Nursing Concepts 5 - Metabolic Mechanisms

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glucose

Back 1

a sugar that is converted from carboyhydrates from digested food

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glycogen

Back 2

excess glucose that is not needed immediately for energy

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fatty acids

Back 3

end products of ingested fat that are transported to the liver from the small intestine

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oxidation

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combining with oxygen

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bile

Back 5

flud that aids in digestion

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emulsify

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break down that fat in the small intestine

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bilirubin

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product of red blood cell destruction

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galllbladder

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pear-shaped hollow organ under the right lobe of the liver; stores and concentrates the bile that has been secreted by the liver; absorbs the bile's water content

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duodenum

Back 9

upper part of the small intestine

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pancreas

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behind the stomach in the upper left side of the abominal cavity; produces both exocrine and endocrine secretions; exocrine-released through various ducts; endocrine - released directly into the bloodstream

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glucagon

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secreted by alpha cells; acts by raising serum glucose levels

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insulin

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secreted by beta cells; lowers blood glucose levels; metabolises carbohydrates, fats, and proteins

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somatostatin

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secreted by delta cells; inhibitory effect on the secretion of glucagon, insulin, and the pituitary hormones, specifically growth hormone

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active transport

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carrying items across cell membranes into cells

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Vitamin A

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essential for normal growth and development, visual acuity, adaptation of the eyes to dark environments, and maintenance of the body's ability to resist infections

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Vitamin D

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calcium and phosphorus absorption and the development of teeth and bones

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Vitamin E

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promotes the stability of red blood cells and may help counter the production of free radicals that results from excess secretionof stress hormones

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Vitamin K

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essential for blood coagulation and the synthesis of prothrombin by the liver; inhibits the growth of oxalate stones and help egulate calcium levels in the blood

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cholelithiasis

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presence or formation of stones in the gallbladder; may obstruct the bile ducts and thereby prevent the flow of bile into the small intestine

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cholecystitis

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bile is restricted from flowing into the duodenum; inflammation of the gallbladder

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guarding

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muscle spasms that occur when the abdomen is palpated over an inflamed or diseased area during examination

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gallbladder series

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patient swallows radiopaque tablets the night before the exam; makes it possible to visualize the gallbladder using x rays

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pigment stones

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calcium based stones

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extracorporeal shock wave lithotripsy

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electrical shock waves moving thorugh water to crush gallstones into smaller pieces so that they can pass through the gallbladder and common bile duct

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intracorporeal lithotripsy

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ultrasound to break up stones

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endoscopic retrograde cholangiopancreatography

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endoscope is inserted through the mouth and then guided internally into the bile duct where stone is crushed and then extracted

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choledochostomy

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formation of an artificial passage through the abdominal wall and into the common bile duct in order to remove gallstones

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choledochotomy

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stones are removed through an incision made directly into the common bile duct

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penrose drain

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covered by a terile dressing may be used to remove blood and any other abdominal drainage

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acute pancreatitis

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inflammation of the pancreas; increase in the secretion of the enzyme trypsin

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trypsin

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enzyme; contains a high acid content and can literally digest the pancrease

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autodigestion

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the act of the pancreas digesting itself

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elastase

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an enzyme that can cause pancreatic hemorrhage

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Turner's sign

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ecchymosis around the flank area

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Cullen's sign

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ecchymosis around the umbilicus

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oral pancreatic enzymes

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may be given with meals to aid in the digestion of fats, proteins and carbohydrates

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chronic pancreatitis

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chronic inflammation of the pancreas that involves decreased secretion of pancreatic juices; disease of fat and protein malabsorption; growth of scar tissue on pancreas; primary factor contributing to its development is chronic alcohol abusecon

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steatorrhea

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frothy and oul stools with high fat content (late sign of pancreatitis)

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pancreatic jejunostomy

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surgical procedure to have pancreatic juices drain into the jejunum

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jejunum

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second chamber of the small intestine

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cirrhosis

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chronic condition that impairs the normal functioning of liver cells and increases the resistance of the liver to blood flow; caused by alcholism, chronic viral hepatitis, and ingestion of toxic substances; caused by fibrosis (scarring)

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postnecrotic cirrhosis

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type of cirrhosis that results from hepatitis and toxic substances

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Laennec's cirrhosis or portal cirrhosis

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associated with chronic alcoholism; more common in men than women; especially prevalent in hispanic, african american, and native americans

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portal vessels

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blood vessels that carry blood to and from the liver

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esophageal varices

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dilated blood vessels in the esophagus

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hepatomegaly

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enlargement of the liver

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hepatic encephalopathy

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changes in mood, personality, and level of consciousness; may result in hepatic coma

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satiety

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feeling of fullness from food

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spider angiomas

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spider shaped capillaries that are visible on the skin

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aspartate aminotransferase (AST)
alanine aminotransferase (ALT)

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liver enzymes; elevated due to cellular eath or necrosis with cirrhosis

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Sengstaken-Blakemore tube

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may be inserted for esophageal varcies: triple lumen; may be inserted into one of the patient's nostrils; two lumens have balloons that press against areas in the stomach and the esophagus and control bleeding when inflated (double-balloon tamponade); 3rd lumen removes blood and other secretions directly from the stomach; primary nursing concert is aspiration since swallowing is not possible when balloons are inflated

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portacaval shunt

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portal vein and vena cava are cut and then connected to each other in order to allow blood to bypass the liver

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portal-systemic encephalopathy

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brain disorder that can result from chronic liver disease; may develop from unhealthy ammonia levels; hypokalemia and internal bleeding may also contribute to this disorder

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asterixis or flapping tumor

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involuntary jerking or flapping movements of the hands; advanced symptom of PSE

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diabetes mellitus

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chronic sidorder of metabolism related to inadequate production or utilization of insulin; can also develop when cells become resistant to insulin; carbohydrate, protein, and fat metabolism are all affected by this condition; one of the most common causes of death in the US

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Type I diabetes or insulin-dependent diabetes (IDDM)

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destruction of the endogenous insulin-secreting beta cells in the pancreas and the subsequent inability of the body to produce any insulin whatsoever

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autoimmune disorders

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body loses its capacity to differentiate the self from what is not the self

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type II diabetes or non-insulin-dependent diabetes mellitus (NIDDM)

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pancrease usually fails to produce enough insulin for adequate glucose metabolism; generally produces enough to prevent fat breakdown and the development of ketoacidosis; insuline resistance

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insulin resistance

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decreased cellular sensitivity to insulin

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gestational diaetes

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occurs during pregnancy; appears to be related to placental hormone secretion

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retinopathy

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blood vessels are damaged in the retina; can result in blindness

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nueropathy

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condition of nerve deterioration that can result in loss of sensation or feelings of numbness, prickling, burning or tingling in the extremities

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osteomyelitis

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bone inflammation and infection

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glucose tolerance test

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fasting blood sample is drawn; drinks a glucose solution and has blood redrawn and retested for glucose at different times throughout the day; if reading is 200mg/dl or higher two hors after consuming the solution, diabetes is generally confirmed

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glycosylation

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excess glucose in the blood coats various tissues and cells

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hyperinsulinism

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rapid drop of blood glucose levels; may lose consciousness with this

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rapid acting insulin

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takes effect in less time than any of the other exogenous insulins; shortest overall impact on the patient; given right before meals; onset is 15-30 mins, peak 1-2 hrs; duration is 3-6 hours; used to treat high glucose levels that can occur after a meal; prevents hypoglycemic attacks in the middle of the night; HUMALOG

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postprandial hyperglycemia

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high serum glucose levels that can occur after a meal

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fast acting insulin

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daily diabetic control and the treatment of life-threatening ketoacidosis; onset 30 mins-1hr; peak 2-3 hrs; duration is 5-7hrs; given 20-30 mins prior to a meal; (R) and crystaline zinc; (R) can be given IV and pumps

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Intermediate Acting INsulin

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routine dibetic control; 30-45 mins prior to a meal; onset is 1-2 hrs, peak 8-12 hrs; duration is 18-24 hrs; Lente, NPH

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Long acting insulin

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routine diabetic control; given 1 hr prior to breakfast; onset is 4-8 hrs; peak is 14-24 rs; duration is 36 hrs; ultralente; may be prone to hypoglycemic reactions in the middle of the night; Lantus - no peak action time

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sulfonylureas

Back 72

oral hypoglycemic; (chlorpropamide) Diabinese, (acetohexamide)Dymelor, (tolazamide)Tolinase, (glipizide)Glucotrol, (glyburide)Micronase, Diabeta

Stimulate the beta cells of the pancvreas to secrete endogenous insulin; not effective with type 1 diabetes

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biguanides

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Metoformin (Glucophage); facilitating glucose metabolism in the muscles and decreasing glucose formation in the liver

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lactic acidosis

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build of lactic acid in the blood; side effect that can occur with alcohol and glucophage are taken concurrently

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glucosidase inhibitors

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Acarbose (Precose); delays carbohydrate digestion and glucose absorption in the intestines; give at the beginning of each meal

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Actos

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oral hypoglycemic; reduces insulin resistance and helps the body use any endogenous insulin that may be present

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glucagon

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hyperglycemic agent and insulin antagonist

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hyperglycemic reactions

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may take hours or even days to develop; can be caused by an overabundance of glucagon, epinephrine, growth hormone, or cortisol

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diabetic ketoacidosis

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serious and severe hyperglycemic reaction that is associated iwth type I diabetes; accompanied by insufficient insulin levels - results in fat breakdown and possible metabolic acidosis because of accumulation of ketone bodies in the blood

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hyperglycemic hypersmolar nonketotic syndrome

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occurs in type II diabetics who still have some insulin being produced in the pancreas; dehydrated patients and frail elderly patients are especially at risk for HHNS; no ketones present; insulin prevents fats from breaking down into ketones; usually related to excess caloric intake; may also develop as a result of acute or chronic diseases that require medications that elevage glucose (steroids and cardiac medications)

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Somogyi effect

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rebound hyperglycemic reaction that is caused by too much insulin

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diabetic exchange diet

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low-sugar complex carbohydrates for 60% of their daily caloric intake and protein for another 15-20%; monounsaturated and polyunsaturated fats should not exceed 30% and saturated fats should be avoided altogether