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Flashcards testing terminology, underlying pathophysiology, diagnostic markers, and pharmacologic management for upper GI, pancreatic, hepatic, and cirrhotic disorders.
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Parietal Cells
Gastric mucosal cells that secrete hydrochloric acid (HCl) when stimulated by histamine (H2 receptors), acetylcholine (muscarinic receptors), and gastrin.
Antacids
Medications such as calcium carbonate or magnesium/aluminum compounds that neutralize acid already present in the stomach for rapid, short-acting symptom relief.
Best to use for rapid relief of occasional symptoms.
Fast relief, relatively short acting
Key nursing considerations:
aluminum/calcium —> constipation
magnesium —> diarrhea
consider renal function
H2 Receptor Antagonists
Medications (e.g., famotidine) that block H2 receptors on parietal cells to decrease histamine-stimulated gastric acid secretion.
Best for mild/intermittent symptoms for moderate acid suppression. These medications provide longer-lasting relief compared to antacids, helping to prevent acid-related disorders. Dose adjustment may be needed with renal impairment.
Proton Pump Inhibitors (PPIs)
Medications (e.g., omeprazole, pantoprazole, esomeprazole) that inhibit the final H+/K+ ATPase proton pump responsible for gastric acid secretion.
Most potent acid suppression; preferred for healing erosive esophagitis. Usually taken once daily before meals to optimize efficacy and provide longer-lasting relief.
Long-term concerns:
possible B12 deficiency
hypomagnesemia
enteric infection
fracture risk
kidney complications
Gastroesophageal Reflux Disease (GERD)
A condition resulting from transient lower esophageal sphincter (LES) relaxation or decreased LES competence, allowing gastric acid and pepsin to reflux into the esophagus and cause mucosal inflammation.
It is characterized by symptoms such as heartburn, regurgitation, sour/bitter taste, epigastric discomfort, symptoms after meals or when lying down or bending over, and sometimes difficulty swallowing. Chronic can lead to more serious complications, including esophagitis or Barrett's esophagus.
GERD Red Flag Findings
Clinical indications requiring advanced diagnostic evaluation, including progressive dysphagia, odynophagia (painful swallowing), GI bleeding, unexplained iron-deficiency anemia, persistent vomiting, and unintentional weight loss.

Barrett's Esophagus
A complication of chronic gastroesophageal reflux where esophageal squamous epithelium undergoes intestinal metaplasia into columnar-type epithelium, increasing the risk for esophageal adenocarcinoma.
Management includes surveillance endoscopy and possible surgical intervention.
NSAID-Induced Gastric Injury
Mucosal degradation caused by cyclooxygenase (COX) inhibition, which reduces prostaglandin synthesis and subsequently impairs gastric mucus production, bicarbonate secretion, and mucosal blood flow. i.e. these interfere with the stomach’s protective mechanisms and increase the risk of ulcers and gastrointestinal bleeding.
Stress-Related Mucosal Injury
Gastric mucosal erosion and ulceration caused by severe physiologic stress and splanchnic hypoperfusion; managed prophylactically with acid suppression in high-risk critically ill patients, those using mechanical ventilation, coagulopathy, major burns, severe trauma, or shock or multi-organ illness.
Autoimmune Gastritis
An autoimmune destruction of parietal cells leading to loss of gastric acid and intrinsic factor, resulting in Vitamin B12 malabsorption and pernicious anemia. Neurologic manifestations can also occur due to deficiencies in Vitamin B12, affecting nerve function and potentially leading to neuropathy.
Bismuth Quadruple Therapy
The recommended treatment regimen for H.pylori eradication, consisting of a Proton Pump Inhibitor, bismuth, tetracycline, and metronidazole.

Sucralfate
A mucosal protective agent that forms a viscous, gel-like barrier over damaged gastric and duodenal ulcers in an acidic environment; must be administered on an empty stomach. It can interfere with the absorption of other medications and can cause constipation.
Misoprostol
A synthetic prostaglandin analog that enhances mucosal protection and prevents NSAID-induced ulcers; contraindicated in pregnancy due to uterine contraction stimulation. Adverse effects: diarrhea, abdominal pain, cramping, headache, and nausea.
Hematemesis
The vomiting of blood, presenting either as bright red blood or dark "coffee-ground" material due to interaction with gastric acid.
Melena
Black, tarry, foul-smelling stool caused by the digestion and oxidation of blood passing through the upper gastrointestinal tract.
Peptic Ulcer Perforation
A full-thickness erosion of the gastric or duodenal wall leading to peritoneal spillage, presenting with sudden severe abdominal pain, guarding, rebound tenderness, and a rigid, board-like abdomen.
Nursing Priorities:
NPO
rapid provider/surgical notification
IV access
IV fluid resuscitation
Laboratory evaluation
Broad-spectrum IV antibiotics as ordered
Pain management
Frequent hemodynamic assessment and monitoring for signs of shock.
Autodigestion
The pathological process in acute pancreatitis where premature intrapancreatic activation of trypsin and other digestive enzymes leads to enzymatic destruction of pancreatic parenchyma, fat necrosis, and tissue injury.
This produces inflammation, edema, cellular injury, fat necrosis, vascular injury, and potential hemorrhage and necrosis
Third Spacing in Pancreatitis
The massive movement of fluid from the intravascular space into peritoneal and retroperitoneal tissue spaces driven by inflammatory vascular permeability.

Cullen Sign
A clinical sign of severe necrotizing pancreatitis characterized by superficial periumbilical ecchymosis resulting from retroperitoneal blood tracking forward.
Grey-Turner Sign
Ecchymosis located along the flanks, indicating retroperitoneal hemorrhage associated with severe acute pancreatitis.
Serum Lipase
A highly specific biomarker for pancreatic tissue injury that remains elevated longer than amylase and is diagnostic for acute pancreatitis when levels are ≥3× the upper limit of normal.

Endoscopic Retrograde Cholangiopancreatography (ERCP)
An endoscopic technique used to visualize and remove obstructing biliary stones in gallstone pancreatitis, which carries an inherent risk of triggering acute pancreatitis.
Pancreatic Enzyme Replacement Therapy (PERT)
Exogenous pancrelipase containing lipase, amylase, and protease administered with meals and snacks to restore nutrient digestion and eliminate steatorrhea in chronic pancreatic exocrine insufficiency.
Administer WITH meals and snacks to improve nutrient absorption and reduce symptoms associated with malabsorption.
Pancreatogenic Diabetes
Type 3c diabetes resulting from progressive autoimmune or inflammatory destruction of pancreatic endocrine islet cells, leading to deficient insulin and glucagon regulation.
AST and ALT
Intracellular hepatic transaminases released into circulation upon hepatocyte cell membrane disruption, acting as primary indicators of active liver cell injury.
A dramatic elevation tells us: A LOT OF HEPATOCYTE INJURY IS OCCURRING
It does NOT independently tell us how well the liver is still performing its essential functions
Prothrombin Time / International Normalized Ratio (PT/INR)
A clinical measure of liver synthetic capacity that reflects hepatic clotting factor synthesis and rapidly changes during acute liver dysfunction due to short coagulation factor half-lives.
In acute severe hepatitis: INR trends may tell us more about worsening synthetic function than albumin.
Hepatitis A Virus (HAV)
A self-limited viral infection transmitted via the fecal-oral route that causes acute hepatitis, does not transition into chronic liver disease, and is preventable by vaccine.
Hepatitis B Virus (HBV)
A bloodborne, sexually, and perinatally transmitted viral infection capable of causing acute or chronic hepatitis, hepatocellular carcinoma, and cirrhosis; preventable via vaccination.
Medications include: antivirals like tenofovir and entecavir.
Hepatitis C Virus (HCV)
A primary bloodborne viral infection that frequently progresses to chronic hepatitis and cirrhosis, managed with direct-acting oral antivirals to achieve a virologic cure.
Sustained Virologic Response (SVR)
The absence of detectable serum HCV RNA after the completion of antiviral therapy, representing a complete virologic cure of Hepatitis C.
Icteric Phase
The symptomatic stage of acute viral hepatitis marked by jaundice, dark urine, pale clay-colored stools, and cutaneous pruritus secondary to conjugated hyperbilirubinemia.
Portal Hypertension
Pathologic elevation of blood pressure within the portal venous system secondary to increased intrahepatic resistance from tissue fibrosis and architectural distortion in cirrhosis.
Ascites
Intraperitoneal fluid accumulation resulting from portal hypertension, splanchnic vasodilation, decreased effective arterial blood volume, hyperaldosteronism, and hypoalbuminemia.
Treatment includes: diuretics (spironolactone and furosemide), paracentesis, and treating underlying liver disease.
Spironolactone
A potassium-sparing aldosterone antagonist used as first-line diuretic therapy in cirrhotic ascites to promote renal sodium and water excretion while conserving potassium.

Abdominal Paracentesis
A procedure involving needle insertion into the peritoneal cavity to evacuate ascitic fluid for diagnostic analysis or therapeutic relief of severe abdominal tension.
Nursing priorities:
monitor
vital signs
weight
abdominal assessment
respiratory status
procedure site
amount and characteristics of removed fluid
watch for
hypotension
dizziness
bleeding
fluid leakage
worsening renal function and infection.
Post-Paracentesis Circulatory Dysfunction
Hypovolemia and secondary acute kidney injury triggered by rapid, large-volume fluid removal during paracentesis; mitigated by Intravenous Albumin administration.
Spontaneous Bacterial Peritonitis (SBP)
An acute bacterial infection of ascitic fluid without an intra-abdominal surgical cause, confirmed by an ascitic polymorphonuclear (PMN) count ≥250cells/mm3.
Esophageal Varices
Engorged, thin-walled submucosal collateral veins in the lower esophagus produced by portal hypertension, susceptible to rupture and massive hemorrhage.
Octreotide
A synthetic somatostatin analog administered continuously via IV in acute variceal bleeding to induce splanchnic vasoconstriction and lower portal venous pressure.
Nonselective Beta Blockers
Medications such as propranolol, nadolol, or carvedilol used for primary prophylaxis of variceal bleeding by reducing cardiac output and splanchnic blood flow.
Asterixis
A bilateral, asynchronous flapping tremor of the hands observed when wrists are extended, representing a characteristic motor sign of hepatic encephalopathy.
Lactulose
A nonabsorbable synthetic disaccharide that lowers systemic blood ammonia levels by acidifying colonic contents, converting NH3 to unabsorbable NH4+, and producing 2–3 soft bowel movements daily. It is used to treat hepatic encephalopathy by promoting ammonia excretion.
Rifaximin
A nonabsorbable oral antibiotic used alongside lactulose to suppress ammonia-producing gut bacteria and reduce recurrent hepatic encephalopathy.
Hepatorenal Syndrome (HRS)
Functional acute kidney injury in advanced cirrhosis triggered by profound splanchnic vasodilation and intense compensatory renal vasoconstriction, resulting in impaired renal perfusion.
Aggressive Factors of the Stomach
Include hydrochloric acid, pepsin, NSAIDs, alcohol, Helicobacter pylori, and other mucosal irritants that contribute to gastric mucosal injury.
Protective Factors of the Stomach
Include mucus, bicarbonate, prostaglandins, tight epithelial junctions, rapid epithelial repair, and blood flow that help maintain gastric mucosal integrity and protect against injury.
Upper Endoscopy- EGD
A procedure using a flexible tube with a camera to examine the upper gastrointestinal tract, including the esophagus, stomach, and duodenum, often used to diagnose conditions like ulcers, esophagitis, strictures, Barrett’s esophagus, or tumors.
Peptic Ulcer Disease (PUD)
A condition characterized by open sores that develop on the lining of the stomach, small intestine, or esophagus, often caused by an infection with H. pylori or prolonged use of NSAIDs. It leads to abdominal pain, bleeding, and can sometimes result in perforation of the gastrointestinal tract.
Symptoms include burning/gnawing epigastric pain, dyspepsia, bloating, nausea, and early satiety.
PUD Treatment
Involves medications such as proton pump inhibitors, bismuth (mucosal protection and antimicrobial activity), antibiotics (tetracycline and metronidazole) for H. pylori, and antacids, along with lifestyle changes to promote healing and prevent recurrence.
Upper GI Bleeding Priorities
ABCs
access airway, breathing, and circulation
large volume hematemesis may also threaten airway
Establish IV Access
typically large-bore peripherally inserted IV access when significant hemorrhage suspected
Obtain Labs
CBC
type and screen/crossmatch
coagulation studies
electrolytes
BUN/creatinine
liver studies when appropriate
Restore Circulating Volume
IV crystalloid and/or blood products depending on the severity and clinical status
Identify and control the source
therapeutic endoscopy
Acute Pancreatitis Causes
Can be caused by gallstones, chronic and excessive alcohol consumption, certain medications, high triglyceride levels, and abdominal trauma.
Acute Pancreatitis
Acute Pancreatitis Diagnosis
Primarily based on clinical presentation, elevated serum amylase and lipase levels, and imaging studies such as abdominal ultrasound or CT scan to identify complications or underlying causes.
Lipase is more informative for diagnosis than amylase, as it remains elevated longer and is more specific to pancreatic injury.
Acute Pancreatitis Labs

Hepatic Encephalopathy
A complex neuropsychiatric syndrome resulting from liver dysfunction, characterized by confusion, altered level of consciousness, and, in severe cases, coma. It often arises from elevated ammonia levels due to liver failure or portosystemic shunting.
It can cause a range of symptoms from subtle changes in mood or personality to severe cognitive impairments, and may be precipitated by factors such as infections, gastrointestinal bleeding, or electrolyte imbalances.
Compensated Cirrhosis
A stage of liver disease where the liver can still perform its vital functions despite structural damage. Patients may remain asymptomatic or exhibit mild signs, but complications can develop.
Decompensated Cirrhosis
A more advanced stage of liver disease where the liver can no longer maintain its functions, leading to significant symptoms and complications such as ascites, jaundice, and hepatic encephalopathy.