Renal-2015 by dr sha..

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Transcript Renal-2015 by dr sha..

RENAL PHYSIOLOGY
DR SYED SHAHID HABIB
MBBS DSDM FCPS
Associate Professor
Dept. of Physiology
College of Medicine & KKUH
Renal Physiology
1)
2)
3)
4)
5)
Introduction
Glomerular Filtration
Tubular Processing
Urine Concentrating Mechanism
Micturition
RENAL PHYSIOLOGY
TUBULAR PROCESSING
TUBULAR
REABSORPTION &
SECRETION
URINE COMPOSITION
pH
usually acidic (pH 6)
range= 4.8 - 7.5
Colour
Volume
Bright Yellow &
transparent
1 - 2 L per day
Glucose
None
REABSORTION PATHWAYS
inulin
urea
gluc
Creat
Urinary Excretion Rate = Filtration Rate – Reabsorption Rate + Secretion Rate
% of Filtered Load
Reabsorbed
Glucose (g/day)
Urea
Glucose
Bicarbonate (mEq/day)
Sodium (mEq/day)
Chloride (mEq/day)
Potassium (mEq/day)
Urea (g/day)
Creatinine (g/day)
100
>99.9
99.4
99.1
87.8
50
0
PROXIMAL CONVOLUTED TUBULE
•
•
•
•
many mitochondria
brush border
tight junctions
lateral intercellular spaces.
GLUCOSE AND AMINO ACID
REABSORPTION IN NEPHRON
TUBULAR TRANSPORT
MAXIMUM
• The Maximum limit/rate at which a
solute can be transported across
the tubular cells of kidneys is
called
TUBULAR
TRANSPORT
MAXIMUM
Tm for Glucose is 375 mg/min
GLUCOSE REABSORPTION
Transport max
375 mg/min
Renal Threshold
200mg/dl
•FBG=60-110 mg/dl
•RBG=110-200 mg/dl
HYDROGEN
•Secreted in
Proximal Tubule
and LOH by
Counter
Transport with
Na
Na-H COUNTER
TRANSPORT
Luminal Membrane
PCT & LOH
PCT
Cotransport
Cotransport
Na
G
Na
AA
water
Reabsoprtion
65%
Na
Na
H+
Countertransport
ATP
K
Cl-
SODIUM HANDLING
Na+ moves by co transport or
exchange from the tubular lumen
into tubular epithelial cells
From cells into interstitium it
moves by primary active transport
In DCT and CT it is under
hormonal control
SODIUM HANDLING
Renal tubular reabsorption
Solute reaborption in the proximal
tubule is isosmotic (water follows solute
osmotically and tubular fluid osmolality
remains similar to that of plasma).
65% of water and sodium reabsorption
occurs in the proximal tubule
 100% of glucose & amino acids
Proximal tubules: coarse adjustment
Distal tubules: fine adjustment
(hormonal control).
THIN LOOP OF HENLE
• few mitochondria
• flattened with few microvilli
THIN DESCENDING LOOP OF HENLE
• few mitochondria
• flattened with few microvilli
Solutes
H2O
THICK ASCENDING LOOP OF HANLE
AND EARLY DCT
Many mitochondria and microvilli, but fewer than in the proximal tubule
ASCENDING LOOP OF HENLE
Many mitochondria and microvilli, but fewer than in the proximal tubule
Solutes
H2O
ECF
Epithelial Cells
Events in
Thick
ALOH
Sodium potassium 2 chloride co transport
Lumen
Absorption through loop of Henle:
Descending limb: is water permeable and allow absorption of 15% of
filtered H2O. It is impermeable to Na-CL.
Thin ascending limb: is impermeable to H2O, but permeable to Na-Cl,
where they are absorbed passively in this part .
Thick ascending limb: is impermeable to H2O.
Na-K-2Cl co-transport occur in this part (25% of Na).
ASCENDING LOOP OF HENLE
Na-H COUNTER
TRANSPORT
Luminal Membrane
HYDROGEN
•Secreted in
Proximal Tubule
and LOH by
Counter
Transport with
Na
PCT & LOH
LATE DCT AND CORTICAL COLLECTING
DUCT
• Mitochondria and microvilli decrease.
• Principal Cells (Na Abs and ADH related Water abs)
• Intercalated Cells (Acid Sec and HCO3 Transport)
DCT AND COLLECTING DUCT
I Cell
P Cell
•Principal Cells (Water reabsortion)
•Intercalated Cells (Acid Secretion)
Events
in
DCT
Intercalated cell
Events in
DCT & CT
Aldosterone
Events in
DCT & CT
Principal Cell
Distal convoluted tubule and
collecting ducts
• What happens here depends on hormonal
control:
• Aldosterone affects Na+ and K+
• ADH – facultative water reabsorption
FACTORS AFFECTING ADH
Increase ADH
↑Osmolarity
↓ Blood volume
↓ Blood pressure
Decrease ADH
↓Osmolarity
↑ Blood volume
↑ Blood pressure
Clinical applications
• Thiazide diuretics
• Loop diuretics:
• K+ sparring diuretics:
MEDULLARY COLLECTING DUCT
REABSORPTION OF WATER IN
DIFFERENT SEGMENTS OF TUBULES
PART OF NEPHRON
Proximal tubules
PERCENTAGE
REABSORBED
65
Loop of Henle
15
Distal tubules
10
Collecting ducts
9.2
Passing into urine
0.8
RENAL PHYSIOLOGY
TUBULAR SECRETION
DR SYED SHAHID HABIB
MBBS, FCPS
TUBULAR SECRETION
• Tubular Secretion may be by Passive or
Active Mechanisms
• The most important secretory
processes are for H, K and Organic
Ions
HYDROGEN
• Secreted in Proximal Tubule by
Counter Transport with Na
• In DCT and CT it is secreted by
Hydrogen ATP ase
• When body fluids are more acidic H
secretory process is accelerated and
Vice Versa
HYDROGEN
•Secreted in
Proximal Tubule
and LOH by
Counter
Transport with
Na
•Secreted in DCT
by H ATP ase
Primary Active
Transport
Na-H COUNTER
TRANSPORT
Luminal Membrane
PCT & LOH
I Cell in DCT
RENAL PHYSIOLOGY
COUNTER CURRENT
MECHANISM
COUNTER CURRENT
MECHANISM
• KIDNEYS HAVE
– MECHANISMS FOR EXCRETING
EXCESS WATER
– MECHANISMS FOR EXCRETING
EXCESS SOLUTES
NEPHRON TYPES
Superficial (cortical) [85 %]
o Capable of forming dilute urine
Juxtamedullary [15 %]
o Capable of forming
concentrated
(> 300 mOsm/kg) urine
EXCRETION LIMITS
• At least 600 mmol of solutes
must be excreted each day
– minimum volume = 600/1200 = 0.5L
– maximum volume = 20 Liters
EXCRETION LIMITS
COUNTER CURRENT MECHANISM
• LOOPS OF HENLE OF JUXTA
MEDULLARY NEPHRONS establish
hyperosmolality of interstitium of
medulla. They are called COUNTER
CURRENT MULTIPLIERS
• VASA RECTA maintain
hyperosmolality established by
counter current multipliers. They are
called COUNTER CURRENT
EXCHANGERS
300
300
200
300
300
250
400
400
300
500
500
400
600
600
500
700
700
600
800
800
800
1000
1000
1000
300
Cortex
Medulla
300
300
400
Osmolality
1200
1200
1200
DISORDERS OF URINARY
CONCENTRATING ABILITY
• Failure to Produce ADH: "Central"
Diabetes Insipidus.
• Inability of the Kidneys to Respond
to ADH: "Nephrogenic"
Diabetes Insipidus.
RENAL PHYSIOLOGY
MICTURITION
DR SYED SHAHID HABIB
MBBS DSDM FCPS
Assistant Professor
Dept. of Physiology
College of Medicine & KKUH
MICTURITION
It is the process by which the
urinary bladder empties when it
becomes filled
 Filling of bladder.
 Micturition reflex.
 Voluntary control.
Nervous Connections of the Bladder
Urogenital diaphragm
Micturition Reflex
• Actions of the internal urethral sphincter and the
external urethral sphincter are regulated by reflex
control center located in the spinal cord.
– Filling of the urinary bladder activates the stretch receptors,
that send impulses to the micturition center.
• Activates parasympathetic neurons, causing rhythmic
contraction of the detrusor muscle and relaxation of the internal
urethral sphincter.
– Voluntary control over the external urethral sphincter.
• When urination occurs, descending motor tracts to the
micturition center inhibit somatic motor fibers of the
external urethral sphincter.
AUTONOMIC SPINAL REFLEX
INNERVATION OF THE BLADDER
Nerves
1
Pelvic nerves
(parasympathetic
fibers)
Characteristic
Function
Both sensory
and motor
nerve fibers
Contraction of bladder
The sensory fibers detect the
degree of stretch in the bladder
wall
S-2 and S-3
2
Pudendal Nerve
somatic nerve
Fibers that innervate and control
the voluntary skeletal muscle of
the sphincter
3
Hypogastric
Nerves
sympathetic
innervation
(L2)
Stimulate mainly the blood
vessels and have little to do with
bladder contraction. Sensory
nerve fibers of the sympathetic
nerves also mediate the sensation
of fullness and pain.
CYSTOMETROGRAM