Gastrointestinal Flashcards
pyloric sphincter
closes to keep food in the stomach, and opens to send food into the small intestine
small intestines
receive digestive enzymes from pancreas and liver, make food into chyme and absorb nutrients
liver functions
produce bile, albumin, cholesterol, converts glucose to glycogen for storage, converts ammonia to urea, metabolizes bilirubin in the breakdowns of RBCs, metabolizes drugs and toxins, produces clotting factors and regulates blood clotting
gallbladder
stores and releases bladder into small intestine
pancreas
regulates blood sugar, and produces and releases digestive enzymes; trypsin, amylase, lipase (released into duodenum)
Large Intestine
absorbs water and electrolytes, produces and absorbs vitamins, forms and propels feces toward rectum for elimination
TPN
delivered intravenously, contains dextrose, amino acids, and electrolytes; central line is preferred
TPN complications
infection, fluid overload hypo/hyper-glycemia, embolism
if TPN runs out and you don’t have anymore what should you do
do not turn off suddenly, give dextrose 10% at same rate the TPN was running
TPN bag and tubing is changed every
24 hours
ondansetron nursing consideration
administer slowly, fast push can cause QT prolongation and VT
antiulcer agents include
H2 receptor blockers, PPIs, antacids, GI protectant
Famotidine
H2 receptor antagonist (antihistamine); blocks release of histamine which blocks acid secretion; separate this class from other medications as they are likely to interact
Famotidine use
short term tx of gastric and duodenal ulcers, GERD, hypersecretion of stomach acid conditions, chronic NSAID use
Omeprazole
PPI; GERD and ulcers, decreases gastric acid production; administer 30-60 minutes, report black, tarry stools
sucralfate
aluminum hyroxide and sucrose; promotes healing of ulcers by providing a barrier over them, short term tx of duodenal or gastric ulcers, peptic esophagitis, NSAID/ASA induced GI damage
surcralfate nursing considerations
take on empty stomach 1 hr before meals or 2 hours after and at bedtime (usually taken 4 times a day), don’t give within 30 min of antacids as it decreases effectiveness, monitor BG in diabetics as it contains sucrose
can decrease availability of warfarin, digoxin, phenytoin, levothyroxine and classes of abx - separate these drugs from sucralfate for at least 2 hrs
NG tube measurement
nose to ear to xiphoid process
blakemore tube
inserted through nose down esophagus and into stomach with balloons that can be inflated to stop bleeding esophageal varices
blakemore tube nursing consideration
must keep a pair of scissors at bedside in case of emergency; if inflate balloon becomes dislodged it can compress the trachea and cause respiratory arrest; if happens cut balloon port to let air escape
hold feeds if gastric residual is greater than
500ml
esophageal varices
dilated submucosal veins in esophagus, can burst and bleed; caused by liver disease and alcoholism tx: blakemore tube and surgery
GERD what is it and tx and complications
acid refluxes from stomach into esophagus causing esophagitis Tx: sit upright after eating, eat small frequent meals, H2 blockers and PPIs, complication: Barrett’s esophagus
Gastritis
inflammatory disorder of gastric mucosa; acute gastritis is associated with H.pylori and NSAID use
gastritis S&S and tx
vague abdominal discomfort, epigastric tenderness, bleeding
tx: healing occurs spontaneously within a few days, no NSAIDs, H2 receptor blockers, PPIs, abx if cause is H. pylori
Barrett’s esophagus
reflux for extended period of time, acid has caused changes to cells of esophagus which are cancerous
Gastric ulcer S&S
pain 1-2 hrs after meals and gets worse when eating, abd pain aggravated by eating, vomiting, weight loss, hematemesis if hemorrhage occurs
Gastric ulcer tx
treat H.pylori infection with abx if this is the cause, reduce stomach acid with PPIs and H2 receptor blocks
duodenal ulcer S&S
pain 2-4 hrs after meals, food may relieve pain, weight gain, melena if hemorrhage occurs
duodenal ulcer tx
treat H.pylori infection with abx if this is the cause, reduce stomach acid with PPIs and H2 receptor blocks
primary action of PPIs is to
increase stomach pH or decrease amount of acid in the stomach
Crohn’s disease
inflammation and erosion of the ileum and anywhere throughout the small and large intestines; affects any part of digestive tract from mouth to anus, skip lesions
ulcerative colitis
inflammation of large intestines, sigmoid colon and rectum, lesions are continuous (no skipped lesions) and are limited to the mucosa and are not transmural
Diverticula
herniation of mucosa through the muscle layers of the colon wall
diverticulosis
asymptomatic diverticular disease
diverticulitis
inflammatory stage of diverticulosis
possible causes of diverticular disease
decreased dietary fiber, abnormal neuromuscular function, alterations in intestinal motility, >60 yrs of age
diverticula disease S&S
rebound tenderness, cramping, diarrhea, vomiting, dehydration, weight loss, rectal bleeding, bloody stools, anemia, fever
diverticula disease tx
low fiber diet, avoid cold or hot foods, no smoking, antidiarrheals, abx, steroids, severe cases may require surgery and ostomy’s
intestinal obstruction
any condition that prevents the flow of chyme through the intestinal lumen or failure of normal intestinal motility in the absence of an obstructing lesion
small intestine obstruction S&S
colicky pains cause by intestinal distention followed by n/v
large intestine obstruction S&S
hypogastric pain and abdominal pain
Appendicitis
inflammation of appendix, begins as a dull steady periumbilical pain, pain progresses an localizes to RLQ, sudden relief of pain may indicate rupture
Appendicitis S&S
RLQ pain, anorexia, increase temp and increased WBCs, nausea, McBurney’s and Psoas sign
McBurney’s sign
indicated when there is significant pain upon palpation of this area in the RLQ
Appendicitis tx
appendectomy; preop: no heat, position on right side low fowlers; postop: IV fluids, abx, pain management, NPO until return of bowel sounds, wound care
pancreatitis
inflammation of the pancreas, number one cause is alcoholism; digestive enzyme activation inside pancreas causes autodigestion of the pancreas
Pancreatitis S&S
pain (increases with eating), distention, ascites, abd mass, rigid abdomen, cullen’s sign, Gray turner’s sign, fever, n/v, jaundice, hypotension, increased WBCs and increase in serum lipase
cullen’s sign
C shaped bruising above belly button
turner’s sign
bruising along flank
cholelithiasis
gallstones, hardened deposits of bile in gallbladder caused by hyperlipidemia or hyperbilirubinemia
gallstone S&S and tx
sudden sharp RUQ pain, pain worsens and radiates to back and between shoulder blades, get worse at night or after fatty meal, n/v
tx: cholecystectomy
cholecystitis
inflammation of gallbladder cause by infection, blocked bile duct, cholelithiasis
rupture of appendix can lead to
peritonitis
cholecystitis S&S and tx
fever, leukocytosis, rebound tenderness, and abdominal muscle guarding
tx: pain management, fluids, fasting, abx if indicated
treatment for perforated gallbladder
immediate cholecystectomy
hepatitis
inflammation of liver that can lead to cirrhosis, caused by different viral infections and severe cases can lead to hepatic coma/encephalopathy
Hep A transmission, prevention, tx
contaminated food or water (fecal-oral)
vaccination, hygiene, sanitation
tx self limited
hep B
contact with infected body fluids (blood, semen, vaginal fluids)
vaccination, blood screening, improved hygiene
acute: supportive, chronic: antiviral therapy
hep C
contact with infected body fluids (IVDU, non sterilized medical equipment)
screening, sanitary environment, sterile needles
direct acting antivirals (DAAs)
hep D
contact with infected body fluids; can only get HDV if already infected with HBV
blood screening, sanitary practices, HBV vaccine helps prevent HDV
hep E
contaminated food or water (fecal - oral)
improved hand hygiene and sanitation
supportive tx
chronic hepatitis includes
B, C, D
Hepatic coma/encephalopathy
increased ammonia levels due to inflammation of liver and it not being able to convert it to urea so it builds up
hepatic encephalopathy S&S
changes in LOC, neuromuscular disturbances, fetor (distinctive musty or sweet breath odor), sleep, mood, and speech problems
hepatic encephalopathy risk factors
high protein diet, infection, hypovolemia, hypokalemia, constipation, GI bleeding, drugs
hepatic encephalopathy tx
decrease ammonia - lactulose, abx, decrease protein in diet
decrease fluid retention - potassium sparing diuretics
avoid CNS depressants - can worse encephalopathy
cirrhosis
chronic disease of the liver marked by degeneration of cells, inflammation, and fibrous thickening of tissue, liver cells destroyed and replaced with scar tissue, this impairs blood flow to liver causing portal htn
causes of cirrhosis
alcoholism, hepatitis B, hepatitis C, diet
cirrhosis S&S
palpable firm liver, ascites, edmea, abd pain, bloating, dyspepsia, poor appetite, spider angiomas, jaundice, low serum albumin, high serum liver enzymes ALT and AST, anemia
anemia can occur in cirrhosis because
liver produces clotting factors, when not working properly becomes bleeding risk and bleeding/blood loss can lead to anemia
cirrhosis tx
paracentesis, strict I&Os, daily weights, be careful with drug doses (liver cannot metabolize as well; especially with narcotics and acetaminophen), antacids, vitamins, diuretics, low protein and sodium diet, bleeding precautions, skin care
avoid _____________ medication in liver pts
acetaminophen
___________________ drugs can worsen encephalopathy
benzodiazepines and opioids
