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SCOLIOSIS AND TREATMENT

What Is Scoliosis?
Scoliosis is a lateral (toward the side) curvature in the normally straight vertical line of the spine. When viewed from the side, the spine should show a mild roundness in the upper back and shows a degree of swayback (inward curvature) in the lower back. When a person with a normal spine is viewed from the front or back, the spine appears to be straight. When a person with scoliosis is viewed from the front or back, the spine appears to be curved.

What Causes Scoliosis?

There are many types and causes of scoliosis, including:


Congenital scoliosis. Caused by a bone abnormality present at birth.

Neuromuscular scoliosis. A result of abnormal muscles or nerves. Frequently seen in people with spina bifida or cerebral palsy or in those with various conditions that are accompanied by, or result in, paralysis.

Degenerative scoliosis. This may result from traumatic (from an injury or illness) bone collapse, previous major back surgery, or osteoporosis (thinning of the bones).

Idiopathic scoliosis. The most common type of scoliosis, idiopathic scoliosis, has no specific identifiable cause. There are many theories, but none have been found to be conclusive. There is, however, strong evidence that idiopathic scoliosis is inherited.

WHAT IS THE HISTORY OF DIABETES

Diseases with the clinical features of diabetes have been recognised since antiquity. The Ebers papyrus, dating from 1550 BC, describes a polyuric state that resembles diabetes.
The word ‘ diabetes ’ was fi rst used by Aretaeus of Cappadocia in the second century AD. Aretaeus gave a clinical description of the disease, noting the increased urine flow, thirst and weight loss, features that are instantly recognizable today.

The sweet, honey - like taste of urine in polyuric states, which attracted ants and other insects, was reported by Hindu physicians such as Sushrut (Susruta) during the fifth and sixth centuries AD. These descriptions even mention two forms of diabetes, the more common occurring in older, overweight and indolent people, and the other in lean people who did not survive for long. This empirical subdivision predicted the modern classification into type 1 and type 2 diabetes.

Diabetes was largely neglected in Europe until a 17th - century English physician, Thomas Willis (1621 – 75), rediscovered the sweetness of diabetic urine. Willis, who was physician to King Charles II, thought that the disease had been rare in ancient times, but that its frequency was increasing in his age ‘ given to good fellowship ’. Nearly a century later, the Liverpool physician Matthew Dobson
(1735 – 84) showed that the sweetness of urine and serum was caused by sugar. John Rollo (d. 1809) was the first to apply the adjective ‘ mellitus ’ to the disease.

LUPUS CAUSES AND TREATMENT

Lupus is a chronic inflammatory disease that occurs when your body's immune system attacks your own tissues and organs. Inflammation caused by lupus can affect many different body systems — including your joints, skin, kidneys, blood cells, brain, heart and lungs.

Lupus can be difficult to diagnose because its signs and symptoms often mimic those of other ailments. The most distinctive sign of lupus — a facial rash that resembles the wings of a butterfly unfolding across both cheeks — occurs in many but not all cases of lupus.

Some people are born with a tendency toward developing lupus, which may be triggered by infections, certain drugs or even sunlight. While there's no cure for lupus, treatments can help control symptoms.

SYMPTOMS

WHAT IS DIABETES MELLITUS

Diabetes mellitus is a condition of chronically elevated blood glucose concentrations which give rise to its main symptom of passing large quantities of sweet - tasting urine ( diabetes from the Greek word meaning ‘ a siphon ’ , as the body acts as a conduit for the excess fluid, and mellitus from the Greek and Latin for honey). The fundamental underlying abnormality is a net (relative or absent) deficiency of the hormone insulin. Insulin is essentially the only hormone that can lower blood glucose.

There are two categories of diabetes: type 1 is caused by an autoimmune destruction of the insulin - producing β cell of the islets of Langerhans in the pancreas (absolute deficiency); and type 2 is a result of both impaired insulin secretion and resistance to its action – often secondary to obesity (relative deficiency).

GALL STONES AND TREATMENTS

Gallstones form in the gallbladder, a small organ located under the liver. The gallbladder aids in the digestive process by storing bile and secreting it into the small intestine when food enters. Bile is a fluid produced by the liver and is made up of several substances, including cholesterol, bilirubin, and bile salts.

What Are Gallstones?

Gallstones are pieces of solid material that form in the gallbladder. These stones develop because cholesterol and pigments in bile sometimes form hard particles.

Gallstones are hardened deposits of digestive fluid that can form in your gallbladder. Your gallbladder is a small, pear-shaped organ on the right side of your abdomen, just beneath your liver. The gallbladder holds a digestive fluid called bile that's released into your small intestine.

Gallstones range in size from as small as a grain of sand to as large as a golf ball. Some people develop just one gallstone, while others develop many gallstones at the same time.

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DIALYSATE COMPOSITION FOR PERITONEAL DIALYSIS

To meet the ultrafiltration requirements of patients on peritoneal dialysis, the peritoneal dialysate is deliberately rendered hyperosmolar relative to plasma, to create an osmotic gradient that favors net movement of water into the peritoneal cavity. In commercially available peritoneal dialysates, glucose serves as the osmotic agent that enhances ultrafiltration. Available concentrations range from 1.5% to 4.25% dextrose. Over time, the osmolality of the dialysate declines as a result of water moving into the peritoneal cavity and of absorption of dialysate glucose.

The absorption of glucose contributes substantially to the calorie intake of patients on continuous peritoneal dialysis. Over time, this carbohydrate load is thought to contribute to progressive obesity, hypertriglyceridemia, and decreased nutrition as a result of loss of appetite and decreased protein intake. In addition, the high glucose concentrations and high osmolality of currently available solutions may have inhibitory effects on the function of leukocytes, peritoneal macrophages, and mesothelial cells. In an attempt to develop a more physiologic solution, various new osmotic agents are now under investigation. Some of these may prove useful as alternatives to the standard glucose solutions.

Those that contain amino acids have received the most attention.

DIALYSIS TREATMENT OF END STAGE RENAL DISEASE

The goal of dialysis for patients with chronic renal failure is to restore the composition of the body’s fluid environment toward normal. This is accomplished principally by formulating a dialysate whose constituent concentrations are set to approximate normal values in the body. Over time, by diffusional transfer along
favorable concentration gradients, the concentrations of solutes that were initially increased or decreased tend to be corrected. When an abnormal electrolyte concentration poses immediate danger, the dialysate concentration of that electrolyte can be set at a nonphysiologic level to achieve a more rapid correction. On a more chronic basis the composition of the dialysate can be individually adjusted in order to meet the specific needs of each patient.

Dialysate Composition for Hemodialysis
In the early days of hemodialysis, the dialysate sodium concentration was deliberately set low to avoid problems of chronic volume overload such as hypertension and heart failure. As volume removal became more rapid because of shorter dialysis times, symptomatic hypotension emerged as a common and often disabling problem during dialysis. It soon became apparent that changes in the serum sodium concentration—and more specifically changes in serum osmolality— were contributing to the development of this hemodynamic instability.

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