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• Is a clear, colourless, watery solution
• Flows from posterior to anterior chamber
• In healthy eye flow against resistance
generates 15 mm hg
• Aqueous formation (F), facility of outflow (C),
and episcleral venous pressure (P0) are the
major intraocular determinants of IOP. These
factors are related to one another by the
Goldmann equation:
F = C (Po - Pv)
P0 is IOP in undisturbed eye
With the discovery of pressure independent
mech the equation is modified
F = C (Po - Pv)+U
U is the sum of pr independent pathways
• Nutrition to lens cornea and iris
• Removes metabolically toxic products
• Refractive index 1.33
• Inflates globe and maintains IOP
• Ascorbate-anti oxidant-uv protection
• Facilitates cellular and humoral response
of eye to inflammation And infection
• Anatomy of aqueous formation and
drainage structures
• Aqueous humor formation
• Aqueous humor outflow
• Primary ocular structures involved are
1.Ciliary body
2.Posterior chamber
3.Anterior chamber
4.Angle of anterior chamber
5.Aqueous outflow system
1.CILIARY BODY
• CILIARY PROCESS
-70-80
-2 mm length and 5mm
width
• Network of capillaries
• Stroma
• Inner pigmented
epithelium
• Outer non pigmented
epithelium
2.POSTERIOR CHAMBER 0.06ml
3.ANTERIOR CHAMBER-0.25ml
4.ANGLE OF ANTERIOR CHAMBER
• Complex pathway
• Ciliary processes are site of aqueous humour
formation
• Mainly by three machanisms
1.Ultra filtration 20%
2.Active transfer 70%
3.Diffusion 10%
1.ULTRAFILTRATION
Process thru which fluids and solutes cross
through semi permeable memb
Capillary blood flow 150ml/min
4%filters thru fenestrations
Favoured by hydrostatic pressure diff b/w
capillary and interstitial pr.
Enough to move fluid to stroma but further req
active transport
Leads to formation of stromal pool
2.ACTIVE TRANSPORT
Energy dependent
Majority production by active secretion
Uses ATP
AA:Decreased by hypoxia, hypothermia and
inhibitors of active metabolism.
Majority of investigators proposed that active
transport of sodium is key in aq humor
formation
• Sodium-70% is actively transported by specific
secretary pump. Rest by diffusion, ultrafiltration.
• Chloride-dependent on sodium
• Ascorbic acid- secreted against large
concentration gradient.
• Amino acids-By 3 carriers.
• Bicarbonate-by carbonic anhydrase mediated
reaction.
3.DIFFUSION
Active Transport of substances described above
lead to osmotic and electrical gradient
To maintain the balance small partices like water
and small plasma constituents move in to post
chamber by diffusion
• Consists of two
pathways
1.Trabecular or
conventional outflow
2.Uveoscleral or
unconventional outflow
UVEOSCLERAL OUTFLOW
 Pressure independent,10-25%
 0.3microl/min and independent of IOP
CILIARY BODY
SUPRA CHOROIDAL SPACE
CILIARY BODY VENOUS CIRCULATION
CHOROID
SCLERA
ORBITAL TISSUE
INCREASE
• Prostaglandins-one of most potent IOP
reducing agents
• Cycloplegics
• Alpha agonists-
epinephrine,brimonidine,apraclonidine
• Atropine
DECREASE
• Pilocarpine
TRABECULAR OUTFLOW
• Pressure dependent,90%
TRABECULAR MESHWORK
SCHEMMS CANAL
INTRASCLERAL CHANNELS
EPISCLERAL AND CONJUNCTIVAL VEINS
CAVERNOUS SINUS
TRABECULAR MESHWORK
• VACUOLATION THEORY:- vesicles and vacuoles in endothelium open and
close intermittently to transport aqueous from TM cells to Schlemm’s canal
Non
Vacuolat
ed state
Early stage
of basal
infolding
Macrov
acuole
formati
on
Vacuolar
transecell
ular
channel
formation
Oclusion
of basal
infolding
SCHLEMMS CANAL
• Endothelial lined oval channel present
circumferentially in Scleral sulcus.
• Cells irregular spindle shaped & contain
giant vacuoles.
• Outer wall contains openings of collector
channels.
• Torus or lip like thickenings near collector
channel help to keep canal open.
• AA: Gaint vacuoles are lost with increasing
age and this is implicated in POAG.
COLLECTOR CHANNELS
• 25-30 intrascleral aqueous vessels
• Valveless,wide at origin
• Direct system
• Indirect system
EPISCLERAL VEINS
• drain ultimately in to cavernous sinus via
ant ciliary and sup ophthalmic veins
• POAG - loss of trabecular endothelial cells.
- collapse of schlemms canal.
- obstruction of collector channels.
• Infantile glaucoma – outflow structures not
developed properly (Trabeculodysgenesis).
• Angle closure glaucoma – peripheral iris
pushed against meshwork.
• Secondary open angle – obstruction by RBCs,
WBCs, tumor cells , pigment & lens particles.
• Rate: 2.4+/-0.6 microL/min
• Volume: 0.31ml( 0.25ml AC, 0.06ml PC)
• Refractive index: 1.336
• Viscosity:1.025-1.040
• Osmotic pressure: 3-5mosm/L
• pH:Acidic,7.2
• Turnover: 1.5-2hrs
• Water -99.9%.
• IgM & IgG ,but no IgA and IgD.
• Plasminogen and its activators but no other
clotting factors.
• Most important- low protein content (200 times
less) and high ascorbate (20 times).ascorbate
acts as anti oxidant and protects ocular
structures from uv light induced oxidative
damage
• Comparision b/w PC and AC aqueous
bicorb and ascorbate pc>Ac
chloride ac>pc
Component (mmol/kg h2o) Plasma conc Aq humor conc
Sodium 146 163
chloride 109 134
Bicarbonate 28 20
Ascorbate 0.04 1.06
Glucose 6 3
Urea 9 7
lactate 4.3 7.4
• The tight junctions
connecting the apical
portions of adjacent non
pigmented epithelial cells
forms the blood aqueous
barrier.
• Responsible for maintaining
the difference in chemical
composition b/w aq and
plasma
Break down
• Proteins appear in aqueous humor:
Plasmoid (Secondary )aqueous
On SLE-Pronounced Tyndall beam
>20mg / 100 ml ,phenomenon of FLARE.
• Fibrinogen enters- clotting of aqueous.
• INFECTIONS-brings mediators of cellular and
humoral immunity
• UVEITIS AND TRAUMA-dev of cataract and
synechiae formation
AA: Rate of penetration of PAH, fluorescein,
Evan’s blue increases-Diagnostic indicator.
• Avg is 2.6-2.8 micro lit/min
• Diurnal variation : maximum in morning hours &
min late at night, due to decreased stimulation
of ciliary epithelium by catecholamines during
sleep.
• Age and sex: similar in males & females , reduces
with age.
• Ocular inflammation ,hypothermia ,systemic
acidosis & anesthetics like halothane ,
barbiturates & ketamine decrease formation.
• Blood flow to ciliary body: profound
vasoconstriction decreases formation.
• Sympathetic system: stimulation by β2 &
inhibition via α2 receptors.
• Parasympathetic system: decreases via M3
receptors.
• Intracelluar regulators: cyclic AMP
increases aqueous formation.
PHYSICAL METHODS-pressure dependent
• -When fluid is introduced in to a closed system
there is intermediate increase in pressure in the
system
• Can be calc using goldmans equation
F = C (Po - Pv)
F- Rate of aqueous outflow (mmHg)
C- Coefficient of outflow facility
(microL/min/mmHg)
Po -Baseline IOP (mmHg)
Pv- Episcleral venous pressure (mmHg)
By
1.Tonography
2.Suction cup
3.Perfusion
tonography
• Non-invasive technique
• Schiotz tonometer placed on eye for 4min ,
raises IOP.
• Rate of flow calculated based on rate of rise
of IOP.
• Normal: 0.28microl/min/mmHg
• Most glaucoma patients have values less than
0.17microl/min/mmHg.
TRACER METHODS
• Measures rate of appearance or
dissappearance of various tracers in ac
• Any aq passing posteriorly to vitreous and
retina cannot be detected
-Photogrammetric estimation
-Radiolabelled isotopes
-Fluorescein technique
-PAH technique
• CLINICAL CONDITIONS
-hypothemia and systemic acidosis
decreases aq production and vice versa
-IDDM decrease aqueous outflow
• PHARMACOLOGICAL AGENTS
INCREASE PRODUCTION
-beta adrenergic agents
-hydrocortisone adm systemically
-intracameral ANP
DECREASED PRODUCTION
-CA inhibitors
-Beta blockers
_ouabain
-cyclodestructive procedures
Aqueous humor dynamics sivateja
Aqueous humor dynamics sivateja
Aqueous humor dynamics sivateja

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ICT role in 21st century education and it's challenges.
 

Aqueous humor dynamics sivateja

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  • 2. • Is a clear, colourless, watery solution • Flows from posterior to anterior chamber • In healthy eye flow against resistance generates 15 mm hg
  • 3. • Aqueous formation (F), facility of outflow (C), and episcleral venous pressure (P0) are the major intraocular determinants of IOP. These factors are related to one another by the Goldmann equation: F = C (Po - Pv) P0 is IOP in undisturbed eye With the discovery of pressure independent mech the equation is modified F = C (Po - Pv)+U U is the sum of pr independent pathways
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  • 5. • Nutrition to lens cornea and iris • Removes metabolically toxic products • Refractive index 1.33 • Inflates globe and maintains IOP • Ascorbate-anti oxidant-uv protection • Facilitates cellular and humoral response of eye to inflammation And infection
  • 6. • Anatomy of aqueous formation and drainage structures • Aqueous humor formation • Aqueous humor outflow
  • 7. • Primary ocular structures involved are 1.Ciliary body 2.Posterior chamber 3.Anterior chamber 4.Angle of anterior chamber 5.Aqueous outflow system
  • 9. • CILIARY PROCESS -70-80 -2 mm length and 5mm width • Network of capillaries • Stroma • Inner pigmented epithelium • Outer non pigmented epithelium
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  • 14. • Complex pathway • Ciliary processes are site of aqueous humour formation • Mainly by three machanisms 1.Ultra filtration 20% 2.Active transfer 70% 3.Diffusion 10%
  • 15. 1.ULTRAFILTRATION Process thru which fluids and solutes cross through semi permeable memb Capillary blood flow 150ml/min 4%filters thru fenestrations Favoured by hydrostatic pressure diff b/w capillary and interstitial pr. Enough to move fluid to stroma but further req active transport Leads to formation of stromal pool
  • 16. 2.ACTIVE TRANSPORT Energy dependent Majority production by active secretion Uses ATP AA:Decreased by hypoxia, hypothermia and inhibitors of active metabolism. Majority of investigators proposed that active transport of sodium is key in aq humor formation
  • 17. • Sodium-70% is actively transported by specific secretary pump. Rest by diffusion, ultrafiltration. • Chloride-dependent on sodium • Ascorbic acid- secreted against large concentration gradient. • Amino acids-By 3 carriers. • Bicarbonate-by carbonic anhydrase mediated reaction.
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  • 19. 3.DIFFUSION Active Transport of substances described above lead to osmotic and electrical gradient To maintain the balance small partices like water and small plasma constituents move in to post chamber by diffusion
  • 20. • Consists of two pathways 1.Trabecular or conventional outflow 2.Uveoscleral or unconventional outflow
  • 21. UVEOSCLERAL OUTFLOW  Pressure independent,10-25%  0.3microl/min and independent of IOP CILIARY BODY SUPRA CHOROIDAL SPACE CILIARY BODY VENOUS CIRCULATION CHOROID SCLERA ORBITAL TISSUE
  • 22. INCREASE • Prostaglandins-one of most potent IOP reducing agents • Cycloplegics • Alpha agonists- epinephrine,brimonidine,apraclonidine • Atropine DECREASE • Pilocarpine
  • 23. TRABECULAR OUTFLOW • Pressure dependent,90% TRABECULAR MESHWORK SCHEMMS CANAL INTRASCLERAL CHANNELS EPISCLERAL AND CONJUNCTIVAL VEINS CAVERNOUS SINUS
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  • 27. • VACUOLATION THEORY:- vesicles and vacuoles in endothelium open and close intermittently to transport aqueous from TM cells to Schlemm’s canal Non Vacuolat ed state Early stage of basal infolding Macrov acuole formati on Vacuolar transecell ular channel formation Oclusion of basal infolding
  • 28. SCHLEMMS CANAL • Endothelial lined oval channel present circumferentially in Scleral sulcus. • Cells irregular spindle shaped & contain giant vacuoles. • Outer wall contains openings of collector channels. • Torus or lip like thickenings near collector channel help to keep canal open. • AA: Gaint vacuoles are lost with increasing age and this is implicated in POAG.
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  • 30. COLLECTOR CHANNELS • 25-30 intrascleral aqueous vessels • Valveless,wide at origin • Direct system • Indirect system EPISCLERAL VEINS • drain ultimately in to cavernous sinus via ant ciliary and sup ophthalmic veins
  • 31. • POAG - loss of trabecular endothelial cells. - collapse of schlemms canal. - obstruction of collector channels. • Infantile glaucoma – outflow structures not developed properly (Trabeculodysgenesis). • Angle closure glaucoma – peripheral iris pushed against meshwork. • Secondary open angle – obstruction by RBCs, WBCs, tumor cells , pigment & lens particles.
  • 32. • Rate: 2.4+/-0.6 microL/min • Volume: 0.31ml( 0.25ml AC, 0.06ml PC) • Refractive index: 1.336 • Viscosity:1.025-1.040 • Osmotic pressure: 3-5mosm/L • pH:Acidic,7.2 • Turnover: 1.5-2hrs
  • 33. • Water -99.9%. • IgM & IgG ,but no IgA and IgD. • Plasminogen and its activators but no other clotting factors. • Most important- low protein content (200 times less) and high ascorbate (20 times).ascorbate acts as anti oxidant and protects ocular structures from uv light induced oxidative damage • Comparision b/w PC and AC aqueous bicorb and ascorbate pc>Ac chloride ac>pc
  • 34. Component (mmol/kg h2o) Plasma conc Aq humor conc Sodium 146 163 chloride 109 134 Bicarbonate 28 20 Ascorbate 0.04 1.06 Glucose 6 3 Urea 9 7 lactate 4.3 7.4
  • 35. • The tight junctions connecting the apical portions of adjacent non pigmented epithelial cells forms the blood aqueous barrier. • Responsible for maintaining the difference in chemical composition b/w aq and plasma
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  • 37. Break down • Proteins appear in aqueous humor: Plasmoid (Secondary )aqueous On SLE-Pronounced Tyndall beam >20mg / 100 ml ,phenomenon of FLARE. • Fibrinogen enters- clotting of aqueous. • INFECTIONS-brings mediators of cellular and humoral immunity • UVEITIS AND TRAUMA-dev of cataract and synechiae formation AA: Rate of penetration of PAH, fluorescein, Evan’s blue increases-Diagnostic indicator.
  • 38. • Avg is 2.6-2.8 micro lit/min • Diurnal variation : maximum in morning hours & min late at night, due to decreased stimulation of ciliary epithelium by catecholamines during sleep. • Age and sex: similar in males & females , reduces with age. • Ocular inflammation ,hypothermia ,systemic acidosis & anesthetics like halothane , barbiturates & ketamine decrease formation.
  • 39. • Blood flow to ciliary body: profound vasoconstriction decreases formation. • Sympathetic system: stimulation by β2 & inhibition via α2 receptors. • Parasympathetic system: decreases via M3 receptors. • Intracelluar regulators: cyclic AMP increases aqueous formation.
  • 40. PHYSICAL METHODS-pressure dependent • -When fluid is introduced in to a closed system there is intermediate increase in pressure in the system • Can be calc using goldmans equation F = C (Po - Pv) F- Rate of aqueous outflow (mmHg) C- Coefficient of outflow facility (microL/min/mmHg) Po -Baseline IOP (mmHg) Pv- Episcleral venous pressure (mmHg)
  • 41. By 1.Tonography 2.Suction cup 3.Perfusion tonography • Non-invasive technique • Schiotz tonometer placed on eye for 4min , raises IOP. • Rate of flow calculated based on rate of rise of IOP. • Normal: 0.28microl/min/mmHg • Most glaucoma patients have values less than 0.17microl/min/mmHg.
  • 42. TRACER METHODS • Measures rate of appearance or dissappearance of various tracers in ac • Any aq passing posteriorly to vitreous and retina cannot be detected -Photogrammetric estimation -Radiolabelled isotopes -Fluorescein technique -PAH technique
  • 43. • CLINICAL CONDITIONS -hypothemia and systemic acidosis decreases aq production and vice versa -IDDM decrease aqueous outflow
  • 44. • PHARMACOLOGICAL AGENTS INCREASE PRODUCTION -beta adrenergic agents -hydrocortisone adm systemically -intracameral ANP DECREASED PRODUCTION -CA inhibitors -Beta blockers _ouabain -cyclodestructive procedures