Diseases

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MARASMUS is a form of severe protein-energy malnutrition characterized by energy deficiency.
A child with marasmus looks emaciated. Body weight may be reduced to less than 80% of the normal weight for that height.[citation needed] Marasmus occurrence increases prior to age 1, whereas kwashiorkor occurrence increases after 18 months. The prognosis is better than it is in kwashiorkor.[1] Signs and symptoms The malnutrition associated with marasmus leads to extensive tissue and muscle wasting, as well as variable edema. Other common characteristics include dry skin, loose skin folds hanging over the glutei, axillae, etc. There is also drastic loss of adipose tissue from normal areas of fat deposits like buttocks and thighs. The afflicted are often fretful, irritable, and voraciously hungry. Causes Marasmus is caused by a severe deficiency of nearly all nutrients, especially protein and calories. Treatment It is necessary to treat not only the symptoms but also the complications of the disorder, including infections, dehydration, and circulation disorders, which are frequently lethal and lead to high mortality if ignored. Ultimately, marasmus can progress to the point of no return when the body's machinery for protein synthesis, itself made of protein, has been degraded to the point that it cannot handle any protein. At this point, attempts to correct the disorder by giving food or protein are futile.

KWASHIORKOR is an acute form of childhood protein-energy malnutrition characterized by edema, irritability,
anorexia, ulcerating dermatoses, and an enlarged liver with fatty infiltrates. The presence of edema caused by poor nutrition defines kwashiorkor.[1] Kwashiorkor was thought to be caused by insufficient protein consumption but with sufficient calorie intake, distinguishing it from marasmus. More recently, micronutrient and antioxidant deficiencies have come to be recognized as contributory. Cases in the developed world are rare.[2] Jamaican pediatrician Dr. Cicely D. Williams introduced the name into the medical community in her 1935 Lancet article.[3] The name is derived from the Ga language of coastal Ghana, translated "the sickness the baby gets when the new baby comes"[4][citation needed], and reflecting the development of the condition in an older child who has been weaned from the breast when a younger sibling comes.[5] Breast milk contains proteins and amino acids vital to a child's growth. In at-risk populations, kwashiorkor may develop after a mother weans her child from breast milk and replaces the diet with foods high in starches and carbohydrates and deficient in protein. Signs and symptoms The defining sign of kwashiorkor in a malnourished child is pedal edema (swelling of the feet). Other signs include a distended abdomen, an enlarged liver with fatty infiltrates, thinning hair, loss of teeth, skin depigmentation and dermatitis. Children with kwashiorkor often develop irritability and anorexia. [1] Victims of kwashiorkor fail to produce antibodies following vaccination against diseases, including diphtheria and typhoid.[6] Generally, the disease can be treated by adding food energy and protein to the diet; however, it can have a long-term impact on a child's physical and mental development, and in severe cases may lead to death.

Possible causes There are various explanations for the development of kwashiorkor and the topic remains controversial.[7] It is now accepted that protein deficiency, in combination with energy and micronutrient deficiency, is necessary but not sufficient to cause kwashiorkor[citation needed]. The condition is likely due to deficiency of one of several types of nutrients (e.g., iron, folic acid, iodine, selenium, vitamin C), particularly those involved with anti-oxidant protection. Important anti-oxidants in the body that are reduced in children with kwashiorkor include glutathione, albumin, vitamin E and polyunsaturated fatty acids. Therefore, if a child with reduced type one nutrients or anti-oxidants is exposed to stress (e.g. an infection or toxin) he/she is more liable to develop kwashiorkor. Ignorance of nutrition can be a cause. Dr. Latham, director of the Program in International Nutrition at Cornell University cited a case where parents who fed their child cassava failed to recognize malnutrition because of the edema caused by the syndrome and insisted the child was well-nourished despite the lack of dietary protein.[citation needed] One important factor in the development of kwashiorkor is aflatoxin poisoning. Aflatoxins are produced by molds and ingested with moldy foods. They are toxified by the cytochrome P450 system in the liver, the resulting epoxides damage liver DNA. Since many serum proteins, in particular albumin, are produced in the liver, the symptoms of kwashiorkor are easily explained. It is noteworthy that kwashiorkor occurs mostly in warm, humid climates that encourage mold growth. In dry climates, marasmus is the more frequent disease associated with malnutrition. This has important consequences for treatment of the patients. Protein should be supplied only for anabolic purposes. The catabolic needs should be satisfied with carbohydrate and fat. Protein catabolism involves the urea cycle, which is located in the liver and can easily overwhelm the capacity of an already damaged organ. The resulting liver failure can be fatal. Other malnutrition syndromes include marasmus and cachexia, although the latter is often caused by underlying illnesses.

ANEMIA (pronounced /əˈniːmiə/, also spelled anaemia and anæmia; from Ancient Greek ἀναιμία anaimia,
meaning lack of blood) is a decrease in normal number of red blood cells (RBCs) or less than the normal quantity of hemoglobin in the blood.[1][2] However, it can include decreased oxygen-binding ability of each hemoglobin molecule due to deformity or lack in numerical development as in some other types of hemoglobin deficiency. Because hemoglobin (found inside RBCs) normally carries oxygen from the lungs to the tissues, anemia leads to hypoxia (lack of oxygen) in organs. Because all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences. Anemia is the most common disorder of the blood. There are several kinds of anemia, produced by a variety of underlying causes. Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). There are two major approaches: the "kinetic" approach which involves evaluating production, destruction and loss [3], and the "morphologic" approach which groups anemia by red blood cell size. The morphologic approach uses a quickly available and cheap lab test as its starting point (the MCV). On the other hand, focusing early on the question of production may allow the clinician more rapidly to expose cases where multiple causes of anemia coexist. Signs and symptoms Anemia goes undetected in many people, and symptoms can be minor or vague. The signs and symptoms can be related to the anemia itself, or the underlying cause. Most commonly, people with anemia report non-specific symptoms of a feeling of weakness, or fatigue, general malaise and sometimes poor concentration. They may also report shortness of breath, dyspnea, on exertion. In very severe anemia, the body may compensate for the lack of oxygen carrying capability of the blood by increasing cardiac output.

The patient may have symptoms related to this, such as palpitations, angina (if preexisting heart disease is present), intermittent claudication of the legs, and symptoms of heart failure. On examination, the signs exhibited may include pallor (pale skin, mucosal linings and nail beds) but this is not a reliable sign. There may be signs of specific causes of anemia, e.g., koilonychia (in iron deficiency), jaundice (when anemia results from abnormal break down of red blood cells — in hemolytic anemia), bone deformities (found in thalassaemia major) or leg ulcers (seen in sickle cell disease). In severe anemia, there may be signs of a hyperdynamic circulation: a fast heart rate (tachycardia), flow murmurs, and cardiac enlargement. There may be signs of heart failure. Pica, the consumption of non-food based items such as dirt, paper, wax, grass, ice, and hair, may be a symptom of iron deficiency, although it occurs often in those who have normal levels of hemoglobin. Chronic anemia may result in behavioral disturbances in children as a direct result of impaired neurological development in infants, and reduced scholastic performance in children of school age. Restless legs syndrome is more common in those with iron deficiency anemia. Less common symptoms may include swelling of the legs or arms, chronic heartburn, vague bruises, vomiting, increased sweating, and blood in stool. Diagnosis Generally, clinicians request complete blood counts in the first batch of blood tests in the diagnosis of an anemia. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells by flow cytometry, which is an important tool in distinguishing between the causes of anemia. Examination of a stained blood smear using a microscope can also be helpful, and is sometimes a necessity in regions of the world where automated analysis is less accessible. In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCH and MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements.

GOITER also called a bronchocele, is a swelling in the thyroid gland,[1] which can lead to a swelling of the neck or
larynx (voice box). Goitre usually occurs when the thyroid gland is not functioning properly. Classification They are classified in different ways:
  

A "diffuse goitre" is a goitre that has spread through all of the thyroid (and can be a "simple goitre", or a "multinodular goitre"). "Toxic goitre" refers to goitre with hyperthyroidism. These are most commonly due to Graves' disease, but can be caused by inflammation or a multinodular goitre. "Nontoxic goitre" (associated with normal or low thyroid levels) refers to all other types (such as that caused by lithium or certain other autoimmune diseases).

Other type of classification:
  

I - palpation struma - in normal posture of head it cannot be seen. Only found when palpating. II - struma is palpative and can be easily seen. III - struma is very big and is retrosternal. Pressure and compression marks.

Signs and symptoms In general, goitre unassociated with any hormonal abnormalities will not cause any symptoms aside from the presence of anterior neck mass. However, for particularly large masses, compression of the local structures may result in difficulty in breathing or swallowing. In those presenting with these symptoms, malignancy must be considered. Meanwhile, toxic goitres will present with symptoms of thyrotoxicosis such as palpitations, hyperactivity, weight loss despite increased appetite, and heat intolerance. Causes Worldwide, the most common cause for goitre is iodine deficiency. In countries that use iodized salt, Hashimoto's thyroiditis is the most common cause. [2] Other causes are:[citation needed] Hypothyroid
  

Inborn errors of thyroid hormone synthesis, causing congenital hypothyroidism (E03.0) Ingestion of goitrogens, such as cassava. Side-effects of pharmacological therapy (E03.2)

Hyperthyroid
  

Graves' disease (E05.0) Thyroiditis (acute or chronic) (E06) Thyroid cancer

Treatment Treatment may not be necessary if the goitre is small. Goitre may be related to hyper- and hypothyroidism (especially Graves' disease) and may be reversed by treatment. Graves' disease can be corrected with antithyroid drugs (such as propylthiouracil and methimazole), thyroidectomy (surgical removal of the thyroid gland), and iodine-131 (131I - a radioactive isotope of iodine that is absorbed by the thyroid gland and destroys it). Hypothyroidism may raise the risk of goitre because it usually increases the production of TRH and TSH. Levothyroxine, used to treat hypothyroidism, can also be used in euthyroid patients for the treatment of goitre. Levothyroxine suppressive therapy decreases the production of TRH and TSH and may reduce goitre, thyroid nodules, and thyroid cancer. Blood tests are needed to ensure that TSH is still in range and the patient has not become subclinically hyperthyroid. If TSH levels are not carefully monitored, it is alleged that levothyroxine may increase the risk of osteoporosis but no peer reviewed studies on levothyroxine replacement of Hypothyroid patients causing this effect have actually been produced. Thyroidectomy with 131I may be necessary in euthyroid goitrous patients who do not respond to levothyroxine treatment, especially if the patients have difficulty breathing or swallowing. 131I, with or without the pre-injection of synthetic TSH, can relieve obstruction and reduce the size of the goitre by thirty to sixty-five percent. Depending on how large the goitre is and how much of the thyroid gland must be removed or destroyed, thyroidectomy or 131I may produce hypothyroidism requiring life-long treatment and may eventually lead to death.

CANCER /ˈkænsər/

(medical term: malignant neoplasm) is a class of diseases in which a group of cells display uncontrolled growth (division beyond the normal limits), invasion (intrusion on and destruction of adjacent tissues), and sometimes metastasis (spread to other locations in the body via lymph or blood). These three malignant properties of cancers differentiate them from benign tumors, which are self-limited, and do not invade or metastasize. Most cancers form a tumor but some, like leukemia, do not. The branch of medicine concerned with the study, diagnosis, treatment, and prevention of cancer is oncology.
( listen)

Causes: Cancers are caused by abnormalities in the genetic material of the transformed cells.[4] These abnormalities may be due to the effects of carcinogens, such as tobacco smoke, radiation, chemicals, or infectious agents. Other cancer-promoting genetic abnormalities may randomly occur through errors in DNA replication, or are inherited, and thus present in all cells from birth. The heritability of cancers is usually affected by complex interactions between carcinogens and the host's genome. Signs and symptoms Symptoms of cancer metastasis depend on the location of the tumor. Roughly, cancer symptoms can be divided into three groups:
 



Local symptoms: unusual lumps or swelling (tumor), hemorrhage (bleeding), pain and/or ulceration. Compression of surrounding tissues may cause symptoms such as jaundice (yellowing the eyes and skin). Symptoms of metastasis (spreading): enlarged lymph nodes, cough and hemoptysis, hepatomegaly (enlarged liver), bone pain, fracture of affected bones and neurological symptoms. Although advanced cancer may cause pain, it is often not the first symptom. Systemic symptoms: weight loss, poor appetite, fatigue and cachexia (wasting), excessive sweating (night sweats), anemia and specific paraneoplastic phenomena, i.e. specific conditions that are due to an active cancer, such as thrombosis or hormonal changes.

Every symptom in the above list can be caused by a variety of conditions (a list of which is referred to as the differential diagnosis). Cancer may be a common or uncommon cause of each item. Prevention Cancer prevention is defined as active measures to decrease the incidence of cancer.[32] Greater than 30% of cancer is preventable via avoiding risk factors including: tobacco, overweight or obesity, low fruit and vegetable intake, physical inactivity, alcohol, sexually transmitted infection, air pollution.[33] This can be accomplished by avoiding carcinogens or altering their metabolism, pursuing a lifestyle or diet that modifies cancer-causing factors and/or medical intervention (chemoprevention, treatment of pre-malignant lesions). The epidemiological concept of "prevention" is usually defined as either primary prevention, for people who have not been diagnosed with a particular disease, or secondary prevention, aimed at reducing recurrence or complications of a previously diagnosed illness.

MYOPIA (Greek: μυωπία, muōpia, "nearsightedness"[1]), is a refractive defect of the eye in which collimated light
produces image focus in front of the retina when accommodation is relaxed. Those with myopia see near objects clearly but far away objects appear blurred. With myopia, the eyeball is too long, or the cornea is too steep, so images are focused in the vitreous inside the eye rather than on the retina at the back of the eye. The opposite defect of myopia is hyperopia or "farsightedness" or "long-sightedness"—this is where the cornea is too flat or the eye is too small. Eye care professionals most commonly correct myopia through the use of corrective lenses, such as glasses or contact lenses. It may also be corrected by refractive surgery, but this does have many risks and side effects. The corrective lenses have a negative optical power (i.e. are concave) which compensates for the excessive positive diopters of the myopic eye. Alternative ideas and methods of treatment exist, most notably the claim that myopia is caused by excessive near sight work Signs and symptoms Myopia presents with blurry distance vision but good near vision.

Cause Because in the most common, "simple" myopia, the eye length is too long, any etiologic explanation must account for such axial elongation. To date, no single theory has been able to satisfactorily explain this elongation. In the mid-1900s, mainstream ophthalmologists and optometrists believed myopia to be primarily hereditary; the influence of near work in its development seemed "incidental" and the increased prevalence of the condition with increasing age was viewed as a "statistical curiosity".[4][5][28] Among mainstream researchers and eye care professionals, myopia is now thought to be a combination of genetic and environmental factors.[9][27][29] There are currently two basic mechanisms believed to cause myopia: form deprivation (also known as pattern deprivation[30]) and optical defocus.[31] Form deprivation occurs when the image quality on the retina is reduced; optical defocus occurs when light focuses in front of or behind the retina. Numerous experiments with animals have shown that myopia can be artificially generated by inducing either of these conditions. In animal models wearing negative spectacle lenses, axial myopia has been shown to occur as the eye elongates to compensate for optical defocus. [31] The exact physiological mechanism of this image-controlled elongation of the eye is still unknown, but the mechanism has been described quantitatively with mathematical precision.[29][32][33] It has been suggested that accommodative lag leads to blur (i.e. optical defocus) which in turn stimulates axial elongation and myopia. Prevention There is no universally accepted method of preventing myopia.[9] Commonly attempted preventative methods include wearing reading glasses, eye drops and participating in more outdoor activities are described below. Some clinicians and researchers recommend plus power (convex) lenses in the form of reading glasses when engaged in close work or reading instead of using single focal concave lens glasses commonly prescribed.[9][58] The reasoning behind a convex lens's possible effectiveness in preventing myopia is simple to understand: Convex lenses' refractive property of converging light are used in reading glasses to help reduce the accommodation needed when reading and doing close work. Although accommodation is irrelevant in Medina's quantitative model of myopia, it reaches the same conclusion. The model teaches a very simple method to prevent myopia.[32]. For people with Presbyopia whose eye's lens can not accommodate enough for very near focus; reading glasses help converge the light before it enters the eye to complement the refractive power of the eye lens so near objects focus clearly on the retina. [59] By reducing the focusing effort needed (accommodation), reading glasses or convex lenses essentially relax the focusing ciliary muscles and may consequently reduce chances of developing myopia. [60] Inexpensive non prescription reading glasses are commonly sold in drug stores and dollar stores. Alternatively, reading glasses fitted by optometrists have a wider range of styles and lens choices. [61] A recent Malaysian study reported in New Scientist[62] suggested that undercorrection of myopia caused more rapid progression of myopia.[63] However, the reliability of these data has been called into question.[64] Many myopia treatment studies suffer from any of a number of design drawbacks: small numbers, lack of adequate control group, failure to mask examiners from knowledge of treatments used, etc. Diabetes mellitus is a common disease in the United States. It is estimated that over 16 million Americans are already caught with diabetes, and 5.4 million diabetics are not aware of the existing disease. Diabetes prevalence has increased steadily in the last half of this century and will continue rising among U.S. population. It is believed to be one of the main criterions for deaths in United States, every year. This diabetes information hub projects on the necessary steps and precautions to control and eradicate diabetes, completely. Diabetes is a metabolic disorder where in human body does not produce or properly uses insulin, a hormone that is required to convert sugar, starches, and other food into energy. Diabetes mellitus is characterized by constant high levels of blood glucose (sugar). Human body has to maintain the blood glucose level at a very narrow range, which is done with insulin and glucagon. The function of glucagon is causing the liver to release glucose from its cells into the blood, for the production of energy. Following are the Causes of Diabetes



         

Hereditary or Inherited Traits : It is strongly believed that due to some genes which passes from one generation to another, a person can inherit diabetes. It depends upon closeness of blood relationship as mother is diabetic, the risk is 2 to 3%, father is diabetic, the risk is more than the previous case and if both the parents are diabetic, the child has much greater risk for diabetes. Age : Increased age is a factor which gives more possibility than in younger age. This disease may occur at any age, but 80% of cases occur after 50 year, incidences increase with the age factor. Poor Diet (Malnutrition Related Diabetes) : Improper nutrition, low protein and fiber intake, high intake of refined products are the expected reasons for developing diabetes. Obesity and Fat Distribution : Being overweight means increased insulin resistance, that is if body fat is more than 30%, BMI 25+, waist grith 35 inches in women or 40 inches in males. Sedentary Lifestyle : People with sedentary lifestyle are more prone to diabetes, when compared to those who exercise thrice a week, are at low risk of falling prey to diabetes. Stress : Either physical injury or emotional disturbance is frequently blamed as the initial cause of the disease. Any disturbance in Cortiosteroid or ACTH therapy may lead to clinical signs of the disease. Drug Induced: Clozapine (Clozaril), olanzapine (Zyprexa), risperidone (Risperdal), quetiapine (Seroquel) and ziprasidone (Geodon) are known to induce this lethal disease. Infection : Some of the strephylococci is suppose to be responsible factor for infection in pancreas. Sex : Diabetes is commonly seen in elderly especially males but, strongly in women and those females with multiple pregnancy or suffering from (PCOS) Polycystic Ovarian Syndrome. Hypertension : It had been reported in many studies that there is direct relation between high systolic pressure and diabetes. Serum lipids and lipoproteins : High triglyceride and cholesterol level in the blood is related to high blood sugars, in some cases it has been studied that risk is involved even with low HDL levels in circulating blood.

Prevention Whether your treatment consists of diet alone, diet and tablets or diet and insulin, you need regular blood tests to keep a check on your blood sugar. Urine sugar test is not a reliable indicator of diabetes control. When blood glucose remains higher than 200mg/dl for 8-10 weeks, the concentration of glycosylated hemoglobin (HbA1c) arises. A (HbA1c) measurement therefore reflects the blood glucose control over a preceding 2-3 months period, while the estimates of blood glucose indicate the glucose value at the time of blood test. HbA1c values between 6-7% indicate very good control on diabetes. You should aim at keeping your blood glucose in the normal range i.e. between 90-130 mg/dl while fasting and less than 180 mg/dl after meals and HbA1c around 7%. Frequent tests for blood glucose are necessary when starting treatment with insulin. If you are doing capillary blood glucose test using a hand held glucometer, do not squeeze the finger to bring out a sample after you have picked. This invariably gives a low glucose value. Ask your diabetes nurse for a demonstration of capillary blood glucose test. Urine test for sugar is not reliable indicator of diabetes control. Although spillage of sugar in urine occurs when the blood glucose exceeds 180 mg/dl in the majority of healthy persons, this is not always so in a patient with diabetes. Most patients with diabetes of many years acquire an increase in the renal threshold for glucose (capacity to prevent spillage of glucose into urine). Hence urine test for glucose is not helpful for assessing control of diabetes. In the presence of urinary infections, the bacteria eats up the sugar present in urine, thereby making urine test for sugar unreliable.

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