DISTAL CONVULATED

TUBULE,LOOP OF HNLE
and Collecting Duct.
 Objectives

Definition of DCT and Collecting Duct

Function of early and late DCT

ADH production and functions

Discuss countercurrent mechanisms.

Formation of urine.

Diuretics

Applied physiology
 Definition of DCT

 It’s a short nephron segment, interposed between the macula densa and
collecting duct.

 Located at the kidney’s cortex, about 5 mm long , made up of typical

absorptive epithelial cells

 It passes close to the afferent and efferent arterioles of the same nephron

 this segment of the renal tubule is lined with simple cuboidal Epithelium
 DCT cont,

It’s called the DCT because it is the segment farthest away in relation
to renal corpuscle.

Renin is secreted by myoepithelioid juxtaglomerular cells in the walls

of the afferent arterioles

Macula densa have a special function in relation to the control of

renin secretion
 Definition cont,

DCT cells are rich in mitochondria, and possess the highest density of Na+/K+-
ATPase along the nephron,

 DCT cells are largely water impermeable, and reabsorb sodium and chloride
across the apical membrane via electroneurtral pathways.

DCT does not act as a mass transporter of magnesium as the ascending loop

It’s the site for many complex influences to determine the final magnesium
excretion

reabsorbs approximately 10% to 15% of the filtered magnesium.

 Early Distal Convoluted Tubule

The role of the early DCT is to actively reabsorbs sodium chloride and calcium.

Mvt of ions depends on Na+/K+ ATPase transporter on the basolateral

membrane of the cells.

 This excretes NA + into the ECF, and brings K+ into the cell

creating a gradient that moves NA into the cell via other channels.
This process is primary active transport, as ATP is directly needed to
set up the gradient.
 Early Distal Convoluted Tubule

it secretes ammonium ions and hydrogen ions.

Regulates the pH of urine by secreting protons and absorbing HCO3-

It forms parts of juxtaglomerular apparatus.

it is relatively impermeable to H20, but in the present of ADH its

permeability to water increases making urine concentrated.
 Definition of collecting duct

The CD runs through the cortex into the medulla and opens into the
renal papilla.

Therefore divided into cortical and medullary portion

 Its Epithelium varies from cuboidal to columnar Epithelium (near the

papilla)

 It is the final segment of the renal tubule.

 Late Distal Convoluted Tubule and Collecting
Duct
There are two types of cells in the region

Principal cells

make up the majority of the tubular cells. They are mainly involved in:

Reabsorbs sodium and water

secretes potassium

Under the control of Aldosterone hormone.

 Late Distal Convoluted Tubule and Collecting
Duct cont,
Intercalated cells

This exchange is again driven by a Na+/K+ ATPase on the basolateral membrane,.

which sets up a gradient for sodium to enter the cell through the ENaC channel.

play a role in acid-base control, by controlling the levels of hydrogen (H+)

and bicarbonate ions (HCO­3–).

These are both produced through the reaction of CO2 (produced from
metabolic processes within the cell) with H2O, by the action of CA enzyme.
Late Distal Convoluted Tubule and Collecting Duct
cont,

The HCO3- cross the basolateral membrane into the ECF through the
anion exchanger channel, for chloride exchange.

H+ are secreted into the lumen via a K+/H+ ATPase antiporter and H+-
ATPase.

 Once inside, H+ ions react with either phosphate (HPO42-) or

ammonia (NH3).
 Late Distal Convoluted Tubule and
Collecting Duct cont,
This prevents the ions from re-entering the cell, as both new compounds
(NH4+ and H2PO4–) are charged.

Hence they are not able to travel back across the membrane, and so are
excreted.

To prevent an accumulation of CL- and K+ within the cell, a K+/Cl– symporter
on the basolateral membrane allows leakage of these ions back into the
extracellular fluid.
 ADH production and transport

ADH is produced in the hypothalamus

stored in the posterior pituitary gland until it is released.

ADH acts on the kidney tubules to increase the number of aquaporin 2 channels
(water channels) in the apical membrane of the tubular cells in the collecting
duct.
 ADH production cont,
ADH binds to V2 r eceptors on the tubule cells, which activate
adenylyl cyclase hence increasing production of c AMP

Subsequently, vesicles containing the aquaporin 2 channels deposit

their contents into the apical membrane of the tubular cells

(the basolateral membrane always contains aquaporin 3 and 4

channels, so is always permeable)
AQUAPORINS
 ADH prod,
It increases the permeability of the cell, thus reabsorb more water
from the filtrate and

Vasopressin makes water moves from hypotonic to cortical collecting

ducts into the interstitium

This makes tubular isotonic leading to 10% of water removal

Isotonic to medullary CD with a Tubule fluid to plasma TF/P inulin of

20
 Functions of collecting duct

Osmolarity of urine is 1200m0sm/kg of H20

When vasopressin is absent, the CD is impermeable to H20

Fluid remains hypotonic and large amounts flow to renal pelvis

Human osmolality can be low as 30 m0sm/kg of H20

2% OF H2O is reabsorbed in absence of vasopressin

However 13% maybe excreted and urine flow reaches 15mls/min or more
COUNTERCURRENT
MECHANISM
 Counter current mechanism

Osmolarity is the number of solute dissolved in 1kg of water and this

reflects the solution’s ability to cause osmosis.

10 sodium ions have the same osmotic activity as10 glucose
molecules or 10 amino acids in the same volume of water.

 The milliosmol (mOsm)- equal to 0.001 osmol, is used as a measure

of osmolarity in terms of mOsm/kg.
 Counter current mechanism

One crucial renal function is to keep the solute load of body fluids
constant at about 300 mOsm,- the osmotic concentration of blood
plasma, by regulating urine concentration and volume.

The kidneys accomplish this feature using countercurrent

mechanisms. Countercurrent means that fluid flows through
adjacent tubes in opposite directions.
 Counter current mechanism

The interaction between the flow of filtrate through the ascending

and descending limbs of the long loops of Henle of juxtamedullary
nephrons (the countercurrent multiplier).

The flow of blood through the ascending and descending portions of

the vasa recta blood vessels (the countercurrent exchanger).
 Counter current mechanism

The countercurrent mechanisms establish and maintain an osmotic

gradient extending from the cortex through the depths of the medulla

This allows the kidneys to vary urine concentration dramatically.

The osmolality of the filtrate entering the PCT is identical to that of

plasma, about 300 mOsm.
 Counter current mechanism
The reabsorption of water and solutes in the PCT lead to an isotonic
filtrate with plasma by the time the descending limb of the loop of Henle
is reached.

 However, its osmolality increases from 300 to about 1200 mOsm in the
deepest part of the medulla.

The increase of concentration lies with the unique workings of the long
loops of Henle of the juxtamedullary nephrons, and the vasa recta.
 Countercurrent multiplier

The countercurrent multiplier functions because of three factors;

1. The descending limb of the loop of Henle is relatively impermeable

to solutes and freely permeable to water.

The osmolality of the medullary interstitial fluid increases all along

the descending limb and water passes osmotically out of the filtrate
all along this course.
 Countercurrent multiplier cont,

The filtrate osmolality reaches its highest point (1200 mOsm) at the
bend of the loop.

2.The ascending limb is permeable to solutes, but not to water.

As the filtrate rounds the bend into the ascending limb, the tubule
permeability changes, becoming impermeable to water and
selectively permeable to salt.
 Countercurrent multiplier cont,

The Na+ and Cl– concentration in the filtrate entering the ascending
limb is very high (and interstitial fluid concentrations of these two
ions are lower).

Na+ and Cl– reabsorption in the ascending limb is both passive (mostly
in the thin segment) and active (via the Na+-K+-2Cl– cotransporter in
the thick segment).
 Countercurrent multiplier cont,

As Na+ and Cl– are extruded from the filtrate into the medullary
interstitial fluid, they contribute to the high osmolality there.

Due to loss of salt but not water, the filtrate in the ascending limb
becomes increasingly dilute until, at 100 mOsm at the DCT, it is hypo-
osmotic, to blood plasma and cortical interstitial fluids.
 Countercurrent multiplier cont,

There is a constant difference in filtrate concentration (200 mOsm)

between the two limbs of the loop of Henle, and between the
ascending limb and the interstitial fluid.

This 200-mOsm gradient by itself would not be enough to allow

excretion of very concentrated urine.
 Countercurrent multiplier cont,
Due to countercurrent flow, the loop of Henle is able to “multiply”
the small changes in solute concentration into a gradient change
along the vertical length of the loop (both inside and outside) that is
closer to 900 mOsm (1200 mOsm – 300 mOsm).

The two limbs of the loop of henle are close enough to influence each
other’s exchanges with the interstitial fluid they share.
 Countercurrent multiplier cont,

Hence, water diffusing out of the descending limb produces the

increasingly “salty” filtrate that the ascending limb uses to raise the
osmolality of the medullary interstitial fluid.

The more NaCl the ascending limb extrudes, the more water diffuses
out of the descending limb and the saltier the filtrate in the
descending limb becomes.
 Countercurrent multiplier cont,

This establishes a positive feedback mechanism that produces the

high osmolality of the fluids in the descending limb and the interstitial
fluid.

Urea recycling contributes to the medullary osmotic pressure.

In the thin limbs of the loop of Henle, urea enters the filtrate by
facilitated diffusion.
 Countercurrent multiplier cont,

As the filtrate moves on, water is reabsorbed but urea is left behind
because the tubule between Henle’s thin limb and the collecting duct is not
permeable to urea.

When filtrate reaches the collecting duct in the deep medullary region,
urea, now highly concentrated, is transported by facilitated diffusion out of
the tubule into the interstitial fluid of the medulla, forming a pool of urea
that recycles back into the thin limb of the loop of Henle.
 Countercurrent multiplier cont,

This pool of urea contributes substantially to the high osmolality in the

medulla.

 Antidiuretic hormone (ADH), which stimulates excretion of highly

concentrated urine, enhances urea transport in the medullary collecting
duct.

When ADH is present, urea recycling is enhanced, the medullary osmotic

gradient is enhanced, and more concentrated urine can be formed.
 Countercurrent Exchanger

The vasa recta function as countercurrent exchangers, maintaining

the osmotic gradient established by the cycling of salt while delivering
blood to cells in the area.

They receive only about 10% of the renal blood supply hence blood
flow through the vasa recta is sluggish.
 Countercurrent Exchanger cont,

They are freely permeable to water and NaCl, allowing blood to make
passive exchanges with the surrounding interstitial fluid and achieve
equilibrium.

 As the blood flows into the medullary depths, it loses water and
gains salt ( hypertonic). Then, as it emerges from the medulla into the
cortex, the process is reversed: It picks up water and loses salt.
 Countercurrent Exchanger cont,

Since blood leaving and reentering the cortex via the vasa recta has
the same solute concentration, the vessels of the vasa recta act as
countercurrent exchangers.

This system does not create the medullary gradient, but it protects it
by preventing rapid removal of salt from the medullary interstitial
space, and by removing reabsorbed water.
 Formation of dilute urine
The tubular filtrate is diluted as it travels through the ascending limb of the
loop of Henle and all the kidney needs to do, to secrete dilute (hypo-osmotic)
urine is to allow the filtrate to continue on its way into the renal pelvis.

This is achieved by inhibiting the release of ADH by the posterior pituitary

gland.

The osmolality of urine can plunge as low as 70 mOsm, about one-fourth the
concentration of glomerular filtrate or blood plasma.
 Formation of dilute urine cont,

The collecting ducts remain essentially impermeable to water due to

the absence of aquaporins in their luminal cell membranes, and no
further water reabsorption occurs.

 Na+ and selected other ions can also be removed from the filtrate by
DCT and collecting duct cells so that urine becomes even more dilute
before entering the renal pelvis.
 Formation of concentrated urine

ADH inhibits diuresis or urine output.

 It accomplishes this via a 2nd -messenger system using cyclic AMP

that causes insertion of aquaporins into the luminal membrane of the
principal cells of the collecting ducts.

Consequently water passes easily into and through the cells into the
interstitial space, and the osmolality of the filtrate becomes equal to
that of the interstitial fluid.
 Formation of concentrated urine cont,

In the distal tubules, the filtrate osmolality is approximately 100 mOsm,
but as the filtrate flows through the collecting ducts and is subjected to
the hyperosmolar conditions in the medulla, water, followed by urea,
rapidly leaves the filtrate.

Depending on the amount of ADH released (which is keyed to the level of

body hydration), urine concentration may rise as high as 1200 mOsm,-----
the concentration of interstitial fluid in the deepest part of the medulla.
 Formation of concentrated urine cont,

With maximal ADH secretion, up to 99% of the water in the filtrate is

reabsorbed and returned to the blood, and half a liter per day of
highly concentrated urine is excreted.

The ability of our kidneys to produce such concentrated urine help us

to survive without water.Water reabsorption that depends on the
presence of ADH is called facultative water reabsorption.
 Formation of concentrated urine cont,

ADH is released more or less continuously unless the blood solute

concentration drops too low.

• Release of ADH is enhanced by any event that raises plasma

osmolality above 300 mOsm such as sweating or diarrhea, or greatly
reduced blood volume or blood pressure.

• The kidneys’ ability to respond to this signal depends on the high

medullary osmotic gradient.
 Diuretics

There are several types of diuretics chemicals that enhance urinary

output.

An osmotic diuretic is a substance that is not reabsorbed and that

carries water out with it (for example, the high blood glucose levels of
a diabetes mellitus patient).

Alcohol, essentially a sedative, encourages diuresis by inhibiting

release of ADH.
 Diuretics cont,

 Other diuretics increase urine flow by inhibiting Na+ reabsorption

and the obligatory water reabsorption that normally follows.

Examples include caffeine (found in coffee, tea, and colas) and many
drugs prescribed for hypertension or the edema of congestive heart
failure.

 Common diuretics inhibit Na+-associated symporters.

 Diuretics cont,

Loop diuretics like furosemide (Lasix) are powerful because they

inhibit formation of the medullary gradient by acting at the ascending
limb of Henle’s loop.

Thiazides like hydrochlorothiazide are less potent and act at the DCT
 Physiological application

Uremia develops when the breakdown of protein metabolism accumulate

in blood

Acidosis is common in CKD due to failure to excrete the acid products of

digestion and metabolism

Abnormal Na+ handling patients with kidney disease retain excessive

amounts of NA+ and become oedematous.

Proteinuria increased permeability of the glomerular capillaries leads to

albumin traced in urine.
MICTURITION
 Objectives

To understand

Definition of micturition

Anatomy and physiology of the bladder

The Innervation of the bladder

Physiology of micturition

Applied physiology
 Definition of micturition

The process by which the urinary bladder empties when it becomes filled

Also known as urination or voiding.

KNOW:
Micturition center of brain: pons
(but heavily influenced by higher centers)
Parasympathetic: to void
Sympathetic: inhibits micturition
Anatomy of the urinary system
 Physiological Anatomy of Urinary System
Kidneys (cortex, medulla, nephron, pelvis )

 Ureters (mucosa, muscle, fibrous) - Conveys urine from kidneys to the bladder

 Urinary Bladder (body, neck), ( mucosa, muscle, fibrous) (detrusor, trigone)

• Stores urine at low pressure.
• Compresses urine for voiding

 Urethra - conveys urine from bladder to outside world

Internal and External sphincters

 Physiologic Anatomy

The urinary bladder is a smooth muscle chamber composed of two main

parts:

The body which is the major part of the bladder in which urine collects

The smooth muscle of the bladder is called the detrusor muscle -

contraction of the detrusor muscle is a major step in emptying the bladder

• Transitional epithelium - Allows expansion of bladder without significant

rise in intravesical pressure
 Anatomy of the bladder
The neck which is a funnel-shaped extension of the body, passing
inferiorly and anteriorly into the urogenital triangle and connecting
with the urethra.

It’s wall is composed of detrusor muscle interlaced with a large

amount of elastic tissue.

 Internal sphincters is made up of smooth muscle.

 External sphincters made up of skeletal muscle.

 Anatomy of the bladder

• Smooth muscle cells of the detrusor muscle fuse with one another so
that low-resistance electrical pathways exist from one muscle cell to
the other.

• Therefore, an action potential can spread throughout the detrusor

muscle, from one muscle cell to the next, to cause contraction of the
entire bladder at once.
Anatomy of urinary bladder
 Innervation of the Bladder

The principal nerve supply is by Parasympathetic nerves transmitted

through pelvic nerve which connect mainly with the S-2 and S-3
segments of the spinal cord

Coursing through the pelvic nerves are both sensory nerve fibers and
motor nerve fibers.
i. Sensory – detect the degree of stretch in the bladder wall
ii. Motor - Contract bladder & inhibit internal sphincter
 Innervation of the Bladder

The motor nerves transmitted in the pelvic nerves are parasympathetic

fibers.

 These terminate on ganglion cells located in the wall of the bladder.

Short postganglionic nerves then innervate the detrusor muscle

 skeletal motor fibers transmitted through the pudendal nerve to the

external bladder sphincter –

It’s somatic nerve fibers that innervate and control the voluntary skeletal
muscle of the sphincter.
 Innervation of the Bladder

The bladder receives sympathetic innervation from the sympathetic

chain through the hypogastric nerves

connecting mainly with the L-2 segment of the spinal cord.

These sympathetic fibers stimulate mainly the blood vessels - sensory

nerve fibers also pass by way of the sympathetic nerves and
important in the sensation of fullness and pain
Innervation of the bladder
 Transport of Urine

Urine flowing from the collecting ducts into the renal calyces
stretches the calyces and increases their intrinsic pacemaker activity,

This initiates peristaltic contractions that spread to the renal pelvis

and then downward along the length of the ureter thereby forcing
urine from the renal pelvis toward the bladder
 Transport of Urine

The walls of the ureters contain smooth muscle and are innervated by both
sympathetic and parasympathetic nerves

Note Peristaltic contractions in the ureter are enhanced by PSN stimulation

and inhibited by SN stimulation

The ureters enter the bladder through the detrusor muscle in the trigone
region, obliquely for several centimeters.

The normal tone of the detrusor muscle in the bladder wall have a tendency
to compress the ureter.
 Transport of Urine

This prevents backflow of urine from the bladder, when pressure

builds up in the bladder during micturition or bladder compression.

Each peristaltic wave increases the pressure within the ureter so that
the region passing through the bladder wall opens and allows urine to
flow into the bladder

Peristaltic waves occur 1-5 times/minute.

 The Cystometrogram

A test done to assess how the bladder and sphincter behave while you
store urine and pass urine.

It shows the approximate changes in intravesicular pressure as the

bladder fills with urine

Empty bladder……Pressure is zero

30-50 ml urine……Pressure is 5-10 cm

 The Cystometrogram cont,

50 – 300 ml urine…. Pressure is 5-10 cm.

this constant level of pressure is caused by intrinsic tone of the

bladder wall.

300 to 400 ml urine…..rapid rise in Pressure as the micturition reflex

is triggered
Normal Cystometrogram
 Micturition
This involves two main steps:

 First, the bladder fills progressively until the tension in its walls rises above a
threshold level

 second step, which is a nervous reflex called the micturition reflex that empties
the bladder or, if this fails, at least causes a conscious desire to urinate.

• Although the micturition reflex is an autonomic spinal cord reflex

• it can also be inhibited or facilitated by centers in the cerebral cortex or brain

stem.
 Micturition reflex cont,
As the bladder fills, many micturition contractions begin to appear.

They are the result of a stretch reflex initiated by sensory stretch receptors in the
bladder wall.

Especially the receptors in the posterior urethra when this area begins to fill with
urine.

Sensory signals from the bladder stretch receptors are conducted to the sacral
segments of the cord through the pelvic nerves
 Micturition reflex cont,
And then reflexively back again to the bladder through the
parasympathetic nerve fibers by way of these same nerves

When the bladder is only partially filled:

 Micturition contractions usually relax spontaneously after a fraction

of a minute.

The detrusor muscles stop contracting.

And pressure falls back to the baseline

 Micturition reflex cont,
As the bladder continues to fill, the micturition reflexes become more

frequent and cause greater contractions of the detrusor muscle.

Once a micturition reflex begins, it is self-regenerative.

This initial contraction of the bladder, activates the stretch receptors

to cause a greater increases in sensory impulses to the bladder and

posterior urethra, which causes a further increase in reflex

contraction of the bladder.

 Micturition
Therefore the cycle is repeated again and again until the bladder has
reached a strong degree of contraction

After a few seconds to more than a minute, the self- regenerative

reflex begins to fatigue and the regenerative cycle of the micturition
reflex stops, permitting the bladder to relax.
The micturition reflex is a single complete cycle of,
a. progressive and rapid increase of pressure.
b. a period of sustained pressure.
c. and return of the pressure to the basal tone of the bladder
 Micturition reflex cont,

Once a micturition reflex has occurred but has not succeeded in

emptying the bladder, the nervous elements of this reflex usually
remain in an inhibited state for a few minutes to 1 hour or more
before another micturition reflex occurs.

 As the bladder becomes more and more filled, micturition reflexes

occur more and more often and more and more powerfully.
 Micturition reflex cont,

Once the micturition reflex becomes powerful enough, it causes another

reflex, which passes through the pudendal nerves to the external urethra

sphincter to inhibit it.

If this inhibition is more potent in the brain than the voluntary constrictor

signals to the external sphincter, urination will occur.

 If not, urination will not occur until the bladder fills still further and the

micturition reflex becomes more powerful.

 Role of the Brain
The micturition reflex is a completely autonomic spinal cord reflex,
but it can be inhibited or facilitated by centers in the brain.

These centers include:

a. strong facilitative and inhibitory centers in the brain stem, located

mainly in the pons, and

b. several centers located in the cerebral cortex that are mainly

inhibitory but can become excitatory.
 Role of the Brain

The micturition reflex is the basic cause of micturition, but the higher
centers normally exert final control of micturition

The higher centers keep the micturition reflex partially inhibited,

except when micturition is desired.
 Role of the Brain
The higher centers can prevent micturition, even if the micturition

reflex occurs, by continual tonic contraction of the external bladder

sphincter until a convenient time presents itself.

When it is time to urinate, the cortical centers can facilitate the sacral

micturition centers to help initiate a micturition reflex

• And at the same time inhibit the external urinary sphincter so that

urination can occur.

 Voluntary urination

Is usually initiated in the following way:

First, a person voluntarily contracts his or her abdominal muscles,

which increases the pressure in the bladder

This allows extra urine to enter the bladder neck and posterior
urethra under pressure, thus stretching their walls.
 Voluntary urination

This stimulates the stretch receptors, which excites the micturition

reflex and simultaneously inhibits the external urethral sphincter.

Ordinarily, all the urine will be emptied, with rarely more than 5 to 10
milliliters left in the bladder
 The applied physiology
Abnormalities of micturition

1. Atonic bladder

2. Automatic bladder

3. The uninhibited neurogenic bladder

4. Urinary incontinence
 Atonic bladder
Due to the destruction of sensory nerve fibers from urinary bladder –
Syphilis.

 Due to the absence of sensory impulses, the detrusor muscle loses

the tone and becomes flaccid. No contraction of muscle

 It is also called overflow dribbling / overflow incontinences / Tabetic

bladder
 Automatic bladder

It’s Caused by Spinal Cord Damage Above the Sacral Region.

If the sacral cord segments are still intact, typical micturition reflexes
can still occur but they are no longer controlled by the brain.

First micturition reflexes are suppressed because of the state of

“spinal shock”
 Automatic bladder cont,

If the bladder is emptied periodically by catheterization to prevent

bladder injury caused by overstretching of the bladder, the excitability of
the micturition reflex gradually increases - then, periodic automatic
bladder emptying occurs.

Some patients can still control urination in this condition by stimulating

the skin (scratching or tickling) in the genital region, which sometimes
elicits a micturition reflex.
 The uninhibited neurogenic bladder

Caused by partial damage in the spinal cord or the brain stem that
interrupts most of the inhibitory signals.

Results in frequent and relatively uncontrolled micturition.

Therefore, facilitative impulses passing continually down the cord keep

the sacral centers so excitable that even a small quantity of urine elicits an
uncontrollable micturition reflex, thereby promoting frequent urination.
 Nocturnal Micturition

• Enuresis or bed wetting.

• Common in infants and children below 3 years

• It is because of the underdevelopment of voluntary control of micturition

which is due to incomplete myelination of motor nerve fibers of the bladder.

• On completion of myelination, voluntary control of micturition develops and

enuresis stops in these children.
 Urinary incontinence
Also known as involuntary urination.

Is any Involuntary leakage of Urine.

Types of urinary incontinence:

1. Urge incontinence

2. Stress incontinence

3. Overflow incontinence

4. Functional incontinence
 Urge incontinence
• It is due to an overactive bladder

• Is a condition where there is a frequent feeling of needing to urinate.

• May occur during the day, at night, or both

• The cause is unknown & amount of urine passed during each

urination is relatively small.

• Risk factors include obesity, caffeine, and constipation

• Poorly controlled diabetes may worsen the symptoms.

 Stress incontinence
The urethra is supported by fascia of the pelvic floor.

When you exercise, laugh, sneeze, or cough the pelvic floor fascia
stretches and weakness .

 Then pressure on your bladder increases and the urethra moves

downwards allowing urine to pass.

Pregnancy and childbirth can stretch and weaken a woman’s pelvic floor
muscles.

Being overweight or obese

 Overflow incontinence

It is the absence of any urge to urinate

Characterized by the involuntary release of urine from an overfull

urinary bladder.

Occurs in people who have a blockage of the bladder outlet e.g.

prostate cancer.
 Functional incontinence
This is when a person is usually aware of the need to urinate, but
unable to get to a bathroom

Can be small leakages to full emptying of the bladder.

Causes can be physical or mental reasons

E.g. confusion, dementia, poor eyesight, impaired mobility or

unwillingness to use the toilet due to depression or anxiety
 Ureterorenal reflex

Ureter is blocked e.g. by a ureteral stone, there will be intense reflex

constriction which is associated with very severe pain.

These pain impulses cause a sympathetic reflex back to the kidney to

constrict the renal arterioles, thereby decreasing urinary output from
that kidney.

Urinary retention Urinary retention Urinary retention, also known as

ischuria, is a lack of ability to urinate.
 References

1. Text book of Medical Physiology 14th Edition Guyton & Hall

2. David Makanjuola, Marta Lapsley, in
Clinical Biochemistry: Metabolic and Clinical Aspects (Third Edition),
2014
3. Vander Human Physiology 8th Edition
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