Ch. 50 Patients with Stomach Disorders Flashcards
Digestion Function
Reservoir of the stomach where it produces acid, enzyme secretion, and gastric motility
Gastritis
Inflammation of the stomach lining (gastric mucosa)
Acute or Chronic
Erose (ulcers in stomach) or Non-Erosive (no erosion such as infection like H pylori)
Acute Gastritis
Sudden onset w/ short duration which could cause GI bleeding, indigestion, perforation, or scarring
Chronic Gastritis
Months to years and typically related to autoimmune disease, pernicious anemia, or chronic H pylori
Acute Gastritis Risk Factors
NSAIDs, alcohol, caffeine, stress, smoking
H Pylori
Autoimmune diseases
Corticosteroids, aldosterone receptor antagonists and serotonin reuptake inhibitors
Acute Gastritis Clinical Manifestations
Dyspepsia (heartburn-indigestion)
Headache
N/V (hematemesis or coffee ground emesis)
Black, tarry stools or Melena (dark tar stool - classic sign of GI bleed)
Acute Gastritis Lab & Diagnostic
CBC
H Pylori Testing
Blood, stool or urea breath test
Upper endoscopy
Acute Gastritis Interventions
Treat symptoms
Pain should subside when cause removed
Drug therapy - H2 antagonist, PPT, antacids, anti-ulcer/mucosal barriers, ABX
Nutrition - bland, non-spicy, small frequent meals
Gastritis Complications
Dehydration
Gastric Bleeding and Hemorrhage
Bleeding - transfusion, fluid replacement, risk for hypovolemic shock
Dumping Syndrome
Complication of chronic gastritis
Rapid release of metabolic peptide following a food bolus; someone has eaten a large meal
Symptoms resolve after having a BM
Clinical Manifestations of Dumping Syndrome
Full after eating (usually 10 min or 3 hr after eating)
Dizziness
Rapid HR (tachycardia)
Abdominal pain
diarrhea
Dumping Syndrome Interventions
Lay down after eating
High protein, high fat, moderate carbohydrate diet
Small meals w/out liquids
Peptic Ulcer Disease (PUD)
GI mucosa defenses become impaired and no protection from acid or pepsin
Can cause ulcers in the stomach
Risk Factors of PUD
Smoking, alcohol, diet, exercise, stress, caffeine
PUD Causes
Bacterial infection (H PYLORI)
Long use of NSAIDs
Genetics
Gastric Ulcers
Inflammation of the stomach mucosa
Pain <60 min after eating
Gastric Ulcers Clinical Manifestations
Pain with food
Hematemesis
Malnourished
Duodenal Ulcers
Inflammation of the upper duodenal mucosa
Most common w/ deep lesions
High gastric secretion (excess acid w/ low pH)
Pain >90 min after eating
Duodenal Ulcers Clinical Manifestations
Pain relieved with eating
Melena stools
Well-nourished
Stress Ulcers
Develop after an acute medical crisis or trauma such as sepsis, head injury, burns, increased ICP, MODS
PUD Lab
CBC (bleeding: low H&H)
Electrolyte imbalance (dehydration - low K, Ca, and phos; high sodium)
Metabolic alkalosis (GI excretion loss) or metabolic acidosis (acute GI bleeding, hypovolemia, shock, severe diarrhea, NG suctioning)
Coagulation studies
H pylori testing
Complications of PUD
1 Perforation - Peritonitis
Pyloric Obstruction
Pernicious anemia and dumping syndrome
#1 complication is hemorrhage from perforation and/or infection
Perforation
Full thickness ulcer that erodes the GI wall spilling contents into peritoneal cavity
S/S: tender, rigid, “board-like abdomen”
Untreated = sepsis, septic shock, and/or hypovolemic shock
Pyloric Obstruction
Blockage
Due to scarring, edema/swelling, inflammation, tumor
S/S: abdomen bloating, fullness pain, N/V
NG tube for gastric decompression
