Some of these include: keeping the feet dry; clipping toenails short; using a separate nail clipper for infected toenails; using socks made from well-ventilated cotton or synthetic moisture wicking materials (to soak moisture away from the skin to help keep it dry); avoiding tight-fitting footwear; changing socks frequently; and wearing sandals while walking through communal areas such as gym showers and locker rooms.According to the Centers for Disease Control and Prevention, "Nails should be clipped short and kept clean. Nails can house and spread the infection." Recurrence of athletes foot can be prevented with the use of antifungal powder on the feet.The fungi (molds) that cause athletes foot require warmth and moisture to survive and grow. There is an increased risk of infection with exposure to warm, moist environments (e.g., occlusive footwear—shoes or boots that enclose the feet) and in shared humid environments such as communal showers, shared pools, and treatment tubs. Chlorine bleach is a disinfectant and common household cleaner that kills mold. Cleaning surfaces with a chlorine bleach solution prevents the disease from spreading from subsequent contact. Cleaning bathtubs, showers, bathroom floors, sinks, and counters with bleach helps prevent the spread of the disease, including reinfection. Keeping socks and shoes clean (using bleach in the wash) is one way to prevent fungi from taking hold and spreading. Avoiding the sharing of boots and shoes is another way to prevent transmission. Athletes foot can be transmitted by sharing footwear with an infected person. Hand-me-downs and purchasing used shoes are other forms of shoe-sharing.
Pathophysiology
The GNAS1 gene involved in both Pseudohypoparathyroidism type 1a and Pseudopseudohypoparathyroidism is greatly affected by imprinting. When a father who has Pseudohypoparathyroidism undergoes spermatogenesis, imprinting of the GNAS1 gene inactivates both copies of his genes: one will be Functional and the other will be defective. Tissues in the body will re-activate different copies of the GNAS1 gene selectively; the kidneys will selectively activate the (functional) maternal copy while keeping the (defective) paternally-derived gene imprinted and inactive, even in normal individuals. Since the maternally-derived GNAS1 gene is functional, renal handling of calcium and phosphate is normal, and homeostasis is maintained in Pseudopseudohypoparathyroidism. However, the rest of the tissues will instead selectively display the defective gene, resulting in haploinsufficiency of the GNAS1 product in most tissues, and giving the phenotype of Pseudohypoparathyroidism type 1a. As a result, there is also a normal response of urinary cAMP to PTH, and normal serum PTH. Diagnosis
The diagnosis is based on the presence of the Albright hereditary osteodystrophy pseudotype but without the PTH resistance. Blood tests including calcium, phosphate, and PTH will exclude other forms of Pseudohypoparathyroidism. X-rays may reveal a short fourth metacarpal. Genetic testing can confirm the diagnosis by showing GNAS gene mutation. Treatment
Treatments focuses on symptoms, with genetic counseling recommended. History
It was characterized in 1952 by Fuller Albright as "pseudo-pseudohypoparathyroidism" (with hyphen). See also
Antidisestablishmentarianism
Floccinaucinihilipilification
GNAS complex locus
Honorificabilitudinitatibus
Longest word in English
Longest words
Parathyroid hormone
Pneumonoultramicroscopicsilicovolcanoconiosis
Supercalifragilisticexpialidocious

References


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