5 sewell gi - ucsf medical education sewell gi.pdf · history"of"stricture"! ......

UCSF, Department of Medicine, CME

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GASTROENTEROLOGY

Jus&n L. Sewell, MD, MPH, FACP Assistant Professor of Medicine Division of Gastroenterology UC San Francisco | San Francisco General Hospital

Disclosures

l No rela&onships or conflicts of interest to disclose

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Agenda

l  Top-‐to-‐boLom overview of GI content most per&nent to IM boards

l  Cases with discussion l  Addi&onal boards-‐relevant informa&on with guideline references

l  Pause for ques&ons aPer each session but ask any&me

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Case #1 l  42 year old Caucasian man with heartburn l  IntermiLent retrosternal burning ~2 years

l  Increasing use of antacids & OTC H2RAs, with only transient relief of symptoms

l  1-‐2 packs cigareLes QD, 1-‐2 glasses wine QHS l  Regurgita&on of sour material at night, but no dysphagia

l  Elevates head of bed and has lost weight without benefit


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Case #1 – What is the most appropriate next step in management?

1.  Perform upper endoscopy 2.  Trial of high-‐dose PPI for 4-‐6 weeks 3.  Stop all caffeine and alcohol 4.  Esophageal pH tes&ng 5.  Take H2RA scheduled rather than prn

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Case #1 – What is the most appropriate next step in management?

1.  Perform upper endoscopy 2.  Trial of high-‐dose PPI for 4-‐6 weeks 3.  Stop all caffeine and alcohol 4.  Esophageal pH tes&ng 5.  Take H2RA scheduled rather than prn

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IndicaEons for endoscopy in GERD

Men and women with: l  Alarm symptoms l  GERD refractory to PPI l  Severe erosive esophagi&s l  Recurrent dysphagia with

history of stricture l  Known BarreL’s esophagus

Men only with: l  GERD>5 years AND

addi&onal risk factors for esophageal cancer (single screening EGD) l  Nocturnal reflux l  Obesity l  Central adiposity l  Smoking l  Hiatal hernia

7 Shaheen NJ. Ann Intern Med 2012; 157(11):808-‐16.

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Case #1

l  Symptoms par&ally improved on PPI à EGD l  EGD: 2 cm tongue of salmon colored mucosa in the distal

esophagus, otherwise unremarkable l  Biopsies: intes&nal metaplasia with no dysplasia


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Case #1 – Which is the most appropriate next step?

1.  Repeat EGD for surveillance within 1 year

2.  Test for H. pylori infec&on and treat if present

3.  Radiofrequency abla&on of the BarreL’s mucosa

4.  Refer to surgeon for an&-‐reflux surgery

5.  Double the dose of his PPI to BID and follow symptoma&cally

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1.  Repeat EGD for surveillance within 1 year

2.  Test for H. pylori infec&on and treat if present

3.  Radiofrequency abla&on of the BarreL’s mucosa

4.  Refer to surgeon for an&-‐reflux surgery

5.  Double the dose of his PPI to BID and follow symptoma&cally

Case #1 – Which is the most appropriate next step?


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Case #1 – BarreL’s surveillance

l  Risk of progression to cancer is low (<1% per year)

l  No dysplasia: EGD every 3-‐5 years l  Low grade dysplasia: repeat 6 months, then annually

l  High grade dysplasia: confirm by 2nd pathologist à abla&on or esophagectomy due to concomitant adenocarcinoma in 30-‐40%

11 ASGE Standards of Prac&ce CommiLee. Gastrointest Endosc 2012; 76(6):1087-‐94.

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Case #1 – BarreL’s management

l  Medical or surgical an&-‐reflux therapies do not cause regression of BarreL’s; goal is to control symptoms and minimize cancer risk

l  Radiofrequency abla&on (RFA) eradicates 80-‐95% of dysplasia and reduces life&me cancer risk from 9% to 1%

l  An&-‐reflux surgery reserved for failures of op&mal medical therapy or pa&ent preference


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Case #1

l  Eradicate H pylori when diagnosed l  Reduces risk of PUD, gastric cancer

l  However this does not affect progression of BarreL’s and could theore&cally worsen GERD

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GERD

l  GERD can cause chest pain but can be difficult to dis&nguish from cardiac source based on history alone l  PPI trial l  Cardiac tes&ng in selected pa&ents

l  GERD can cause globus and dysphagia à PPI trial l  Func&onal heartburn and non erosive reflux disease are

common and are less responsive to acid suppression l  Esophageal pH monitoring required to diagnose

l  PPI should be taken 30-‐60 minutes before ea&ng for op&mal acid suppression


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GERD

l  GERD can be exacerbated by l  Impaired salivary flow (Sjögrens, XRT) l  Esophageal dysmo&lity (scleroderma) l  Gastric distension (gastroparesis, dietary habits) l  Reduced LES pressure (chocolate, alcohol, nico&ne, CCBs, nitrates, an&depressants, progesterone, benzodiazepines)

l  Atypical (extraesophageal) GERD manifesta&ons include: chronic cough, hoarseness, laryngi&s, asthma

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Dysphagia

l  Dysphagia: source suggested by symptoms l  IntermiLent solid: Schatzki ring, eosinophilic esophagi&s l  Progressive solid: stricture/achalasia (slow) or neoplasm (rapid) l  Solid and liquid: dysmo&lity

l  EGD usually first test though can consider esophagram l  Manometry tes&ng if EGD nondiagnos&c

l  Achalasia: lack of peristalsis and non-‐relaxing LES l  Oropharyngeal dysphagia usually due to neuromuscular

disorders, and is associated w/ coughing, nasal regurgita&on, choking


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Eosinophilic esophagiEs

l  Eosinophilic esophagi&s l  IntermiLent solid food dysphagia or food impac&on, M>F

l Ringed or “feline” esophagus l Eosinophilic infiltrate on biopsy l Treat with elimina&on diet, swallowed inhaled steroids, PPIs

Dellon ES. Gastroenterology 2014; 147(6):1238-‐54.

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Case #2

l  62 y/o woman with 4 months of epigastric abdominal pain, worse post-‐prandially

l  Incompletely relieved by OTC H2RAs l  Occasional nausea but no vomi&ng l  Mild anorexia l  5 pound weight loss l  ASA 81mg/d and PRN ibuprofen for arthri&s l  PEx: mild epigastric TTP, otherwise unremarkable


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Case #2 Which of the following is the best approach at this Eme? 1.  Empiric H pylori treatment

2.  H pylori tes&ng and treatment if posi&ve

3.  Empiric proton pump inhibitor Rx

4.  Upper endoscopy

5.  Switch ibuprofen to a COX-‐2 NSAID

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Case #2 Which of the following is the best approach at this Eme? 1.  Empiric H pylori treatment

2.  H pylori tes&ng and treatment if posi&ve

3.  Empiric proton pump inhibitor Rx

4.  Upper endoscopy

5.  Switch ibuprofen to a COX-‐2 NSAID


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Non-‐invasive H. pylori tesEng

H. pylori negaEve

Chronic dyspepsia

H. pylori posiEve

EradicaEon therapy Empiric treatment: Proton pump inhibitor

Endoscopy

Improvement Improvement No improvement

YES

NO

Alarm signs or symptoms Age > 55

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Case #2 – H pylori tesEng

l  Rarely treat empirically l  Ac&ve infec&on: urea breath test, stool an&gen, endoscopic biopsy

l  Ac&ve/prior infec&on: serology


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Case #2 – Empiric PPI

l  Empiric acid-‐suppression has some efficacy in dyspepsia, and is reasonable in young pa&ents with no alarm symptoms

l  COX-‐2 selec&ve NSAIDs have less GI toxicity l  New dyspepsia in pa&ents over age 50, dyspepsia with alarm symptoms or family history of gastric cancer, should have EGD to rule out cancer

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H pylori

l  Usually acquired in childhood, person to person transmission l  Inverse associa&on with socioeconomic status l  OPen asymptoma&c

l  10-‐20% PUD l  <0.01% gastric CA

l  Treatment: l  Triple: PPI, clarithromycin, amoxicillin x 10-‐14 days l  Quadruple: PPI, bismuth, metronidazole, tetracycline x 10-‐14 days l  Other an&bio&c op&ons include levofloxacin, rifabu&n, nitazoxanide


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PepEc ulcer disease

l  GUs require biopsy & repeat EGD to exclude CA l  Mul&ple non-‐healing ulcers, or ulcers w/ diarrhea: suspect ZES. Best ini&al test: fas&ng serum gastrin

l  Elevated gastrin seen in gastric outlet obstruc&on, PPI use, pernicious anemia, renal insufficiency, diabetes, and gastrinoma

l  Gastrin levels >1000 highly suspicious for ZES; 200-‐1000 best evaluated with secre&n s&mula&on test (paradoxical rise in gastrin aPer secre&n administered)

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UGI bleed

l  High risk GIB pa&ents taking NSAIDS: l  Known PUD, advanced age, warfarin l  Test and treat for H pylori l  Co-‐prescribe PPI

l  Stress, caffeine, prednisone do not cause PUD


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UGI bleed

l  UGIB may present as hematochezia if brisk, and conversely, slow right-‐sided colonic bleeding may cause melena

l  NG tube only 85% sensi&ve in UGIB l Most UGIB will stop spontaneously l Most UGIB can be effec&vely managed by EGD or angiography

l  Surgery indicated if persistent or recurrent exsanguina&on

Common causes of upper GI bleeding

PUD (50%)

Mallory-‐Weiss tear (10%)

Varices / portal hypertension (20%)

Erosive gastri&s (10%)


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UGI bleed

l Mortality risk ~10% l  Increased with advance age, shock, hematochezia, cirrhosis

l  EGD: diagnos&c, therapeu&c, prognos&c l  IR and surgery are backup l Medical therapy with PPI bolus + con&nuous infusion

l  No role for H2RA’s

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Case #3

l  47 y/o male execu&ve admiLed with severe abdominal pain radia&ng to his back

l  Drinks 2-‐3 cocktails per day, occasionally more l  PEx notable for mid-‐abdominal tenderness with hypoac&ve bowel sounds

l  Lipase 9,200 l  Ini&al management: NPO, analgesia and hydra&on


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Case #3

l  Addi&onal labs: l WBC 11,000 l Bili 1.6, AST 95, ALT 32, AlkP 120 l Triglycerides 220 l Calcium 8.5

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Case #3 What is the most appropriate next diagnosEc step? 1.  Ultrasound of the abdomen 2.  Empiric an&bio&cs 3.  MRCP 4.  Surgical consulta&on 5.  Trend liver tests and lipase, follow exam

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Case #3 What is the most appropriate next diagnosEc step? 1.  Ultrasound of the abdomen 2.  Empiric an&bio&cs 3.  MRCP 4.  Surgical consulta&on 5.  Trend liver tests and lipase, follow exam

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Case #3

l U/S: normal GB and CBD, pancreas is “obscured by overlying bowel gas”

l  An&bio&cs not recommended l  By hospital day #8, his lipase has normalized but his abdominal pain is worsening slightly, and he has developed new fevers to 101.8, with a rising WBC

Tenner S. Am J Gastroenterol 2013; 108(9):1400-‐15.


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Case #3 Which of the following is the best approach at this Eme? 1.  Ini&ate oral feeds, as lipase is normal

2.  Empiric an&bio&cs

3.  Epidural catheter and PCA

4.  ERCP

5.  CT scan of the pancreas

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Case #3 Which of the following is the best approach at this Eme?

1.  Ini&ate oral feeds, as lipase is normal

2.  Empiric an&bio&cs

3.  Epidural catheter and PCA

4.  ERCP

5.  CT scan of the pancreas


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Case #3 – CT scan with necrosis

Normal enhancement

Lack of enhancement

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Case #3 – PancreaEc necrosis

l  Persistent symptoms with acute pancrea&&s should raise concern for complica&ons

l  Pancrea&c necrosis predicts poor outcome l  An&bio&cs not recommended unless high suspicion

or documented infected necrosis l  Carbapenems have excellent pancrea&c penetra&on l  If pa&ent appears infected and has pancrea&c

necrosis, consider FNA with gram stain/culture l  Infected necrosis (posi&ve gram stain) predicts high

mortality rate and requires surgical debridement



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Case #3 – ERCP for pancreaEEs

l  ERCP if biliary source for pancrea&&s suspected l  ALT is first to rise followed by bilirubin and alkP l  Biliary dila&on (US, CT, MRCP)

l  Wait for pancrea&&s to improve unless obstruc&ng CBD stone on imaging or suspected cholangi&s

39 Tenner S. Am J Gastroenterol 2013; 108(9):1400-‐15.

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Case #3 – Acute pancreaEEs management

l  Can assess prognosis w/ Ranson or APACHE II l  Serial amylase/lipase levels not useful in predic&ng course

l  Obtain CT if severe pancrea&&s is suspected (organ failure, lack of improvement, increasing pain, fever, WBC, hypotension)

l  Necrosis on CT has worst prognosis



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l  Prophylac&c an&bio&cs not indicated l  Early studies evaluated agents with poor pancreas penetra&on and included pa&ents with mild disease

l  Best therapy is good suppor&ve care and aggressive hydra&on (250-‐500 mL/hour, bolus if hypovolemic)


Case #3 – Acute pancreaEEs management

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Case #3 – When to feed

l  Pa&ents can eat when pain-‐free and hungry l  Liquid diet and low-‐fat solid diet are equivalent l  Post-‐duodenal enteral feeding may be appropriate in pa&ents with acute pancrea&&s but does not improve outcomes compared with on-‐demand oral feeding

Bakker OJ. New Engl J Med 2014; 371(21):1983-‐93. Tenner S. Am J Gastroenterol 2013; 108(9):1400-‐15.


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Acute pancreaEEs – eEologies

l  Most common e&ologies: gallstones and alcohol l  Less common: hypertriglyceridemia, post‑ERCP, pregnancy, hypercalcemia, viral, hereditary, autoimmune

l  Medica&ons: Erythromycin, tetracycline, 6‑MP/AZA, sulfas, 5‑ASAs, NSAIDs, estrogens, thiazides

Chronic pancreaEEs

l  Exocrine and endocrine manifesta&ons l  Imaging: dilated duct, calcifica&ons l  Enzymes beLer for steatorrhea than pain l  For pain can consider celiac plexus block, surgical op&ons

l  Can cause biliary obstruc&on l  Pancreas divisum: failure of fusion of dorsal and ventral glands; found in 5% of popula&on; may predispose to chronic pancrea&&s

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Let’s take a detour into… radiology

l  Common abdominal x-‐rays you might see on boards

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What is this?

1.  Toxic megacolon 2.  Small bowel

obstruc&on 3.  Sigmoid volvulus 4.  Perforated viscus

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What is this?



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What is this?



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What is this?



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What is this?



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What is this?



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What is this?



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What is this?



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Case #4

l  22 y/o man c/o 1 year of worsening bloa&ng & gas l  Frequent malodorous, floa&ng, greasy stools l  20 lb weight loss in 6 months l  Denies abdominal pain, but has decreased food intake as it provokes diarrhea

l  He also complains of an itchy rash on his knees and elbows


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Case #4

l  Pex: short stature, mucosal pallor, angular cheilosis, scaLered papules and vesicles with excoria&on over the knees and elbows, and mild pre&bial edema

l  Lab tests are significant for microcy&c anemia and a low serum albumin

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GI rashes you need to know…

Derma&&s Herpe&formis E. nodosum Pyoderma


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Case #4 Which of the following is the most likely cause of this paEent’s syndrome and malnutriEon?

1.  Whipple’s Disease

2.  Crohn’s Disease

3.  Celiac Disease

4.  Pancrea&c exocrine insufficiency

5.  Small bowel bacterial overgrowth

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Case #4 Which of the following is the most likely cause of this paEent’s syndrome and malnutriEon?

1.  Whipple’s Disease

2.  Crohn’s Disease

3.  Celiac Disease

4.  Pancrea&c exocrine insufficiency

5.  Small bowel bacterial overgrowth


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Case #4

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Case #4

l  Severe celiac disease with profound malabsorp&on l  Gluten bound by par&cular HLA types results in

inflammatory cascade damaging SB mucosa l  Presenta&on ranges from asymptoma&c to mild iron

deficiency to IBS symptoms to severe malabsorp&on l  Dx: EGD (villous atrophy, increased IELs) and/or

serologic markers (an&-‐&ssue transglutaminase Ab) l  Small bowel mucosa and auto-‐an&bodies can

normalize with gluten free diet

Green PH. New Engl J Med 2007; 357(17):1731-‐43.


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Case #4 l  Tx : gluten-‐free diet l  New agent = larazo&de (prevents &ght junc&on opening à decreased gluten uptake)

l  Long-‐term complica&ons include elevated risk of SB CAs (AdenoCA, lymphoma) and osteoporosis

l  Associa&on with other autoimmune diseases, such as RA and thyroid disease

l  Whipple’s disease, bacterial overgrowth, Crohn’s disease & pancrea&c insufficiency can also cause malabsorp&on

Green PH. New Engl J Med 2007; 357(17):1731-‐43.

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Case #5

l  48 year old man complains of watery diarrhea of 4 months’ dura&on

l  He has 4-‐6 large volume watery movements daily

l  He has required hospitaliza&on twice for dehydra&on

l  On each admission, exam, labs, cultures unrevealing


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Case #5 Which of the following studies would provide the strongest evidence for a secretory eEology for his diarrhea?

1.  The presence of fecal leukocytes

2.  A history of recent an&bio&c use

3.  A history of lactose intolerance

4.  High stool osmolar gap

5.  A fas&ng fecal volume >2.5L / 24 hours

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1.  The presence of fecal leukocytes

2.  A history of recent an&bio&c use

3.  A history of lactose intolerance

4.  High stool osmolar gap

5.  A fas&ng fecal volume >2.5L / 24 hours

Case #5 Which of the following studies would provide the strongest evidence for a secretory eEology for his diarrhea?


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Case #5

l  Main diarrhea mechanisms are secretory, osmoEc / malabsorpEve, inflammatory, funcEonal

l  Differen&ate on analysis of stool for fat and WBC, response to fas&ng, stool osmolar gap

l  Osmolar gap

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Case #5

l  Secretory diarrhea is typically large volume (>1L/d) and does not diminish with fas&ng

l  Causes of secretory diarrhea: l  Bacterial and parasi&c infec&ons l  Bile salt malabsorp&on from ileal resec&on l  Medica&ons l  Small intes&nal bacterial overgrowth (SIBO) l  Hormone secre&ng tumors l  Microscopic coli&s


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Diarrhea

l  Celiac disease can cause both secretory and osmo&c (malabsorp&ve) diarrhea

l  Osmo&c diarrhea: lactose intolerance, magnesium intake

l  Inflammatory diarrhea: usually due to bacterial coli&s or IBD

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Steatorrhea

l  Elevated fecal fat suggests maldiges&on or malabsorp&on

l  FaLy diarrhea can be due to defec&ve: l  Lipolysis (pancrea&c insufficiency) l  Micellariza&on (bile salt insufficiency) l  Absorp&on (intes&nal epithelium) l  Delivery (lympha&cs)

+ à


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Other diarrheal syndromes

l  E coli 0157:H7 associated with HUS (renal failure, thrombocytopenia, hemoly&c anemia)

l  Diabe&c with diarrhea: consider SIBO, osmo&c (sorbitol), “diabe&c diarrhea”

l  Consider fac&&ous diarrhea in medical personnel with unexplained diarrhea

l  In hospital-‐acquired diarrhea, consider C difficile and medica&ons

carbohydrates fats

proteins magnesium

trace elements vitamins Water and

electrolytes

short chain faLy acids

iron, calcium, copper folate

vitamin B12 bile salts

Colonic disease does not cause malabsorp@on

What’s (mal)absorbed where?


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C difficile

l  Risk factors: hospitaliza&on, an&bio&cs, chemotherapy, immune suppression, PPIs

l  Community acquired C. difficile increasingly common

l  C. difficile spores are hardy and highly infec&ous l  Have a high index of suspicion in the elderly, immunosuppressed, immunocompromised, and pa&ents with IBD

Case #6

l  87 y/o man with history of AFib, HTN, CAD, and DM presents to ER with 1 day of crampy leP lower quadrant abdominal pain and bloody stool

l  PEx: BP 106/75, pulse 112, mild LLQ TTP, and maroon stool on rectal exam

l  Hct 36%, WBC 12K l  CT Abd shows leP colon wall thickening l  The pa&ent is admiLed to the hospital and gentle fluid resuscita&on is ini&ated


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Case #6 Which of the following is the most appropriate next step?

1.  Visceral angiogram

2.  Flexible sigmoidoscopy

3.  Thromboly&c therapy

4.  Renal dose dopamine

5.  Stool for C difficile toxin

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Case #6 Which of the following is the most appropriate next step?

1.  Visceral angiogram

2.  Flexible sigmoidoscopy

3.  Thromboly&c therapy

4.  Renal dose dopamine

5.  Stool for C difficile toxin


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Case #6

l  Ischemic coli&s: seen with older age, atherosclerosis, arrhythmias and hypotension

l  Younger individuals: s&mulant drug use, endurance athletes

l  Classic presenta&on is sudden, crampy abdominal pain associated with hematochezia


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Case #6

l  Watershed regions most commonly involved though studies suggest mul&ple distribu&ons

l  Rectal sparing due to collateral flow via the hemorrhoidal plexus (internal iliac artery)

l  Embolic disease usually more severe

Brandt LJ. Am J Gastroenterol 2015; 110(1):18-‐44.

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Case #6

l  Flex sig will reveal rectal sparing and localized signs of mucosal ischemia (ulcera&ons, hemorrhage)

l  Not pathognomonic, but highly sugges&ve l  Presenta&on not sugges&ve of C difficile (typically nonbloody and would not see these endoscopic findings)



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Case #6

l  Suppor&ve management with goal of euvolemia, normotension

l  Pressors may worsen visceral vasoconstric&on l  Worsening abdominal exam with peritoneal signs, lac&c acidosis suggest toxic megacolon and/or perfora&on à requires urgent surgical evalua&on

l  Prognosis is generally good l  80% resolve, 15% chronic ischemia, 5% fulminant


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Vascular bowel disease

Ischemic coliEs Acute mesenteric ischemia

Chronic mesenteric ischemia

Bowel site Colon Small bowel Small bowel

Onset Acute Acute Chronic/recurrent

Typical pathophysiology

Hypoperfusion Embolism Thrombosis

Atherosclerosis

PresentaEon Acute cramping and hematochezia

Acute, severe pain “out of propor&on to examina&on”

Recurrent post-‐prandial pain “food fear”

Natural course 80% resolves 15% chronic 5% fulminant

Death if not rapidly treated

Gradual chronic worsening

Treatment Conserva&ve Emergent surgery Elec&ve surgical or endovascular therapy


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ColiEs

l  IBD results from uncontrolled immune response in the gut

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ColiEs

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Environmental triggers

Moderately inflamed

Failure to down- regulate

Chronic uncontrolled inflammation = IBD

Down- regulate

Normal gut controlled inflammation

Normal gut controlled inflammation


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Pathologic features UlceraEve ColiEs Crohn’s disease

Transmural involvement No (except fulminant) Yes

“Skip lesions” No Yes

Fibrosis Minimal Common

Fistulae No Common

Granulomas No Yes, in 20%

Small bowel disease No Yes, 75%

Rectal involvement Always Occasional

Clinical features UlceraEve ColiEs Crohn’s disease

Diarrhea Very common Common

Blood per rectum Very common Occasional

Abdominal pain Common Very common

Cons&tu&onal symptoms Common Common

Strictures/abscesses/fistulae No Common

Perianal disease No Common

Extra-‐intes&nal manifesta&ons Occasional Occasional

Recurrence aPer surgery No Common, >50%

Malignancy Occasional Occasional

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ColiEs

l  NSAID use may result in symptoms mimicking IBD or may exacerbate exis&ng IBD

l  Risk CRC in IBD propor&onal to extent of colon involved and dura&on of illness

l  EIM: arthri&s, uvei&s, erythema nodosum, pyoderma gangrenosum, sclerosing cholangi&s


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Medical therapy

5ASA

An&bio&cs

Steroids

Immuno-‐modulators

Biologics

Suppor&ve agents

Cancer screening in IBD

l Ulcera&ve coli&s proximal to the rectum or Crohn’s disease with significant colonic involvement

l Disease dura&on > 8 years l  Colonoscopy q1-‐2 years with targeted biopsies plus random biopsies OR chromoendoscopy

86 Laine L. Gastrointest Endosc 2015; 81(3):489-‐501.


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Lower GIB

l  10% w/ hematochezia have UGI source l  >80% LGIB stops spontaneously, 25% recur l  Diver&culosis most common cause l  Tagged RBC scan (blood loss 0.1 cc/min, 6 cc/hr) l  Angiography (blood loss 0.5 cc/min, 30 cc/hr) l  Colonoscopy can be pursued but requires rapid prep

DiverEcular disease

l  Common in elderly l No treatment indicated l  Complica&ons: LGIB and diver&culi&s l Diagnosis of diver&culi&s warrants future colonoscopy to rule out cancer

l  Consider surgery if recurrent diver&culi&s

88


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Case 7

l  A 62 y/o man has a posi&ve FOBT collected via digital rectal exam

l  Takes a daily low-‐dose ASA for cardioprotec&on l  Reports occasional BRB when he wipes with toilet paper for years, especially with straining

l  No family history of colorectal cancer l  No other GI symptoms

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Case 7 Which of the following is the best approach at this Eme?

1.  Repeat FOBT on spontaneously defecated stool

2.  Colonoscopy

3.  Flexible Sigmoidoscopy

4.  Barium Enema

5.  CT colonography


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Case 7 Which of the following is the best approach at this Eme?

1.  Repeat FOBT on spontaneously defecated stool

2.  Colonoscopy

3.  Flexible Sigmoidoscopy

4.  Barium Enema

5.  CT colonography

92


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Case #7

l  Could be false posi&ve FOBT due to DRE or hemorrhoids, but a posi&ve test always requires a complete colonoscopy

l  No role for “confirmatory” retes&ng

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Colorectal cancer screening

l  Approved CRC screening methods: l  Colonoscopy (q 10 years) l  Flexible sigmoidoscopy (q 5 years) l  CT colonography (q 5 years) l  FOBT/FIT (annually) l  BE has fallen out of favor (q 5 years)

l  Any posi&ve exam à colonoscopy l  CEA not used for screening l  Fecal DNA not widely used

Levin B. Gastroenterology 2008; 134(5):1570-‐95.


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Polyps & colorectal cancer

l  Increased CRC risk l  Personal or family history of polyps or cancer

l  10 years before age of affected family member or age 40, whichever is earlier

l  IBD l  APer 8-‐10 years of disease

l  Subsequent colonoscopy intervals if average risk l  10 years if no polyps l  5 years is < 2 small adenomas l  3 years if >2 small, or any large (10mm+) adenomas

Lieberman DA. Gastroenterology 2012; 143(3):844-‐57.

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Cancer syndromes

l  Familial Adenomatous Polyposis: AD, 1/3 new muta&ons, cancer in 30s w/o colectomy

l  Gardner's = FAP w/ extracolonic osteomas, desmoid tumors, congenital hypertrophy of the pigmented re&nal epithelium

l  Both caused by same muta&on (APC), a tumor suppresser gene

l  Main cause of death in FAP and Gardner’s pa&ents s/p colectomy is periampullary neoplasia; next are desmoid tumors


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l  Turcot's = FAP w/ CNS malignancies l  Lynch Syndrome = Hereditary Non-‐Polyposis Colorectal Cancer (HNPCC). AD, incomplete penetrance, R-‐sided CRCs, beLer prognosis than FAP l  Increased risk of ovarian, endometrial, breast, gastric,

ampullary CA l  Caused by muta&ons in DNA mismatch-‐repair genes

Cancer syndromes

98

CASE #8

l  59 y/o Chinese woman recently immigrated to US with 4 months of progressive dyspepsia, described as a periumbilical gnawing or fullness

l  12 lb weight loss and early sa&ety l  EGD reveals diffuse gastric atrophy and a 1.5cm ulcer in the fundus with exophy&c edges l  Ulcer biopsies – granula&on &ssue l  Gastric body biopsies – organisms consistent with H

pylori


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99

CASE #8 Which of the following is the best approach at this Eme?

1.  Treat for H pylori, then repeat EGD

2.  Treat for H pylori, repeat EGD if symptoms persist

3.  Treat for H pylori, check UGIS if symptoms persist

4.  Treat for H pylori, no need to repeat EGD

5.  PPI BID, no need to treat for H pylori if symptoms resolve

100

1.  Treat for H pylori, then repeat EGD

2.  Treat for H pylori, repeat EGD if symptoms persist

3.  Treat for H pylori, check UGIS if symptoms persist

4.  Treat for H pylori, no need to repeat EGD

5.  PPI BID, no need to treat for H pylori if symptoms resolve

CASE #8 Which of the following is the best approach at this Eme?


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101

102

CASE #8

l  Proximal loca&on, H pylori, recent Asian immigrant, exophy&c margins concerning for malignancy


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103

CASE #8

l  All gastric ulcers require repeat endoscopy aPer medical treatment to confirm healing and exclude neoplasia

l  Pa&ent with mul&ple, small, antral ulcers, especially with known risk factors (such as NSAIDs) is the excep&on

l  Repeat EGD not required for typical duodenal ulcers, as cancer risk is very low

ASGE Standards of Prac&ce CommiLee. Gastrointest Endosc 2010; 71(4): 663-‐8.

104

Gastric cancer

l  Risk factors: H pylori, achlorhydria (par&al gastrectomy, atrophic gastri&s), intes&nal metaplasia, adenomatous gastric polyps, smoking, alcohol abuse

l  Majority is adenocarcinoma l  Gastric lymphoma is the most common site of extranodal lymphoma

l  MALT lymphoma: related to H pylori, can oPen be cured with HP eradica&on alone


53

105

Esophageal cancer

l  Esophageal adenocarcinoma risk factors: male gender, Caucasian, BarreL’s, smoking, obesity, alcohol abuse

l  Squamous cell esophageal cancer risk factors: alcohol abuse, smoking, caus&c inges&on, achalasia, tylosis, dietary nitrates

l  Stage with CT scan à endoscopic ultrasound if no mets on CT

106

l  Very uncommon, but can include adenocarcinoma, carcinoid, GIST, lymphoma

l  Risk factors: celiac disease, Crohn’s disease, familial polyposis, HIV (lymphoma)

Small bowel cancer


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107

PancreaEc cancer

l  Incidence increasing, now the 4th leading cause of cancer death in US (lung, colon, breast)

l  Risk factors: smoking, alcohol abuse, chronic pancrea&&s

l  Mainly adenocarcinoma, 70% in pancrea&c head l  Systemic manifesta&ons of Panc CA: polyarthri&s, subcutaneous fat necrosis, migratory thrombophlebi&s

108

Other pancreaEc cancers

l  IPMN, cystadenocarcinoma, neuroendocrine l  Islet cell tumors:

l  insulinomas → hypoglycemia l  glucagonomas → hyperglycemia & rash (necroly&c migratory erythema)

l  gastrinoma → pep&c ulcer disease, diarrhea l  VIPoma → watery diarrhea, hypokalemia


55

PancreaEc cysts

l  Serous cystadenoma (or carcinoma), mucinous cystadenoma (or carcinoma), IPMN, pseudocysts

l  Common incidentalomas

109

PancreaEc cysts – new guidelines

l High risk features: >3 cm in size, solid component, dilated PD

l  0-‐1 high-‐risk feature: MRI in 1 year then q2 years x 2

l  >1 high-‐risk feature: EUS with FNA l  If EUS without concerning features à MRI l  If lesion in tail, easier to resect surgically

110 Vege SS. Gastroenterology 2015; 148(4):819-‐22.


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The End

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