ELDER TIP As the body ages, the cells become more resistant to insulin, thus reducing the older adult’s ability to metabolize glucose. In addition, the release of insulin from the pancreatic beta cells is reduced and delayed. These combined processes result in hyperglycemia. In the older patient, sudden concentrations of glucose cause increased and more prolonged hyperglycemia.
The “other specific types” of DM result from various conditions (such as a genetic defect of the beta cells or endocrinopathies) or from use of or exposure to certain drugs or chemicals. GDM is considered present whenever a patient has any degree of abnormal glucose during pregnancy. This form may result from weight gain and increased levels of estrogen and placental hormones, which antagonize insulin.
Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage in the fat deposits. Insulin deficiency compromises the body tissues’access to essential nutrients for fuel and storage.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Diabetic complications during pregnancy:
Causes
(Professional Guide to Diseases (Eighth Edition))
In diabetes mellitus, glucose is inadequately utilized either because insulin isn’t synthesized or because tissues are resistant to the hormonal action of endogenous insulin. During pregnancy, the fetus relies on maternal glucose as a primary fuel source. Pregnancy triggers protective mechanisms that have anti-insulin effects: increased hormone production (placental lactogen, estrogen, and progesterone), which antagonizes insulin’s effects; degradation of insulin by the placenta; and prolonged elevation of stress hormones (cortisol, epinephrine, and glucagon), which raise blood glucose levels.
In a normal pregnancy, an increase in anti-insulin factors is counterbalanced by an increase in insulin production to maintain normal blood glucose levels. However, females who are prediabetic or diabetic are unable to produce sufficient insulin to overcome the insulin antagonist mechanisms of pregnancy, or their tissues are insulin-resistant. As insulin requirements rise toward term, the patient who’s prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control, whereas the patient who’s insulin-dependent may need increased insulin dosage.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Hereditary fructose intolerance:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Transmitted as an autosomal recessive trait, hereditary fructose intolerance results from a deficiency in the enzyme fructose-1-phosphate aldolase. The enzyme operates at only 1% to 10% of its normal biological activity, thus preventing rapid uptake of fructose by the liver after ingestion of fruit or foods containing cane sugar.
In some European countries, hereditary fructose intolerance may have an incidence as high as 1 in 20,000 people.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Protein-calorie malnutrition:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Both kwashiorkor (edematous PCM) and marasmus (nonedematous PCM) are common in underdeveloped countries and in areas in which dietary amino acid content is insufficient to satisfy growth requirements. Kwashiorkor typically occurs at about age 1, after infants are weaned from breast milk to a protein-deficient diet of starchy gruels or sugar water, but it can develop at any time during the formative years. Marasmus affects infants ages 6 to 18 months as a result of breast-feeding failure, or a debilitating condition such as chronic diarrhea.
In industrialized countries, PCM may occur secondary to chronic metabolic disease that decreases protein and calorie intake or absorption, or trauma that increases protein and calorie requirements. In the United States, PCM is estimated to occur to some extent in 50% of elderly people in nursing homes. Those who aren’t allowed anything by mouth for an extended period are at high risk of developing PCM. Conditions that increase protein-calorie requirements include severe burns and injuries, systemic infections, and cancer (accounts for the largest group of hospitalized patients with PCM). Conditions that cause defective utilization of nutrients include malabsorption syndrome, short-bowel syndrome, and Crohn’s disease.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Cholelithiasis and related disorders:
Causes and incidence
(Professional Guide to Diseases (Eighth Edition))
Cholelithiasis, stones or calculi (gallstones) in the gallbladder, results from changes in bile components. Gallstones are made of cholesterol, calcium bilirubinate, or a mixture of cholesterol and bilirubin pigment. They arise during periods of sluggishness in the gallbladder due to pregnancy, hormonal contraceptives, diabetes mellitus, celiac disease, cirrhosis of the liver, and pancreatitis. Cholelithiasis is a common health problem, affecting about 1 out of every 1,000 people. The prognosis is usually good with treatment unless infection occurs, in which case the prognosis depends on its severity and response to antibiotics.
One out of every 10 patients with gallstones develops choledocholithiasis, or gallstones in the common bile duct (sometimes called “common duct stones”). This occurs when stones passed out of the gallbladder lodge in the hepatic and common bile ducts and obstruct the flow of bile into the duodenum. Prognosis is good unless infection occurs.
Cholangitis, infection of the bile duct, is commonly associated with choledocholithiasis and may follow percutaneous transhepatic cholangiography or occlusion of endoscopic stents. Predisposing factors may include bacterial or metabolic alteration of bile acids. Widespread inflammation may cause fibrosis and stenosis of the common bile duct. The prognosis for this rare condition is poor without stenting or surgery.
Cholecystitis, acute or chronic inflammation of the gallbladder, is usually associated with a gallstone impacted in the cystic duct, causing painful distention of the gallbladder. Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery. The acute form is most common during middle age; the chronic form usually occurs among elderly patients. The prognosis is good with treatment.
Cholesterolosis, polyps or crystal deposits of cholesterol in the gallbladder’s submucosa, may result from bile secretions containing high concentrations of cholesterol and insufficient bile salts. The polyps may be localized or speckle the entire gallbladder. Cholesterolosis, the most common pseudotumor, isn’t related to widespread inflammation of the mucosa or lining of the gallbladder. The prognosis is good with surgery.
Biliary cirrhosis, ascending infection of the biliary system, sometimes follows viral destruction of liver and duct cells, but the primary cause is unknown. This condition usually leads to obstructive jaundice and involves the portal and periportal spaces of the liver. It’s nine times more common among women ages 40 to 60 than among men. The prognosis is poor without liver transplantation.
Gallstone ileus results from a gallstone lodging at the terminal ileum; it’s more common in the elderly. The prognosis is good with surgery.
Postcholecystectomy syndrome commonly results from residual gallstones or stricture of the common bile duct. It occurs in 1% to 5% of all patients whose gallbladders have been surgically removed and may produce right upper quadrant abdominal pain, biliary colic, fatty food intolerance, dyspepsia, and indigestion. The prognosis is good with selected radiologic procedures, endoscopic procedures, or surgery.
Acalculous cholecystitis is more common in critically ill patients, accounting for about 5% of cholecystitis cases. It may result from primary infection with such organisms as Salmonella typhi, Escherichia coli, or Clostridium or from obstruction of the cystic duct due to lymphadenopathy or a tumor. It appears that ischemia, usually related to a low cardiac output, also has a role in the pathophysiology of this disease. Signs and symptoms of acalculous cholecystitis include unexplained sepsis, right upper quadrant pain, fever, leukocytosis, and a palpable gallbladder.
Each of these disorders produces its own set of complications. Cholelithiasis may lead to any of the disorders associated with gallstone formation: cholangitis, cholecystitis, choledocholithiasis, and gallstone ileus. Cholecystitis can progress to gallbladder complications, such as empyema, hydrops or mucocele, or gangrene. Gangrene may lead to perforation, resulting in peritonitis, fistula formation, pancreatitis, limy bile, and porcelain gallbladder. Other complications include chronic cholecystitis and cholangitis.
Choledocholithiasis may lead to cholangitis, obstructive jaundice, pancreatitis, and secondary biliary cirrhosis. Cholangitis, especially in the suppurative form, may progress to septic shock and death. Gallstone ileus may cause bowel obstruction, which can lead to intestinal perforation, peritonitis, septicemia, secondary infection, and septic shock.
In most cases, gallbladder and bile duct diseases occur in people who are older than age 40 and are more prevalent in women and Native Americans.
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Source: Professional Guide to Diseases (Eighth Edition), 2005
Diabetes insipidus:
Causes
(Handbook of Diseases)
Pituitary diabetes insipidus results from intracranial neoplastic or metastatic lesions, hypophysectomy or other neurosurgery, a skull fracture, or head trauma that damages the neurohypophyseal structures. It can also result from infection, granulomatous disease, and vascular lesions; it may be idiopathic and, rarely, familial.
The hypothalamus synthesizes vasopressin. The posterior pituitary gland (or neurohypophysis) stores vasopressin and releases it into the general circulation, where it causes the kidneys to reabsorb water by making the distal tubules and collecting duct cells water-permeable.
In pituitary diabetes insipidus, the absence of vasopressin allows the filtered water to be excreted in the urine instead of being reabsorbed. In renal diabetes insipidus, the kidney doesn’t respond to vasopressin, which is usually present in high concentrations.
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Source: Handbook of Diseases, 2003
Diabetes mellitus:
Causes
(Handbook of Diseases)
The effects of diabetes mellitus result from insulin deficiency. Insulin transports glucose into the cell for use as energy and storage as glycogen. It also stimulates protein synthesis and free fatty acid storage. Insulin deficiency or resistance compromises the body tissues’access to essential nutrients for fuel and storage.
Type 1A results from autoimmune beta-cell destruction, resulting in insulin deficiency. Type 1B leaves these immunologic markers but results in insulin deficiency and kerosis.
Other risk factors include the following:
❑ Obesity contributes to the resistance to endogenous insulin.
❑ Physiologic or emotional stress can cause prolonged elevation of stress hormone levels (cortisol, epinephrine, glucagon, and growth hormone). This raises blood glucose levels, which, in turn, places increased demands on the pancreas.
❑ Pregnancy causes weight gain and increases levels of estrogen and placental hormones, which antagonize insulin.
❑ Some medications can antagonize the effects of insulin, including thiazide diuretics, adrenal corticosteroids, and hormonal contraceptives.
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Source: Handbook of Diseases, 2003
Diabetic complications during pregnancy:
Causes
(Handbook of Diseases)
In diabetes mellitus, glucose is inadequately used either because insulin isn’t synthesized (as in type 1, insulin-dependent diabetes) or because tissues are resistant to the hormonal action of endogenous insulin (as in type 2, non–insulin-dependent diabetes).
Protective mechanisms
During pregnancy, the fetus relies on maternal glucose as a primary fuel source. Pregnancy triggers protective mechanisms that have anti-insulin effects: increased hormone production (placental lactogen, estrogen, and progesterone), which antagonizes the effects of insulin; degradation of insulin by the placenta; and prolonged elevation of stress hormones (cortisol, epinephrine, and glucagon), which raise blood glucose levels.
In a normal pregnancy, an increase in anti-insulin factors is counterbalanced by an increase in insulin production to maintain normal blood glucose levels. However, women who are prediabetic or diabetic can’t produce sufficient insulin to overcome the insulin antagonist mechanisms of pregnancy, or their tissues are insulin-resistant.
As insulin requirements rise toward term, the patient who is prediabetic may develop gestational diabetes, necessitating dietary management and, possibly, exogenous insulin to achieve glycemic control. The insulin-dependent patient may need increased insulin dosage.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Protein-calorie malnutrition:
Causes
(Handbook of Diseases)
Both marasmus (nonedematous protein-calorie malnutrition) and kwashiorkor (edematous protein-calorie malnutrition) are common in underdeveloped countries and in areas where dietary amino acid content is insufficient to satisfy growth requirements. Kwashiorkor typically occurs at about age 1, after infants are weaned from breast milk to a protein-deficient diet of starchy gruels or sugar water, but it can develop at any time during the formative years. Marasmus affects infants ages 6 to 18 months as a result of breast-feeding failure or a debilitating condition such as chronic diarrhea.
In industrialized countries, protein-calorie malnutrition may occur secondary to chronic metabolic disease that decreases protein and calorie intake or absorption or trauma that increases protein and calorie requirements. In the United States, protein-calorie malnutrition is estimated to occur to some extent in 50% of surgical and 48% of medical patients. Those who aren’t allowed anything by mouth for an extended period are at high risk for developing protein-calorie malnutrition. Conditions that increase protein-calorie requirements include severe burns and injuries, systemic infections, and cancer (accounts for the largest group of hospitalized patients with protein-calorie malnutrition.) Conditions that cause defective utilization of nutrients include malabsorption syndrome, short-bowel syndrome, and Crohn’s disease.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
Cholelithiasis, cholecystitis, and related disorders:
Causes
(Handbook of Diseases)
The origin and frequency of gallbladder and biliary tract disease vary with the particular disorder.
Cholelithiasis
The presence of stones or calculi (gallstones) in the gallbladder results from changes in bile components. Gallstones are made of cholesterol, calcium bilirubinate, or a mixture of cholesterol and bilirubin pigment. They arise during periods of sluggishness in the gallbladder resulting from pregnancy, use of oral contraceptives, diabetes mellitus, Crohn’s disease, cirrhosis of the liver, pancreatitis, obesity, and rapid weight loss.
Cholelithiasis is the fifth leading cause of hospitalization among adults and accounts for 90% of all gallbladder and duct diseases. The prognosis is usually good with treatment unless infection occurs, in which case the prognosis depends on the infection’s severity and response to antibiotics.
Cholecystitis
Cholecystitis, an acute or chronic inflammation of the gallbladder, is usually associated with a gallstone impacted in the cystic duct; the inflammation develops behind the obstruction. Cholecystitis accounts for 10% to 25% of all patients requiring gallbladder surgery.
The acute form is most common during middle age; the chronic form, among elderly people. The prognosis is good with treatment.
Biliary cirrhosis
Primary biliary cirrhosis is a chronic, progressive disease of the liver characterized by autoimmune destruction of the intrahepatic bile ducts and cholestasis. This condition usually leads to obstructive jaundice and pruritus and involves the portal and periportal spaces of the liver. It affects women between the ages of 40 and 60 nine times more often than men. The prognosis is poor without liver transplantation.
Cholangitis
An infection of the bile duct, cholangitis is commonly associated with choledocholithiasis and may follow percutaneous transhepatic cholangiography. Predisposing factors include bacterial or metabolic alteration of bile acids. Widespread inflammation may cause fibrosis and stenosis of the common bile duct. The prognosis for this rare condition is poor without stenting or surgery.
Choledocholithiasis
One out of every 10 patients with gallstones develops choledocholithiasis, or gallstones in the common bile duct (sometimes called common duct stones). This occurs when stones passed out of the gallbladder lodge in the hepatic and common bile ducts and obstruct the flow of bile into the duodenum. The prognosis is good unless infection occurs.
Cholesterolosis
Cholesterol polyps or cholesterol crystal deposits in the gallbladder’s submucosa may result from bile secretions containing high concentrations of cholesterol and insufficient bile salts. The polyps may be localized or may speckle the entire gallbladder. Cholesterolosis, the most common pseudotumor, isn’t related to widespread inflammation of the mucosa or lining of the gallbladder. The prognosis is good with surgery.
Gallstone ileus
Gallstone ileus results from a gallstone lodging in the terminal ileum. It’s more common in elderly people. The prognosis is good with surgery.
Postcholecystectomy syndrome
Postcholecystectomy syndrome commonly results from retained or recurrent common bile duct stones, spasm of the sphincter of Oddi, functional bowel disorder, technical errors, or mistaken diagnoses. It occurs in 1% to 5% of all patients whose gallbladders have been surgically removed and may produce right upper quadrant abdominal pain, biliary colic, fatty food intolerance, dyspepsia, and indigestion. The prognosis is good with selected radiologic procedures, endoscopic procedures, or surgery.
Complications
Each disorder produces its own set of complications. Cholelithiasis may lead to any of the disorders associated with gallstone formation: cholangitis, cholecystitis, choledocholithiasis, or gallstone ileus.
Cholecystitis can progress to gallbladder complications, such as empyema, hydrops or mucocele, or gangrene. Gangrene may lead to perforation, resulting in peritonitis, fistula formation, pancreatitis, limy bile, and porcelain gallbladder. Other complications include chronic cholecystitis and cholangitis.
Choledocholithiasis may lead to cholangitis, obstructive jaundice, pancreatitis, and secondary biliary cirrhosis. Cholangitis, especially in the suppurative form, may progress to septic shock and death. Gallstone ileus may cause bowel obstruction, which can lead to intestinal perforation, peritonitis, septicemia, secondary infection, and septic shock.
» READ BOOK EXCERPT ONLINE »
Source: Handbook of Diseases, 2003
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