Anatomy and physiology Vitreous ppt final.pptx

Anatomy and physiology Vitreous ppt final.pptx

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  ANATOMY AND PHYSIOLOGY OF VITREOUSHUMOUR PRESENTED BY; DR. RAHUL GUPTA 1ST YR.RESIDENT DEPT. OPHTHALMOLOGY DATE: 24TH SEPT, 2023
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  CONTENTS Introduction Embryology Anatomy Proper Biochemical composition Physiologicalproperties Blood vitreous barrier Age related changes
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  INTRODUCTION  Vitreous humoris inert, transparent, colorless, hydrophilic gel  pH = 7.2  Boundaries;  Anterior: Lens and Ciliary body  Posterior: Retina  Weight: 4g approx.  Volume: 4cc, approx. 2/3rd of the entire volume  Function;  Allows light to reach retina  Helps in diffusion of nutrients from ciliary body to retina  Imp supporting structure to eyeball
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  • Develops betweenlens and optic cup mostly derived from mesoderm with minimal contribution from ectoderm. • Formation of vitreous occurs in three stages : 1. Primary vitreous 2. Secondary vitreous 3. Tertiary vitreous EMBRYOLOGY
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  Primary vitreous –1st month • Mixed mesenchymal and ectodermal in origin. Fully formed by 8th WOG. • It is a vascular structure network of delicate cytoplasmic process which occupy the space between lens vesicle and inner layer of optic cup. • It is composed of fibrils (ectoderm) and mesenchymal cells(mesoderm) which constitutes primary vitreous. • Mesodermal cells migrate via choroidal fissure and are joined by hyaloid system(vasa hyaloidea propria).
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  Secondary vitreous-2nd month • Startsto form after closure of choroidal fissure in 8th WOG. • secreted by neuroectoderm of optic cup, avascular gel like substances occupying the space between primary vitreous and retina. • As hyaloid system regresses and primary vitreous cell differentiates into hyalocytes which synthesis type II collagen and hyaluronic acid which constitutes secondary vitreous Secretion of vitreous continues in 3rd month of development. • By 5th-6th month primary vitreous and Hyaloid vessels undergoes atrophy. • Atrophied hyaloid vessels become hyaloid cannal which remain throughout the life as Cloquet canal.
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  Tertiary vitreous-3rd month •Developed from neuroectoderm. • It is Formation of zonular fiber between the ciliary body and lens capsule. • Collagen fibrils synthesized by ciliary epithelium becomes more condensed and extends to the lens equator and become zonular fiber of lens which constitutes the tertiary vitreous.
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  Related images
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  Applied anatomy( vitreousbody) • Mittendorf’s dot: remnants of anterior end of hyaloid artery associated with posterior polar cataract & attached to posterior lens capsule • Subluxation/Ectopia lentis: Partial or total failure in Tertiary vitreous development • Bergmeister’s Papillae: -flakes of glial tissue -projecting from the optic disc • Persistent Primary hyperplastic vitreous:Its occurs due to failure of primary vitreous and hyaloid vessels to regress. Presents as leukocoria- white pupillary reflex
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  DEVELOPMENTAL ANOMALIES Persistent fetalvascular (PFV) syndrome/persistent hyperplastic primary vitreous (PHPV)  Anterior PFV  cataract formation  shallowing of the anterior chamber  angle-closure glaucoma  Iris vessel engorgement and recurrent intraocular hemorrhage  Posterior PFV consists of a prominent vitreous fibrovascular stalk that originate from the optic nerve and courses anteriorly
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  ANATOMY STRUCTURE; Largest but simplestconnective tissue found in the body. Divided into 3 parts  Hyaloid layer  Anterior hyaloid /Anterior limiting membrane  Posterior hyaloid/Posterior limiting membrane  Cortical vitreous  Medullary vitreous
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  HYALOID LAYER
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  Ligamentous attachments of anteriorhyaloid membrane  Hyalociliary zonules: AHM- Ciliary processes  Retrolental ligament : AHM- Lense  Coronary ligament : AHM- inner face of posterior third of cillary processes circumferentially  Median ligament : AHM- midzone of pars plana
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   From vitreousbase upto optic disc  Lies in contact with Internal Limiting membrane of retina from which it is cilinically indistinguishable  But it may become evident in presence of subhyaloid hemorrhage and PVD. Posterior Hyaloid Membrane
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  CORTICAL VITREOUS  Itrefers to entire peripheral zone 100 microns width  Consists of relatively condensed fibrillar vitreous  Occupies only 2% of the total vitreous volume  Main metabolic site due to presence of hyalocytes
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  HYALOCYTES  10-15 micronin diameter.  Fusiform /stellate shaped with prominent lobulated nuclei.  Cytoplasm contain : PAS positive granules, SER, Golgi apparatus lysosomal granules containing enzymes necessary for phagocytosis. Function; Synthesis of hyaluronic acid  Phagocytosis
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  MEDULLARY VITREOUS  Similarto cortical vitreous but has less fibrillar structure and contains no hyalocytes
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  VITREOUS TRACTS Fine sheetlike condensation of vitreous tissue radiating into vitreous space from ciliary body and anterior retina.
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  VITREOUS ATTACHMENTS  Attachedfirmly around  The ora serrata  Optic disc  Post. of lens  Foveal regions  Strongest to the pars plana and at ora serrata, known as Vitreous base.
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  VITREOUS BASE
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  PHYSIOLOGY OF VITREOUS BIOCHEMICALCOMPOSITION Consist of 3 major components  Water  Collagen fibers  Hyaluronic acid (GAG)
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  COLLAGEN Stickler syndrome Marshall syndrome
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  HYALURONIC ACID  Mucopolysaccharidecomposed of equivalent amount of N-acetyl glucosamine and glucuronic acid  Present as unbranched linearly arranged polymer, coils upon itself producing large sponge like spheroidal network interwined among collagen fibers.  Responsible for viscosity of vitreous.  Produced by hyalocytes.  Concentration  Highest in posterior cortex  lesser in central  lowest in anterior periphery
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  Soluble proteins :Acid glycoproteins and albumin Low molecular weight constituents  Sugar: glucose , galactose, fructose, glucuronic acid and glucosamine  Ascorbic acid  Amino acid
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  ELECTROLYTE  Na, Ca:almost equal to Aqueous humor and plasma  K: 9.5 mM/kg, higher then AH(5mM/kg) and plasma (5.6mM/kg)  Active transport through ciliary body and anterior capsule of lense to posterior chamber  Passive diffusion through posterior capsule of lense  Chloride : higher then AC, PC and Plasma  HCO3, Phosphate : Lower  Lactic acid : Higher
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  BIOCHEMICAL AND PHYSIOLOGICALACTIVITIES PHYSIOCHEMICAL PROPERTIES  Optical properties  Transparency  Soluble proteins : prevents light scattering  RI: 1.3349  Transmit about 90%of light between 300 -1400 nm
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   Plasticity  Viscoelasticity Gel stability  Vitreous expansion and contraction
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  FUNCTION OF VITREOUSBODY  Supportive Function for the retina and filling function of the vitreous body cavity  Diffusion barrier (ant/post segment)  Metabolic buffer function  Establish an unhindered path for transmission light
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  SUPPORT FUNCTION  Preventor retard the development of retinal detachment  Shock absorber: absorb external forces and prevent deformation of the globe  Supports lens during trauma
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  BARRIER FUNCTION  Diffusionbarrier between anterior and posterior segment  Reason : Diffusion is slow and movement by bulk flow is very much limited in vitreous  Significance  Topically administered drug is prevented from reaching retina and optic nerve head in significant concentrations  Entrance of systemic drugs is also impeded in vitreous
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  METABOLIC BUFFER  Substancespresent in or produced in the retina are diluted by diffusion.  Glucose and glycogen in the vitreous body supplement retinal metabolism.  Vitamin C act as an anti-oxidant.
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  BLOOD VITREOUS BARRIER Tight junctional complexes  Retinal vascular endothelium  Pigment epithelium of retina  Non – pigmented epithelium of ciliary body  Basal lamina of the vitreoretinal junction  Vitreous cortex
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  AGE-RELATED VITREOUS CHANGES Infant - very homogeneous, gel-like body  With maturation-gel volume decreases and the liquid volume increases(vitreous liquefaction or vitreous synersis).  By age 40 years - 80% gel and 20% liquid,  By 70 or 80 years - 50% liquid (most of the liquefaction occurring in the central vitreous)  Plasminogen (proteolytic enzymes) increases vitreous concentrations  Weakening of adhesion at the vitreoretinal interface (between the cortical vitreous gel and the inner limiting lamina)
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  In old ageadvanced liquefaction (synchesis) occurs with ultimate collapse (syneresis) of the vitreous and PVD. True PVD is a separation between the posterior vitreous cortex and the ILL of the retina
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  VITREOUS OPACITIES  Muscaevolitantes( floaters)  Vitreous haemorrhage  Asteroid hyalosis  common degenerative process  calcium pyrophosphate particles collect within the vitreous gel.  numerous tiny round yellow– white opacities of varying size and density
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  Synchysis scintillans;  Occursas a consequence of chronic vitreous haemorrhage  Composed of cholesterol and are derived from plasma cells or degraded products of erythrocytes  Numerous flat golden-brown refractile particles Amyloidosis;  Extracellular deposition of fibrillary protein  Vitreous involvement typically occurs in familial amyloidosis  Characterized by polyneuropathy, prominent corneal nerves and pupillary light near dissociation.
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  Vitreous cyst