Pathophys & tests for upper GI pathology Flashcards
H pylori serology
Infection elicits a local and systemic IgG-mediated immune response
ELISA and rapid office-based immunoassays
Serology is the test of choice when endoscopy is not indiated
90% sensitivity, specificity
-‘s: antibody titres can remain high for up to a year, cannot test for eradication
Urea breath test
Carbon-labeled urea
H. pylori can hydrolyze urea
sensitivity and specificity >95%
ingest urea labelled with either 14C or 13C - 13C requries mass spec, but 14C radiation
Urea metabolized to ammonia and labelled bicarb in the presence of H. pylori
Less expensive than endoscopy, samples the entire stomach
false-negatives can occur if the test is done too soon afte treatment, so test 4 weeks post-tx
best method to test for eradication
Esophagogastroduodenoscopy (EGD)
Visualization and biopsy
Surgical procedure
Recommended with suspicious of esophagitis, but not required for every patient undergoing reflux evaluation
Method of choice for PUD
Biopsy from esophagus, stomach, and duodenum for histology and H. pylori
Hemostatic therapy
Barium X-ray (upper GI)
can often demonstrate peptic ulcers Radiation exposure lack of technicians visualize obstructions/strictures limited utility in modern practice
Esophageal manometry
assessment of LES pressure and relaxation, peristaltic activity (contraction amplitude, duration, and velocity
generally not indicated in evaluation of uncomplicated GERD because most have a normal resting LESP.
24h ambulatory pH monitoring
GERD
Indications:
- document excessive acid reflux in suspected GERD but withoud endoscopic esophagitis
- evaluate efficacy of surgical/medical therapy
Achalasia
Poorly relaxing LES without known cause
Diffuse esophageal spasm
normal peristalsis intermittently interrupted by simultaneous contractions with uncertain cause
Hypercontractile esophagus
Esophageal contraction pressure above normal (2SD)
“Nutcracker” esophagus when high pressure occurs in esophageal body and hypertensive LES when resting LES pressures are raised
Hypocontracting esophagus
non-specific motility disorders
motility tracings characterized by:
- low amplitude (<30 mmHg) peristalsis
- simultaneous contractions in distal esophagus
- failed peristalsis: wave does not transverse entire length of distal esophagus
Secondary esophageal motility abnormalities
abnormal motility patterns secondary to systemic disease
e.g. scleroderma, Chagas’ disease, Amyloidosis
GERD
transient relaxation of LES, allowing for spontaneous or stress (increased abdominal pressure) reflux
other causing factors:
- decreased clearance of acid from esophagus due to decreased peristalsis, or salivary secretion
- reduced resistance of esophageal mucosa to gastric content
- delayed gastric emptying
Risk factors for GERD
hiatal hernia pregnancy diabetes mellitus CT disorder obesity chocolate, caffeine, alcohol, high fat foods) NSAIDs, opioids, anticholinergics
Stress gastritis
stress-related mucosal erosions and subepithelial hemorrhages typically found in critically ill patients
Despite normal/decreased acid secretion
H. pylori gastritis
causes gastric mucosal inflammation with PMNs and lymphocytes despite not being invasive
Pernicious anemia gastritis
autoimmune, involves fundic glands
resultant achlorhydria and vit B12 malabsorption (gastritis caused by autoimmune disorder, anemia caused by decreased IF released from damaged parietal cells, therefore less B12 absorbed)
Peptic ulcer disease
disruption of mucosal integrity of the stomach/duoenum caused by local inflammation resulting from imbalance between damaging effects of noxious substances and ability of mucosa to defend against them
Etiology: H. pylori, NSAIDs and acid hypersecretory states such as Zollinger-Ellison syndrome
Risk factors: smoking, alcohol, stress, cocaine, FHx
H. pylori ulcer formation
survival due to urease activity
Epithelial cell disruption from secretion of CagA, VacA
Induction of local immune responses and cytokine secretion
increased gastrin and gastric acid secretion due to cytokine-induced gastrin secretion, reduced antral somatostatin secretion, local alkaline environment
other factors contributing to local tissue injury
Gastric cancer
diffuse: poorly differentiated, lacks glandular structure, poorer prognosis
Intestinal form: gland-like tubular structures mimicking intestinal glands, closely linked to environmental and dietary factors, also H. pylori, cigarette smoking
S/S: weight loss, abdominal pain, fatigue, early satiety, hematemesis, melena, nausea, vomiting, supraclavicular lymphadenopathy, periumbilical lymphadenopathy (Sister Mary Joseph Nodes)
GIST tumours
gastrointestinal stromal tumours
most common mesenchymal tumour in the digestive tract
most are symptomatic and large lesions can ulcerate and bleed
Barrett’s esophagus
Distal squamous mucosa replaced by metaplastic columnar epithelium with goblet cells due to prolonged injury from GERD
gross: red velvety GI Type mucosa between pale squamous mucosa of lower esophagus and lush pink gastric mucosa
Major risk for gastric adenocarcinoma - higher risk >2cm Barrett’s esophagus
Diagnosis: endoscopic appearance and histological findings
long segment: >3cm from GE junction
need endoscopy every 1-2 y
Esophageal cancer
Most common: squamous (smoking/alcohol) and adenocarcinoma (likely from GERD)
Both carry a poor prognosis
Risk factors: tobacco, alcohol, GERD, obesity, history of head and neck cancer, history of breast cancer treated with radiotherapy, frequent consumption of extremely hot beverages
S/S: weight loss, dysphagia, odynophagia, GERD
Lymphadenopathy in Virchow’s node, hepatomegaly, pleural effusion
Diagnostic: barium swallow (esophagogram)
Tx: chemo/radiotherapy, surgery
Triple therapy for H. pylori
patient has not received a macrolide previously
PPI + clarithromycin + amoxicillin
if allergic to penicillin - PPI + clarithromycin + metronidazole
eradication rate 70-85%
Quadruple therapy for H. pylori
Allergic to penicillin, or failed triple therapy
Bismuth + metronidazole + tetracycline + PPI
eradication rate 75-90%
