UCSF, Department of Medicine, CME GASTROENTEROLOGY Fernando Velayos - - PDF document

UCSF, Department of Medicine, CME 1

UCSF, Department of Medicine, CME 1

GASTROENTEROLOGY

Fernando Velayos MD MPH

Associate 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 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

• ccasional 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

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Case #1-3

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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 of the Barrett’s mucosa

4.

Refer to surgeon for anti-reflux surgery.

5.

Double the dose of his PPI to BID and repeat endoscopy 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 of the Barrett’s mucosa

4.

Refer to surgeon for anti-reflux surgery.

5.

Double the dose of his PPI to BID and repeat endoscopy 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

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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 not decrease 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.

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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.

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Case #1-11 Esophagus Pearls

 Eosinophilic Esophagitis

increasingly diagnosed

 Intermittent solid food dysphagia

• r food impaction

 M>F  “ringed” or corrugated esophagus  Tx with swallowed inhaled

steroids, PPIs

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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.

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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

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

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Case #2-3 ANSWER

 Test-and-treat strategies for Hp have

shown some benefit in uninvestigated dyspepsia, 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

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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,

• r 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

• minous 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)

UCSF, Department of Medicine, CME 23

Case #2-7 Gastric Pearls

 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

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

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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

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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.

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

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

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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.

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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

• f 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

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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.

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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’

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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)

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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

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.

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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

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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

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.

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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

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

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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

UCSF, Department of Medicine, CME 56

Case #5-5 Diarrhea Pearls

 Main mechanisms are secretory and

• smotic / malabsorptive

 Differentiate on analysis of stool for fat;

• smolar 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)

UCSF, Department of Medicine, CME 57

Case #5-6 Diarrhea Pearls

 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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Case #5-7 Diarrhea Pearls

 E coli 0157:H7 ass’d with HUS (renal failure,

 plts and hemolytic anemia)

 Diabetic with diarrhea: consider bacterial

• vergrowth ( 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 → 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)

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

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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

• ther 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

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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

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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

• ften 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

• r 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

• f 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

• r 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

• n 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, on spontaneously defecated stool, while

• n

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, on spontaneously defecated stool, while

• n

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

• perating characteristics are unacceptable for

widespread adoption, including need for preparation and low sensitivity, and not currently endorsed as first line screening test

• r ‘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-op levels 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

• f 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,

• thers 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;