DIGESTIVE DISTURBANCES: CONSTIPATION
When the bowels do not move with their accustomed frequency or when waste material is passed in small, hard masses, sometimes with pain, the symptom is called constipation. Accompanying the condition one may have a sense of fullness or tightness in the abdomen, and sometimes pain. Other associated symptoms include headache, weakness, indigestion, belching, aching muscles, and even painful urination.
Constipation is not a disease – it is a symptom indicating that the fundamental difficulty lies in improper diet, wrong eating habits, a variety of diseases or abnormalities of structure, and, quite frequently, emotional difficulties or disorders of personality.
Most people have one or two actions of the bowel daily, usually after breakfast or after the largest meal of the day. Irregularity of eating or sleeping brings on irregularity of bowel action. Travel, stress, complete changes in nature of food, also disturb regularity of bowel action.
In old people blocking of the lower bowel may occur, due to inefficiency of the bowel musculature and lessened sensitivity of the nervous system. Exceedingly old people, who spend much of their time in bed, note particularly the tendency to less frequent action of the bowel. Most people under sixty years of age may be trained to proper rhythm by teaching good habits aided by a carefully selected diet.
The simplest materials for use in ordinary cases are the lubricants such as paraffin oil or mineral oil, which must not be used routinely because it picks up vitamin A; also useful are bulk materials, such as agar or cellulose, which are available in special preparations.
Spasticity of the colon and sensitivity to various foods such as chocolate, onions, garlic, cabbage, or other common sensitizers must be investigated.
The frequently used laxatives contain phenolphthalein, or senna, or magnesia; stronger are salts and castor oil.
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CHRONOLOGY OF LANDMARKS IN DIABETES MELLITUS (HISTORY): HISTORY OF OHA (ORAL HYPOGLYCAEMIC AGENTS)
Herbals and minerals for ages :
1918 : Watnbe Expt. proof of guanidine’s hypoglycaemic properties. 1926 : Frank – modified guanidine Synthalin A , Decreased use of Synthalin due to Hepatotoxicity.
1932 : Ruiz – Hypoglycaemic effect of sulfas noted. 1942 : Janbon Loubatiers – Trial of 225 RP in typhoid cases. Symptoms of hypo noted – Confirmed in animals
1955 : Frank and Fuchs – Use of BZ55 as an anti-infective agent; rediscovery of ‘Hypo’ effect in sulfas.
1956-1960 : Era of 1st Generation Sulfonylureas, 1957 : UNGER – Reintroduced guanidine compound – phenformin. 1961-1970 : Controversial UDGP study. 1969 : Onwards 2nd generation sulfonylureas.
1977 : New Compound Acarbose. Novel Compound (New) for NIDDM : These are: lYoglitazone, Repaglinide,
Glimepiride (Amaryl) already marketed in India is having good response.
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TYPE 2 DIABETES: COMPLICATIONS OF NEUROPATHY
Peripheral sensory polyneuropathy is present in 5-10%of people at the time of diagnosis of type 2 diabetes. In prospective studies with standard management, 40-50% have evidence of peripheral sensory neuropathy after 10 years of type 2 diabetes. The diagnosis is usually made by a careful history and physical examination. The symptoms of peripheral sensory polyneuropathy in diabetes are listed in Table 5. Significant physical findings may suggest the presence of peripheral sensory polyneuropathy. Finally, the diagnosis may be confirmed by sensory testing with simple, user-friendly instruments.
The 10-gram monofilament is used to assess pressure sensation and has been shown to be a good test for predicting ulceration. Insensitivity is defined as no sensation after a force sufficient to cause the filament to buckle. Generally, testing is done on at least one of four plantar sites on the forefoot, including the great toe and the first, third, and fifth metatarsal heads. Decreased to absent vibration sensation, as assessed by a tuning fork over the great toe or malleoli, is also a predictor of ulceration.
Numerous cross-sectional studies have been done in attempts to define risk factors for peripheral sensory polyneuropathy. Longitudinal studies, although less numerous, are preferable for multivariate analysis. In the Seattle Prospective Foot Study, hyperglycemia was a predictor of monofilament insensitivity. There was a 15% increase in risk for each 1% increase in HbAlc. In a prospective study of type 2 diabetics in Finland, glycemia was a predictor of peripheral sensory polyneuropathy. Evidence from the UKPDS and the Kumomoto Study that intensive glycemic management delays progression of sensory neuropathy in type 2 diabetes lends strong support to the concept that hyperglycemia is the predominant risk factor for peripheral sensory polyneuropathy. Other risk markers include age, height, ethnicity (American Indians), alcohol abuse, and increased urinary albumin excretion.
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