GIGI Flashcards
GI disorders
gastroesophageal disease (GERD), pyloric stenosis, barret’s esophagus, gastritis, peptic ulcer disease, dumping syndrome, constipation, diarrhea, crohns disease, ulcerative colitis, diverticulitis/diverticulosis, appendicitis, pancreatitis
GERD
backflow of gastric and duodenal contents into the esophagus; caused by incompetent lower esophageal sphincter, pyloric stenosis, motility disorder
causes of lower esophageal sphincter weakening
overeating regularly- u=increased pressure on LES, smoking- increases acidity, drinking alcohol- relaxes LES muscles, specific medications, certain acidic foods- citrus, tomatoes, coffee, chocolate, fried food, fatty meals, carbonation
meds that cause weakening of LES
progestins, nitrates, beta blockers, calcium channel blockers, dopamine agonists, anticholinergics
GERD assessment
heartburn, cough, regurgitation, dysphagia, laryngitis, chest pain (may mimic MI); obtain HX and info about diet
GERD interventions
avoid food triggers, GERD friendly diet- smaller more frequent meals high in fiber alkaline and fluids, elevate HOB and encourage sitting up for 30 min following meal, medications- proton pump inhibitors and H2 receptor blockers, monitor for aspiration
pyloric stenosis
thickening/swelling of the pylorus; common in children but rare in adults; congenital in children and secondary in adults; causing back up and fullness in stomach
causes of pyloric stenosis in adults
ulcers, cancer, adhesions after abdominal surgery
pyloric stenosis assessment
dyspepsia (epigastric pain), nausea, regurgitation, odynophagia (pain when swallowing), hypersalivation
pyloric stenosis interventions
avoid foods that increase LES pressure or esophageal irritation, low fat high fiber diet, avoid eating 2 hours before bed, elevated HOB, avoid anticholinergics and NSAIDs, take prescribed meds- antacids, H2 receptor antagonists, PPIs, prokinetic medications; extreme cases may require endoscopic dilation or pyloroplasty (widening)
Barrett’s esophagus
normal lining of esophagus is damaged by acid reflux and thickens and reddens; presence of metaplasia causes increased risk of esophageal cancer; long-term effect of gerd
H. pykori
type of bacteria that infects stomach and duodenum causing inflammation; no symptoms present unless complicated by something else; main cause of peptic ulcer disease and chronic gastritis
gastritis
inflammation of the stomach or gastric mucosa; can be acute or chronic
acute gastritis causes
ingestion of food contaminated with disease-causing microorganisms, food that is irritating or too highly seasoned, overuse of ASA/NSAIDs/corticosteroids, alcohol, bile reflux, radiation therapy
chronic gastritis causes
benign or malignant ulcers, H. pylori, autoimmune diseases, dietary factors, medications, alcohol, smoking, reflux
gastritis assessment
gastritis interventions
peptic ulcer disease
ulceration in mucosal wall of stomach, pylorus, duodenum, or esophagus in portion accessible to gastric secretions; erosion can extend through muscle to peritoneum; usually occurs alone and in people aged 30-60
gastric ulcers
ulceration of the mucosal lining that extends to the submucosal layer of the stomach
duodenal ulcers
break in the mucosa of the duodenum
risk factors for developing gastric/duodenal ulcers
stress, smoking, use of corticosteroids, NSAIDs, alcohol, hx of gastritis, family hx of gastric ulcers, infection with H. pylori
complications with ulcers
hemorrhage, perforation, pyloric obstruction
gastric ulcer assessment
gnawing sharp pain; left to mid epigastric region; occurs during or 30-60 minutes after eating; hematemesis
duodenal ulcer assessment
burning pain; mid-epigastric region; occurs 1.5-3 hours following a meal and during the night; melena; pain relieved by eating
interventions for peptic ulcer disease
monitor VS for signs of bleeding, small frequent bland meals, H2 receptor agonist or PPI to decrease gastric acid secretion, antacids to neutralize secretions, mucosal barrier protectants 1 hr before meal, prostaglandins for protecting and antisecretory actions, avoid alcohol caffeine chocolate smoking NSAIDs
peptic ulcer disease active bleeding interventions
monitor VS for dehydration, hypovolemic shock (tachy, hypoten., hypotherm.), respiratory compromise; maintain NPO status and give fluids; monitor Hgb and hematocrit; admin meds to vasoconstrict and reduce bleeding
peptic ulcer disease surgical interventions
gastroduodenostomy/billroth I- partial gastrectomy and remaining segment connected to duodenum; gastrojejunostomy/billroth II- partial gastrectomy and remaining segment is connected to jejunum; total gastrectomy- removal of the stomach and attach esophagus to jejunum or duodenum; pyloroplasty- enlargement of pylorus to prevent/decrease pyloric obstructing increasing gastric emptying
dumping syndromeq
rapid emptying of gastric contents into the small intestine following a gastric resection
constipation
less than 3 bowel movements per week; caused by surgery, chronic laxative, immobility, diet, ignoring urge, lack of exercise
diarrhea
over 3 bowel movements per day; can be acute, persistent, or chronic; caused by infections, meds, tube feeds, endocrine and metabolic disorders, IBS
irritable bowel syndrome
chronic recurrent diarrhea, constipation, and/or abdominal bloating/pain; idiopathic but can be triggered by environmental, stress, hormonal, or genetic
IBS assessment
alterations in bowel patterns, pain, bloating, distention
IBS interventions
increase dietary fiber, drink 8-10 cups of liquid per day, exercise, sleep, med therapy
ulcerative colitis
large intestine and rectum are affected; migrates in continuous pattern; inner layer of intestinal lining; cure is colectomy with ileostomy
crohns disease
cobblestone appearance of distal ileum and ascending colon mainly but can affect entire all intestines; edematous bleeding lesions and ulcers; entire bowel wall; there is no cure but can be managed
crohns disease vs ulcerative colitis
crohns disease is patchy inflammation throughout small and large bowel; UC is continuous and uniform inflammation in the large bowel
crohsn disease assessment
fever; cram like colicky pain in RLQ after meals that does not relieve with BM; chronic diarrhea with mucus and pus; abdominal distention; tenderness; anorexia, N/V; dehydration; weight loss; anemia; malnutrition; electrolyte imbalance
UC assessment
anorexia causing weight loss malnutrition and dehydration; electrolyte imbalance; vitamin K deficiency; malaise; abdominal tenderness in LLQ with cramping; severe diarrhea with blood and mucus; anemia
diagnostics testing for UC
imagine- CT scan, MRI, abdominal x-ray, colonoscopy with biopsies, ultrasound; labs- CBC, WBC, ESR/CRP, low albumin, electrolyte imbalance
interventions for crohns/UC
NPO, fluids IV, lectrolytes, parenteral nutrition, restrict movement to reduce intestinal activity, monitor BS/tenderness/cramping, monitor stools, administration of meds- salicylate/corticosteroids/antibx/immunosuppressants/antidiarrheals, avoid gas forming foods/whole wheat grains/nuts/raw fruits/veg./alcohol/smoking
crohns disease and UC surgical interventions
restorative proctocolectomy with ileal pouch anal anastomosis: removal of entire colon and rectum but keeps anal sphincter; total proctocolectomy with permanent ileostomy: removes all the large intestine and small intestine through and opening
stoma care
want bright beefy red stoma; pale pink is sign of low Hgb; purplish/black is sign of compromised circulation
diverticulosis
outpouching herniation of the intestinal mucosa and/or all layers without inflammation; can occur in any part of intestine but mostly in sigmoid colon
diverticulitis
inflammation of 1 or more diverticula that occurs from penetration of fecal matter through thin-walled diverticula; result in local abscess formation and perforation; perforated diverticula can progress to intra-abdominal perforation with generalized peritonitis; usually left lower quadrant
diverticulosis/diverticulitis assessment
LLQ abdominal pain increasing with coughing, straining, and lifting; flatulence; cramp-like pain; abdominal distention and tenderness; palpable tender rectal mass may be present; blood in stools; elevated temp.; N/V
diverticulitis/diverticulosis inteventions
bed rest, NPO with clear liquids; introductiNon of fiber containing diet gradually once inflammation resolves; admin antibx/analgesics/anticholinergics; refrain from strenuous activities (lifiting coughing);
NG tubes
decompress stomach by removing fluids and gas; administration of meds to those unable to swallow; prove nutrition by acting as feeding tube; can be used to irrigate stomach and remove toxins; can feed as bolus (30-60 min q3-6 hours), continuous, or cyclical (8-16 hours overnight)
admin of tube feeds
high fowlers, assess bowel sounds and hold if absent; assess tube placement via aspirating and check pH; warm feed to room temp.; maintain upright position for 30 min following bolus feed; flush with 30-50mL after feeding and then clamp 30-60 min after; tubing changed q24 hours
parental nutrition
is used as a last resort for supplying nutrients; supplies nutrients via veins and can be partial or total; supplies fats carbs and proteins; prevent fat and muscle protein from being broken down; is a hypertonic saline d/t ihgh glucose and amino acids
indications for admin of parenteral nutrition
dysfunctional or non-functional GI tract that cannot process nutrients; not enough oral nutrition; multiple GI surgeries or trauma; intolerance to enteral feeding; used when need to heal bowel; no other nutritional alternatives available
PPN
admin though large distal vein either standard PIV or midline/PICC or subclavian or IJ/EJ
TPN
continuous administration over 24 hours or cyclical overnight through central vein/PICC; must infuse via pump; admin D10W when TPN runs dry and waiting for new bag; watch for sclerosis, phlebitis, swelling; moitor glucose
when discontinuing TPN
need evaluation by nutritionist; gradually decrease flow for 1-2 hours while increasing oral intake; change IV dressing after removal until healed; encourage PO nutrition; record IO, weight, lab results of electrolytes and glucose levels
Parenteral nutrition interventions
validated by 2 RNs to ensure proper prescribed components; IV meds and blood not given through PN lines; blood can be drawn from central line but need to be stopped; monitor PT and PTT if receiving anticoags; monitor BGL, monitor for refeeding syndrome (rapid drop in K, Mg, and Phosph.), monitor central line infection; monitor liver/kidney function; refrigerate PN and admin within 24 hours
appendicitis
most common cause of acute abdomen in US; leading reason for emergency abdominal surgery; common ages are 10-30; higher incidence in men; familiar predisposition
diagnosing appendicitis
elevated WBC, elevated C-reactive proteins within 12 hours and may normalize after 24 hours; CT or ultrasound for confirmation; UA to rule out UTI or renal calculi
appendicitis assessment
initial- vague dull poorly localized periumbilical pain, anorexia/loss of appetite; progression- pain shift to RLQ and is sharp and localized, nausea with low grade fever
physical findingsing of appendicitis
local tenderness at McBurneys point on pressure (RLG 1/3 way from anterior iliac spine to umbilicus), rebound tenderness, rovisings sign (LLQ palpation causes RLQ pain)
appendicitis complication
ruptured appendix is emergency and can cause spread of infection and bacteria
appendicitis interventions
immediate surgery; pain relief, fluid balance, anxiety reduction; infection prevention, atelectasis, skin issues; optimal nutrition; high fowlers; discharge instructions for wound care
pancreatitis
self-digestion by pancreatic enzymes; gallstone obstruct flow of pancreatic juice activating the enzymes; enzyme act. leads to vasodilation, increased permeability, necrosis, erosion, hemorrhage
causes of pancreatitis
infections, mumps complications, trauma, peptic ulcers, vascular issues, HLD, hypercalcemia, alcohol, tobacco, hereditary
interstitial edematous pancreatitis
mild common form characterized by gland enlargement due to edema; minimal organ dysfunction that resolves in 6 months; risk of shock, fluid electrolyte imbalance, sepsis
necrotizing pancreatitis
severe rare form with tissue necrosis in or around pancreas; enzymes damage blood vessels leading to bleeding and thrombosis; necrosis may extend retroperitoneal; can cause organ failure
acute pancreatitis assessment
severe abdominal pain that radiates to back that is aggravated by meals and unrelieved by antacids; abdominal guarding; rigid abdomen if peritonitis, bruising in flank (turners sign) or umbilicus (Cullens sign); n/v, fever, jaundice; hypotension, tachycardia, cyanosis, cold skin, resp. distress, hypoxia, AKI, hypocalcemia, hyperglycemia, coag issues
chronic pancreatitis manifestation
recurring severe abdominal pain and back pain, attacks become more frequent severe and longer, weight loss d/t decreased intake and malabsorption, frothy foul smelling diarrhea, calcification of gland and formation of calcium stones
diagnosis acute pancreatitis
2 of 3 following- upper abdominal pain hx, amylasee/lipase elevation, typical imaging
