The Urinary System

DR ENE CHIDIEBERE BROWN

• The urinary system is the main excretory system and consists of the
following structures:
• 2 kidneys, which secrete urine,
• 2 ureters, which convey the urine from the kidneys to the urinary
bladder,
• the urinary bladder where urine collects and is temporarily stored,
• the urethra through which the urine passes from the urinary bladder to
the exterior.
• Urine is stored in the bladder and excreted by the process of micturition
An overview of the urinary system
The main functions of the kidneys are:
• formation and secretion of urine, which regulates total body water,
electrolyte and acid–base balance and enables excretion of waste
products
• production and secretion of erythropoietin, the hormone that
stimulates formation of red blood cells
• production and secretion of renin, an important enzyme in the control
of blood pressure
• The kidneys produce urine that contains metabolic waste products,
including the nitrogenous compounds urea and uric acid, excess ions
and some drugs.
A longitudinal section of the right kidney.
• Kidneys are bean-shaped organs, about 11 cm long, 6 cm wide, 3 cm
thick and weigh 150 g.
• They are embedded in, and held in position by, a mass of fat
• The kidney is composed of about 1–2 million functional units,
the nephrons, and a smaller number of collecting ducts.
• The collecting ducts transport urine through the pyramids to the
calyces and renal pelvis, giving the pyramids their striped appearance
A nephron and associated blood vessels
Blood Supply to the Kidney
• The kidneys receive about 20% of the cardiac output.
• After entering the kidney at the hilum the renal artery divides into smaller
arteries and arterioles.
• In the cortex an arteriole, the afferent arteriole, enters each glomerular
capsule and then subdivides into a cluster of tiny arterial capillaries,
forming the glomerulus.
• Between these capillary loops are connective tissue phagocytic mesangial
cells, which are part of the monocyte–macrophage system
• The blood vessel leading away from the glomerulus is the efferent
arteriole
• The afferent arteriole has a larger diameter than the efferent arteriole
• whic increases pressure inside the glomerulus and drives filtration
across the glomerular capillary walls.
• The efferent arteriole divides into a second peritubular (meaning
‘around tubules’) capillary network, which wraps around the
remainder of the tubule, allowing exchange between the fluid in the
tubule and the bloodstream
• Venous blood drained from this capillary bed eventually leaves the
kidney in the renal vein, which empties into the inferior vena cava.
The series of blood vessels in the kidney
• The blood vessels of the kidney are supplied by both sympathetic and
parasympathetic nerves.
• The presence of both branches of the autonomic nervous system
controls renal blood vessel diameter and renal blood flow
independently of autoregulation
Formation of urine
• The composition of urine reflects exchange of substances between
the nephron and the blood in the renal capillaries.
• Waste products of protein metabolism are excreted, electrolyte levels
are controlled and pH (acid–base balance) is maintained by excretion
of hydrogen ions.
• There are three processes involved in the formation of urine:
• Filtration
• Selective reabsorption
• Secretion.
Filtration
• This takes place through the semipermeable walls of the glomerulus
and glomerular capsule.
• Water and other small molecules pass through, although some are
reabsorbed later.
• Blood cells, plasma proteins and other large molecules are too large
to filter through and therefore remain in the capillaries.
• The filtrate in the glomerulus is very similar in composition to plasma
with the important exceptions of plasma proteins and blood cells.
Filtration in the glomerulus.
The glomerulus and glomerular capsule
Constituents of glomerular filtrate and
glomerular capillaries
• Filtration takes place because there is a difference between the blood
pressure in the glomerulus and the pressure of the filtrate in the
glomerular capsule.
• Because the efferent arteriole is narrower than the afferent arteriole,
a capillary hydrostatic pressure of about 7.3 kPa (55 mmHg) builds up
in the glomerulus.
• This pressure is opposed by the osmotic pressure of the blood,
provided mainly by plasma proteins, about 4 kPa (30 mmHg), and
by filtrate hydrostatic pressure of about 2 kPa (15 mmHg) in the
glomerular capsule.
• The volume of filtrate formed by both kidneys each minute is called
the glomerular filtration rate (GFR).
• In a healthy adult the GFR is about 125 ml/min, i.e. 180 litres of
filtrate are formed each day by the two kidneys.
• Nearly all of the filtrate is later reabsorbed from the kidney tubules
with less than 1%, i.e. 1 to 1.5 litres, excreted as urine.
• The differences in volume and concentration are due to selective
reabsorption of some filtrate constituents and tubular secretion of
others.
Autoregulation of filtration
• Renal blood flow is protected by a mechanism called autoregulation, whereby
renal blood flow is maintained at a constant pressure across a wide range of
systolic blood pressures (from around 80 to 200 mmHg).
• Autoregulation operates independently of nervous control, i.e. if the nerve
supply to the renal blood vessels is interrupted, autoregulation continues to
operate.
• It is therefore a property inherent in renal blood vessels; it may be stimulated
by changes in blood pressure in the renal arteries or by fluctuating levels of
certain metabolites, e.g. prostaglandins.
• In severe shock, when the systolic blood pressure falls below 80 mmHg,
autoregulation fails and renal blood flow and the hydrostatic pressure decrease,
impairing filtration within the nephrons.
Selective Reabsorption
• Most reabsorption from the filtrate back into the blood takes place in the proximal
convoluted tubule.
• Materials essential to the body are reabsorbed here, including some water,
electrolytes and organic nutrients such as glucose.
• Some reabsorption is passive, but some substances are transported actively.
• Only 60–70% of filtrate reaches the loop of the nephron.
• Much of this, especially water, sodium and chloride, is reabsorbed in the loop, so only
15–20% of the original filtrate reaches the distal convoluted tubule.
• More electrolytes are reabsorbed here, especially sodium, so the filtrate entering the
collecting ducts is actually quite dilute.
• The main function of the collecting ducts therefore is to reabsorb as much water as
the body needs.
Directions of selective reabsorption and secretion in the
nephron
• Active transport takes place at carrier sites in the epithelial
membrane, using chemical energy to transport substances against
their concentration gradients.
• Some ions, e.g. sodium and chloride, can be absorbed by both active
and passive mechanisms depending on the site in the nephron.
• Some constituents of glomerular filtrate (e.g. glucose, amino acids) do
not normally appear in urine because they are completely reabsorbed
unless blood levels are excessive.
• Reabsorption of nitrogenous waste products, such as urea, uric acid
and creatinine is very limited.
• The kidneys’ maximum capacity for reabsorption of a substance is
the transport maximum, or renal threshold.
• For example, the normal blood glucose level is 3.5 to 8 mmol/l (63 to 144
mg/100 ml) and if this rises above the transport maximum of about 9
mmol/l (160 mg/100 ml), glucose appears in the urine.
• This occurs because all the carrier sites are occupied and the mechanism for
active transport out of the tubules is overloaded.
• Other substances reabsorbed by active transport include sodium, calcium,
potassium, phosphate and chloride.
• The renal threshold, of some substances varies according to body need at a
particular time, and in some cases reabsorption is regulated by hormones.
Hormones that influence selective reabsorption
• Parathyroid hormone
• This comes from the parathyroid glands and together
with calcitonin from the thyroid gland regulates the reabsorption of
calcium and phosphate from the distal collecting tubules.
• Antidiuretic hormone
• Also known as ADH, this is secreted by the posterior lobe of the
pituitary gland and increases the permeability of the distal convoluted
tubules and collecting tubules, increasing water reabsorption.
• Secretion of ADH is controlled by a negative feedback system
Negative feedback regulation of secretion of
antidiuretic hormone (ADH)
• Aldosterone
Secreted by the adrenal cortex, this hormone increases the
reabsorption of sodium and water, and the excretion of potassium.
• Secretion is regulated through a negative feedback system
• Atrial natriuretic peptide
• Also known as ANP, this hormone is secreted by the atria of the heart
in response to stretching of the atrial wall. It decreases reabsorption
of sodium and water from the proximal convoluted tubules and
collecting ducts.
• Secretion of ANP is also regulated by a negative feedback system
Negative feedback regulation of aldosterone secretion. ACE = angiotensin converting enzyme
Negative feedback regulation of secretion of atrial natriuretic
peptide (ANP)
Tubular Secretion
• Filtration occurs as the blood flows through the glomerulus.
• Substances not required and foreign materials, e.g. drugs including
penicillin and aspirin, may not be cleared from the blood by filtration
because of the short time it remains in the glomerulus.
• Such substances are cleared by secretion from the peritubular
capillaries into the convoluted tubules and excreted from the body in
the urine.
• Tubular secretion of hydrogen ions (H+) is important in maintaining
normal blood pH.
Summary of urine formation
The three processes involved – filtration,
selective reabsorption and tubular secretion
Composition of urine
• Water 96%
• Urea 2%
• Others are;
• Uric acid
• Creatinine
• Ammonium
• Potassium
• Chlorides
• Phosphates
• Sulphates
• Oxalates
• Urine is clear and amber in colour due to the presence of urobilin, a
bile pigment altered in the intestine, reabsorbed then excreted by the
kidneys.
• The specific gravity is between 1020 and 1030, and
• The pH is around 6 (normal range of 4.5 to 8).
• A healthy adult passes 1000 to 1500 ml per day.
• The amount of urine produced and the specific gravity vary according
to fluid intake and the amount of solute excreted.
• Urine production is decreased during sleep and exercise.
Water balance and urine output
• The source of most body water is dietary food and fluid, and a small amount
(called ‘metabolic water’) is formed by metabolic processes.
• Water is excreted as the main constituent of urine, in expired air, faeces and
through the skin as sweat.
• The amount lost in expired air and faeces is fairly constant, and the amount of
sweat produced is associated with environmental and body temperatures
• The balance between fluid intake and output is controlled by the kidneys.
• The minimum urinary output, i.e. the smallest volume required to excrete body
waste products, is about 500 ml per day.
• Urinary volume in excess of this is controlled mainly by antidiuretic hormone
(ADH) released into the blood by the posterior lobe of the pituitary gland.
• Sensory nerve cells in the hypothalamus (osmoreceptors) detect
changes in the osmotic pressure of the blood.
• Nerve impulses from the osmoreceptors stimulate the posterior pituitary
to release ADH.
• When the osmotic pressure is raised, i.e. the blood is becoming more
concentrated, ADH output is increased and as a result, water
reabsorption by the distal convoluted tubules and collecting ducts is
increased, reducing the blood osmotic pressure and ADH output.
• This negative feedback mechanism maintains the blood osmotic
pressure (and therefore sodium and water concentrations) within
normal limits
• The feedback mechanism may be suppressed when there is an
excessive amount of a dissolved substance in the blood.
• For example, in diabetes mellitus when the blood glucose level is
above the transport maximum of the renal tubules, excess water is
excreted with the excess glucose.
• This polyuria may lead to dehydration despite increased production of
ADH but is usually accompanied by acute thirst and increased water
intake.
• When blood volume is increased, stretch receptors in the atria of the
heart release atrial natriuretic hormone (ANP).
• This reduces reabsorption of sodium and water by the proximal
convoluted tubules and collecting ducts, meaning that more sodium
and water are excreted.
• In turn, this lowers blood volume and reduces atrial stretching, and
through the negative feedback mechanism ANP secretion is switched
off.
• Raised ANP levels also inhibit secretion of ADH and aldosterone,
further promoting loss of sodium and water.
Electrolyte balance
• Changes in the concentration of electrolytes in the body fluids may be
due to changes in:
• the body water content, or
• electrolyte levels.
• There are several mechanisms that maintain the balance between
water and electrolyte concentration.
Sodium and potassium balance
• Sodium is the most common cation (positively charged ion) in extracellular fluid and
potassium is the most common intracellular cation.
• Sodium is a constituent of almost all foods and salt is often added to food during
cooking.
• This means that intake is usually in excess of the body’s needs.
• It is excreted mainly in urine and sweat.
• The amount of sodium excreted in sweat is insignificant except when sweating is
excessive.
• This may occur when there is pyrexia (fever), a high environmental temperature or
during sustained physical exercise.
• Normally the renal mechanism described below maintains the concentration of
sodium and potassium within physiological limits.
Renin–angiotensin–aldosterone system
• Sodium is a normal constituent of urine and the amount excreted is
regulated by the hormone aldosterone, secreted by the adrenal cortex.
• Cells in the afferent arteriole of the nephron release the enzyme reninin
response to sympathetic stimulation, low blood volume or by low arterial
blood pressure.
• Renin converts the plasma protein angiotensinogen, produced by the liver,
to angiotensin 1.
• Angiotensin converting enzyme (ACE), formed in small quantities in the
lungs, proximal convoluted tubules and other tissues, converts angiotensin
1 into angiotensin 2, which is a very potent vasoconstrictor and increases
blood pressure.
• Renin and raised blood potassium levels also stimulate the adrenal
gland to secrete aldosterone.
• Water is reabsorbed with sodium and together they increase the
blood volume, leading to reduced renin secretion through the
negative feedback mechanism.
• When sodium reabsorption is increased potassium excretion is
increased, indirectly reducing intracellular potassium.
Calcium balance
• Regulation of calcium levels is achieved by coordinated secretion of
parathyroid hormone (PTH) and calcitonin.
• The distal collecting tubules reabsorb more calcium in response to
PTH secretion, and reabsorb less calcium in response to secretion of
calcitonin.
pH balance
• In order to maintain the normal blood pH (acid–base balance), the
cells of the proximal convoluted tubules secrete hydrogen ions.
• In the filtrate they combine with buffers:
• Bicarbonate, forming carbonic acid
• Ammonia, forming ammonium ions
• Hydrogen phosphate, forming dihydrogen phosphate
• Carbonic acid is converted to carbon dioxide (CO2) and water (H2O),
and the CO2 is reabsorbed, maintaining the buffering capacity of the
blood.
• Hydrogen ions are excreted in the urine as ammonium salts and
hydrogen phosphate.
• The normal pH of urine varies from 4.5 to 8 depending on diet, time
of day and a number of other factors.
• Individuals whose diet contains a large amount of animal proteins
tend to produce more acidic urine (lower pH) than vegetarians.
Micturition
• When 300 to 400 ml of urine have accumulated in the bladder,
afferent autonomic nerve fibres in the bladder wall sensitive to
stretch are stimulated.
• In the infant this initiates a spinal reflex and micturition occurs.
• Urine passed in the response to parasympathetic stimulation of the
bladder, causing contraction of the detrusor muscle and relaxation of
the internal urethral sphincter.
• Urine is expelled from the bladder and passes through the urethra
before leaving the body.
Reflex control of micturition when conscious
effort cannot override the reflex action
• When the nervous system is fully developed, the micturition reflex is
stimulated but sensory impulses also pass upwards to the brain and
there is awareness of the need to pass urine.
• By learned and conscious effort, contraction of the external urethral
sphincter and muscles of the pelvic floor can inhibit micturition until it
is convenient to empty the bladder
 Control of micturition after bladder control is
established
• In adults, urine is passed when the detrusor muscle contracts, and there
is reflex relaxation of the internal sphincter and voluntary relaxation of
the external sphincter.
• It can be assisted by increasing the pressure within the pelvic cavity,
achieved by lowering the diaphragm and contracting the abdominal
muscles (Valsalva’s manoeuvre).
• Overdistension of the bladder is extremely painful, and when this stage
is reached there is a tendency for involuntary relaxation of the external
sphincter to occur allowing a small amount of urine to escape, provided
there is no mechanical obstruction.
• Involuntary loss of urine is known as incontinence.
Common signs and symptoms of disorders of the urinary system
Diseases of the kidneys
• Glomerulonephritis (GN)
• This term suggests inflammatory conditions of the glomerulus, but
there are several types of GN and inflammatory changes are not always
present.
• In many cases immune complexes damage the glomeruli.
• These are formed when antigens and antibodies combine either within
the kidney or elsewhere in the body, and they circulate in the blood.
• When immune complexes lodge in the walls of the glomeruli they often
cause an inflammatory response that impairs glomerular function.
• Other immune mechanisms are also implicated in GN.
Effects of glomerulonephritis
• Haematuria
• Asymptomatic proteinuria
• Acute nephritis; This is characterised by the presence of:
• • oliguria (<400 ml urine/day in adults)
• • hypertension
• • haematuria
• • uraemia.
• Loin pain, headache and malaise are also common.
• Nephrotic syndrome
• Chronic renal failure
Nephrotic syndrome
• This is not a disease in itself but is an important feature of several
kidney diseases.
• The main characteristics are:
• marked proteinuria
• hypoalbuminaemia
• generalised oedema
• hyperlipidaemia.
• When glomeruli are damaged, the permeability of the glomerular membrane is
increased and plasma proteins pass through into the filtrate.
• Albumin is the main protein lost because it is the most common and is the smallest of
the plasma proteins.
• When the daily loss exceeds the rate of production by the liver there is a significant fall
in the total plasma protein level.
• The consequent low plasma osmotic pressure leads to widespread oedema and
reduced plasma volume.
• This reduces the renal blood flow and stimulates the renin–angiotensin–aldosterone
system, causing increased reabsorption of water and sodium from the renal tubules.
• The reabsorbed water further reduces the osmotic pressure, increasing the oedema.
Stages of development of nephrotic syndrome
• Nephrotic syndrome occurs in a number of diseases.
• In children the most common cause is minimal-change
glomerulonephritis.
• In adults it may complicate:
• most forms of glomerulonephritis
• diabetic nephropathy
• systemic lupus erythematosus
• infections, e.g. malaria, syphilis, hepatitis B
• drugs, e.g. penicillamine, gold, captopril, phenytoin.
Diabetic nephropathy
• Renal failure is the commonest cause of death in young people with diabetes mellitus and
is more common if hypertension and severe, long-standing hyperglycaemia are present.
• Diabetes causes damage to large and small blood vessels throughout the body, although
the effects vary considerably between individuals.
• In the kidney, these are known collectively as diabetic nephropathy or diabetic kidneyand
include:
• progressive damage of glomeruli, proteinuria and nephrotic syndrome
• ascending infection leading to acute pyelonephritis, sometimes complicated by renal
papillary necrosis
• atheroma of the renal arteries and their branches leading to renal ischaemia and
hypertension
• chronic renal failure.
Hypertension and the kidneys
• Hypertension can be the cause or the result of renal disease.
• Essential and secondary hypertension both affect the kidneys when
there is renal blood vessel damage, causing ischaemia.
• The reduced blood flow stimulates the renin–angiotensin–
aldosterone system, raising the blood pressure still further.
• Essential hypertension
• Benign hypertension
• Malignant hypertension
• Benign hypertension
• This causes gradual and progressive damage to the glomeruli, which may lead
to renal failure after the renal reserve has been lost or to malignant
hypertension.
• Malignant hypertension
• This causes arteriolosclerosis which spreads to the glomeruli with subsequent
destruction of nephrons, leading to a further rise in blood pressure and a
variable degree of renal impairment in most people.
• In a few people there are more serious effects; increased permeability of the
glomeruli allows escape of plasma proteins and red blood cells into the filtrate
causing proteinuria and haematuria, which may progress to renal failure.
• Secondary hypertension
• This is caused by long-standing kidney diseases and may lead to chronic renal
ischaemia, worsening hypertension and renal failure.
• Acute pyelonephritis
• This is acute bacterial infection of the renal pelvis and calyces, spreading to the
kidney substance causing formation of small abscesses.
• The infection may travel up the urinary tract from the perineum or be blood-borne.
• It is accompanied by fever, malaise and loin pain.
• Ascending infection
• Upward spread of microbes from the bladder is the most common cause of this
condition.
• Blood-borne infection
• The source of microbes may be from septicaemia or elsewhere in the
body, e.g. respiratory tract infections, infected wounds or abscesses.
• Due to their large blood flow (20% of cardiac output) the kidneys are
susceptible to infection by blood-borne microbes.
Renal failure
• Acute renal failure
• There is a sudden and severe reduction in the glomerular filtration rate
and kidney function that is often reversible over days or weeks if treated.
• There is oliguria or anuria accompanied by metabolic acidosis due to
retention of H+; electrolyte imbalance; accumulation of other mainly
nitrogenous waste products; and, if not associated with severe fluid loss,
retention of water, i.e. substances normally excreted in urine are
retained in the body.
• This occurs as a complication of a variety of conditions not necessarily
associated with the kidneys.
• The causes of acute renal failure are classified as:
• • prerenal: the result of reduced renal blood flow, especially as a
consequence of, e.g., severe and prolonged shock
• • renal: occurs due to damage to the kidney itself due to, e.g., acute
tubular necrosis, glomerulonephritis
• • postrenal: arises from obstruction to the outflow of urine, e.g.
disease of the prostate gland, tumour of the bladder, uterus or cervix,
large calculus (stone) in the renal pelvis.
Chronic renal failure
• This occurs when the renal reserve is lost and there is irreversible
damage to about 75% of nephrons.
• Onset is usually slow and asymptomatic, progressing over several years.
• The main causes are diabetes mellitus, glomerulonephritis and
hypertension.
• The effects on glomerular filtration rate (GFR), selective reabsorption and
tubular secretion are significant.
• GFR and filtrate volumes are greatly reduced, and reabsorption of water
is seriously impaired.
• This results in production of up to 10 litres of urine per day.
• Reduced glomerular filtration leads to accumulation of waste
substances in the blood, notably urea and creatinine.
• When renal failure becomes evident, blood urea levels are raised and
this is referred to as uraemia.
• Some of the signs and symptoms that may accompany this condition
include nausea, vomiting, gastrointestinal bleeding, anaemia and
pruritus (itching)
• Others are polyuria, acidosis, electrolyte imbalance, anemia,
hypertension etc
End-stage renal failure
• When death is likely without renal replacement therapy, such as
haemodialysis, peritoneal dialysis or a kidney transplant, the
condition is referred to as end-stage renal failure.
• The excretory functions of the kidneys are lost, acid–base balance
cannot be maintained and endocrine functions of the kidney are
disrupted.
• Towards the end of life anorexia, nausea and very deep (Kussmaul’s)
respirations occur as uraemia progresses.
• In the final stages there may be hiccoughs, itching, vomiting, muscle
twitching, seizures, drowsiness and coma.
Renal calculi
• Calculi (stones) form in the kidneys and bladder when urinary constituents
normally in solution are precipitated.
• The solutes involved are usually oxalates and phosphates.
• They are more common in males and after 30 years of age and the condition is
often recurrent.
• Most originate in the collecting tubules or renal papillae.
• They then pass into the renal pelvis where they may increase in size.
• Some become too large to pass through the ureter and may obstruct the
outflow of urine, causing kidney damage.
• Others pass to the bladder and are either excreted or increase in size and
obstruct the urethra
Predisposing factors to renal calculi include:
• Dehydration. This leads to increased reabsorption of water from the
tubules but does not change solute reabsorption, resulting in a reduced
volume of highly concentrated filtrate in the collecting tubules.
• pH of urine. When the normally acid filtrate becomes alkaline, some
substances may be precipitated, e.g. phosphates. This occurs when the
kidney buffering system is impaired and in some infections.
• Infection. Necrotic material and pus provide foci upon which solutes in
the filtrate may be deposited and the products of infection may alter the
pH of the urine. Infection sometimes leads to alkaline urine (see above).
• Metabolic conditions. These include hyperparathyroidism and gout.
Tumours of the kidney
• Benign tumours are relatively uncommon.
• Malignant tumours- These are most common in the bladder or kidney.
• Renal cell carcinoma
• Previously known as hypernephroma or Grawitz’s tumour, this tumour of tubular
epithelium is more common after 50 years of age, especially in males.
• Clinical features include haematuria, back or loin pain, anaemia, weight loss and
fever.
• Local spread involves the renal vein and leads to early blood spread of tumour
fragments, most commonly to the lungs and bones.
• The causes are unknown although there is an increased incidence in cigarette
smokers.
• Nephroblastoma (Wilms’ tumour)
• This is one of the most common malignant tumours in children under
10 years, usually occurring in the first 4 years.
• Clinical features include hamaturia, hypertension, abdominal pain
and, sometimes, intestinal obstruction.
• It is usually unilateral but rapidly becomes very large and invades the
renal blood vessels, causing early blood spread to the lungs.
Cystitis
• This is inflammation of the bladder and may be due to:
• upward spread of microbes that are commensals of the bowel from the perineum via
the urethra, especially in women
• trauma, with or without infection, following health-care interventions, e.g. radiotherapy,
insertion of a urinary catheter or instrument into the bladder.
• The effects are inflammation, with oedema and small haemorrhages of the mucosa,
which may be accompanied by haematuria.
• The sensory nerve endings in the bladder wall become hypersensitive and are
stimulated before the bladder has filled, leading to frequency of micturition and dysuria.
• The urine may appear cloudy and have an unpleasant smell. Lower abdominal pain
often accompanies cystitis. If untreated, upward spread may cause acute pyelonephritis
or septicaemia.
• Cystitis is uncomplicated when it occurs in otherwise healthy
individuals with a normal urinary tract.
• When it affects people with structural or functional abnormalities of
the urinary tract or those with pre-existing conditions, e.g. diabetes
mellitus or urinary outflow obstruction, it is described as complicated.
• Complicated UTIs sometimes cause permanent renal damage,
whereas this is very rare in uncomplicated infections.
• Recurrence is fairly common, especially in women, either when the
original infection is not eradicated or reinfection occurs.
Predisposing factors
• These include stasis of urine in the bladder and the shorter female urethra,
which is close to the anus, and the moist perineal conditions there that may
harbour commensal microbes.
• Sexual intercourse may cause trauma to the urethra and transfer of
microbes from the perineum, especially in the female.
• Hormones associated with pregnancy relax perineal muscle, and cause
relaxation and kinking of the ureters.
• Towards the end of pregnancy, pressure caused by the fetus may obstruct
the outflow of urine.
• In the male, prostatitis provides a focus of local infection or an enlarged
prostate gland may cause progressive urethral obstruction.
Urinary incontinence
• In this condition normal micturition is affected and there is involuntary loss of urine. Several
types are recognised.
• Stress incontinence
• This is leakage of urine when intra-abdominal pressure is raised, e.g. on coughing, laughing,
sneezing or lifting.
• It usually affects women when there is weakness of the pelvic floor muscles or pelvic
ligaments, e.g. after childbirth or as part of the ageing process.
• It occurs physiologically in young children before bladder control is achieved.
• Urge incontinence
• Leakage of urine follows a sudden and intense urge to void and there is inability to delay
passing urine.
• This may be due to a urinary tract infection, calculus, tumour or overactivity of the detrusor
muscle.
• Overflow incontinence
• This occurs when there is overfilling of the bladder and may be due to:
• retention of urine due to obstruction of urinary outflow, e.g. enlarged
prostate gland or urethral stricture, or
• a neurological abnormality affecting the nerves involved in micturition,
e.g. stroke, spinal cord injury or multiple sclerosis.
• The bladder becomes distended and when the pressure inside overcomes
the resistance of the external urethral sphincter, urine dribbles from the
urethra.
• The individual may be unable to initiate and/or maintain micturition.
The Nephron
• The nephron consists of a tubule closed at one end, the other end opening into a
collecting tubule.
• The closed end which is indented to form the cup-shaped glomerular
capsule (Bowman’s capsule), which are made of tiny arterial capillaries,
the glomerulus.
• Continuing from the glomerular capsule, the remainder of the nephron is about 3
cm long and is described in three parts:
• the proximal convoluted tubule
• the medullary loop (loop of Henle)
• the distal convoluted tubule, leading into a collecting duct.
• The collecting ducts unite, forming larger ducts that empty into the minor calyces.