Upload
others
View
31
Download
0
Embed Size (px)
Citation preview
UCSF, Department of Medicine, CME
1
UCSF, Department of Medicine, CME 1
GASTROENTEROLOGY
Fernando Velayos MD MPHAssociate Professor of MedicineDivision of GastroenterologyUniversity of California San Francisco
Case #1-1 42 year old Caucasian man with heartburn Intermittent retrosternal ‘burning’ >12 years Increasing use of antacids & OTC H2RAs, with only
transient relief of symptoms 1-2 packs cigarettes QD, 1-2 glasses wine QHS Denies chest pain, but notes regurgitation of ‘sour’
material occasionally at night Sleeps on 2 pillows in attempt to decrease this, without
much success.
UCSF, Department of Medicine, CME 3
Case #1-2
Denies dysphagia, odynophagia or weight loss Admits to recurrent sore throats with ‘laryngitis’, and
occasional dyspnea on exertion Put on a daily PPI, scheduled for EGD in 4 weeks EGD: 4 cm of salmon colored mucosa in the distal
esophagus (bx’d), otherwise unremarkable Biopsies: intestinal metaplasia (intestinal type
epithelium with goblet cells) with no dysplasia Sxs improved somewhat, but incompletely, on PPI
UCSF, Department of Medicine, CME
2
UCSF, Department of Medicine, CME 4
Case #1-3
UCSF, Department of Medicine, CME 5
Case #1-4 Which of the following is the most appropriate next step?
1. Repeat EGD for surveillance in 5 years
2. Test for H. pylori infection and treat if present
3. Photodynamic therapy (PDT) or RF ablation ofthe Barrett’s mucosa
4. Refer to surgeon for anti-reflux surgery.
5. Double the dose of his PPI to BID and repeatendoscopy for surveillance in one year.
UCSF, Department of Medicine, CME 6
Case #1-4 Which of the following is the most appropriate next step? (CORRECT ANSWER)
1. Repeat EGD for surveillance in 5 years
2. Test for H. pylori infection and treat if present
3. Photodynamic therapy (PDT) or RF ablation ofthe Barrett’s mucosa
4. Refer to surgeon for anti-reflux surgery.
5. Double the dose of his PPI to BID and repeatendoscopy for surveillance in one year.
UCSF, Department of Medicine, CME
3
UCSF, Department of Medicine, CME 7
Case #1-5 ANSWER
Endoscopy (with bx): best test to dx Barrett’s Definition: intestinal metaplasia distal esophagus EGD indicated as a ‘once in a lifetime’ procedure in
pts with chronic GERD symptoms (duration undefined), particularly in Caucasian men who have the highest rate of Barrett’s and AdenoCA
Medical or surgical anti-reflux therapies do not cause regression of Barrett’s; endpoint of Rx is same as non-Barrett’s GERD: to ameliorate Sxs
UCSF, Department of Medicine, CME 8
Case #1-6 ANSWER
Anti-reflux surgery should not be done solely due to presence of Barrett’s, but for failures of optimal medical therapy or patient preference
Progression of Barrett’s to AdenoCA (app 0.5%/year) has promoted endoscopic surveillance programs EGD yearly X2, then Q2-3 years if no dysplasia Low grade dysplasia: surveillance every 6-12 mos High grade dysplasia: confirm by a 2nd ‘expert’
pathologist, ablation or esophagectomy due to concomitant adenoCA in 30-40%
UCSF, Department of Medicine, CME 9
Case #1-7 ANSWER
PDT, argon plasma & (most recently, likely dominant) radiofrequency (RF) ablative Rxs are emerging for HGD (maybe LGD, and still controversial in non-dysplastic disease).
While eradication of Hp does decrease PUD recurrence and maybe gastric CA, it does notdecrease the risk of esophageal AdenoCA, in fact might be protective, with a possible inverse association, ie Hp may be protective for reflux / Barrett’s / esophageal AdenoCA (but not causative)
UCSF, Department of Medicine, CME
4
UCSF, Department of Medicine, CME 10
Case #1-8 Esophagus Pearls
GERD is the most common cause of unexplained (non-cardiac) chest pain, and is highly treatable; empiric trial of acid suppression reasonable.
Panic disorder is present in 25-40% of patients with non-cardiac chest pain syndromes, also treatable.
GERD symptoms may mimic cardiac symptoms; history cannot reliably distinguish between these two etiologies of chest pain.
Globus sensation is also commonly due to GERD; empiric treatment also reasonable.
UCSF, Department of Medicine, CME 11
Case #1-9 Esophagus Pearls
Factors which impair salivary flow (eg Sjogrens, XRT), esophageal motility (eg PSS), or gastric emptying (eg DM) may aggravate GERD.
Be aware of extraesophageal or ‘atypical’ GERD: chronic cough, hoarseness, laryngitis, asthma.
Atypical GERD often requires high-dose PPI treatment for prolonged periods of time
Chocolates, alcohol, nicotine, CCBs, nitrates, antidepressants, progesterone, benzodiazepines reduce LES pressure and can exacerbate GERD.
UCSF, Department of Medicine, CME 12
Case #1-10 Esophagus Pearls
Dysphagia: etiology usually evident by Sxs Intermittent solid: Schatzki Ring (“steakhouse syndrome”). Progressive solid: stricture (slow) or neoplasm (rapid). Solid and liquid: motility disturbance.
Esophagram helpful as ‘road-map’ to plan EGD Rx Patients with achalasia have esophageal contractions
which are never peristaltic and incomplete LESRs. Oropharyngeal (or ‘transfer’) dysphagia is usually due to
neuromuscular disorders, and is associated w/ coughing, nasal regurgitation, choking.
UCSF, Department of Medicine, CME
5
UCSF, Department of Medicine, CME 13
Case #1-11 Esophagus Pearls
Eosinophilic Esophagitis increasingly diagnosed Intermittent solid food dysphagia
or food impaction M>F “ringed” or corrugated esophagus Tx with swallowed inhaled
steroids, PPIs
UCSF, Department of Medicine, CME 14
Case #1-12 Esophagus Pearls
Medications can cause “pill” esophagitis: tetracycline, quinidine, iron, ascorbic acid, fosamax, potassium, and are a common iatrogenic cause of chest pain.
Empiric fluconazole is the best initial therapy in AIDS pts with dysphagia and thrush, reserve endoscopy for those not responding.
Causes of esophageal ulcers in AIDS patients: CMV, HSV, idiopathic.
UCSF, Department of Medicine, CME 15
Case #2-1
62 y/o woman w/ 4 months of abdominal pain Epigastric, worse post-prandially, and somewhat,
but incompletely relieved by OTC H2RAs Occasional nausea but has not vomited 5 pound weight loss (5%IBW), which she attributes
to decreased food intake ASA 81mg/d and PRN motrin for OA PEx: epigastric TTP, otherwise unremarkable.
UCSF, Department of Medicine, CME
6
UCSF, Department of Medicine, CME 16
Case #2-2Which of the following is the best approach at this time?
1. Empiric H pylori treatment
2. Hp testing and treatment if positive
3. Empiric proton pump inhibitor Rx
4. Upper endoscopy
5. Switch ibuprofen to a COX-2 NSAID
UCSF, Department of Medicine, CME 17
Case #2-2 Which of the following is the best approach at this time? (CORRECT ANSWER)
1. Empiric H pylori treatment
2. Hp testing and treatment if positive
3. Empiric proton pump inhibitor Rx
4. Upper endoscopy
5. Switch ibuprofen to a COX-2 NSAID
UCSF, Department of Medicine, CME 18
UCSF, Department of Medicine, CME
7
UCSF, Department of Medicine, CME 19
Case #2-3 ANSWER
Test-and-treat strategies for Hp have shown some benefit in uninvestigateddyspepsia, presumably due to effect in the subset (10-20%) with active PUD
Large RCTs have failed to show a benefit in non-ulcer dyspepsia (NUD), ie after ulcer disease has been ruled out
UCSF, Department of Medicine, CME 20
Case #2-4 ANSWER With widely available, accurate, and
relatively inexpensive tests available, there is no role for empiric Hp therapy
Hp testing in an untreated patient: UBT or stool antigen testing or serology (poor PPV)
If endoscopy is indicated, Hp testing can be easily and accurately done at that time
After Rx, Ab titers do not predictably decline, thus repeat serology useless; use UBT or stool Ag
UCSF, Department of Medicine, CME 21
Case #2-5 ANSWER Empiric acid-suppression has some efficacy in
dyspepsia, and is reasonable in young patients with no alarm symptoms (bleeding, dysphagia, or weight loss), esp in low risk Hp populations
New dyspepsia in patients over age 50 (as well as this patient’s weight loss) should be evaluated with an endoscopy to r/o more ominous pathologies, particularly CA
While COX-2 selective NSAIDs do have GI toxicity, this patient needs endoscopy.
UCSF, Department of Medicine, CME
8
UCSF, Department of Medicine, CME 22
Case #2-6 Gastric Pearls
Hp acquired in childhood, person:person transmission Inverse association with socioeconomic status. Only small percentage of patients infected will get
symptomatic disease 10% PUD (the commonest cause, with NSAIDs) 1000 highly suspicious for Z-E syndrome; 200-1000 best evaluated with secretin stimulation test
UCSF, Department of Medicine, CME 24
Case #2-8 Gastric Pearls
High risk GIB patients taking NSAIDS: Hx PUD, advanced age, warfarin Use COX-2 agents or co-prescribe PPI
Steroids not considered ulcerogenic alone; may be synergistic with NSAIDs.
No convincing evidence that stress, alcohol, or caffeine cause gastritis/PUD.
Gastric Outlet Obstruction: PUD and CA
UCSF, Department of Medicine, CME
9
UCSF, Department of Medicine, CME 25
Case #2-9 Gastric Pearls
GIB increasing in the elderly due to NSAIDs No indication for surgery in the acute
presentation of PUD without exsanguination NG tube only 85% sensitive in UGIB (can
bleed post-pyloric, heavily, and NPV low) UGIB may present as BRBPR if brisk, and
conversely, slow right-sided colonic bleeding may cause melena
UCSF, Department of Medicine, CME 26
Case #2-10 Gastric Pearls
Overall mortality of UGIB is 10% High Risk: Age, shock, BRB, cirrhosis
EGD: diagnostic, therapeutic, prognostic H2 blockers: no improved outcomes in UGIB PPIs (IV, continuous infusion) probably do
diminish re-bleeding in high risk PUD (active bleeding, visible vessels) after endoscopy
UCSF, Department of Medicine, CME 27
Case #3-1
47 y/o executive is admitted with severe abdominal pain radiating to his back
He drinks 2-3 cocktails per day, and more recently during a business trip
PEx notable for mid-abdominal tenderness with hypoactive bowel sounds
WBC 11,000, lipase is 9200 Rx: NPO, analgesia and hydration
UCSF, Department of Medicine, CME
10
UCSF, Department of Medicine, CME 28
Case #3-2
U/S: normal GB and CBD, pancreas is “obscured by overlying bowel gas”
By hospital day #8, his lipase has normalized but his abdominal pain persists, and he has developed new fevers to 102.8, with a rising WBC count.
UCSF, Department of Medicine, CME 29
Case #3-3Which of the following is the best approach at this time?
1. Initiate oral feeds, as lipase is normal
2. Broad spectrum antibiotics
3. Epidural catheter and PCA for analgesia
4. ERCP
5. CT scan of the pancreas
UCSF, Department of Medicine, CME 30
Case #3-3Which of the following is the best approach at this time? (CORRECT ANSWER)
1. Initiate oral feeds, as lipase is normal
2. Broad spectrum antibiotics
3. Epidural catheter and PCA for analgesia
4. ERCP
5. CT scan of the pancreas
UCSF, Department of Medicine, CME
11
UCSF, Department of Medicine, CME 31
Case #3 – CT scan with necrosis (non-enhancement)
UCSF, Department of Medicine, CME 32
Case #3-4 ANSWER
Persistent Sxs in pt with acute pancreatitis (AP) should raise concern for complications
Pancreatic necrosis (non-opacification on rapid-bolus CT scan) is most powerful predictor of adverse outcome, predicting sepsis syndrome / MIF
If necrosis is present especially with worsening clinical picture, an FNA & gram stain on the smear should be done.
UCSF, Department of Medicine, CME 33
Case #3-5 ANSWER Infected necrosis (positive gram stain)
predicts high mortality rate and generally requires surgical debridement
Role of prophylactic Abx conflicting Early studies evaluated agents that had poor
pancreatic penetration and included patients with mild disease who are unlikely to benefit
Imipenim seems to have excellent pancreatic penetration and is a reasonable choice in patients with severe disease, but is not a substitute for assessing necrosis
UCSF, Department of Medicine, CME
12
UCSF, Department of Medicine, CME 34
Case #3-6 ANSWER
Oral feedings should generally be withheld until sx improvement is evident, irrespective of labs / lipase levels
Post-duodenal enteral feeding, particularly with elemental formulations, is gaining favor in patients with acute pancreatitis
ERCP is generally not performed in AP, for fear of worsening the inflammation, unless a biliary origin is suspected, suggested by elevated bilirubin or ductular dilation
UCSF, Department of Medicine, CME 35
Case #3-7 Pancreas Pearls
Gallstones, alcohol most common etiologies, less common: hypertriglyceridemia, post-ERCP, pregnancy, hypercalcemia, viral.
Medications: Erythro, tetracycline, 6-MP/Imuran, sulfas, 5-ASAs, NSAIDs, estrogens, thiazides, DDI, pentamidine.
Serial amylase/lipase levels not useful in predicting course of acute pancreatitis.
Lipase more specific, remains longer, useful later in course for dx (but not prognosis)
UCSF, Department of Medicine, CME 36
Case #3-8 Pancreas Pearls
Assess prognosis w/ Ranson or APACHE II Necrosis by dynamic CT best prognosticator Obtain CT whenever severe dz is suspected,
ie organ failure, lack of improvement, increasing pain, fever, WBC, or hypotension
Ultrasound is more sensitive than CT for imaging the biliary tree but overlying bowel gas precludes complete pancreatic visualization in 1/3. Use to evaluate for biliary source
UCSF, Department of Medicine, CME
13
UCSF, Department of Medicine, CME 37
Case #3-9 Pancreas Pearls
Best therapy AP is good supportive care and aggressive hydration.
Role of prophylactic Abx unclear Imipenim if severe dz reasonable
Infected necrosis major complication, CT/FNA if suspected, surgery if present.
Endoscopic intervention within first 48hrs in biliary pancreatitis with suspected biliary sepsis (ie. cholangitis, jaundice) improves outcome.
UCSF, Department of Medicine, CME 38
Case #3-10 Pancreas Pearls
Acute or chronic pancreatitis can result in splenic vein thrombosis and bleeding from isolated gastric varices.
Pancreatic ‘colonization’ with CMV, cryptosporidia, microsporidia, is common in AIDS by autopsy, but generally does not cause clinical pancreatitis.
UCSF, Department of Medicine, CME 39
Case #3-11 Pancreas Pearls
Diffuse pancreatic calcification seen in only 30% of pts with CP, implies loss of >90% of glands exocrine function.
Biliary disease is a very uncommon cause of chronic pancreatitis.
Chronic pancreatitis can result in stenosis of the intrapancreatic portion of the CBD resulting in an elevated alk phos, jaundice, and occasionally cholangitis or secondary biliary cirrhosis.
UCSF, Department of Medicine, CME
14
UCSF, Department of Medicine, CME 40
KUBs you need to know
Chronic panc Ca++ SBO with ‘ladder’ and AFLs
UCSF, Department of Medicine, CME 41
And one more…
Sigmoid volvulus‘coffee bean’
UCSF, Department of Medicine, CME 42
Case #3-12 Pancreas Pearls
ERCP or MRCP to diagnose CP Pancreas divisum: failure of fusion of dorsal
and ventral glands; found in 5% of normals; may predispose to chronic pancreatitis.
Rx of chronic pancreatitis: ? pancreatic enzymes Peustow for large duct disease Nerve blocks ineffective for CP (work for CA)
UCSF, Department of Medicine, CME
15
UCSF, Department of Medicine, CME 43
Case #4-1
A 22 y/o man c/o 1 year of bloating & gas Stools frequency, floating, & malodorous 20 lb weight loss (200->180 lbs) in 6 months Denies abdominal pain, but has decreased
food intake as it provokes diarrhea He also complains of some tongue soreness,
and an itchy rash on his knees and elbows
UCSF, Department of Medicine, CME 44
Case #4-2
PEx short stature, mucosal pallor, angular cheilosis, evidence of weight loss, abdominal distention with tympany, scattered papules and vesicles with excoriation over the knees and elbows, and mild pretibial edema
Lab tests are significant for macrocytic anemia and a low serum albumin
Endoscopy is remarkable for a scalloped small bowel mucosa with biopsies revealing flattened duodenal epithelium.
UCSF, Department of Medicine, CME 45
UCSF, Department of Medicine, CME
16
UCSF, Department of Medicine, CME 46
GI Rashes you need to know…
Dermatitis Herpetiformis E. nodosum NME
UCSF, Department of Medicine, CME 47
Case #4-4 Which of the following is the most likely cause of this patient’s syndrome and malnutrition?
1. Whipple’s Disease
2. Crohn’s Disease
3. Celiac Sprue
4. Pancreatic exocrine insufficiency
5. Small bowel bacterial overgrowth
UCSF, Department of Medicine, CME 48
Case #4-4 Which of the following is the most likely cause of this patient’s syndrome and malnutrition? (CORRECT ANSWER)
1. Whipple’s Disease
2. Crohn’s Disease
3. Celiac Sprue
4. Pancreatic exocrine insufficiency
5. Small bowel bacterial overgrowth
UCSF, Department of Medicine, CME
17
UCSF, Department of Medicine, CME 49
CASE #4-5 ANSWER
Severe celiac sprue (= gluten-sensitive enteropathy = non-tropical sprue) with profound malabsorption (most cases milder)
Dx: EGD (villous atrophy) or serologic markers (anti-endomysial Ab, anti-gliadin Ab and anti-tissue transglutaminase Ab)
Reversal of villous atrophy after strict gluten free diet is most confirmatory, but not always performed these days
UCSF, Department of Medicine, CME 50
CASE #4-6 ANSWER
Whipple’s disease, bacterial overgrowth, Crohn’s disease & pancreatic insufficiency can all cause malabsorption but would not show severe villous atrophy on biopsy, nor the rash of dermatitis herpetiformis
Tx sprue: lifelong gluten-free diet Long-term complications include SB CAs
(AdenoCA, lymphoma) and osteoporosis Association with other autoimmune
diseases, such as RA and thyroid disease
UCSF, Department of Medicine, CME 51
CASE #5-1
48 year old man complains of watery diarrhea of 4 months duration
It varies in severity, but he has 4-6 large volume watery movements daily
He has required hospitalization twice for dehydration/rehydration
On each admission, exam, labs, cultures unrevealing.
UCSF, Department of Medicine, CME
18
UCSF, Department of Medicine, CME 52
CASE #5-2 Which of the following studies would provide the strongest evidence for a secretory etiology for his diarrhea.
1. The presence of fecal leukocytes
2. A history of recent antibiotic use
3. A history of lactose intolerance
4. 290 - [Na + K] X 2 = 150mEq/L
5. A fasting fecal volume >2.5L / 24 hours
UCSF, Department of Medicine, CME 53
CASE #5-2 Which of the following studies would provide the strongest evidence for a secretory etiology for his diarrhea. (CORRECT ANSWER)
1. The presence of fecal leukocytes
2. A history of recent antibiotic use
3. A history of lactose intolerance
4. 290 - [Na + K] X 2 = 150mEq/L
5. A fasting fecal volume >2.5L / 24 hours
UCSF, Department of Medicine, CME 54
CASE #5-3 ANSWER
Secretory diarrhea is typically large volume (>1L/d) and changes little with fasting
Causes of secretory diarrhea: Bacterial toxins Bile salt malabsorption from ileal resection Non-osmotic laxative abuse Villous adenoma Hormone secreting tumors such as VIPoma,
carcinoid, medullary carcinoma of the thyroid, and Zollinger-Ellison Syndrome
UCSF, Department of Medicine, CME
19
UCSF, Department of Medicine, CME 55
CASE #5-4 ANSWER
Lactose intolerance is an osmotic diarrhea Celiac sprue, like all disease processes
impairing small bowel function, results in a diarrhea of malabsorption (osmotic)
Osmolar gap: 290 – 2[Na+K] Gap >125 suggests a pure osmotic diarrhea Gap
UCSF, Department of Medicine, CME
20
UCSF, Department of Medicine, CME 58
Case #5-7 Diarrhea Pearls
E coli 0157:H7 ass’d with HUS (renal failure, plts and hemolytic anemia)
Diabetic with diarrhea: consider bacterial overgrowth ( gastric/SB motility) vs sorbitol in ‘diabetic’ foods
Consider factitious diarrhea in medical personnel with unexplained diarrhea
In hospital-acquired diarrhea, consider C. diff and medications
UCSF, Department of Medicine, CME 59
Case #5-8 Diarrhea Pearls
The ileum absorbs B12 and bile salts. Ileal resections:
100 cm → in bile acid depletion and steatorrheic diarrhea.
Duodenum absorbs iron, and IDA may be the first, and sometimes only, sign of celiac dz
Whipple’s disease: diarrhea, adenopathy, arthritis, neuro sxs (PAS+ macros on bx)
UCSF, Department of Medicine, CME 60
Case #5-9 Diarrhea Pearls C diff: Abx, but also chemoRx, IBD, PPIs, HIV C. diff can be transmitted person to person
(gloves!), and survive in hospital environment in spores, thus infection clusters can occur, including non-Abx patients
All antibiotics have been associated with the development of C. difficile enterocolitis Commonest: clindamycin, PCNs, quinolones Rare: metronidazole, tetracycline, vancomycin,
aminoglycosides
UCSF, Department of Medicine, CME
21
UCSF, Department of Medicine, CME 61
Case #5-10 Diarrhea Pearls
AIDS patients with diarrhea: Infrequent but high volume, watery: consider
MAI, cryptosporidium, microsporidium, and if cultures negative, consider EGD with bx
More frequent but smaller volume, bloody, tenesumus and urgency: consider CMV or other proctitis, consider F/S with bx
C diff also a common pathogen in HIV+ pts
Case #6-1 87 y/o man with history of AFib, HTN, CAD, and
DM presents to ER with 1 day of crampy left lower abdominal pain and bloody stool
PEx: BP 106/75, pulse 112, mild LLQ TTP, and maroon stool on rectal exam
Hct is 36%, WBC 12,000 KUB: unremarkable CT Abd shows left colon wall thickening The patient is admitted to the hospital and gentle
fluid resuscitation is begun.
UCSF, Department of Medicine, CME 63
Case #6-2 Which of the following is the most appropriate next step?
1. Visceral angiogram
2. Flexible sigmoidoscopy
3. Thrombolytic therapy
4. ‘Renal dose’ dopamine
5. Stool for C. Diff toxin
UCSF, Department of Medicine, CME
22
UCSF, Department of Medicine, CME 64
Case #6-2 Which of the following is the most appropriate next step? (CORRECT ANSWER)
1. Visceral angiogram
2. Flexible sigmoidoscopy
3. Thrombolytic therapy
4. ‘Renal dose’ dopamine
5. Stool for C. Diff toxin
UCSF, Department of Medicine, CME 65
UCSF, Department of Medicine, CME 66
Case #6-3 ANSWER
Ischemic colitis: seen with older age, atherosclerosis, arrhythmias and hypotension
Younger individuals, esp w/ drug use (cocaine or methamphetamines), or in endurance athletes
The classic presentation is sudden, crampy, mild LLQ abdominal pain associated with hematochezia
UCSF, Department of Medicine, CME
23
UCSF, Department of Medicine, CME 67
Case #6-4 ANSWER Pathophysiology: non-occlusive, non-embolic,
due to ‘low-flow’ state and often vasoconstriction (“ATN of colon”)
The ‘watershed’ colon (splenic flexure, at the junction of the IMA and SMA circulation) is most commonly involved
Rectal sparing due to collateral flow via the hemorrhoidal plexus (from the iliac artery)
UCSF, Department of Medicine, CME 68
Case #6-5 ANSWER
Flex sig (gentle) will reveal rectal sparing and signs of mucosal ischemia (ulcerations, hemorrhage) in the left colon
Not pathognomonic, but highly suggestive in this scenario above, and excludes other dxs
Typical peudomembranes can be seen in C. Diff colitis, but absence of antecedent Abx & bloody stool make this an unlikely diagnosis
UCSF, Department of Medicine, CME 69
Case #6-6 ANSWER Unlike acute small bowel infarction, which is
often thromboembolic & fatal w/o emergent intervention, ischemic colitis can be treated conservatively in most pts with bowel rest, IVF, empiric Abx, and maximizing perfusion
Angiogram can be both diagnostic and therapeutic when a focal vascular narrowing or thrombus is amenable to angioplasty or stenting, but is not routinely warranted, nor is there a role for systemic thrombolysis
UCSF, Department of Medicine, CME
24
UCSF, Department of Medicine, CME 70
Case #6-7 ANSWER Pressors should be avoided, may worsen
visceral vasoconstriction Worsening abdominal exam, peritoneal signs,
fever, leukocytosis, or lactic acidosis suggest colonic perforation and require urgent laparotomy
The prognosis for recovery is generally good, although ischemic colitis is a common cause of chronic colonic stricturing (with Div Dz).
UCSF, Department of Medicine, CME 71
Case #6-8 Colitis/LGIB Pearls
UC: continuous involvement from rectum proximally Crohn's: M2A, "skip" areas, perianal disease NSAID use may result in symptoms mimicking IBD
or may exacerbate existing IBD IBD: risk CRC proportional to extent of colon
involved and duration of illness Extraintestinal manifestations of IBD: arthritis,
uveitis, erythema nodosum, pyoderma gangrenosum, sclerosing cholangitis
UCSF, Department of Medicine, CME 72
Case #6-9 Colitis/LGIB Pearls
Serum ANCA (Antineutrophil Cytoplasmic Abs) common in UC
ASCA (Anti-Saccharomyces cerevisiae Abs) more common in CD
Crohn's patients more likely to smoke, U.C. patients less likely. Nicotine may Rx UC
Gallstones (CD) and renal (oxalate) stones (CD & UC) can complicate IBD
UCSF, Department of Medicine, CME
25
UCSF, Department of Medicine, CME 73
Case #6-10 Colitis/LGIB Pearls
Sulfasalazine and mesalamine (5-ASA) are main Rx for colonic IBD. Intolerance to sulfasalazine is secondary to SULFA, switch to 5-ASA compounds (Asacol, Pentasa, Lialda etc)
Immuran/6-MP can be steroid sparing but may take months to work
IV Prednisone or Cyclosporine for severe acute flares; anti-TNF Abs (infliximab, adalimumab) for CD (emerging for UC)
In acute or severe disease, avoid antidiarrheal agents which can predispose to toxic megacolon
UCSF, Department of Medicine, CME 74
Case #6-11 Colitis/LGIB Pearls
10% pts w/ hematochezia have UGI source 80%+ LGIB stops spontaneously, 25% recur Diverticulosis, AVMs most common causes AVMs and aortic stenosis? Controversial 99Tc RBC scan detects intermittent bleeding for
48 hours; screening test for angiogram. “Rapid Purge” with PEG over 3-4 hours can
clear the colon and permit urgent colonoscopy
Case #6-12 Diverticular Disease
Common in elderly in ‘western’ world “Precocious” disease in younger men No Rx for incidental disease Complications: LGIB and diverticulitis Abx for diverticulitis: anaerobes & GNRs Consider surgery after 2nd or 3rd
complication, esp if localized disease
UCSF, Department of Medicine, CME 75
UCSF, Department of Medicine, CME
26
UCSF, Department of Medicine, CME 76
Case 7-1
A 62 y/o man is undergoing a routine PEx at which time he is noted to be hemoccult (FOBT) positive on a single slide done during a digital rectal exam
Takes a daily baby ASA for cardioprotection Reports occasional BRB when he wipes with toilet
paper for years, especially with straining, which he attributes to hemorrhoids
He has no family history of colorectal cancer, and no other GI symptoms.
UCSF, Department of Medicine, CME 77
Case 7-2 Which of the following is the best approach at this time?
1. Repeat the hemoccult testing with six cards, onspontaneously defecated stool, while on a‘hemoccult’ diet
2. Colonoscopy
3. Flexible Sigmoidoscopy
4. Barium Enema
5. CT (‘virtual’) colonography
UCSF, Department of Medicine, CME 78
Case 7-2 Which of the following is the best approach at this time? (CORRECT ANSWER)
1. Repeat the hemoccult testing with six cards, onspontaneously defecated stool, while on a‘hemoccult’ diet
2. Colonoscopy
3. Flexible Sigmoidoscopy
4. Barium Enema
5. CT (‘virtual’) colonography
UCSF, Department of Medicine, CME
27
UCSF, Department of Medicine, CME 79
UCSF, Department of Medicine, CME 80
Case #7-3 ANSWER Although his positive test may indeed be a false
positive due to his hemorrhoids or dietary hemoglobin, or ASA, any positive test requires a complete colonic evaluation, most appropriately with a colonoscopy
There is no role for any repeat testing after a positive test, and no difference between one positive card or six…a positive is a positive.
If the pt were heme (-), other screening options would be appropriate, including annual FOBT with F/S Q5 years
UCSF, Department of Medicine, CME 81
Case #7-4 ANSWER
BE mainly utilized today when colonoscopy is either unsuccessful technically or deemed too high a risk (due to the sedation)
While CT colography holds promise as a screening test in the future, it’s current operating characteristics are unacceptable for widespread adoption, including need for preparation and low sensitivity, and not currently endorsed as first line screening test or ‘approved’ by CMS as 1st line test
UCSF, Department of Medicine, CME
28
UCSF, Department of Medicine, CME 82
Case #7-5 CRC/Polyps Pearls
False positive GUAIAC can be caused by peroxidase activity in animal hemoglobin and some fruits and vegetables (turnips, horseradish, broccoli). FIT more accurate
Vitamin C can cause false negative test Only 50% of patients with CRC are FOBT + CEA is NOT a useful screening test - it
should be used for F/U in patients with resected colon CA with elevated pre-oplevels that drop after surgery.
UCSF, Department of Medicine, CME 83
Case #7-6 CRC/Polyps Pearls Increased CRC risk: chronic IBD (>10 yrs),
personal hx polyps/cancer, 1st or 2nd degree relatives with polyps/CRC,?hx of breast/GYN CA
Distal colonic adenomas associated with a 30-50% incidence of proximal adenomas and mandate proximal colon evaluation if seen on F/S; hyperplastic polyps do not
Colonoscopic follow up for polyps every 3-5 years (depending on size, number and histology); after negative colonoscopy: f/u 10 yrs in avg risk screening population
UCSF, Department of Medicine, CME 84
Case #7-7 CRC/Polyps Pearls Familial Adenomatous Polyposis: AD, 1/3
new mutations, cancer in 30s w/o colectomy Gardner's = FAP w/ extracolonic osteomas,
desmoid tumors, congenital hypertrophy of the pigmented retinal epithelium.
Both are caused by same mutation (APC), a tumor suppresser gene on Chromosome 5q
Main cause of death in FAP and Gardner’s patients s/p colectomy is periampullary neoplasia; next are desmoid tumors
UCSF, Department of Medicine, CME
29
UCSF, Department of Medicine, CME 85
Case #7-8 CRC/Polyps Pearls
Turcot's = FAP w/ CNS malignancies Lynch Syndrome = Hereditary Non-Polyposis
Colorectal Cancer (HNPCC). AD, incomplete penetrance, R-sided CRCs, better prognosis
Lynch II with ovarian, endometrial, breast CAs ('cancer family syndrome'). Caused by mutations in DNA mismatch-repair genes
UCSF, Department of Medicine, CME 86
Case #7-9 CRC/Polyps Pearls
Adjuvent XRT and 5-FU improves survival in Stage II and III rectal cancer
5-FU and levamisole adjuvant therapy improves survival in Stage III (Duke’s C) colon cancer (?IIb)
UCSF, Department of Medicine, CME 87
CASE #8-1 A 59 y/o Chinese woman presents with 4 mos
of progressive dyspepsia, described as a periumbilical gnawing or fullness
Reports a 12 lb weight loss (10% IBW) over this period and a sensation of early satiety
EGD reveals diffuse gastric atrophy (loss of rugal folds) and a 1.5cm ulcer in the fundus with exophytic, heaped up edges Ulcer bxs reveal only granulation tissue Gastric body bxs reveal atrophy, with organisms
consistent with H pylori present.
UCSF, Department of Medicine, CME
30
UCSF, Department of Medicine, CME 88
CASE #8-2 Which of the following is the best approach at this time?
1. Repeat the EGD soon for further biopsies
2. UGI series
3. H pylori Rx, no need to repeat EGD
4. PPI BID, no need to repeat EGD
5. Screening family members for H pylori
UCSF, Department of Medicine, CME 89
CASE #8-2 Which of the following is the best approach at this time? (CORRECT ANSWER)
1. Repeat the EGD soon for further biopsies
2. UGI series
3. H pylori Rx, no need to repeat EGD
4. PPI BID, no need to repeat EGD
5. Screening family members for H pylori
UCSF, Department of Medicine, CME 90
UCSF, Department of Medicine, CME
31
UCSF, Department of Medicine, CME 91
CASE #8-3 ANSWER
Although the bxs were negative, this patient has a worrisome presentation for gastric malignancy, and repeat bxs should be undertaken soon
While benign appearing gastric ulcers may be treated and re-endoscoped in 3 months, this patients presentation should encourage earlier evaluation
UCSF, Department of Medicine, CME 92
CASE #8-4 ANSWER
As dogma, all gastric ulcers require repeat endoscopy after medical treatment to confirm healing and exclude neoplasia
Not true for duodenal ulcers, as the risk of cancer is low
The occasional patient with multiple, small, antral/pre-pyloric ulcers, especially with known risk factors (such as NSAIDs) is the exception to this rule
UCSF, Department of Medicine, CME 93
CASE #8-5 GI Oncology Pearls
Gastric CA Risk Factors: achlorhydria (partial gastrectomy, atrophic gastritis, ?PPIs), gastric polyps, H pylori
The incidence of gastric cancer is decreasing in US (?declining Hp); remains high in Japan.
Majority of gastric cancer is adenocarcinoma Gastric lymphoma is the most common site of
extranodal lymphoma MALT lymphoma: related to H. Pylori, low-
grade, may regress with Abx Rx, then XRT
UCSF, Department of Medicine, CME
32
UCSF, Department of Medicine, CME 94
CASE #8-6 GI Oncology Pearls
Esophageal Cancer Risk Factors: smoking, alcohol, achalasia, lye ingestion, Plummer-Vinson Syndrome, men>women, Barrett’s Esophagus (AdenoCa)
Adenocarcinoma of the esophagus is rapidly increasing in rate (2nd only to melanoma).
Esophageal cancer: stage with CT scan and endoscopic ultrasound if neg for mets (EUS staging standard for esoph and panc CA).
UCSF, Department of Medicine, CME 95
Small intestinal malignancy uncommon Small intestinal cancer Risk Factors: celiac
sprue, Crohn’s disease, familial polyposis, HIV (lymphoma)
Small bowel tumors: AdenoCa (proximal), Carcinoid (distal), GIST, lymphoma (distal).
CASE #8-7 GI Oncology Pearls
UCSF, Department of Medicine, CME 96
CASE #8-8 GI Oncology Pearls
Pancreatic Cancer Risk Factors: smoking, alcohol, chronic pancreatitis, ? diabetes
Pancreatic cancer has increasing incidence, now the 4th leading cause of cancer death in US (lung, colon, breast)
Pancreatic neoplasms mainly adenocarcinoma, with 70% arising in HOP, others APUD/neuroendocrine
UCSF, Department of Medicine, CME
33
UCSF, Department of Medicine, CME 97
CASE #8-9 GI Oncology Pearls
Extraintestinal manifestations of Panc CA: polyarthritis, subcutaneous fat necrosis, migratory thrombophlebitis
Pancreatic islet cell tumors: insulinomas → hypoglycemia glucagonomas → hyperglycemia & rash
(necrolytic migratory erythema) gastrinoma → peptic ulcer disease, diarrhea VIPoma → watery diarrhea, hypokalemia;