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contraindications to GI endoscopy

recent MI
combative pt
intestinal perforation


EGD is procedure of choice for:

eval odynophagia,to determine presence of peptic ulcer
upper GI bleed workup, always before PUD surgery, w/up for GERD with failed tx, eval ingested foreign body, persistent dyspepsia, dysphagia-after barium swallow


ERCP - endoscopic retrograde cholangiopancreatography, after this procedure

*60% have increased amylase
*5-20% develop acute pancreatitis


before ERCP in patient with suspected bile duct obstruction

treat with antibiotics prior to ERCP


indications for ERCP

*find otherwise undetectable common bile duct stone
*find cause of pancreatic duct obstruction
*dx chronic pancreatitis
*to r/o primary sclerosing cholangitis(MRCP is better tho)
*to tx choledoccholithisis with cholangitis


ERCP is contraindicated in ACUTE pancreatitis EXCEPT in these conditions

*impacted gallstones
*ascending cholangitis-(bacterial infection causing cholangitis)


MRCP-magnetic resonance cholangiopancratography is used to

*dx chronic pancreatitis
*assess lack of clinical improvement in acute pancreatitis
*test of choice for primary sclerosing cholangitis


endoscopic ultrasonography-u/s probe put thru biopsy port of endoscope.
used to evaluate

*pancreatic diseases
*biliary duct dz when ERCP contraindicated:gallstone pancratitis, pregnancy
*to confirm MRCP findings


dysphagia is

swallow that for any reason does not proceed in normal fashion


odynophagia is

pain with food bolus passage


3 categories/causes of dysphagia

*transfer disorders
*anatomic or structural disorders
*motility disorders


transfer disorders causing dysphagia

*neurologic deficit-CVA,ALS
see difficulty transfer food from mouth to esophagus, causing oropharyngeal muscle dysfunction
*symptoms: cough, gag, nasal regurg, immediate upon swallow


motility disorders causing dysphagia

problem in transport food from upper esophagus to stomach
*failure of effective peristalsis &/or failure of LES relaxation
*endogenous and exogenous causes


dysphagia-always do

work up! do not do just empiric treatment


dysphagia work up

**Barium swallow** first test
EGD if needed is done after barium swallow-except in patient with hx reflux and slight -moderate dysphagia to Solids-high likely this is stricture from chronic reflux
*esoph. manometry only if barium and EGD were negative



*neuronal denervation & gangion cell degeneration=> no organized peristalsis in esophageal body and LES increased pressure and does not relax with swallowing


achalasia-characeristic features in patient history

*dysphagia to solids and liquids
* LONGSTANDING symptoms-years
*regurg of food, especially at night
*no age or gender predilection


achalasia-dx tests in this order

*barium swallow: dilated esophagus-often fluid filled.see "bird beak" narrowing distally due to LES tight
*EGD:use to confirm dx and r/o tumor
*esophageal manometry:last test to confirm dx


pseudoachalasia and secondary achalasia

*tumor at esophagogastric junction
*consider if: onset of symptoms RAPID
patient > age 60
symptoms progressive and see profound weight loss


complications of achalasia

*aspiration pneumonia
*weight loss


Tx achalasia

*pneumatic dilation at LES opening
*surgical myotomy
*botulism toxin every 6-12 months-good in high risk patient
*calcium blockers and nitrates-only temporary partial relief


diffuse esophageal spasm

"irritable bowel of the esophagus"
*simultaneous, non peristaltic contraction of esophagus
*often precipitated by cold or carbonated liquids
*symptoms: dysphagia, atypical CP


diffuse esophageal spasm

Dx and Tx

Dx: barium swallow-usually normal but can see classic "corkscrew", manometry confirms diagnosis, EGD not helpful
Tx: reassurance, if needs rx-1st line:diltiazem or imipramine


anatomical obstruction of esophagus

*see slowly progressive dysphagia, first to solids then to liquid
* symptoms can be intermittant or constant
YOUNG-usually schatzki ring
OLDER-cancer or stricture


schatzki ring-lower esophageal ring, is always assoc with

hiatal hernia


classic history of patient with schatzki ring

*very slow progression of intermittent solid food dysphagia- esp to meat, bread
*may have hx of regurgitaion of impacted bolus for relief


schatzki ring, Dx & Tx

barium swallow-ring 13mm or less in diameterr to cause symptoms
Tx:dilation then PPI


symptoms of esophageal stricture

slow progression
solid food s


causes of esophageal stricture

* #1: long hx inadeq tx reflux
*prolonged NG tube
*lye ingestion decades prior-these pt also incr risk esophageal cancer


esophageal stricture Dx & Tx

dx-barium swallow:narrowing-usually esophagogastric junction


history of dysphagia in malignant esophageal obstruction-either esophageal malignancy or compression from non-esophageal ca

rapid progression of symptoms
dysphagia: solid>soft foods>liquids


plummer-vinson syndrome

*dysphagia due to a web in the cervical esophagus
*see in females with iron def anemia- unknown why
*slight incr risk of esophageal cancer


dysphagia due to neurologic dysfunction (CVA,parkinsons, ALS,MS,bulbar palsy) see symptoms

*dysphagia to solid & liquids from the ONSET


aspiration due to dysphagia

*can occur with any type dysphagia
*usually well tolerated and no tx unless pulmonary problems
*s/s:choking,gag,cough, nasal regurg
*trach usually does not cure, may need PEG
*eval with video swallow study



shiny hard thick skin


systemic sclerosis

when scleroderma also involves internal organs
*#1 most common conn. tissue dz of esophagus
*weak or absent peristalsis of esoph, & LES is wide open
*severe reflux and damage from it.
* polymyositis & dermatomyositis can do same as above


Eosinophilic (allergic) esophagitis

*chronic inflammatory disorder, Involves IL-5, most incr IgE
* most in males, 30% have peripheral eosinophils
*main symptom:recur attacks dysphagia with food impaction


eosinophilic esophagitis : EGD findings, Dx, Tx

EGD: classic SCALLOPED appearance with ridges or rings in esophagus
Dx: biopsy >20eos/hpf in MIDesophagus biopsy
Tx: difficult, allergy testing and avoid allergens,fluticasone BID or viscous budesonide, PPI if reflux present



painful swallowing


most common causes of odynophagia

pill induced esophagitis
opportunistic infections-candida, HSV, CMV-tx cause,if no improvement do EGD w biopsy


Most common drugs that can cause pill induced odynophagia

*esp if take with little water or before lying down
*doxycycline, KCL,ASA,NSAIDS
**dx made by hx alone (abrupt onset and taking the med)
Tx-stop med, reassure and educate pt


GERD due to

inappropriate transcient relaxation of LES
hiatal hernia often present


suspect GERD if

*nocturnal cough,frequent sore throat
*hoarse,laryngitis,clearing throat
*loss of dental enamel
*exac of asthma
*vocal cord dysfunction


GERD assoc with these 2 respiratory disorders

*Asthma-even if no s/s GERD,PPI may improve asthma in some but recent study did not show improved asthma control with GERD tx
*vocal cord dysfxn:spasm of vocal cords assoc inspir stridor-wheeze at night


vocal cord dysfunction seen in

young pt in competitive sports: more stress rxn in most but 10% of exercise induced asthma in likely misdiagnosed VCD



if only heartburn trial PPI, EGD if fails to control symptoms-62% will have normal esophagus (non-erosive reflux dz)


ALARM signals in GERD patient-they need EGD

*N/V, dysphagia, odynophagia
*blood in stool, wt loss, anorexia, anemia, abnl phys exam
* family hx PUD, long duration of symptoms (esp white male >45)
*fail full dose PPI
*suspect barretts


Indications for 24 hour esophageal pH monitor

*atypical cases of GERD
*refractory symptoms and normal EGD
*failure of response to PPI
*hoarse,cough, atyp CP, and no classic symptoms of GERD


severe GERD (grade 2 or worse esophagitis)

PPI tx indefinately or corrective surgery


in pt w GERD symptoms that dont respond to PPI, look for these meds that cause delay gastric emptying causing reflux

*calcium channel blockers


indications for antireflux surgery

*refractory to medical tx
*young pt with severe dz
*need for longterm PPI
-outcome best in those that respond to PPI, 60% p surg need PPI
-must do motility study pre op-poor peristalsis-post op dysplasia


Barrett esophagitis

*change cell type from squamous>metaplasia
*highest risk:heartburn>10yr,>age 50, white male
*if chronic GERD: 10%male, 2% female have barretts. large # pt have barretts but no GERD symptoms


Barretts assoc with only this type cancer

*PPI and antireflux surgery never change to cellular changes of Barretts


risk of adenocarcinoma in barretts

0.4% per year in pt w barretts
risk relates to: length of the barretts changes, presence of hiatal hernia, degree of dysphagia, **concurrent smoking**


Monitoring of barretts or those at risk

*2 EGD w Bx within 1 year, if both neg for dysplasia, reck 3 yrs
*if low grade dysplasia Bx #1, reck within 6 mo,, if no higher dysplasia on this bx, do yearly until no dysplasia on 2 consecutive yearly EGD w Bx


if high grade dysplasia on a EGD w Bx

*repeat EGD w Bx within 3 month
*any bx w high grade and mucosal irreg>endoscopic resection
*if 3 mo bx w high grade again but no mucosal irregularity, 3 ways to handle: 1. resection 2. reck EGD w bx every 3 month 3. radiofreq ablation c freq EGD follow ups


2 types of esophageal cancer

squamous cell


adenocarcinoma of esophagus

slightly >50% of cancers
distal 1/3 of esophagus
assoc w Barretts


squamous cell of esophagus

slight <50%
proximal 2/3 of esophagus
causes: smoking, alcohol-these have synergistic carcinogenic(NOT additive),head & neck cancers, achalasia, lye stricture, Plummer-vinson syndrome,strong assoc diet & environ


dx esophageal cancer

barium swallow then EGD w bx
CT scan and endoscopis U/S to stage


tx esophageal cancer

*small & localized: surgical resection
*large or metastasized:combo chemotherapy + radiation prior to surgery-2 year survival 38%


zenker diverticulum

outpouch of upper esophagus
#1cause of transfer (trouble initiating swallow) dysphagia to solid foods
*s/s: foul breath, regurg food eaten several days prior,often elderly


stomach physiology

G cells in pyloric antrum-incr pH & amino acid from food brkdown>G cell releases gastrin>that acts on parietal cells in fundus>secretes HCL(gastric acid)via proton pump
gastrin>enterochromaffin like cells (ECL) produce histamine-local effect via H2 receptors of parietal cells(paracrine)
acetylcholine from vagus nerve (neurocrine) w direct effect on parietal cells


parietal cells are affected by

endocrine (gastrin)
neurocrine (acetylcholine)
paracrine (histamine)


inhibitors of gastrin

somatostatin & secretin
*decr pH> stim these (negative feedback) to regulate pH


achlorhydria patients (autoimmune gastritis) or those with pernicious anemia, or if PPI tx leads to achlorhydria

gastrin levels skyrocket due to loss of inhibitory effect, can see gastrim levels >500


gastric acid and pepsin(made from pepsinogen in presence of acid)

digest food and also attack mucosal defenses



recurrent upper abdominal pain or discomfort


s/s dyspepsia

epigastric fullness
gnawing pain (not severe)


causes of dyspepsia

*most functional
*meds:ASA NSAIDS iron
*if *PUD,GERD,gastritis,biliary colic, gastroparesis,pancreatitis,cancer


gastritis, classified by

histology or etiology


histologic classifications of gastritis

*acute gastritis-superficial-neutrophil infiltrate
*atrophic gastritis- medications, lymphocytes
*gastric atrophy-late, gastropathy


etiology classification of gastritis

Type A: autoimmune,atrophic,pernicious anemia,achlorhydria
*affects proximal stomach (body and fundus)
*autoantibodies against both intrinsic factor & parietal cells-progress to pernicious anemia & achlorhydrea w secondary hypergastrinemai and gastrin level >1000


Type B gastritis

*most common - 80% of chronic gastritis-due to H pylori


H pylori is linked to

*gastritis, PUD
*gastric adenocarcinoma
*gastric B cell lymphoma (MALT)


medications that require gastric acid for best absorption

* thyroxine
*itraconazole, ketoconazole **fluconazole does NOT
*50% AIDS pts have decr stomach acid w incr rate of itraconazole failure


erosive gastropathy

*not inflam response so is not a gastritis
*assoc: NSAID, alcohol, severe physiologic stress-ICU,surgery,burns


SRMD-stress related mucosal damage

causes and prevention

*causes: ICU,burns,CNS injury, surgery, vent,coagulopathy
*prevent: H2 block, antacid, PPI, early feedings
**Most effective: continuous infusion H2 receptor antagonist-NO increased risk of aspiration pneumonia


when to test for H pylori

*any hx PUD-esp duodenal ulcer
*current EGD w ulcer,erosive gastritis or duodenitis
*if MALT lymphoma is present
*family hx gastric cancer
*test & treat: dyspepsia pt


Gold standard H pylori test

biopsy with histology of antral mucosa on EGD


h pylori test that is good to check active disease and response to treatment

urease test (CLO and rapid urease tests)
*95% sens & specificity
*less accurate if on antibiotic or PPI


non invasive H pylori tests

*urea breath tests-first choice to check effectiveness of H.pylori tx-need to be of PPI for 2 week prior to test
*fecal antigen tests-good for primary dx, best test if on PPI to test effectiveness of treatment
*serologic-dont use, poor for checking effectiveness of tx


H pylori treatment

*triple drug -2 antibiotic (biaxin & amox) & PPI
* in US, flagyl less effective due to resistance


universal post treatment testing of H pylori is not recommended unless:

*hx H pylori assoc ulcer
*persistent dyspepsia symptoms
*H pylori assoc MALT lymphoma
*resection of early gastric carcinoma
** test no sooner than 4 weeks after finish treatment


4 causes of peptic ulcer disease

* #1: H pylori-if irradicated, ulcer does not recur
*high acid secreting states-Zollinger
*crohn dz of duodenum/stomach


NSAID induced peptic ulcer disease

*10-40% of patients taking med, many small & no s/s
*gastric & duodenal ulcers
*if has and needs NSAID: enteric coated NSAID,nonacetylaed ones-salsalate; non acidic ones-relafen, PPI or cytotec, COX2


risk factors for NSAID PUD

*first 3 mo of use, high dose, elderly, Hx PUD/UGI bleed,heart dz, concurrent steroids, serious illness, concurrent ASA


smoking and PUD

*exaccerbate duodenal and gastric ulcers
*decreases healing rates
*increase recurrance and perforation rates


Do Not cause ulcers



EGD in PUD if:

*assoc dysphagia or odynophagia
*follow up healing gastric ulcer
*UGI bleed
*foreign body
*family hx duodenal ulcers
*abnl UGI or CT scan


perforated gastric and duodenal ulcers

*often free air in peritoneal space-do upright abd films
*pain is usually severe


absense of an ulcer crater means

there is no risk of hemorrhage, perforation or scarring


tx of nonbleeding PUD

*H pylori treatment
*decrease acid secretion-H2, PPI
*stop smoking, NSAIDS


indications for surgery in PUD

*#1: UGI bleed-unable to stop endoscopically
*gastric outlet obstruction w failed balloon dilation
* perforation
*recur/refractory ulcers
*Z-E syndrome-to remove gasrinoma


causes duodenal ulcers

*H pylori
*Z-E syndrome


causes of gastric ulcers

NOT H pylori assoc
*tx PPI x 3mo as slower to heal
* all non healing ones need EGD w at least 6 bx samples to r/o ca


bleeding peptic ulcers

*#1cause: NSAID
*bleed risk is dose related
*incr risk NSAID->age 60, female
*no perfectly safe dose ASA
*risk bleed on COX2-close to nl pt but if also ASA same as NSAID


dx & tx emergently for UGI bleed



EGD finding that increase chance of rebleed

*larger size of ulcer
*visible vessels on non-bleeding ulcer (incr risk to 50% rebleed)
*visible clot (0%)


ulcer with clean base-no bleed, no clot, no visible vessels

very low chance of rebleed


tx bleeding peptic ulcer

*initial if active bleed, adherent clot, or visible vessel= combo injection epinephrine, saline,alcohol then either thermal or laser coagulation or hemoclip
*incr gastric pH >6: bid dosing PPI IV or po


treatments that do not work for bleeding peptic ulcer

*gastric lavage
*IV vasoconstrictors


non ulcer causes of UGI bleeds

*osler-weber-rendu:hereditary hemorrhagic telangiectasia
*AVM-usually stomach, duodenum
*Peutz-Jegher syndrome-hamartomatous polyps stomach to rectum (see dark melanin spots lips, buccal mucosa, hand/feet)


Zollinger Ellison syndrome

gastrinoma-produce gastrin continuously
*refractory ulcers-duodenal bulb & stomach
* s/s: ulcers, #1presentation-diarrhea, +/- steatorrhea
90% in "ZE triangle":porta hepatis,mid duod.,head pancreas
*80% sporadic, 20% assoc MEN type I


consider Z-E in patient with

*severe esophagitis and chronic diarrhea
*ulcer and chronic diarrhea
*duodenal ulcer + big folds stomach d/t parietal cell hyperplasia
*recur ulcer and no risk factors
*post bulbar duodenal ulcers


dx and tx of Z-E syndrome

Dx: gastrin level off PPI, if increase gastrin: do abd CT, endoscopic U/S, somatostatin receptor imaging
Tx: surg exploration, 1/3 cured by primary tumor resect,even c mets, resect to decr mass effect
PPI at higher doses and long erm


conditions assoc with high gastrin levels

*Z-E syndrome
*vitiligo *gastric carcinoids
*renal failure, hyperthyroidism
*achlorhydria due to PPI use
*chronic type A gastritis


gastric carcinoid

rare,due to chronic hypergastrinemic states(but not shown due to PPI increased gastrin level)
*usually not metastatic or symptomatic
*almost never causes carcinoid syndrome
*autoimmune gastritis,pern anemia, ZE,MEN I,spontaneous


4 types of gastric cancer

*adenocarcinoma 95%
*GIST-gastrointestinal stromal tumor(leiomyosarcoma)


risk factors assoc with gastric cancer

*chronic H pylori
*chronic metaplastic atrophic gastritis
*menetrier dz-lg intest folds due to epith. cell hyperplasia
*adenomatous gastric polyps


acanthosis nigrans

*usually d/t obesity & insulin resistance
*can be due to various GI and lung cancers (gastric ca mostly)



*due to H pylori
*dx-EGD w bx
*when tx H pylori-MALT may resolve


alcohol and gastric ulcers do not cause



tx gastric cancer

*surg resection w adjacent lymph nodes
*adjuvant combo chemo prolongs survival


Postgastrectomy syndromes

*dumping syndrome
*blind loop syndrome
*afferent loop syndrome


post gastrectomy dumping syndrome

*postprandial vasomotor symptoms:palpitation,sweating,lighthead
*early type:30" after eat, unclear etiology
*late type: 90" or more after eating-due to hypoglycemia
*tx both-restrict sweets & lactose, small freq meals


post gastrectomy blind loop syndrome

*bacterial overgrowth in a loop
*manifests: fat & B12 malabsorption
*low D-xylose absorption test


post gastrectomy afferent loop syndrome

*at bypass site, afferent loop still has bile and pancreatic fluids flow
*abd bloating and pain 20-60" after eating
*vomiting often relieves symptoms& see bile colored emesis


gastroparesis in diabetes

more in type I
*longterm DM.slow gastric emptying>incr blood sugar levels due to delay of insulinemic and glycemic response to carbs
*motor dysfxn w N/V, early saity, predisp to bezoars


causes of gastroparesis

*autonomic: diabetes, amyloid neuropathy
*infiltrative process of smooth muscle:scleroderma,amyloidosis
*other:CNS-stress,parkinson,tumor,MS; spinal cord injury or ganglion problem - post vagotomy


work up and tx gastroparesis

*w/up: r/o obstruction first, confirm dx w radioisotope labeled solid meal
*tx; hydration, nutrition, tight glycemic control, metoclopramide or emycin liguid


inflammatory bowel disease comprised of

ulcerative colitis


common factors with inflam bowel dz

*family at incr risk of dz
*incr risk of GI cancer-esp UC
*toxic megacolon-complication-barium enema contraindicated if acute exac of the dz


smoking assoc with IBD

increase risk-crohns
decrease risk-ulcerative colitis



*sulfasalazine-split by bacteria in colon>mesalamine (ineffective if small bowel involved)
*mesalamine (5-ASA):colon dz-rectal enema, proctitis-suppository, oral form for distal ilium/colon
*metronidazole-perianal abscess&fistula in crohn, combo w 5asa in chrone
*budesonide - use specifically for small bowel crohns
*6 mercaptopurine & azathioprine(metab to 6MP)-prednisone sparing drug-use both dz
*remicade, humira,cimzia-monoclonal ab to TNF-a


drugs that decrease relapse rate in crohns

6 MP
*smoking cessation decreases relapse


drugs that decrease relapse rate in ulcerative colitis

all standard drugs
**stopping smoking increases relapses



*any age, most 20-30 and smaller peak 70-80s
*increase risk GI cancer, esp after 20yrs of dz
*screen longterm pts every other year for cancer
*more indolent than UC so less responsive to tx, hard to get off steroids-osteoporosis common


crohn dx

biopsy of ulcer pathognomonic
patchy, focal,apthous ulcers & deep transmural ulcers with occ. strictures, fistulas, granulomas


Tetrad for crohns colitis

*skip lesions
*perirectal disease
*rectal sparing
*contiguous ileocolic disease


"string sign"

classic but uncommon
see on small bowel follow thru for crohns, lumen is edematous and fibrotic so contrast appears as string
*if see elsewhere in colon "apple core"lesion=suggests cancer


bowel involvement in crohns

30%colon only
40% small bowel only
30% both


in 15% of IBD-definate dx cant be made and these labs can help

P-ANCA assoc with ulcerative colitis

ASCA-(anti saccharomyces antibody) assoc crohns


problems related to crohns resection of terminal ileum (not UC)

*calcium ox kidney stones
*pigment gallstones
*B12 def, hypocalcemia-due to Vit D malabsorption
*bile acid induced diarrhea
*nutrient malabsorption


surgery in crohns

*only for intractable dz and serious complicationa
*the worse the dz where surgery is the more likely recur at that site
*colectomy & ileostomy-best result for crohn colitis with no ileal inflammation , >60% no recurrence


ulcerative colitis

*uniform,continuous mucosal inflam w shallow ulcers
*always starts rectum and extends proximally
*area of unvolvement usually remains the same
*70% are pANCA +, ESR & CRP usually elevated
*main symptoms:abd pain, bloody diarrhea


extraintestinal manifestations of Uc (can see in crohns of colon)

*E.nodosum, pyoderma gangrenosum
*peripheral polyarthritis,ankylosing spondylitis
*iritis,episcleritis, uveitis
*venous thrombosis
*pericholangitis, primary sclerosing cholangitis


cancer in UC

risk high 0.5% per year
increase risk with duration of UCand extent of UC-pancolitis high, if only proctitis-no increased risk


colonoscopy in UC

usually after 10 years of UC, then every 1-3 years


tx of UC

complete colectom-cures, not done routinely
medical tx as with crohns with good response rates, 30% remission in 2 mo of tx


indications for complete colectomy in UC

*dysplasia on bx in mass lesion or highgrade in flat lesion
*intractable dz, perforation, growth retardation in kid
*toxic megacolon, stricture
*steroid dependence, exsanginating hemorrhage
*complication from therapy


diarrhea definition

>200-250gm/day of stool
*normal 150-180 gm/d, small volume, loose stool not diarrhea
*acute 4wks


acute diarrhea -causes

*usually infectious-invasive or non-invasive
*food poisoning
*drug side effect


acute diarrhea work up

*diet & travel hx
*check fecal leukocytes-+in invasive, if + do:C&S*c difficile if suspect
*if suspect E. coli 0157:H7 MacConkey-sorbitol agar for stool


tx acute diarrhea

*invasive:general -bactrim, campylobactor-macrolide,amebiasis-flagyl
*salmonella-no abx- they prolong the illness
*Ecoli 0157:H7-abx are contraindicated


chronic diarrhea

*stool total osmolality=serum osm in all types
*secretory diarrhea
*osmotic diarrhea
*increased motility diarrhea


secretory diarrhea

*stool often >1 liter/day,risk electrolyte deficiency
*causes: enterotoxin,e coli, cholera,s.aureus
villous adenoma, gastrinoma, bile acids. VIPomas
microscopic colitis, collagenous colitis
*24-48h fast doesnt decr it except w fatty acid & bile acid diarrhea


osmotic diarrhea

*serum osm >50 gap
*due to nonabsorbable osmotic agent
*24h fast resolves the diarrhea, if persists after fast suspect ingestion of magnesium antacid


common causes of osmotic diarrhea

*#1 lactase deficiency
*Mg++containing laxatives and antacid-esp castor oil
*poorly absorb.CHO-lactulose,sorbitol, fructose
*nutrient malabsorption:pancreatic insuff,celiac dz,bacterial overgrowth


diarrhea due to increased motility

causes: antibiotic assoc (not c diff)-emycin
irritable bowel


chronic loose stools

lactase deficiency


laxative abuse

*urine for bisacodyl,anthraquinones, phenolphthalein
*stool osmotic gap >100 - Mg+ containing
*stool measurement of phosphate & sulfate
*if stool osm is low, pt could be adding water or urine to stool


causes of malabsorption

*decreased small bowel mucosal transport-something wrong with intestinal uptake
* decreased digestion-not enough digestive enzymes


Big 6 labs for work up of malabsorption

(low values of below labs)
*calcium, cholesterol, carotene
*serum iron
*prolonged PT


decreased mucosal transport causes of malabsorption

*celiac dz,tropical sprue
*common variable immune deficiency w hypogammaglobulinemia
*whipple dz, intestinal lymphoma
*eosinophilic gastroenteritis, bacterial overgrowth
*other small bowel disease


Celiac disease (celiac sprue, nontropical sprue)

*common, 1% populaton,d/t gluten-wheat,barley,rye
*autoimmune intestinal disorder>villous atrophy>malabsorption
*can cause growth retardation
*assoc HLA DQ2 & DQ8


extraintestinal manifestations of celiac disease

*#1-iron def anemia-low hgb,MCV, ferritin
*abnormal serum aminotransferases
*dermatitis herpetiformis
*neuro psych, dental enamel defect,prim. intestinal lymphoma


deficiencies caused by celiac disease

*folic acid
*vit D & B12


4 requirements for dx celiac disease

*evidence of malabsorption-steatorrhea,wt loss,iron def anemia
*+antiendomysial Ab or +tissue transglutaminase AB
*positive response to gluten free diet
*abnormal small bowel biopsy


do antibody test for celiac disease in patient with these presentations

*16 y/o with bipolar
*33 y/o with bone pain spine/legs
*28 y/o with purulent papalovesicular eruptions
*30 y/o anemia w low hgb,MCV,Ferritin


only disorder assoc with low ferritin

iron deficiency


collagenous sprue

unusual, possible celiac variant
*bx small bowel:flat mucosa w large masses of subepithelial eosinophilic hyaline material in lamina propria


tropical sprue

*found equatorial areas
*probably infectious etiology
*often pt w megaloblastic anemia
*tx-bactrim x 3-6 months, folic acid alone or w abx


Whipple disease

*rare,<1000 cases,d/t tropheryma whippelii gm+ actinomycele
*cardinal tetrad: arthralgia (#1), abd pain,wt loss, diarrhea
*severe malabsorption w marked decr albumin & neuro s/s
*Dx: EGD w sm bowel bx:foamy macrophages, PAS +
*Tx:pcn or roceph IV x14d then bactrim x 1 year


eosinophilic gastroenteritis

*N/V/D, abd pain,wt loss, albumin wasting,iron def anemia
*often see eosinophilia on CBC (r/o strongyloides that can cause eosinophilia
*tx: corticosteroids x 6wks and avoid causative foods


short bowel syndrome

*occurs after massive bowel resection
*if <100cm sm bowel left-may need TPN for life
*tx;low fat diet, vitamins


malabsorption d/t decreased digestion 2main causes

pancreatic insufficiency
bile acid deficiency


pancreatic insufficiency

*chronic pancreatitis,pancreatic cancer, cystic fibrosis
*see undigested muscle fibers in stool exam
*confirm: + response to tx w pancreatic enz, or d-xylose absorp
* do CT scan to r/o pancreatic cancer if >age 55


bile acid deficiency

*ileal resection >100cm,or ileal dz or dz that decreases bile acid uptake, severe liver dz, ZE syndrome, bacterial overgrowth


best indicator of malabsorption

steatorrhea >14g/d of fecal fat
*sudan stain stool-best screening for fat
*gold standard-3 day quanitative fecal fat


steatorrhea due to pancreatic insufficiency

>40 g/d fecal fat


Irritable bowel syndrome

*15% population, female
*s/s: freq sm stools w mucus, abd pain relieved by BM
*Dx: exclude others-celiac, lactose intol..., look for chara s/
*Tx: *reassure,fiber,probiotics,antispasmotic, TCA, loperamide, amitiza for constipation prominent IBS


colon cancer risk factors:
*4% lifetime risk
*age >50, obesity, smoking
*Hx adenomatous polyps
*UC, crohns

*BRCA1 mutation
*fam hx colon ca,,familial polyposis syndr, hereditary nonpolyposis colon cancer
*diet high in calories and animal fat


red flags for colon cancer

*anorexia, wt loss, anemia, fever, heme + stool
*change in bowel habits-esp nocturnal BM
*onset of symptoms after age 45


endocarditis due to this organism is often associated with colon cancer and need work up

**strep bovis or clostridium


full dose ASA helps decrease risk of

colon cancer


colon adenomas with advanced features

*high grade dysplasia
*villous histology
*size >10mm


colon adenomas

*need follow up. only 1% ever become malignant but most GI cancers arise from adenomas

**hyperplastic polyps <1cm -no incr risk- 10 yr follow up as normal


guidelines colon adenomas

1-2 sm tubular adenoma w low grd dysplasia-re ck 5-10 years
3-10 adenoma, or 1 adenoma>1cm,any villous feature or high grade dysplagia-re ck 3 years
>10 ademomas-re ck 3 years
sessile w piecemeal removal-re ck 2-6 mo to verify removal


Inherited colon cancers

*Familial polyposis syndrome:(all autosomal dominant)
familial adenomatous polyposis, Gardner syndrome, Peutz-Jeghers syndrome, Juvenile polyposis
*Hereditary nonpolyposis colon cancer: Lynch syndrome


Familial adenomatous polyposis

*100s of adenomas in colon
*100% risk of cancer if not tx
**MUST have proctocolectomy by age 20!
*cont to monitor as often get duodenal cancer from polyps


Gardner syndrome

*variant of familial adenomatous polyposis
*100% risk of cancer-tx same as above
*often see soft tissue tumors & bone lesions - osteomas, so if see these do colonoscopy


Peutz-Jeghers syndrome

*multiple hamartomatous polyps t/o small bowel, occ colorectal and stomach
*melanotic pigmentation (freckles) on lips and buccal mucosa
*benign tumors but 50% risk cancer by age 60


Juvenile polyposis

*no malignant potential and no special follow up needed


Hereditary nonpolyposis colon cancer (Lynch syndrome)

*definition: occur of colon ca in at least 3 1st degree relatives over at least 2 generations & one of those dx *females in these families higher risk ovarian and endometrial cancer, also renal,urethral,stomach,pancreas, biliary tree cancer
*start screening age 25


colon screening

yearly fecal occult blood testing in low risk pt but misses 1/3 of advanced cancers


colon screening in asymptomatic pt =/> age 50 with negative family history

*colonoscopy every 10 years
OR one of these every 5 years:
*flex sig
*double contrast BE
*CT colonography


adenomatous polyp on screening colonoscopy

re check in 3 years


"10 year" rule for colonoscopy screening

*high risk patients-start 10 years earlier than age of person in family with colon cancer or age 40-whichever is first


Indications for colonoscopy

*occult bleeding,iron def anemia without other explanation
*gross lower GI bleed (except BRB in young person), abnl BE
*adenomatous polyp, 1st degree relative w colon ca, familial syndromes,ischemic colitis,persistent diarrhea,4-8wk after onset presumed new diverticulitis, strep bovis/clostridium bacteremia


CEA testing

*only for checking for recur of colon cancer and only if it was elevated before surgery and declined after surgery


Colon cancer staging TNM

*stage 1: T1 cancer into submucosa,T2 into muscularis
*stage 2: T3 into tissue,T4a visceral peritoneum,T4b direct invasiv
*stage 3: as above plus + nodes (no mets)
*stage 4: + nodes and + distant mets


colon cancer always mets first to

liver via portal cirulation

*exception is RECTUM-blood supply bypasses portal circulation so no liver mets


rectal cancer metastasizes to

Lung, bone, brain
* not to liver


tx colon cancer

*tx choice - surg resection-potential cure
*radiation then surg-ONLY RECTAL cancer
*adjunct chemo -only stage 3 orr locally adv 2-FOLFOX
*solitary liver mets-hepatic resection-improve survival


if remove cancerous polyp MUST do

bowel resection if it extends to either blood vessel or cautery line


most common cause of colon bleed in elderly

*diverticular bleeding
*#2: angiodysplasia-more severe bleeding usually-us. stops spont.


tx and dx diverticular bleed

*r/o UGI source w NG aspirate or EGD
*colonoscopy only if bleed doesnt stop
*DX:severe or continued bleeding-colonoscopy or taged RBC scan angiography


Indications for angiography in GI disease

*chronic & acute mesenteric ischemia
*severe lower GI bleed
*some duodenal ulcers or rare UGI bleed
*TIPS in variceal bleed
*tx use:embolization, vasopressin


diverticulitis usually due to



usual s/s of diverticulitis

LLQ pain
increased WBC
(no bleeding)


dx diverticulitis

CT most useful-thickened sigmoid colon, colic fluid

**No colonoscopy


cause of 50% all GI bleeds in children

Meckel diverticula- can cause obstruction & intussusception

*Dx: technetium scan


angiodysplasia and lower GI bleed

*usually R colon-cecum, ascending


Hereditary hemorrhagic telangiectasis (Osler-Rendu-Weber)

*multiple AVM's all organs-brain,lung,skin,m membr,GI tract-esp Upper GI
** these people have history of epistaxis


Ischemic colitis characterized by

abdominal pain
maroon stools


video capsule endoscopy

*use when EGD & colonoscopy negative and pt has some form of GI bleeding, looks at small bowel or occult bleed


#1 cause of small bowel obstruction

adhesions from prior surgery


3 most common causes of colon obstruction



dx bowel obstruction

*flat and upright abdominal films: excess air in small bowel and no air in colon-air fluid loops


tx bowel obstruction

IVF,, NG suction. work up if not resolved 1-2 days


4 types of intestinal ischemia

*ischemic colitis
*chronic mesenteric ischemia
*acute mesenteric ischemia
*mesenteric venous thrombosis


Ischemic colitis

*nonocclusive-inferior mesenteric-esp splenic flexure to sigmoid
*most no specific cause
*s/s:sudden LLQ pain, urge to defecate then pass red/maroon
*KUB-thumbprint, DX-CT
*TX:bowel rest, abx, fluids


chronic mesenteric ischemia "intestinal angina"

*classic triad: wt loss, abd bruit, abd pain p meals-pain out of proportion to exam-1-3hrs of dull, gnawing pain shortly p eat
*dx:symptoms, MRI or CT angiogram
*Tx: surgical bypass or angioplasty


acute mesenteric ischemia- do angiography unless perforation thenbowel resection and possible embolectomy

*MORTALITY 70% even with treatment-d/t acute loss of blood flow to part or all small bowel and ascending colon (emboli #1)
*often chronic intestinal angina then develop acute illness w N/V/D and occult blood-bowel infarct>acidosis, incr lactate and incr amylase


Meseneric venous thrombosis

*assoc with hypercoag. states
*dx CT scan
*tx: acute-thrombolytics & long term anticoag.


causes of acute pancreatitis

*#1-alcohol abuse. #2 gallstones
*ERCP,DKA,hyper TG, hyper CA+,trauma, pancr ca,CF,hereditary
*drugs:valp.,hypogly,TCN,sulfa,lasix , HCTZ,estrogen,HIV meds, 5-ASA meds , azothioprine


acute pancreatitis lab

amylase >3x early is usual and decr in 2-3 days of onset
lipase elevates slower but stays incr 7-1 days


hyper TG and acute pancreatitis

TG>1000can cause pancreatitis but high TG can also cause a spuriously normal amylase level


severity of pancreatitis

directly relates to degree of pancreatic necrosis (10% have necrosis) and whether the necrotic tissue gets infected
*overall mortality 5-10%


severe pancreatitis can cause multisystem organ failure and will likely see

P02 <3.2


assessing severity of acute pancreatitis

*erythema of flanks-extravasated pancreatic exudates
*severe necrotizing-Cullen sign-faint blue periumbil.=hemoperitoneum. Grey-Turner-blue to purple -brown discoloration flank=catabolism of hemoglobin =retroperitoneal blood dissecting along tissue planes


scoring system for pancreatitis severity: BISAP

Bun >25
Impaired mental status
Age >60
Pleural effusion


SIRS-systemic inflammatory response syndrome
*easy to do bedside & repeated daily
*categorizes severe illnesses in general
*requires 2 of the following

*T 38
*HR> 90
* RR >20 or PCO2 12K or 10% bands


independent risk factors acute pancreatitis

BMI >30-mortality incr 2 times
Hemoconcentration >44%
age >75
organ failure


pancreatic necrosis confirm with

dynamic CT or MRI


Fluid/masses in acute pancreatitis

*acute fluid collection
*necrotic tissue
*infected necrosis


acute fluid collection in acute pancreatitis

50% within 48hr of pain onset
symptomatic transudative Left pleural effusion freq. occurs and resolve spontaneously


necrotic tissue in acute pancreatitis

*onset 1-2 weeks
*differentiate from pseudocyst by ultrasound
*serious and may need drainage


infected necrosis in acute pancreatitis

* usually need endoscopic or CT guided drainage or surgery within 2 weeks
*DX: CT guided aspiraion and bacterial smear and culture



* think this in pt recovering normally from pancreatitis and suddenly gets worse

*develops in 10-15%
*requires about 4 or more weeks after acute attack
*small-spont resolve
*>5 cm-may not resolve, if persists >3-6 mo surg drainage


pseudocysts can be assoc with serious complications, they need removal if not resolving

*rupture- 15% mortality
*hemorrhage w rupture-60% mortality


abscess assoc with acute pancreatitis

*4-6 wks after onset of acute with severe pancreatic necrosis
*"soap Bubble" sign on upright KUB
*very serious with fever and shock
*Dx: CT guide aspir, immed surgical debridement and drainage


in acute pancreatitis, if amylase is still increaed by day 10, something else is going on like:

leaking pseudocyst
pancreatic duct leak


recur of pancreatitis and no hx of alcohol and no gallstones, think

microlithiasis and consider cholecystectomy


gastric varices without esophageal varices ONLY occurs in

splenic vein thrombosis- a complication of severe acute or chronic pancreatitis


with pancreatitis, ERCP not done acutely unless

sepsis or cholangitis


criteria to resume oral feeding with pancreatitis

*bowel sounds present and passing gas/stool
*not requiring narcotics
*pt expresses hunger


conditions that cause abdominal pain and incr amylase

*acute pancreatitis and cholecystitis
*intestinal infarction, perforated ulcer
*salpingitis, ectopic pregnancy


causes of chronic pancreatitis

#1 chronic (>10 yr)alcohol abuse -70%
idiopathic 30%
hereditary 10%
*rare: autoimmune, hyperparathyroid, cystic fibrosis


Dx chronic pancreatitis - triad

*pancreatic calcification
only see <20% and is late stage disease


dx chronic pancreatitis,start with CT abdomen, positive if

see calcification, atrophic pancreas, dilated pancreatic duct
*if CT nondiagnostic and still suspect-MRCP (preferred over ERCP) or ERCP-as MRCP doesnt cause pancreatitis as ERCP can. positive will see large duct dz , "chain of Lakes" appearance


most sensitive test for pancreatic function

secretin test-not done much=complicated


complications of chronic pancreatitis

*persistant and severe abd pain
*4% develop pancreatic cancer after 20 yrs of the disease
*gastric varices,B12 malabsorption, jaundice,pleural effusion
*brittle DM-prone to hypoglycemia-but dont get retinopathy or nephropathy unless they are alcoholic as cause


skin condition assocc with chronic pancreatitis

tender red nodules due to fat necrosis-similar to erythema nodosum


TX chronic pancreatitis

*pancreatic enzymes:minimun 20,000 u lipase per meal
*decr dietary fat, add medium chain TG to diet
*stop alcohol and smoking
*short term opiods with amitryptyline if that fails, little will help


autoimmune pancreatitis

*2X normal
TX: steroids


pancreatic cancer

80% present with advanced disease


risk factors for pancreatic cancer

*smoking 2X risk
*pancreatic cancer in two 1st degree relatives
*chronic or hereditary pancreatitis


pancreatic cancer usually presents with

*abdominal pain
*weight loss


dx pancreatic cancer

helical CT
CT angiography
endoscopic ultrasound


Tx pancreatic cancer

*resection-only hope for cure-whipple
*chemo may incr survival few months
*ERCP only use in this is to stent for biliary obstruction



*glucagon secreting alpha cell tumor of pancreas


Unique clinical findings of glucagonoma

*scaly necrolytic erythema
*persistent hyperglycemia
*plasma glucagon >1000
*weight loss



very rare
insulin secreting beta cell tumor of pancreas



see in Z-E syndrome, 24% occur in pancreas



2/3 occur in pancreas
>50% malignant
DX: incr serum VIP level and hypokalemia



usually asymptomatic
not assoc with high cholesterol
80% are radiolucent cholesterol stones


cholelithiasis assoc with

*clofibrate treatment
*ileal disease or resection


Dx cholelithiasis

*HIDA-best to confirm acute cysic duct obstruction


tx cholelithiasis

*surgery only if symptomatic
* in those can do surgery-ursodeoxycholic acid(oral bile acid)


acalculous cholecystitis

*only see in seriously ill-major trauma,burns, surgery
*Dx-ultrasound or CT-large, tense thick GB, no stones


common duct stone

*incr alk phos and bili >4 - suggests it
*can see in post chole pt with persistent pain
*can cause cholangitis
*TX: ERCP possible endoscopic sphincterotomy



*can be obstructive (common duct stones) or hepatocellular
*both see retention of substrates that normally are released into bile
*see incr LFT,incr alk phos, incr conjugated bilirubin, bilirubinuria



*common complication of common bile duct blockage-stone or cancer
*acute-see Charcots triad: biliary colic, fever/chills, jaundice


suppurative cholangitis

charcot triad plus:mental confusion, bacteremia, septic shock
*DX/TX: ERCP w sphencterotomy or surgery if ERCP not available.
*antibiotic to cover anaerobic &aerobic - NO ROCEPHIN-can cause biliary sludge and no anaerobic coverage


Porcelain gallbladder

xray-calcified outline of GB
**suggests CANCER
TX: open cholecystectomy needed


primary biliary cirrhosis

*slow onset, etiology unknown, usually mid aged females
*chara: non supperative, progressive, destructive cholangitis
*some are hereditary, 70% have altered immunity
*chronic bile duct inflammation>obstr. jaundice and liver cirrhosis


Hallmark of primary biliary cirrhosis

90% have + antimitochondrial antibody (>1:40)
*degree of elevation does NOT correlate with disease severity


symptoms of primary biliary cirrhosis (symptoms develop but disease is already advanced when they develop)

*fatigue, itching(esp palms and soles first)
*high alk phos
*eventual:jaundice, hyperpigmentation,inflam arthropathy, keratoconjunctivitis &/or xerostomia. accelerated osteoporosis


prognosis of primary biliary cirrhosis

*about 10 yr after onset symptoms
*if bilirubin is at 10, most die shortly unless liver transplant


Dx & Tx primary biliary cirrhosis

Dx: liver bx-granulomas, **high hepatic copper level
Tx: urosodiol-improves LFT & decr symptoms-doesnt slow dz
*Puritis-cholestyramine tx,oteomalacia-vit d and calcium.
malabsorption -decr diet fat, add med chain TG
*late dz-liver transplant


Primary sclerosing cholangitis

*develop inflam and sclerosis of entire biliary tract>obstr jaundice>cirrhosis
*indolent, cause unknown
8-15% develop cholangiocarcinoma


90% of patient with primary sclerosing cholanitis have

**ulcerative colitis-**screen all with PSC with colonoscopy!!
can also be seen in crohn dz of COLON
**screen all patients for PSC if alk phos >2X normal
average pt : male (70%), age 45


symptoms (only in advanced dz) of PSC

weak, fatigue
abdominal pain


Dx of primary sclerosing cholangitis

*ERCP, transhepatic cholangiography
see "beaded"appearance
**liver bx: "onion skin" fibrosis in portal triads


Tx primary sclerosing cholangitis

liver transplant only-no ursodiol


secondary causes of sclerosing cholangitis

*bacteria-stone or bile duct stricture
*atypical anatomy-congenital or prior surgery
*bile duct neoplasms
*AIDS assoc cholangiopathy


more specific liver enzyme



alcoholic hepatitis

alcohol damages mitochondria which are the source of AST


viral hepatitis

ALT>AST-more toxic to liverr



ALT/AST ratio >2:1


histologic features of acute viral hepatitis

*diffuse liver cell injury and swelling
*increased macrophages
*accelerated apaptosis-the normal programmed cell death
*inflammatory periportal infiltrate


histologic features of chronic viral hepatitis

*interface hepatitis - PIECEMEAL NECROSIS


if see elevated liver enzymes, order

*alk phos, recheck LFT
*total and direct bilirubin, albumin
**if still elevated, do Hep A-B-C, iron & ferritin


since alk phos comes from bone and liver, to determine if liver do

GGT-it parallels alk phos form liver


next in eval of incr LFT

ultrasound of abdomen
do antimtochondrial antibody of indicated


first marker of hep B

HBsAg-patient producing hep B virus-acute or chronic, if + means past exposure or vaccine, usually indicates "cure"



appears early in disease and persists for life- IgM then IgG


best marker of previous exposure to HBV (doesnt tell if active or cured)




*making hep B virus and highly infectious if +
* appears several weeks after the illness
*quantity of intact virus


these 2 hep b markers indicate active disease and highly infective



only hepatitis composed of DNA

hepatitis B


incubation for hepatitis B

1-6 months
*window between HBsAg turning positive can be this long, must do HBcAb IgM to confirm acute Hep B


lab marker to confirm acute Hep B



Hepatitis B is strongly assoc with

PAN-polyarteritis nodosa-30%


prodrome symptoms of hep B

*fever, arthritis,urticaria, angioedema
*above resolve as pt develops jaundice, elevated LFT with liver swelling and tenderness



if given in hep B helps decrease severity of illness only but doesnt protect from the disease
*effective prophylaxis when given early


Hep B vaccine

*composed of HBsAg- 2 types of vaccine, both = effective and safe in pregnancy
*give both to household contacts and partners (HBG & vaccine)


several months after Hep B infection, check these markers to be sure not chronic Hep B state

*loss of HBsAg


chronic hep B two types of carrier states

*inactive carrier-if get immunocompromised can get severe disease>ie develop cancer of some type and on chemo can get active dz so drug LAMIVUDINE is given with chemo in these pts to blunt viral replecation
*chronic active hepatitis


confirm dx of chronic hep B

liver biopsy


chronic hep B is

*serious illness
*often >cirrhosis
*strong assoc Hepatocellular carcinoma-20% lifelong risk
is screened for with AFP and ultrasound every 6 months


who to treat with hepatitis B

*all with HBV-DNA >20,000 and ALT > 2x normal
*HBeAg (-) start immediate tx
*new dx HBeAg (+) delay tx 3-6 mo to see if seroconvert
*if cirrhosis: tx if HBV DNA >2000(compensated) or >200 (decompensated)


tx chronic hep B

*interferon:35% complete remission, S/E may be severe, esp if young and wanting pregnancy
*Lamivudine-safe in preg, high rate drug resistance
*liver transplant-only end stage-tx new liver with antivirals


Hepatitis A

*RNA virus,fecal-oral transmission, can be sexually transmitted
*No carrier or persistant states
*incubation 15-50 days
*onset jaundice is 3 weeks (3 months in HepB)
*vaccine 2 dose 6 mo apart age 2,mark decr risk


DX Hepatitis A

*acute: high anti HAV IgM
*prior Hep A: anti HAV IgG (+) in prior disease and in vaccinated


indications for HAV vaccine

*high risk sexual behavior, IVDU
*all >age2
*chronic liver dz, all pt with Hep C ( If they get hep A can be fulminant)
*travel to high risk countries


Hep C

*ssRNA virus
*#2 most common liver disease (#1 is NAFLD)
*90% transmittted prior to 1990s
*#1 genotype in US: genotype 1


those at risk for Hep C

*IVDU,prisioners, needlesticks
*tatoo, piercings,shared razor, toothbrushes
*renal dialysis personnel
*snorting cocaine,high risk sex,w prostitute/STD
*blood transfusion prior 1990


Hepatitis C "Rule of 2's" (2%)

*US population
*risk with needlestick transmission
*risk neonatal transmission
*risk spouse transmission
*cirrhosis w hep C develop hepatocellular ca/yr (aka hepatoma)


HIV & Hep C

*30% pt with HIV are coinfected with HCV
*progress faster to cirrhosis
*best tx:interferon & ribavirin


extrahepatic disease with HCV

*small vessel vasculitis w glomerulonepritis, neuropathy
*mixed cryoglobulinemia
* porphyria cutanea tarda-only assoc with hep C


porphyria cutanea tarda

ONLY assoc with Hep C- so if see skin blisters-think Hep C


Hep C serology

*2-4 mo p episode hepC : check i loss of HCV RNA (PCR)to ensure hasnt become chronic
*in pt HCV Ab (+), check for active virus w HCV RNA


Chronic Hep C

*70-80% acute HCV become chronic!!
*hep C viral counts are lower so mor insidious nature: only 25% acute infections are symptomatic
*low transmission sexually in monogamous couples: 2% after 10-20years


chronic hep C

25% only carriers
50% no symptoms but abnormal LFT
25%chronic disease with symptoms-end stage cirrhosis after 20-25 yrs
1-4% of those w cirrhosis develop hepatocellular Ca / year


screening for hepatocellular carcinoma (HCC)

*AFP and ultrasound of abdomen every 6 months

*same for chronic hep B , Hep C and alcoholic cirrhosis


#1 cause of liver transplant in the US

chronic hep C


55% w chronic hep C have mixed cryoglobulinemia and presents with small vessel vasculitis w "palpable purpura" crops of purple papules. also see mixed cryoglob in

chronic hepatitis
chronic liver disease
connective tissue disease


Tx chronic hepatitis C

peg INF alpha injections and oral ribavirin (also decr risk HCC)
*measure response to tx w HCV RNA-if no response @12 wk D/C
*if (+) response, tx genotype 1 for 1 year, type 2 & 3 tx 6 months


hepatitis E

*fecal/oral-water p monsoon flood. no chronic form
*VERY high risk fulminent hepatitis in 3rd trimester preg-20%fatal
*acute hep in traveler and negative hep A & B think E


autoimmune chronic hepatitis

*insiduous onset, young female, 50% have other alt immunity
*Dx:liver bx , r/o other dx with labs
Tx:rapid reversal of symptoms, incr survival w prednisone +/- azathioprine(steroid sparing) **INF alpha-contraind-makes worse
No cure. Px freq progress cirrhosis, some HCC, transplant endst


drug related chronic hepatitis:

*lab often +ANA,hypergammaglobulinemia
TX-stop med

*OCP,MTX,acetaminophen, trazadone,nitrofurantoin,methyldopa,valproate,emycin,halothane,INH -but more common for it to cause acute hepatitis


#1 cause of fulminant hepatitis in the US

acetaminophen toxicity


acetaminophen toxicity

*metabolism:90% glucouronidation path, 5% cP450>NAPQI that is toxic intermediary that is rapidly reduced by glutathione.
*w OD glutathione is depleted rapidly and toxic liver by NAPQI
*w chonic acetam,alcohol,malnutr,illness, normal dose toxic as those conditions produce more NAPQI thats rapid reduced


lab that is disproportionately high in alcoholic is

GGT as alcohol induces it
*also see : AST/ALT ratio 3:1
AST always <300


OCP assoc with these liver conditions

*benign hepatic adenoma
* peliosis hepatis-blood filled sinusoids
*focal nodular hyperplasia of liver
** young female on OCP w liver mass -likely adenoma


aspirin and Reye's syndrome

*always *assoc w influenza,chicken pox and concurrent aspirin (other virus
*fatty liver and progressive encephalopathy-
*lab: incr AST,ALT,PTT,NH3 and hypoglycemia-due to severe liver failure


other causes of chronic hepatitis

*wilson disease
*alpha 1 antitrypsin defic


Non alcoholic fatty liver disease- NAFLD aka NASH

*pattern opposite of alcoholic liver disease:
* higher fibrosis


NAFLD assoc with

*obesity, diabetes, protein malnutrition, hyperlipidemia,prolonged IV
*amiodarone, corticosteroids, hyperalimentation
*DROP aka metabolic syndrome


DROP- metabolic syndrome

*insulin Resistance
*increased blood Pressure



*all factors can modify/ control
*low fat diet
*avoid alcohol


Hepatocellular canncer - hepatoma

* 75% have cirrhosis, chronic liver any cause can do this
*assoc with aflatoxin-in raw peanuts -esp asia
*80% incr AFP
*interferon alpha tx of chronic hep C decr risk of HCC


Hepatocellular carcinoma assoc with

tender hepatomegaly
bruit in RUQ, bloody ascites
incr alk phos, incr AFP, hypercalcemia, hypoglycemia,
water diarrhea
Fever unknown origin


causes of cirrhosis

*#1 alcohol, Hep B or C, biliary dz, alpha 1 antitrypsin deficiency
*hemochromatosis, wilson dz, schistosomiasis
*post necrotic-ie drugs, toxins
*severe prolonged right side CHF


stigmata of cirrhosis

*hepatosplenomegaly, jaundice, ascites
*caput medusae, telangiectasis, palmar erythema,fetor hepaticus
*male:gynecomastia, atrophy of testes
*asterixis-hepatic encephalopathy
*clubbing-biliary causes of cirrhosis


complications of cirrhosis

*esophageal variceal hemorrhage
*hepatic encephalopathy
*hepatorenal syndrome
*prolonged prothrombin time


esophageal variceal hemorrhage

*1/3 w varices bleed, 1/3 of bleeds die
*prophylaxis of pt with varices:propranolol w/wo isosorbide dinitrate-give to all with large varices, no prophyl. if small one
**only large varices bleed


active variceal bleed

*primary tx:endoscopic band or sclerotherapy-somastatin,octreotide are splanchnic vasoconstrictors and used endoscopically.
*prophylactic antibiotic to prevent SBP
*prevent rebleed-propranolol or nadolol



*rare use, major complication is encephalopathy
*only use in those that rebleed or for ascites d/t cirrhosis
*it decompresses portal vein


hepatic encephalopathy can be precipitated by

*GI bleed, hypovolemia,hypoxia
*incr dietary protein
*alkalosis,infection, sedatives, tranquilizers


signs of hepatic encephalopathy

*fetor hepaticus-unique musty odor to breath and urine
*altered mental status


Tx hepatic encephalopathy

*restrict dietary protein
*lactulose-in GI it inhibits bacterial growth which decr NH3 production so is inactive NH4
*neomysin or flagyl/rifampin/vanco used more now
*acarboise, probiotics


hepatorenal syndrome

renal failue due to renal vasoconstriction during severe, uncompensated cirrhosis
*usually fatal
**urine sodium is very low in this disorder


causes of hepatorenal syndrome

*diuretics, NSAIDS,aminoglycosides, IV contrast
*GI bleed


Tx hepatorenal syndrome

careful volume management
*midodrine - (alpha 1 agonist )plus octreotide (stimulates fluid absorption from GI)


prolonged prothrombin time in alcoholic

*malabsorption of vitamins, including vit K>prolonged PT
*easily corrects with vit K IM


causes of ascites

*CHF,constrictive pericarditis
*cirrhosis,alcoholic hepatitis, fulminent hepatitis
*hepatic veno occlusive dz-incl Budd Chiari
*hypoalbuminemia,chylous ascites,pseudochylos
*myxedema,nephrogenic, pancreatic pseudocyst, duct obstr


cirrhosis induced ascites

*acidic fluid is resorbed via peritoneal surface at a max of 900cc/d so if draw off more than that its at the expense of intravascular volume


chylous ascites

*due to lymph blockage:trauma, tumors (esp lymphoma), TB, filariasis


Dx ascites

peritoneal fluid analysis,cellcounts, albumin, protein


coloration of peritoneal fluid

*bloody-consider tumor
*milky-lymphatic obstruction


peritoneal fluid cell count >250 PMN

do C & S and start antibiotic


SAAG > 1.1 (serum ascites albumin gradient)
*low albumin
*portal HTN

* #1-cirrhosis, Budd Chiari syndrome
*fulminant liver failure


SAAG <1.1
*high albumin
*no portal HTN

*TB peritonitis
*nephrotic syndrome
*peritoneal carcinomatosis


ascites protein level = or > 2.5

*TB peritonitis, bacterial or fungal peritonitis
*nephrotic syndrome
*peritoneal carcinomatosis


ascites protein level <2.5

*cirrhosis, liver failure
*Budd Chiari


spontaneous bacterial peritonitis (SBP)

*peritoneal fluid >250 PMN
*e.coli, s.pneumoniae, klebsiella
**may NOT have abdominal pain


ascites with any of following, consider SBP

*new onset confusion
*renal failure
*hepatic encephalopathy


risk factors for SBP

*acites protein <1.0
* hx variceal bleed
*hx prior SBP
**those at risk need intermittent (preferred) or continuous antibiotic prophyl-Quinolone or bactrim


initial tx of new onset ascites or with severe refractory ascites

*can do up to 4 liters/d if renal function normal and no gi bleed, sepsis or encephalopathy. give 8gm albumin for each liter removed with large volume paracentesis
*give IV abx in life threatening ascites



main finding in hereditary liver dz
*unconjugated bili too bound and complex too large for glomerulus
*conjugated less bound to albumin and 5% unbound easily passed into urine



only from conjugated hyperbilirubinemia=its an indication of cholestasis-see post op usually benign


unconjugated bili=indirect=no bili in urine

see above


Gilbert syndome

*7% population, chronic, benign, mild unconjugated hyperbilirubinemia, jaundice on & off due to physical stress,fasting, and alcohol ingestion
*Dx:incr unconjug. bilirubin after prolonged fast
Tx-none needed


alpha 1 antitrypsin deficiency

*autosomal recessive
*chronic hepatitis>cirrhosis
*Dx: electrophoresis
Tx: liver transplant-does NOT recur


2 types of hemochromotosis



acquired hemochromotosis

*due to mult blood transfusions or iron loaded chronic anemia with secondary erythroporesis (sideroblastic anemia or thalassemia)
*most age 40-60


genetic hemochromatosis

HFE gene, autosomal recessive


symptomatic hemochromatosis

most in males (10X) due to menses in female with iron loss


both types of hemochromotosis see increased intestinal iron absorption>

*deposits in tissues>
fibrosis and organ damage>
heart, liver,pancreas, pituitary


clinical findings in hemochromotosis

*hepatomegaly 95%
*gray hyperpigmentation 90%
*secondary DM 65%-suspect >50y new diabetic
*arthropathy-esp 2nd & 3rd MCP joint wrist 40%
*secondary hypogonadism-depresses hypothal-pit axis
*30% risk HCC in pt with cirrhosis
*heart involvement 15%


Dx hemochromatosis

*suggested by:high iron, high ferritin, high transferrin levels
*transferrin sat >45% most helpful
*confirm: liver bx and staging of fibrosis **do bx ferritin >1000
*confirm hereditary type: HFE gene assay


tx hemochromatosis

*if early-no cirrhosis>normal life w tx/monitoring
*initial tx-weekly phlebotomies then 4x/yr
*GOAL: ferritin 50-100
*most symptoms of dz return to near normal, loss of secondary sex characteristics do not return to normal


Wilson disease

*autosomal recessive
*present most age 15-25
*due to impaired excretion of copper into bile>excess copper in body tissue


S/S wilson disease

*liver disease
*neurologic/psych dysfxn in adolescent
**Kayser-Flescher rings-brown corneal ring PATHOGNOMONIC


Dx wilson disease

Screen: (*confirm dx:liver biopsy (PBC & PSC have incr copper also)


wilson dz treatment

*Phase I: decr copper level by chelation-penicillamine *Must give pyridoxine with this drug!! or tx trientine if pen. not tol,or give zinc
*Phase 2: maint w lower dose of above me
*liver transplant-CURES
*low copper diet


fulminent wilson disease

*severe hemolytic anemia
*high copper level due to release copper from liver
**Penicillamine NOT effective
*ONLY TX: liver transplant


AVOID these foods in wilsons due to high copper content

NO: nuts,peas,chocolate,mushrooms, shellfish,liver


liver dz in pregnancy

*1st trim: hyperemesis gravidarum-mild incr AST/ALT,N/V &dehyd
*2nd trim:best time for GB surg if severe symptoms
*3rd trim:Hep E-fulminent hepatitis
Fatty liver of pregnancy-very serious,microvasc fat deposit in liver as in Reye's syndrome


Fatty liver of pregnancy presentation

*modest incr AST/ALT/bili, hypoglycemia,renal failure
*pre eclampsia,pancreatitis
**Must deliver the baby


Intrahepatic cholestasis of pregnancy

*causes itching
*incr alk phos, incr bili, incr AST/ALT


contraindications-absolute-to liver transplant

*pre-existing advanced or uncontrolled non liver disease
*active drug or alcohol abuse
*life-threatening systemic disease
*metastatic cancer
*many relative contraind-especially advanced age


indicators seen in end stage chronic liver disease

*bilirubin 10-15, albumin 3-5s above normal
*intractable pruritis, hepatic encephalopathy
*bacterial peritonitis
*intractable ascites
*development of HCC


DDX jaundice

*viral hepatitis, alcoholic liver dz,gallstones & complications
*sickle cell dz, PBC, PSC
*drug induced, chronic hepatitis, pancreatic cancer
*gilbert syndrome
*ascariasis-esp recent foreign travel & incr eosinophil count


most with jaundice fall into 3 main groups

*acute viral hepatitis-esp *chronic cirrhosis-most age 40-60
*obstructive jaundice-most age 60-80


work up of jaundice: careful history, liver panel, ultrasound with U/S results determining next step as below

*dilated ducts & stones: ERCP
*dilated duct to pancreas & no stone: CT scan
*dilated intrahepatic ducts: CT scan
*dilated duct to r/o PSC: MRCP
*no dilated ducts: liver biopsy


deficiency of water soluable vitamins B,C and mg++ causes

*muscle stiffness and cramps
*crohns patient may see tetany


zinc deficiency

*poor wound healing


copper deficiency

*hypochromic, microcytic anemia


vit k deficiency

*prolonged PT


selenium deficiency

*hemolytic anemia


chromium deficiency

*glucose intolerance
*peripheral neuropathy


vitamin B1 deficiency (thiamine): beriberi

*usually alcoholic or chronic dialysis patient
*WET beriberi:heart failure,ascites,peripheral edema common
*DRY:peripheral neuropathy (symmetric sensory, motor or reflex loss), wernicke encephalopathy, Korsakoff syndrome


Wernicke encephalopathy symptoms

*mental deterioration


Tx wernicke encephalopathy

*medical emergency
*immed. thiamine 50mg IM or IV daily
*glucose may precipitate it so see in closet drinker who comes in sick and give glucose and develop symptoms
*thiamine usually cures this


Korsakoff Syndrome symptoms

*poor recent memory and learning
*only 50% reversible with thiamine and only 25% fully recover


vitamin B2 ribaflavin

*normocytic normochomic anemia
*sore throat with hyperemic mucosa and glossitis
*cheilosis, angular stomatitis
*seborrheic dermatitis-esp perineal and scrotal
Tx reverses symptoms


Vit B6-pyridoxine

*general malabsorption syndromes
*chronic alcoholic, Meds : INH, cycloserine, penicillamine
*symptoms: seizures, vomiting, glossitis, cheilosis


vit B12

*macrocytic anemia
*smooth tongue
*subacute,combined degen. of sp cord-initial pin-needles then decrease vibration and proprioception stocking glove


Niacin (nicotinic acid) causes pellagra

not vitamin, made in body from tryptophan
*is in grain so rare
*see deficiency in carcinoid (uses tryptophan) and INH tx


S/S pellegra

* 3 Ds: dementia, diarrhea,dermatitis
*glossitis-"bald tongue". stomatitis
*some may have hyperpigmentation


vitamin C-ascorbic acid-scurvy, symptoms

*petechial hemorrhage and ecchymosis first then
*hyperkeratotic papules around hair follicles
*sjogren syndrome,hemorrhage into muscle and joint, purpura
*splinter hemorrhages
*child:bone formation and intracerebral hemorrhage


vitamin A deficiency

*major cause of blindness in developing countries
*night blindness -earliest symptom***


vitamin D deficiency

*rickets in children
*osteomalacia in adults
*causes decr absorb calcium from gut>decr resorp from kidney & stimulates release PTH to incr gut absorb & leech it from bone


main causes of vit D deficiency

*decr production in skin-less sun exp.,elderly decr synthesis
*kidney disease
*decr intestinal absorption-decr dietary intake, steatorrhea


vitamin E - antioxidant

*fat malabsorption and deficiency other fat soluble vitamins
decr vibration and position sense


hypervitaminosis A

*chronic ingestion of 25,000u/d: arthralgia,anorexia,dry skin, hairloss, low grade fever, hepatosplenomegaly


enteric feeding vs TPN

*enteric feeding is better option


simple clues to malnutrition

*IBW <6 female)
*greater than 10% wt loss in 6 months


23 yo male w intermittent dysphagia, after swallows large amount of food-esp big bite of steak.never with liquids. occurs 1-2 times a month then goes away. no active heartburn symptoms. whats next approp. test in diagnosis

*upper endoscopy

(anatomic obstructive symptoms)


68 yo female difficulty swallowing. 4 mo ago trouble with big pieces of food,now difficult with thick liquids. 10# weight loss,due to lack appetite. no GERD. + tobacco 80 pack years.Exam normal except pale. likely etiology?

squamous cell carcinoma of the esophagus


42 y/o male difficulty swallow solid food. began 3 yr ago,at first with steak large pieces not chewed well.gradual worsening needs to chew careful and lots wt loss. no fever, noc N/V or abd smoke, no alcohol. Dx?

peptic stricture


28 y/o female long hx alternating diarrhea & constipation. not progressive. diffuse lower abd cramping w the loose stools. worse with stress. colonoscopy 1 yr ago normal.eats alot fast foods.exam normal. next step?

reassure pt and start high-fiber diet and referral for stress management clinic

Irritable bowel syndrome


30 y/o male for routine exam. no c/o.PMH -, no bad habits. dad with colon ca age 55,paternal uncle colon ca age 42, brother age 35 w mult polyps on recent colonoscopy. what to recommend?

colonoscopy now

concern Hereditary non-polyposis (lynch) syndrome


25 y/o female w 3 yr hx diarrhea & abd camping, worse w stress.diarrhea can wake her, tried high fiber & dicyclomine-no help. hx (-) exan -neg except some fullness and tencer colonoscopy, normal exc at R colon-shallow ulcers. ileum edematous w shallow ulcers. Bx-chronic inflam & ulcer. Tx


Tx-mesalamine 400mg po TID


60 y/o female -sudden onset cramping abd pain in lower abd assoc with passing several maroon stools. pain severe but intermittent. began 4 hours ago. no prior similar. PMH: CAD w stents. daily aspirin, no smoke x 20 yrs no alcohol. exam (-)except mild tender LLQ.lab mild edema. next test?

Dx-ischemic colitis

Test-flex sig


29 y/o female long hx crohns sudden onset RUQ pain during noc.pain x 1 hour now gone, no hx of similar pain. hx resection R colon & terminal ileum 7 yr ago, 5 yr ago documented recur ileum dz recur. exam normal but mild RUQ tender, labs ok. what next?

gallbladder ultrasound


35 y/o/ male new diarrhea x 3 days. watery at first then bloody too. assoc abd cramps, some N/V. PMH only + for freq fast food meals. exam-mild dehydr, mild tender RLQ. Hgb 16, WBC 12k. stool studies, culture + E.coli 0157:H7, others pending. what antibiotic do recommend?

No antibiotic - contraindicated with this infection


40 y/o female w chronic heartburn & diarrhea x 2 years.omeprazole some heartburn relief. 5-6 loose BM/day and some epigastric discomf. EGD grade III esophagitis, mult shallow ulcers duod. bulb and 2nd portion duodenum.what recommended?

order fasting serum gastrin after stopping omeprazole X 7 days

Dx: Z-E syndrome


68 y/o female c/o weakness and fatigue X 2 mo.only other symptom is DOE. Hx unremarkable . only med estrogen. exam-some paleness, stool brown and heme+ Hgb 9.6, MCV 72, liver-wnl. what to order next?


Dx iron def anemia


36 y/o male new patient to est care. no complaints. PMH dx as teen w familial polyposis coli, his dad and brother have it also.age 20 he had total abdominal colectomy w ileorectostomy and has done well since. 4 BMs daily since the surgery. exam normal. you get flex sig-10 polyps residual rectum-adenomatous, next?

upper endoscopy


24 y/o female malaise 2-3 mo. no meds,PMH (-)ros otherwise -. exam normal except + hepatomegaly and slight tender. Lab: AST 1020, ALT 1220, bili 1.0, alk phos 120.other tests come back for hepatitis screen : +HCV Ab positive, anti sm musc + 1:250,antimitochondrial antibody + 1:40. liver Bx-chronic active hepatitis. next best tx?

start oral prednisone and azathioprine 50mg/d

Dx: autoimmune hepatitis


60 y/o female acute RUQ pain and fever.prior episode lasting less than 30 minutes. pain now for 2 hours. No meds or PMH.exam:tender RUQ, alk phos 400, total bili 3.0, AST 120, ALT 110. ultrasound, many stones,and dilated bile duct with several apparent stones. you start antibiotic, what next?


Dx-acute cholangitis


17 y/o female w chronic abd pain , colicky in RLQ.she has no weight gain for 1 year and has delayed puberty. exam-pale, thin, no secondary sex chara, abd slight distended, mild tender RLQ w palp loop of bowel, stool is heme+, w RBC & WBC. stool cultures are negative. what to do to confirm diagnosis?

upper and lower endoscopy with mucosa biopsy

Dx: crohn disease, must have biopsy dx


16 y/o male with flu and jaundice. history of "doing this all the time"when ill. father and uncle do the same. indirect bili is 4. rest labs are normal. next step?

reassure this is benign condition

Dx Gilbert syndrome


60 y/o white male w dysphagia. for 2 years to solid and liquids. slightly progressive. some noc regurgitation .omeprazole no help. PMH:CAD, EF 20%, cardiomyopathy, copd. Upper GI -dilated esophagus that tapered at junction to stomach. EGD-same. dilated esoph. w retained food,no mass effect. best tx?

botox injection into the LES

Dx: seriously chronically ill patient with achalasia


40 y/o female w scleroderma. new onset dysphagia, gradually worse past 6 months.dysphagia to bread and meats. never for liquids. no other complaints, no other PMH. exam as expected for scleroderma. what to recommend?

EGD and dilate if narrowed area of esophagus

Dx scleroderma and esophageal stricture


28 y/o recent develop acne, he started on doxycycline and now has sudden onset of pain with swallowing anything for 2 days. exam normal and no signif history than above.what do you recommend ?

supportive care

DX: pill esophagitis


60 y/o male long hx reflux symptoms, mostly controlled on PPI. also has adult onset asthma thats more bothersome. asthma for 20 years less responsive to inhalers and prednisone. upper GI-small hiatal hernia and reflux. EGD-linear esophageal erosion. what tests recommended?

evaluate for antireflux surgery


55 y/o male several month hx upper abd discomfort and fullness, freq belches. no hx of similar. has been on pepcid bid for 8 weeks. PMH: HTN, on ACE. No asa or NSAIDS. exam-benign. Upper GI:gastric ulcer w benign appearance. next step?

EGD now

** eval ulcers that occur on H2 and age 55 or older


35 y/o female, dx crohns age 19. one resection of cecum & terminal ileum age 23. prednisone x 2 in past 5 years. 2-3 soft BM daily, occassional abd cramps. mesalamine 2.4gm/d. ROS otherwise -.colonoscopy 1 yr ago-recur dz at anastamosis, 15cm into ileum. next step?

bone mineral density now

crohns predisposes to early onset osteoporosis


40 y/o male dx ulcerative colitis age 25. 1-2 flares a year, not seen doctor past 5 years. colonoscopy 5 yr ago- UC entire colon. other hx and exam are normal.what recommend?

start sulfasalazine 2 gm/day


70 y/o female w 6 mo hx watery diarrhea.assoc mild cramping and abd pain, never wakes at noc for BM or pain.PMH-hypothyroid. lab and stool workup were normal. stool output was 500g/day. what test to order now?

colonoscopy with biopsy

microscopic colitis


32 y/o male est as new patient. dx age 19 familial polyposis coli and total colectomy & ileorectostomy age 19. 3 BM/d. no symptoms.has flex sig with removal of mult small adenomatous polyps. EGD-mult large polyps body and fundus stomach.duodenum mult tiny, white plaques=adenoms,what now?

repeat EGD in 1-2 years


25 y/o college student to ER p passing large, bloody maroon stool. 3rd time in 2 years. 6 mo ago needed 4 unit RBC.colonoscopy then was normal.EGD normal, upper GI negative. now hgb 8.8,HR120 BP 90/60 what next?

has had 99m tech. pertechnetate scan and confirms dx. now need surgery

Dx:Meckels diverticulum


65 y/o female w fatigue x 2 months, no other symptoms. no nsaids or aspirin, exam normal except heme + stools. Hgb 7.8, MCV 65. EGD is normal, colonoscopy attempted, not adequate exam of colon, tortuous. what next?

air contrast barium enema

signif risk of colon cancer-need to evaluate entire colon


27 y/o female recent dx ulcerative colitis with 3 month hx rectal bleeding, abd cramps and diarrhea. started on mesalamine with some improvement, 3 wk later severe epigastric pain radiate to back. N/V. ER>dx pancreatitis,tx and mesalamine stopped ,home.2 wk later to ER with same but lesser degree of pain.amylase and lipase in 300 range. what do you recommend?

tx conservative measures, bowel rest and IV fluids

*management of pancreatic cyst


68 y/o ICU x 2 wk,elective resect colon ca cecum, aspiration pneum.,resp failure/vent> acute RF,prolonged ileus>TPN for nutrition. antibiotic, abdomen distended. afebile x 1 week, now temp 102. U/S abdomen-GB wall thickening and sm amt fluid around GB, AST 110,ALT 90 Bili 1.6 next step?

has acalculous cholecystitis, interventional radiology to place a percutaneous cholecystostomy drainage tube


60 y/o prior rock n roller, went to donate blood, told may have hepatitis, no complaints or symptoms. IVDU 20 yr ago. no other health problems. beer on sunday only. exam normal except tatoos. LFT wnl, HCV antibody +, HBsurface antigen -, HBcore -. 2 week recheck LFT are again normal. recommend/

no tx at this time

Dx hep C


24 y/o male to ER w symptoms of esophageal food impaction for 2 hr p ate chicken. salivating and spitting frothy secretions. cant drink water without regurgitation. this is his 4th episode. exam, lab, CXR all normal. next step?

GI consult for EGD to remove food bolus


70 y/o asian male , no doc for 20 years, presents to you with not eating and weight loss. progressive difficulty swallowing, 6 mo ago could swallow soft, now difficulty with liquids as well. long history of smoking and alcohol use.exam-muscle wasting. hgb 10, MCV 72, barium swallow: 3cm segment severe narrow distal esoph. what next step?

refer to GI for EGD
at risk of squamous cell carcinoma


70 y/o w hematemesis & melena. started one hour prior hx or similar.takes NSAIDS for OA. was 100/60, HR 120, given IV fluids and now 130/80, HR 96. exam normal except NG tube with coffee ground material, hgb 10, EGD 2 cm ulcer in antral ares, raised protuberance in crater, clot and large volume blood in fundus, several non bleeding erosions in antrum and duodenum. next step in management?

endoscopic treatment with a heater probe to visible vessel

*visible vessels need intervention!!


60 y/o w diarrhea x 2 yrs.extensive w/up negative.colonoscopy neg x 2 , 6 watery stools/d, progressive over 2 years. 3 days ago nausea and profuse vomiting, no meds, no PMH. exam negative. EGD done-severe ulcer esophagitis w large volume secretions in stomach. pH 1.0 mult ulcers duod. incl descending duod. fasting gastrin 5000. CT negative, next step?

endoscopic ultrasound

Has Z-E syndrome


30 y/o female long standing crohns. 3 yr ago 24" of ileum and cecum removed. on eval x 3 2 mo hx of intermittent RLQ pain and loose stools. exam tender RLQ but no mass. LFT & CBC normal. likely diagnosis?

exacerbation of crohns=classic presentation after ileal resection


35 y/o female belching and indigestion-substernal discomfort lasting all day, no regurg. for 2 years and progressive, belching constantly and abd distention. BMs are normal. on PPI BID x 1 month and no help. prior EGD and pH monitor were normal. no other symptoms or history. what to do next?

psychiatric referral or anti anxiety med

Dx aerophagia


27 y/o female w crohns x 5 yr.hosp now with 3rd episode of small bowel obstr in past 6 months. fiber worsens and distends abd. colonoscopy 1 yr ago no active crohn, terminal ileum stenotic and could not pass scope into ileum. sm bowel series> tight 10 cm area distal ileum. Best plan of action?

refer for surgical resection of terminal ileum


25 y/o female with ulcerative colitis for 5 years, presents 8 weeks pregnant. past colonoscopy dx distal disease=proctosigmoiditis, 2-3 flares a year. has been on incr dose mesalamine 3.2 gm/d with fewer flares. all else negative. best tx now pregnant?

continue mesalamine at current dose


16 y/o male to ER w 3 day hx diarrhea initally watery now bloody. vomiting for last 1 day. abd cramps and discomfort. no hx of similar. Hx unremarkable. exam: skin turgor decr, dry mucous membr., slight abd distention and mild right abd tenderness. WBC 14.5, stool + e.colo 0157:H7 at risk of what complication?

hemolytic uremic syndrome


40 y/o with acute diarrhea and for about 1 year but getting worse, 6 watery, occ foul smelling stools/d. hx negative except travel to Mexico 6 mo ago and 2 yrs in Indonesia.Lab: hgb 13, MCV 108 B12 normal. folate depressed significantly. O & P negative. what appropriate tx?

trial of tetracycline

tropical sprue


55 y/o female onset mod-severe abd cramping and maroon, bloodys stools ,abd tender to palpation LLQ and incr bowel sounds, IV fluids given, sigmoidoscopy: nl rectum, 25cm from anus, abrupt transition to edema, purple mucosa thats circumferential. best tx based on these findings

IV metronidazole

Ischemic colitis


78 y/o female with recent flagyl tx for c. diff toxin, but n/v with flagyl and didnt complete tx. now with same symptoms and + fecal leukocytes and + c. diff toxin. what appropriate tx?

vancomycin 250mg po QID x 14 days


50 y/o male to ER with c/o passing 3 large maroon stools, no pain or cramping, exam normal. takes asa daily. no other health problems . VSS . Most likely cause?

diverrticulosis- ** painless maroon stool


24 y/o with intermittent diarrhea for 3 years, alternating with constipation. mild abdominal cramps. beer on weekends, 2 glassed milk each day. no other problems or history. best plan of action

trial of lactose-free, sorbitol-free diet


35 y/o female with constipation since college. otc laxatives some relief . 2 BMs a week,but hard pass. some abd distention. history entirely negative. labs normal. barium enema-few diverticula in sigmoid colon. what intervention ?

regimen of fiber supplementation and increased water intake



60 y/o with 3 episodes of melana, negative workup 3 yr ago. now 2 day of dark, tarry stool, never maroon stools. father and uncle with recurrent GI bleeding, patient had recur epistaxis in his 20s. exam: telectasias lips and fingertips, nasalmucosa,stool heme+. endoscopy 4 well defined AV malform in stomach & same duodenum. colonoscopy - except diverticulosis, no AVMs. DX?

Osler-weber-rendu syndrome


24 y/o male with 2 day hx severe N/V/D and fever. pmh otherwise negative. does eat raw oysters 1 week ago and 3 beers/wk. exam fairly benign but + scleral icterus. labs all normal except total bili 4.0 likely cause of jaundice?

Gilberts syndrome


man calls ER and says his family of 4 including himself have all gotten sick in past hour with profuse vomiting, some now with diarrhea and abd cramping, no fevers. teens ate fast food lunch, all went for chinese dinner. mom threw bad mayo away yesterday, likely cause of their illness?

food poisoning with B. cereus- see with ingestion infected fried rice so chinese they all ate is the cause


54 y/o rocker w 10 yr hx hep C, tx interferon x6mo,no f/up c/o except occ weakness.hx otherwise negative. exam liver and spleen enlg,trace ascites, no edema.lab:ptl 98k,bili 2, ast 56,alt 50,INR 1.1.EGD-large, grade 4 esoph varices,some w red markings,no bleed,stomach eryth mosaic pattern, next?

initiate propranolol and titrate dose until pt HR


55 y/o male for health check, no complaints, no meds. screening colonoscopy w 1.2cm polyp snared, bx tubular adenoma w low-grade dysplasia. when needs follow up colonoscopy?

3 years


22 y/o male w negative history,complains of turning yellow, noticed yellowing in eyes yesterday. today skin turning yellow. no other complaints. drinks 12-18 beers on weekends. exam: scleral icterus, liver enlarged,slight tender, spleen tip palpable. Lab: anti HAV IgM positive whats diagnosis?

acute hepatitis A


NOT an indication for colonoscopy

bright red blood on toilet paper in 19 yr old college student


lab that indicates hepatitis B infection that has resolved?

HBsAg (-)
HBcAb IgG (+)
HBs Ab (+)


cause of diarrhea that will typically have fecal leukocytes



4 people who were at picnic all get sick about same time with sudden onset severe N/V then profuse diarrhea and severe weakness. they all ate multiple mayo based foods brought by various people, 2 went swimming in local creek. all got sick about 4 hours after eating.afebrile, Hr 140 BP 80/40. IVF given, next?

staph aureus food poisoning
no antibiotic tx indicated
supportive care


anti HAV IgM looks for

acute hepatitis A


HBsAg looks for

acute infection and chronic carrier states


anti HBc IgM looks for

acute infection in the "window"


anti HBc IgG looks for

if the person has been infected with hep B in the past
**does not tell if person is still infected


Hepatitis C antibody

tells if person has been infected w hepatitis C
**does not tell you if chronic C or if resolved


remember there is no chronic form of

hepatitis A


extrahepatic manifestations of Hepatitis B

*polyarteritis nodosa-multisyst dz w foot drop or wrist drop
*mixed cryoglobulinemia, polyneuropathy


extrahepatic manifestations of hepatitisC

*mixed cryoglobulinemia
*leukocytoclastic vasculitis, porphyria cutanea tarda-blister/scar on sun exposed areas,arthritis, Sjögren's syndrome
*membranoproliferative GN type 1
*lymphocytic sialadenitis


most common cause of acute hepatitis and jaundice in the WORLD

hepatitis E


tx of ascites

*low Na intake(1-2gm/d), water restrict if Na1 in urine suggests effective dose
*diuretic resistant ascites-large volume paracentesis, TIPS


Budd Chiari syndrome

*cause:hepatic venous outflow tract obstruction (hepatic vein or suprahepatic IVC) due to :50%myloproliferative disorder, Bechets, antiphos antibody syndr., OCPs, invasion or compression from malignancy


causes of toxigenic diarrhea

*staph aureus-1-6hr incubation, tx supportive
*c. perfringens-only diarrhea,7-16hr incub-supportive tx
*E coli-travelers-watery diarrhea, tx empiric-cipro or azith 1 gm
*bacillus cereus-contaminated fried rice-vomit,diarrhea-support
*vibrio cholera-severe watery diarrhe-doxycycline 300mg singledose
*giardia-hikers drink contam. water, acute-diarrhea, cramps. wt loss. chronic-steatorrhea. tx flagyl or tinidazole 2gm single dose



cipro 750mg daily x 3 days or azith 500mg daily x 3 days



azith 500mg daily x 3 days


nontyphoid salmonella

watery diarrhea or bloody with fever
* tx only if age65,on steroids, IBD, immunosuppressed, hemoglobinopathies, hemodialysis, aortic aneurysm, prosthetic heart valve


e.coli 0:157:H7 or non -O157

*no fever, Hemolytic uremic syndrome
*dx: shiga toxin 1 & 2 in stools, stool culture
*tx supportive only


vibrio parahaemolyticus

shellfish and seafood, tx as shigella


vibrio vulnificus

*raw oysters,shellfish,seafood
*incr risk with chronic liver disease
*tx : doxycycline plus 3rd gen ceph.



*stool antigen best Dx test
*may mimic UC, sigmoidoscopy w bx of colon ulcer edge may show organism
*tx:flagyl 7-10days followed by paromomycin or diiodohydroxyquin


yersinia enterocolitica

*watery or bloody diarrhea
*pseudo appendicitis picture
*tx cipro


42 y/o male no symptoms, has mild hepatmagaly and elevated liver enz . Lab AST70, ALT 120, GGTP 150, nl a phos, hepatitis neg, chol 280, TG 450, HDL 30. abdominal u/s incr echogenicity consist w fatty infiltrate, liver bx:steatosis, infiltr PMNs, hepatocyte ballooning, spotty necrosis & mallory hyaline. DX?

non alcoholic steatohepatitis


30 y/o male w 6 mo of abd discomfort, flatulence, bloat, diarrhea, wt loss. exam:vesicular erup both elbows, Lab hgb 10, MCV 70,serum iron 20, TIBC 500 (incr), ferritin 8 (15-200) what to order next?

IGA antiendomysial and or anti-tissue transglutaminase antibody


27 y/o admit w acute pancreatitis. 4 days later worsening abd pain and high fever. CT scan:severe pancreatic necrosis, CT guided needle aspir shows gram negative organism on gram stain . what is recommended now

IV antibiotic plus insertion of ct guided percutaneous drain tube


36 y/o female with longstanding ulcerative colitis on sulfasalazine for 8 years, now c/o wt loss, jaundice, RUQ pain , pruritis. Labs: AST 60, ALT 56, bili 10, alk phos 840. ultrasound abd normal. best test to confirm dx?



52 y/o white female on routine exam has this lab: alk phos 500, GGT 300, chol 400, normal AST,ALT,bili. hx of excess itching, no other complaints. abd ultrasound negative. what test to confirm her diagnosis?

antimitochondrial antibody


68 y/o male w 1 day hx fever, chills, RUQ abd pain. exam: T 103, RUQ tender, no rebound. Lab: WBC 15K, AST 150, ALT 160, alk phos 400, sonogram and CT show dilated common bile duct and no gallstones. blood cultures done and started on antibiotics. what now recommended?

ERCP w possible sphincterotomy


49 y/o male presents w incr abd girth for few months, Hx hepatitis 10 yrs ago. exam:tense ascites, Lab: albumin 3.2,AST 80, ALT 76, alk phos 68, abd paracentesis clear fluid w 10 mononuclear cells, total protein 2.0, albumin 1.5. whats most likely cause of his ascites?

cirrhosis with portal hypertension


52 y/o female w progressive dysphagia both solid and liquids w choking/cough at nite, intermittent regurg of undigested food and wt loss. started 1 yr ago and has lost 30#. hx occ chest discomfort, not relieved w antacids, CXR shows widened mediastinum. likely diagnosis?



32 y/o alcoholic male presents w 4 hour severe retrosternal CP. pain worse w breathing and swallow. auscultation over LSB-superficial crackling, EKG normal, CXR-left pleural effusion and air in the mediastinum. best way to confirm diagnosis?

gastrograffin swallow study


32 y/o male w severe epigastric pain radiating to back, N/V, fever and chills few hours. exam: T 103, epigastric & RUQ tender, hypoactive bowel sounds, lipase & amylase markedly increased. ultrasound-gallstones & dilated common bile duct. he is started on IVF, antibiotic and NG suction. you also recommend

ERCP and sphincterotomy within 24 hours and cholecystectomy prior to discharge from the hospital.


32 y/o female long hx ulcerative colitis on sulf. for many years, is now having severe bloody diarrhea, marked weakness, fever, abd pain. exam: T 102, HR 110, 110/70,abd distended w diffuse tender, sigmoidoscopy-friable colonic mucosa w sev. ulcers. tx IV hydrocortisone, NG tube, antibiotics, 48 hr later still same symptoms, repeat xray abdomen shows transverse colon dilated to 10 cm, was 7 cm initially. what to do now?

total colectomy


44 y/o female w chronic diarrhea and wt loss. 4-5 bulky foul smelling stools/day. hx of crohns mor than 100cm sm. bowel resected about 2 yr ago. stool fat is 20gm/24hours and sed rate is normal. what to recommend now?

low fat diet and add medium chain triglycerides to diet


72 y/o male admit CCU w anteroseptal MI, he develops a. fib needing cardioversion. 4 days after admit sudden onset severe colicky abd pain w vomiting. exam-diffuse abd tender and distended. xray-few distended loops. stools + occult blood. WBC 12K, amylase 300. now recommend?

abdominal angiogram


40 y/o female w elevated bilirubin. she was admit w acute appy w emerg. appendectomy 3 days ago, still NPO on IVF and clinda and gent. no abd pain Lab: bili 5, indirect 4.2, other liver tests normal. no blood transfusions . now recommend?

no further dx tests


38 y/o male c recur epig. pain & chronic diarrhea. long hx PUD , partial gastrectomy w Bilroth II one yr ago. upperGI - stomal ulcer and hypertrophy of gastric folds. H pylori negative. fasting serum gastrin 500, after IV secretin, gastrin 900.

*diarrhea d/t inactivation of pancreatic lipase due to high acid production
* CT scan likely to show pancreatic tumor
*hypercalcemia may be assoc w this disorder


80 y/o w left sided abd pain and recur bright red rectal bleeding for 2 days, exam: left side tender, no rebound. abd xray-thumb printing in descending colon. sigmoidoscopy-friable colonic mucosa w mult ulceration. WBC 11K. now recommend?

continued close observation


70 y/o hosp x 2 days w fever, LLQ abd pain, constipation. exam: T101, tender LLQ w localized rebound in area. WBC 15K, amylase normal. abd xray-nonspecific bowel gas, no free air, now recommend?

ct scan abdomen, IVF, antibiotics


52 y/o w 5 yr hx of pernicious anemia now 2 wk hx epigastric discomfort after eating. on B12 IM monthly. Lab: +serum antibody to parietal cell and intrinsic factor. fasting gastrin level 3400.

*high gastrin levels are due to achlorhydria due to atrophic gastritis
*higher incidence of developing gastric carcinoma and gastric carcinoid in this patient


true statements about H. pylori

*major factor in cause of PUD
*ulcer recurrences can be more effectively prevented by eradication of this organism than by continuous acid suppression


true statements about NSAID use

*they increase risk of bleeding in patient w ulcer disease
*concomitant steroid use increases the risk of toxicity
*NSAID induced gastric toxicity can be prevented by concomitant use of misoprostol


true statements about spontaneous bacterial peritonitis

*more common in ascites w total protein content 250
*blood cultures are positive in <50%


alpha interferon has been found to be effective in the treatment of these forms of chronic hepatitis

hepatitis B,C,D


seen in the majority of patients with ulcerative colitis

rectal involvement


ulcerative proctitis is best treated by

local steroid or 5-ASA enemas


in patients with ulcerative pancolitis of >8 yrs duration, surveillance colonoscopy w mucosal biopsies shoud be done every

1-2 years


travellers diarrhea is most commonly caused by

enterotoxigenic E. coli


Enterohemorrhagic E. coli (0157:H7) may cause

hemolytic uremic syndrome


Bacillus cereus is assoc with ingestion of

fried rice


Vibrio parahemolyticus is assoc w ingestion of

uncooked shellfish


true statements about malabsorption syndrome

*fecal fat >40gms suggests pancreatic insufficiency
*bacterial overgrowth causes malabsorption by deconjugation of bile salts.
*malabsorption in patients with extensive small bowel resection occurs due to loss of bile salts