Luvox

By P. Tizgar. Marlboro College.

Oral med- angle glaucoma is much less common ications for the treatment of glaucoma than chronic open-angle glaucoma buy luvox 50mg free shipping, it is work by decreasing the production of a medical emergency and must be treat- aqueous humor discount luvox 100mg with visa. For example, arteriosclerot- medical supervision, not only to monitor ic retinopathy is due to changes that occur the condition itself but also to identify any in blood vessels in the retina because of side effects of the medication. Hypertensive retinopathy is When intraocular pressure cannot be due to changes that occur in blood vessels successfully controlled with medication, in the retina because of high blood pres- individuals with chronic open-angle glau- sure. In both instances, treatment of the coma may have a surgical procedure primary underlying condition can control called trabeculectomy that relieves pressure the progress of retinopathy. Individuals may also need and the most common cause of blindness, to continue using eye drops or oral med- is diabetic retinopathy. Diabetic retinopathy ication after surgery to control pressure; is the result of damage to the retina and is however, in some instances surgery may a complication of diabetes mellitus (see eliminate the need for medication. Treatment of Acute Closed-Angle Glaucoma Consequently, regular comprehensive eye examinations by a physician are impor- Acute closed-angle glaucoma results tant in helping to prevent visual loss. Nonproliferative diabetic retinopathy miotics constrict the pupil, thus enlarging 2. Proliferative diabetic retinopathy the drainage passageway and facilitating the outflow of aqueous humor. Because of Nonproliferative diabetic retinopathy is the emergency nature of acute closed- caused by changes in blood vessel walls angle glaucoma, oral or intravenous med- that allow fluids to leak into retinal tissue. As a rior chamber of the eye, thus preventing result, retinal tissues receive too little oxy- further eye damage by relieving built-up gen (ischemia) and growth of new vessels pressure. At times iridotomy abnormally fragile and prone to bleed, may also be performed prophylactically in causing hemorrhage into the vitreous the unaffected eye after an acute attack. Vessels Retinopathy may burst, filling the back of the eye with blood and resulting in significant visual Any disease or disorder of the retina is loss. Retinopathies are often named ated with new vessels can pull on the reti- 132 CHAPTER 4 CONDITIONS OF THE EYE AND BLINDNESS na so that it detaches from underlying tis- scleral buckling is sometimes used to treat sue. Scleral buckling Surgery may be performed to remove mechanically restores contact of the reti- vitreous gel and hemorrhage (vitrectomy), na with the choroid. The area of the scle- or laser treatment may be performed to ra that lies over the retinal defect is stop the bleeding. Laser photocoagulation is depressed with an implant so that the a procedure in which an intense beam of choroid and retina are pressed together. The laser beam Retinitis Pigmentosa passes through the lens of the eye and vit- reous fluid without harming the struc- A hereditary condition, retinitis pig- tures. It then is directed to a very precisely mentosa, involves the slowly progressive defined area to destroy fragile vessels loss of peripheral vision. Although there prone to hemorrhage or diseased areas of is progressive restriction of the visual field the retina in which there may be addition- due to loss of peripheral vision, the re- al proliferative vessel changes. Laser pho- maining central visual acuity is often tocoagulation may help reduce the risk of good. Frequently the first symptom of visual loss, but it does not stop the pro- retinitis pigmentosa is difficulty with gression of diabetic retinopathy. Laser night vision (night blindness), which usu- treatment is usually performed on an out- ally begins in late youth or early adult- patient basis. Total bilateral loss of vision can occur in later stages of the disease. There Retinal Detachment is no cure or treatment for the condition; however, a number of assistive devices With detached retina, the sensory lay- may be utilized to enhance function. De- tached retina may result from a sudden Macular Degeneration blow to the head, a tumor in the choroid layer, retinal degeneration caused from Degenerative changes in the macula, conditions such as arteriosclerosis, or the part of the eye needed for seeing fine hemorrhage with conditions such as dia- detail and central vision, results in a con- betic retinopathy. Symptoms may develop suddenly or Macular degeneration usually occurs slowly over time. Individuals may notice after the age of 50, from no apparent flashes of light or a loss of vision in dif- cause. Painless loss of central visual acu- ferent areas of the visual field, or they may ity is usually slow, with visual distortion experience a complete loss of vision in the or blurring of vision being the first symp- affected eye. Retinal detach- a blind spot in the center of their field of ment in one eye may indicate an in- vision that gradually increases in size as creased risk of detachment in the other the condition progresses.

These cells gradually become engulfed in their own cartilage and are replaced by new cells on the cartilage surface buy luvox 50 mg lowest price, allowing the process to continue luvox 100 mg fast delivery. The cartilage gradually becomes calci- fied, and the embedded chondrocytes die. The calcified cartilage begins to erode, and osteoblasts migrate into the area. Osteoblasts secrete osteoid, which eventually be- comes mineralized, and new mature bone is formed. In the epiphyseal plate, therefore, the continuing processes of cartilage synthesis, calcification, erosion, and osteoblast in- vasion result in a zone of active bone formation that moves away from the middle or center of the bone toward its end. Insulin-like growth factor I (IGF-I), primarily produced by the liver in response to growth hormone, serves as a primary stimulator of chondrocyte activity and, ultimately, of bone growth. Insulin and thyroid hormones provide an additional stimulus for chondrocyte activity. Beginning a few years after puberty, the epiphyseal plates in long bones (as in the legs and arms) gradually become less responsive to hormonal stimuli and, eventu- The location and relationship of the three ally, are totally unresponsive. For exam- Long-Term Regulation of Plasma Calcium and ple, those in the fingers, feet, skull, and jaw remain re- Phosphate Concentrations sponsive, which accounts for the skeletal changes seen in acromegaly, the condition of growth hormone overpro- The hormonal mechanisms described here have a large ca- duction (see Chapter 32). It may take several minutes or hours for the bone structure generally referred to as remodeling. However, modeling occurs along most of the outer surface of the bone, these are the principal mechanisms that regulate plasma making it either thinner or thicker, as required. Remodeling is an The Chemistry of Parathyroid Hormone, Calcitonin, and adaptive process that allows bone to be reshaped to meet 1,25-Dihydroxycholecalciferol and the Regulation of changing mechanical demands placed on the skeleton. One of the primary regulators of allows the body to store or mobilize calcium rapidly. Synthetic peptides containing the first 34 amino terminal residues appear to be as active as the REGULATION OF PLASMA CALCIUM native hormone. AND PHOSPHATE CONCENTRATIONS There are two pairs of parathyroid glands, located on Regulatory mechanisms for calcium include rapid nonhor- the dorsal surface of the left and right lobes of the thyroid monal mechanisms with limited capacity and somewhat gland. Because of this close proximity, damage to the slower hormonally regulated mechanisms with much parathyroid glands or to their blood supply may occur dur- greater capacity. There are also similar mechanisms in- ing surgical removal of the thyroid gland. The primary physiological stimulus for PTH secretion is a decrease in plasma calcium. It is actually a de- Buffer Small Changes in Plasma Concentrations crease in the ionized calcium concentration that triggers an of Free Calcium increase in PTH secretion. The net effect of PTH is to in- The calcium bound to plasma proteins and a small fraction of that in bone mineral can help prevent a rapid decrease in the plasma calcium concentration. The association of calcium with 700 proteins is a simple, reversible, chemical equilibrium process. Protein-bound calcium, therefore, has the capacity to serve as a buffer of free plasma calcium concentrations. This effect 3,000 600 is rapid and does not require complex signaling pathways; however, the capacity is limited, and the mechanism cannot 500 serve a long-term role in calcium homeostasis. Recall that approximately 99% of total body calcium is 300 present in bones, and a healthy adult body has about 1 to 2 kg of calcium. Most of the calcium in bones exists as 1,000 200 mature, hardened bone mineral that is not readily ex- changeable but can be moved into the plasma via hor- monal mechanisms (described below). However, approx- imately 1% (or 10 g) of the calcium in bones is in a simple chemical equilibrium with plasma calcium. This readily 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 exchangeable calcium source is primarily located on the Serum calcium (mg/dL) surface of newly formed bones. Any change in free cal- cium in the plasma or extracellular fluid results in a shift FIGURE 36. Simultaneous measurements of calcitonin and parathyroid against changes in free calcium concentrations, it is lim- hormone in the pig.