Stomach & Duodenum Flashcards
ACUTE injury to the gastric mucosa caused by NSAIDs or chmicals like ALCOHOL which DOES NOT HAVE an INFLAMMATORY INFILTRATE on histology?
ACUTE REACTIVE GASTROPATHY (not gastritis as there is no inflammatory infiltrate)
To accurately diagnose the varois forms of GASTRITIS, where must biopsies be obtained from?
Microaerophilic, Gram-Negative, Urease-producing Spiral bacteria?
Helicobacter Pylori
What does H.pylori cause in most individuals?
ASYMPTOMATIC CHRONIC ACTIVE GASTRITIS (can cause peptic ulcers and cancer) - presence of NEUTROPHILS and LYMPHOCYTES
Genta, Giemsa, Warthin-Starry?
Immunohistochemical stains to identify H.pylori
What is the ONLY thing that needs to be measured when checking H.pylori exposure SEROLOGICALLY?
H.pylori IgG (many false positives in low-prevalence areas, but if negative, it is reliable)
What is the DIFFERENCE between gastric EROSIONS and gastric ULCERS?
EROSIONS do NOT penetrated the MUSCULARIS MUCOSA, ULCERS DO
Wahat test is POOR for H.pylori if there is gastric BLEEDING?
Biopsy
What are the REQUIREMENTS of a UREA BREATH test and FECAL ANTIGEN TEST to avoid FALSE NEGATIVE results when testing for H.pylori?
Pt MUST be off PPI for 2 WEEKS and off ANTIBIOTICS for 4 WEEKS (H2 blockers do NOT affect this)
What is a LOW-GRADE B-CELL malignancy that can be caused by H.pylori and if not eradicated, it can undergo malignant transformation?
MALT
Pts who are about to start CHRONIC NSAID therapy, have unexplained chronic iron-deficiency ANEMIA, have ACTIVE or prior PUD, gastgric MALT lymphoma, and s/p early gastric CANCER, are ALL indications for testing for what?
H.pylori
In which patients is the use of Clarithromycin + Amoxicillin + PPI appropriate therapy for H.pylori infection?
Those who have NOT used a MACROLIDE before, and come from an area with LOW prevalence (<15%) of clarithromycin-resistance)
In which patients is the regimen to treat H.pylori consising of BISMUTH + PPI + TETRACYCLINE + METRONIDAZOLE used?
Those who are PENNICILIN ALLERGIC or who failed prior therapy, or PRIOR MACROLIDE EXPOSURE
In which patients is the regiment to treat H.pylori consisting of PPI + CLARITHROMYCIN + AMOXICILLIN + METRONIDAZOLE + TINIDAZOLE used?
What regimens to treat H.pylori are available for thos who have had PRIOR MACROLIDE therapy?
BISMUTH QUADRUPLE therapy or LEVOFLOXACIN-based tripple therapy
What should be done in ALL patients whp have been treated for H.pylori?
Test for ERADICATION
In a patient who FAILED prior H.pylori therapy, what regimens are available for re-treatment?
Bismuth QUADRUPLE therapy or,
LEVOFLOXACIN + PPI + AMOXICILLIN or
RIFABUTIN + PPI + AMOXICILLIN
Is GASTRITIS symptomatic?
NO (histologic diagnosis only, by presendce of neutrophils and lymphocytes)
Abdominal pain, anorexia, occult bleeding, weight loss and HYPOalbuminemia with EGD findgins of HYPERtrophic gastric folds, association with CELIAC disease, mucosal NODULARITY with EROSIONS, volcano-like lesions?
LYMPHOCYTIC gastritis
What is the MOST IMPORTANT management of LYMPHOCYTIC gastritis?
Rule-out MALT lymphoma (EUS or full-thickness biopsy) - anti-ulcer therapy, steroids
Mucosal ULCERATION, DYSMOTILITY (impaired gastric emptying), abdominal PAIN, luminal OBSTRUCTION and is treated with steroids?
EOSINOPHILIC gastritis - presence of PERIPHERAL EOSINOPHILIA, check for PARASITES
What type of GASSTRITIS is CROHN’s, SARCOIDOSIS and SYPHILIS associated with?
GRANULOMATOUS gastritis
A type of GASTRITIS that is ANTRUM-SPARING, involving the BODY of the stomach, with HYPERgastrinemia, ACHLORHYDRIA, decreased PEPSINOGEN-1 and IF-deficiency and is associated with gastric CARCINOIDS?
AUTOIMMUNE ATROPHIC gastritis (anti-IF Abs, anti-parietal cell Abs, B12-deficiency)
GIANT gastric FOLDS sparing the antrum, massive FOVEOLAR hyperplasia with CYSTIC dilation?
Menetrier’s Disease - eradicate H.pylori if this is the cause
What manifestation do PARIETAL-CELL mass, Zollinger-Ellison Syndrome, gastric LYMPHOMA, LYMPHOCYTIC gastritis, gastric ADENOCARCINOMA and AMYLOIDOSIS all have in common?
HYPERtrophied Gastric Folds
How do GASTROPATHIES differ from GASTRITIS?
Gastropathies have little to NO INFLAMMATION
Prior history of PUD, Elderly, taking HIGH-DOSE or MULTIPLE NSAIDs and those who ALSO take CORTICOSTEROIDS, ANTICOAGULANTS or SSRIs are pre-disposed to what?
Gastric ULCERS
What can be used as ulcer PROPHYLAXIS in patients taking NSAIDs?
PPIs (or misopropstol which is poorly-tolerated)
For a patient who had a prior BLEEDING ULCER while in NSAID therapy, what is recommended if they require anti-inflammatories?
PPIs + COX-2 inhibitor (Celecoxib)
Patients who suffered CNS INJURY, PROLONGED VENTILATION and BURNS are at HIGH RISK of what?
PUD due to HYPERsecretion of gastric acid and require PPI (OMEPRAZOLE) or continuous H2-blockers or Sucralfate treatment
Nocturnal abdominal pain RELIEVED with ANTACIDS usually indicates what?
PUD (also relived with FOOD)
Which ULCERS DO NOT required endoscopic therapy and can be treated with PO PPIs?
CLEAN-BASED ulcers (no visible vessel, have not bled, no stigmata)
What is a gastroduodenal ULCER called when it affects the liver or the pancreas and how is it treated?
PENETRATING ULCER, it is treated expectantly with OBSERVATION
How effective is SUCRALFATE?
As effective as H2-blockers in treating duodenal ulcers and same as Misoprostol (causes diarrhea)
Serum GASTRIN >100 pg/mL with PUD, REFLUX ESOPHAGITIS and DIARRHEA?
Zollinger-Ellison Syndrome form a GASTRINOMA - Basal Acid Output >15 meq/Hr and POSITIVE SECRETIN TEST or SOMATOSTATIN SCAN (25% part of MEN-I: Pancreas, Pituitary, Parathyroid) Gastrinomas are found in the pancreas and duodenum
If a patient NOT on PPI therapy is found to have MULTIPLE GASTRIC POLYPS (fundic-gland type) what should be advised and why?
COLONOSCOPY (may have FAP)
Hyperplastic Gastric polyps are most often associated with what?
Autoimmune Atrophic gastritis or H.pylori
How should GASTRIC ADENOMAS be treated?
Endoscopic REMOVAL with surveillance
In what region of the UPPER GI TRACT are polyps in FAP with the HIGHEST risk for MALIGNANT transformation?
By the AMPULLA of VATER
Atrophic Gastritis, Intestinal Metaplasia and Dysplasia are all associated with this condition?
Gastric Adenocarcinoma
Which H.pylori STRAIN is associated with GASTRIC ADENICARCINOMA?
cagA (cytotoxin-associated gene A)
How is GASTRIC ADENOCARCINOMA staged after it is diagnosed?
EUS LOCALLY and CT or PET for any metastatic disease
What GENE is expressed by GIST and diagnosed by testing for this?
cKIT
How are malignant GISTs treated?
IMATINIB (low-grade GISTs can just be observed)
NESTS of small, bland-looking cells, functional or non-functional and may release SEROTONIN and occur in the FUNDUS, BODY of the stomach in patients with ATROPHIC (autoimmune) gastritis and PERNICIOUS ANEMIA and the DUODENUM
CARCINOID Tumors - can be removed endosocopically
Type II CARCINOID tumors are known to be associared with MEN-I and ZES, therefore what must be done when these are found?
Look for any PANCREATIC lesions (3P’s of MEN-I)
This GASTRIC CARCINOID tumor has NORMAL GASTRIN levels, is derived from EC (enterochromaffin cells) and carries a HIGH RISK of malignant transformation?
Type-III Carcinoid tumor (normal gastrin)
Which types of MALT lymphomas can be treated by EARDICATING H.pylori?
LOW-GRADE Lymphomas ONLY (HIGH-grade lymhomas require surgical resection) - CT and EUS staging
Epigastric PAIN, 1.5 cm SUBEPITHELIAL gastric mass, NEUROENDOCRINE cells on EUS/FNA, no gastric atrophy on biopises and no PUD noted, what is the NEXT STEP?
NO GASTRIC ATROPHY on biopsies, so NOT TYPE I (multiple lesions) - elevated gastrin
NO associated PUD, so NOT TYPE II (multiple lesions, MEN-I, ZES) - elevated gastrin
TYPE III - so MUST STOP the PPI and check SERUM GASTRIN and if NORMAL - SURGERY (high malignant potential)
What is the EXPECTED histologic finding of ALCOHOLIC GASTRITIS?
EROSIONS and SUBEPITHELIAL HEMORRHAGES
CHRONIC DIARRHEA, POST-BULBAR DUODENAL ULCER, SEVERE EROSIVE ESOPHAGITIS are all aspectss of what CONDITION?
ZOLLINGER-ELLISON SYNDROME (test for FASTING SERUM GASTRIN)
PROTEIN LOSING ENTEROPATHY (low albumin, low total protein, DIARRHEA, EDEMA) with HYPERTROPHIED gastric folds (also in H.pylori, lymphoma, gastrinoma, amyloidosis) is likely due to what condition and how is it TESTED for?
MENETRIER’s DISEASE (ELEVATED α-1 antitrypsin in the STOOL)
Are biopsies in the setting of BLOOD useful for H.pylori?
NO
If there is HIGH suspicion for H.pylori infection, should you START TREATMENT BEFORE positive testing for H.pylori?
NO, there is NO urgency in starting H.pylori treatment
Bothersome SYMPTOMS of epigastric pain, burning, early satiety and early post-prandial fulness in the ABSENCE of any STRUCTURAL disease on EGD is undicative of what condition?
FUNCTIONAL DYSPEPSIA
ATROPHIC GASTRITIS and INTESTINAL METAPLASIA only require SURVIELLANCE when?
When STAGE 3-4
What is recommended for the management of FUNDIC GLAND POLYPS?
OBSERVATION, NO SURVEILLANCE
WHEN should HYPERPLASTIC polyps be removed?
When >1 cm (MODERATE risk of malignant transformation)
Severe ATROPHIC GASTRITIS, severe INTESTINAL METAPLASIA, FAMILY HISTORY and SMOKING are all risk factors for what?
GASTRIC CANCER
cKIT (CD117) positive, RESECT if >2 cm, can metastasize to LIVER, treat with IMATINIB if metastatic?
GIST
Is INJECTION MONOTHERAPY with sclerosant such as epinephrine recommended for a bleeding ulcer?
NO
If an ULCER has a FLAT HEMATIN SPOT, does it REQUIRE ENDOSCOPIC treatment?
NO (<10% chance of re-bleed)
How should be patients with a CLEAN BASED ULCER be treated?
NO ENDOSCOPIC therapy required, dishcarge HOME on PPI
How should a patient with BLEEDING ULCER or tightly-adherent CLOT be treated?
AFTER endoscopic therapy, with IV PPI BOLUS and DRIP for 72 HOURS
When are ORAL PPIs appropriate for treatment of ULCERS?
When there are NO ENDOSCOPIC findings of HIGH-RISK BLEEDING STIGMATA
In which patients are UPPER GI ANGIODYSPLASIAS noted?
Those with CHRONIC RENAL FAILURE, LVAD
WHEN might you use ESTROGEN/PROGESTERONE therapy in treatment of GIB caused by vascular ectasias?
In cases such as OSLER-WEBER-RENDU or CREST wehre these are very numerous and bleed often
This consition occurs in OLDER WOMEN with IRON-DEF ANEMIA, histologically you see DILATED VENULES, FOCAL THROMBOSIS and FIBROMUSCULAR HYPERPLASIA and besides ENDOSCOPY, can be treated with IRON SUPPLEMENTATION?
GAVE
HYPOPERFUSION due to COMORBIDITY with MULTIPLE SUPERFICIAL ULCERS in the PROXIMAL stomach with bleeding from superficial vessels (respiratory failure, burns, coagulopathy, sepsis and organ failure) - treated PREVENTIVELY and with CIMETIDINE INFUSION or OMEPRAZOLE with BICARBONATE?
STRESS ULCERS
Patients with which BLEEDING STIGMATA of PUD have the HIGHEST RISK of re-bleeding and require endoscopic therapy with adjuvant IV PPI?
Those with a VISIBLE VESSEL in the ULCER BED (not those with clot, 50% vs 15% risk)
If NEGATIVE EGD and COLONOSCOPY in a patient with SYMPTOMATIC IRON DEFICIENCY ANEMIA, what is RECOMMENDED NEXT?
VIDEO CAPSULE ENTEROSCOPY (if negative too, supplement iron)
Does IV PPI INFUSION therapy have any ROLE in esophageal VARICEAL BLEEDING?
NO
What does PRE-TREATMENT of a patient with an UPPER GI BLEED do ENDOSCOPICALLY?
DOWNGRADES ENDOSCOPIC STIGMATA and therefore REDUCES the need for ENDOSCOPIC INTERVENTION of the lesion
Is there ANY EVIDENCE of ANY LONG-TERM RISK of HIGH DOSE PPI THERAPY?
NONE (no osteoporosis, no renal disease, nothing)
What is the MEDICAL treatment in PUD of an ACTIVE GIB, NON-BLEEDING VISIBLE VESSEL or ADHERENT CLOT after EGD?
IV PPI BOLUS + INFUSION x 72 HOURS (if pigmented flat spot, ORAL PPI ONLY)
In a patient with GIB, endoscopically you find a CLEAN-BASED ULCER or a PIGMENTED FLAT SPOT, besides ORAL PPI therapy, what intervention should be done endoscopically?
NOTHING
If ASPIRIN is used in PRIMARY PREVENTION of CV disease, what should be done with it if patient presents and is treated for an UGIB?
DISCONTINUE IT (continue for SECONDARY prevention)
What is the RECOMMENDED treatment for SLOW, RECURRENT GIB from AVMs?
Maintenance IRON therapy
How is ANEMIA due to the slow bleed from PHG or Cameron’s Lesions treated?
PPIs and IRON SUPPLEMENTATION
What are the TWO HIGHEST RISK FACTORS for GIB in patients admitted to the ICU who develop STRESS ULCERS?
RESPIRATORY FAILURE and COAGULOPATHY