urine.
The urinary system helps maintain proper calcium
concentrations not only by directly adjusting the retention and excretion of
calcium but also by activating vitamin D. Fully activated vitamin D from the
kidneys is needed for adequate absorption of calcium by the small intestine and
proper calcium retention by the kidneys.
The urinary system helps regulate oxygen levels. When oxygen
levels are low, the kidneys secrete a hormone (erythropoietin)
that stimulates red blood cell production in bone marrow. When red blood cells
increase, more oxygen enters the blood in the lungs. Conversely, high oxygen
levels inhibit erythropoietin production, leading to slower RBC production. As
the number of RBCs declines through normal attrition, oxygen levels decrease.
Since the kidneys are virtually identical to each other in
structure and functioning, we will consider only the right kidney here.
As shown in
Fig.
12.1, blood vessels enter and leave the
kidney where it is indented. The arteries branch into smaller vessels as they
pass through the inner region (medulla) of the kidney (Fig.
12.2). These branches curve over the segments of the medulla and then send
smaller arterial branches to the outer region (cortex). Within
the cortex, each of the smallest branches (afferent arterioles) leads into a
tuft of capillaries called a glomerulus. Another tiny artery
(efferent arteriole) leaves the glomerulus and leads into another group of
capillaries (peritubular capillaries), which surround small kidney tubules.
Blood from these capillaries is collected into veins, which carry it back
through the medulla and out of the kidney.
The capillaries that constitute each glomerulus are much
more porous than are other capillaries. Blood pressure causes much of the water
and most small molecules in the blood, including both desirable and undesirable
substances, to pass through the glomerular wall by the process of filtration.
The filtrate that has passed through the glomerular wall is captured by a
double layer of kidney cells called Bowman's capsule, which
surrounds the glomerulus. The filtrate then passes into a twisted tube called
the renal tubule, which has three sections, the proximal
convoluted tubule, the loop of Henle, and the distal convoluted tubule. (Fig.
12.3). Meanwhile, blood cells, large molecules such as proteins, and some
water and small molecules remain in the glomerulus and then flow through the
efferent arteriole.
Different types of kidney cells compose each region of the
renal tubule, and one region of the tubule (the loop of Henle) passes through
the center of the kidney. As the filtrate passes through each region of the
tubule, the tubule cells send desirable materials in the filtrate into the
blood in the surrounding capillaries. These materials include essentially all
the glucose and amino acids, much of the water and sodium, and smaller amounts
of minerals such as calcium. This retrieval process is called reabsorption
(Fig.
12.4). At the same time, the tubule cells cause undesirable materials
remaining in the blood to move into the fluid within the tubule by the process
called secretion (excretion). Finally, more water
is reabsorbed as the fluid passes through the collecting duct.
The solution of wastes, toxins, and other undesirable materials remaining in
the collecting duct is urine. Urine passes from the kidney into
the ureter, which transports it to the urinary bladder.
The kidney has approximately 1 million glomeruli, each of
which is associated with a Bowman's capsule and a renal tubule. The combination
of these three structures is called a nephron (Fig.
12.2,
Fig.
12.3). All nephrons function in a similar though not an identical manner.
One noteworthy difference is that nephrons with glomeruli close to the medulla
(juxtamedullary nephrons) seem to be especially important for reabsorbing
water.
Urine formation involves the three processes of filtration,
reabsorption, and secretion. The rate and amount of each of these processes are
carefully adjusted so that blood leaving the kidneys can compensate for any
factors that tend to disturb homeostasis with respect to waste and toxin
levels, osmotic pressure, the concentrations of many individual substances,
acid/base balance, and blood pressure. Adjustments are made based on the
quality of blood passing through the kidney and many regulatory substances
including hormones, nitric oxide (*NO), and sympathetic nerves. Tubule cells
also add correct amounts of vitamin D and erythropoietin to the blood. Thus,
the kidneys perform all the urinary system functions for homeostasis.
Under favorable living conditions, such as having
comfortable temperatures, proper diet, and moderate exercise, as little as 30
percent of the working capacity of both kidneys is needed to maintain
homeostasis. The additional reserve capacity becomes important when conditions
are less favorable, such as when high temperatures cause profuse sweating or
the diet contains excess water. However, even the most fully functional kidneys
can be overburdened by extreme conditions such as complete water deprivation.
Therefore, in healthy adults there is a range of living conditions within which
the kidneys can maintain homeostasis. Conditions outside this range overwhelm
the powers of compensation of the kidneys and lead to loss of homeostasis, cell
and body malfunction, illness, and possibly death.
Aging causes the kidneys to gradually decrease in length,
volume, and weight. The decline in size may begin as early as age 20, and the
resulting changes are evident by age 50. Shrinkage of the kidneys continues
thereafter.
The loss of kidney mass seems to result primarily from
declining blood flow through the kidneys caused by degenerative changes in the
smaller arteries and glomeruli. The smaller arteries, including arterioles
attached to glomeruli, become irregular and twisted. Glomeruli can be injured
by *FRs, glycation of proteins, imbalances between substances causing
vasodilation and vasoconstriction, and by excess cell formation. Functional
glomeruli are lost gradually, beginning before age 40. By age 80, 40 percent of
the glomeruli may stop functioning. From 20 to 30 percent of glomeruli that
stop functioning become solidified, and this stops all blood flow through them.
Increasing numbers of other glomeruli have their capillaries replaced by one or
a few arterioles that permit blood flow while preventing filtration. These
shunts develop predominantly in glomeruli close to the medulla. Many remaining
glomeruli become smoother and have thicker and declining surface area. These
latter changes reduce their filtration rates.
The amount of blood flowing through kidney vessels is called
renal blood flow (RBF), and age changes in kidney
vessels significantly decrease RBF. The decline may begin as early as age 20
and is apparent in most individuals during the fifth decade. The average
decline in RBF is 10 percent per decade, though many individuals have more
rapid decreases with age. There is a greater decline in blood flow through
peripheral cortical nephrons than through glomeruli close to the medulla
(juxtamedullary nephrons) and the medulla itself.
This decline seems to be the main reason for most reductions
in the functional capacity of the kidney, including filtration, reabsorption,
and secretion. In addition, age changes seem to reduce the ability of kidney
vessels to dilate and constrict and therefore to adjust kidney blood flow. This
change reduces both the speed of kidney functioning and the extent to which it
may increase or decrease to meet alterations in body conditions. The greater
decline in blood flow in the cortical region compared with the medulla also
seems to contribute to the decline in the ability of the kidneys to reduce
water loss. This change reduces the ability to compensate for high osmotic
pressure.
Some older individuals are at risk for even greater
reductions in RBF and kidney functioning because certain abnormal or disease
conditions cause less blood to pass through the kidneys. Examples include
dehydration, atherosclerosis of kidney arteries, weak heart function, and edema
from protein malnutrition or cirrhosis. Renal blood flow is also reduced by certain
pain-relieving medications, such as nonsteroidal anti-inflammatory drugs
(NSAIDs), which lead to vasoconstriction of kidney arterioles.
One main effect of age changes in glomeruli and a declining
RBF is a declining rate of filtration through the glomeruli [glomerular
filtration rate (GFR)]. The GFR usually begins to drop
between ages 30 and 35. However, both the age at which GFR begins to drop and
the rate of decline vary greatly among individuals. In some older individuals
GFR may remain steady or improve for years before declining again.
A decline in GFR is important because it reduces the
elimination rate of many undesirable substances by filtration and secretion.
Examples include acids, urea, uric acid, creatinine, toxins, and certain
antibiotics, NSAIDs, and other drugs. Therefore, these substances may
accumulate in the body and reach hazardous levels. Reductions in GFR also limit
the ability of tubules to adjust the retention or elimination of materials such
as water, sodium, and potassium.
Normal individual variability in the changes in GFR,
together with difficulties in accurately measuring GFR, increases the
possibility of making errors in establishing GFRs for older individuals. Such
errors can lead to other errors in making dietary recommendations or
prescribing drug doses.
Age changes in blood vessels are accompanied by age changes
in tubules. The tubules become thicker, shorter, and more irregular as their
cell numbers decrease. These changes seem to have little effect on the
functioning of individual tubules. However, the total capacity for reabsorption
and secretion by kidney tubules is reduced because of the decrease in GFR,
which supplies filtrate to the tubules, and because whole nephrons stop
functioning, shrink, and are lost. The loss of nephrons whose glomeruli are
close to the medulla exceeds the loss of more peripheral nephrons.
Little information about age changes in collecting ducts is
available, suggesting that these ducts undergo few age changes. There are
conflicting views about whether there is an age-related decline in the
responsiveness of the collecting ducts to hormones that promote water
reabsorption.
Renin One way by which the kidneys regulate blood
pressure is by adjusting the production of renin. The kidneys
also produce renin when osmotic pressure or sodium concentrations are abnormal.
Renin indirectly causes tubules to reabsorb more sodium and secrete more
potassium. Therefore, adjusting renin production helps regulate blood pressure,
along with osmotic pressure and concentrations of sodium and potassium.
Aging causes a gradual decrease in renin production by the
kidneys, and the kidneys become less sensitive to messages initiated by renin.
These changes decrease further the ability of the kidneys to maintain
homeostasis of osmotic pressure, sodium and potassium concentrations, and blood
pressure.
Vitamin D Activation Aging causes a decline in vitamin D
activation by the kidneys, especially after age 65. Lower vitamin D activation
promotes calcium deficiencies, bone fractures, and osteoporosis.
Women experience dramatic decreases in vitamin D activation
before age 65 because estrogen, which stimulates vitamin D activation, drops precipitously
at menopause (approximately age 50). In women, the combination of aging of the
kidneys and hormonal changes results in a greatly reduced vitamin D supply and
is a major reason for the higher incidence of osteoporosis among postmenopausal
women.
In summary, there is an age-related decline in the reserve
capacity of the kidneys for maintaining homeostasis of osmotic pressure,
concentrations of sodium and potassium, acid/base balance, and blood pressure.
Elimination of wastes and toxins becomes slower, and less vitamin D is
activated. As with age changes in other parts of the body, these changes begin
at different times and progress at different rates. The ability to produce
erythropoietin to regulate oxygen levels declines, which increases the risk of
anemia. Age changes in the ability to regulate substances such as calcium and
magnesium have not been well studied.
In spite of the gradual decline in many kidney functions,
healthy people enter adulthood with enough kidney reserve capacity so that
under favorable living conditions there is ample functioning to maintain
homeostasis regardless of age. However, the declining kidney capacity results
in a narrowing of the range of conditions over which the kidneys can provide
compensatory adjustments. This narrowing in range, together with certain age
changes and many age-related abnormal and disease changes, increases the
chances that excessive demands will be placed on the kidneys. Therefore, as
people get older, there is a greater likelihood that the frequency, extent, and
duration of excursions outside the urinary system's adaptive capacity and beyond
the bounds of homeostasis will occur. This necessitates greater conscious
effort to prevent such excursions and, when they occur, to correct the
conditions causing them.
The relationships between the kidneys and medications change
in several ways as age increases. Age changes in the kidneys reduce their
ability to destroy some drugs (e.g., morphine) and to eliminate others in the
urine (e.g., aspirin, NSAIDs, antibiotics). The effects of these age changes
may be enhanced or reduced by diseases (e.g., circulatory diseases, cirrhosis,
urinary tract infections, kidney diseases), by some medications (e.g., NSAIDs,
diuretics), and by age-related decreases in total body water and increases in
percent body fat. Therefore, as age increases, types and doses of all
medications should be selected in a more individualized and careful manner to
provide effective therapy while minimizing the risks of complications.
Abnormal and Disease Changes in Kidneys
Aging is associated with an increase in the risk of
developing kidney diseases such as infections. However, the age-related rise in
most kidney diseases results from an increase in factors outside the urinary
system that cause adverse changes in the kidneys. Examples include age changes
such as reduced white blood cell functioning, abnormal conditions such as
autoimmune problems and drug toxicity, and diseases such as high blood
pressure, atherosclerosis, diabetes mellitus, and prostatic hypertrophy.
Abnormal and disease conditions in the kidneys can be prevented or minimized by
avoiding, compensating for, or treating these nonurinary factors.
Abnormal and disease conditions of the kidneys become more
important with age because aging has already reduced some kidney functions.
Many conditions are serious threats since the kidneys play several essential
roles in maintaining homeostasis. However, abnormal and disease conditions of
the kidneys are not discussed in this book because they become neither
sufficiently more frequent nor unusual in the elderly and are not among the
most common disorders in older people.
For a photo of urinary bladder stones, go to Preserved
Specimen Photos .
Urine passes through the ureter from each
kidney and enters the urinary bladder (Fig.
12.1). Occasional waves of peristalsis in the muscle layer in each ureter
pump urine toward the bladder. Gravity may assist the flow of urine through the
ureters. The ureters seem to undergo no significant age changes.
The urinary bladder is located in the lower
part of the abdominal cavity (Fig.
12.1). It has a smooth inner lining, a middle layer of smooth muscle, and
an outer fibrous layer. The muscle layer, the detrusor muscle, is
fairly thick (Fig.
12.5).
As urine enters the bladder from the ureters, the bladder
wall is stretched. It can expand enough for the bladder to accommodate
approximately 1 liter of urine, though the bladder usually empties before it
has been filled to capacity. Emptying is accomplished by contraction of the
muscular wall of the bladder and simultaneous relaxation of muscles in and
around the urethra. Once emptying begins, reflexes cause it to continue until
all urine has been voided. However, voluntary impulses and muscle contractions
can stop bladder emptying before all urine has been eliminated. Since emptying
involves the coordinated actions of the bladder, the urethra, and other muscles
and nerves, this function is discussed in detail after the section on age
changes in the urethra.
Aging causes the bladder to become smaller. Bands of tissue
develop within the bladder and fibrous material in the bladder wall increases.
These changes reduce the bladder’s ability to stretch and contract.
Consequently, the bladder empties less completely and the maximum capacity of
the bladder declines. Incomplete emptying of the bladder increases the risk of developing
urinary tract infections from bacteria that remain in the bladder. The
declining bladder capacity results in frequent emptying, which becomes
inconvenient. When the bladder must be emptied three or more times during the
night, the condition is called nocturia. Nocturia disrupts sleep
and increases the risk of falls from nighttime visits to toilet facilities.
Age-related factors that increase urine production also contribute to nocturia.
Finally, the age-related increase in spontaneous spastic contraction of bladder
muscle (i.e., unstable bladder) increase nocturia and the risk of unintentional
release of urine.
The urethra begins at the base of the bladder, extends
through the layer of voluntary skeletal muscle at the bottom of the pelvis, and
ends at an opening on the surface of the body, the external urethral meatus.
The male urethra is several inches longer than the female urethra because it
extends through the penis (Fig.
12.5)
The urethra has the same three layers found in the bladder,
though the muscle layers in the urethra are thinner. In addition, the beginning
of the urethra contains a ring of smooth muscle, the internal urethral
sphincter. When contracted, this sphincter prevents urine from flowing
from the bladder into the urethra. A second ring, composed of voluntary
skeletal muscle (external urethral sphincter), encircles the
urethra where it passes through the floor of the pelvis. Contraction of both
this sphincter and the muscular floor of the pelvis can also prevent urine from
passing through the urethra. Note that in men the prostate gland,
which functions as part of the reproductive system, encircles the urethra just
below the bladder.
The urethra as a whole becomes thinner with aging, causing
increased susceptibility to injury. Thinning of the skeletal muscle seems to
cause weakening of the external urethral sphincter. These changes are greater
in women and seem to result largely from the decrease in estrogen after
menopause.
The combination of urethral thinning and weakening of the
urethral sphincter reduces the control of urination. However, significant
problems such as urethral inflammation and urinary incontinence
(inappropriate elimination of urine) develop only when other factors contribute
to them.
Elimination of urine from the bladder is called urination,
micturition, or voiding. This process is similar in
operation to the elimination of feces. When the bladder is empty, its muscular
wall is relaxed and the internal urethral sphincter is contracted. As urine
from the ureters enters the bladder, the bladder stretches outward. After 200
to 300 ml of urine has entered the bladder, pressure in the bladder rises and
is detected by sensory neurons. Impulses are sent by nerves to the spinal cord
and brain, causing the person to perceive the need to void. At this point
autonomic impulses from the spinal cord reflexively stimulate contraction of
the detrusor muscle and relaxation of the internal urethral sphincter, causing
urine to flow out through the urethra. However, urination can be prevented by
voluntary impulses from the brain that suppress the impulses from the spinal
cord and cause contractions of the external urethral sphincter and muscles in
the pelvic floor.
If urination is voluntarily prevented, the perception of
fullness and pressure in the bladder subsides. Bladder filling, bladder
stretching, and increasing pressure continue until the sensory neurons are
stimulated enough to again cause the sensation of fullness. Once again reflex
voiding is initiated, and bladder emptying can be voluntarily prevented. This
process can be repeated until the pressure rises high enough and impulses from
neurons that detect bladder pressure become powerful enough to override efforts
to retain the urine.
In most circumstances, maximum bladder filling and very high
pressures do not develop because voluntary impulses that suppress voiding are
purposely stopped. Then reflex contraction of the bladder, together with
relaxation of both urethral sphincters and the pelvic floor muscles, results in
forceful elimination of urine through the urethra. Once initiated, voiding
usually continues reflexively until the bladder is empty, at which point the
bladder relaxes and the internal urethral sphincter contracts again. Voiding
can be stopped before complete emptying has been achieved by voluntarily
contracting the external urethral sphincter and pelvic floor muscles.
Urination can occur voluntarily as long as the bladder
contains some urine. Then voluntary contraction of abdominal muscles causes
bladder pressure to rise, initiating the voiding reflex. Then voluntary
relaxation of the external sphincter and pelvic floor muscles permits urine
flow.
Age changes in the sensory nerves associated with the
bladder cause a declining ability to detect bladder stretching and pressure;
some individuals lose all ability to perceive bladder fullness. These sensory
changes increase the risk of prolonged urine retention and therefore urinary
incontinence. However, the effects of age changes in the bladder usually
override the effects of changes in the sensory neurons and cause voiding to
occur more frequently and at lower bladder volumes.
Adequate control of urination is retained regardless of age
unless abnormal or disease conditions reduce it. Since the incidence and
severity of many of these conditions and diseases increase with age, the
incidence of abnormal and inadequate control of urination also rises with age.
One form of inadequate control that becomes more common as
age increases is urinary incontinence. Estimates of its incidence vary widely
depending on both the strictness applied in defining this condition and the
techniques used to identify it. Among noninstitutionalized people over age 65,
5 percent to 15 percent of men and 11 percent to 50 percent of women have at
least temporary urinary incontinence. However, at least 50 percent of
institutionalized elderly people have urinary incontinence. The ratio of
occurrence between elderly hospitalized women and men is approximately 2:1.
The very high incidence of urinary incontinence among
institutionalized individuals occurs because incontinence is a main reason for
institutionalizing older individuals and because many other conditions leading
to institutionalization contribute to it. Examples include dementia, strokes,
and severe physical disability.
Types Four distinct types of urinary incontinence
can be identified. Some individuals may have two or more types simultaneously. Overflow
incontinence is due to excess pressure in the bladder caused by
excessive urine retention. This type of incontinence, which is less common than
the other types, may or may not be accompanied by a strong sensation of bladder
fullness. Urge incontinence is accompanied by a strong perception
that urination is necessary even though the bladder is not filled to capacity.
It is often due to excess bladder contractions. Stress incontinence
involves urine loss from factors that weaken muscles in the sphincter and
pelvic floor. Incontinent events often occur when a rise in abdominal pressure
causes higher bladder pressure, such as during coughing, laughing, sneezing,
and strenuous effort such as standing up and lifting a heavy object. Stress
incontinence is much more common in women than in men because women have
shorter urethras and postmenopausal thinning and weakening of structures used
for retaining urine. Functional incontinence results from factors
that reduce the cognitive functions needed to control urination. Factors
include dementia, stroke, and strongly psychoactive medications. This type of
incontinence involves no abnormalities or diseases of the urinary system. Some
people have more than one type of urinary incontinence, a condition called mixed
incontinence.
Overflow incontinence causes elimination of small volumes of
urine. Stress, urge, and functional incontinence may result in loss of urine
volumes ranging from a few drops to several hundred milliliters. Urge and functional
urinary incontinence may cause complete bladder emptying.
Contributing Factors Urinary incontinence results from excess
bladder pressure caused by excess urine production, urine retention, or
stimulation of the bladder; from inadequate contraction of pelvic floor muscles
due to muscle weakness or nervous system malfunction; or from a combination of
these conditions. A person may have two or more factors acting simultaneously
or in various sequences.
Effects and Complications Urinary incontinence has the same
undesirable results that characterize fecal incontinence. These include skin
inflammation, sores, and infection; social and psychological disruptions; and
institutionalization. Costs for devices and supplies (e.g., absorbent
undergarments) for adults with urinary incontinence reach 10 billion dollars
per year.
Prevention and Treatments Some cases of urinary incontinence can be
prevented by avoiding factors that substantially increase the risk of
developing this condition. Examples include certain medications (e.g.,
diuretics, psychoactive drugs) and limited access to toilet facilities.
Many individuals with urinary incontinence can reduce their
incidents of incontinence substantially or can be cured. As with fecal
incontinence, the nature and extent of interactions between care givers and
persons with urinary incontinence can influence the degree of success achieved.
Steps can also be taken to reduce the impact of incidents of urinary
incontinence. The first step is to identify the factors leading to
incontinence. This procedure may involve taking a patient history, performing a
physical examination that includes special tests for urinary function,
evaluating nervous system function, and scrutinizing the medications being
taken. Once the type of incontinence and the contributing factors have been
identified, an individualized care plan can be developed (Table 12.1).
Table
12.1 TREATMENTS FOR URINARY INCONTINENCE
Regulate intake of fluids and diuretics (e.g., alcohol,
caffeine, drugs) to reduce urine formation
Regulate all medications affecting urinary or nervous system
functioning
Assure accessibility to facilities such as bedpans, urinals,
and care giver assistance
Urinate at scheduled times
Cure urinary tract infections to reduce bladder instability
Exercise sphincter and pelvic floor muscles to increase
strength (e.g., Kegel exercises)
Use estrogen therapy in women to increase urethral strength
Take medications to modify bladder and internal sphincter
function
Undergo surgery to remove obstructions (e.g., prostate
surgery), enlarge the bladder, denervate the bladder, or implant an artificial
sphincter
Use behavioral modification and training
Use biofeedback control to increase awareness of need to
void and gain better control of muscles
Use electrical stimulators to control muscles
Use absorbent pads or male condom catheters to catch urine
Perform skin care to avoid complications
Use catheters to drain urine (can lead to complications such
as infections and bladder instability)
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Salisbury University, Maryland
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