صفحه 1:
®Urine Formation by the Kidneys:
Glomerular Filtration, Renal
Blood Flow, and Their Control
Dr. Mard
صفحه 2:
یس
The kidneys serve multiple functions, including the
following:
© Excretion of metabolic waste products and
foreign chemicals
© Regulation of water and electrolyte balances
® Regulation of body fluid osmolality and
electrolyte concentrations
© Regulation of arterial pressure
© Regulation of acid-base balance
® Secretion, metabolism, and excretion of
hormones
© Gluconeogenesis
صفحه 3:
-
© Excretion of metabolic waste products and
foreign chemicals : include
® urea (from the metabolism of amino acids)
© creatinine (from muscle creatine),
® uric acid (from nucleic acids)
® end products of hemoglobin breakdown
(such as bilirubin)
® metabolites of various hormones
© most toxins and other foreign substances
such as pesticides, drugs, and food additives.
صفحه 4:
®Regulation of Water and_ Electrolyte
Balances. For maintenance of homeostasis,
excretion of water and electrolytes must precisely
match intake. =
Intake = Output (excret we
4-202 4 6 8 1012 4
Time (cays)
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صفحه 5:
© Regulation of Arterial Pressure
Long-term regulation of arterial pressure by
excreting variable amounts of sodium and
water.
Short-term arterial pressure regulation by
secreting vasoactive factors or substances,
such >
Renin angiotensin II
صفحه 6:
® Regulation of Acid-Base Balance
The kidneys contribute to acid-base regulation,
along with the lungs and body fluid buffers, by
excreting acids and by regulating the body fluid
buffer stores. The kidneys are the only means of
eliminating from the body certain types of
acids, such as sulfuric acid and phosphoric acid,
generated by the metabolism of proteins.
صفحه 7:
© Regulation of Erythrocyte Production
hire erythroperesm RBC
production
een > Porarwis
CRF (hemodialysis)
صفحه 8:
©The kidneys produce the active form of
vitamin D, 1,25-dihydroxyvitamin D3
(calcitriol), by hydroxylating this vitamin at
the "number 1" position.
صفحه 9:
® Physiologic Anatomy of the Kidneys
Location : posterior wall of the abdomen
(retroperitoneal)
Weight : 150 gr
Hilum : entrance of renal pedicles and ureter
Fibrous capsule : The kidney is surrounded by a
tough, that protects its delicate inner
structures.
صفحه 10:
The kidney composed of : two major regions that can be visualized
are the outer cortex and the inner region (medulla).
Renal pyramids : The medulla is divided into multiple cone-shaped
masses of tissue called renal pyramids.
The base of each pyramid originates at the border between the
cortex and medulla and terminates in the papilla, which projects
into the space of the renal pelvis.
Renal pelvis : a funnel-shaped continuation of the upper end of the
ureter. The outer border of the pelvis is divided into open-ended
pouches called major calyces that extend downward and divide
into minor calyces
صفحه 11:
Ow
Minor calyces : collect urine from the tubules of
each papilla.
contractile elements : The walls of the calyces,
pelvis, and ureter contain contractile elements
that propel the urine toward the bladder
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Blood flow: is normally about 22% of the C.O or
1100 ml/min.
The renal artery enters the kidney through the hilum
and then branches progressively to form :
Afferent arteric?e= glomeru®r capillaries
Effexgnt arteriole
peritubular capillaries
صفحه 14:
GFR
Maximum urine flow
Normal urine flow
Minimum urine flow
Renal blood flow 1100 mL/min
Renal plasma flow 625 mL/min
125 mL/min
20 mLimi
1 mU/min|
0.4 mL/min
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صفحه 15:
صفحه 16:
mal circulation is unique-in-that it
glomerular and peritubular capillaries, which are arranged (in series),
which help regulate the hydrostatic pressure in both sets of capillaries.
© High hydro-static pressure in the glomerular capillaries (60 mm
Hg) causes rapid fluid filtration,
© Whereas a much lower hydrostatic pressure in the peritubular
capillaries (about 13 mm Hg) permits rapid fluid reabsorption.
© By adjusting the resistance of the afferent and efferent
arterioles, the kidneys can regulate the hydrostatic pressure in
both the glomerular and the peritubular capillaries, thereby
changing the rate of glomerular filtration, tubular reabsorption
صفحه 17:
۳ 89 tional L
~~ Kidney
Each kidney (1 million nephrons)
Each nephrons capable of forming urine.
The kidney cannot regenerate new nephrons
Therefore, with renal injury, disease, or normal aging, there is a gradual
decrease in nephron number.
After age 40, the number of functioning nephrons usually decreases about
10 per cent every 10 years.
Each nephron contains :
(1)The glomerulus
(2)a long tubule in which the filtered fluid is converted into urine on its
way to the pelvis of the kidney
صفحه 18:
e glomerulus contains a network of branching
and anastomosing glomerular capillaries that,
compared with other capillaries, have high
hydrostatic pressure (60 mm Hg).
The glomerular capillaries are covered by
epithelial cells, and the total glomerulus is
encased in Bowman's capsule. Fluid filtered from
the glomerular capillaries flows into Bowman's
capsule and then into the proximal tubule
صفحه 19:
Thick segment of
ascending limb
Thin segment of
ascending limb
Descending limb
© Elsevier. Guyton & Hall: Textbook of Medical Physiology 11e - www.studentconsult.com
صفحه 20:
وب سس
Bladder
Figure 26-7. Innervation af the urinary bladder
صفحه 21:
Pain sensation in ureter
© Reflex. The ureters are well supplied with pain
nerve
© fibers. When a ureter becomes blocked (e.g., by a
ureteral stone), intense reflex constriction occurs,
which is associated with severe pain. Also, the pain
impulses cause a sympathetic reflex back to the
kidney to constrict the renal arterioles, thereby
decreasing urine output from the kidney. This
effect is called the ureterorenal reflex and is
important for preventing excessive flow of fluid
into the pelvis of a kidney with a blocked ureter.
صفحه 22:
vation of the Bladder.___ ۳
© principal nerve supply of the bladder-the pelvic nerves, which connect with the
spinal cord through the sacral plexus, ($2 and $3)
The sensory fibers detect the degree of stretch in the bladder wall.
Stretch signals from the posterior urethra are especially strong and are mainly
responsible for initiating the reflexes that cause bladder emptying.
The motor nerves transmitted in the pelvic nerves are parasympathetic fibers.
In addition to the pelvic nerves, two other types of innervation are important in
bladder function. Most important are the skeletal motor fibers transmitted through
the pudendal nerve to the external bladder sphincter.
‘These fibers are somatic nerve fibers that innervate and control the voluntary
skeletal muscle of the sphincter.
Also, the bladder receives sympathetic innervation from the sympathetic chain
through the hypogastric nerves, connecting mainly with the L2 segment of the
spinal cord. These sympathetic fibers stimulate mainly the blood vessels and have
little to do with bladder contraction.
Some sensory nerve fibers also pass by way of the sympathetic nerves and
may be important in the sensation of fullness and, in some instances, pain.
صفحه 23:
Volume (milliliters)
Figure 26-8. A normal cystometrogram, showing also acute pres-
sure waves (dashed spikes) caused by micturition reflexes.
صفحه 24:
e 26-8 shows the approximate
intravesicular pressure as the bladder fills with urine.
When there is no urine in the bladder, the intravesicular
pressure is about 0, but by the time 30 to 50 milliliters of
urine have collected, the pressure rises to 5 to 10
centimeters of water.
© Additional urine—200 to 300 milliliters—can collect with
only a small additional rise in pressure; this constant level
of pressure is caused by intrinsic tone of the bladder wall.
Beyond 300 to 400 milliliters, collection of more urine in
the bladder causes the pressure to rise rapidly.
© Superimposed on the tonic pressure changes during filling
of the bladder are periodic acute increases in pressure that
last from a few seconds to more than a minute. The
pressure peaks may rise only a few centimeters of water or
may rise to more than 100 centimeters of water. These
pressure peaks are called micturition waves in the
cystometrogram and are caused by the micturition reflex.
صفحه 25:
As the bladder fills, many superimposed micturition contractions begin to appear, as shown by the dashed
spikes. They are the result of a stretch reflex initiated by sensory stretch receptors in the bladder wall,
especially by the receptors in the posterior urethra when this area begins to fill with urine at the higher
bladder pressures.
® Sensory signals from the bladder stretch receptors are conducted to the sacral segments of the cord through
the pelvic nerves and then reflexively back again to the bladder through the parasympathetic nerve fibers by
way of these same nerves.
® When the bladder is only partially filled, these micturition contractions usually relax spontaneously after a
fraction
® of a minute, the detrusor muscles stop contracting, and pressure falls back to the baseline
® As the bladder continues to fill, the micturition reflexes become more frequent and cause greater
contractions of the detrusor muscle.
® Once a micturition reflex begins, itis “self-regenerative.” That is, initial contraction of the bladder activates
the
® stretch receptors to cause a greater increase in sensory impulses from the bladder and posterior urethra,
which
® causes a further increase in reflex contraction of the bladder; thus, the cycle is repeated again and again
until
® the bladder has reached a strong degree of contraction.
® Once the micturition reflex becomes powerful enough, it causes another reflex, which passes through the
pudendal
٩ “nerves to the external sphincter to inhibit it. If this inhibition is more potent in the brain than the voluntary
® constrictor signals to the external sphincter, urination will occur. If not, urination will not occur until the
bladder fills still further and the micturition reflex becomes more powerful
صفحه 26:
صفحه 27:
known as the macula densa
© Distal tubule : Beyond the macula densa, fluid enters
the distal tubule, which, like the proximal tubule, lies in
the renal cortex. This is followed by the connecting
tubule and the cortical collecting tubule, which lead to
the cortical collecting duct.
۰
© The initial parts of 8 to 10 cortical collecting ducts join
to form a single larger collecting duct that runs
downward into the medulla and becomes the medullary
collecting duct.
© The collecting ducts merge to form progressively
larger ducts that eventually empty into the renal pelvis
through the tips of the renal papilla
In each kidney, there are about 250 of the very large
collecting ducts, each of which collects urine from
about 4000 nephrons.
صفحه 28:
egional Differences in Nephron Structure
(Length of Henle & the vascular structures)
Cortical :
1. Glomeruli located in the outer cortex
2. They have short loops of Henle that penetrate only a short distance into the medulla
3. The entire tubular system is surrounded by an extensive network of peritubular capillaries
Juxtamedullary Nephrons (20 to 30 % of the nephrons) :
1, glomeruli that lie deep in the renal cortex near the medulla
2.These nephrons have long loops of Henle that dip deeply into the medulla
3. long efferent arterioles extend from the glomeruli down into the outer medulla
and then divide into specialized peritubular capillaries called vasa recta (this
specialized network of capillaries in the medulla plays an essential role in the
formation of a concentrated urine).
صفحه 29:
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jppew ۵
صفحه 30:
© Urine Formation Results from Glomerular Filtration,
Tubular Reabsorption, and Tubular Secretion
© The rates at which different substances are excreted in
the urine represent the sum of three renal processes,
shown in
© (1) glomerular filtration
© (2) reabsorption
© (3) secretion
Expressed mathematically:
Urinary excretion rate= Filtration rate-
Reabsorption rate + Secretion rate
صفحه 31:
4. Filtration
2, Reabsorption
3, Secretion
4. Excretion
Urinary excretion
exoretica rote= Pirotica rote- Reubsorpicg rate + Georetiva rate و(
صفحه 32:
Ultrafiltation :
© Urine formation begins when a large amount of fluid
that is virtually free of protein is filtered from the
glomerular capillaries into Bowman's capsule. Most
substances in the plasma, except for proteins, are
freely filtered, so that their concentration in the
glomerular filtrate in Bowman's capsule is
almost the same as in the plasma.
صفحه 33:
Fitration only Filtration, partal
reabsorption
Substance A Substance B
vine Urine
C. Fitton, complete Fitaion, secretion
reabsorption
‘Substance C ‘Substance D
urine Urine
صفحه 34:
IA is freely filtered by the glomeru ut is
neither reabsorbed nor secreted. Therefore, its excretion rate
is equal to the rate at which it was filtered (such as
creatinine)
Panel B, the substance is freely filtered but is also partly
reabsorbed from the tubules back into the blood (rate of
urinary excretion < rate of filtration): electrolytes
In this case, the excretion rate is calculated as the filtration rate
minus the reabsorption rate.
Panel C, the substance is freely filtered at the glomerular
capillaries but is not excreted (comp[letly absorbed) shuch
as : nutritional substances (amino acids and glucose)
Panel D is freely filtered at the glomerular capillaries and is
not reabsorbed, but additional quantities of this substance are
secreted from the peritubular capillary blood into the renal
tubules (organic acids and bases.
The excretion rate in this case is calculated as filtration rate
plus tubular secretion rate.
صفحه 35:
8 on, absorpt
Different Substances
In general, tubular reabsorption is quantitatively more important
than tubular secretion in the formation of urine, but secretion
plays an important role in determining the amounts of K and H ions
Most substances that must be cleared from the blood, especially the
end products of metabolism such as urea, creatinine, uric acid,
and urates, are poorly reabsorbed and are therefore excreted in
large amounts in the urine.
صفحه 36:
\re Large Amounts of S
absorbed by the Kidneys?
One might question the wisdom of filtering such large amounts
of water and solutes and then reabsorbing most of these
substances.
1. One advantage of a high GFR is that it allows the kidneys to
rapidly remove waste products from the body that depend
primarily on glomerular filtration for their excretion.
2. A second advantage of a high GFR is that it allows all the
body fluids to be filtered and processed by the kidney
many times each day. Because the entire plasma volume is
only about 3 liters, whereas the GFR is about 180 L/day, the
entire plasma can be filtered and processed about 60 times
each day. This high GFR allows the kidneys to precisely and
rapidly control the volume and composition of the body fluids.
صفحه 37:
1
21105
Filtrate composition s
Free from proteins and devoid of cellular elements, including
red blood cells.
The concentrations of other constituents of the glomerular
filtrate, including most salts and organic molecules, are
similar to the concentrations in the plasma.
Exceptions for calcium and fatty acids because of almost one
half of the plasma calcium and most of the plasma fatty acids
are bound to proteins
صفحه 38:
low
GFR is determined by:
)1( 200 ۲
(2) the capillary filtration coefficient (Kf) [the product of the
permeability x A]
K, of glomerular capillaries=400 other
capillaries
صفحه 39:
Efferent
Glomerular
‘oncotic
pressure
(32 mm Hg)
Bowman's
capsule
pressure
(18 mm Hg)
Glomerular
hydrostatic
pressure
(60 mm Hg)
Afferent
arteriole
Net filtration
pressure
(10mm Hg)
صفحه 40:
_ the average adult human, the GFR is = out 125
ml/min, or 180 L/day.
The fraction of the renal plasma flow that is filtered
(the filtration fraction) averages about 0.2; this
means that about 20 % of the plasma flowing
through the kidney is filtered through the
glomerular capillaries
Filtration fraction : GFR/Renal plasma flow
صفحه 41:
merular Capillary
Membrane
The glomerular capill membrane i:
similar to that of other capillaries
except that it has three (instead ©
the usual two) major layers:
© Endothelium
© A basement membrane
* A llayer of epithelial cells
(podocytes,
Alfeent arteriole
Etlerent arteriole
Together, these layers make up the
filtration barrier, which, despite
the three layers, filters Several
hundred times as much water anc مهو
solutes as the usual capillary
membrane. تست
membrane
Ultra-filtration : Even with this
high rate of filtration, the
glomerular capillary
membrane normally prevents 8 هه
filtration of plasma proteins.
Endothelin
صفحه 42:
Lumen of Bowman's capsule
Basement
membrane
Filtration slit
~
Capillary endothelium
Filtered
material
Capillary lumen
Bowman's capsule
epithelium
endothelium
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صفحه 43:
Their Size
The glomerular capillary membrane is thicker than most
other capillaries, but it is also much more porous and
therefore filters fluid at a high rate. Despite the high
filtration rate. the alomerular filtration barrier is selective
in deterr Table 26-4 their
size and_ Filterability of Substances by Glomerular Capillaries Based
‘on Molecular Weight
Substance Molecular Weight Filterability
Water 18 1.0
Sodium 23 1.0
Glucose 180 1.0
Inulin 5500 1.0
Myoglobin 17,000 0.75
Albumin 69,000 0.005
صفحه 44:
© The molecular diameter of the plasma, protein albumin is only
about 6 nm, whereas the pores of the glomerular membrane are
thought to be about 8 nanometers
© Albumin is restricted from filtration, however, because of its negative
charge. and the electrostatic repulsion exerted by negative charges of
the glomerular capillarv wall proteoalvcans
—Poiyeationie dextvan
Neutral dextran
—Polyanionic dextran
18 2 26 30 4 38 42
Efective molecular radius (A)
صفحه 45:
In certain kidney diseases, the negative charges
on the basement membrane are lost even before
there are noticeable changes in kidney
histology, a condition referred to as minimal
change nephropathy. As a result of this loss of
negative charges on the basement membranes,
some of the lower-molecular-weight proteins,
especially albumin, are filtered and appear in
the urine, a condition known as proteinuria or
albuminuria.
صفحه 46:
GFR is determined by
(1) the sum of the hydrostatic and colloid osmotic
forces across the glomerular membrane, which
gives the net filtration pressure, and
(2) the glomerular capillary filtration coefficient, Kf.
Expressed mathematically, the GFR equals the
product of Kf and the net filtration pressure:
*
GFR = Kf “Net filtration pressure
صفحه 47:
hy drostatic and colloid osmotic 0۳06
or oppose filtration across the glomerular eapillaries.
© These forces include (1) hydrostatic pressure inside the
glomerular capillaries (glomerular hydrostatic pressure,
PG), which promotes filtration
© (2) the hydrostatic pressure in Bowman's capsule (PB)
outside the capillaries, which opposes filtration
© (3) the colloid osmotic pressure of the glomerular
capillary plasma proteins (mG), which opposes filtration
© (4) the colloid osmotic pressure of the proteins in
Bowman's capsule (mB), which promotes filtration.
(Under normal conditions, the concentration of protein
in the glomerular filtrate is so low that the colloid
osmotic pressure of the Bowman's capsule fluid is
considered to be zero.)
© The GFR can therefore be expressed as
GFR = K; x (Pg — Pp - 10 + Tp)
صفحه 48:
® Increased Glomerular Capillary Filtration Coefficient
Increases GFR
K, = GFR/Net filtration pressure
صفحه 49:
Pressure Decreases GFR
In certain pathological states associated with obstruction of the
urinary tract, Bowman's capsule pressure can increase markedly,
causing serious reduction of GFR. For example, precipitation of
calcium or of uric acid may lead to "stones" that lodge in the
urinary tract, often in the ureter, thereby obstructing outflow of
the urinary tract and raising Bowman's capsule pressure. This
reduces GFR and eventually can damage or even destroy the
kidney unless the obstruction is relieved.
صفحه 50:
Filtration
traction
‘osmotic pressure
(mm Hg)
Glomerular colloid
Filtration
fraction
8 8 8 8 م 88
2016086000 المت 10
end
Distance along end
glomerular capillary
صفحه 51:
Glomerular
filtration
SS ۰ وراد
كاهش baw 5 GFR
#تنكى متوسط وابران م
: افزایش oy GFR
ناشی از افزایش فشار هیدروستاتیک
: شدید وابران x
از افزایش cb GFR
اسمزی کلوئیدی
صفحه 52:
Ow
© Increased Glomerular Capillary Colloid Osmotic Pressure
Decreases GFR
صفحه 53:
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صفحه 54:
out 60 mm under normal conditions. Changes in
glomerular hydrostatic pressure serve as the primary means for
physiologic regulation of GFR. Increases in glomerular hydrostatic
pressure raise GFR, whereas decreases in glomerular hydrostatic
pressure reduce GFR.
e مت یت hydrostatic pressure has been estimated to
© Glomerular hydrostatic pressure is determined by three variables,
each of which is under physiologic control: (1) arterial pressure, (2)
afferent arteriolar resistance, and (3) efferent arteriolar resistance.
صفحه 55:
ا -
Factors That Can Decrease the Glomerular Filtration Rate
Physiologic/Pathophysiologic Causes
Renal disease, diabetes mellitus,
hypertension
Urinary tract obstruction (e.g... kidney
stones)
4 Renal blood flow, increased plasma
proteins
4 Arterial pressure (has only small effect
due to autoregulation)
4 Angiotensin II (drugs that block
angiotensin II formation)
T Sympathetic activity, vasoconstrictor
hormones (e.g. norepinephrine,
endothelin)
R
(GFR)
Physical Determinants*
LK) >1GFR
1 ل + و۲ 6
176 كه ل
ل ل ع وم ل
مج مه 1
LRE > LPG
TR»A> IPG
* Opposite changes in the determinants usually increase
K,, glomerular filtration coetficient: P,, Bowman's capsule hydrostatic pres-
sure; X;, glomerular capillary colloid csmotic pressure; Po, glomerular capil-
lary hydrostatic pressure:A,. systemic arterial pressure: R,. efferent arteriolar
resistance; R afferent arteriolar resistance.
صفحه 56:
© Renal Blood Flow
®Ina و man, the combined blood flow through both kidneys
is about 1100 ml/min (22 % of the CO).
Considering the fact that the two kidneys constitute only about
0.4 % of the TBW, one can readily see that they receive an
extremely high blood flow compared with other organs.
Aims of the highly BF :
© Supplies nutrients and removes waste products
© The purpose of this additional flow is to supply enough plasma
for the high rates of glomerular filtration that are necessary for
precise regulation of body fluid volumes and solute
concentrations.
As might be expected, the mechanisms that regulate renal blood
flow are closely linked to the control of GFR and the excretory
functions of the kidneys.
صفحه 57:
© The kidneys oxygen consumption=2 times of
brain
© Thus, the oxygen delivered to the kidneys far
exceeds their metabolic needs
© A large fraction of the oxygen consumed by the
kidneys is related to the high rate of active
sodium reabsorption by the renal tubules.
© Therefore, renal oxygen consumption varies in
proportion to renal tubular sodium reabsorption,
which in turn is closely related to GFR and the
rate of sodium filtered.
صفحه 58:
‘Sodium reabsorption
(mEq/min per 100 و kidney weight)
10 15 20
5
95
8 86
0
۳
صفحه 59:
© Determinants of Renal Blood Flow
© Renal blood flow is determined by the
pressure gradient across the renal
vasculature (the difference between renal
artery and renal vein hydrostatic pressures),
divided by the total renal vascular resistance:
(Renal artery pressure — Renal vein pressure)
Total renal vascular resistance
صفحه 60:
of the renal
major segments: interlobular arteries, afferent
arterioles, and efferent arterioles.
© Resistance of these vessels is controlled by the
sympathetic nervous system, various hormones, and
local internal renal control mechanisms, as discussed
later.
© An increase in the resistance of any of the vascular
segments of the kidneys tends to reduce the renal
blood flow, whereas a decrease in vascular
resistance increases renal blood flow if renal artery
and renal vein pressures remain constant
صفحه 61:
ough changes in arterial pressure
on renal blood flow,
©The kidneys have effective mechanisms for maintaining
renal blood flow and GFR relatively constant over an
arterial pressure range between 80 and 170 mm Hg, a
process called autoregulation (myogenic and metabolic
regulations).
© This capacity for autoregulation occurs through
mechanisms that are completely intrinsic to the kidneys
صفحه 62:
— = سا _ ۶
© Blood Flow in the Vasa Recta of the
Renal Medulla Is Very Low Compared
with Flow in the Renal Cortex
© Blood flow in the renal medulla
accounts for only 1 to 2 % of the total
renal blood flow.
صفحه 63:
9 Physiologic Control of Glomerular
Filtration and Renal Blood Flow
© The determinants of GFR include
1. the glomerular hydrostatic pressure
2. and the glomerular capillary colloid
osmotic pressure.
These variables, in turn, are influenced by
1. the sympathetic nervous system
2. hormones and autacoids (vasoactive
substances that are released in the
kidneys and act locally)
صفحه 64:
pathetic_Nervo
Decrease
5
Strong activation : constrict the renal arterioles and
1. decrease renal blood flow and 2. GFR.
Moderate or mild has little influence on renal blood
flow and GFR.
Under normal condition, sympathetic tone appears to
have little influence on renal blood flow.
صفحه 65:
. Norepinephrine
. Epinephrine
. Endothelin Constrict Renal Blood Vessels and.
Decrease GFR.
ده تب
NE and Epinephrine (severe hemorrhage)
constrict afferent and efferent arterioles GFR and
ی
RBF
Endothelin (vascular injury, such as toxemia of pregnancy,
acute renal failure, and chronic ro
renal vasoconstriction and GFR
صفحه 66:
aglandins and Brady
Increase GFR.
PGE2 and PGI2 and bradykinin cause
1. Vasodilation
2. increased renal blood flow
3. and GFR
These agents # sympathetic effect
Under stressful conditions, such as volume depletion or after
surgery, the administration of nonsteroidal anti-inflammatory
agents, such as aspirin, that inhibit prostaglandin synthesis
may cause significant reductions in GFR.
صفحه 67:
۱ 6۳8 ۴
صفحه 68:
Autoregulation of GFR and Renal
Blood Flow
Feedback mechanisms intrinsic to the kidneys
normally keep the RBF and GFR relatively
constant, despite marked changes in
arterial blood pressure.
This relative constancy of GFR and renal blood
flow is referred to as autoregulation.
صفحه 69:
1 In the kidneys, the normal blood
flow is much higher than that
required for these functions.
The major function of autoregulation in the
kidneys is to maintain a relatively
constant GFR and to allow precise control
of renal excretion of water and solutes
صفحه 70:
تسه سس
igure 26-16 Autoregulation of renal blood flow and glomerular
filtration rate but lack of autoregulation of urine flow during
changes in renal arterial pressure.
1600 100 ¢
مب 1
مه و ORE
=e 2
se Feral boos fow
38 fae 5
8
5 8
ae
85 م
ge
5 2
50 100 150 200
Arterial pressure
(mm Hg)
a a a دس ی ی ی ار و یس
صفحه 71:
e GFR __ normally remains
autoregulated (that is, remains
relatively constant), despite
considerable arterial pressure
fluctuations that occur during a
person's usual activities (a decrease in arterial
pressure to as low as 75 mm Hg or an increase to as high as
160 mm Hg changes GFR only a few percentage points).
صفحه 72:
nee of =
Preventing Extreme Changes in Renal
Excretion
The autoregulatory mechanisms of the kidney are not
100 per cent perfect, but they do prevent
potentially large changes in GFR and renal
excretion of water and solutes that would
otherwise occur with changes in blood pressure.
صفحه 73:
ormally, GFR is about 180 L/day and tubular
reabsorption is 178.5 L/day, leaving 1.5 L/day of
fluid to be excreted in the urine.
In the absence of autoregulation, a relatively small
increase in blood pressure (from 100 to 125 mm Hg)
would cause a similar 25 per cent increase in GFR
(from about 180 to 225 L/day). If tubular reabsorption
remained _constant_at_178.5 L/day, this would
increase the urine flow to 46.5 L/day
صفحه 74:
ut in reality, such a change in arterial pressure exerts
much less of an effect on urine volume for two reasons:
(1) renal autoregulation prevents large changes in GFR
that would otherwise occur, and
(2) there are additional adaptive mechanisms in the renal
tubules that allow them to increase their reabsorption
rate when GFR rises, a phenomenon referred to as
glomerulotubular balance
صفحه 75:
@ of Tubuloglomerular in
Autoregulation of GFR
© To perform the function of autoregulation, the kidneys have a
feedback mechanism that links changes in NaCl concentration
at the macula densa with the control of renal arteriolar
resistance. This feedback helps ensure a relatively constant
delivery of NaCl to the distal tubule and helps prevent spurious
fluctuations in renal excretion that would otherwise occur.
صفحه 76:
juxtaglomerular com sists
of
1- macula densa cells in the initial portion of the
distal tubule and
2- juxtaglomerular cells in the walls of the
afferent and efferent arterioles.
The macula densa is a specialized group of
epithelial cells in the distal tubules that comes
in close contact with the afferent and efferent
arterioles.
The macula densa cells contain Golgi apparatus, which
are intracellular secretory organelles directed toward
the arterioles, suggesting that these cells may be
secreting a substance toward the arterioles.
صفحه 77:
se a
lation of Afferent Arterioles
Increased Renin Release
and
one ae CO ae تب henge: in
olume ivery to the distal tugule.
flow rate in the logs Henle
reab¥orption NaCl
NaCl at the macula densa cells initiates a
signal from the macula densa that has two effects
صفحه 78:
re.
giotensinogaa=a=> angiot
angiotensin II
Angiotensin II constricts the efferent arterioles,
thereby increasing Pc and returning GFR toward
normal.
صفحه 79:
Glomerular
هه
۳9 ل ‘membrane
tubule
© Elsevier Guyton & Hall: Textbook of Medical Physiology 11¢ - wwvr.studentconsult.com
صفحه 80:
© Elsevier La, Bere ota: Physioloay SE ww. studentconsult.comt
صفحه 81:
fa lee
0
Glomerular hydrostatic 9
تک pressure ~
1
وعه 37
4 Angiotensin it
۱
Etferent Aferent
۸ ۱
resistance resistance
© Elsevier. Guyton & Hall: Textbook of Medical Physiology 11¢ - www.studentconsult.com
صفحه 82:
سح
oa ter
During Renal Hypoperfusion
As discussed earlier, a preferential constrictor action of angio II on
efferent arterioles helps prevent serious reductions in Pc and
GFR when renal perfusion pressure falls below normal. The
administration of drugs that block the formation of angio II
(inhibitors) or that block the action of angio II (angio II
antagonists) causes greater reductions in GFR than usual when
the renal arterial pressure falls below normal. Therefore, an
important complication of using these drugs to treat patients who
have hypertension because of renal artery stenosis (partial
blockage of the renal artery) is a severe decrease in GFR that
can, in some cases, cause acute renal failure.
صفحه 83:
Nevertheless, angiotensin II-blocking drugs can be _ useful
therapeutic agents in many patients with hypertension, congestive
heart failure, and other conditions, as long as they are monitored
to ensure that severe decreases in GFR do not occur.
صفحه 84:
High Protein Intake and Increased Blood Glucose
صفحه 85:
Urinary excretion = Glomerular filtration - Tubular reabsorption
+ Tubular secretion
صفحه 86:
Tubular Reabsorption Is Selective and
Quantitatively Large
Filtration = Glomerular filtration rate* Plasma
concentration
صفحه 87:
Table 2-4
Filtration, Reabsorption, and Excretion Rales of Different Substances by the Kidneys
‘Ament Filtered ‘Amount Reabsortiod ‘Amount Exereted ‘Ye of Filtered Load Reabsorbed
Glucose (gay) ۳ 180 0 ۳
Bicarbonate (mEqiday) 4200 4318 2 5009
Sodium (mEqiday) 25540 اد 1 ous
Chloride (mEqldey] 19.40 19260 8 91
Potassinm (mEday) 156 64 2 11
tea (gia) 468 24 BA 3
Creatinine (giday) 18 1 18 0
صفحه 88:
Peritubular Tubular ۱33 ال
cells ۷ مامه
Lumen
ih oe Peraceltier
ow, ۳ 0
م
Active كو
& Passive
(difusion) Sales
Dsmosie¢— H,0 هد
REABSORPTION مسج
۱
Figure 27-4
Reabsorptian of filtered water and solutes from the tubular humen
across the tabalar epithelial cll through the renal interstitium, and
back into the blood. Solute: are transported through the cells (trans-
cellar route) by passive diffusion or active transport, or betwosn
the cells (paracellular route) by diffusion, Water is transported
through the cells and between the tubular cells by osmosis. Trans-
port of water and soluves from the interstdial uid into the per-
‘ubuler capillaries occurs by ultsaflration (bulk flow).
صفحه 89:
Interstitial Tubular Tubular
fluid cells. lumen,
Co-transport
ay Glucose
Na*
eon,
Amino ai
—_ <>"
-70mV
-
Counter-transport
Figure 27-3
‘Mechanisms of secondary active transport. The upper cell shows the
صفحه 90:
900.
800.
Transport
maximum /Reabsorption
Glucose filtered load, reabsorption
‘or excretion (mg’min)
100.
B00 700 B00 500 400 300 200 100 و
Plasma glucose concentration
تن
Figure 27-4
Relations among the fitered load of glucose. the rate of glucose
reabsorption by tho ronal twbules and the rate of glucose exeration
inthe urine, The ransport main fs the ual ext ut whlch
glucose can be reabsorbed from the tubules. The dhreshold for
iEhicore rofore tothe fltrad load of glucose at which alacose frst
‘opine to be excreted in the urine
صفحه 91:
Substance Transport Maximum
mgimin 375 میاه
Phosphate تاه وله
Sulfate 01.06 mMimin
‘Amino acids 15 m/min
Urate 15 mgimin
Lactate 75 mgmin
Plasma protein 306 متصاعس
Transport Maximums for Substances That fre Actively
Secreted. Substances that are actively secreted also
exhibit transport maximums as follows:
Substan Transport Maximum
Creatinine 16 mpmin
Para-aminchippurie acid 90 mp/min
صفحه 92:
Na* reabsorption
4
HO reabsorption
1 |
Lumen Luminal
Luminal CE
negetive urea
Ares مه ٩ سس
Passive Cr Pastive urea
reabsorption reabsorption
Figure 27-5
Mechenisas by which water, chloride, and urea reabsorption are
coupled with sodiam reabsorption.
صفحه 93:
Collulor ultrastructure and primary troneport charscteristies of the
proximal tubule. The proximal tubules renbsorb about 65 per cent
Of the tltered sedium, chloride, biearbonste, and potassium and
sseontially all the filtered glucore and amino acids, The prosimal
{nibs also secrete organic acids. bases, ané hyclrogen ions into the
tubular lumen,
صفحه 94:
100
Creatinine,
Nav
20 40 6080
% Total proximal tubule length
ابم
plasma concentration
°
صفحه 95:
Loop oP Wee
Thick ascending
Toop of Hone
Collar uluestructure and vansport characteristics of the thin
| oop of Henle (tp) and ie Ihek ascending sexe nt of
the loop of Heute (bo) The descending pat the tia sexe
tthe lop of Heals ily peeneable to water and moderately
Permeable tonto! welts bul her few mitochondria and ite ene
[Stne reorption The thc atcending ly of the lonp of Neale
ب كه بد لي the flier lone sedan باه
nd potest, as well 9 large emis of eae, bieareonats
{nd mngnestum, Ths spre also secretes hysrogen fons imo the
tabular ten
صفحه 96:
Renal حك
intact Tubular
cial all
یوب ۳ 0
=
©
Loop diuretics
Furosemide
*Ethacrynie acid
Bumetanide
مه بو
Mechasiins of nom, chliie, and pansion موه ithe
thick ascending lop of Henle The soda petasism A Pee pam
Inthe howlnter! cll membrane. mantnine 8 (ow toc: ar
featiam conesntatin anda negate eer potent thee
“Tho Iseium, 2 chloride, -potassim c-tansporer i thofeminal
هو vauspocs these eee fom om the tba fale fate
‘hocells sig ho جات هناد fleas by dito of sodium,
میات هه ول xraieat into the cells Solari ale
‘ansportd ot the tua cellby sodium ogen eousterrans
fot. the pontine charge (28 mV) of the tabula hc eae To
frome mt othe interstt!H vate parce pth
صفحه 97:
Renal Tubular
interstitial Tubular humen
‘ie calls tom
Oppronertely G% oP te Phered bed oP 9
te redeorbed i fe Poly - باه 0ك
cid سلطا oo
over رس
Thiazide diuretics:
Figure 27-10
chloride transport in the early dtl tubo موه ام دوس
Sodiun and chloride me transported from the tubular Inner Into
the cell by co-iransporter tt le Inkibited by thlazde diuretics
Sodium ie pumped out of tho eal by socium potassium ATPace and
‘hlorige diffuse nto the interstitial eid va chloride chaanela
صفحه 98:
tubule ما رارمع
صفحه 99:
Mecha
وی
‘mela collating Set Tho mein clletng duce actly
Feabsorb sium and secrete nrogea fons and are permeable ©
‘on hi is oubwotbed la thew tubular sine Ts absorp
ono tern esl cing dt contro he et
‘uation of antidiuretic
صفحه 100:
0 luidiplaema concentration
Proximal
tubule 1 Hone 1 tubule mbit t
Figure 27-44
(Changes in average concentrations of diferent substances at difer-
{ont points nthe tubal system rolative tothe concentration of that
Subance in the psa and inthe glomerular fiat. vakteof 10
Indicates thatthe concentration ofthe subwiance Inthe tuba Bid
{sth same the concentration of that substance inthe plasms,
‘Vales love Li indicate thot the substance = eahsorbed more
avidly Wan ater, whereas valves bv (ince tht he nab
Stance ie reebeorbod ts lssr extent than water orf eerste into
نا
صفحه 101:
Tubular Tubular ی
capillary fuid cells lumen
Wer
۳
Netreabsorption 0
۳ 0
is
Figure 27-15,
Summary of the hydrostatic and colloid osmotic forces that deter-
imine fuid reabsorption by the peritubular capillaries. The aumeri=
cal values shown are estimates of the normal values for humans. The
net reabsomptive pressure is normally about 10 mm Hg. causing fluid
and sohutes to be reabsorbed into the peritubular capillaries as they
fare trarsported across the ronal tubular calls. ATP. adonosins
iphospliate; P,, peritubular capillary Lydrostatie pressure; Py inter
stitial fluid hydrostatic pressare: ™, peritubular capillary colloid
osmotic pressure: My. interstitial uid colloid osmotic pressure,
صفحه 102:
Factors That Can Influence Peritubular Capillary
Reabsorption
TP. 4 Reabsorption
۰۱ رز
۰ 1ج 1 زا
۱
T دیع T Reabsorption
Tmotn
1ب ۲۲۲ و
TK, > T Reabsorption
۳: peritubular capillary hydrostatic pressure: Ra and Re, afferent and elfer-
ent arteriolar resistances, respectively: يج peritubular capillary colloid osmotic
pressure; Xa, arterial plasma colloid osmotic pressure; FF, filtration traction;
K,, peritubular capillary filtration coetticient,
صفحه 103:
incensed دب
‘backloak >
صفحه 104:
Normal
0
‘tas cals
“Fiure 27-16,
sora sonditins ep) and during doctewsal porta ری
‘Sronini Searhces oo
اس سا te ز
صفحه 105:
تا
1 NaCl, HAO reabsorption, 1 K”soeretion
1 NaC. HO reabsorption, THY secretion
70 reabsorption
4 NaCl reabsorption
4 PO; reabsorption, T Co” reabsorption
| Table 27-3
Hormones that Regulate Tabular Reabsorption
Hormone Sito of Aetion
Aldosterone Collccting tubule ond duct
‘Angiotensin IL Proximal tubule. tick ascending leop of Henleldistal
‘ubuk, collecting tubule
Antidiuretie hormone Distal mbule/colleeting tubule and duct
‘Atrial natriuretic peptide Distal tubulo‘colecting tubule and éuct
Parathyroid hormone Proximal tubule, thick ascending loop of
‘enleldistal tubule
صفحه 106:
Praia = 1 09۱
Amount filtered = Amount excreted
GFR X Prin = Ulin XV
۷ نا
GFR = in XY
3
6۳8 - 125 ۷
Unuiin < 125 ۳9۷۷
۷۰۱ ملام
© Elsevier. Guyton & Hall: Textbook of Medical Physiology 11e - www.studentconsult.com
صفحه 107:
Sorum creatinine
concentration (mg/dl)
Creatinine production and
Tena excretion (g/day)
© Elsevier, Guyton & Hall: Textbook of Madical Physiology 116 - www.studentconsult.com
صفحه 108:
او 5.86 > بيرجلا
۱ ۶ ۷
Elsevier. Guyton & Hall: Textbook of Medical Physiology 11e - www.studentconsult.com ©
صفحه 109:
&
>
5
8
4
8
5
1
a
60
GFR (mL/min)
{© Else, Cao: Esoi'sIntzaratad Physiology - wr. sadentconsult com
صفحه 110:
سا
ماه
None
salina
مه
min
oF min ام ولج
nl, evclinin, mg in
موه مه رصم شاوی
Gna SY
۷ سول
Tha
اتسار
Use of Clearance to Quantity Kidney Function
سس
دنا
0
(Clearance rato
سمت دمع
Con
“Enany” (Pn Vesna
Pon
REF
Ror.
T-Hematoe
Excretion ate = Uc
Reabnorption rate Pllered loa - Excretion rate
[ares t)=,2¥)
Excretion ate Flee los
Secretion rte
tem
مه سس
{Gomera ration rato (GER)
سس ratio
renal plasm fw (ERPF) ملسا
‘Rona plasma flow (RPP)
Rona blood ow (RIF)
rate ماما
Reabsoepion rte
suri me corer: Howe pam امو PAE, are لفق لوج مجاه oa aera PA ene Eg PA
تساه six Voy الا یه cmc
صفحه 111:
® Urine
concentration
صفحه 112:
Ow
600 mOsm/day be
7200 mi 1 0.5 L/day
— Usa * V
Com ۳ osm
صفحه 113:
Ow
=V—Com = V — Un XV)
Cio =V Com = VE
Pysn = 2.1 x Plasma sodium concentration
صفحه 114:
NaCl H,0
7
حچست 6000
i
1
© Elsevier. Guyton & Hall: Textbook of Medical Physiology 11e - www.studentconsult.com
صفحه 115:
fia {€) Countercurrent exchange in the vasa recta يميه سا سس لت سيب سا سسا اناري
of ions in his region creates
‘Acne reabecrption|
2
صفحه 116:
(© Hever Guylon& Hal Textbook of Medical Physloloay Le - ww studenkeonsulteom
صفحه 117:
/
-> ورد ایو
medula a
١
۱
1
i
'
1
!
© Elsevier. Guyton & Hall: Textbook of Medical Physioloay 11e - www.studentconsult.com
صفحه 118:
Inner
medulla
FIGURE 38-17 Operation of the vasa recta as
‘countercurrent exchangers in the kidney. NaCl and urea diffuse out
of the ascending limb of the vessel and into the descending limb,
whereas water difluses out of the descending and into the ascending
limb of the vascular loop.
صفحه 119:
۱
‘Vasopressin makes the eotecting act permeable to water.
{ayer manima esopresi, he cotecing ducts reay permeable (eo te absence چا وی ما وهی اه
10 water War leaves Dy osmosis and scarred ay by he vasa Ipereanito water ana ie umes ute
‘cla captarss, Una conoonraou
oe |
امه مود
موه
Vasa recta
900 mom
530530
صفحه 120:
Cross sation at
وی duct
صفحه 121:
Glomerulus
capsule
Proximal 1) Filrate isotonic to plasma
tubule:
a @ Proximal woe eabeorton 900
wy»
@Pe0 veabsorved: NaC! and vba. 1000
Interstitial diffuse in
) SF) fluid osmolarity
300 mOsm —(@) Tight unctions water 400,
impermeable — NaCl acthely
منم
400 0۵0
160 ی
‘impermeable — NaCl actey
reabsorbed
مه مق
مه ام ie ADH. ro
@ aon ator eavsnood
ithe ADH. no wntereaborbed
Oe
Vino ACH, no air eaboatod
© Else Cao: Esoa'sIntearatad Physlloay - won. sudentconsuitcom
صفحه 122:
osmotarty ماه رز
J ADH secretion
(posterior pituitary)
|
J Pasme ADH
|
HO permeatilty in
distal tubules,
collecting ducts
|
‘41,0 reabsorption
|
{ieee
© Elsevier. Guyton & Hall: Textbook of Medical Physioloay 11e - www.studentconsult.com
صفحه 123:
Summary of Tubule Characteristics—Urine Concentration
‘Active Nac Permeabiity
1۳200000. 1۵ 1۵۵ Urea
Proximal tubule + مد +
Thin descending limb 0 بو
‘Thin ascending limb 0 o + +
Thick ascending limb 4 إلى 8 0
Distal tubule ADH 0
Cortical collecting + 4ADH 0 3
‘bul
Inner medullary + الاصهد 00 ADEE
collecting duct
inna lve active tamper permeability; moderate level active
وا ماه مج مه feel of سره سدع
ADH, permeability to walcr or urea inceased by ADH
صفحه 124:
1250
Osmolarity (mOsmiL)
صفحه 125:
صفحه 126:
1
sine
مه
«معنالاة میدوب و شهب سیر مه بسرت اوم ©
صفحه 127:
۳
© Isovolemic osmoiic increase
Pyyp = 1.3 6-017 0
we = 13
40
35
30
25
20
18
10
5
0
171000 هه وه وه
Per cent change
© Elsevier. Guyton & Hall: Textbook of Medical Physioloay 11e - www.studentconsult.com
Plasma ADH (pg/ml)
صفحه 128:
Regulation of ADH Secretion
J Plasma osmolarity
T Blood volume
T Blood pressure
Drugs:
Alcohol
Clonidine (antihypertensive drug)
Haloperidol (dopamine blocker)
Increase ADH
T Plasma osmolarity
4 Blood volume
4 Blood pressure
Nausea
Hypoxia
Drugs:
Morphine
Nicotine
Cyclophosphamide
صفحه 129:
صفحه 130:
152
148
144
140
Plasma sodium concentration (mEq/L)
136
0 30 60 90 120 150 180
‘Sodium intake (mEqj/day)
© Elsevier. Guyton & Hall: Textbook of Medical Physioloay 11e - www.studentconsult.com
صفحه 131:
Decrease Thirst
{ Osmolarity
T Blood volume
T Blood pressure
4 Angiotensin II
Gastric distention
Control of Thirst
Increase Thirst
T Osmolarity
+ Blood volume
{ Blood pressure
Angiotensin
Dryness of mouth
صفحه 132:
© 30 60 90 120 150 180 210
‘Sodium intake (mEq/L)
© Elsevier. Guyton & Hall: Textbook of Medical Physiology 11e - www.studentconsult.com
صفحه 133:
H,0 filtered load =
125 mL/min
© Else, Cao: Esoar'sIntearatad Physiology - won sudentconsuitcom
صفحه 134:
۱
Thin descending Thin ascending
Loop of Henle
{Else Cao: Eso'sIntearatad Physiology - wom. sudantconsultcom
صفحه 135:
Collecting
duct
K+ filtered load = 0.5 mEq/min
Medullary
Thin descending
Loop of Henle
© Else, Cao: Esov'sIntarated Physlloay - wom sudantconsutcom
صفحه 136:
Urea filtered ۱0۵0 - 6 ۵۸
Collecting
Thin descending
Thin ascending
صفحه 137:
اسلام بر خلاف مذاهب دیگری که توجیه کننده ی فقر را مناسبات
زندگی اجتماعی میدانند. بزرگترین آموزش یافته ی مکتبش ابوذر
میگوید: "وقتی فقر وارد خانه ای میشود. دین از درب دیگر خارج میشود"
و یا پیامبر اسلام حضرت محمد (ص) که بنیانگذار مکتبی است که همه
ما مسلمانان به آن اعتقاد راسخ داریم چه شیوا و ساده بیان فرموده است:
"من لا معاش له لا معاد له" کسی که زندگی مادی ندارد زندگی معنوی
aaa
چون؛ شکم خالی هیچ ندارد. جامعه ای که دچار کمبود اقتصادی و مادی
است مسلماً کمبود های معنوی بسیاری خواهد داشت و آنچه را که در
جامعه های فقیر آنرا اخلاق و مذهب می نامند» متاسفانه معنویت در آن
جایی ندارد.
صفحه 138:
© میخواهم بگویم؛ فقر همه جا سر میکشد ...
© فقرء گرسنگی نیست. عریانی هم نیست ...فقر محتی گاهی زیر شمش های طلا خود را پنهان میکند...
© فقر. چیزی را "نداشتن" است ؛ ولی آن چیز پول نیست ؛ طلا و غذا هم نیست .
© فقر. ذهن هارا مبتلا ميكند ...
© فقر ء اعجوبه ايست كه بشكه هاى نفت در عربستان را تا ته سر ميكشد
* فقر» همان گرد و خاکی است که بر کتابهای فروش نرفته ی یک کتابقروشی می نشیند ...
© فقرء تیه های برنده ماشین بازیافت است که روزنامه های برگشتی را خرد میکند .
* فقرء کتیبهی سه هزر ساله ای است که روی آن یلدگاری نوشته اند .-
© فقر. يوست موزی است که از پنجره یک اتومبیل به خیابان انداخته میشود ... فقر . همه جا سر میکشد ...
© فقر. شب را "بی غذا" سر کردن نیست .. فقر :روز را "بی اندیشه" سر کردن است ...
صفحه 139:
Kt intake
100 mEq/day>
Extracellular Intracellular
fluid K* fluid K*
4.2mEqL 140 mEq/L
x14 x28L
59m Eq 3920 mEq
K+ output gz
Urine 92 mEqiday
Feces 8 mEqiday
mEq/day
Figure 29-41
Normal potassium intake, distribution of potassium in the body
fiuids, and potassium output from the body.
صفحه 140:
# تنظیم غلظت پتاسیم. کلسیم و....مایع خارج سلولی
© -غلظت طبيعى يتاسيم يلاسما برابر با ۴/۲ میلی ایکی والان در ليتر
© -افزايش يتاسيم يلاسما منجر به ايست قلبى مى گردد
© توزيع يتاسيم در بخش هاى مختلف به ترتيب ذيل است
108-9896 ©
ECF=2%®
* بنابراین سلول ها می توانند در ایجاد تعادل پتاسیم یعنی هوموستاز آن نقش مهمی داشته باه
© An overflow site for excess ECF potassium during
hyperkalemia
© A resource of potassium during hypokalemia
© Therefore, redistribution of k+ between the intra- and extra-
cellular compartments provides a first line of defense
against changes in ECF potassium concentration
صفحه 141:
فاکتورهای افزایش دهنده جذب سلولی پتاسیم
#انسولین ۰ آلدوسترون. تحریک بتا آدرنریک و آلکالوز
فاکتورهای کاهش دهنده جذب سلولی پتاسیم
# ديابت» آدیسون, بلوک بتا آدرنرژیک ۰ تخریب سلولی (سلول خونی و عضلانی) ۰
ورزش سنگین و افزایش یافتن اسمولاریته خارج سلولی
#س: در صورت عدم وجود مکانیزم های تنظیمی دریافت مقدار ۱۰۰ ملی
ایکی والان پتاسیم چه تاثیری بر پتاسیم پلاسما و عملکرد بدن داشت؟
صفحه 142:
‘and blood pressur ing aldosterone
Secretion, underscoring the integrated functions of the
Fenal and cardiovascular systems. ANG I increases.
bload pressure both directly and indirectly through four
‘ational pathways (Fig, 20-10)
11 ANG i! increases vasopressin secretion. ANG I
receptors in
the hypothalamus initiate this reflex. Fluid retention in
the
kidney under the influence of vasopressin helps
blood volume, thereby maintaining blond pressure
2 ANG I! stimulates thirst. Fluid ingestion is a behavioral
response that expands blood volume and raises blood
pressure,
3 ANG ilis one of the mast potent vasoconstrctors
inown
in humans, Vasoconstriction causes blood pressure to
without a change in blood volume.
4 Activation of ANG It receptors inthe cardiovascular
ccontrot
© center increases sympathetic output tothe heart and
Blood
"© vessels. Sympathetic stimulation increases cardiac
output
‘© and vasoconstriction, both of which increase blood
© pressure,
© 5.ANG I! increases proximal tubule Nareabsorption.
ANGI
‘© stimulates an apical transporter, the Na-Hexchanger
"© (WHE). Sodium reabsorption inthe proximal tubule is
followed
© by water reabsorption, so the net effe
صفحه 143:
صفحه 144:
ااا لس
|Table 20-1
Factors That Can Alter Potassium Distribution Between the
Intra- and Extracellular Fluid
Factors That Shift K° into Cells Factors That Shift K* Out of Cells
(Decrease Extracellular [K"]) (Increase Extracellular (K*])
* Insulin * Insulin deficiency (diabetes
« mellitus)
* B-adrenergic stimulation * Aldosterone deficiency
* Alkalosis (Addison’s disease)
* B-adrenergic blockade
* Acidosis
© Cell lysis
* Strenuous exercise
* Increased extracellular fluid
osmolarity
صفحه 145:
#اختلالات اسید و باز:
#اسیدوز متابولیک منجر به هیپرکالمی
آلکالوز متابولیک منجر به هیپوکالمی
#علل احتمالی هیپرکالمی در اسیدو
پمپ سدیم-پتاسیم
اثیر منفی یون هیدروژن تجمع يافته بر فعالیت
® Acute acidosis: a decrease in potassium secretion
due to Na/K pump inhibition
® Chronic acidosis: an increase in potassium
secretion due to inhibition of reabsorption of water
and sodium in proximal tubule lead to increase
delivery them to distal portions of nephron which
should reabsorb in these segments and also an
increase in GFR.
صفحه 146:
= SSS ۳ مرور
© هر چه مقدار فیلتراسیون گلومرولی بیشتر باشد میزان دفع؟
میزان بازجذب پتاسیم در لوله نزدیک ۶۵ درصد و بخش ضخیم هنله ۲۷ درصد
# ترشح پناسیم که سلول های اصلی متخصص این امر بوده و در حالت طبیعی روزانه ۳۱
میلی اکی والان برابر ۴ درصد از پتاسیم را ترشح می کنند.
® در صورتی که روزانه مقدار دریافت پتاسیم ۱۰۰ میلی اکیوالان باشد کلیه ها باید
حدود AY درصد آن را دفع کنند و از این مقدار ۳۱ درصد در بخش های انتهایی نفرون
جمع آوری می گردد.
-حدود ۸ میلی اکیوالان از طریق مدفوع دفع می گردد.
© کته ٩۰ درصد سلول های توبول دور و مجاری جمع کننده سلول اصلی هستند.
© ترشح پتاسیم بوسیله سلول های اصلی یک فرآیند دو مرحله است
© ١-ورود يتاسيم به سلول از طیق غشا قاعده ای بوسیله پمپ سدیم-چتاسیم
-خروج پتاسیم از سلول های فوق از طریق غشا لومینال
صفحه 147:
Luminal membranes of principal cells are highly permeable
to potassium. They have epithelial potassium channels in this
membrane.
e
© Intercalated cells can reabsorb potassium during potassium
depletion.
© It maybe occurs through K-H ATPase located in the luminal
membrane.
۰
© Key factors stimulate potassium secretion by principal cells
© [K*] بو 2. Aldosterone increment and 3. High flow rate of
tubular fluid
۰
© The most potent releaser of aldosterone is hyperkalemia.
© If potassium concentration increases from 3.5 to 6, plasma
aldosterone levels increase up to 10 times.
صفحه 148:
Control of renal calcium excretion
and calcium ECF concentration
©[Ca].cp=2.4 meq/L
°©50% as ionized or free form
©40%= bound to plasma proteins
©10%=complex with phosphate and citrate.
© Hypocalcemia leads to neuronal hyper-excitability
(Tetany)
۰
© Hypercalcemia leads to decrease neuronal excitability
(Coma)
© Unlike other ions such as sodium, potassium and ..., a
large share of calcium excretion occurs in the feces.
۰
صفحه 149:
Pin
© Day to day regulation of calcium concentration is
mediated in large part by the effect of PTH on
bone resorption
© This hormone
© 1. Stimulate bone resorption
© 2. Activate vitamin D and
© 3. directly increases renal tubular calcium
reabsorption
صفحه 150:
چون کلسیم ترشح نمی گردد بنابراین میزان دفع آن از فرمول ذیل محاسبه می گردد
Renal calcium excretion=Ca filtered-Ca ©
reabsorbed
٩ درصد کلسیم به ترتیب در لوله نزدیک (۶۵» ضخیم هنله (۲۵-۳۰)و لوله دور و جمع
كتنده (20-5) بازتجذب.مى كردق
عوامل افزايش دهنده بازجذب كلسيم
PTH, Hypocalcemia, hypotention,
hyperphostamemia, metabolic acidosis, VitD
#عوامل کاهش دهنده بازجذب کلسیم
عکس موارد فوق
در زمان هیپرتانسیون ی افزایش حجم مایع خارج سلولى به دليل بالا بودن 61718 و
افزایش سرعت مایع توبولی بازجذب؟؟؟؟
صفحه 151:
ار
© توبول هاى كليوى براى بازجذب
نشان می دهند.
هر گاه خی پلاسمایی از :1۸ - میلی مولار بیقتر شود در امرار ظاهر می گرده:
CC (Plasma) 0.8mM 1000©
©125CC(GFR) 0.1mM
این ترکیب کاینیتیک حداکثر اشباع (۰.۱
ن قشک لیدودر دفع ف سفاندارد
#منيزيم
محل بازجذب توبول نزدیک (۳۵) ضخيم هنله (۶۵) و لوله دور درصد
# در شرایط هیپرمنیزمی, هیپرکلسمی و افزایش ECF exe میزان دفع منیزیم
افزايش مى يابد.
صفحه 152:
#مکانیزم های کلیوی کنترل حجم مایع خارج سلولی
8 حجم مایع خارج سلولی به وسیله تعادل بین دریافت آب و نمک تعیین می
گردد.
#دفع سدیم به وسیله دو متغیر 23718-۱) و ۲- میزان بازجذب کنترل می
گردد.
® Sodium excretion= GFR-Reabsorption.
درصورتی که اختلالی هریک از دو متفیر فوق را تحت تاثیر قرار دهد
مکانیزم های بافری وارد عمل می گردد
® Glomerulotubular balance
® Macula densa feedback
صفحه 153:
C— +—_ ک
@ FIGURE QUESTION
Map the cardiovascular
reflex patnway
represented by me@.
صفحه 154:
اهمیت دیورز و ناتریورز فشاری در تنظیم تعادل آب و سدیم
© تعريف ديورز؟
#به اثر فشار خون بر دفع سديم ناتريورز فشارى و بر دفع آب ديورز فشاری
كويند.
#دو يديده فوق مكانيزم هاى فيدبكى كليدى بدن براى تنظيم مايعات بدن و
فشار شريانى مى باشند
افزایش دریافت آب و نمک: افزایش حجم مایع 2617 : افزایش حجم خون:
افزایش میانگین فشار پرشدگی عروقی: افزایش با زگشت وریدی: افزایش برون ده
قلبی: افزایش فشار خون: افزايش *۵1) : دیورز فشاری
# بنابراين تغییرات بزرگ در دریافت مایع و نمک در شرایط فیزیولوژیک تاثیر کمی بر
حجم خون . فشار خون و حجم sable wales ECF
صفحه 155:
bution of ECF be
and plasma
#در صورتى كه مقدار كمى مايع به دليل نوشيدن زياد يا کاهش برون ده کلیوی در
خون تجمع یابد حدود ۲۰-۳۰ درصد آن پس از مدتی به 19۳ وارد شده مابقی در
سیستم عروقی باقی خواهد ماند
ولی اگر میزان تجمع مایع زیاد باشد ۵۰ درصد از آن به 15 وارد می شود که این
مساله باعث ایجاد ادم می گردد ولی از طرفی ورود این بار اضافی به فضاى ميان
بافتی در شرایط تحت Overload 3) o& قلب می کاهد (نقش کاردیوپروتکتیو).
صفحه 156:
‘and hormonal mechanism:
with the pressure natriuresis and pressure diuresis,
making them more effective in minimizing the changes in
blood volume, ECF volume and arterial pressure that occur
in response to day-to-day challenges.
کنترل دفع کلیوی: رفلکس گیرنده بارورسپتو شریانی و گیرنده حجمی
Hemorrhage: a decrease in pressure of pulmonary blood
vessel: activation of sympathetic system leads to
Vasoconstricing the afferent arteriole 1
2decrease GFR
Activation of RAS 3
4And ultimately increase tubular reabsorption (water and
salt)
صفحه 157:
افزایش تكلا"نا باتولوزيى ۸00102 تاثیر قابل ملاح
ظ ندارد زیر
افزایش آنژیو۲: احتباس آب و سدیم توسط کلیه ها: افزايش حجم 3۳ :
افزایش 13 : دیورز و ناتریورز فشاری: تصحیح حجم خارج سلولی.
آلدوسترون نیز با بازجذب سدیم منجر به احتباس آب و سدیم و دفع پتاسیم می گردد.
فرار آلدوسترونی:
# در صورت انفیوژن آلدوسترون یا تومور غده فوق کلیه (سندرم كن ) افزايش بازجذ
توبولی سدیم و کاهش دفع ادراری آن گذرا خواهد بود. زیر:
یک تا سه روز پس از احتباس آب و سدیم: افزایش حجم "3.623 به میزان ۱۰-۱۵
درصد: افزايش هم زمان 13۳ : دیورز فشاری (در اين زمان کلیه ها از احتباس آب و
نمک فرار کرده و از آن پس مقادیر ورودی با خروجی برابر خواهد بود)
* فقدان آلدوسترون یا کاهش يافتن ترشح آن: افت شدید حجم ۳6/۳
The most important role of aldosterone is to ©
maintain the volume of ECF
صفحه 158:
ترشح ADH تاثير اندکی بر حجم BP , ECF دارد.
افزايش ](۸1 نیز تاثیر اندکی بر بر حجم 30/۳ و 3 دارد که به دلیل
ایجاد دیورز فشاری می باشد.
#ولى افزايش 21011 می تواند منجر به هیپوناترمی گردد (هم رقیق شدن سطح
پلاسمایی سدیم به دلیل افزایش بازجذب آب و هم ایجاد دیورز فشاری)
صفحه 159:
FIGURE 40-1 Secretion of acid by proximal tubular cells in
the kidney. H* is transported into the tubular lumen by an antiport in
exchange for Na*. Active transport by Na, K ATPase is indicated by ar-
rows in the circle. Dashed arrows indicate diffusion.
صفحه 160:
Regulation of Acid-Base
Balance
صفحه 161:
FIGURE 40-2 Feat crates audi ange
{orl Top fabio iteedeiatortn CO, Mae:
ای ره 0غ
۱ ا
صفحه 162:
خب + ولا هس ربا
Catarina SUS مدای NH?
Glutamic
واوتهاناوماهكاه امعط نامدا مسسنتخ + ۱
FIGURE 40-3 Major reactions involved in ammonia
production in the kidneys.
صفحه 163:
FIGURE 29-5 summary دوع و فصو اوه 99اه ۱۵ mutate of akostroesertion by angetanshl Ths ps
maronsreatonctenn itera Ineingsaphirereio-ar yore yan; tease ده إن م ngee a ٠
تخاس
صفحه 164:
Definitions :
Acids : Molecules can release hydrogen ions in solutions
(HCl & H2CO3)
Bases : A base is an ion or a molecule that can accept an H+.
For example, HCO3 & HPO4
The proteins in the body also function as bases, because some
of the amino acids that make up proteins have net negative
charges that readily accept H+. The protein hemoglobin in
the RBCs and proteins in the other cells of the body are
among the most important of the body’s bases.
صفحه 165:
1فرار : اسیدهائی که Wo توانند توسط ریه ها دفع شوند
(4112003
2) غیرفرار : به طور عمده توسط متابولیسم پروتئین ها
تولید می شوند و نمی توانند توسط ریه ها دفع شوند
بدن روزانه حدود 80 10۳76 اسید غیرفرار تولید می کند
(از متابولیسم پروتئین ها که فقط توسط کلیه ها باید دفع
دد
صفحه 166:
synonymously
An alkali is a molecule formed by the combination
of one or more of the alkaline metals—sodium,
potassium, lithium, and so forth—with a highly
basic ion such as a hydroxyl ion (OH-).
The base portion of these molecules reacts quickly
with H+ to remove it from solution; they are,
therefore, typical bases. For similar reasons, the
term alkalosis refers to excess removal of H+
from the body fluids, in contrast to the excess
addition of H+, which is referred to as acidosis.
Alkalosis pH>7.4, Acidosis pH<7.4
صفحه 167:
rong and
A strong acid is one that rapidly dissociates and releases
especially large amounts of H+ in solution (HCl).
Weak acids ............ H2CO3
A strong base is one that reacts rapidly and strongly with
H+ and, therefore, quickly removes these from a solution
(example is OH-, which reacts with H+ to form water
(H20)
A typical weak base is HCO3 because it binds with H+ much
more weakly than does OH-
Most of the acids and bases in the ECF that are involved in
normal acid-base regulation are weak acids and bases
صفحه 168:
Buffer systems do not eliminate H+ from or add them to the
body but only keep them tied up until balance can be
reestablished.
1. Chemical B. : a few seconds
2. Respiratory B. system : a few minutes (acts within a few minutes
to eliminate CO2 and, therefore, H2CO3 from the body).
3. Kidneys B. (a few hours to days) : can eliminate the excess
acid or base from the body, the strongest system.
H ions origin :
In the body : 0.00004 mEq/L (40 nEq/L).
Produced during or ingested : 80 mEq/day
(Without buffering, the daily production and ingestion of acids
would cause huge changes in body fluid H+ concentration)
صفحه 169:
pH and H* Concentration of Body Fluids
pH
7.40
7.35
7.35
6.0 to 7.4
45 to 8.0
08
Ht Concentration (mEq/L)
40x10
45x 10"
45x10"
1x 10 to 4x 10°
3x 107 to 1x 10%
160
Extracellular fluid
Arterial blood
Venous blood
Interstitial fluid
Intracellular fluid
Urine
Gastric HCl
صفحه 170:
1
۳
For example, the normal ]111[ is 40nEq/L
(0.00000004 Eq/L). Therefore, the normal pH is
pH =-log [0.00000004]
pH=7.4
=-log[H"]
pH =log
صفحه 171:
Buffering of Hydrogen Ions in the Body
Fluids
A buffer is any substance that can reversibly
bind H+.
The general form of the buffering reaction is
Buffer +H* <——~ H Buffer
صفحه 172:
(Puvtors thot detercoicates the ubiliy oP buPPer systesw
Cd.0CQ spstew
سدس امج دومج لو S.QuPPer
اه بر موی جر خأن جصتدانيج 8), 9
اد
صفحه 173:
Bicarb
The bicarbonate buffer system consists of a water solution
that contains two ingredients:
(1) a weak acid, H2CO3, and
(2) a bicarbonate salt, such as NaHCO3.
H2CO3 is formed in the body by the reaction of CO2 with
H20.
0
002 + H20*— 3
H2CO3 ۲1+ + 37
Carbonic anhydrase is especially abundant in the walls of the lung
alveoli, where CO2 is released & also present in the epithelial cells
of the renal tubules, where CO2 reacts with H20 to form H2CO3.
صفحه 174:
HCO; ~~ ۲۲۳ +۲
۷ص :1:۱0 سح 60:11:0
لاك
۹
Nat
صفحه 175:
bicarbonate buffer solution, the increased H+
released from the acid (HCl H + Cl) is buffered
by HCO3
O¢vLCOD => Oui + 09 + الراك
As a result, more H2CO3 is formed, causing increased CO2 and
H20 production
صفحه 176:
with H2CO3 to foun additional HCO3.
Thus, the weak base NaHCO3 replaces the strong base
NaOH. At the same time, the concentration of H2CO3
decreases (because reacts with NaOH), causing more CO2
to combine with H20 to replace the H2CO3
NaOH + H,CO; —> NaHCO, + HO
The net result, therefore, is a tendency for the CO2 levels in
the blood to decrease, but the decreased CO2 in the blood
inhibits respiration and decreases the rateof CO2
expiration.The rise in blood HCO3 that occurs is
compensated for by increased renal excretion of HCO3
صفحه 177:
100
75
‘added احج
Heo,
Per cant of buffer in form of
50
25
وت
pK
H,CO, and CO,
ام
سس Acid adie هس
er cent of buffer i form of
8
Figure 30-4
Tiration curve for bicarbonate butfer system showing the pH of
extraceluer fLid when the percentages of fufler in the form of
HCO, “and CO, (or H.C.) are اه
صفحه 178:
Bicarbonate Buffer System
1. PK=6.1
2. Concentration of ingredients regulates by
kidneys and respiratory system
Thus, Bicarbonate Buffer System is the most
important and strongest system in ECF
صفحه 179:
“Phosphate Buffer System ——
1. The phosphate buffer system is not important
as an ECF buffer
2. It plays a major role in buffering renal tubular
fluid and ICF
3. The main elements of the phosphate buffer
system are H2PO4 and HPO4
۳۱۳۵ ۳۱۳0۵
صفحه 180:
“When a strong سس سس 5
mixture of these two substances, the hydrogen
is accepted by the base HPO4 and converted to
H2P04
HCl + Na;sHPO, —> NaH>PO, + NaCl
When a strong base, such as NaOH, is added to
the buffer system, the OH is buffered by the
H2PO4to form additional amounts of HPO4 +
H’ NaOH + NaH.PO, —> NaHPO, + HO
صفحه 181:
1. pK = 6.8 which is not far from the normal pH = 7.4 in the body fluids
2. Its concentration in the ECF is low (about 8 % of the
concentration of the bicarbonate buffer)
In contrast to its rather insignificant role as an extracellular buffer
, the phosphate buffer is especially important in the tubular fluids of the kidneys
and intracellular fluid
1. It usually becomes greatly concentrated in the tubules
2. the tubular fluid usually has a considerably lower pH than
the ECF does, bringing the operating range of the buffer closer to the pK (6.8)
of the system
3.The concentration of phosphate in this fluid (ICF) is many times that in the
ECF
4.. Also, the pH of intracellular fluid is < that of ECF and therefore is
usually closer to the pK of the phosphate buffer system compared with the ECF.
صفحه 182:
roteins: I 5
Buffers
Proteins are among the most plentiful buffers in the body because of their
high concentrations, especially within the cells.
The pH of the cells, although slightly < in the ECF, nevertheless changes
approximately in proportion to ECF pH changes.
There is a slight amount of diffusion of H+ and HCO3 through the cell
membrane, although these ions require several hours to come to
equilibrium with the extracellular fluid, except for rapid equilibrium that
occurs in the red blood cells.
C02, however, can rapidly diffuse through all the cell membranes. This
diffusion of the elements of the bicarbonate buffer system causes the pH in
intracellular fluid to change when there are changes in extracellular pH.
For this reason, the buffer systems within the cells help prevent changes in
the pH of ECF but may take several hours to
become maximally effective.
صفحه 183:
buffer, as follows:
H* + Hb —— HHb
Approximately 60 to 70 % of the total chemical
buffering of the body fluids is inside the cells, and
most of this results from the intracellular proteins.
In addition to the high concentration of proteins in
the cells, another factor that contributes to their
buffering power is the fact that the pKs of many
of these protein systems are fairly close to
7.4.
صفحه 184:
tory Re
The second line of defense against acid-base disturbances is
control of ECF CO2 concentration by the lungs.
t Ventilarom—>f co, 2۳۳۳
[E+] مین
كت حت
Ventilation CO, Elimination
مین ۱۳1۹1
صفحه 185:
Agents that determine the concentration of CO2
1. metabolic formation rate
2. pulmonary ventilation.
Increasing alveolar ventilation to about twice normal
raises the pH of the ECF by about 0.23 (PH 7.4
7.63) محر
reducing the ventilation to one fourth normal reduces
the pH to 6.95.
صفحه 186:
25
05 10 15 20
Rate of alveolar ventilation
(normal = 1)
668
52
Lit
in body fluids
°
1
0.13 ع
O24
pH change
bb
S28
صفحه 187:
70 71
Alveolar ventilation (normal
72,73 74 75 76
pH of arterial blood
Ena
Effect of blood pH on the rete of alveolar ventilation,
صفحه 188:
اس 5 _
و6 كص ج02) م19 مسل را ۶و اون
T{H*] > TAlveolar ventilation
کارآنی کننرل تنقسن غلظت بون هبدروژن :
کنترل تنفسی کاملا قادر به برگرداندن ۲ به میزان طبیعی نیست یعنی اینکه
موثر بودن این سیستم به میزان 50 تا 75 درصد است.
به عنوان مثال قادر است 2 با" را به میزان 0/2 تا 0/3 ارتقاء دهد یعنی رج
رصح
صفحه 189:
بافرهای شیمیائی بدن
Buffer potency comparison
respiratory system >> chemical
system
قدرت بافری سیستم تنفسی یک تا دو برابر بیشتر از قدرت
بافری تمام بافرهای دیگر موجود در "120۳ است
صفحه 190:
کلیه ها با تغيير دادن 253 ادرار, 213 مایعات خارج سلولی را
تنظیم می کنند
در شرایط اسیدوز
دفع ادرار اسیدی : بازجذب بیشتر ۲1003 و ترشح بیشتر یون ۲1
در شرایط آلکالوز
دفع ادرار بازی : بازجذب کمتر ۲1003 و کاهش ترشح پون 1
صفحه 191:
1)ترشح یون های هیدروژن
2 با زجذب یون های بیکربنات فیلتره شده
3)تولید یون های بیکربنات جدید
صفحه 192:
78 0
Rosbeoration of bicarbonate in differ
feni segmenis of te tenal tubule, The
percentages of the tered losd of
Bicarbonate absorbed by the various
lubuiar segments ste shown, as wel
faethe numbsr of millecuvalente
Feebsoibed per day under nommal
condivons,
85%
(2672 mEqiéay)
4320 mEqiday
10%
(492 mE lay)
وود
رت
رلا وعد م
صفحه 193:
onal Tubular
oral “Tubular cells timer
fat Na+ HCO,
هيا + يمع
Calla mechanisms for (1) acne secretion hydrogen ins ito
the renal ube ©) buat ressasrpion cr Hicabenate fe by
combination van hydrogen ns term carbons acid uth c
fecintes erm cotbon douse snd wate and (3) sod um fon
‘eahcerion in exchange for hyciogen ions secreted. Th pater
دی مارا تسده مامت مط موش tubule Wide
مرسمه segment ofthe lop ol Henle, and the earl, dal
iba
صفحه 194:
Rona! “Tubular
عم مهن از
ع
Primary acive sectetion of fyctogen ions theuah the lumina
‘membrane ofthe hetcalted epthelaloele of te Ine dat and
Soieeing ules Nets that ane Hleabona an :د مسا ج
‘ach halogen kn secreted and « chixide ion is. pecoively
Secreted slong withthe hydrogen ion
صفحه 195:
O.LCOF ard WOPOFP bevowe cvareuirated io the tubular Puid bemouse oF their retaively
poor جومم سر
©. جما له اوه له ure te ski acide, ood the utc pL t& crar he AK = 0.0
oP the phosphdte buPPer systew.
wherever بلا" جد seoreted tity te tuber keoed oowbker wi ober voter tar LOO9, te
wet PP Pent i addiica oP a eu/LOO9 te the bbod.
صفحه 196:
Renal Tubular
interstitial Tubular cells lumen
fluid Na*+NaHPO,-
Nat “oO.
H+ NaHPO,-
==-HCO,-+ Ht
H,CO, NaH,PO,
Carbonic
anhydrase |
از
3
co,
Figure 30-7
Buffering of secreted hydrogen ions by filtered phosphate
(NaHPO,). Note that a new bicarbonate ion is returned to the
blood for each NaHPO,; that reacts with a secreted hydrogen ion
صفحه 197:
Under normal conditions, much of the filtered
phosphate is reabsorbed, and only about 30 to 40
mEq/day is available for buffering H+. Therefore,
much of the buffering of excess H+ in the tubular
fluid in acidosis occurs through the ammonia
buffer system.
صفحه 198:
۱0۵۳ 0۲ ۴۱6655 ۷۲00
Generation of New Bicarbonate by the
Ammonia Buffer System
A second buffer system in the tubular fluid that is even more
important quantitatively than the phosphate buffer system is
composed of ammonia (NH3) and the ammonium ion (NH4).
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 proximal tubules, thick ascending limb of
the loop of Henle, and distal tubules (Figure 30-8).
Once inside the cell, each molecule of glutamine is metabolized in a
series of reactions to ultimately form two NH4 and two HCO3.
The HCO3 generated by this process constitutes new
bicarbonate.
صفحه 199:
Tubular =
lumen
Renal
interstitial
fluid
Proximal
tubular cells
Glutamine ——————_ Guta
~€---2HCO,- 2NH,* |
“ON cr
Na+ Nat
Figure 30-8
Production and secretion of ammonium ion (NH,*) by proximal
tubular cells. Glutamine is metabolized in the cell, yielding NH,*
and bicarbonate. The NH,° is secreted into the lumen by a
sodium-NH,* pump. For each glutamine molecule metabolized,
two NH." are produced and secreted and two HCO, are returned
to the blood.
صفحه 200:
The addition of NH4 to the tubular fluids occurs
through a different mechanism (Figure 30-9).
Here, H is secreted by the tubular membrane
into the lumen, where it combines with NH3 to
form NH4, which is then excreted. The
collecting ducts are permeable to NH3, which
can easily diffuse into the tubular lumen.
However, the luminal membrane of this part of
the tubules is much less permeable to NH4;
therefore, once the H has reacted with NH3 to
form NH4, the NH4 is trapped in the tubular
lumen and eliminated in the urine.
For each NH4 excreted, a new HCO3 is
generated and added to the blood.
صفحه 201:
Renal Tubular —_
Collecting ۱ نس
a tubular cells lumen
cr
دس ۱60+ ۴
H,CO,
Carbonic NH,*+ Cr
anhydrase
0 0
+
co,
Figure 30-9
Buffering of hydrogen ion secretion by ammonia (NH.) in the col-
lecting tubules. Ammonia diffuses into the tubular lumen. where it
reacts with secreted hydrogen ions to form NH,*, which is then
excreted. For each NH,' excreted, a new HCO, is formed in the
tubular cells and returned to the blood
صفحه 202:
One of the most important features of the renal
ammonium-ammonia buffer system is that it is
subject to physiologic control.
t ۱۳۲۱ عع = t stimulates renal glutamine
t كك
formation of NH4 New HCO3 to be used
in H buffering;
A decrease in H+ concentration has the opposite effect.
صفحه 203:
لس وه طولب(
۳۲۶ له موه عل روا مه بل خاب امجمه systew uovouts Por
bout SO per cect of the uid excreted und GO per cect oP the ce
WOOO yeuersied by the عولط
وله سا
0 و Dhe rote oP OWE excretivg co reuse 7 os work
wEqday. Therefore, wi chrooic uctdosis, the dowiccdt weckodisc by
whic acid is elevated is excretioa oP OWE.
This usv provides the wost ispportiat weohodisw Por yeurrotiggy سوه
۱ dura chrouir uvidosis.
صفحه 204:
Factors That Increase or Decrease H* Secretion and HCO;
Reabsorption by the Renal Tubules
Increase H* Secretion and Decrease H* Secretion and
HCO; Reabsorption HCO, Reabsorption
T Pcoz 4 Pco;
11 HCO; LH’, T HCO:
4 Extracellular fluid volume T Extracellular fluid volume
7 Angiotensin II 4 Angiotensin I
7 Aldosterone 4 Aldosterone
Hypokalemia Hyperkalemia
صفحه 205:
Characteristics of Primary Acid-Base Disturbances
pH HY Pco, HCO,”
Normal 7.4 40mEq/L 40mmHg 24 mEq/L.
Respiratory acidosis 1 ٩ 11 1
Respiratory alkalosis T 1 dW L
Metabolic acidosis L of 4 dw
Metabolic alkalosis oT J 1 11
‘The primary event is indicated by the double arrows (17 or 11). Note that
respiratory acid-base disorders are initiated by an increase or decrease in
PCO, whereas metabolic disorders are initiated by an increase or decrease in
HCO.
صفحه 206:
كً ———
=a
TA pH? I 274
aed i is mn Hg stat fat <40 mia wat
سس تست ۳ امد con
HCO, HCO,
الو 2 و0 oad a Hg 4
Analysis of simple acid-base disorders, If the compensatory
responses are markedly different from those shown at the bottom
of the figure, one should suspect a mixed acid-base disorder.
صفحه 207:
| © 79 50 0 انر
i Ha) ی
eid-bae9 nomogran. showing
‘teal blood pl avail pl
HOO" “and Poo. values. The
Cantal open ciclo’ shove tho
Spprocmate is for ده تاد
Status In normal people. The
Shae! ena in the nemaqea
Show the epprouats mits
lasma [HCO] mE!)
با و ۵ ۵ 9 ۶ ۵ ۵ ٩ 8
Arterial
hone for the ‘norma, compensations:
respiratory bused by simple melnbalic and
falas Pl (mmHg) Foepratery dserdete For vate
areas, نهاك ددن لكات ورا
شاه suspect amie رده
2 0 7 0 |
‘terial blood oH Cogan MG, Recter Fe dr Asie
gee Dsorders nthe Richey ro
3. Phiacepis. NB. Saunders,
1365)
صفحه 208:
Table ata
Metabolle Acidosis Assoelaed with Normal or Iereased
Plasma anion Gap
Ineease fon Gap ‘Honma Anion Gap
(tormoeoromia) تسس
Diabetes malin: (Ketaedosis)Diarrhou
ste aides Renal tabular acidosis
(Chronic ena ite ها مس رل لت
رقم نوالسوهاه مریم Adow's elsease
Métharel posoning
Etiylene shoe! pesoning