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CHAPTER III: PATHOPHYSIOLOGY

Predisposing/Non-Modifiable Precipitating/ Modifiable Factors

Factors Smoking
• (+) Family History of: Excessive Drinking of Alcohol
o Glaucoma Unhealthy Diet
o Hypertension Sedentary Lifestyle
o Diabetes Mellitus Lack of Exercise
• Aging (Usually 40 y/o and Long Term-Ultra Violet Exposure
above) Exposure to Radiation
• Genetics Job/Work
• Sex/Gender (Females) Usage of Corticosteroids & Ezetimibe
Secondary to other Diseases like Uveitis or
Inflammation of the Inner Layer of the Eye.

Progressive Oxidative Damage to the Lens

↓ Antioxidants, Vitamins, & Enzymes

↓ H2O Content ↑ Destruction & ↓ Sodium (Na)

Breakdown of CHON

Disrupts the Normal Fibers in the Eyes

↑ Density of Lens

Opacity/Clouding of the Lens

CATARACT FORMATION

↓ Vision Loss of Transparency

BLINDNESS

Table 1. [Mature] Cataract Schematic diagram Book Based

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A. Pathophysiology

 The pathophysiology behind cataracts is complex and yet to be fully understood. In

all probability, its pathogenesis is multifactorial involving complex interactions
between various physiologic processes. As the lens ages, its weight and thickness
increases while its accommodative power decreases. As the new cortical layers are
added in a concentric pattern, the central nucleus is compressed and hardened in a
process called nuclear sclerosis. Progressive oxidative damage to the lens with aging
takes place, leading to cataract development. Various studies showing an increase in
products of oxidation (e.g.: oxidized glutathione) and a decrease in antioxidant
vitamins and the enzyme superoxide dismutase underscore the important role of
oxidative processes in cataractogenesis.
 Cataract can be classified into 3 main types: nuclear cataract, cortical cataract, and
posterior subcapsular cataract. Nuclear cataracts result from excessive nuclear
sclerosis and yellowing, with consequent formation of a central lenticular opacity. In
some instances, the nucleus can become very opaque and brown, termed a brunescent
nuclear cataract. Changes in the ionic composition of the lens cortex and the eventual
change in hydration of the lens fibers produce a cortical cataract. Formation of
granular and plaquelike opacities in the posterior subcapsular cortex often heralds the
formation of posterior subcapsular cataracts.
 Among the transparent tissues of the eye, the lens is a rather bradytrophic
compartment having a relatively xenobiotic metabolism. It is composed of specialized
proteins, whose optical properties are dependent on the fine arrangement of their
three-dimensional structure and hydration. Protein-bound SH-groups of the crystallins
are protected against oxidation and cross-linking by high concentrations of reduced
glutathione. Their molecular composition as well tertiary and quaternary structures
provide a high spatial and timely stability (heat-shock proteins) especially of the
larger crystallins, who are able to absorb radiation energy (shortwave visible light,
ultraviolet and infrared radiation) over longer time periods without basicly changing
their optical qualities. This provides considerable protective function also for the
activity of various enzymes of the carbohydrate metabolism. The glucose metabolic
pathway is functioning rather anaerobicly with low energetic efficiency, nevertheless
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it has to provide the metabolic energy for protein synthesis, transport and membrane
synthesis. In addition, the syncytial metabolic function of the denucleated fiber cells
has to be maintained by the epithelium and the small group of fiber cells, which still
have their metabolic machinery. This results in a steep inside-out metabolic gradient,
which is complicated by the fact that the lens has a kind of repair system shutting of
damaged groups of fiber cells (wedge- or sectorial cataracts). All epithelial cells of
the lens are subjected to light and radiation stress leading to alterations of the genetic
code. Because defective cells cannot be extruded, these are either degraded
(apoptosis, necrosis), or they are moved to the posterior capsular area, where they
contribute to the formation of posterior subcapsular cataracts. Ageing generally
reduces the metabolic efficiency of the lens thus increasing its succeptability to
noxious factors. Ageing provides the grounds where cataract noxae can act and
interact to induce the formation of a variety of cataracts, many of them being
associated with high protein-related light scattering and discoloration.