Monday, 9 November 2015

Online Assignment

                                                      
                                PANCREAS
                                         The pancreas is a glandular organ in the digestive system and endocrine system of vertebrates. In humans, it is located in the abdominal cavity behind the stomach. It is an endocrine gland producing several important hormones, including insulin, glucagon, somatostatin, and pancreatic polypeptide which circulate in the blood. The pancreas is also a digestive organ, secreting pancreatic juice containing digestive enzymes that assist digestion and absorption of nutrients in the small intestine. These enzymes help to further break down the carbohydrates, proteins, and lipids in the chyme.
                                      The pancreas is an endocrine organ that lies in the abdomen, specifically the upper left abdomen. It is found behind the stomach, with the head of the pancreas surrounded by the duodenum. The pancreas is about 15 cm (6 in) long.
                                     Anatomically, the pancreas is divided into a head, which rests within the concavity of the duodenum, a body lying behind the base of the stomach, and a tail, which ends abutting the spleen. The neck of the pancreas lies between the body and head, and lies anterior to the superior mesenteric artery and vein. The head of the pancreas surrounds these two vessels, and a small uncinate process emerges from the lower part of the head, lying behind the superior mesenteric artery.

The pancreas is a secretory structure with a internal hormonal role (endocrine) and an external digestive role (exocrine). It has two main ducts, the main pancreatic duct, and the accessory pancreatic duct. These drain enzymes through the ampulla of Vater into the duodenum.

Function:-

The pancreas is a dual-function gland, having features of both endocrine and exocrine glands.

Endocrine

The part of the pancreas with endocrine function is made up of approximately a million[8] cell clusters called islets of Langerhans. Four main cell types exist in the islets. They are relatively difficult to distinguish using standard staining techniques, but they can be classified by their secretion: α alpha cells secrete glucagon (increase glucose in blood), β beta cells secrete insulin (decrease glucose in blood), Δ delta cells secrete somatostatin (regulates/stops α and β cells) and PP cells, or γ (gamma) cells, secrete pancreatic polypeptide.[9]
The islets are a compact collection of endocrine cells arranged in clusters and cords and are crisscrossed by a dense network of capillaries. The capillaries of the islets are lined by layers of endocrine cells in direct contact with vessels, and most endocrine cells are in direct contact with blood vessels, either by cytoplasmic processes or by direct apposition.

Exocrine

The pancreas also functions as an exocrine gland that assists the digestive system. It secretes pancreatic fluid that contains digestive enzymes that pass to the small intestine. These enzymes help to further break down the carbohydrates, proteins and lipids (fats) in the chyme.
In humans, the secretory activity of the pancreas is regulated directly via the effect of hormones in the blood on the islets of Langerhans and indirectly through the effect of the autonomic nervous system on the blood flow.[11]
The exocrine component of the pancreas, often called simply the exocrine pancreas, is the portion of the pancreas that performs exocrine functions. It has ducts that are arranged in clusters called acini (singular acinus). Pancreatic secretions are secreted into the lumen of the acinus, and then accumulate in intralobular ducts that drain to the main pancreatic duct, which drains directly into the duodenum.
Control of the exocrine function of the pancreas is via the hormones gastrin, cholecystokinin and secretin, which are hormones secreted by cells in the stomach and duodenum, in response to distension and/or food and which cause secretion of pancreatic juices.
Secretion
Cell producing it
Primary signal
digestive enzymes
Basophilic cells
Pancreatic secretions from ductal cells contain bicarbonate ions and are alkaline in order to neutralize the acidic chyme that the stomach churns out.
The pancreas is also the main source of enzymes for digesting fats (lipids) and proteins. (The enzymes that digest polysaccharides, by contrast, are primarily produced by the walls of the intestines.).The cells are filled with secretory granules containing the precursor digestive enzymes. The major proteases which the pancreas secretes are trypsinogen and chymotrypsinogen. Secreted to a lesser degree are pancreatic lipase and pancreatic amylase. The pancreas also secretes phospholipase A2, lysophospholipase, and cholesterol esterase.

 Clinical relevance

A puncture of the pancreas, which may lead to the secretion of digestive enzymes such as lipase and amylase into the abdominal cavity as well as subsequent pancreatic self-digestion and digestion and damage to organs within the abdomen, generally requires prompt and experienced medical intervention.
It is possible for one to live without a pancreas, provided that the person takes insulin for proper regulation of blood glucose concentration and pancreatic enzyme supplements to aid digestion.
Inflammation of the pancreas is known as pancreatitis. Pancreatitis is most often associated with recurrent gallstones or chronic alcohol use, although a variety of other causes, including measles, mumps, some medications, the congenital condition alpha-1 antitrypsin deficiency and even some scorpion stings, may cause pancreatitis. Pancreatitis is likely to cause intense pain in the central abdomen, that often radiates to the back, and may be associated with jaundice. In addition, due to causing problems with fat digestion and bilirubin excretion, pancreatitis often presents with pale stools and dark urine.[14]
In pancreatitis, enzymes of the exocrine pancreas damage the structure and tissue of the pancreas. Detection of some of these enzymes, such as amylase and lipase in the blood, along with symptoms and findings on X-ray, are often used to indicate that a person has pancreatitis. A person with pancreatitis is also at risk of shock. Pancreatitis is often managed medically with analgesics, removal of gallstones or treatment of other causes, and monitoring to ensure a patient does not develop shock.[14]

Pancreatic cancers, particularly the most common type, pancreatic adenocarcinoma, remain very difficult to treat, and are mostly diagnosed only at a stage that is too late for surgery, which is the only curative treatment. Pancreatic cancer is rare in those younger than 40, and the median age of diagnosis is 71.[15] Risk factors include: smoking, obesity, diabetes, and certain rare genetic conditions including: multiple endocrine neoplasia type 1 and hereditary nonpolyposis colon cancer among others. About 25% of cases are attributable to tobacco smoking, while 5-10% of cases are linked to inherited genes.
There are several types of pancreatic cancer, involving both the endocrine and exocrine tissue. Pancreatic adenocarcinoma, which affects the exocrine part of the pancreas, is by far the most common form. The many types of pancreatic endocrine tumors are all uncommon or rare, and have varied outlooks. However the incidence of these cancers has been rising sharply; it is not clear to what extent this reflects increased detection, especially through medical imaging, of tumors that would be very slow to develop. Insulinomas (largely benign) and gastrinomas are the most common types.[18] In the United States pancreatic cancer is the fourth most common cause of deaths due to cancer.[19] The disease occurs more often in the developed world, which had 68% of new cases in 2012.[20] Pancreatic adenocarcinoma typically has poor outcomes with the average percentage alive for at least one and five years after diagnosis being 25% and 5% respectively.[20][21] In localized disease where the cancer is small (< 2 cm) the number alive at five years is approximately 20%.[22] For those with neuroendocrine cancers the number alive after five years is much better at 65%, varying considerably with type.[20]

Preventing Pancreatitis
There are ways you can protect your pancreas and reduce your risk for pancreatitis and other serious health problems like EPI:
1. Limit alcohol consumption. By drinking less or not at all, you can help protect your pancreas from the toxic effects of alcohol and reduce your risk for pancreatitis. A number of studies, including a population-based study in Denmark involving 17,905 people, found that high alcohol intake is associated with an increased risk of pancreatitis in both men and women.
2. Eat a low-fat diet. Gallstones, a leading cause of acute pancreatitis, can develop when too much cholesterol accumulates in your bile, the substance made by your liver to help digest fats. To reduce your risk for gallstones, eat a low-fat diet that includes whole grains and a variety of fresh fruits and vegetables. To help prevent pancreatitis, specific foods to avoid include fatty or fried foods as well as full-fat dairy products. High triglyceride levels, or the amount of fats carried in your blood, can increase your risk for acute pancreatitis. So, it's also important to limit foods high in simple sugars, such as sugary sweets and high-calorie beverages, that could raise your triglyceride levels.
3. Exercise regularly and lose excess weight. People who are overweight are more likely to develop gallstones, putting them at greater risk for acute pancreatitis. Losing extra pounds gradually and maintaining a healthy weight by eating a balanced diet and engaging in regular physical activity can help prevent gallstones from forming.
4. Skip crash diets. The caveat to losing weight is to do it gradually. When you go into crash-diet mode, prompting quick weight loss, your liver ramps up cholesterol production in response, which increases your risk for gallstones.

5. Don't smoke. Studies show that smoking cigarettes is linked to acute pancreatitis. Researchers in Sweden followed 84,667 healthy women and men between the ages of 46 and 84 to examine how smoking affected their risk for acute pancreatitis. The study, published in the journal Gut, revealed that people who smoked the equivalent of at least one pack of cigarettes a day for 20 years had more than double the risk for non-gallstone-related acute pancreatitis than non-smokers had. Quitting smoking reduced the smokers' risk for acute pancreatitis to the same level as that of non-smokers.
RICKETS

                          Rickets is defective mineralization or calcification of bones before epiphyseal closure in immature mammals due to deficiency or impaired metabolism of vitamin D, phosphorus or calcium, potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets (cases of severe diarrhea and vomiting may be the cause of the deficiency). Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition, usually resulting from famine or starvation during the early stages of childhood.



Signs and symptoms


                                                                   Widening of wrist
                                                          
Signs and symptoms of rickets include:
·         Bone tenderness[4]
·         Dental problems[4]
·         Muscle weakness (rickety myopathy)]
·         Increased tendency for fractures (easily broken bones), especially greenstick fractures
·         Skeletal deformity[4]
·         Toddlers: Bowed legs and double malleoli (genu varum)[5]
·         Older children: Knock-knees (genu valgum) or "windswept knees"
·         Cranial deformity (such as skull bossing or delayed fontanelle closure)
·         Pelvic deformity
·         Spinal deformity (such as kyphoscoliosis or lumbar lordosis)
·         Growth disturbance
·         Hypocalcemia (low level of calcium in the blood)
·         Tetany (uncontrolled muscle spasms all over the body)
·         Craniotabes (soft skull)
·         Costochondral swelling (aka "rickety rosary" or "rachitic rosary")
·         Harrison's groove[4]
·         Double malleoli sign due to metaphyseal hyperplasia
·         Widening of wrist[5] raises early suspicion, it is due to metaphyseal cartilage hyperplasia.
An X-ray or radiograph of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance (Caput Quadratum). These deformities persist into adult life if not treated. Long-term consequences include permanent bends or disfiguration of the long bones, and a curved back.

Cause
The primary cause of rickets is a vitamin D deficiency.[7] Vitamin D is required for proper calcium absorption from the gut. Sunlight, especially ultraviolet light, lets human skin cells convert vitamin D from an inactive to active state. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in hypocalcaemia, leading to skeletal and dental deformities and neuromuscular symptoms, e.g. hyperexcitability. Foods that contain vitamin D include butter, eggs, fish liver oils, margarine, fortified milk and juice, portabella and shiitake mushrooms, and oily fishes such as tuna, herring, and salmon. A rare X-linked dominant form exists called vitamin D-resistant rickets or X-linked hypophosphatemia.
Cases have been reported in Britain in recent years[8] of rickets in children of many social backgrounds caused by insufficient production in the body of vitamin D because the sun's ultraviolet light was not reaching the skin due to use of strong sunblock, too much "covering up" in sunlight, or not getting out into the sun. Other cases have been reported among the children of some ethnic groups in which mothers avoid exposure to the sun for religious or cultural reasons, leading to a maternal shortage of vitamin D;[9][10] and people with darker skins need more sunlight to maintain vitamin D levels. The British Medical Journal reported in 2010 that doctors in Newcastle on Tyne saw 20 cases of rickets per year. Rickets had been a significant malaise in London, especially during the Industrial Revolution. Persistent thick fog and heavy industrial smog permeating the city blocked out significant amounts of sunlight so much so that up to 80 percent of children at one time had varying degrees of rickets in one form or the other. Diseases causing soft bones in infants, like hypophosphatasia or hypophosphatemia can also lead to rickets.[11]

Diagnosis


Wrist X ray showing changes in rickets. Mainly cupping is seen here.

Chest X ray showing changes consistent with rickets. These changes are usually referred to as "rosary beads" of rickets.
Rickets may be diagnosed with the help of:
·         Blood tests:[19]
·         Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high from bones or changes in the shape or structure of the bones. This can show enlarged limbs and joints.
·         Bone biopsy is rarely performed but will confirm rickets.[19]

Types

·         Vitamin D-related rickets[20]
·         Vitamin D deficiency
·         Vitamin D-dependent rickets[20]
·         Type 1 (25-Hydroxyvitamin D3 1-alpha-hydroxylase deficiency)
·         Type 2 (calcitriol receptor mutation)
·         Hypocalcemia-related rickets
·         Hypocalcemia
·         Chronic renal failure (CKD-BMD)
·         Hypophosphatemia-related rickets
·         Congenital
·         Autosomal recessive hypophosphatemic rickets (ARHR)[21]
·         Hypophosphatemia (typically secondary to malabsorption)
·         Fanconi's syndrome
·         Seconary to other diseases
·         Tumor-induced osteomalacia
·         McCune-Albright syndrome
·         Epidermal nevus syndrome
·         Dent's disease

 

 

Differential diagnosis

Infants with rickets often have bone fractures. This sometimes leads to child abuse allegations. This issue appears to be more common for solely nursing infants of black mothers, in winter in temperate climates, suffering poor nutrition and no vitamin D supplementation.[22] People with darker skin produce less vitamin D than those with lighter skin, for the same amount of sunlight.[23]

 

Treatment and prevention



The most common treatment of rickets is the use of Vitamin D.[24] However, surgery may be required to remove severe bone abnormalities.[20]

Diet and sunlight

Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet B light (most easily obtained when the sun is highest in the sky), cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.
A sufficient amount of ultraviolet B light in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned people need to be exposed longer to the ultraviolet rays. The replacement of vitamin D has been proven to correct rickets using these methods of ultraviolet light therapy and medicine.[25]
Recommendations are for 400 international units (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance.

 

 

Supplementation

Sufficient vitamin D levels can also be achieved through dietary supplementation and/or exposure to sunlight. Vitamin D3 (cholecalciferol) is the preferred form since it is more readily absorbed than vitamin D2. Most dermatologists recommend vitamin D supplementation as an alternative to unprotected ultraviolet exposure due to the increased risk of skin cancer associated with sun exposure. Endogenous production with full body exposure to sunlight is approximately 250 µg (10,000 IU) per day.[26]
According to the American Academy of Pediatrics (AAP), all infants, including those who are exclusively breast-fed, may need Vitamin D supplementation until they start drinking at least 17 US fluid ounces (500 ml) of vitamin D-fortified milk or formula a day.[27]