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1. What is the volume of daily gastric secretion? And what
is its content?
2. What are the classes of medications that are used to
treat peptic ulcers and what are their mechanisms of
action?
3. e patient undrgoes emergency laparotomy, and a
large friable perforated duodenal ulcer is found that
could not be closed with a patch. e surgeon decides
to perform distal gastrectomy with Roux-en-Y gastrojejunostomy. What are the potential complications of
gastrectomy?
4. Why does dumping syndrome develop?
OSCE Scenario 10.5
A 65-year-old female patient with background of smoking
and hypertension presents with chronic postprandial pain
(sitophobia), weight loss and loose stools. She is found to
be cachexic due to food fear and admission is for urgent
investigations and addressing nutritional problems with
total parenteral nutrition (TPN).
1. A CT abdomen is arranged (Fig. 10.5Q). What is the
main nding on this CT scan? What is the diagnosis?
2. What are the pros and cons of enteral and parenteral
feeding?
3. How would you treat this condition?
CHAPTER 10 Gastrointestinal System
Fig. 10.5Q CT angiogram of abdominal aorta.
231
4. Five days aer her admission, the patient is found to
have low levels of K, Mg and PO4. What is this condition called? And why does it develop?
Answers in Appendix pages 451–454
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
11
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Urinary System
COMPONENTS
e urinary system is composed of:
• kidneys
• ureters
• bladder
• urethra.
Functions
e functions of the urinary system include:
• maintenance of electrolyte balance
• maintenance of uid balance
• maintenance of acid–base balance
• storage and excretion of urine
• hormone production: renin, erythropoietin, 1,25-di hydrocholecalciferol.
Structure
• See Chapter 2 for further anatomical detail of the kid-
neys, ureter, bladder and urethra.
• Macroscopically the kidney can be divided into:
• outer region: cortex
• inner region: medulla, pelvis.
• Medulla is divided into several pyramids that project
into the pelvis.
• e renal pyramids divide the renal pelvis into two to
three areas known as the major calyces.
• e functioning portion of the kidney is the nephron;
each nephron consists of a glomerulus; this consists of
a collection of capillaries that are connected to aerent
(a = arrive) and eerent (e = exit) arterioles.
• Each glomerulus is surrounded by epithelium, which
forms Bowman’s space.
• e glomerulus is the site of plasma ltration.
• From Bowman’s space the ltrate passes in turn through
the proximal convoluted tubules, loop of Henle, distal
convoluted tubule and the collecting duct. e resulting
urine passes through the papilla in the renal pyramids
into the renal pelvis.
RENAL BLOOD SUPPLY
Renal Circulation
• Renal artery enters the hilum → branches to form interlobar arteries, which ascend between the pyramids →
interlobar arteries branch to form arcuate arteries →
arcuate arteries branch to form interlobular arteries →
aerent arteries arise from the interlobular arteries.
• Aerent arterioles give rise to glomerular capillaries
within Bowman's capsule → leave the glomerulus as the
eerent arterioles.
• Eerent arterioles have two distinct courses:
• supply of capillaries to the renal tubules → peri-
tubular capillaries
• descending vessels called the vasa recta; these pro-
vide the blood supply to the medulla; the ascending
vasa recta drain into the arcuate veins → interlobar
vein → renal vein.
Regulation of Renal Blood Flow
• Total renal blood ow (RBF) is approximately 1.25 L/
min or 25% of the cardiac output.
• Renal blood ow is maintained by intrinsic mechanisms; it shows very little variation over a range of arterial pressures; this is termed autoregulation.
• Autoregulation fails at systolic blood pressures <80 mmHg.
• e mechanisms underlying autoregulation of renal
blood ow can be divided into:
• myogenic: ↑ in pressure due to ↑ in ow causes dis-
tension of the vessels; this elicits smooth muscle
contraction and thus ↑ vascular resistance and thus
↓ blood ow
• metabolic: metabolites from active renal tissue
induce vasodilatation.
• Renal blood ow can also be inuenced by:
• humoral factors
• prostaglandins (vasodilatation)
• nitric oxide (vasodilatation)
• adrenaline (vasoconstriction)
232
CHAPTER 11 Urinary System
To proximal
233
Bowman's
space
Podocyte
Foot
Glomerular
capillary
P
Fenestrated
endothelium
Fig. 11.1 Microscopic structure of the glomerulus.
P = hydrostatic pressure, π = osmotic pressure.
(From McGeown JG. Physiology, 2nd edn. Churchill
Livingstone, Edinburgh, 2002, with permission.)
p
processes
or pedicels
convoluted
tubule
Basement
membrane
• noradrenaline (vasoconstriction)
• angiotensin I (vasoconstriction)
• angiotensin II (vasoconstriction).
• Renal nerves:
• sympathetic (vasoconstriction)
• parasympathetic (vasodilatation).
Glomerulus (Fig. 11.1)
Microscopic Structure
• e endothelium and the epithelium of Bowman’s capsule have several features which allow them to perform
the role of ltration:
• the capillary endothelium is perforated by small
pores; it is referred to as a fenestrated capillary; it
permits the free passage of water and electrolytes
• negative charge of glycoproteins in the basement
membrane results in greater permeability to positively or neutrally charged molecules than negatively
charged molecules
• the epithelium of Bowman’s capsule contains special-
ized cells called podocytes. ese cells do not form a
continuous layer, and instead they are spread over the
basement membrane and pass out processes known
as pedicels or ‘foot processes’. is leaves gaps, which
allow ltration to occur.
• In addition, the numerous glomeruli throughout the
kidney produce a large surface area to allow ltration.
• e fenestrated nature of the endothelium and the gaps
between podocyte processes produce low resistance to
uid movement.
Glomerular Filtration
• e glomerulus is the initial site of urine formation.
• As a result of the factors mentioned above, the kidneys
show a high rate of ltration: 120 mL/min.
• e forces governing ltration are identical to ltration
forces in peripheral capillaries:
• hydrostatic pressure
• osmotic pressure.
• Hydrostatic pressure is higher than in normal capillaries; approximately 50 mmHg; this is generated by the
high resistance to outow caused by the eerent arteriole. Pressure within Bowman’s capsule is approximately 10 mmHg; this leaves a hydrostatic pressure of
40 mmHg.
• Plasma proteins generate osmotic pressure; they are not
ltered and therefore produce an opposing absorption
pressure to the hydrostatic pressure. Osmotic pressure
is about 25 mmHg; therefore, the net ltration pressure
is around 15 mmHg.
• As ltration proceeds, the remaining plasma proteins
exert a greater osmotic pressure until it equals that of
the ltration pressure and thus no further removal of
uid occurs.
• e uid that is ltered by the glomerulus is identical
to plasma, apart from the lack of plasma proteins and
blood cells; it is oen referred to as an ultraltrate.
• e osmolality of the ultraltrate is around 300mosmol/L.
Proximal Convoluted Tubule
• e proximal convoluted tubule absorbs 70% of the
ltered sodium; chloride follows by electrostatic attraction; water follows the absorption of NaCl as a result of
the osmotic gradient.
• e volume of the ultraltrate is decreased but as
the NaCl solution is isosmotic with the plasma, the
osmolality of the ltrate reaching the loop of Henle is
unchanged.
• e transport of Na+ is an energy dependent process; it
relies on an ATP-dependent pump.
• e proximal tubular cells are particularly vulnerable to
ischaemic damage as a result of the energy requirements.
Loop of Henle
• e descending loop of Henle is permeable to NaCl
and water. Due to the high osmolality of the surrounding medulla, water is removed from the ultraltrate and
NaCl is added as ions move down the concentration
gradient between the medulla and the ultraltrate.
234
From PCT To DCT
Flow of fluid
Medulla
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SECTION II Physiology
• e ultraltrate in the descending loop of Henle is
concentrated by the passive addition of NaCl from the
medulla and the reduction in volume due to the absorption of water.
• e ascending loop of Henle is responsible for the
active reabsorption of Na+ (which again leads to passive
Cl− absorption). However, this region is impermeable
to water; the transport of NaCl leads to a decrease in
the osmolality of the ultraltrate but an increase in the
osmolality of the surrounding medullary parenchyma.
• e osmolality of the ultraltrate entering the loop
of Henle is approximately 300mosmol/L. As uid is
removed and ions added in the descending loop, the
osmolality increases to around 1200mosmol/L at the
bottom. As the uid enters the ascending limb, ions
are removed but water remains, as this area is impermeable to water. e osmolality is decreased as ions are
removed; the concentration of the ultraltrate entering
the convoluted tubule is about 100mosmol/L.
Countercurrent Multiplier Mechanism (Fig. 11.2)
• e changes in osmolality of the ultraltrate as it moves
through the loop of Henle produce very high ion concentration within the medulla, providing the necessary
osmotic pressure for water reabsorption from the collecting ducts.
• e mechanism by which the high medullary osmolality is produced is called the countercurrent multiplier
mechanism.
• e explanation for countercurrent exchange lies in
its ‘U’ shape and repeated cycles of ion pumping and
uid movement. is allows uid to be concentrated
several times (osmolality changes from around 300–
1200mosmol/L, which equates to a fourfold increase in
concentration); this is signicantly greater than could
be achieved with a parallel system.
• e ‘U’ shape of the loop of Henle allows solute to be
continuously recycled in order to generate the high
medullary osmolality.
• e other facet of the countercurrent mechanism is
the fact that the vasa recta (medullary blood supply) is
arranged in a similar ‘U’ shape; this allows the continuous recycling of solute and prevents the removal of solute and resulting decrease in medullary osmolality.
Distal Convoluted Tubule and Collecting Ducts
• e distal convoluted tubule and the collecting ducts
have two important functions:
• water reabsorption
• Na+ reabsorption.
• e ultraltrate that enters the distal tubule has a
low osmolality and thus water is reabsorbed. Further
100
Cortex
300
H
H
O
2
O
2
1200
+
Na
CI
Active
–
Passive
H2O
Fig. 11.2 The osmolality of the fluid entering the descending loop of Henle is approximately 300mosmol/L.
The descending loop is permeable to Na+ and Cl− and H2O, thus there is osmotic removal of H2O and an
increase in the osmolality due to the influx of Na+ and Cl−. In the ascending limb there is an active pumping of
Na+ (Cl− following passively), but this region is impermeable to water and thus the fluid becomes more dilute.
CHAPTER 11 Urinary System
235
uid absorption occurs in the collecting ducts as they
descend through the medulla.
• e absorption of water in the distal tubule and collecting
ducts leads to a decrease in the volume of urine and an
increase in its concentration; therefore, under normal circumstances concentrated urine of low volume is excreted.
• e distal tubule and collecting duct also function to
reabsorb the remaining Na+. is process is energy
dependent and requires ATP. A proportion of the Na+
absorption is under the control of the hormone aldosterone (see later).
REGULATION OF NA+ AND WATER
REABSORPTION
• ree hormones are involved in the control of the extracellular uid (ECF) volume via their actions on Na+ and
water absorption; these hormones are:
• antidiuretic hormone (ADH or vasopressin)
• renin–angiotensin–aldosterone (RAS) system
• atrial natriuretic hormone.
Antidiuretic Hormone
• Produced in the supraoptic nucleus in the hypothalamus; it is then released from the posterior pituitary.
• Stimulation of ADH release is via osmoreceptors in the
hypothalamus; they detect increases in the osmolality of
the ECF and stimulate drinking.
• Other factors that stimulate ADH secretion include:
• ↓ circulating blood volume
• ↓ arterial pressure
• angiotensin II.
• e actions of ADH include:
• ↑ water permeability of the distal tubule and collect-
ing ducts
• ↑ arterial blood pressure by vasoconstriction.
• e secretion of ADH leads to the production of concentrated low-volume urine.
• Inhibition (i.e. alcohol), absence (cranial diabetes insipidus) or failure to respond to ADH (nephrogenic diabetes insipidus) leads to the production of urine with a low
osmolality and a high volume.
• Juxtaglomerular cells are specialized smooth muscle
cells that lie in the wall of the aerent arteriole and
secrete the hormone renin.
• Renin catalyses the reactions in the RAS system; release
from the juxtaglomerular cells is stimulated by:
• decrease in aerent arteriole pressure
• reduction in Na+, detected by the macula densa
which monitors the Na+ load in the distal tubule
• stimulation by renal sympathetic nerves.
• Renin stimulates the conversion of the plasma protein
angiotensinogen to angiotensin I; this is then converted
to angiotensin II in the lungs by the enzyme angiotensin
converting enzyme (ACE).
• Angiotensin II has a number of actions:
• stimulates arterial vasoconstriction
• stimulates the release of ADH
• stimulates drinking
• stimulates the release of aldosterone.
• Aldosterone is released from the adrenal cortex and
stimulates the reabsorption of Na+ and water from the
distal tubule and collecting ducts (see Chapter 12 for
more details).
Atrial Natriuretic Peptide (ANP)
• Released by the heart in response to an increase in the
ECF—stimulation is via atrial stretch.
• e actions of ANP are:
• increases glomerular ltration
• inhibits reabsorption of Na+.
• e actions of ANP lead to increased excretion of both
Na+ and water.
Ion and Nutrient Reabsorption
Potassium
• Active reabsorption of K+ occurs in the proximal tubule
and the ascending loop of Henle in conjunction with Na+
and Cl− transport. By the time it reaches the distal tubule,
approximately 90% of the ltered K+ has been reabsorbed.
• e amount of K+ present in the urine is regulated by
aldosterone.
• Aldosterone stimulates the secretion of K+ into the distal tubule and thus into the urine.
Renin–Angiotensin–Aldosterone System (RAS)
• e RAS system is a complex interaction of hormones
that inuences the ECF volume and also interacts with
the vascular system and aects blood pressure.
• e juxtaglomerular apparatus in the kidney is a key
mechanism in monitoring changes in the ECF and renal
circulation; it is composed of the juxtaglomerular cells
of the aerent arteriole and the macula densa cells in the
distal tubule that lie in close association.
Calcium and Phosphate
• Calcium and phosphate are actively absorbed in the
proximal tubule and ascending loop of Henle; any
remaining is absorbed in the distal tubule and collecting duct. Only 1% of the ltered calcium is excreted.
• Absorption in the distal tubule and collecting ducts is
controlled by parathormone (PTH) (see Chapter 12).
• PTH stimulates calcium reabsorption and phosphate
excretion.
236
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SECTION II Physiology
Hydrogen and Bicarbonate (Fig. 11.3)
• e regulation of H+ and HCO
taining adequate acid–base balance and a normal pH.
−
is essential in main-
3
• e majority of the ltered bicarbonate is reabsorbed in
the proximal tubule and the loop of Henle.
• Intercalated cells in the distal tubule dier from proximal tubular cells in that they actively secrete ions,
namely H+, rather than actively absorb them.
• H+ and HCO
the dissociation of carbonic acid (formed from CO2 and
−
are generated in the intercalated cells by
3
H2O and catalysed by carbonic anhydrase).
• H+ is then transported in the distal tubular lumen and
the HCO
stream, thus maintaining electrical neutrality.
• H+ secretion drives the reaction with HCO
carbonic acid, which in turn dissociates to H2O and
−
passively diuses into the peritubular blood-
3
−
; this forms
3
CO2; the CO2 diuses into the tubular cell and begins
the reaction between CO2 and H2O to produce H+ and
−
HCO
.
• ese reactions are able to react to changes in acid–base
3
balance in several ways:
• with a metabolic alkalosis there will be an increase in
the ltered HCO
secreted H+ and will be excreted
• with a metabolic acidosis the amount of HCO
reabsorbed can be increased; this occurs when the
secreted H+ reacts with other buers in the urine,
and leaves HCO
−
, thus the HCO
3
−
to diuse into the bloodstream.
3
−
will swamp the
3
−
3
Glucose and Amino Acids
• Glucose is ltered by the glomerulus and has an identical concentration to plasma.
• As the concentration of glucose in the ultraltrate and
plasma are identical, it cannot be reabsorbed along a
concentration gradient; it therefore requires an energydependent process. e transport of glucose utilizes the
gradient of Na+ between the ultraltrate and the plasma;
Na+ and glucose bind to a carrier protein and the movement of Na+ along the concentration gradient draws the
glucose with it. e glucose leaves the cell by a separate
cell membrane transport protein.
• e same mechanism is responsible for the absorption
of amino acids.
• e process occurs in the proximal tubule, and under
normal circumstances leads to the absence of glucose or
amino acids in the urine.
• e uptake mechanism of glucose can be saturated;
in these instances the excess glucose will be lost in
the urine (glycosuria); the renal threshold for glucose
absorption is around 11 mmol/L. Glycosuria is one of
the main symptoms in diabetes mellitus.
ECF Tubular
–
HCO
3
epithelium
HCO
3
H2CO
H2O + CO
–
+ H
+
3
CA
2
A
ECF Tubular
–
HCO
3
CO
2
epithelium
–
HCO
3
H
2CO3
CO2 + H2O
+ H
+
CA
B
ECF Tubular
–
HCO
3
CO
2
C
Key :-
epithelium
–
HCO
3
H2CO
CO
+ H2O
2
+ H
3
CA
NH
3
+
Active
secretion
Passive
diffusion
Filtrate
H+ + HCO
H
2CO3
CO2 + H2O
Urine
Filtrate
+
H
+ HPO
H
2PO4
Urine
Filtrate
+
H
+ NH
+
NH
4
Urine
–
3
2–
4
–
3
Fig. 11.3 Mechanisms for regulation of the pH of extra-
cellular fluid. Tubular secretion of H+ leads to reabsorption of filtered HCO
protonate filtered phosphates (B) or ammonia (C) and
−
(A). Secreted H+ can also
3
is then excreted. (From McGeown JG. Physiology,
2nd edn. Churchill Livingstone, Edinburgh, 2002, with
permission.)
CHAPTER 11 Urinary System
U: urine concentration
(a
×−
Pelvic splanchnic
of urethra
237
Urea
• Urea is a waste product formed in the liver during protein metabolism. It is not actively absorbed, but as water
is drawn out the concentration of urea in the tubules
rises and therefore there is a small amount of passive
reabsorption as urea moves down the concentration
gradient.
Glomerular Filtration Rate (GFR) and Renal
Plasma Flow
• e concept of clearance can be used to calculate both
GFR and renal plasma ow.
• Clearance is a quantitative measure of the rate of
removal of a waste product from the blood by the kidneys; it is calculated from its urinary concentration,
multiplied by the volume per unit time and divided by
the plasma concentration:
Clearance
Measuring GFR
• ere are a number of mechanisms that can be used to
calculate GFR:
1. Inulin clearance: inulin is used as it closely obeys the
following criteria needed of a substance to measure
GFR:
• must be ltered by the glomerulus
• must not be reabsorbed
• must not be secreted
• must not be metabolized
• this technique is the ‘gold standard’ for measuring GFR; however, it is not widely used in clinical
practice.
2. Creatinine clearance: used in clinical practice as creatinine occurs naturally; production is relatively constant but a small amount is secreted by the tubules;
this can be signicant at low GFR.
3. EDTA: has similar kinetics to inulin; it can be radioactively labelled and GFR determined from subsequent blood tests.
4. Dynamic renography: an estimate of GFR can be
made from DTPA and MAG3 scans.
5. Cockro–Gault equation: this equation can be used
to estimate creatinine clearance, and thus GFR:
Clearance
UV
V: urine volume
P
P: plasm=aa concentration
( ) or ()
123104 140..
×
=
(weight [kg]
Serum creatinine ( mol/L) µ
ge)
))
Measuring Renal Plasma Flow
• Measurement of renal plasma ow requires that a substance be completely removed from the plasma in a
single pass through the kidney.
• Para-aminohippuric acid (PAH) is used for this test and
is injected into the bloodstream; clearance is then calculated using UV/P.
• Renal plasma ow is around 650 mL/min.
Micturition
• Urine is formed at the rate of 1 mL/kg/h.
• Urine is transported from the renal pelvis to the bladder
by the ureters by waves of peristaltic contraction.
• Urine is then stored in the bladder.
• e pressure within the bladder (intravesical pressure) is around 3cmH2O. e bladder will ll to a volume of about 200–300 mL of urine before the desire
to urinate is felt. Before this point there is little change
in intravesical pressure. As the volume increases, the
intravesical pressure rises steeply and the desire to
urinate increases; at this point the volume is around
400–450 mL.
• ese changes in volume are sensed by stretch receptors that send impulses to the spinal cord via the pelvic
nerves.
• e nervous control of bladder function is from both
parasympathetic and sympathetic systems (Fig. 11.4):
Sympathetic trunk
Inferior hypogastric plexus
S2
S3
S4
nerve
Bladder
Pudendal nerve
External
sphincter
Urethra
Fig. 11.4 Innervation of the bladder and urethra.
238
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SECTION II Physiology
• parasympathetic: these run in the sacral outow
(S2–3) and innervate the bladder (detrusor muscle)
and internal sphincter. Parasympathetic bres also
run in the pudendal nerve and control the external
sphincter. ey stimulate micturition by ↑ detrusor contraction and ↓ contraction of the internal
sphincter
• sympathetic: these run in the hypogastric plexus;
they act to inhibit micturition by ↓ detrusor contraction and ↑ contraction of the internal sphincter.
• erefore, parasympathetic input initiates micturition
and sympathetic input inhibits it.
• Once micturition is initiated, the sympathetic impulses
are inhibited by impulses from the brainstem and parasympathetic impulses lead to bladder contraction and
relaxation of the internal sphincter.
• Voluntary contraction of the abdominal muscles aids
bladder emptying.
• In the rst few years of life micturition is a reex occurrence with no voluntary control; however, later in life
it becomes a voluntary response; descending impulses
inhi bit parasympathetic bres and also stimulate somatic
im pulses along the pudendal nerve, which allow contraction of the external sphincter.
Clinical Physiology
Bladder Function and Spinal Injury
• A normal bladder has the following innervation:
• L1–2: sympathetic outow (see above)
• S2–4: parasympathetic (see above)
• eerent sensory bres enter the spinal cord at L1–2
and S2–4.
• Following spinal injury there are three common bladder
abnormalities; these are:
• atonic bladder
• automatic reex bladder
• autonomous bladder.
• Atonic bladder: occurs during the initial phase of spinal
shock and may last several weeks; the following abnormalities are seen:
• bladder wall muscle is relaxed
• sphincter vesicae is contracted
• sphincter urethrae is relaxed
• bladder becomes distended and eventually empties
by overow. If the level of the spinal injury is above
L1–2 then the patient is unaware of the bladder distension; if the injury is below L1–2 then the patient
is aware of the distended bladder.
• Automatic reex bladder: this is seen once the spinal
shock has subsided in patients with a spinal injury
above the parasympathetic outow (S2–4). e bladder
empties reexively every 3–4 h rather than by simple
distension and overow.
• Autonomous bladder: occurs if the sacral area of the
spinal cord is damaged. The bladder is flaccid and
its capacity greatly increases; the bladder fills to
capacity and then overflows. Partial emptying can
be performed by compression of the lower abdomen;
however, backpressure leading to vesicoureteric reflux and hydronephrosis is unavoidable, and leads
to frequent infections and eventually chronic renal
failure.
Hormone Production
Renin
• Produced by the juxtaglomerular apparatus in the
kidney.
• e action of renin is to cleave angiotensin I from
angiotensinogen.
• e release of renin is stimulated by:
• reduction in renal perfusion
• stimulation of the sympathetic nervous system
• catecholamine release
• hyponatraemia.
Erythropoietin
• Majority is secreted in the kidney, although small
amounts are made in the spleen and liver.
• It acts by accelerating dierentiation of marrow stem
cells into erythrocytes.
• ere are numerous stimuli that increase the rate of
erythrocyte production:
• haemorrhage
• respiratory disease
• high altitude
• vasoconstriction
• ↑levels of red blood cells degradation products.
• In general these causes result in low tissue PO2; this is
the main stimulus for erythropoietin secretion.
1α-Hydroxylase
• 1α-hydroxylase is secreted by the kidney in response to
↓Ca2+; it converts 25-hydroxycholecalciferol to 1,25-di -
hydroxycholecalciferol.
• 1,25-dihydroxycholecalciferol promotes Ca2+ reabsorption and decreases urinary loss (see Chapter 12 for further details on calcium homeostasis).
OSCE SCENARIOS
CHAPTER 11 Urinary System
239
OSCE Scenario 11.1
A 70-year-old male is two days post-repair of a ruptured
abdominal aortic aneurysm. Urine output has been poor,
the last 4 h having been 20 mL, 10 mL, 5 mL and 5 mL per
hour, respectively. e patient has been haemodynamically
unstable.
1. How would you dene oliguria?
A specimen of urine is sent for examination and reveals
the following results:
Specic gravity >1020
Urine osmolality >500mosmol/L
Urine sodium <20 mmol/L
Fractional sodium excretion <1
2. What is the likely cause of the oliguria?
3. What action would you take based on these results?
Appropriate measures fail to produce a diuresis. Serum
creatinine is now 350 mmol/L and urine analysis reveals
the following:
Specic gravity <1010
Urine osmolality 290mosmol/L
Urine sodium >40mosmol/L
Fractional sodium excretion >2
4. What is now the cause of the patient's renal dysfunction?
5. What techniques are available for renal replacement
therapy in this patient?
6. What are the absolute indications for renal replacement
therapy?
7. Which mode of renal replacement therapy will be the
most appropriate in this patient?
OSCE Scenario 11.2
A 19-year-old male is admitted to A&E having been
stabbed in the abdomen. On examination he is pale, sweating, with a tachycardia of 120 and a systolic blood pressure
of 80 mmHg.
1. What are the grades of haemorrhagic shock?
2. What is renal blood ow autoregulation and how is it
aected by shock?
3. Describe the hormonal response to shock with specic
reference to ADH, aldosterone and the renin–angiotensin system.
OSCE Scenario 11.3
A 75-year-old male with a known lung malignancy is
admitted in an acute confusional state. He is found to have
a sodium level of 117 mmol/L. He is not dehydrated and
has no signs of sepsis.
1. What possible explanation is there for the electrolyte
abnormality?
2. What other tests would help conrm it?
3. Which type of lung cancer most commonly causes it?
4. How would you treat it?
OSCE Scenario 11.4
A 40-year-old male who was a restrained driver in a motor
vehicle crash was found to be paraplegic at the level of T10.
Aer primary and secondary survey, he was admitted to
the high-dependency unit and abdominal examination
revealed a palpable bladder.
1. What is the normal innervation to the urinary bladder?
2. What are the three bladder abnormalities that can occur
following spinal injury?
3. Describe the bladder function following the initial
phase of spinal injury.
OSCE Scenario 11.5
A 70-year-old man is admitted to the emergency surgical unit
with suprapubic pain and inability to pass urine for 12 h. He
reported recent history of hesitancy, weak stream and nocturia. Abdominal examination revealed a palpable distended
bladder. His creatinine is found to be 220 μmol/L and GFR
of 32 mL/min/1.73 m2, while his baseline test 2 months ago
showed Cr of 87 μmol/L and GFR of 60 ml/min/1.73 m2.
1. What volume in the bladder normally triggers the urge
to urinate?
2. What is the dierential diagnosis?
3. What is the likely cause of his renal function
deterioration?
4. e patient was found to have been recently com-
menced on tamsulosin by his GP. How does tamsulosin
work?
Answers in Appendix pages 454-456
Please check your eBook at https://studentconsult.inkling.com/ for more self-assessment questions. See inside cover for
registration details.
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Endocrine System
INTRODUCTION
• e function of the endocrine system is the secretion
of hormones into the circulation and their regulation of
cellular responses by binding to target cells and initiating a particular response.
• Hormones can be divided into:
• steroids: derived from cholesterol
• peptides
• altered amino acids, e.g. thyroid hormones are com-
posed of two tyrosine residues.
• e secretion of hormones can be stimulated by:
• level of a substance, e.g. glucose and insulin secretion
• stimulation by another hormone, e.g. TSH stimu-
lates the thyroid gland to secrete thyroid hormones
• nervous control, e.g. catecholamines during the
‘ght or ight’ response.
• Hormones interact with receptors to exert their eects;
there are three main types:
1. Receptors on the cell surface: usually protein or peptide
hormones, they initiate conformational changes in the
receptor that lead to the production of second messengers, which in turn modify the cell’s response.
2. Cytoplasmic receptors: steroid hormones interact with
receptors in the cytoplasm (or nucleus). e receptor–
hormone complex then enters the nucleus and binds to
a specic area of DNA and stimulates translation of a
protein product.
3. Nuclear receptors: thyroid hormone receptors are found
in the nucleus of cells; thyroid hormone enters the cell
in conjunction with the receptor and enters the nucleus
to exert its eect.
PITUITARY AND HYPOTHALAMIC
FUNCTION
• e hypothalamus lies in the forebrain in the oor of
the third ventricle; it is linked to the thalamus above and
the pituitary below via the hypophyseal stalk.
• e pituitary is divided into anterior and posterior.
• anterior pituitary (adenohypophysis): derived from
an outpouching of tissue from the oral cavity (ectoderm); it is linked to the hypothalamus via the
hypophyseal portal system
• posterior pituitary (neurohypophysis): derived from a
downgrowth of neural tissue; it is continuous with the
hypothalamus. Nuclei (paraventricular and supraoptic) lie within the hypothalamus and send axons into
the posterior pituitary. ese axons are specialized
and release hormones into the bloodstream.
Control of Pituitary Function
Anterior Pituitary
• Regulation of hormone secretion from the anterior
pituitary is by hormones secreted along the hypophyseal
tract from the hypothalamus.
• ese releasing or inhibiting hormones act on secretory
endocrine cells in the anterior pituitary.
• Release of the hormone from the target organ is regulated by feedback inhibition, either by the releasing/
inhibiting hormone or by the hormone released from
the target organ.
Posterior Pituitary
• e posterior pituitary stores two hormones, which are
produced by two nuclei in the hypothalamus.
• ese two hormones are transported to the ends of the
axons that connect the hypothalamus and the posterior
pituitary; they are released into the circulation following
an appropriate stimulus.
Anterior Pituitary Hormones
Adrenocorticotrophic hormone (ACTH)
• Secreted in response to corticotrophin-releasing hormone (CRH) from the hypothalamus.
• Stimulates the release of glucocorticoids from the adrenal cortex; also stimulates the release of β-endorphin and
precursors of melanocyte-releasing hormone (MSH).
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