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82 Cards in this Set

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  • Back
glucose
a sugar that is converted from carboyhydrates from digested food
glycogen
excess glucose that is not needed immediately for energy
fatty acids
end products of ingested fat that are transported to the liver from the small intestine
oxidation
combining with oxygen
bile
flud that aids in digestion
emulsify
break down that fat in the small intestine
bilirubin
product of red blood cell destruction
galllbladder
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
duodenum
upper part of the small intestine
pancreas
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
glucagon
secreted by alpha cells; acts by raising serum glucose levels
insulin
secreted by beta cells; lowers blood glucose levels; metabolises carbohydrates, fats, and proteins
somatostatin
secreted by delta cells; inhibitory effect on the secretion of glucagon, insulin, and the pituitary hormones, specifically growth hormone
active transport
carrying items across cell membranes into cells
Vitamin A
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
Vitamin D
calcium and phosphorus absorption and the development of teeth and bones
Vitamin E
promotes the stability of red blood cells and may help counter the production of free radicals that results from excess secretionof stress hormones
Vitamin K
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
cholelithiasis
presence or formation of stones in the gallbladder; may obstruct the bile ducts and thereby prevent the flow of bile into the small intestine
cholecystitis
bile is restricted from flowing into the duodenum; inflammation of the gallbladder
guarding
muscle spasms that occur when the abdomen is palpated over an inflamed or diseased area during examination
gallbladder series
patient swallows radiopaque tablets the night before the exam; makes it possible to visualize the gallbladder using x rays
pigment stones
calcium based stones
extracorporeal shock wave lithotripsy
electrical shock waves moving thorugh water to crush gallstones into smaller pieces so that they can pass through the gallbladder and common bile duct
intracorporeal lithotripsy
ultrasound to break up stones
endoscopic retrograde cholangiopancreatography
endoscope is inserted through the mouth and then guided internally into the bile duct where stone is crushed and then extracted
choledochostomy
formation of an artificial passage through the abdominal wall and into the common bile duct in order to remove gallstones
choledochotomy
stones are removed through an incision made directly into the common bile duct
penrose drain
covered by a terile dressing may be used to remove blood and any other abdominal drainage
acute pancreatitis
inflammation of the pancreas; increase in the secretion of the enzyme trypsin
trypsin
enzyme; contains a high acid content and can literally digest the pancrease
autodigestion
the act of the pancreas digesting itself
elastase
an enzyme that can cause pancreatic hemorrhage
Turner's sign
ecchymosis around the flank area
Cullen's sign
ecchymosis around the umbilicus
oral pancreatic enzymes
may be given with meals to aid in the digestion of fats, proteins and carbohydrates
chronic pancreatitis
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
steatorrhea
frothy and oul stools with high fat content (late sign of pancreatitis)
pancreatic jejunostomy
surgical procedure to have pancreatic juices drain into the jejunum
jejunum
second chamber of the small intestine
cirrhosis
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)
postnecrotic cirrhosis
type of cirrhosis that results from hepatitis and toxic substances
Laennec's cirrhosis or portal cirrhosis
associated with chronic alcoholism; more common in men than women; especially prevalent in hispanic, african american, and native americans
portal vessels
blood vessels that carry blood to and from the liver
esophageal varices
dilated blood vessels in the esophagus
hepatomegaly
enlargement of the liver
hepatic encephalopathy
changes in mood, personality, and level of consciousness; may result in hepatic coma
satiety
feeling of fullness from food
spider angiomas
spider shaped capillaries that are visible on the skin
aspartate aminotransferase (AST)
alanine aminotransferase (ALT)
liver enzymes; elevated due to cellular eath or necrosis with cirrhosis
Sengstaken-Blakemore tube
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
portacaval shunt
portal vein and vena cava are cut and then connected to each other in order to allow blood to bypass the liver
portal-systemic encephalopathy
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
asterixis or flapping tumor
involuntary jerking or flapping movements of the hands; advanced symptom of PSE
diabetes mellitus
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
Type I diabetes or insulin-dependent diabetes (IDDM)
destruction of the endogenous insulin-secreting beta cells in the pancreas and the subsequent inability of the body to produce any insulin whatsoever
autoimmune disorders
body loses its capacity to differentiate the self from what is not the self
type II diabetes or non-insulin-dependent diabetes mellitus (NIDDM)
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
insulin resistance
decreased cellular sensitivity to insulin
gestational diaetes
occurs during pregnancy; appears to be related to placental hormone secretion
retinopathy
blood vessels are damaged in the retina; can result in blindness
nueropathy
condition of nerve deterioration that can result in loss of sensation or feelings of numbness, prickling, burning or tingling in the extremities
osteomyelitis
bone inflammation and infection
glucose tolerance test
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
glycosylation
excess glucose in the blood coats various tissues and cells
hyperinsulinism
rapid drop of blood glucose levels; may lose consciousness with this
rapid acting insulin
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
postprandial hyperglycemia
high serum glucose levels that can occur after a meal
fast acting insulin
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
Intermediate Acting INsulin
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
Long acting insulin
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
sulfonylureas
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
biguanides
Metoformin (Glucophage); facilitating glucose metabolism in the muscles and decreasing glucose formation in the liver
lactic acidosis
build of lactic acid in the blood; side effect that can occur with alcohol and glucophage are taken concurrently
glucosidase inhibitors
Acarbose (Precose); delays carbohydrate digestion and glucose absorption in the intestines; give at the beginning of each meal
Actos
oral hypoglycemic; reduces insulin resistance and helps the body use any endogenous insulin that may be present
glucagon
hyperglycemic agent and insulin antagonist
hyperglycemic reactions
may take hours or even days to develop; can be caused by an overabundance of glucagon, epinephrine, growth hormone, or cortisol
diabetic ketoacidosis
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
hyperglycemic hypersmolar nonketotic syndrome
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)
Somogyi effect
rebound hyperglycemic reaction that is caused by too much insulin
diabetic exchange diet
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