week 5- upper GI Flashcards
• What are the types of esophageal CA?
o Benign tumors: many types, may cause dysdphagia, ulcer, leiomyoma most common, good px
o CA: Primary: SCC, adenocarcinoma, other malignant tumors (sarcoma, melanoma, etc)
o Secondary: often from melanaom, breast CA, seed loose CT stroma around E
• What is prevalence and risk factors of E SCC?
o In proximal 2/3 of E
o ~8000/yr. in US
o 4-5x more in African-Americans than whites
o M>F (2-3x)
o Worldwide more in Asia and South Africa
o Risks: alcohol, tobacco, achalasia, HPV, lye ingestion, sclerotherapy, Plummer-Vinson, irradiation, esophageal webs
• What is prevalence of E adenocarcinoma? Risks? Ddx?
o 50% of E carcinoma in whites (4x more common)
o Risks: smoking but NOT alcohol, most arise in Barrett’s E
o Ddx: adenocarcinoma of gastric cardia invading distal E
• What are ssx of esophageal CA?
o early is asx!!! (often sxs don’t occur until lumen <14mm)
o Progressive dysphagia (solid → semisolid →liquid →saliva)
o Weight loss
o Hoarseness (compressed recurrent laryngeal n → vocal cord paralysis)
o Horner’s syndrome (compressed sympathetic n)
o Nerve compression: spinal pain, hiccups, diaphragm paralysis
o Dyspnea (dt pleural effusion, mets)
o (intraluminal): odynophagia, vomiting, hematemesis, melena, IDA, aspiration, cough
• What is work-up for E cancer? Px?
o Endoscopy w bx, then CT and endoscopic US
o Px: metastasis to lung, liver. overall poor (5-yr. survival <5%)
• What are E varices? Ssx?
o Dilated veins in distal E/stomach dt hi P in portal veins, usu dt cirrhosis
o Ssx: sudden, painless, upper GI bleeding, often massive; mb ssx of shock
• What is work-up for E varices? Px?
o Eval for coagulopathy, CBC w platelets, PT, PTT, LFT
o Endoscopy
o Px: bleeding resolves spontaneously in 80%, >50% mortality (assoc w liver dz); common recurrence
• What causes foreign bodies in E? ssx? Tx?
o usu in narrow space (cricopharyngeus, aortic arch, above GEJ)
o Intentional: kids, mentally ill, smugglers
o Unintentional: swallowing poorly chewed food, dentures elderly, inebriated
o Ssx: Complete obstruction: vomiting; Drooling if can’t swallow saliva
o Tx: removal w endoscopy
• What are the conditions of the stomach?
o H. pylori o Gastritis o PUD o Gastric CA o Bezoars o Foreign bodies
• What is H. pylori infection? Etio? Prevalence?
o In stomach → gastritis, PUD, gastric adenocarcinoma, low grade gastric lymphoma.
o Etio: Oral-fecal route
o In US: 50% by 60; more in blacks, Hispanics, Asians; Nurses and gastroenterologists at high risk
o 3-6x more likely to develop stomach CA
• What is the pathophysiology of H. pylori infection?
o Depends on location in stomach
o Antral: ↑ gastrin dt local impairment of somatostain → acid hypersecretion → mb prepyloric, duodenal ulcers
o Body: ↑ IL-1→ gastric atrophy, ↓acid → mb gastric ulcer, adenocarcinoma
o Mixed: combo
• What are ssx of H. pylori? Work-up?
o Mb asx, mb gastritis, PUD
o Work-up: only in sx pts
o Non-Invasive tests: Serologic (Sn, not Sp), Urea breath test, stool Ag assay
o Invasive: Endoscopy (only if more ddx requires), mucosal bx rapid urease test (RUT), histology
• What causes gastritis? Ssx? Work-up?
o inflammed gastric mucosa
o etio: Infection (H. Pylori), Drugs (NSAIDs, Alcohol), Stress, AI (atrophic gastritis)
o many asx, Dyspepsia, GI bleeding
o Work-up : endoscopy
• What are the types of gastritis?
o Erosive, non-erosive, post-gastrectomy, uncommon gastritis syndromes, AI Metaplastic Atrophic Gastritis (AMAG)
• What is erosive gastritis? Causes?
o gastric mucosal erosion dt damaged mucosal defenses
o usu acute, w bleeding (or subacute, chronic)
o Cause: NSAIDS, alcohol, stress, Radiation, viral infx (eg CMV), vascular infx, direct trauma
• What are ssx of erosive gastritis? Dx?
o Often asx. Dyspepsia, N/V. Often 1st sign is hematemesis, melena, blood in nasogastric → aspirate in 2-5 days. bleeding mild-mod, or massive if deep ulcer
o Dx: endoscopy
• What is non-erosive gastritis? Ssx? Dx?
o mainly dt H. Pylori
o ssx: usu asx, or mild dyspepsia
o Dx: Endoscopy (st incidental)
• What is postgastrectomy gastritis?
o gastric atrophy after partial or subtotal gastrectomy
• what are the uncommon gastritis syndromes?
o Ménétrier’s dz o Eosinophilic gastritis o Mucosa-associated lymphoid tissue (MALT) lymphoma o dt systemic dos o dt physical agents o Infectious (septic)
• What is Autoimmune Metaplastic Atrophic Gastritis (AMAG)? Work-up?
o Genetic, attacks parietal cells →hypochlorhydria ↓IF
o Consequences: Atrophic gastritis, B12 malabsorption, Pernicious anemia, 3x risk gastric adenocarcinoma
o Work-up: labs mb macrocytic anemia; endoscopic bx
• What is PUD? Prevalence? Etio?
o erosion in GI mucosa, usu stomach (GASTRIC ULCER) or proximal duodenum (DUODENAL ULCER), penetrates muscularis mucosae
o any age, usu middle age
o Etio: H. Pylori (50-70% of duodenal ulcers, 30-50% of gastric ulcers)
o NSAIDs, smoking, FHx (50-60% duodenal ulcers)
o Zollinger-Ellison Syndrome (gastrin tumor, ↑HCl)
• What are general ssx of PUD? Gastric and duodenal ulcers?
o Ssx: mb asx, pain common (epigastrium, burning, gnawing), relieved by food, antacids; course often chronic, recurrent
o Gastric: no consistent pattern (eating st exacerbates, not relieve pain)
o Duodenal: More consistent pain, none after wake in am, starts mid-am, relieved by food, recurs 2-3 hrs. after meal. Awakens at night
• What is work-up for PUD?
o dx by endoscopy (must r/o stomach CA); st serum gastrin levels
• what are some complication of PUD?
o Hemorrhage (most common) hematenesis (fresh or “coffee ground”), Hematochezia, melena, weakness, orthostasis, syncope, thirst
o Penetration (confined perforation): pain persistent, intense, referred (usu back). CT or MRI to dx
o Free perforation: sudden, intense, continuous epigastric pn, spreads rapidly thru abdomen, RLQ, may refer to shoulders, deep breathing worsens (lie still), diminished or absent bowel sounds, painful abdominal palpation, rigidity, rebound tenderness. Dx: w CT or x-ray (lateral) w air under diaphragm, in peritoneal cavity
o Gastric Outlet Obstruction: mb dt scarring, spasm, infiltration of ulcer. Recurrent, large-volume vomiting, more at end of the day, mb 6 hr after meal. Loss appetite, bloat, full, after eating
o Recurrence: mb dt refractory H. Pylori (>50% recurrence when not eradicated), NSAIDs, smoking, gastrinoma (less common)
o Gastric Cancer: only pts w H. pylori-assoc ulcers at inc risk gastric cancer later in life (3-6x)
• What are the types of gastric cancer? Incidence? Risk factors?
o Gastric adenocarcinoma most common (95%)
o Less: gastric lymphomas and leiomyosarcoma
o Incidence: varies by country; ↑ w age
o Risk: H. Pylori, AI atrophic gastritis, Gastric polyps,
o Dietary, risky foods: smoked, salted meat, pickled veg (nitrates, nitrites → bacteria convert to carcinogen)
• What are ssx of gastric CA?
o Initial: non-specific, eg dyspepsia
o Later: early satiety if CA obstructs pyloric region
o Weight loss, weakness
o Dysphagia if obstructs GEJ
o Uncommon: massive hematemesis or melena
o Occasionally 1st sx dt metastasis
• What is found on PE for gastric CA? work-up? Px? Ddx?
o PE: May be unremarkable
o Late: Epigastric mass; umbilical, L supraclavicular (Virchow’s) or L axillary LN; HM; Pulmonary, CNS, bone lesions; (+) hemoccult
o Work-up: Endoscopy, bx, CT and endoscopic US
o Px: overall poor (5 yr survival <5-15%), usu present w advanced dz.
o Ddx: Peptic ulcer and its complications
• What are bezoars? Ssx? Imaging?
o tightly packed, partially/un-digested material, can’t exit stomach. In pts w abn gastric emptying: Diabetic gastroparesis, post-gastric surgery
o Ssx: usu asx, mb post-prandial fullness, N/V, pain, GI bleeding
o Imag: Endoscopy; detectable as mass lesion on most tests (x-ray, US, CT)
• What are the 3 types of bezoars?
o Phyto: vegetable matter; mb dt Hypochlorhydria, ↓antral motility, incomplete mastication (all more common in elderly)
o Tricho: hair, usu w psychiatric dos
o Pharmaco: medications
• What are the complications of foreign bodies in the stomach?
o Usu asx, unless obstruction or perforation
o 80-90% pass spontaneously
o 10-20% require non-operative intervention
o ≤ 1% require surgery
• What are the dos of the pancreas?
o Acute/chronic pancreatitis
o Pancreatic CA
o Pancreatic endocrine tumors
• What is acute pancreatitis? Etio? Pathophysiology?
o Inflammation (mild-severe) of pancreas (st adjacent tissue) dt release of activated pancreatic enzymes o Etio: 80% biliary tract dz or alcoholism; drugs, infx, heredity, mechanical, toxins o Path: enzymes activated in pancreas → damage tissue, activate complement, cytokines→ inflammation, edema, necrosis
