In normal skin, the rate of production equals the rate of loss; about two weeks are needed for a cell to migrate from the basal cell layer to the top of the granular cell layer, and an additional two weeks to cross the stratum corneum.The dermis is the layer of skin between the epidermis and subcutaneous tissue, and comprises two sections, the papillary dermis and the reticular dermis. The superficial papillary dermis interdigitates with the overlying rete ridges of the epidermis, between which the two layers interact through the basement membrane zone. Structural components of the dermis are collagen, elastic fibers, and ground substance. Within these components are the pilosebaceous units, arrector pili muscles, and the eccrine and apocrine glands. The dermis contains two vascular networks that run parallel to the skin surface—one superficial and one deep plexus—which are connected by vertical communicating vessels. The function of blood vessels within the dermis is fourfold: to supply nutrition, to regulate temperature, to modulate inflammation, and to participate in wound healing.The subcutaneous tissue is a layer of fat between the dermis and underlying fascia. This tissue may be further divided into two components, the actual fatty layer, or panniculus adiposus, and a deeper vestigial layer of muscle, the panniculus carnosus. The main cellular component of this tissue is the adipocyte, or fat cell. The structure of this tissue is composed of septal (i.e. linear strands) and lobular compartments, which differ in microscopic appearance.
Continued damage to the optic nerve results in the development of optic atrophy, classically seen as temporal pallor of the optic disc. Cause
Toxic optic neuropathy
There are several causes of toxic optic neuropathy. Among these are: ingestion of methanol (wood alcohol), ethylene glycol (automotive antifreeze), disulfiram (used to treat chronic alcoholism), halogenated hydroquinolones (amebicidal medications), ethambutol and isoniazid (tuberculosis treatment), and antibiotics such as linezolid and chloramphenicol as well as chloroquine and the related hydroxychloroquine (for lupus and rheumatoid arthritis) where it is known as chloroquine retinopathy. Tobacco is also a major cause of toxic optic neuropathy. Nutritional optic neuropathy
The predominant cause of nutritional optic neuropathy is thought to be deficiency of B-complex vitamins, particularly thiamine (vitamin B1), cyanocobalamin (vitamin B12) and recently copper. Deficiency of pyridoxine (vitamin B6), niacin (vitamin B3), riboflavin (vitamin B2), and/or folic acid also seems to play a role. Those individuals who consume excessive amounts of alcohol and use tobacco are at greater risk because they tend to be malnourished. Those with pernicious anemia are also at risk due to an impaired ability to absorb vitamin B12 from the intestinal tract. Pathophysiology
All of the above risk factors impact mitochondrial oxidative phosphorylation. Thus, the toxic and nutritional optic neuropathies are actually acquired mitochondrial optic neuropathies. The clinical picture that they produce is akin to that of the congenital mitochondrial optic neuropathies, e.g., Lebers hereditary optic neuropathy and Kjers optic neuropathy. Diagnosis
The diagnosis of toxic or nutritional optic neuropathy is usually established by a detailed medical history and careful eye examination.