Gastroenterology Flashcards
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
contraindications to GI endoscopy
recent MI
combative pt
intestinal perforation
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
achalasia
*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
constant
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
Tx-dilation
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
- rare
- 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
scleroderma
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
odynophagia
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
*iron,alendronate,quinidine
**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
GERD
young pt in competitive sports: more stress rxn in most but 10% of exercise induced asthma in likely misdiagnosed VCD
Dx GERD
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
- antihistamines
- tricyclics
- anticholinergics
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
- adenocarcinoma
* 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
adenocarcinoma
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
Tx-surgery
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
dyspepsia
recurrent upper abdominal pain or discomfort
s/s dyspepsia
epigastric fullness
belch,bloating
gnawing pain (not severe)
heartburn
causes of dyspepsia
- most functional
- meds:ASA NSAIDS iron
- if <age 5, test for H. pylori
- 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 <age 55 & no alarm symptoms
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
- NSAIDS
- 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
- alcohol
* corticosteroids
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
- EGD & UGI are CONTRAINDICATED
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
- NSAIDS
- 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
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
- carcinoid
- adenocarcinoma 95%
- lymphoma
- 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)
MALT-lymphoma
- due to H pylori
- dx-EGD w bx
- when tx H pylori-MALT may resolve
alcohol and gastric ulcers do not cause
cancer
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
crohns
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
Tx IBD
- 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
azathioprine 6 MP MTX remicade *smoking cessation decreases relapse
drugs that decrease relapse rate in ulcerative colitis
all standard drugs
**stopping smoking increases relapses
crohns
- 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<O&P
- 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
hyperthyroidism
carcinoid
irritable bowel
chronic loose stools
<200g/d
lactase deficiency
IBS
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
- albumin
- 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
- osteoporosis,osteomalacia
- neuro psych, dental enamel defect,prim. intestinal lymphoma
deficiencies caused by celiac disease
- iron
- folic acid
- calcium
- 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
- acromegaly
- 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
hamartomas
*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 <age 50
- 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
- stabilize
- 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
microperforations
usual s/s of diverticulitis
LLQ pain
fever
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