Exam 4 - Chapter 20 Flashcards
Islets of Langerhans
Endocrine tissue containing α, β, and δ cells which regulate insulin and glucagon secretion
Alpha Cells (α)
Stimulate the release of glucagon and glycogen stores and promote gluconeogenesis which target all cells, particularly in the liver, muscle, and fat
Beta Cells (β)
Stimulate the release of insulin and lower the blood glucose level which target all cells, particularly in the liver, muscle, and fat
Delta Cells (δ)
Inhibit glucagon and insulin secretion via somatostatin, which inhibit α and β cells
Acute Pancreatitis
Inflammation and hemorrhage of the pancreas due
to auto digestion of pancreatic parenchyma by
pancreatic enzymes.
Causes: Premature activation of trypsin leads to activation of other pancreatic enzymes. Most commonly due to alcohol and gallstones; other causes include trauma, hypercalcemia, hypertriglyceridemia
Pathology: Liquefactive hemorrhagic (white fat necrosis), calcium soap deposition, necrosis of parenchyma. Elevated serum lipase and amylase; lipase is more specific for pancreatic damage
Symptoms: Epigastric and LUQ abdominal pain that radiates to the back, nausea and vomiting, fever after increased alcohol intake, hypocalcemia (calcium is consumed during saponification in fat necrosis). Can result in pancreatic pseudocyst—formed by fibrous tissue surrounding liquefactive necrosis and pancreatic enzymes, and pancreatic abscess—often due to E coli
Treatment: Food restriction, IV fluids, Demerol (for pain), nasogastric tube
Chronic Pancreatitis
Fibrosis of pancreatic parenchyma with destruction of Acini (exocrine tissue) but Islets spared
Causes: alcohol (adults) and cystic fibrosis
(children), idiopathic, acute pancreatitis
Pathology: Calcified concretions, pseudocyst formation. “Chain of Lakes Pattern” (due to dilation of pancreatic ducts, normal serum lipase and amylase
Symptoms: Abdominal and back pain, pancreatic insufficiency (malabsorption with steatorrhea and fat-soluble vitamin deficiencies and diabetes), increased risk for pancreatic carcinoma
Treatment: Enzyme and insulin replacement for pancreatic insufficiency
Pancreatic Carcinoma (Adenocarcinoma)
Adenocarcinoma arising from the pancreatic ducts, most commonly seen in the elderly
Causes: Smoking, chronic pancreatitis, alcohol, high-fat diet, chronic gallbladder disease, and diabetes
Pathology: 60% in head of pancreas, 15% body, 5% tail, 20% diffuse (whole organ). Dilated intrahepatic ducts, tumor cells form clusters, anaplastic cuboidal epithelium. Increased ALP, increased CEA levels, serum tumor marker is CA 19-9
Symptoms: Often clinically silent until widespread metastasis. Epigastric upper abdominal pain
and weight loss, Trousseau syndrome, obstructive jaundice with pale stools. Tumors that arise in the head can cause palpable gallbladder. Tumors associated in the body or tail cause secondary diabetes mellitus, Courvoisier’s sign (gallbladder distention)
Treatment: Very poor prognosis and 1-year survival is
Pancreatic Carcinoma (Gastrinoma)
Zollinger-Ellison syndrome with multiple ulcers unresponsive to medical therapy; may be part of MEN1 (multiple endocrine neoplasia)
Diabetes Mellitus (Type I)
Insulin deficiency leading to a metabolic disorder characterized by hyperglycemia
Causes: Autoimmune destruction of beta cells by T lymphocytes, genetic susceptibility (HLA-DR3 and HLA-DR4), environmental factors
Pathology: Inflammation of Islets, hyperglycemia leads to polyuria and polydipsia, insulin deficiency leads to polyphagia and weight loss, fat catabolism leads to ketoacidosis
Symptoms: Hyperglycemia (from gluconogensis, glycogenolysis, and lipolysis via glucagon), glucosuria, polydipsia, polyuria, polyphagia, weight loss, weakness, ketosis and diabetic ketoacidosis. Kussmaul respirations, fruity breath, ketonemia, ketonuria. Osmotic diuresis
Treatment: Lifelong insulin
Diabetes Mellitus (Type II)
End-organ insulin resistance leading to a metabolic
disorder characterized by hyperglycemia. Mostly in
middle-aged, obese adults
Causes: Strong genetic predisposition, decreased number of insulin receptors due to obesity, decreased response of β cells to glucose
Pathology: Amyloid replaces Islets and deposits in pancreas, high insulin levels early on but low levels later
Symptoms: Same as Type I, non-ketotic hyperosmolar coma
Complications: Nonenzymatic Glycosylation (NEG) leads to trapping of LDL in endothelial cells. Ocular - cataracts, glaucoma, proliferative retinopathy. Atherosclerosis leads to MI, gangrene, stroke. Microangiopathy - NEG leads to delayed wound healing and increased risk of infection. Nephropathy - due to NEG damage to basement membranes. Peripheral and Autonomic Neuropathy - Loss of sensation, nerve pain, numbness, leading to amputation of distal limbs.
Diagnosis: Normal - 70-120 mg/dL. Diagnosed when random glucose > 200 mg/dL, fasting glucose > 126 mg/dL (two times). Glucose tolerance test with a serum glucose level >200 mg/dL two hours after glucose loading
Treatment: Dietary changes and oral drugs to
stimulate insulin production and increase receptor
effectiveness, hypoglycemic drugs, and treating any complications
Diabetic Emergencies of Type I (Ketoacidosis)
Buildup of ketones in body which leads to acidosis. Life-threatening
Causes: Body can’t metabolize any glucose (carbs) so it metabolizes fat, which leads to the buildup of ketones
Symptoms: Hyperglycemia (> 300 mg/dL), Kussmaul respirations, dehydration, hyperkalemia, nauseau, vomiting, fruity breath (due to acetone)
Treatment: Fluids, insulin, and potassium to replenish electrolyte loss
Diabetic Emergencies of Type II (Hyperosmolar Coma)
Hyperglycemic Hyperosmolar Non-ketotic Coma (HHNC) - Diuresis with hypotension leads to coma. Life threatening
Causes: Hyperglycemia (> 500 mg/dL)
Symptoms: Marked dehydration, no ketones because small amounts of insulin circulate the blood
Treatment: Fluids and insulin
Hypoglycemia
Blood sugar
