GI Exam: The Gut Flashcards
What does the upper esophageal sphincter do?
Prevents aspiration of esophageal contents
What does lower esophageal sphincter do?
Prevents reflux of gastric contents, allows food bolus to pass into stomach
What phases of swallowing are voluntary? Involuntary?
Voluntary: oropharyngeal phase; tongue moves bolus
Involuntary: esophageal phase; peristalsis
What is oropharyngeal dysphasia?
–Difficulty transferring bolus out of mouth
–Associated w/ coughing & aspiration
What are known causes of oropharyngeal dysphasia?
–Mechanical/obstructing lesions •Zenker’s diverticulum, tumors, osteophytes –Neurologic disorders •Stroke, ALS, Parkinson’s –Skeletal muscle disorders •Muscular dystrophy –Neuromuscular transmission disorders •Myasthenia gravis
What is esophageal dysphasia?
–Sense of bolus “sticking in chest”
What are known causes of esophageal dysphasia?
–Mechanical causes •Tumors, strictures •Eosinophilic esophagitis –Motility disorders •Achalasia •Chagas’ disease •Scleroderma •Diffuse esophageal spasm
What happens to swallowing in scleroderma?
Characterized by vascular obliteration and fibrosis of the esophageal smooth muscle
Results in aperistalsis and weak lower esophageal sphincter (no contraction)
What happens to swallowing in achalasia?
Due to ganglion cell loss in myenteric plexus
Impaired relaxation of lower esophageal sphincter (always contracted), aperistalsis
How can you treat achalasia?
•Pharmacologic:
–Calcium channel blockers
–Botulinum toxin
•Pneumatic balloon dilation
•Heller myotomy (cut through LES), may be accompanied by a “loose wrap” of the fundus
•POEM (peroral endoscopic myotomy), fix w/ endoscopy
What is GERD?
•Definition: the reflux of gastric contents into the esophagus that results in troublesome symptoms and/or complications
•Most common reason for visit to GI specialist
–Significant health care impact: costs, quality of life, loss of productivity
What are typical and atypical symptoms of GERD?
•Typical symptoms
–Heartburn
–Regurgitation
•Reflux chest pain
•Atypical symptoms
–Wheezing, cough, hoarseness, globus, dyspepsia, nausea
Typical can occur without atypical; much less common for atypical to occur without typical
What are common causes of GERD?
Defective esophageal clearance Lower esophageal sphincter dysfunction (transient LES relaxations) Hiatal hernia Increased intra-abdominal pressure Delayed gastric emptying
What are transient lower esophageal sphincter relaxations?
•Transient LES relaxations (tLESRs)
–Primary mechanism underlying most acid reflux episodes
–Not associated with swallowing
–Last longer than swallow LESRs (10+ seconds)
•Can be caused by certain foods as well as gastric distention
•Can be inhibited by GABA type B agonists (baclofen)
–Clinical trial results disappointing
How should mild to moderate GERD be treated?
–Dietary modification
•Avoidance of fatty food, alcohol, caffeine, carbonated beverages
•Smaller meals
–Weight loss
–Raise head of bed if pt has nighttime symptoms
–Stop smoking
–Antacids (neutralize refluxate)
•Magnesium trisilicate, aluminum hydroxide, and calcium carbonate
•Neutralize pH of low pH refluxate
How should moderate to severe GERD be treated?
•Reduce gastric acid production (increase pH of refluxate)
–Histamine-2 receptor antagonists (H2RAs)
•Cimetidine, famotidine, ranitidine
•Block H2 receptor on gastric parietal cells
•pH about 4
-PPIs (pH 6-7); inhibited acid secretion into gastric lumen by binding covalently to cysteine residues of H+/K+ ATPase
When should PPIs be used?
– h/o erosive esophagitis
• Erosive esophagitis is a chronic condition – high rate of relapse (up to 80%)
– Barrett’s esophagus
– GERD sx responsive to PPIs and not controlled by less potent rx
What are the potential adverse effects of PPIs?
Higher rates of c diff
Bone fracture rate increases
Vitamin B12 deficiency (gastric acid releases B12 from protein-bound state and can then bind to R proteins)
What pathologic changes are seen in GERD?
•Inflammation –Eosinophils*, Lymphocytes, Neutrophils •Basal cell hyperplasia •Hyperplasia of stromal papillae •Erosions/ulcers •Barrett’s Esophagus (late complication)
What is Barrett’s Esophagus?
•Complication of chronic GERD
•Definition:
–Proximal displacement of squamocolumnar junction
–Columnar-lined epithelium with intestinal metaplasia (goblet cells)
•Primary precursor lesion to esophageal adenocarcinoma
–Lifetime esophageal cancer risk is about 5-10%
•Prevalence: is about 1-2% of general population
•Risk factors:
–*GERD, white, male, older age, smoking, obesity, H. pylori (inverse)
What is eosinophilic esophagitis?
•Allergen mediated esophagitis – assoc autoimmune disorders/atopy
–Most often diagnosed in children and young adults
–70% of cases in males
•Symptoms
–Children: feeding intolerance, heartburn, regurgitation, dysphagia, food impaction, failure to thrive, diarrhea
–Adults: dysphagia (to solids), food impaction, heartburn, chest pain
What are the findings of eosinophilic esophagitis on endoscopy?
- White papules
- Linear furrows
- Rings (felinization, trachealization)
- Strictures
How is eosinophilic esophagitis treated?
•Dietary modifcation
–Avoidance of triggers
•Six-food elimination diet: milk, egg, soy, wheat, peanuts/tree nuts, fish/shellfish
•More effective in children than adults
–Elemental diet (amino acid-based formulas)
•Steroids
–Topical (fluticasone, beclomethasone)
–Systemic steroids, other immunosuppressants
•No FDA-approved treatments for EoE
•Frequent relapses when therapy discontinued
How is the histology seen in eosinophilic esophagitis?
•Diagnosis requires combination of sx of EoE combined with histologic findings: –15+ eosinophils in a high-power field –Basal cell hyperplasia –Subepithelial fibrosis –Eosinophilic microabscesses –Degranulated eosinophils –Superficial clustering
What is HSV esophagitis?
- Most common viral esophagitis
- Self limited in healthy pts. Can disseminate in immunosupressed
- Ulcers
- Secondary bacterial and fungal infections common
- Dx generally made by bx
- Primarily infects squamous cells
What are the common drugs that can cause esophagitis?
NSAID tetracyclines bisphosphonates potassium vitamin C iron
What is radiation esophagitis?
•Acute and chronic damage possible •Acute: within 2-3 wks of RT –Ulceration, necrosis, mucosal denudation –Sx: odynophagia, chest pain –Eventually resolves spontaneously •Chronic: at least 3-6 months after RT –Fibrosis and stricturing –Sx: dysphagia –Rx: dilation, stents
What is metaplasia?
Change from 1 cell lineage to another
What is a hamartoma?
Malformation
What does adeno- mean?
Glandular
What is a carcinoma?
Malignant epithelial neoplasm
What is a sarcoma?
Malignant mesenchymal neoplasm
What do chief cells excrete?
pepsinogen
What do parietal cells excrete?
HCl and instrinsic factor
What are the layers of the stomach?
- Mucosa – delineated by muscularis mucosae (thin muscle)
- Submucosa – between muscularis mucosae and muscularis propria
- Muscularis propria – thick muscle
- Serosa – outermost thin lining of the organ
What is seen in histo in chronic gastritis?
Increased plasma cells
Lymphocytes
What is seen in active (acute) in chronic gastritis?
PMNs (acute inflammation)
What is the progression of h pylori?
- Infection
- Acute inflammation
- Chronic inflammation
- can then cause no atrophy or possible intestinal metaplasia - Multifocal atrophy
- Intestinal metaplasia
- Dysplasia
- Adenocarcinoma
What is autoimmune atrophic gastritis?
- Caused by autoantibodies to parietal cell (more common) or intrinsic factor
- F more common than M, about 1-2% of population, elderly women about 4-5%
- Stomach body-centered disease (antrum is spared)
- Can lead to iron deficiency anemia or vitamin B12 anemia (“pernicious anemia”)
- Can lead to neuroendocrine tumors and even adenocarcinoma
What are the histo features of autoimmune atrophic gastritis?
- Atrophy (loss of oxyntic glands)
- Inflammation (variable)
- “Antralization”
- Intestinal metaplasia
- Enterochromaffin-like cell hyperplasia
What is granulomatous gastritis?
• Pattern of injury, not specific disease
• Granuloma = nodular collection of
histiocytes
• Differential includes: Crohn’s disease, Sarcoidosis, Infection (mycobacterial, rarely H. pylori), Drug effect
What can cause lymphocytic gastritis?
Celiac disease, lymphoma, H pylori
What is CMV gastritis?
• Typically seen in immunosuppressed patients
• Infects epithelial, endothelial and stromal
cells
• Histologic features:
–Large cells, large nuclei
–Red-purple nuclear inclusion (larger)
–Basophilic cytoplasmic inclusion (smaller)
What is reactive gastropathy and what does it look like on histo?
•Caused by NSAIDS, duodenal reflux (bile)
•AKA “chemical” gastritis
•Histologic features of:
–Foveolar hyperplasia with mucin reduction
–Smooth muscle proliferation
–Mucosal edema, fibrosis and congestion
–Minimal chronic inflammation
What is a hyperplastic polyp?
• Benign, likely reparative (very rarely can see dysplasia) • Most common • Usually in antrum • Dilated and distorted mucous glands • Serrated epithelium may be seen
What is a fundic gland polyp?
- Almost always benign, usually secondary to hypochloridia (PPI treatment)
- Considered hamartomatous
- Dysplasia can be seen (esp. patients with FAP)
- Dilated oxyntic glands
What is a peptic ulcer?
- A punched-out mucosal defect that can be round or linear, appearing white with depth, which penetrates the wall deeper than the muscularis mucosa, and which occurs in the presence and partly as a consequence of acid and pepsin.
- Usually 3+ mm, distinct from erosions
- Simple or complex, anywhere in upper GI tract
- PUD implies tendency to recur
- Lifetime prevalence of PUD ~ 10%
What is the difference between an erosion and an ulcer?
Erosion only gets down to the muscularis mucosa and does not penetrate it; ulcer may go below it
How do peptic ulcers typically present?
•Simple ulcers –Symptomatic: Dyspepsia (Differential diagnosis includes non-ulcer dyspepsia (NUD), GERD, medications, pancreatobiliary disease, gastric cancer.) –Asymptomatic •Complicated ulcers –Bleeding –Perforation (or penetration). –Obstruction (gastric outlet obstruction) –Death
What is hematochezia?
bright red blood per rectum
What are major causes of upper GI bleeding?
–PUD (50%), esophageal varices/portal HTN (20%), Mallory Weiss tears (5-10%; usually caused by vomiting), angiodysplasia/AVM (7%), erosive gastritis (10%), esophagitis (2%), neoplasms (< 1%)
What are major causes of peptic ulcer dz?
H pylori
NSAIDs
