Emailing urinary answered essay asm 2019 team (1)

Urinary system .
Previous exams answered essay questions
ASM 2019 team

‫النية‬ ‫جدد‬^_^ ‫جهاد‬ ‫المذاكرة‬ ..
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1- Histology(4 marks for essay Qs)
1. Compare between the renal cortex & medulla.
Renal medullaRenal cortex
it's the-
 Inner
 Pale layer
 Striated appearance
Due to presence of renal tubules &
surrounding vasculature.
 (5-10%) of blood passes through
medulla.
-extensions from medulla into cortex
known as >> medullary rays
Contain :
Straight tubules and collecting ducts.
it's the-
 Outer
 Dark layer
 granular appearance
Due to presence of vascular renal
corpuscles.
 (90-95%) of blood passes through
cortex.
-extensions from cortex into medulla
known as >> renal columns
:Contain
Interlobar blood vessels.
2. Discuss the basis of renal lobulation then mention the contents of the renal
lobes & lobules
 kidney is a compound tubular gland
 Divided into lobes and lobules according to:
 the subdivisions of renal artery within renal parenchyma
 And drainage of the uriniferous tubules
 It lacks the presence of connective tissue septa.
Renal lobe Renal lobule
Formed of medullary pyramid + mass of
cortical tissue surrounding it (1/2 of
each adjacent renal column)
Formed of a medullary ray + mass of
cortical tissue surrounding it .

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3. Mention the structures within the renal interstitium.
 Renal interstitium is >> the C.T filling spaces between the renal parenchyma
 It's more abundant in MEDULLA
Composed of:
a-network of reticular fibers supports parenchyma
b-collagen bundles around B.Vs
c-highly hydrated matrix of mucopolysaccarides
d-Connective tissue cells including macrophages & fibroblasts.
have the following characteristics:Medullary fibroblasts
 Perpendicular to axis of tubules & their processes are closely attached to them
 Rich in actin filaments & show subplasmalemmal densities >> so considered
myofibroblasts.
 Supportive in function
 Release prostaglandins & medullipin peptide for control of systemic blood pressure
4. Enumerate parts of the nephron.
 Renal corpuscle ( Bowman's capsule, glomerulus and mesangium)
 Proximal convoluted tubule
 Loop of Henle
 Distal convoluted tubule
5. Classify nephrons according to the position of renal corpuscles.
Juxtamedullary nephronsIntermediate nephronsSubcapsular neohrons
-renal corpuscles found
deep in cortex near
medulla.
- have very long loops of
Henle.
-renal corpuscles in the
midregion of cortex.
-have loops of Henle of
intermediate length.
-renal corpuscles lying
under the capsule.
-have very short loops of
Henle.

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6. Mention the structural features of renal vasculature that help create a high
hydrostatic pressure in the glomerular capillaries
a)the short course of renal artery arising directly from abdominal aorta.
b)coiled course of glomerular tuft o capillaries.
c)well developed internal elastic lamina of the afferent arteriole.
7. Enumerate the structures of intrarenal arterial vasculature.
 Each kidney receives direct branch from abdominal aorta >> RENAL ARTERY.
 RENAL ARTERY divides into Anterior & Posterior branches
 On entering hilum , the main branches further divide into >> INTERLOBAR ARTERIES
<which reach cortex and ends as CAPSULAR CAPILLARIES>.
 INTERLOBAR ARTERY bends sharply at corticomedullary junction forming >> ARCUATE
ARTERIES.
 Which In turn give >> INTERLOBULAR ARTERIES.
 Which give off >> Afferent arterioles>> divide into
 glomerular capillaries (1ry capillary network) >> reunite forming
 efferent arterioles >>give rise to
 2ry capillary network .
8. Discuss the intrarenal venous drainage at the different levels of the kidney.
Outer zone of cortex Deep zone of cortx The medulla
Drained by
Superficial cortical veins
Join to drain into
↓
Stellate veins
Which drain into
↓
Drained by
deep cortical veins
which drain into
↓
Interlobular veins
↓
Arcuate veins
Drained by veins that
directly pour into
Interlobar veins

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Interlobular veins
↓
Arcuate veins
↓
Interlobar veins
↓
Interlobar veins
The interlobar veins unite to form the→ renal vein at level of hilum which drains finally into
→inferior vena cava
9. Mention the characteristic features of the fenestrated capillaries in the
glomerulus.
-The glomerular capillaries are lined by fenestrated endothelium and differ from fenestrated
capillaries elsewhere in the body by:
 Their larger size (70-90nm)
 More numerous
 Irregular outlines
 Lack a diaphragm over the fenestra
10. Discuss the functions of the mesangial cells.
 Supportive function >> support glomerular capillary wall where podocytes are lacking.
 Phagocytic f.
-phagocytosis of filtration residues so keeping glomerular filter free of debris continuous
turnover of basal lamina
 Contractile f. >> contraction decreases GFR by reducing blood flow through glomerular
capillaries
 Secretion of
- interleukin-1 / platelet-derived growth factor / prostaglandins causes vasodilatation >>
increase glomerular filtration
 Mesangial cells possess receptors for angiotensinogen II ,vasopressin , noradrenaline &
atrial natriuretic factor so control systemic blood pressure.
11.Compare between light microscopic features of a cross section in proximal &
distal convolutes tubules.

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PCRT DCRT
-The longest among all segments of
nephron(14 mm long).
-About (1 mm).
-more frequently seen near renal
corpuscles in cortex.
-less frequently seen near renal
corpuscles in cortex.
-Rounded or oval cross sections
-lined by 3-5 tall pyramidal-shaped
cuboidal cells.
-Smaller cross section
-Lined by a 5-8 cells per section
-cells show well-developed apical brush
border
-cells show less distinctive apical brush
border
Narrower lumen Wider lumen
Indistinct boundaries between adjacent
cells.
Cell boundaries are distinct.
Deep eosinophilic cytoplasm Pale eosinophilic cytoplasm
Spherical nucleus located nearer to the
base.
Spherical nuclei pushed towards the
apical cytoplasm.
12. Discuss the structure of the renal filtration barrier.
A)fenestrated endothelium of glomerular capillaries (70-90 nm)
 Form initial barrier to the passage of blood constituents from capillary lumen to
Bowman's capsule.
 Their negatively charged glycocalyx (CELL COAT) contributes to the selective filtration
function.
B) The thick basal lamina (is the common between endothelium & podocytes)
By E.M , it has a central electron-dense zone extending between 2 lucent layers .
It’s the principal component of filtration barrier and acts as :
 Physical barrier,where collagen type IV in lamina densa holds macromolecules.
 Electrical barrier, where polyanions (mainly heparin sulphate) in lamina rara interna &
externa prevent negatively charged molecules from passing the lamina
C)filtration slits between pedicles of podocytes bridged by diaphragms
Hold particles with a diameter > 10 nm

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13. Compare between the two types of cells in the collecting ducts.
There are 2 types of cells in collecting ducts which are :- the principal cells and intercalated
cells.
Principal cells
Light or clear cells
Intercalated cells
Dark cells
Site : in all collecting tubules & ducts Absent in inner medullary ducts
Number : the majority Few in number
Cytoplasm : electron-lucent More electron-dense
Organelles :
-scanty organelles
-few mitochondria
-rich in organelles
-abundant apical vesicles & numerous
mitochondria
Apical surface :
-few short microvilli & a single central
flagellum(sensor).
-microplica ( large, unequally tall apical
projections)
Lateral membrane :
--------------------------------- -many intercellular lateral membrane
folds
Basal membrane :
-basal infoldings -------------------------
14. Mention the lining epithelium in the different parts of the collecting tubules
& ducts.
The lining cells vary along the course of the collecting tubules and ducts as follows :
 The collecting tubules & cortical collecting ducts are lined by cuboidal cells.
 In medullary collecting ducts , they start as cuboidal cells with transition into columnar
as the ducts increase in size.
 The papillary ducts of Bellini are lined by columnar cells.
There are 2 types of cells in collecting ducts which are :-
# the principal cells >> present in all collecting tubules & ducts
#and intercalated cells >> Absent in inner medullary ducts.

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15. Mention the lining epithelium of the different segments of the Loop of
Henle.
The lining epithelium along the segments of of loop of Henle shows
Intercellular fenestrations & lateral membrane interdigitations depending on the degree of permeability
to water ,salts & urea . therefore , it has four segments:-
 1)the descending thick limb with lining epithelium similar to that of proximal convoluted
tubules with moderate intercellular fenestrations
 2)the descending & the ascending thin limbs lined by >> simple squamous epithelium
 3)the ascending thick limb with lining epithelium nearly similar to that of distal convoluted
tubules with wide intercellular fenestrations to allow diffusion o urea molecules into
interstitium
16. Ibrahim has been working in leather factory for 15 years.he uses aniline dyes
to treat leather & prepare it for staining.a month ago, he was admitted to the
nephrology department at Alexandria unirversity educational hospital & was
diagnosed as a case of chronic renal failure caused by chronic aniline dyes
toxicity.
Enumerate 2 structural components in urinary bladder epithelium that protect
its wall against toxic products in urine.
Answer :-
The osmotic barrier (urinary bladder barrier) between the hypertonic urine in bladder lumen &
interstitium of bladder . it consists of
 1)thickened luminal membrane of superficial cells by plaques
 2)intercellular occluding junctions between superficial cells
Explain the structure to function adaptation of musculosa of urinary passages
Answer :-
Musculosa of ureters
 formed of well-developed smooth muscle fibers >> responsible for slow peristaltic contractions
forcing urine in unidirectional pulses down into bladder.

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 Muscle fibers are spirally arranged , there is predominantly inner longitudinal & outer circular
layer>> patent lumen of ureter
 Bundles of muscle fibers are separated by abundant connective tissue fibers >> to allow
distensibility of the wall when filled with urine.
 As the ureter opens into trigone of bladder (lower 1/3 of ureter) , the wall is thickened by
additional outer longitudinal layer.
Musculosa of urinary bladder
 Musculosa is formed of spirally arranged smooth muscle fibers , there is predominantly inner &
outer longitudinal muscle layers & a middle circular layer >> patent lumen
 Muscle fibers are separated by abundant connective tissue >> to allow bladder distention
 At the neck of bladder , dense fibers of circular smooth muscles surround the urethra forming
internal urethral sphincter(involuntary )
17. Discuss the histological adaptations of the ureter to its function.
Mucosa:
 Transitional epithelium rests on corrugated basement membrane . it's supported by loose
aereolar lamina propria rich in elastic fibers to allow stretch during full state .
Musculosa
 formed of well-developed smooth muscle fibers >> responsible for slow peristaltic contractions
forcing urine in unidirectional pulses down into bladder.
 Muscle fibers are spirally arranged , there is predominantly inner longitudinal & outer circular
layer>> patent lumen of ureter
 Bundles of muscle fibers are separated by abundant connective tissue fibers >> to allow
distensibility of the wall when filled with urine.
 As the ureter opens into trigone of bladder (lower 1/3 of ureter) , the wall is thickened by
additional outer longitudinal layer.
Adventitia :
A fibroelastic coat containing B.Vs , lymphatics & nerves separating ureter rom surrounding
retroperotitoneal structures.
)‫احتياطي‬ ‫(نكتبها‬

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18. Discuss the lining epithelium of the female urethra.
It's lined by:
 Transitional epithelium at its beginning
 Pseudostratified columnar epithelium in the middle
 Stratified squamous epithelium at its end
19. Compare between parts of the male urethra.
Penile urethraMembranous urethraProstatic urethra
14 cm
Runs through corpus
spongium of penis.
Lined by pseudostratified
columnar epithelium except
at its end where the lining
changes into stratified
squamous epithelium.
Contains openings of ducts
of bulbourethral glands
& mucus secreting glands of
Littre.
1 cm
Runs through urogenital
diaphragm & surrounded by
skeletal muscles forming the
external urethral sphincter.
Lined by pseudostratified
columnar epithelium.
3 cm
Runs through prostate.
Lined by transitional
epithelium.
It's posterior wall contains
the openings of:
Prostatic utricle
Ejaculatory ducts
Ducts of prostatic glands
20.discuss the consistency & function of the urinary bladder barrier.
The (urinary bladder barrier) is the osmotic barrier between the hypertonic urine in bladder lumen &
interstitium of bladder . it consists of
 1)thickened luminal membrane of superficial cells by plaques
 2)intercellular occluding junctions between superficial cells
It serves to (functions)
 Prevent the bladder epithelium from toxic wastes present in urine.

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 Prevent the dilution of urine from capillaries in the lamina propria.
21. Compare between the bladder in the full & empty states.
Empty stateFull state
-epithelium attains its full thickness (6 layers
or more )
-epithelium becomes stretched & much
thinner (2 – 3 cells thick)
-superficial cells are >> Dome-shaped-cells are flattened
-relative wide intercellular spaces-minimal cellular interdigitations
- smaller
As plaques are detached from luminal
surface of superficial cells by the filaments &
are internalized as vesicles to reside in the
apical cytoplasm thus returning bladder
surface to its original size.
-bladder surface area>> bigger
As the filaments in the superficial cells pull
the vesicles to the luminal surface to which
they become inserted as plaques & thus
increasing surface area.
- more-number of vesicles >> less
- thinner-plaques layer >> thicker
22.Name the components labeled 1,2 & 3 in the illustration below . mention the
structure they form together & their functional correlation.

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:Answer
1-filtration slits between pedicles of podocytes(bridged by diaphragms)
2-endothelium fenestrae of glomerular capillaries.
3-thick basal lamina (of epithelial & endothelial cells)
kidney.the filtration barrier of thethey form >>Together
-fenestrated endothelium of glomerular capillaries (70-90 nm)
 Form initial barrier to the passage of blood constituents from capillary lumen to
Bowman's capsule.
 Their negatively charged glycocalyx (CELL COAT) contributes to the selective filtration
function.
-The thick basal lamina (is the common between endothelium & podocytes)
By E.M , it has a central electron-dense zone extending between 2 lucent layers .
It’s the principal component of filtration barrier and acts as :
 Physical barrier,where collagen type IV in lamina densa holds macromolecules.
 Electrical barrier, where polyanions (mainly heparin sulphate) in lamina rara interna &
externa prevent negatively charged molecules from passing the lamina
-filtration slits between pedicles of podocytes bridged by diaphragms
Hold particles with a diameter > 10 nm

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2- Anatomy & embryology (6 marks )
1) Mention the nerve supply of the bladder.
1- Motor supply:
a- Sympathetic : preganglionic nerve cell in L1,2 spinal segments
b- From S2,3,4 nerves and reach the ureter through pelvic splanchnic nerves
2) In which perineal pouch are the following structures found?
- Membranous urethra.
Deep perineal pouch
3) Enumerate the structures related to the anterior surface of the left kidney
1- Stomach
2- Spleen
3- Suprarenal gland
4- Body of pancreas & splenic artery
5- Descending colon
6- Coils of small intestine & ascending branch of left colic artery
( 3 S + 2 intestine + body pancreas)
4) Give the position, relations and peritoneal coverings of the urinary
bladder in both sexes.
Position :
5) What is the widest and most dilatable part of male urethra? Mention 2
openings in this part.
Prostatic urethra
1- Prostatic utricle at summit of colliculus

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2- Ejaculatory ducts at each side of opening of prostatic utricle
6) Name the parts of the male urethra. In which do the ejaculatory ducts
open ?
1- Prostatic urethra
2- Membranous urethra
3- Spongy or penile urethra
- Open on the prostatic urethra
7) Name the structures related to the posterior surface of the urinary
bladder in males.
1- Two seminal vesicles
2- Two ampulla of vas deferens
3- Rectum
4- Rectovesical pouch
8) Give a full account on the anterior relations of the right kidney.
1- Suprarenal gland
2- 2nd part duodenum
3- Right lobe of the live
4- Right colic flexure
5- Part of small intestine & ascending branch of right colic artery
9) Mention the relations of the left kidney.
1- Anterior relations: See Qs N. 3
( 3 S + 2 intestine + body pancreas)
2- Posterior relations : (N.B : same in right and left kidney)
(4 muscles , 3 nerves , 1 vessel)
1- Diaphragm behind the upper 1/3
3 muscles behind the lower 2/3
2- Psoas major
3- Quadratus lumborum
4- Transversus abdominus
3 nerves & 1 vessel (from medial to lateral)

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1- Subcostal vessels
2- Subcostal nerve
3- Iliohypogastric nerve
4- Ilioinguinal nerva
10) Discuss the blood supply and lymphatic drainage of the kidney.
- Arterial :
Renal artery from abdominal aorta at the level of L2
- Venous :
Renal vein which drain into inferior vena cava
- Lymphatics :
Para-aortic lymph nodes at the level of L2
embryology
1- Describe the development of the ovary?
The female has XX sex chromosome ---the primitive sex cord dissociate into
irregular cell clusters.
Those contain primitive germ cells, occupy the medullary cords. Later they
disappear and replaced by vascular stroma that will form (medulla of ovary)
The surface epithelium continue to grow and give 2nd
generation cords
(cortical cord)
Cortical cord increase in size, the primordial germ cells are incorporated
into them.
The cortical cords are split into primordial follicles each one contain one
oogonia surrounded by follicular cells .

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2- Describe the development of the uterus &mention its congenital
anomalies?
Develops from paramesonephric duct ,it divided into 3 parts :
1-the cranial vertical part(uterine tubes)
2- middle horizontal part (uterus)
3- caudal vertical part called uterovaginal canal (body of uterus ,cervix
,upper3/5 of vagina )
its congenital anomalies
1-anomalies due to failure of fusion of 2 paramesonephric duct:
A) Double uterus double vagina
b) Double uterus double cervix one vagina
c) Double uterus one cervix one vagina
d) Bipartite uterus
e) Arcuate uterus
2- Anomalies due to complete or partial atresia of 2 paramesonephric duct:
a) Atresia of cervix
b) Atresia of vagina
c) Imperforate hymen
d) Bicornate uterus with a rudimentary horn

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3- Describe the development of metanephros &mention its congenital
anomalies?
Primordia: ureteric bud and metanephric cap.
It begins development early in the 5th week.
It is Functioning at 9 weeks.
Urine produced and released into amniotic fluid.
It starts in the pelvis, and has 2 origins:
a)Collecting part. B)Secretory part.
The collecting part
The ureteric bud arises as an outgrowth from the lower end of the
mesonephric duct near the cloaca and invaginate the nephrogenic cord
which is now called metanephrogenic cap or blastema.
The ureteric bud elongates forming the ureter, renal pelvis, major calyces,
minor calyces and collecting ducts &tubules.
The secretory part
The metanephric cap which forms from the caudal portion of the
intermediate mass, it divides into small masses one opposite each of the
collecting tubules. Part of metanephric cap canalizes to form vesicles which
elongates and canalizes to form tubules.
 These tubules form parts of the nephron:
a. Glomerulus. c. Convoluted tubule
b. Bowman's capsule. d. Loop of Henle
Formation of the nephrons of the permanent kidney begins at 8th week.
The tubules directly contact the arched collecting tubules.

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The metanephric tubules are lobulated and remain this way until after
birth.
Contact with the collecting tubule is essential to produce proteases which
break down the extracellular matrix between the metanephric tubule and
the collecting tubule.
These tubules then become continuous to form the early nephron.
mention its congenital anomalies
1- Renal agenesis: It means failure of formation of one or the two kidneys.
It is always associated with oligohydraminos.
2-Polycystic kidney: It means abnormal development of the collecting
system, or failure of the collecting tubules and nephrons to join. It may lead
to renal failure.
3- Pelvic kidney: It is due to failure of the kidney to ascend to the abdomen
where it is kept in the pelvis.
4-Horseshoe kidney: Both kidneys fail to ascend, and their lower poles fuse
together.
4- mention the embryological basis of 5 anomalies of kidney ?
1- Renal agenesis: It means failure of formation of one or the two kidneys.
It is always associated with oligohydraminos.
2-Polycystic kidney: It means abnormal development of the collecting
system, or failure of the collecting tubules and nephrons to join. It may lead
to renal failure.

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3- Pelvic kidney: It is due to failure of the kidney to ascend to the abdomen
where it is kept in the pelvis.
4-Horseshoe kidney: Both kidneys fail to ascend, and their lower poles fuse
together.
5- double ureter : early splitting ureter completely, ureters open into the
bladder separately or unite and open as usual.
5) Complete:
- The trigone of the urinary bladder is developed from…….(mesodermal in origin)
- The uterine tube is developed from…….(from paramesonephric duct
the cranial vertical part)
- The ureter is developed from…...(caudal part of mesonephric duct)
6-Mention the congenital anomalies of the urinary bladder?
1- Urachal fistula: caused by persisting allantois, urine may drain from
umbilicus.
2- urachal cyst : caused by failure of obliteration of middle part of allantois
3- urachal sinus : caused by failure of obliteration of proximal or distal part of
allantois
4- Ectopia vesicae (extrophy of the bladder): the absence of the anterior
abdominal wall& anterior wall of bladder .
5- Congenital recto-vesical fistula.
7) Describe the urogenital derivatives of the coloaca?

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It is terminial part of hind gut ,endodermal in origin divided by cloacal septum
into primitive urogenital sinus & postrtior anorectal canal which forms rectum
& upperpart of anal canal
1- The primitive urogenital sinus is divided by constriction where the
mesonephric duct is opened into cranial & caudal part
a) The cranial + constriction: called primitive urinary bladder, the caudal
called definitive urogenital sinus.
b) The primitive urogenital sinus is continues with allantois at its apex
and the 2 mesonephric duct open into its dorsal surface.
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8) Describe the derivatives of the paramesonephric duct.
Arise from the longitudinal epithelium invagination lateral to mesonephric
duct
They shift from the lateral to median side then meet and diffuse to form
uterovaginal canal without any septa.
Develops from paramesonephric duct ,it divided into 3 parts :
1-the cranial vertical part(uterine tubes)
2- middle horizontal part (uterus)
2- caudal vertical part called uterovaginal canal (body of uterus ,cervix
,upper3/5 of vagina )
3-Pathology (6 marks)

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4- Physiology (12 marks)
- Discuss Role of the kidney in acid-base balance. (2002)
- Give an account on Role of the kidney in regulation of blood pH
All diagrams for these two Qs are very important
The kidneys regulate the blood pH by secretion of hydrogen ions and by
regulating the concentration of HCO3 in plasma
A) Tubular secretion of hydrogen ions
The epithelial cells of the proximal, distal tubules, and collecting ducts all secrete
hydrogen ions into the tubular fluid.
B) Regulation of plasma HCO3
The kidneys regulates the plasma HCO3 by two mechanisms:
1. Reabsorption of filtered bicarbonate
In we had to go deeper into details, In
PCT and early DCT hydrogen is
secreted by secondary active
transport, In Late DCT and
intercalated cells of collecting ducts
hydrogen ions is secreted by primary
active transport.

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- Blood CO2 is in equilibrium with CO2 in the tubular cells. In the cell CO2
reacts with H2O in the presence of carbonic anhydrase to form carbonic
acid. Carbonic acid dissociate into hydrogen ions and bicarbonate ions.
- The hydrogen ions is secreted from the brush border of the tubular cells
into the tubular fluid by sodium-hydrogen counter-transport (To maintain
electro-neutrality inside the cell)
- In the tubular fluid, hydrogen ions are buffered with the filtered
bicarbonate forming carbonic acid. This carbonic acid is dissociated to CO2
and water. The CO2 molecules moves across the epithelium.
- The bicarbonate ion generated in step 1 passes passively across the tubular
cell membrane to peritubular fluid accompanied by reabsorbed sodium
ions. In this way, filtered sodium bicarbonate is returned to the blood.

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2. Generation of new bicarbonate
The kidneys generate HCO3
-
to replace the HCO3
-
lost in buffering the various
strong acids formed in the body. About 100 mmol of H+
is added to the body
fluids each day from fixed acids produced during the metabolism. The body’s
buffer systems, particularly the bicarbonate buffer, provides the most immediate
defense against this H+
For example. Sulphoric acid produced during the metabolism of sulpher
containing amino acids is buffered by HCO3
-
CO2 formed in this reaction is eliminated by the lungs. The net result of the
reaction is loss of two HCO3 Ions from the body, which must be replaced by the
kidneys.
The main buffer in the tubular fluid is the bicarbonate buffer (HCO3
-
). However
since the reaction between H and HCO3
-
results in the reabsorption of filtered
HCO3
-
, excess H must be excreted by combining with non-bicarbonate buffer s
in the tubular fluid, the most important of which are ammonia and phosphate.
 Ammonia
Ammonia (NH3) is a highly effective buffer for secreted H as a result of two
important factors:
First factor
H2SO4 + 2NaHCO3 Na2SO4 + 2H2CO3 Na2SO4 + 2CO2 + 2H2O

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Ammonium ion is synthesized from glutamine which comes mainly from the
metabolism of amino acids in the liver. The glutamine delivered to the kidneys is
transported into the epithelial cells of the PCT, thick ascending limb of loop of
Henle, and DCT.
Once inside the cell, each molecule of glutamine is metabolized in a series of
reactions to ultimately form 2NH4 and 2HCO3 ions.
About 60% of the NH3 synthesized in the epithelial cells is derived from
glutamine. The enzyme glutaminase is abundant in the mitochondria of tubular
epithelial cells.
Glutamine + glutminase  glutamic acid + NH3
Glutamic acid + glutamic acid dehydrogenase  NH3 + alpha ketoglutarate
The remaining 40% of NH3 synthesized in the epithelial cells is derived from
other amino acids particularly glycine and alanine.
Second factor
NH3 and NH4 have different solubility characteristics. NH3 is highly lipid soluble
an can passively diffuse across cellular membrane. In contrast, NH4 is highly
polar and crosses membrane poorly.
Thus, as NH3 is synthesized and its concentration in the epithelial cells increases,
it diffuses out of the cells. Although it can diffuse into either the tubular lumen of
the peritubular capillaries, its diffusion into the lumen (i.e. NH3 secretion) is

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favored because secreted NH3 immediately reacts with previously secreted H to
form NH4.
Ammonium ion due to its electrical charge combines with chloride ion forming
ammonium chloride which is very weakly acidic. Sodium ion is exchanged with
hydrogen and is absorbed to the blood as new sodium bicarbonate.
From this reaction 2 NH3 molecules are formed and 2 new HCO3 are generated
and enter the blood.
Sufficient NH3 is therefore secreted to react with virtually all the secreted H+
that
cannot be buffered by the low capacity phosphate buffer system, allowing the 50-
100 mmol of excess H must be excreted per day to be excreted with a minimum
fall in the tubular fluid pH.
The formation of NH3 in the epithelial cells increases in acidosis, and decrease in
alkalosis.

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 Phosphate
In the distal nephron the phosphate concentration in the tubular fluid is
significantly increased due to the reabsorption of water in excess of phosphate.
Sodium mono-hydrogen phosphate (NaH2PO4) changes to the more acidic
sodium di-hydrogen phosphate (NaH2PO4). One sodium ion is replaced by one
hydrogen ion secreted by tubular cells.
Sodium ion is reabsorbed with the generated bicarbonate into the blood. Thus, for
each hydrogen ion combined with phosphate, one molecule of new sodium
bicarbonate is added to the blood.
In normal man the amount of phosphate delivered to the distal nephrons allows
only 12-40 mmol of H to be excreted as NaH2PO4 each day. However, the
amount of available phosphate remains relatively constant even in acidotic
conditions.

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- Discuss the Juxta-glomerular hypothesis for autoregulation of glomerular
filtration rate (2005)(2003)(2006)
Juxtaglomerular hypothesis
In case of hypotension, there’s are two special feedback mechanisms
 The afferent arteriolar vasodilator feedback mechanism
- Too little flow of the glomerular filtration into the tubules causes decreased
sodium and chloride ion concentration at the macula densa
- The decreased ion concentration causes afferent arteriolar dilatation
- This increases the rate of blood flow into the glomerulus and increases the
glomerular pressure.
- The increased glomerular pressure increases the glomerular filtration rate
back toward the required level
 The efferent arteriolar vasoconstrictor feedback mechanism
- Too low glomerular filtration rate causes excess reabsorption of sodium
and chloride ions from the filtrate, reducing the concentration of these ions
at the macula densa
- The low concentration of these ions then causes the JG cells to secrete renin
from their granules
- The renin causes formation of angiotensin II
- Angiotensis II constricts the efferent arterioles, which causes the pressure
on the glomerulus to rise

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- The increased pressure then causes the glomerular filtration rate to return
back toward normal
In case of hypertension
The GFR increases, this in turn increases the concentration of sodium and
chloride ions at the macula densa; this causes afferent arteriolar constriction
which decreases the glomerular filtration rate.

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Try to draw it simply but it’s important
- Discuss the autoregulation of GFR (2012)
A) Myogenic hypothesis
The myogenic hypothesis attributes the increase in renal vascular resistance
accompanies an increase in systemic arterial pressure to contraction of the
afferent arteriolar smooth muscle in response to stretch. On the other hand, a
decrease in systemic arterial pressure decreases the stretch on the afferent
arteriolar smooth muscle and leads to afferent arteriolar dilatation.
B) juxtaglomerular hypothesis
Mentioned above

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- The concentrating mechanisms of the kidney (2001)
- Discuss the role of loob of Henle in the concentrating mechanism of the
kidney (2013)
- Discuss the causes of renal medullary interstitial hyperosmolality and the
role of vasa recta in its maintenance. (2007)
(U can just outline the words written in blue then go ahead in explaining the countercurrent mechanism)
In order to excrete the excess of ingested electrolytes, or in case of inadequate
water supply, the kidney excretes concentrated urine, so that excess solutes are
eliminated with a little loss of water from the body.
The basic requirements for forming concentrated urine:
- A high level of ADH which increases the permeability of the DCT and
collecting duct to water, thereby allowing these tubular segments to
eagerly reabsorb water
- A high osmolality of the renal medullary interstitial fluid which provides
osmotic gradient necessary for water reabsorption to occur in the presence
of high levels of ADH
The renal medullary interstitium surrounding the collecting duct is normally
hyperosmotic, so when ADH levels are high, water moves through the tubular
membrane by osmosis into the renal interstitium, from there it’s carried away by
the vasa recta back into the blood.

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Thus, the urine concentrating ability is limited by the level of ADH and by this
degree of hyper-osmolality of the renal medulla.
The mechanism by which this hyper-osmolality is obtained is the counter current
mechanism.
Countercurrent system is a system in which the inflow runs parallel, counter to,
and adjacent to the outflow. The counter current mechanism depends on the
special arrangement of the loop of Henle and the vasa recta. About 25% of the
nephrons are juxtamedullary nephron with loops of Henle and vasa recta that go
deeply into the medulla, Where there’s four solute concentrating mechanisms are
responsible for this hyper-osmolality :
1. The principle cause is active transport of sodium ions with secondary
active transport of chloride and potassium ions out of the thick portion of
the ascending limb of loop of Henle into the outer medullary interstitial
fluid. Which increases the osmolality of the medullary interstitium.
2. Passive reabsorption of Na and Cl ions from the thin ascending limb of the
loop of Henle. This passive reabsorption process depends upon the prior
existence of the medullary gradient to reabsorb water from the thin
descending limb, thereby increasing the conc. of Na and Cl ions in the
tubular fluid delivered to the thin ascending limb
3. ADH helps reabsorption of urea from the inner medullary part of the
collecting ducts. This part becomes moderately permeable to urea and
highly permeable to water; water is rapidly reabsorbed and this greatly
increases the urea concentration. Urea diffuse by concentration gradient
through the collecting duct into the medullary interstitium, its conc in the

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medullary interstitium is increased and increase the inner medullary fluid
osmolality
4. Active reabsorption of sodium from the collecting ducts into the medullary
interstitial fluid associated with electrogenic passive absorption of chloride
ions
The net result of these mechanisms is the increase in the medullary interstitial
fluid osmolality to 1200-1300 mOsm/Kg water in the pelvic tip of the medulla.
The combination of these mechanisms is called “Counter current multiplier
mechanism” because it multiplies or increases the medullary interstitial fluid.
When the conc. of ADH is high, the epithelium of the late part of the distal
convoluted and the collecting duct becomes highly permeable to water and water
is reabsorbed into the highly concentrated medullary interstitial fluid.
If you have time in the exam,
try to illustrate it in a simple
diagram. It would be very
good.

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Counter current exchange mechanism
The medullary blood flow has two characteristics for maintaining the high solute
concentration in the medullary interstitial fluid constant.
First, the medullary blood flow is very small in quantity, amounting to only 1-2
percent of total blood flow of the kidney. Because of this very small and sluggish
flow, removal of solutes is minimized.
Second, the vasa recta functions as a counter-current exchanger that prevents
washout of solutes from the medulla.
Operation of vasa recta as counter current exchangers in the kidney
As blood flows down the descending limb in the vasa recta, its osmolality is
slightly lower than the osmolality of the medullary interstitial fluid, so sodium
chloride and urea diffuse from the interstitial fluid into the blood while water
diffuses out into the interstitium. The osmolality of the blood in the vasa recta
increases to 1200mOsm/Kg water at its tip.
Then, as the blood flows back up in the ascending limb, the osmolality of the
blood is slightly higher than the osmolality of the medullary interstitial fluids, so
sodium chloride and urea diffuse back out of the blood into the interstitium and
water diffuses back into the blood, thus, the blood of vasa recta removes a little
amount of solutes from the interstitial fluid.
There’s a diagram for vasa recta in the book page 38

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- Mechanisms controlling water balance (2001)
Mechanisms regulating water balance (ADH thirst system)
A. Increase in plasma osmolality
the increase in plasma osmolality is produced by:
- Excess sodium and negative ions that go with it excite the osmoreceptors
located in the hypothalamus which cause release of ADH that increase the
permeability of the late distal tubules and collecting ducts, causing
increased conservation of water by the kidneys.
the conservation of water with the loss of sodium and other osmolar
substances in the urine causes dilution of the sodium and other substances
in the ECF, thus correcting the initial increase in plasma osmolality.
- Decrease in blood volume (total body water)
Mechanism exciting osmoreceptors
Increased osmolality in the ECF pulls water out of the osmoreceptors, causing
them to shrink and thereby increasing their rate of discharge. The osmorecepotrs
respond to changes in ECF sodium concentration but not to changes in potassium
concentration and only slightly to changes in urea and glucose concentrations.
The reason is probably that these substances can penetrate the osmoreceptors cell
membrane and therefore cause little or no osmotic effect.
B. Decrease in blood volume

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The decrease in blood volume causes the arterial pressure to fall and activates the
arterial baroreceptor reflex. Moreover, the volume receptor reflex is activated
when the pressure in the two atria, in the pulmonary artery and in other low
pressure areas of the lesser circulation fall below normal.
The net result is to activate the ADH-thirst system and thereby to increase the
body fluid volume.
- Functions of PCT. (2012)(2007)(2002)(2004)(2006) very Imp
* Sodium reabsorption: About 65% of sodium in the glomerular filtrate is
actively reabsorbed from proximal tubules
* Cloride and bicarbonate reabsorption: Their reabsorption is a passive
process created by diffusion by an electrochemical gradient through the
tubular membrane
* The wall of the PCT is freely permeable to water
Absorption of the solutes results in passive transport of water by osmosis.
65% of the water is reabsorbed and this fraction is called “Obligatory
water reabsorption” since it’s osmotically obligated to the absorbed
solutes. And it’s not under the control of ADH
* Water leaving the PCT has the same osmolality of the plasma, solutes
which are not reabsorbed become concentrated due to absorption of
water, such substances undergo diffusion by concentration gradient
provided that the membrane is permeable to them, like urea
* Glucose reabsorption: Under normal conditions, glucose is completely
reabsorbed in the PCT by secondary active process (Na-Co transport)
because it can occur against concentration gradient.

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Glucose is bound to a carrier which transports Na at the same time. The
electrochemical gradient for Na provides the energy for the transport of
glucose across the brush border to the inside of the cell.
The transport of glucose from inside the cell to the peritubular fluid
occurs by another carrier and down its concentration gradient “Facilitated
diffusion”
* Potassium reabsorption: 65% of the K in the glomerular filtrate is
reabsorped from the proximal tubules by a secondary active transport
mechanism in a parallel fashion to sodium reabsorption
* Phosphate reabsorption: Reabsorption of phosphate is restricted to the
PCT. Phosphate reabsorption is a secondary active process, it’s under
control of parathormone which inhibits its absorption. In absence of
parathormone, phosphate absorption is increased, phosphate conc in the
blood is in turn increased and consequently ca conc decreases in blood
and tetany occur.
* Secretion, most of the H ions are secondary actively secreted by PCT
but without marked decrease in urine pH
If u have time in the exam it would be good if u draw a very simple diagram for PCT illustrating what is
reabsorbed and what’s excreted
Discuss:
- GFR and factors affecting it. (2002)
- Four factors affecting the GFR (2013)
 Renal blood flow
An increase in the rate of blood flow through the nephron greatly elevates
the glomerular pressure and increase GFR

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Normally, a large amount of plasma is filtered through the glomerular
membrane, thus the colloid osmotic pressure in the glomerulus rises very
high and opposes further filtration because of retained colloids.
Filtration stops until new plasma flows into the glomerulus; consequently
the greater the rate of the plasma flow in the glomerulus, the greater is the
filtration rate.
 Diameter of glomerular blood vessels
Afferent glomerular arteriole
- Arteriolar constriction decreases the rate of blood flow into the glomerulus,
decreases the glomerular pressure and thus, decreases filtration rate.
- Arteriolar dilatation increases the glomerular blood flow and glomerular
pressure, which increases the filtration rate
Efferent glomerular arteriole
- Arteriolar dilatation lowers the glomerular pressure and decreases the
filtration rate
- Arteriolar constriction
Mild arteriolar constriction: increases the glomerular pressure and
increase the filtration force
Sever or moderate constriction: decreases the glomerular flow rate and
decreases the filtration rate. The plasma will remain for a longer period of
time in the glomerulus, and extra large amounts of plasma will filter out.

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This increases the plasma colloid osmotic pressure and a paradoxical
decrease in GFR occurs despite the increase in the glomerular pressure.
 Sympathetic stimulation
During sympathetic stimulation e.g. stress conditions, the afferent arterioles
are constricted, both renal flow and filtration decreases. With very strong
stimulation, the glomerular flow and pressure are so greatly reduced that
the urinary output can fall to zero.
 Arterial blood pressure
An auto-regulatory mechanism prevents significant rise in the glomerular
pressure corresponding to a rise in the systemic blood pressure. Automatic
afferent arteriolar constriction occurs in case of high arterial pressure.
However, glomerular filtration rate increases only a few percent if the
increase in blood pressure is not sever.
 Intrapelvic pressure
A rise of pressure in the renal pelvis will produce back pressure in the
intracapsular pressure which antagonize the filtration force. A pressure
higher than 28 mmHg will stop the filtration and consequently urine
formation, the reason could be renal pelvic stones or tumors
 Colloid osmotic pressure
The colloid osmotic pressure of the plasma proteins antagonizes filtration.
Hypo-proteinemia will increase the filtration rate.
 Permeability of the glomerular capillaries
Increased permeability of the glomerular capillaries increase the GFR.
The permeability of the glomerular capillaries and bowmen’s capsule is
absent for substances of molecular weight higher than 70,000.

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In case of plasma proteins, the serum albumin has a molecular weight of
70,000. Globulin 165,000. Fibrinogen 200,000. Accordingly, serum
globulin and fibrinogen cannot pass through, serum albumin can pass
through but the amount filtered is very small and therefore it would be
reabsorbed back in the renal tubules; normally urine if free of plasma
proteins.
If kidney became diseased, the permeability increases and so serum
albumin will appear in large amounts in urine.
When the disease of the kidney is advanced, serum globulin will appear in
urine, fibrinogen will never appear.
The molecular weight of haemoglobin is 68,000 but it’s normally protected
by being enclosed inside the membrane of RBCs. If hemolysis occur Hb will
be set free and because its molecular weight it will pass through glomeruli
and this is dangerous because in renal tubules the reaction is acidic and so
haemoglobin will be participated as acid haematin which block renal
tubules leading to anuria and death.
- Discuss dynamics of glomerular filtration (2012)
Dynamics of GFR
1. Glomerular pressure
The glomerular pressure is about 60 mmHg
2. Pressure in bowmen’s capsule
Pressure in the capsule is about 18 mmHg
3. Colloid osmotic pressure in the glomerular capillaries

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Approximately one fifth of the plasma in the capillaries filters into the
capsule, thus the protein concentration increases about 20 percent as the
blood passes from the arteriolar to the venous ends of the glomerular
capillaries. If normal colloid osmotic pressure of blood entering the
capillaries is 28 mmHg, it rises to approximately 36 mmHg by the time the
blood reaches the venous ends of the capillaries, and the average colloid
osmotic pressure is about 32 mmHg.
4. Filtration pressure
It’s equal to the glomerular pressure minus glomerular colloid osmotic
pressure and capsular pressure.
Therefore, the normal filtration pressure is about 60 – (32+18) = 10 mmHg
- Define glomerular filtration rate, mention its value, dynamics and factors
affecting it ()
Any diagram that show the direction
of the forces would be more than
enough !

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GFR
The volume of fluid filtered out of the plasma through glomerular capillary walls
into Bowman's capsules per unit of time. It equals 125ml/min.
The rest of the question is answered above in the previous Qs
- Mention the causes of metabolic acidosis and explain the mechanism of
compensation. (2006)
- Define metabolic acidosis. Discuss its causes, manifestations and
compensation (2012)
Metabolic acidosis
The primary abnormality is a decrease in P(HCO3). Most cases of metabolic
acidosis results from abnormal accumulation of organic acids.
This condition of accumulation of acids without enough bicarbonate results
imbalance in the pH
Causes:
- Diarrhea: the gastrointestinal secretions normally contain large amounts of
sodium bicarbonate. Therefore, excessive loss of these secretions in t a bout
of diarrhea is exactly the same as excretion of large amounts of sodium
bicarbonate in urine.

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- Hypovolemia and other forms of circulatory shock in which lactic acid
may accumulate (lactic acidosis)
- Uncontrolled DM, in which acetoacetic acid and B-OH-butyric acid may
accumulates (Diabetic ketoacidosis)
- Severe renal failure: failure of the kidney to get rid the body even of the
normal amounts of acid formed each day by metabolic processes of the
body
Compensation:
Metabolic acidosis is compensated by the lungs, then the kidneys act to correct
the pH back to normal
The decreased arterial pH stimulates the chemoreceptors in the carotid bodies
which in turn initiates a reflex stimulation of alveolar ventilation.
The increase in the ventilation results in decrease in P(CO2). Thus although
P(HCO3) remains low, the P(HCO3)/P(CO2) and hence arterial pH increases 50%-
70% towards normal.
Manifestations:
The major effect of acidosis is depression of the CNS. Therefore, patients dying of
diabetic, uremic, and other types of acidosis usually die in a state of coma.
In metabolic acidosis, the high H ion concentration increases the rate an depth of
respiration, therefore, one of the diagnostic signs of metabolic acidosis is
increased pulmonary ventilations.

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On the other hand, in respiratory acidosis, respiration is usually depressed
because this is the cause of acidosis.
- Explain the role of non-bicarbonate buffers in tubular fluid in buffering
excess H ions. (2005)(2006)
- Discuss the role of the kidney in generation of new bicarbonate into
blood (2012) these non-bicarbonate buffers results in the formation of new bicarbonate as would be
explained and illustrated
The main buffer in the tubular fluid is the bicarbonate buffer (HCO3
-
). However
since the reaction between H and HCO3
-
results in the reabsorption of filtered
HCO3
-
, excess H must be excreted by combining with non-bicarbonate buffer s
in the tubular fluid, the most important of which are ammonia and phosphate.
 Ammonia
Ammonia (NH3) is a highly effective buffer for secreted H as a result of two
important factors:
First factor
Ammonium ion is synthesized from glutamine which comes mainly from the
metabolism of amino acids in the liver. The glutamine delivered to the kidneys is
transported into the epithelial cells of the PCT, thick ascending limb of loop of
Henle, and DCT.
Once inside the cell, each molecule of glutamine is metabolized in a series of
reactions to ultimately form 2NH4 and 2HCO3 ions.

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About 60% of the NH3 synthesized in the epithelial cells is derived from
glutamine. The enzyme glutaminase is abundant in the mitochondria of tubular
epithelial cells.
Glutamine + glutminase  glutamic acid + NH3
Glutamic acid + glutamic acid dehydrogenase  NH3 + alpha ketoglutarate
The remaining 40% of NH3 synthesized in the epithelial cells is derived from
other amino acids particularly glycine and alanine.
Second factor
NH3 and NH4 have different solubility characteristics. NH3 is highly lipid soluble
an can passively diffuse across cellular membrane. In contrast, NH4 is highly
polar and crosses membrane poorly.
Thus, as NH3 is synthesized and its concentration in the epithelial cells increases,
it diffuses out of the cells. Although it can diffuse into either the tubular lumen of
the peritubular capillaries, its diffusion into the lumen (i.e. NH3 secretion) is
favored because secreted NH3 immediately reacts with previously secreted H to
form NH4.
Ammonium ion due to its electrical charge combines with chloride ion forming
ammonium chloride which is very weakly acidic. Sodium ion is exchanged with
hydrogen and is absorbed to the blood as new sodium bicarbonate.

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From this reaction 2 NH3 molecules are formed and 2 new HCO3 are generated
and enter the blood.
Sufficient NH3 is therefore secreted to react with virtually all the secreted H+
that
cannot be buffered by the low capacity phosphate buffer system, allowing the 50-
100 mmol of excess H must be excreted per day to be excreted with a minimum
fall in the tubular fluid pH.
The formation of NH3 in the epithelial cells increases in acidosis, and decrease in
alkalosis.
 Phosphate
In the distal nephron the phosphate concentration in the tubular fluid is
significantly increased due to the reabsorption of water in excess of phosphate.

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Sodium mono-hydrogen phosphate (NaH2PO4) changes to the more acidic
sodium di-hydrogen phosphate (NaH2PO4). One sodium ion is replaced by one
hydrogen ion secreted by tubular cells.
Sodium ion is reabsorbed with the generated bicarbonate into the blood. Thus, for
each hydrogen ion combined with phosphate, one molecule of new sodium
bicarbonate is added to the blood.
In normal man the amount of phosphate delivered to the distal nephrons allows
only 12-40 mmol of H to be excreted as NaH2PO4 each day. However, the
amount of available phosphate remains relatively constant even in acidotic
conditions.
- Draw a diagram representing the role of the kidney in acid-base balance.
(2008)
The kidneys regulate the blood pH by secretion of hydrogen ions and by
regulating the concentration of HCO3 in plasma

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A) Tubular secretion of hydrogen ions
B) Regulation of plasma HCO3
1. Reabsorption of filtered bicarbonate
2. Generation of new bicarbonate

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Don’t forget that these non-bicarbonate buffers which are ammonia and
phosphate results in formation of new bicarbonate as illustrated in the
diagram

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- Role of bicarbonate buffers in the tubular fluid in buffering excess
hydrogen ions.
In the tubular fluid, hydrogen ions are buffered with the filtered bicarbonate
through the process of reabsorption of filtered bicarbonate in the following steps
- Blood CO2 is in equilibrium with CO2 in the tubular cells. In the cell CO2
reacts with H2O in the presence of carbonic anhydrase to form carbonic
acid. Carbonic acid dissociate into hydrogen ions and bicarbonate ions.
- The hydrogen ions is secreted from the brush border of the tubular cells
into the tubular fluid by sodium-hydrogen counter-transport (To maintain
electro-neutrality inside the cell)
- In the tubular fluid, hydrogen ions are buffered with the filtered
bicarbonate forming carbonic acid. This carbonic acid is dissociated to CO2
and water. The CO2 molecules moves across the epithelium.
- The bicarbonate ion generated in step 1 passes passively across the tubular
cell membrane to peritubular fluid accompanied by reabsorbed sodium
ions. In this way, filtered sodium bicarbonate is returned to the blood.

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- Discuss glucose tubular transport (2013)
Glucose is transported from the tubular lumen through the brush border by a
process called “Sodium co-transport” which is a secondary active transport
process.
The glucose binds with the same sodium carrier molecule in the brush border
that transports sodium ions through this membrane, then as the sodium diffuses
inward through the membrane down its concentration gradient it pulls the
glucose along with it.
Once inside the epithelial cell, the sodium and the glucose split from the carrier.
The glucose then diffuses through the basal membrane of the cell and thence into
the peritubular capillaries by a carrier down their concentration gradient
“Facilitated diffusion”

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- Discuss the diluting mechanism of the kidney (2012)
The late distal tubule and the collecting ducts are impermeable to water
when the antidiuretic hormone is not present in the circulating body
fluids.
In case of haemodilution , absorption of solutes only takes place at these
sites as the ADH is not secreted and is present in low concentration.
- At the thick portion of the loop of Henle and the first segment of the
distal tubule (Diluting segments) there is active absorption of sodium ions
and secondary active absorption of chloride and potassium ions.
The osmolality of the fluid in the ascending limb of the loop of Henle
decreases progressively to about 100 milliosmoles per Kg water by the
time the fluid leaves the tubular segment.
- In the late distal tubules and collecting ducts, there’s an active absorption
of sodium and passive absorption of anions e.g. chlorides. The osmolality
of the tubular fluid decreases as little as 65-70 milliosmoles per Kg water
by the time it leaves the collecting duct to enter the urine.
To summarize, the process for excreting a dilute urine is one of absorbing
solutes at the distal segments of the tubules, while water fail to be
reabsorbed.

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- Estimation of renal blood flow (2003)
Renal plasma flow is commonly measure by infusing PAH at low doses
(3mg/100ml)
PAH is cleared from the plasma by filtration through glomeruli and secretion in
the PCT, so that its extraction ratio =
arterial concentration−venous concentration
𝑎𝑟𝑡𝑒𝑟𝑖𝑎𝑙 𝑐𝑜𝑛𝑐𝑒𝑛𝑡𝑟𝑎𝑡𝑖𝑜𝑛
] is
high. About 90% of PAH in the arterial blood is remove in a single circulation
through the kidney, only about one tenth remains in the renal venous plasma
after leaving the kidney.

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Effective renal plasma floe ERPF is the plasma passing through functioning
nephrons and so cleared from PAH. The rest of the plasma passes to areas do not
contain functioning nephrons like the renal medulla, capsule, perirenal fat .. etc.
𝐸𝑅𝑃𝐹 =
𝑈 𝑃𝐴𝐻 x V
𝑃 𝑃𝐴𝐻
= 630 ml/min
ERPF can be converted to actual renal plasma flow
Average PAH extraction ratio = 0.9
𝐴𝑐𝑡𝑢𝑎𝑙 𝑅𝑃𝐹 =
ERPF
𝑒𝑥𝑡𝑟𝑎𝑐𝑡𝑖𝑜𝑛 𝑟𝑎𝑡𝑖𝑜
=
630
0.9
= 700 ml/min
From the renal plasma flow, the renal blood flow can be calculated after
estimation of the hematocrit value.
If hematocrit = 45%
Renal blood flow = RPF
1
1−Ht
= 700 𝑥
1
0.55
= 1273 𝑚𝑙/𝑚𝑖𝑛

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5- Biochemistry (2 marks)
1- Explain briefly the role of the kidney as endocrine organ .
a) production of erythropoietin
- it's glycoprotein hormone that controls erythropoiesis
- produced by renal cortex in respond to hypoxia
- it stimulates bone marrow to produce more blood cells to increase o2 carrying
capacity of the blood .
- In renal insufficiency the decreased production of it leading to anemia
b) formation of active form of vitamin D
- by formation 1 alfa hydroxylase enzyme which is the key regulatory enzyme in
formation the active form of vit. D
- In renal failure patient the formation of Vit. D is diminished leading to
hyperparathyroidism
secretion of renin (renin is enzyme not hormone ‫بس‬‫الدكتور‬‫قالت‬‫في‬
‫المحاضرة‬‫قالت‬‫ممكن‬‫نقو‬‫له‬‫عادي‬‫مع‬‫السؤال‬‫ده‬‫باعتبار‬‫إنه‬‫حيتشغل‬‫على‬
aldosterone w angiotensin II
‫فنقوله‬‫بالمرة‬ ):
Kidney secretes Renin which activates renin-angiotensin aldosterone system ,
and that is very important in long term regulation of the blood pressure
(activation of this system occure in hypotension to increase absorption of NACL
and then water to rise the blood pressure)
2- Write a short note on proteinuria:
Proteinuria is increase protein level in urine above normal which is it can
be of 2 types
1- Albuminuria :
Increase level of albumin in urine above normal which is (30-200 mg/day ) , it can
be ,
- Physiologically (less than 500 mg/day) :
after severe muscle exercise , prolonged standing , high protein meal , pregnancy
- Pathological :
Prerenal : e.g. heart failure
Renal : e.g. nephritis and nephrosis
Postrenal : in lower urinary tract e.g. cyctitis
Albumin is detected in urine by heat coagulation test
2- Bence-Jones proteins:
Abnormal globulin appear in urine in cases of :

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Multiple myeloma – leukemia – lymphosarcoma
Urine in this condition undergo 3 phases : clotting when heated to 60 , redissolve at 100
, reclotting by cooling.
3- Mention 2 roles of the glutamine aminoacids in kidney metabolism
1- It is one of the most important substrates in renal cortical gluconeogenesis
and thus important role in maintaining glucose hemostasis by the kidney
2- Used in ammonia production by the action of glutaminase enzyme , it's
important to produce enough NH3 from glutamine to buffer the non-
volatile acids .

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N.B :
Pharma – micro – para : NO essay , only MCQs
‫واآلخرة‬ ‫الدنيا‬ ّ‫بخيري‬ ‫لنا‬ ‫الدعاء‬ ‫نسألكم‬ ، ‫هللا‬ ‫بحمد‬ ‫تم‬^__^
ASM 2019 team 

Emailing urinary answered essay asm 2019 team (1)

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