M9 Gastrointestinal Disorders

GI system

includes mouth, esophagus, stomach, small intestine, large intestine, liver, pancreas, gallbladder, colon, rectum

responsible for intake, breakdown, absorption, elimination of food

examples of GI disorders

gastroesophageal reflux disease (GERD), gastritis, peptic ulcer disease (PUD), GI bleed, irritable bowel syndrome (IBS), appendicitis, diverticulitis/diverticulosis, Crohn’s disease, ulcerative colitis (UC), parenteral nutrition, pancreatitis

gastroesophageal reflux disease

aka GERD, backflow of gastric/duodenal contents into esophagus

caused by incompetent lower esophageal sphincter (LES), pyloric stenosis, motility disorder

causes of weakened LES

regular overeating or obesity (stomach swells/puts P on LES, LES loses shape/strength over time, gastric contents backflow into esophagus, reflux further damage to esophagus), smoking (raises acidity of stomach fluids and exposes esophagus to toxins/chemicals that damage it), alcohol (relaxes muscles of LES), specific meds (CCBs, nitrates, albuterol, progestins), certain foods (citrus, tomatoes, cofee, chocolate, fried foods, fatty meats, carbonated beverages)

GERD management

avoid situations that decrease LES pressure or cause irritation (smoking, excess alcohol, etc.)

meds → antacids (Ca carbonate, Al/Mg hydroxide), H2 receptor antagonists (famotidine), PPIs (pantoprazole, omeprazole)

gastritis

inflammation of gastric mucosa, can be acute or chronic

gastritis causes

acute → ingestion of food comtaminated w/ disease-causing microorganisms, irritating/overly seasoned food, overuse of ASA/NSAIDs/corticosteroids, alcohol, bile reflux, radiation therapy

chronic → benign/malignant ulcers, H. pylori, autoimmune diseases, dietary factors, NSAIDs/ASA/steroids, alcohol, smoking, reflux

H. pylori

type of bacteria that infects stomach/duodenum → inflammation

s/s → none, unless complicated by something else

diagnosis → H. pylori breath test

treatment → PPI & antibiotics

*main cause of chronic gastritis and PUD

gastritis assessment

acute → abdominal discomfort, anorexia, N/V, headache, hiccuping reflex, bleeding (if erosive)

chronic → anorexia, N/V, belching, heartburn after eating, sour taste in mouth, B12 deficiency d/t malabsorption, bleeding (if erosive)

diagnosing gastritis

endoscopy w/ biopsy, H. pylori breath test

gastritis interventions

• NPO until symptoms resolve

• acute → avoid irritating foods/fluids, may need NGT, decrease acid w/ meds, IV fluids

• meds → antibiotics, antacids, vit. B12 injections if deficient

• monitor for signs of hemorrhagic gastritis

• decrease anxiety, promote optimal nutrition, maintain fluid balance

• relieve pain

peptic ulcer disease

aka PUD, ulceration in mucosal wall of stomach/pylorus/duodenum/esophagus in portions accessible to gastric secretions, erosion can extend through muscle to peritoneum

gastric vs. duodenal ulcers

gastric → ulceration of mucosal lining that extends to submucosal layer of the stomach, gnawing/sharp pain, left to mid-epigastric region, hematemesis, 30-60min after eating meal

duodenal → break in the mucosa of the duodenum, burning pain, mid-epigastric region, melena, pain relieved by eating, 1.5-3hrs after eating meal and during night

gastric/duodenal ulcers risk factors

stress, smoking, corticosteroid use, NSAIDs, alcohol, h/x of gastritis/gastric ulcers, H. pylori infection

gastric/duodenal ulcers complications

hemorrhage, perforation, pyloric obstruction

PUD nursing interventions

• monitor v/s for bleed

• small, frequent, bland meals

• H2 receptor antagonist or PPI → decrease gastric acid secretion

• antacids → neutralize secretions and help w/ pain

• mucosal barrier protectants 1hr before meal (ex: sucralfate)

• prostaglandins → protecting, antisecretory actions

• optimize nutrition → avoid alcohol, caffeine, chocolate, smoking, NSAIDs

PUD active bleeding interventions

• monitor v/s (dehydration, hypovolemic shock, respiratory compromise)

• maintain NPO status, give IV fluids

• monitor Hgb/Hct (transfuse blood as Rx’ed)

• prep for endoscopy w/in 12hrs to find/stop bleed

• post-op complications → hemorrhage, dumping syndrome, diarrhea, hypoglycemia, vit. B12 deficiency

GI bleed

acute → sudden onset; often d/t peptic ulcers, varices, tears in GI tract; can lead to significant blood loss and hemodynamic instability

chronic → slow/persistent bleeding; often d/t colorectal cancer, IBD, angiodysplasia; leads to anemia over time

GI bleed clinical manifestations

acute → hematemesis, melena, hematochezia (bright red blood per rectum, if severe), signs of shock (tachycardia, HOTN, pallor)

chronic → fatigue, pallor, iron-deficiency anemia, occult blood in stool

GI bleed management

nrsg interventions → monitor v/s and O2 sat, establish IV access for fluid resuscitation, prep for possible blood transfusions, admin meds as Rx’ed (ex: PPIs)

medical mgmt → endoscopy for diagnosis/treatment (e.g., banding, clipping), surgery if bleeding is uncontrolled, meds to reduce acid production and manage underlying conditions

PUD surgical interventions

gastroduodenostomy (Billroth I) → partial gastrectomy, remaining segment connected to duodenum

gastrojejunostomy (Billroth II) → partial gastrectomy, remaining segment connected to jejunum

total gastrectomy → removal of stomach, attach esophagus to jejunum/duodenum

pyloroplasty → enlargement of pylorus to prevent/decrease pyloric obstruction, enhancing gastric emptying

dumping syndrome

rapid emptying of gastric contents into SI following gastric resection

assessment → 30min after eating, N/V/D, abdominal fullness/cramping, tachycardia, palpitations, perspiration, weakness, dizziness, borborgymi (loud gurgling sounds)

pt education → avoid sugar/salt/milk, high protein, high fat, low carb, small meals, avoid fluids during meal, lie down after meal for 30min, med as Rx’ed (ex: octreotide)

irritable bowel syndrome

aka IBS, chronic/recurrent diarrhea and/or constipation, abdominal pain/bloating, idiopathic (triggers can be environmental, genetic, hormonal, stress)

IBS clinical manifestations

alteration in bowel patterns, pain, bloating, distention

IBS management

increase dietary fiber, drink 8-10cups liquid/day, exercise, sleep, medication therapy (depends on predominant IBS s/s)

appendicitis

most common cause of acute abdomen in the US, leading reason for emergency abdominal surgery

occurs mainly btw age 10-30, slightly higher incidence in males, familial predisposition

inflammation can be caused by kinking, obstruction by fecalith, lymphoid hyperplasia, foreign bodies/tumors, increased intraluminal pressure, edema, orifice obstruction

appendicitis clinical manifestations

initial → vague periumbilical pain (dull, poorly localized), anorexia
progression → pain shifts to RLQ, pain changes to sharp/well-localized parietal pain, nausea (50%), low-grade fever
manifestations → local tenderness at McBurney’s point on pressure, rebound tenderness (pain intensifies on pressure release), Rovsing’s sign (palpating LLQ causes pain in RLQ)

appendicitis treatment

immediate surgery → appendectomy indicated upon diagnosis to prevent complication, antibiotic prophylaxis for 1-5 days depending on perforated vs. nonperforated

appendicitis nursing interventions

• pain relief, fluid balance, anxiety reduction

• prevention of infection, atelectasis, skin issues

• optimal nutrition, thoracic expansion promotion

• High-Fowler position to reduce tension and promote breathing

diverticulosis

outpouching/hernation of intestinal mucosa and/or all layers w/o inflammation

diverticulitis

inflammation of 1 or more diverticula that occurs from penetration of fecal matter through thin-walled diverticula, results in local abscess formation/perforation

perforated diverticulum can progress to intra-abdominal perforation w/ generalized peritonitis

diverticulosis/diverticulitis manifestations

LLQ abdominal pain (increases w/ coughing, straining, lifting), elevated temp, N/V, flatulence, cramp-like pain, abdominal distention/tenderness, palpable/tender rectal mass, blood in stool

diverticulosis/diverticulitis nursing interventions

• bedrest during acute phase

• maintain NPO status, provide clear liquids during acute

• introduce fiber-containing diet gradually once inflammation resolved

• analgesics, anticholinergics, antibiotics if complicated/hospitalized

• refrain from lifting, straining, coughing, bending

• 2500-3000mL fluids per day

• eat high-fiber soft foods

• avoid gas forming foods

• surgery → colon resection, colostomy

Crohn’s disease

cobblestone appearance, distal ileum & ascending colon, edematous/bleeding lesions/ulcers, skip lesions, entire bowel wall, no cure → managed

ulcerative colitis

large intestine & rectum, migrates in continuous pattern, inner layer of intestinal lining, cure → colectomy w/ ileostomy

Crohn’s disease manifestations

fever, cramp-like/colicky pain in RLQ after meals that doesn’t resolve w/ BM, chronic diarrhea (semisolid) w/ mucus/pus, abdominal distention, tenderness, anorexia, N/V, dehydration → wt loss, anemia, malnutrition, electrolyte imbalance

ulcerative colitis manifestations

anorexia → wt loss, malnutrition, dehydration, electrolyte imbalances, vit. K deficiency, malaise, abdominal tenderness in LLQ, cramping, severe diarrhea w/ blood/mucus → anemia

complications → toxic megacolon, perforation, bleeding

Crohn’s disease/ulcerative colitis diagnostic studies

imaging → CT scan, MRI, abdominal x-ray (UC), colonoscopy w/ biopsies, ultrasound (UC)

labs → CBC, WBC, ESR/CRP, low albumin levels (UC), electrolyte imbalances

Crohn’s disease/ulcerative colitis nursing interventions

• acute phase → NPO, IV fluids/electrolytes, parenteral nutrition

• sub-acute phase → move from clear to low-fiber/high-protein diet

• restrict movement to reduce intestinal activity

• monitor bowel sounds

• monitor stools

• avoid gas forming foods

• avoid smoking

Crohn’s disease/ulcerative colitis surgical interventions

• restorative proctocolectomy w/ ileal pouch-anal anastomosis (RPC-IPAA) → removes entire colon/rectum but keeps anal sphincter (performed in extreme cases if medical management is unsuccessful)

• total proctocolectomy w/ permanent ileostomy → removes colon/rectum, end of ileum forms the opening/stoma

parenteral nutrition

supplies nutrients via veins, can be partial (PPN) or total (TPN)

supplies carbs (dextrose), emulsified fats, amino acids, vitamins, minerals, electrolytes, water

prevents subQ fat/muscle protein being broken down for energy

hypertonic d/t high glucose and amino acids

parenteral nutrition indications

severe dysfunctional/impaired GI tracts that can’t process nutrients, inadequate oral intake, multiple GI surgeries, trauma, intolerance to enteral feedings, obstructions, severe nutritionally deficient conditions (cancer, burn injuries), no other nutritional alternative available

parenteral nutrition administration

PPN → peripheral vein, less hypertonic than TPN, not nutritionally complete, lipids given w/ it to protect vein

TPN → administered through central vein (ex: PICC), must infuse through pump, watch for sclerosis/phlebitis/swelling

continuous → infused continuously over 24 hours or cycled overnight, mostly used in hospital setting, monitor glucose levels closely

discontinuing → eval by nutritionist before PN discontinued, gradually decrease flow for 1-2hrs while increasing oral intake, after removing IV change dressing daily until heals, encourage oral nutrition, record I&O/wt/labs

(if TPN runs empty and waiting for new bag, infuse D10W instead at prescribed rate)

parenteral nutrition nursing interventions

• validation by 2 RNs to ensure prescribed components

• IV meds/blood not given through PN lines → dedicated line

• blood can be drawn from central line, TPN needs to be stopped

• monitor PT/PTT if receiving anticoagulants

• monitor blood glucose levels

• monitor for refeeding syndrome (rapid drop in K, Mg, phosphate)

• monitor liver/kidney fxn

• PN should be refridgerated (take out 30-60min before infusing, admin w/in 24hrs)

• monitor for central line infection

pancreatitis

inflammation of pancreas, self-digestion by pancreatic enzymes

gallstones obstruct flow of pancreatic juice activating enzymes → leads to vasodilation, increased permeability, necrosis, erosion, hemorrhage

mortality rate 2-10% (often d/t shock, anoxia, imbalances), higher at 10-30% w/ severe disease (ex: necrosis)

pancreatitis causes

• infections (bacterial, viral), mumps complication

• trauma

• peptic ulcers

• vascular issues

• hyperlipidemia

• hypercalcemia

• alcohol/tobacco use

• acute idiopathic pancreatitis

• hereditary pancreatitis

acute pancreatitis manifestations

• severe abdominal pain, may radiate to back

  • mid-epigastrium location, often diffuse/acute

  • aggravated by meals, unrelieved by antacids

• acutely ill appearance

• abdominal guarding

• possible rigid abdomen indicating peritonitis

• bruising (ecchymosis) in flank/umbilicus

• N/V (gastric/bile stained)

• fever, jaundice, mental confusion, agitation

• HOTN, tachycardia, cyanosis, cold skin

• respiratory distress, hypoxia, pulmonary infiltrates

• AKI, hypocalcemia, hyperglycemia, coagulation issues

acute pancreatitis diagnosis

2 of 3 criteria → upper abdominal pain history, amylase/lipase elevation, typical imaging

serum amylase/lipase rise w/in 24hrs, amylase returns to normal in 48-72hrs

elevated urinary amylase/WBC count, hypocalcemia and elevated bilirubin in some

acute pancreatitis diagnostic imaging/tests

• X-ray, u/s, CT scans, MRI used to identify pancreatic ∆

• Hgb/Hct levels monitor bleeding risk

• elevated pancreatic enzymes in peritoneal fluid

• ERCP rarely for diagnosis but useful for gallstone pancreatitis treatment

acute pancreatitis severity classification

mild → no organ failure/complications

moderately severe → transient organ failure, complications

severe → persistent organ failure

various different risk stratification systems predict complications/severity, importance of early severity prediction for treatment decisions and optimal care

acute pancreatitis acute management

• withhold all PO intake (to minimize pancreatic stimulation)

• enteral/parenteral feeding

• administer analgesics (typically opioids)

• avoid high-dose opioids d/t GI paralysis and ileus risk

• correct fluid/albumin imbalances, maintain fluid V

• may require ICU care

• insulin for hyperglycemia

• aggressive care d/t diaphragm elevation, atelectasis risk

• semi-fowler’s → decrease P of abdomen on diaphragm

• surgery → biliary drains/stents used to reestablish pancreatic drainage

• surgical postop care w/ drains and open incision management

acute pancreatitis post-acute nursing interventions

• weak/debilitated after acute episode

• regaining strength and returning to previous activity level may take weeks to months

• patient’s memory might be affected d/t severity of illness

• repitition and reinforcement of patient education are crucial

• educate about factors causing acute pancreatitis onset

• avoid high-fat foods, heavy meals, alcohol

• educate on what s/s to report to primary provider

• referral for home care

• address risk of returning to previous drinking habits

chronic pancreatitis medical management

directed by probable cause of chronic pancreatitis, prevent/manage acute attacks, relieve pain, manage exocrine/endocrine insufficiency, nonsurgical approaches include endoscopy (ERCP) for stone removal/stenting, diabetes management, pancreatic enzyme replacement

hypomagnesemia

serum Mg <1,8mg/dL

causes → diarrhea, NG suction, fistulas, malabsorption (IBD), refeeding, alcohol use disorder, diuretics, PPIs

s/s → neuromuscular irritability, increased reflexes, positive Trousseau/Chvostek signs, confusion, seizures if severe, dysrhythmias (torsades de pointes), often occurs w/ low K/Ca

mgmt → replace Mg PO/IV, seizure precautions if severe, teach foods (green leafy veggies, nuts, legumes)

Trosseau’s sign

place BP cuff around arm, inflate cuff for 1-4mins, if hands/fingers go into spasm in palmar flexion = positive

indicates low Ca/Mg

Chvostek’s sign

tap face just below/in front of ear, if facial twitching occurs on one side of mouth/nose/cheek → positive

indicates low Ca/Mg

hypermagnesemia

serum Mg >3.0mg/dL

causes → kidney injury (most common), Mg-containing laxatives/antacids, excess IV Mg

s/s → drowsiness, lethargy, muscle weakness, decreased/absent DTRs, HOTN, brady cardia, respiratory depression if severe

mgmt → stop all Mg sources, IV Ca to counter cardiac/neuromuscular effects, loop diuretics/IV fluids if kidneys work (dialysis if severe), teach pts w/ kidney disease to check before taking OTC products

hypophosphatemia

serum phosphorus <2.5mg/dL

causes → refeeding syndrome (malnutrition, alcohol use disorder), malabsorption (Crohn’s, celiac, chronic diarrhea), hyperparathyroidism, antacids that bind phosphorus

s/s → muscle weakness/pain, respiratory muscle weakness, confusion, seizures if severe, rhabdomyolysis, HF if severe

mgmt → start feedings gradually in malnourished pts, oral phosphate w/ vit. D (IV only ig <1mg/dL), monitor IV site and Ca/P levels, teach foods (dairy, meat, beans)

hyperphosphatemia

serum phosphorus >4.5mg/dL

causes → kidney injury, CKD (most common), phosphate containing laxatives/enemas, chemotherapy, hypoparathyroidism

s/s → signs of low Ca (tetany, muscle cramps), hyperactive reflexes, Ca deposits in soft tissue (longterm)

mgmt → phosphate binders w/ meals, limit phosphate-rich foods (dairy, nuts, meats), avoid phosphate-containing laxatives/enemas, monitor Ca

hypokalemia

serum K <3.5mEq/L

muscle weakness, fatigue, cramping, palpitations, constipation

hypocalcemia

serum Ca <8.5mg/dL

seizures, tetany, paresthesia, heightened neuromuscular excitability (Trosseau’s/Chvostek’s), QTC prolongation