UCSF, Department of Medicine, CME · 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

UCSF, Department of Medicine, CME

1

UCSF, Department of Medicine, CME 1

GASTROENTEROLOGY

Fernando Velayos MD MPHAssociate Professor of Medicine

Division of Gastroenterology

University 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 onlytransient 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, withoutmuch success.


Case #1-2

Denies dysphagia, odynophagia or weight loss

Admits to recurrent sore throats with ‘laryngitis’, andoccasional dyspnea on exertion

Put on a daily PPI, scheduled for EGD in 4 weeks

EGD: 4 cm of salmon colored mucosa in the distalesophagus (bx’d), otherwise unremarkable

Biopsies: intestinal metaplasia (intestinal typeepithelium with goblet cells) with no dysplasia

Sxs improved somewhat, but incompletely, on PPI


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Case #1-3


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.


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.


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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


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%


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)


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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.



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.



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.


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Eosinophilic Esophagitis increasingly diagnosed Intermittent solid food dysphagia

or food impaction

M>F

“ringed” or corrugated esophagus

Tx with swallowed inhaled steroids, PPIs



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.


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.


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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


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



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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


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


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.


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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) <0.01% gastric CA (adenoCA and MALToma)

Testing / Rx indicated for bona fide PUD, gastric CA Standard Rx:

Triple: PPI, clari 500, amox 1g BIDX10d (PCN allergy: metronidazole) Quad: PPI, PB, metronidazole, tetracycline (old, now back due to

increasing clarithro resistance)



GUs require bx & repeat EGD to exclude CA; not true for DUs.

Ectopic/non-healing ulcers, or ulcers w/ diarrhea: suspect ZES. Best test: fasting serum gastrin

gastrin seen in gastric outlet obstruction, acid suppression, pernicious anemia, renal insufficiency, diabetes, and gastrinoma

Gastrin levels >1000 highly suspicious for Z-E syndrome; 200-1000 best evaluated with secretin stimulation test



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


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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



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 dodiminish re-bleeding in high risk PUD (active bleeding, visible vessels) after endoscopy


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


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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.


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


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


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Case #3 – CT scan with necrosis (non-enhancement)


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.


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


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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


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)



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


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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.



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.



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.


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KUBs you need to know

Chronic panc Ca++ SBO with ‘ladder’ and AFLs


And one more…

Sigmoid volvulus‘coffee bean’



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)


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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


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.



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GI Rashes you need to know…

Dermatitis Herpetiformis E. nodosum NME


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


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


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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


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


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.


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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


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


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


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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 <50 suggests a pure secretory diarrhea


Case #5-5 Diarrhea Pearls

Main mechanisms are secretory and osmotic / malabsorptive

Differentiate on analysis of stool for fat; osmolar gap; and response to fasting (osmotic, malabsorptive improve)

Stool is always iso-osmolar (and assumed to equal serum, ie we use 290 instead of measuring actual Osm in calculating gap)

Hypo or hyperosmolar stool implies adding hypo or hypertonic fluid (ie factitious)



Many fecal WBCs suggests infectious (Shigella, Salmonella, Campylobacter, Yersinia, E. coli) or IBD.

Fecal fat is useful in chronic diarrhea Qualitative ‘spot’ Sudan black stained smear Quantitative 24h collection (on 100g/day diet)

fecal fat can be due to defects in the lipolytic (pancreas), micellarization (bile salts), cellular (intestinal epithelium) or delivery (lymphatics) stages of fat assimilation


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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



The ileum absorbs B12 and bile salts. Ileal resections:

<100 cm → bile-acid mediated (excess BAs in colon) secretory diarrhea (cholerrhea)

>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)



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


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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.


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


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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



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


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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)


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


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


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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).


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



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


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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



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



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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.


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


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


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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


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


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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.



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



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


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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



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)


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.


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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


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



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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


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


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


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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).


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).




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


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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;

Documents

UCSF, Department of Medicine, CME · 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