Levitra Super Active
That it is due to “catching something” purchase levitra super active 40 mg erectile dysfunction after radiation treatment for prostate cancer, not eating what we should quality levitra super active 20mg erectile dysfunction treatment ottawa, like roughage or vitamins, or not doing what we should, like dressing properly, exercising or going to bed on time. The current concepts on disease causation blaming our actions and our genes are simply not logical. After you have found the parasite interlopers hiding in your body you can kill them electronically. And after you have iden- tified the pollutants stuck in your organs you can stop eating them, breathing them or putting them on yourself. In response, your body will begin to heal, just as surely as a mosquito bite heals. It will be an exciting adventure to watch yourself lose your symptoms and get stronger. Self Health The entire purpose of this book is to enable you to diag- nose and treat yourself for any disease. You have three new approaches that make this wish a reality: the understanding that only pollution and parasites make you sick, the quick and inex- pensive diagnostic circuit that lets you find which pollutants and parasites they are, and the zapper or herbal recipe that kills the parasites. Suppose your doctor has already diagnosed you as having “Atypical Lateral Sclerosis” or “Shoulder-Hip Girdle Metas- table Aplasia. And so a new gift is given to humanity, like the gift of music or the art of cooking. How To Heal Your body has been trying to rid itself of its parasites and pollutants all your life! Can you help your body get rid of these accumulations and sweep itself clean again? Sweeping your liver clean is the most powerful way of helping your body to heal itself after the parasites are gone. In days, not weeks or months, you can feel the healing effects of clearing gallstones and kidney stones from your body. But there are miles of bile ducts (50,000 ducts) in the liver; the herbal recipes that do this are used over and over, patiently, until all, the “trash” is removed. So, although you can stop your disease very quickly from progressing, the healing process may not be complete for years. Organs that have been damaged beyond the ability of our simple methods to reverse can be treated with the magic of modern surgery. Killing parasites, removing pollutants and clearing gallstones and kidney stones from your body is a powerful combination of treatments. Should you stop taking your prescription medicine while you are treating yourself? Remember that the medicine is buying you the time to cure yourself, something to be grateful for. Parasites are things that live on us, using up our food and giving us their wastes. Pollutants are toxic things in us making it difficult for our organs to do their work. Our hair turns gray, we develop cataracts, the spine bends, nerves and muscles die. Second, we will remove the toxic molds, metals and chemi- cals in our foods and body products. Third, we will clear away and wash away the stones, secre- tions and debris already formed, that hinder healing. Fourth, we will use herbs and special food factors to hasten healing, being very careful to use pure products. What could be more exciting than finding the tremor is out of your arm or the pain is out of your shoulder? Fortunately for us, pain killers are at hand to get us through it and buy us the time it takes to solve the real problem behind it. As we turn to electrical pain killing the need for addicting drugs should decline. There are other very useful pain killers: acupuncture, massage, listening to music, feedback devices, contemplation, hypnotism, and prayer. But we will focus on getting rid of the cause of pain and healing the organs that are in pain so none of these methods are needed. I am not talking about the pain of a broken bone, twisted ankle, bee sting or sunburn. I am not talking about the pain of a misaligned vertebra or stretch trauma in your leg muscles or arm muscles. All of these may have special names like rheumatoid arthritis, cluster headache, fibromyalgia, bursitis, tennis elbow and so on, but they are all the same phenomenon. Knowing that parasites and pollutants are the real culprits, let us get right down to the job of finding out which they are, where they come from, and how to get rid of them. Our cells try to keep their doorways tight-shut but, of course, they have to open to let food in, or hormones, or other life-signals. There is probably a specific electrical attraction between them and an exact physical fit. Your white blood cells are waiting for them, and will gobble them up in a grand feast. Step Three is to find the pollutants and identify them because this gives us a clue as to their source. An intriguing question will pop into your head as you search your organs for parasites and pollutants. Or do the bacteria come first, jamming open the doorways so the pollutants can enter? The only ones that get away are those that are stuck in doorways and ‘channels with pollutants in them! Fortunately we do not have to know exactly how parasites and pollution make us sick in order to get well. Searching For Bacteria In order to find which organs have the bacteria and which bacteria are present you will need to learn the new technology that makes all of this possible. This technology is a simple electronic circuit that is capable of trapping frequencies in such a way that you can hear them. If your pain returned how would you know if it was the same old bacteria or a new one? What You Will Find First we will study and cure pains of all kinds, starting with the toes and working our way up the body. The inside of your eyeball, the testi- cle, the interior of gallstones, the middle of a tooth abscess or the bowel contents are such places. Your zapper current, because it is high frequency, prefers to “go around” these items, rather than through them.
In addition discount 20 mg levitra super active with amex erectile dysfunction 3 seconds, two other cally and pathologically in any other disease clinical varieties of oral leukoplakia have been entity buy levitra super active 40 mg cheap smoking weed causes erectile dysfunction. The available data show that the preva- described: proliferative verrucous leukoplakia, lence rate of leukoplakia ranges from 0. Some of the leukoplakias are tobacco- cal removal, and hairy leukoplakia, which is a related, whereas in other cases predisposing fac- unique lesion in patients infected with human tors, such as local irritation, Candida albicans, immunodeficiency virus. It is characterized ini- alcohol, industrial products, and possible viruses tially by a slightly raised, poorly demarcated, and have been incriminated. However, it must be corrugated white patch with late formation of emphasized that nonsmokers with leukoplakia are prominent projections, and frequently it appears Fig. This classifi- the floor of the mouth, followed by the tongue and cation has practical clinical significance, since the the lip. Clinical signs suggesting a potential malig- speckled leukoplakia is four to five times more nancy are: speckled surface, erosion or ulceration likely to result in malignant transformation than in the lesion, development of a nodule, induration homogeneous leukoplakia. Proliferative verru- of the periphery, and the location of the lesion cous leukoplakia also shows an increased risk, (high-risk sites). However, the aforementioned whereas the hairy leukoplakia has not been clinical criteria are not totally reliable and all described as progressing to malignancy. However, the most frequent locations are clinical oral leukoplakia exhibits histologically the buccal mucosa and commissures, followed by epithelial dysplasia, carcinoma in situ, or invasive the tongue, palate, lip, alveolar mucosa, gingiva, carcinoma at the time of initial biopsy. The studies of oral leukoplakia have found a frequency lesions may be small or large and the sites of of malignant transformation ranging from 0. The differential diagnosis includes hypertrophic slightly elevated or flat fiery red plaque of varying lichen planus, chronic hyperplastic candidosis, size, with a smooth and velvety surface that is well chemical burn, leukoedema, discoid lupus demarcated from the adjacent normal mucosa erythematosus, and several genetic syndromes (homogeneous form). Histopathologic examination is floor of the mouth, retromolar area, mandibular the most important test to define the nature and alveolar mucosa, and mucobuccal fold are the the relative risk of oral leukoplakic lesions. The presence of epithelial dysplasia signifies a precan- most common sites of involvement, followed by the soft palate, the buccal mucosa, and the tongue cerous lesion. Oral leukoplakia sometimes regresses throplasia exhibit histologically severe epithelial after discontinuation of tobacco use. In addition, dysplasia, carcinoma in situ, or invasive squamous the elimination of any irritating factor is manda- cell carcinoma at the time of diagnosis. The tory, and good oral hygiene and follow-up of the remaining 9% also shows mild or moderate patients is indicated. The differential diagnosis includes local irritation, lichen planus, discoid lupus erythematosus, erythematous candidosis, tuberculosis, and early Erythroplasia squamous cell carcinoma. Histopathologic examination is lesion frequently occurring on the glans penis and essential to establish the accurate diagnosis and to rarely on the oral mucosa. The term "oral erythroplasia" is now used in a clinical descriptive sense, and it is clinically characterized by a red nonspecific plaque on the mucosa that cannot be attributed to any other known disease. There is no sex predilection, and it occurs most frequently between 50 and 70 years of age. Candidal Leukoplakia The differential diagnosis includes leukoplakia, hypertrophic form of lichen planus, white sponge Candidal leukoplakia, or nodular candidosis, is nevus, and other genodermatoses associated with classified by some investigators as a precancerous white oral lesions. It has been shown that croscopic examination is helpful in establishing in 50 to 60% of oral leukoplakia cases with severe the presence of C. Clinically, candidal trimazole, miconazole, or in severe cases systemic leukoplakia is characterized by an intensely white, administration of ketoconazole or fluconazole well-defined plaque not easily detached, which were found to be beneficial. If the lesion does not occasionally shows mild erythema or erosions regress, surgical excision is recommended. The Plummer-Vinson syndrome "a generalized state associated with a significantly may be associated with oral epithelial atrophy and increased risk of cancer. However, this risk of malignant transforma- deficiency dysphagia), involves mainly women tion does not seem to be as high in Europe and between the fourth and sixth decade of life. Plummer-Vinson syndrome, atrophy of the dorsum of the tongue and early leukoplakia. Precancerous Conditions Atrophic Glossitis in Tertiary Syphilis and 40 years of age. Clinically, it is characterized by an intense burning sensation and vesicle forma- Formerly, syphilis was considered to be an impor- tion (particularly on the palate), followed by shal- tant predisposing factor in the development of low ulcers, excessive salivation, or sometimes oral carcinoma. Later the oral mucosa becomes tionship has been exaggerated in the past, and the smooth, atrophic, and inelastic, simulating only relationship that exists is between atrophic scleroderma. It is known lae, the uvula is destroyed, and multiple fibrotic that atrophic glossitis is a manifestation of tertiary bands appear on the entire oral mucosa (Fig. It has The patient develops difficulty in opening the been suggested that the atrophic epithelium is mouth, mastication, and swallowing. The fact that more vulnerable to the action of carcinogenic 13 to 14% of all cases histologically show epithe- agents, resulting in leukoplakia and carcinoma lial dysplasia confirms the precancerous nature of (Fig. In India 40 to 50% of oral cancer now very rare because of early diagnosis and coexist with submucous fibrosis. Submucous Fibrosis The differential diagnosis includes scleroderma, Plummer-Vinson syndrome, pernicious anemia, Submucous fibrosis is a chronic disease of atrophic lichen planus, and chronic bullous dis- unknown cause affecting the oral mucosa and eases. The diagnosis is confirmed by Asians, although sporadic cases have been histopathologic examination. Systemic and the use of chili, betel nut chewing, and and local use of corticosteroids have only a tem- tobacco are considered as etiologic agents. Atrophic glossitis in tertiary syphilis associated with leukoplakia and early squamous cell carcinoma. Submucous fibrosis, squamous-cell carcinoma development on the tongue of patient in Figure 430, 3 years later. Precancerous Conditions Epidermolysis Bullosa Dystrophica Lichen Planus Epidermolysis bullosa dystrophica is a rare The precancerous nature of lichen planus (see p. Many investigators deny the recessive variants of the disease lead to severe premalignant potential of the disease, whereas atrophy and scarring of the skin and mucous mem- others have reported malignant transformation branes. It has been suggested neoplasms, usually squamous cell carcinoma of that particularly the erosive and atrophic forms of the skin and less commonly of the oral mucosa oral lichen planus show an increased risk for (Fig. However, the available data are scar formation in recessive dystrophic epidermoly- unreliable and the possible precancerous nature of sis bullosa is associated with a persistent growth- oral lichen planus needs further clarification. This chronic growth activation state or failure of cells to differentiate in a normal fashion may be linked to the high incidence of squamous-cell carcinomas. Oral clinicians should keep in mind the possi- bility of development of squamous-cell carcinoma in the atrophic oral lesions of epidermolysis bul- losa dystrophica, despite the fact that few cases have been reported so far. It is a systemic disease that usually begins between the first and third year of life, with predominating skin, ocu- lar, and neurologic abnormalities. Clinically, the skin is dry, atrophic, with numerous freckles, erythema, and telangiectasias. Pigmentation, scales, scars, and precancerous actinic keratosis are common manifestations as well. About 50% of the patients with xeroderma pigmentosum develop multiple malignant tumors predominantly on sun-exposed skin (squamous and basal cell carcinoma, melanoma) leading to death, usually before the age of 20 years. Squamous cell car- cinoma occasionally develops on the lower lip and rarely intraorally (Fig.
Additionally buy levitra super active without prescription erectile dysfunction drugs in ghana, atrial flutter or fibrillation may be evident in patients with significant right atrial enlargement cheap levitra super active 20 mg with visa erectile dysfunction opiates. Echocardiography The anatomy of Ebstein’s anomaly can usually be well delineated by 2D-echocardiography. Anatomic details of the tricuspid valve, its attachments, and the extent of displacement into the right ventricle can be evaluated. Cross and Ra-id Abdulla and function of the right atrium, atrialized right ventricle, and true right ventricle can be determined. Color flow Doppler is also an important aspect of the echocardiographic evaluation of Ebstein’s anomaly that can yield information regarding the extent of tricuspid insufficiency, direction and extent of any shunting, and degree of outflow tract obstruction. In severe forms of Ebstein’s anomaly, there can also be dyssynchronous motion of the interventricular septum causing left ventricular outflow tract obstruction that can be evident on 2D-echocardiography. Transesophageal echocardiography or cardiac magnetic resonance imaging can be used to image older patients with Ebstein’s anomaly who may have limited echocardiographic windows. Cardiac Catheterization Cardiac catheterization is rarely needed to diagnose or assess patients with Ebstein’s anomaly. However, it can be useful in rare cases to measure right atrial, right ventricular, or pulmonary artery pressures. Quantification of right-to-left shunting and cardiac output performed in the catheterization laboratory may also be useful in the management of more severe forms of Ebstein’s anomaly. Angiographic evaluation of right ventricular outflow tract or pulmonary artery obstruction can be helpful, particularly in cases where interventional catheterization techniques can be used to relieve the obstruction. It is of historical significance to note that the simultaneous measurement of pressure and intracardiac electrocardiogram in the atrialized portion of the right ventricle demonstrates atrial pressures with ventricular electrical tracings. Treatment/Management There is a wide variability in the medical management of Ebstein’s anomaly that correlates with the severity of the heart disease. In the cyanotic newborn with mild to moderate Ebstein’s anomaly, close observation and clinical support may be all that is needed until the normal drop in pulmonary vascular resistance occurs. As the pulmonary vascular resistance decreases, there is increasing forward flow through the right ventricle resulting in less cyanosis secondary to atrial level shunting. These patients often benefit from oxygen to stimulate lowering of the pulmonary vascular resistance, and in some cases, the use of prostaglandin E1 to maintain ductal patency may be required to ensure adequate pulmonary blood flow. Infants with mild Ebstein’s anomaly may remain completely asymptomatic and require no medical management. Those with more severe forms of Ebstein’s anomaly experience congestive heart failure symptoms and benefit from anticongestive 24 Ebstein’s Anomaly 289 therapy with diuretics, and may also require inotropic support if there is significant compromise in cardiac output. Patients with associated Wolff–Parkinson–White syndrome can be managed conservatively, but if they experience supraventricular tachycardia then appropriate antiarrhythmic medications should be started or the patient should be considered for electrophysiology study and ablation therapy. Surgical management of Ebstein’s anomaly is also variable and dictated by the degree of cyanosis or heart failure. Patients with cyanosis and right ventricular outflow tract obstruction may benefit from interventional catheterization or sur- gery to relieve the obstruction. These patients would then usually be considered for a Glenn cavopulmonary anastomosis at several months of age. Newborns with sig- nificant tricuspid insufficiency pose a particularly difficult surgical challenge. Patients have undergone varying types of tricuspid valve repairs in the newborn period, but usually with only limited success. Older patients with progressive tri- cuspid insufficiency may benefit from tricuspid valve repair or replacement. Indications for surgery include progressive cyanosis, worsening heart failure, arrhythmias, and paradoxical emboli due to right-to-left atrial shunting. Long-term Follow-up Children with significant tricuspid insufficiency require long-term anticongestive therapy with diuretics and possibly digoxin. However, those patients with mild degrees of tricuspid insufficiency may remain asymptomatic and require no treatment in the early years. It is not uncommon, however, for these patients to develop worsening congestive heart failure or cyanosis due to progressive tricuspid insufficiency during the second or third decade of life. These patients would then need to be treated medically for the heart failure symptoms and surgical repair or replacement of the tricuspid valve should be considered. Patients should be followed closely for the evidence of cyanosis, increasing shortness of breath, increasing fatigue, or for the evidence of arrhythmias. Prognosis The prognosis of Ebstein’s anomaly is directly related to the severity of the valve abnormality and degree of tricuspid insufficiency. It is estimated that the overall mortality rate in the first year of life is around 20%. The average life expectancy for early survivors is 20 years, but there are ample reports of patients with milder forms of Ebstein’s anomaly who live much longer. Cross and Ra-id Abdulla Case Scenarios Case 1 About 6 h after an uncomplicated delivery, it is noted that a full term female infant appears to be cyanotic. Heart examination reveals increased right precordial activity with a right-sided heave. There is a 3/6 systolic regurgitant murmur of tricuspid insufficiency heard along the left lower sternal border and a wide split first heart sound is heard. Chest X-ray demonstrates a markedly enlarged cardiac silhouette and the lung fields are dark, consistent with diminished pulmonary blood flow. An echocardiogram is obtained and shows severe apical displacement of the tricuspid valve into the right ventricle, and there is severe tricuspid valve insuffi- ciency. The right atrium is moderately enlarged and a small atrial septal defect is present. This newborn has severe Ebstein’s anomaly with severe tricuspid valve insuf- ficiency. The right ventricle is unable to produce adequate pressure to overcome the high pulmonary vascular resistance in this newborn. There is also right to left shunting of deoxygenated blood across the atrial septum sec- ondary to the tricuspid insufficiency and high right atrial pressures. The baby needs to be followed over the following days as the pul- monary vascular resistance drops to determine if forward pulmonary blood flow across the small right ventricle improves. The baby can most likely be tried off the prostaglandin E1 in 3–4 days to determine if there is adequate pulmonary blood flow after the pulmonary vascular resistance has decreased. In severe cases, the child may eventually require a univentricular repair (Fontan procedure), however, this is unlikely. His past medical history is unremarkable, although his mother had been told in the past that he had a faint murmur. Chest X-ray demonstrates a mildly enlarged cardiac silhouette, but is otherwise normal.
The peripheral ameloblastoma probably arises fromdental lamina rests or frombasal epithelial cells cheap levitra super active online american express erectile dysfunction facts and figures. Clinical features Peripheral ameloblastoma is rare and accounts for about 1–2% of all ameloblastomas buy 40 mg levitra super active erectile dysfunction treatment houston. It usually presents as a painless, slow- growing, nonulcerated, sessile red mass (Fig. The posterior alveolar mucosa and the gingiva of the mandible are more frequently affected. The clinical diagnosis should be confirmed by a biopsy and histopathological examination. Differential diagnosis Pyogenic granuloma, peripheral giant cell gran- uloma, fibroma, squamous-cell carcinoma, extraosseous calcifying epi- thelial odontogenic tumor, extraosseous calcifying epithelial odontogen- ic cyst, odontogenic myxoma. Sturge–Weber Angiomatosis Definition Sturge–Weber angiomatosis, or encephalotrigeminal an- giomatosis, is a relatively rare, sporadic congenital capillary vascular malformation typically involving areas innervated by the trigeminal nerve. Clinical features The main clinical features are characterized by uni- lateral hemangiomas of the facial skin, oral mucosa, and leptomeninges, brain calcification, ocular disorders, epilepsy, and occasionally mild mental handicap. Oral hemangiomas have a bright red or purple color and are usually flat but may also be raised, causing tissue enlargement (Fig. Dentists and oral surgeons must be careful during tooth ex- traction and periodontal surgery so as to avoid bleeding complications. Facial hemangiomas have a bright red color and are asymptomatic Laskaris, Pocket Atlas of Oral Diseases © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license 81 3 Black and Brown Lesions Pigmented oral lesions are a large group of disorders in which the dark or brown color is the essential clinical characteristic. Usually, the dark color of the lesions is due to melanin production by either melanocytes or nevus cells. In addition, exogenous deposits and pigment-producing bacteria can also produce pigmented lesions. Benign disorders, deposits, benign and malignant neoplasms, and systemic diseases are included in the group of pigmented lesions. O Normal pigmentation O Lentigo O Amalgam tattoo O Lentigo maligna O Heavy-metal deposition O Pigmented nevi O Drug-induced pigmentation O Nevus of Ota O Smoker’s melanosis O Melanoma O Black hairy tongue O Addison disease O Ephelis O Peutz–Jeghers syndrome Laskaris, Pocket Atlas of Oral Diseases © 2006 Thieme All rights reserved. Usage subject to terms and conditions of license 82 Black and Brown Lesions Normal Pigmentation Definition and etiology Increased melanin production and deposition in the oral mucosa may often be a physiological finding, particularly in dark-skinned individuals. Clinical features This type of pigmentation is persistent and symmet- rical, and clinically presents as asymptomatic black or brown areas of varying size. The gingiva are most commonly affected, followed by the buccal mucosa, palate, and lips (Fig. The pigmentation is more prominent in areas of pressure or friction, and usually becomes more intense with increasing age. Differential diagnosis Addison disease, smoker’s melanosis, drug-in- duced pigmentation, pigmented nevi, melanoma, amalgam tattoo. Clinical features The condition presents as a well-defined irregular or diffuse flat area, with a bluish-black discoloration of varying size (Fig. The most common sites of involvement are the gingiva, alveolar mucosa, and buccal mucosa. Differential diagnosis Pigmented nevi, lentigo, freckles, melanoma, normal pigmentation, other metal tattoo. Usage subject to terms and conditions of license 84 Black and Brown Lesions Heavy-Metal Deposition Definition and etiology Heavy-metal deposition is a rare oral condi- tion caused by ingestion or exposure to bismuth, lead, silver, mercury, and other heavy metals. Clinical features Clinically, the most common pattern (bismuth, lead) is a bluish line along the marginal gingiva, or similar spots within the gingival papillae (Fig. Drug-Induced Pigmentation Definition Drug-induced oral pigmentation is a relatively common condition, caused by increased melanin production or drug metabolite deposition. Etiology Antimalarials, tranquilizers, minocycline, azidothymidine, ke- toconazole, phenolphthalein, and others are the most common drugs that induce pigmentation. Clinical features The clinical picture varies, and the condition may appear as irregular brown or black macules or plaques, or diffuse mela- nosis (Fig. The buccal mucosa, tongue, palate, and gingiva are the most commonly affected sites. Differential diagnosis Normal pigmentation, Addison disease, Peutz– Jeghers syndrome. Usage subject to terms and conditions of license 86 Black and Brown Lesions Smoker’s Melanosis Definition Smoker’s melanosis, or smoking-associated melanosis, is a benign abnormal melanin pigmentation of the oral mucosa. Clinical features Clinically, it appears as multiple brown pigmented areas, usually located on the anterior labial gingiva of the mandible (Fig. Pigmentation of the buccal mucosa and palate has been asso- ciated with pipe smoking. Differential diagnosis Normal pigmentation, drug-induced pigmenta- tion, pigmented nevi, melanoma, Addison disease. Cessation of smoking is usually associated with a return of normal mucosal pigmentation. Usage subject to terms and conditions of license 88 Black and Brown Lesions Ephelis Definition Ephelides, or freckles, are discrete brown macules, com- monly seen on sun-exposed skin and rarely in the mouth. Clinical features Clinically, the lesions appear as solitary and well- demarcated asymptomatic round brown macules, less than 5 mm in diameter (Fig. Differential diagnosis Lentigo, pigmented nevi, melanoma, drug-as- sociated pigmentation, Peutz–Jeghers syndrome, Albright syndrome. Treatment No treatment is required, except for aesthetic or diagnostic considerations. Clinical features The condition presents as small round flat spots, brown or dark brown in color, usually less than 0. Differential diagnosis Ephelis, pigmented nevi, melanoma, Peutz– Jeghers syndrome. Usage subject to terms and conditions of license 90 Black and Brown Lesions Lentigo Maligna Definition Lentigo maligna, or Hutchinson’s freckle, is a premalignant lesion of melanocytes that probably represents in-situ melanoma. Clinically, it appears as a slowly expanding black or brown plaque, with irregular borders (Fig. The lips, buccal mucosa, palate, and floor of the mouth are the common sites affected. Pigmented Nevi Definition Pigmented cellular nevi are benign malformations of me- lanocytes and “nevus cells,” common in the skin and rare in the oral mucosa. Clinical features Based on histological criteria, oral pigmented nevi are classified into four types: intramucosal, junctional, compound, and blue. Clinically, the lesion appears as an asymptomatic, well-demarcated, flat or slightly elevated, brown, black, or blue spot or plaque (Fig. Usage subject to terms and conditions of license 92 Black and Brown Lesions Nevus of Ota Definition Nevus of Ota, or oculodermal melanocytosis, is a hamar- tomatous disorder of the melanocytes that predominantly involves the skin of the face and eyes, and mucous membranes.
By N. Javier. Rogers State University.