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
If an AORTO-ENTERIC fistula is suspected, what is the TEST of choice?
ANGIOGRAPHY
In a patient with OCCULT-OBSCURE GIB who is <50 yo, and continues to bleed with NO IDENTIFIABLE source, what SHOULD be tested for?
MECKEL’s Scan
What can be RARELY used when there is continued OCCULT-OBSCURE GIB with NO identifiable source in spite of EGD, COLONOSCOPY, VCE, CTA, NM BLEEDING SCAN, PUSH ENTEROSCOPY?
PROVOCATIVE TESTING (use HEPARIN and be ready to scope)
What regulates gastric MOTILITY (relaxation, accomodation, food grinding and propulsion)?
ENTERIC Nervous System, VAGUS nerve and SPINAL
POST-INFECTION, patient presents with NAUSEA, EARLY SATIETY, WEIGHT LOSS. What is the mechanism?
IMPAIRED ACCOMODATION due to FUNCTIONAL DYSPEPSIA caused by post-infection effect
What determies and controls the ANTRAL PUMP responsible for GRINDING and PROPULSION of food ACCOMODATED in the GASTRIC BODY?
The GASTRIC PACEMAKER, located in the MID-BODY of the stomach (controls velocity, frequency and direction)
What are the FIRST THREE tests to use in working-up GASTROPARESIS if IDIOPATHIC (majority of cases) and not diabetic, or neurological (parkinson’s)?
1. UGI Series (excludes anatomic and mechanical obstruction)
2. EGD - presence of BEZOAR without GOO
3. Nuclear Gastric Emptying Study
What is considered NORMAL GASTRIC EMPTYING at 30 min, 1 HOUR, 2 HOUR and 4 HOUR?
30 min (70%)
1 HOUR (30-90%)
2 HOURS (60%)
4 HOURS (10%)
What are the DIETARY MODIFICATIONS recommended in GASTROPARESIS?
- SMALL FREQUENT MEALS
- AVOID FIBER (causes BEZOAR)
- REDUCE FAT
- LIQUID CALORIE supplementaion
What DRUG for GASTROPARESIS should NOT be used in patients with HYPERPROLACTINEMIA?
METOCLOPRAMIDE
NEW drug for GASTROPARESIS that IMPROVES gastric EMPTYING, and REDUCES VOMITING?
RELAMORELIN
What SURGICAL PROCEDURE is available for GASTROPARESIS with good symptomatic relief?
COMPLETION GASTRECTOMY (total gastrectomy)
Cyclical Vomiting syndrome (nasuea, vomiting, abdominal pain) COMPULSIVE HOT SHOWERS, does NOT respond to TCAs?
CANNABINOID HYPEREMESIS
What other NEUROLGICAL condition is NON-CANNABINOID Cyclical Vomiting Syndrome associated with ?
MIGRAINE HEADACHES
What are the NEUROMUSCULAR components of the small bowel responsible for PERISTALTIC movement?
- MYENTERIC (Auerbach’s) PLEXUS between circular and longitudinal muscle layer
- SUBMUCOSAL (Meissner’s) PLEXUS - secretory
What are the EXCITATORY and INHIBITORY neurotransmitters in the small bowel?
- EXCITATORY (acetylcholine, substance P, serotonin - 5HT)
- INHIBITORY (vasoactive intestinal polypeptide - VIP and nitric oxide)
What is RESPONSIBLE for the FREQUENCY and PROPAGATION of GASTRIC and DUODENAL CONTRACTIONS?
Interstitial cells of CAJAL
What is the GASTRIC and INTESTINAL MOTOR pattern of the INTERDIGESTIVE (fasting) STATE?
MIGRATING MOTOR COMPLEX (MMC) - in the FED state, the stomach (3/min), proximal small intestine (12/min) and distal small intestine (8/min) - MMC is TIRGGERED by MOTILIN and INHIBITED by GASTRIN (so food can be digested in stomach and moved away when ready)
What DETERMINES the RATE of PERISTALSIS in the FED state?
CALORIC content of foods (FASTER for triglycerides and SLOWER for proteins) - this is MESSED UP by OPIOIDS (causes SIMULTANEOUS contractions throughout the intestine)
MYOPATHIES (familial, collagen, amyloidosis) and NEUROPATHIES (Hirschprung, Chagas, paraneoplastic) affect the small bowel by causing HYPOacitve motility - myopathies, or HYPERactive motility - neuropathies. What condition does this result in?
INTESTINAL PSEUDOOBSTRUCTION
Clinical manifestations of GI DYSMOTILITY (gasgtroparesis, SIBO, small bowel diverticula, intestinal pseudoobstruction) are seen in this MIXED neuropahty/myopathy causing nausea, vomiting, intestinal cramps, abdominal distention, weight loss, malabsorption, diarrhea and constipation?
Systemic Sclerosis
Which CONDITIONS are associated with PARANEOPLASTIC INTESTINAL PSEUDOOBSTRUCTION?
SMALL CELL LUNG CANCER and CARCINOID TUMORS - DYSMOTILITY PRECEDES DIAGNOSIS of CANCER (patients with NEW onset dysmotility and abnormal gastric emptying or manometry) - DO CXR, CT CHEST
Anti Neuronal Nuclear Antibodies (ANNA-1 and ANNA-2), N-type calcium channel antibody, and the Purkinje cell cytoplasmic antibody (PCA-1) are all associated with what conditions?
PARANEOPLASTIC INTESTINAL PSEUDOOBSTRUCTION
Where in the INTESTINAL TRACT do you test for AMYLOIDOSIS if an INTESTINAL PSEUDOOBSTRUCTION is suspected?
RECTAL BIOPSY
In a patient with MOTILITY issues such as in INTESTINAL PSEUDOOBSTRUCTION, evidence of STEATORRHEA and VIT B12 deficiency suggests what?
SIBO
How is INTESTINAL PSEUDOOBSTRUCTION treated in the ACUTE hospital setting and maintenance?
In the HOSPTIAL - IV ERYTHROMYCIN at 3 mg/kg every 8 HOURS for 5-7 DAYS
Metoclopramide for MAINTENANCE
In a patient with RECURRENT BEZOAR formation who does NOT HAVE SIBO, what can be used for effective treatment of their dysmotility?
SUBCUTANEOUS OCTREOTIDE qHS
What is the MOST IMPORTANT dietary STIMULANT for the GASTROCOLONIC RESPONSE where taking in food causes COLONIC MOTILITY?
FAT
What is the ONLY VISCERAL SENSATION the colon can feel which is elevated in conditions like IBS and IBD?
WALL DISTENTION (NON-FOCAL)
In a patient s/p resolution of an ACUTE ILLNESS with lingering symptoms of nausa, vomiting and weight loss, bloating and diarrhea with no response to a gastroparesis diet, UGIS, EGD and GES normal, what is the BEST TREATMENT?
FUNCTIONAL DYSPEPSIA - due to impaired gastric accomodation and hypersensitivity to gastric distention - treat with BUSPIRONE (no effect of TCAs or SSRIs if not gastroparesis)
Does BOTOX play a role in patients with GASTROPARESIS?
NO (no better than SHAM injections)
How is POST-INFECTIOUS GASTROPARESIS best treated?
IV ERYTHROMYCIN (do NOT start with metoclopramide)
In WHICH patients with REFRACTORY GASTROPARESIS has the gastric PACEMAKER been shown to be the most EFFICACIOUS?
DIABETIC PATIENTS with NAUSEA and VOMITING
Episodes of VOMITING and ABDOMINAL PAIN separated by SYMPTOM-FREE intervals?
CYCLICAL VOMITING SYNDROME (if cannabinoid related - relieved by hot showers and abstinence from cannabinoids; if idiopathic, responds to TCAs and associated with migraines)
MEGADUODENUM (also affects esophagus and anorectum) is seen on UGIS in patients with this CONDITION
SCLERODERMA (often manifests as SIBO and MALABSORPTION - hydrogen breath test)
What MEDICATIONS have been shown to DELAY GASTRIC EMPTYING causing GASTROPARESIS?
TCAs, OPIOIDS, PPIs, LITHIUM, CANNABINOIDS, TOBACCO
UGIS with RETENTION of BARIUM, WITHOUT OBSTRUCTION, EGD with BEZOAR WITHOUT OBSTRUCTION, abnormal SOLID GES?
GASTROPARESIS
Does ACCELERATING GASTRIC EMPTYING improve symptoms of GASTROPARESIS?
NO
What is the MECHANISM of GI MUCOSAL DAMAGE (ulcers, etc.) that occurs with NSAID use?
The systemic INHIBITION of PROSTAGLANDIN SYNTHESIS
Chronic GASTRIC ANTRAL INFLAMMATION caused by THIS, can decrease the number of ANTRAL D-cells and level of SOMATOSTAIN leading to an increased rate of gastric acid secretion and duodenal ulcer formation?
Helicobacter Pylori
Which MEDICATION is CONTRAINDICATED in the TREATMENT of PUD in the PREGNANT patient?
MISOPROSTOL (almost all antacids are safe including H2 blockers, PPIs and Sucralfate)
What should be done for ALL patients who TEST POSITIVE for H.pylori?
ALL should be OFFERED TREATMENT
ALL patients with H.pylori and GASTRIC ADENOCARCINOMA, or EXTRA-NODAL MARGINAL ZONE B-CELL LYMPHOMA (MALTOMA) or FIRST-DEGREE RELATIVES of H.pylori-INFECTED patients with GASTRIC ADENOCARCINOMA should be treated HOW?
H.pylori TREATMENT
How do you TREAT PREGNANT patients with H.pylori infection?
ACID-SUPPRESSION ONLY!! TREAT FULL COURSE, ONLY AFTER DELIVERY (DO NOT TEST WHEN PREGNANT)
Which ENVIRONMENTAL FACTOR is MOST ASSOCIATED with PUD?
SMOKING
What is the MOST COST-EFFECTIVE way of testing for H.pylori in a PREVIOUSLY UNTESTED or UNTREATED patient?
SEROLOGIC Ab TESTING (highest sensitivity and specificity)
POSITIVE ANTI-PARIETAL CELL Ab, POSITIVE ANTI-INTRINSIC FACTOR Ab, HIGH GASTRIN LEVEL, LOW Vit B-12 LEVEL are found in what CONDITION?
AUTOIMMUNE (ATROPHIC) GASTRITIS (older white women, antrum and fundus) - loss of parietal cells causes a low-acid state stimulating gastrin cell hyperplasia
What is HIGHLY-SUGGESTIVE when LYMPHOCYTIC GASTRITIS is histologically found on BIOPSY?
H.pylori INFECTION
In what CONDITION on GASTRIC BIOPSY do you see FIBRIN THROMBI, dilted mucosal cappilaries, fibromuscular hyperplasia of the lamina propria and almost NO inflammation?
GAVE
In what CONDITION on GASTRIC BIOPSY do you see CONGESTIVE VASCULOPATHY?
PORTAL HYPERTENSIVE GASTROPATHY
In what CONDITION on GASTRIC BIOPSY do you see SUPERFICIAL LAMINA PROPRIA HEMORRHAGE?
ACUTE EROSIVE GASTRITIS
In what CONDITION on GASTRIC BIOPSY do you see INFLAMMATION with EOSINOPHILIC INFILTRATE?
EOSINOPHILIC GASTRITIS
What is the MOST LIKELY cause for a GASTRIC ULCER in a patient with HIV and CD <200?
CMV infection (CENTER of the ULCER BIOPSY - VASCULAR ENDOTHELIAL INVOLVEMENT with ENLARGED CELL INTRANUCLEAR INCLUSIONS) - Owel’s Eyes
In a patient with HIV infection with LOW CD count (<200) and a gastric ULCER, WHERE DO YOU TAKE BIOPSIES?
CENTER of the ulcer (CMV) and EDGES of the ulcer (HSV)
In a patient with HIV infection with LOW CD count (<200) and a gastric ULCER on which biopsies reveal NUCLEAR INCLUSIONS with MULTINUCLEATION, MARGINATION and MOLDING?
HSV (EDGE of ULCER BIOPSY)
In a patient with HIV infection with LOW CD count (<200) and a gastric ULCER on which biopises reveal INTENSE PLASMA CELL INFILTRATION and MONONUCLEAR VASCULITIS with a POSITIVE SILVER WARTHIN-STARRY STAIN?
SYPHILIS
In a patient with HIV infection with LOW CD count (<200) and a gastric ULCER on which biopsies reveal MARKED LYMPHOPLASMACYTIC INFLAMMATION and NEUTROPHILS?
CHRONIC ACTIVE GASTRITIS from H.pylori INFECTION
In CHEMICAL GASTROPATHY caused by BILE SALTS, ALCOHOL, NSAIDs, it is important to do WHAT, before increasing frequency and dosage of PPIs?
ELIMINATE the causative factors (ALCOHOL and NSAIDs)
Is CHOLESTYRAMINE likely to be HELPFUL for excess BILE SALTS in the stomach as far as RELFUX is concerned?
NO
What is the most COMMON CAUSE of GRANULOMATOUS GASTRITIS?
CROHN’s DISEASE (52% of cases)
FLUSHING, DIARRHEA, WHEEZING and HEART DISEASE are symptoms of WHAT GI PATHOLOGY and WHERE is it MOST COMMONLY FOUND?
CARCINOID - SMALL BOWEL (JEJUNUM, etc.) - with mets to the LIVER
Is CHROMOGRANIN A measurement a good SCREENING TEST for the diagnosis of a CARCINOID TUMOR?
NO
IN which DISEASE PROCESS is EGD SCREENING for GASTRIC CANCER RECOMMENDED?
FAP
The REALTIVE RISK of H.pylori infection leading to GASTRIC ADENOCARCINOMA is greatest in whom?
YOUNG patients <29 yo
Nearly HALF (50%) of GASTRIC CANCERS in DEVELOPING COUNTRIES are ATTRIBUTED TO?
H.pylori infection
WHERE in the STOMACH do GASTRIC CANCERS associated with H.pylori develop?
BODY and ANTRUM (distal stomach)
In which of these EASTERN EUROPE, AUSTRALIA, WESTERN SOUTH AMERICA, JAPAN and EAST ASIA, is the INCIDENCE of GASTRIC CANCER the LOWEST?
AUSTRALIA
A patient has a GLUCAGON LEVEL >1,000 pg/mL and a BLOOD GLUCOSE LEVEL of >200 mg/dL and pt has DIARRHEA, what is this and WHERE is it found?
GLUCAGONOMA (in the PANCREAS and usually with METS to the LIVER) - UNRESECTABLE
In the GUT, ACTIVATION of PARASYMPATHETIC OUTFLOW to NON-SPHINCTERIC SMOOTH MUSCLE are components of EXTRINSIC NEURAL CONTROL that PROMOTE what?
INTESTINAL TRANSIT
Parkisnon’s Disease, DM, MS, Anticholinergics are ALL NEUROPATHIC DISORDERS of GUT MOTILITY, which is a MYOPATHIC DISORDER?
DERMATOMYOSITIS
The presence of GAS or FLUID in an OBSTRUCTED ORGAN (GOO) on abdominal auscultation while moving patient?
SUCCUSSION SPLASH
WHICH CANCER can CAUSE a PARANEOPLASTIC PSEUDO-OBSTRUCTION of the STOMACH, SMALL BOWEL and COLON?
SMALL CELL LUNG CANCER (SMOKER)
In what MANNER are LIQUIDS EMPTIED from the STOMACH?
EXPONENTIAL (not linear)
HOW LARGE can an INDIGESTIBLE SOLID be to EXIT the STOMACH during an MMC?
2 CM
WHAT is the MAXIMUM SPEED at which GASTRIC CONTRACTIONS OCCUR during an MMC?
3 CYCLES/MINUTE
WHAT is EMPTIED from the STOMACH after an INITIAL LAG PHASE followed by a LINEAR EMPTYING PHASE?
SOLIDS
What SHOULD be done with SHARP OBJECTS when swallowed BEFORE the REACH and INJURE the SMALL BOWEL?
REMOVE by EGD
In a patient with HIV and LOW CD COUNT, with FEVER, WEIGHT LOSS and SEVERE DIARRHEA, with MESENTERIC LNs and on EGD you note patchy areas of EDEMA, ERYTHEMA and NODULARITY with FROSTED YELLOWISH PLAQUES in the DUODENUM, what is the CAUSATIVE AGENT?
MAC (mycobaterium avium-intracellulare complex)
A patient with HIV was noted to have these LESIONS in their DUODENUM, what is the CAUSATIVE AGENT?
Kaposi Sarcoma (HSV-8)
A CHRONICALLY-ILL patient with HIV presents with BLOODY DIARRHEA, FEVER and ABDOMINAL PAIN. Colonoscopy demonstrates PATCHY ULCERATIONS, INTRANUCLEAR INCLUSIONS, PERINUCLEAR HALO and CYTOPLASMIC INCLUSIONS?
CMV infection
A CHRONICALLY-ILL patient with HIV presents with BLOODY DIARRHEA, FEVER and ABDOMINAL PAIN. Colonoscopy demonstrates PATCHY ULCERATIONS, GROUND-GLASS NUCLEI, EOSINOPHILIC INTRANUCLEAR INCLUSIONS and MULTINUCLEATE CELLS?
HSV infection
A CHRONICALLY-ILL patient with HIV presents with BLOODY DIARRHEA, FEVER and ABDOMINAL PAIN. Colonoscopy demonstrates TERMINAL ILEUM EDEMA, MILD VILLOUS ATROPHY with APICAL INTRACELLULAR, EXTRACYTOPLASMIC ICLUSIONS?
CRYPTOSPORIDIUM
Which MEDICATIONS have been IMPLICATED in CAUSING PANCREATITIS in patients with HIV infection?
DIDANOSINE, PENTAMIDINE, DAPSONE, TMP-SMX, FUROSEMIDE, METRONIDAZOLE and NELFINAVIR
HIV patient presents with 12-WEEKS of WATERY, NON-BLOODY DIARRHEA and WEIGHT LOSS, NO fever or chills, no nausea, vomiting, abdominal pain?
ENTEROADHERENT E.coli (chronic diarrhea) - can also cause ACUTE DIARRHEA in travelers and children who are NOT immunocompromised
HIV patients easily get INFECTED with this AGENT which causes CHRONIC WATERY DIARRHEA - treated with CIPROFLOXACIN?
ENTEROADHERENT E.coli (chronic diarrhea) - can also cause ACUTE DIARRHEA in travelers and children who are NOT immunocompromised
What is found in a patient that is infected with ENTEROHEMORRHAGIC or ENTEROINVASIVE E.coli?
SHIGA TOXIN in stool cultures, fecal LEUKOCYTES, and BLOODY DIARRHEA
WATERY DIARRHEA found MOSTLY in TRAVELERS is caused by this E.coli?
ENTEROTOXIGENIC E.coli
WATERY DIARRHEA MOST COMMON in CHILDREN <6 yo is caused by this E.coli?
ENTEROPATHOGENIC E.coli
WELL TREATED HIV PATIENTS who stick to their medication protocols and AVOID TROUBLESOME SUBSTANCES, who present with DYSPHAGIA, are generally found to have WHAT?
GERD with ESOPHAGITIS (not CMV, not EOE)
HIV patient with POOR MEDICAL COMPLIANCE and LOW CD COUNT, handles FISH and presents with PAINFUL SWOLLEN AREA around CUT in ARM which is ENLARGING and PAINFUL?
VIBRIO VULNIFICUS (wound infections with cellulitis, myositis and fasciitis)
What do VIBRIO mimicus, parahemolyticus**, **cholerae and fluvialis CAUSE?
DIARRHEA
SLOW DECREASE in Hb after the TREATMENT of a BLEEDING ULCER is INDICATIVE of WHAT?
REEQUILIBRATION (no repeat EGD or intervention is required)
POST UGIB, a FORMED BLACK STOOL vs LIQUID BLACK STOOLS is consistent with WHAT?
RECENT bleed (clearing of GIT), NOT ACTIVE bleed
WHERE are the MAJORITY of DIEULAFOY lesions found?
UPPER STOMACH
What is RECOMMENDED for the TREATMENT of a DUODENAL ULCER AFTER EGD intervention?
ONCE-DAILY PPI for 4 WEEKS
What happens when a patient with an UGIB is tested for H.pylori with a RAPID UREASE TEST?
FALSE-NEGATIVE with an UGIB
What is the RISK of RE-BLEED in a patient with PUD WITHOUT a CORRECTABLE CAUSE? HOW DO YOU TREAT?
30% in the next 5 YEARS
Treat with ONCE DAILY PPI LIFE-LONG
GIB after NECROTIZING PANCREATITIS is caused by WHAT and HOW is it TREATED?
Bleeding from a PSEUDOANEURYSM (via pancreatic duct)
IR ANGIOGRAPHIC EMBOLIZATION
LARGE-VOLUME STOOL with BLOOD and PAINLESS ABDOMEN with NORMAL Hb and MINOR ORTHOSTATIC CHANGE, VAGAL-INDUCED SYNCOPE associated with MULTIPLE RED STOOLS?
DIVERTICULAR BLEED
WHERE in the GIT is it COMMON to find an AORTO-ENTERIC FISTULA?
DISTAL 3rd of DUODENUM
WHERE in the GIT is it COMMON to find a DUODENAL ULCER associated with the POSTERIOR GASTRODUODENAL ARTERY?
POSTERIOR DUODENAL BULB
WHERE in the GIT is it COMMON to find an ULCER ASSOCIATED with the LEFT GASTRIC ARTERY?
LESSER CURVATURE of the STOMACH
An ADHERENT CLOT over a DUODENAL BULB ULCER that is NOT ACTIVELY BLEEDING has WHAT RISK of BLEED if LEFT UNTREATED? HOW DO YOU TREAT?
25% RISK of RE-BLEED
TREAT with EGD CLOT REMOVAL+ INTERVENTION + IV PPI
CONSTANT ABDOMINAL PAIN with URGE to have BROWN BOWEL MOVEMENT followed by LOOSE BLOODY TOOLS, no fever or chills, on COLONOSCOPY you see a WELL-DEMARCATED AREA of ULCERATION, EDEMA and ERYHTEMA?
ISCHEMIC COLITIS (WELL DEMARCATED) - use of TRIPTAN (migraines)
YOUNG patient with CHRONIC VASCULAR THROMBOSIS with OCCLUSION of the IVC (inferior vena cava) is SUGGESTIVE of what pathology?
FACTOR V LEIDEN genetic mutation
HYPERTHYROIDISM with a tender thryoid (nervousness, loose stools, weight loss, a-fib) and a NEW, PERIUMBILICAL PAIN without much TENDERNESS on PALPATION (mesenteric ischemia) which is most likely CAUSED by WHAT?
SMA OCCLUSION (embolus - a-fib)
POST-OP (cholecystectomy), pt with CAD, DM, HTN, CANNOT BE WEANED off NGT and imaging shows a MILD, NON-SPECIFIC DILATION of a FEW SMALL BOWEL LOOPS WITH INCREASED GAS and FLUID but NO TRANSITION POINT (ILEUS), what is RECOMMENDED?
CHECK for SMALL BOWEL VASCULAR DISEASE (doppler US of abdominal arteries)
What DIAGNOSTIC TEST SHOULD BE AVOIDED in a patient with elevated Cr?
CONTRAST STUDIES (CT, including enterography)
WHEN SHOULD a SPLENIC ARTERY ANEURYSM (SYMTOMATIC or NOT) be TREATED (IR)?
ALL SYMPTOMATIC ANEURYSMS (abd pain, nausea) - HIGH risk of BLEED
ASYMTOMATIC ANEURYSMS >2 cm
ABDOMINAL PAIN AFTER MEALS (30 min), DULL, ACHY, PERIUMBILICAL and lasts ~1 HOUR, with WEIGHT LOSS, FEVERS, FATIGUE, ARTHRALGIA and HTN, LIVEDO RETICULARIS with LE EDEMA, ELEVATED ESR and Cr?
POLYARTERITIS NODOSA (mesenteric angiography - MICROANEURYSMS)
A patient with HEREDITARY HEMORRHAGIC TELANGIECTASIA (HHT) will have symptoms of HF and LIVER INVOLVEMENT (VASCULAR MALFORMATIONS). What are the THREE (3) DIFFERENT TYPES of ABNORMAL LIVER COMMUNICATIONS that can form?
- PORTAL VEIN - HEPATIC VEIN (PORTOVENOUS) FISTULA
- HEPATIC ARTERY - HEPATIC VEIN (ARTERIOVENOUS) FISTULA
- HEPATIC ARTERY - PORTAL VEIN (ARTERIOPORTAL) FISTULA
What are the THREE LIVER MANIFESTATIONS that can OCCUR CLINICALLY in patients with HEREDITARY HEMORRHAGIC TELANGIECTASIA (HHT)?
HIGH-OUTPUT CARDIAC FAILURE
BILIARY ISCHEMIA
PORTAL HTN
What is the most COMMON MANIFESTATION of HEREDITARY HEMORRHAGIC TELANGIECTASIA (HHT) due to LIVER INVOLVEMENT?
HEPATIC ARTERY - HEPATIC VEIN (ARTERIOVENOUS) FISTULA causing HIGH-OUTPUT HEART FAILURE (fatigue, dyspnea on exertion, orthopnea, JVD, systolic murmur, LE edema)
INTERMITTENT EPISODES of PAINLESS HEMATOCHEZIA, REQUIRING TRANSFUSIONS, no melena. ONE of his LEGS is LARGER than the OTHER, one of his LEGS has CUTANEOUS HEMANGIOMAS and BOTH LE’s have VENOUS VERICOSITIES. Why is he bleeding?
KTW (Klippel-Trenaunay-Weber Syndrome) - RECTAL HEMANGIOMAS
A CONGENITAL VASCULAR DISORDER with LIMB HYPERTROPHY, CUTANEOUS HEMANGIOMAS and VARICOSITIES - also CARVERNOUS HEMANGIOMAS of RECTUM with catastrophic bleeds?
Klippel-Trenaunay-Weber syndrome (KTW)
YOUNG patient presents with SEVERE, DIFFUSE ABDOMINAL PAIN for 12 HOURS ASSOCIATED with NAUSEA and CONSTIPATION and this has been happening over the PAST 5 YEARS with HTN and TACCHYCARDIA. WHAT is it and how is it TREATED?
INTERMITTENT PORPHYRIA
TREAT PAIN with acetaminophen, meperidine or morphine
TREAT NAUSEA ONLY with ONDANSETRON (not promethazine)
IV HEMIN and glucose
Why do patients with SCLERODERMA often present with NAUSEA, VOMITING, ABDOMINAL PAIN, DISTENDED ABDOMEN with DIMINISHED BOWEL SOUNDS? How do you TREAT?
CHRONIC INTESTINAL PSEUDO-OBSTRUCTION (CIPO) - intestinal stasis
TREAT with antibiotics (CIPROFLOXACIN) - causes SIBO
What can be used to TREAT the chronic intestinal pseudo-obstruction that causes SIBO due to intestinal STASIS in SCLERODERMA patients (besides antibiotics) that promotes small bowel MOTILITY?
LOW-DOSE OCTREOTIDE (20 mcg SC) - high-dose does not work
PROGRESSIVE SOLID-FOOD DYSPHAGIA, SMALL-CALIBER ESOPHAGUS, MUCOSAL RINGS, MIDDLE-AGED WOMAN, PROXIMAL ESOPHAGUS STRICTURE with DENSE SUBEPITHELIAL LYMPHOCYTIC INFILTRATE, INTRAEPITHELIAL LYMPHOCYTES and MULTIPLE EOSINOPHILIC NECROTIC KERATINOCYTES?
Esophageal LICHEN PLANUS (systemic corticosteroids, topical tacrolimus)
This DISEASE occurs almost EXCLUSIVELY in MIDDLE-AGED WOMEN and MIMICS EOE?
Esophageal LICHEN PLANUS (systemic corticosteroids, topical tacrolimus)
What is the MOST COMMON SITE of GUT INVOLVEMENT of AMYLOIDOSIS?
DUODENUM (then colon, then esophagus)
