GI

The page includes some notes on hepatitis .


The Gospel of Fagel 


Dan Fagel, M.D.
2012 Instructor of the Year
St. Elizabeth Hospital Edgewood


General Notes

  • Need 25 to 35 gm of fiber QD
  • 1 bowel raisin bran - 8gm, also Fiber1 & Kashi, Wheat Chex
  • Probotic recommended - Phillips Colon Heathy (for gas)
  • Adkins diet (all meat) decreases gas
  • Recommends the Cooper Clayton Smoking Cessation plan
  • Age 50 & thin = runner or smoker :)
  • The colon extends from the cecum to the rectum
  • Nexium 40 mg is equivalent to Prilosec 20 mg
  • Parietal cells make acid in the stomach 
  • Pepcid and Tagamet block H1 receptors to decrease acid secretion.
  • Prilosec blocks the pump as does Omeprazole
  • Protonix, Prevacid, Acafex and Dexalon work via the same mechanism.
  • Give vitamin E for fatty liver.
  • GI tract transit time is 8 hr to 3 days - variability is in the colon.
  • Sigmoid colon has diverticuli first b/c it's smallest diameter and greatest pressure. - confirm
  • Senna causes melanosis.
  • Minocycline causes pill esophagitis.
  • Azathyoprine - can judge efficacy through the wbc count.
  • UC is urgency due to inflammation at the edge of the rectum.
  • Sacrolilitis is assoc with UC.
  • Gapping around scope pathogneumonic for hiatal hernia.
  • Posterior wall gastric ulcers have greater cancer potential.
  • If a great deal of inflammation is seen on EGD in duodenum or below it's like ZE.
  • Dexalon and Prevacid are the same - dex is the R-handed isomer, Prevacid is L-handed.
  • Psyllium grows only in India.


  Irritable Bowel Syndrome (IBS)
  1. Cause is unknown.
  2. Identify environmental triggers.
  3. Establish a good relationship with the pt.
  4. Constipation predom. and mixed are MC.
  5. Sometimes just meet pt to follow.
  6. For constip predom NNT = 6, medication ?
  7. DDX: celiac ds, colorectal ca, hypothyroidism, lactose intolerance. (REF), microscopic and collagenous colitis, atypical Crohn's ds. (REF).

 Inflammatory Bowel Disease (IBD)
  • Crohn's Disease
  • Ulcerative Colitis
  • Infectious Colitis
  • Ischemic Colitis
  • Diverticulitis

 

Patient Example   
- Pt p/w bili/alk phos 1.5/96 -> 1.8/140 in 3 months. 
- Simvastatin had been D/C's 2 months ago.
- There was h/o Tricor use 10 years ago resulting hospitalization for hyperbilirubinemia.
- Etiology: Hepatocellular vs Biliary
- DDX for this presentation:
  1. EtOH
  2. Fatty Liver ds - would usu present with ALT>AST but her LFT were NL
  3. Hemochromatosis
  4. PBC
  5. PSC - 80% have UC. 5% of UC patients have PSC.
  6. Autoimmune Hepatitis
  7. Chronic viral Hepatitis - only 20% of pts clear Hep C, 95% of pts clear Hep B. Chlorcyclizine inhibited Hep C in mice
  8. Alpha-1 anti-trypsin deficiency
  9. Wilson's ds
  10. Gall stones
  11. Tumors
  12. Gilbert's disease
  13. Medication induced
  14. Other hepatocellular disease.
 


 Chronic Liver Disease Panel    
  1. Hepatitis screen
  2. Iron studies
  3. ANA, AMA, ASNA
  4. Alpha-1 anti-trypsin
  5. Cu ceruplasmin
  6. Thyroid studies
  7. Alpha Fetoprotein
  8. US - r/o stones, focal liver lesions
 


 General Approach to GI   

Is it an upper or lower GI problem ?

Upper GI problems:
  1. Related to meals.
  2. Associated with burning and gnawing.
  3. Associated with N/V & early satiety.
  4. An upper bleed is an ulcer til proven OTW.
  5. Gastritis doesn't bleed.

Lower Gi problems:

  1. Can be anywhere, often related to bowel problems and are associated with bloating and gas. Crohn's ds sx are related to bowel movements.
  • Interesting note: IBS can be reproduced by placing a balloon in the sigmoid colon and inflating it. The pain was found to migrate even when the balloon was re-inflated in the same place.  The enteric nervous system is primitive - visceral afferents vary greatly from person to person. Note - don't be depressed b/c Cope is about the acute abdomen and these are chronic problems.
  • DDX of IBS: Hypothyroidism, Celiac DS, Lactose Intolerance, Colorectal CA. 

 


 Esophagus

  1. Acid and non-acid reflux are mc problems.
  2. Reflux affects 44% (60m) adults, 7% daily.
  3. Is one foot in length.
  4. First 1/3 is striated, second 2/3 is smooth.
  5. Non-keratinized stratified sq epithelium.
  6. Innervated by the enteric NS.
  7. Only job is to deliver food to the stomach.
  8. More problems here than anywhere in GI.
  9. Measure eso time with trickle and scope !
  10. Upper sphincter opens & closes.
  11. LES stays relaxed throughout bolus.
  12. END - LES, diaphragmatic hiatus, squamocolumnar junction. 
  13. Normally the 3 are all at the same place.
  14. Barret's - lining of the stomach creeps up into the esophagus such that the squamocolumnar junction is above the LES and diaphragmatic hiatus.
  15. Hiatal hernia - finish
  16. Lines in eso are pathogneumonic for eosinophilic esophagitis.
  17. Pearl - GERD (acid reflux) causes hiatal hernia by shrinking the eso and pulling it up above the diaphragm resulting in the hiatal hernia. 
  18. Pearl - Large hiatal hernia may be the only finding in a patient with microcytic anemia. So hiatal hernia and microcytic anemia can be treated at the same time with a PPI and Fe.
  19. Diaphragm separates chest from abdomen.
  20. Cameron lesions are caused by the esophageal folds rubbing together.
 
  • Very important - hiatal hernia may be the only finding in a patient with microcytic anemia.
  • Can lose up to a cup of blood per day due to friction of the hernia and have no melena.

 Stomach

  1. Is one foot in length.
  2. 3 layers of mm - circ, long, oblique.
  3. body, fundus, cardia - same tissue, acid-secreting, parietal (red) - acid, chief (blue) - pepsinogen.
  4. antrum - different - secretory cells.
  5. Gastric acid's primary purpose is to kill bacteria and other things as needed.
  6. Requires 2 - 4 hours for stomach to empty.
  7. Liquids empty with linear kinetics, solids with zero order (same % over time).
  8. Stomach defense - mucous layer w/ pH gradient from 1 to 7. 
  9. Prostaglandins and blood supply stimulate the mucous layer
  10. ASA and motrin decrease the mucous layer causing ulcers.
  11. Atrophic gastritis - H. Py., Autoimmune (pernicious anemia) in older person.
  12. Ring dysphagia - acid reflux
  13. Job - temporary storage (maintains wt), pyloris regulates gastric emptying, food won't leave stomach until it's ground to 1-2 mm. Grinding, Mixing. (3 jobs).
  14. CTX 3X / min, small bowel 14X / min.
  15. Pepsinogen, CCK, Gastrin - activated when pH increases.  PPIs cause hyperplasia. HCL.
  16. Parietal cells is the only mammalian cell that makes an inorganic acid.

  Gastritis 
acute hemorrhagic superficial chronic active  chronic atrophic 
- loss of surface layer
- vascular with dilated capillaries
- non-infiltrated
- cx by NSAIDS, coffee, cigs
- sx abd pain, guaic+, with HbB 15 and no orthostasis
- tx PPIs, remove irritants
- mucosa will recover after an hr
- p/w dyspepsia, burning, gnawing 
- synonymous w/ H.Pylori
- bx shows CAG
- tx eradicated by 3 therapy

  • Was ubiquitous, now primarily in developing countries and lower economic classes.
  • Was thought initially to be Campylobacter.
  • Helicobacter Pylori is G-, motile, splits urea and makes it's own acid environment to live in.
  • H. Py. is the only bug that can live in the stomach.
  • H. Py. lives in the mucous layer - It can't live in the antrum or acid would kill it, can't live in the mucosa or the immune system would kill it. 
  • H. Py. is spread person to person via fecal oral route.
  • H. Py. is associated with gastric cancer and non-childhood obesity.
  • Grehlin / leptin (appetite suppressants) increased by H. Py. which decreases activity.
  • H. Py - most get it before age 12, at > 60 most have it but < 40 ~ 20% have it so they weren't exposed and probably won't get it.
  • Index + - 70% of family get it, Index - 20% of family will get it.
  • H. Py. was rediscovered in 1982 by Barry Marshall - at that time a partial gastrectomy for ulcer ds was as common as cholecystecomy. Went from .5 million to 5,000 as a result of rediscovery of H. Py. Marshall cultured it in the lab, swallowed it, he got sick, then got an ulcer. Won the Nobel prize. As of '91 we test and treat it. Why from "maybe" to certain in 3 years ? Tons of publications.
  • PEARL - 90% of duodenal ulcers associated with H.Py., 50% of gastric ulcers but H. Py. can live only in the stomach. ANS: Duodenal ulcer is a gastric ulcer in the duodenum b/c must have metaplasia. After meals duodenal ulcers have increased acid and decreased bicarb from Brenner's glands. 1% develop gastric cancer.
- cx: autoimmune pernicious anemia or long standing H. Py. 
- loss of gastric pits
- you don't see glandular cells
- PA - much more severe
- H. Py work up
- anyone w/ dyspepsia 
- anyone with ulcers

 


 Erosions vs Ulcers
  1. Erosions are < 3 mm deep.
  2. Ulcers are > 3 mm deep, lose surface area.
  3. Upper bleeds are ulcer until proven OTW.
  4. Gastritis doesn't bleed.
  5. Varacies will bleed as much as an ulcer.
  6. Plicaque circularis.
  7. Stomach is only part of GI tract with 3 layers.
 


Upper GI
5 things to know.
 Lower GI
4 things to know.
  1. reflux - mc
  2. ulcer ds and gastrits
  3. gastroparesis
  4. pancreatobiliary
  5. celiac disease - 1/133 in US.
  • Reflux is greatly affected by weight gain sometimes as little as 5-10 lb. Losing weight can often be the best tx. Increasing fiber may also help.
  1. diverticulitis
  2. IBS
  3. inflammatory bowel disease
  4. polyps & cancer
  • If pt presents w/ diarrhea and wt loss with diverticuli, do a clean out and sometimes will improve. In this case it was likely due to bacterial overgrowth.  Bacteria can proliferate and gobble up nutrients which can then lead to malabsorption. Can put some of these pts on ciprofloxacin and they improve. Bacterial overgrowth can also occur 2/2 decreased motility in the setting of Perocet use and gastroparesis.
  • The remainder of lower GI problems, such as Meckel's diverticulum are very uncommon.

More random pearls.
  • Crohn's symptoms are related to bowel movements.
  • 10% of lower GI bleeds are caused by upper GI bleeds
  • Lipomas exist and are common in the GI tract "pillow sign" seen on colonoscopy.
  • Lipomas aren't removed b/c they are attached to the submucosa.
  • Zollinger woke up pts in 1940s during cholecystectomy and squeezed the GB. Pts reported mid-epigastric pain, NOT RUQ pain.  Ask the most likely places again (see my drawing).
  • Cholecystitis is constant, steady, burning, severe, 
  • GI cocktail - lidocaine, antacid + donatol which is an anticholinergic which causes the bile duct to relax and if there is a stone there the pain subsides. This can be deceived b/c you may be tempted to give antacid and advise F/U because you thought it was pyrosis or dyspepsia. Pt then comes back to the ER with gall stone pancreatitis almost dead and you just, plain missed it.
  • Pt reports LLQ pain w/ dull pain to the hip. GI usu doesn't go to the hip. Pain increases with activity. Some relief with bowel movement. Endometrium causes pain immed before mensus. This is an example of colon with external pressure on it from endometrium.  Interesting.
  • 6X / day we have the "major migratory complex" which starts in eso and goes to colon, which is the major "house cleaning" function.
  • MMC is lacking in gastroparesis.
  • In gastroparesis can only rid yourself of seeds and nuts via emesis.
  • MC causes of gastroparesis is idiopathic.
  • Having 1 colonoscopy decreases chance of colon ca by 80%.
DDX of mid-epigastric pain:
  1. acid reflux (GERD) - "pyrosis" - "fire", "pyre", like funeral pyre
  2. ulcer ds and gastritis - "dsypepsia"
  3. biliary colic

 "pyrosis"  "dsypepsia"  biliary colic
  1.  burning mid-epigastric pain
  2. occurs after meal
  3. radiates to throat
  4. relieved by antacids
  5. sensory afferents relay to brain & it's associated with burning
  6. gastrin stimulates blue (chief) cells and parietal (red) cells.
  7. MC in Western civilization.
  1. gnawing, empty stomach before meal
  2. unbuffered acid irritates ulcer
  3. food brings relief
  4. duodenal ulcers make you want to eat all the time.

  1. severe, radiates to back
  2. no relief to emesis
  3. no relief to tagemet
  4. midepigastric
  5. brings people to the ER
  6. if misdiagnosed as reflux and the pt returns to the ER with gallstone pancreatitis then you messed up.
  7. episodic (like q 6 mo) - vs pyrosis & dyspepsia which happens all the time.

 
 Acid reflux (GERD), pyrosis workup / treat
 First of all, what to work up:
  1. long standing disease.
  2. age > 50 at presentation.
  3. complications.
  4. no response to treatment.
  5. atypical chest pain.
 Treatment:
  1. BX by EGD - most sensitive for Barrett's esophagus.
  2. Barium swallow - if symptoms persist after EGD.
  3. Manometry - If considering for a Nissan. If there isn't enough pressure won't be able to swallow after Nissan. Also for eval of eso spasm and achalasia.
  4. pH monitoring - Bravo pH strip is placed 5 cm above the LES. Use this when pts aren't responding to medications. Also try different medications. If no improvement then increase to BID or change PPIs. 
  5. If no response then surgery. 
  6. Note that Dexalon and Nexium be more efficacious for severe reflux.
  7. Note that Barrett's may also be a risk for increased gastric cancer. 
  8. Pts usu return because they are undertreated, so use full dose.  H2 blockers quit working when tachyphylaxis occurs. Also, Prilosec label says use no more than 14 days b/c they don't want to mask other pathologies. Difficulty swallowing is another complication. 
 Complications:
  1. Stricture (10-20% w/ lax LES), Barrett's, hiatal hernia, eso ulcers & bleeding (both uncommon).
  2. LES is most accurate way to find the end of the eso.
  3. Large non-reduced hiatal hernia can cause esosinophilc esophagitis.
  4. Z-line ?
 Pathogenesis:
  1. LES - 80% of patients have an abnormal LES.
  2. TLESR - Transient lower eso relaxations. Too much acid.  Primary peristaltic wave is the swallow, in secondary peristaltic wave the reflex is cleared, in tertiary peristaltic wave is spontaneous, causing eso spasms and presbyesophagus. Iceburg effect - most people (20% with GERD) present with stricture and Barrett's. Usu caused by lax LES. So TLESR don't present as often. Consider a Nissan for lax eso and hiatal hernia.  ZE - lots of acid created & there is reflux.
  3. Gastroparesis - N/V early satiety, bloating. Reglan - use smallest possible dose (SE = TD), Domperidone only available outside US. 
  4. Eso clearance. Volume clearance is by second wave. We swallow saliva which is alkalotic on the esophagus. Scleroderma affects motility. Increase motility with hard candy and jaw ?
  5. Cytoprotection - lining is stratified squamous non-keratinized epithelium.  Herthle cells for tight jn. Pathogenesis in breakdown is eosinophil and neutrophil infiltration, tight jn change or anything that breaks the barrier.  Must have sx for 2-3 yrs for damage to be done.

NERD - non-acid reflux
  1. Tissue injury into esophagus.
  2. Common and chronic.
  3. All ages.
  4. Greater in Western civilizations, assoc w/ obesity.
  5. > Barrets and eso in older men ?DK?
 

Some anatomy during colonoscopy: how to identify the iliocecal junction.
  1. appendiceal orifice - looks like a "D" (see drawing).
  2. 3 tinea mms forming the crow's foot.
  3. iliosecal valve
  4. Not that the terminal ilium has villa.
  5. Ilium has the most elongated villi.
  6. Bruner's glands are in duodenum and make bicarb.
  7. Duodenum has plicqae circularis.
The five valves of the GI tract.
  1. Upper esophageal
  2. Lower esophageal
  3. Pyloris
  4. Ilieosecal
  5. Anus
Colon
  1. 5-7 meters in length
  2. most of the food is in the right colon
  3. 1 liter of H2O is delivered to the colon QD
  4. absorbs H2O and salt
  5. Fish have cloaca b/c they don't care about H2O
  6. Some absorption of carbs occurs in the colon in herbivores.
  7. Carnivores have short colons.
Ascending and Transverse colon anatomy:
  1. Triangular with haustral folds
  2. Triangles are caused by tinea.
  3. There are no villi in the transverse colon.
  4. The liver is blue
  5. Endometriosis is most often in the left colon.



Fissures
Hemorrhoids
  1. painful - fissures are a tear in the lining.
  2. hard stool
  3. tenesmus
  1. painless
  2. dripping blood is pathogneumonic
  3. lar ?



 Small Intestine

  1. Digestive organs - stomach, small bowel, liver (bile - ADEK abs and fat digestion), pancreas (trypsin, chymotrypsin, amylase, lipase).
  2. Disaccharidases
  3. Peptidases
  4. Area will cover a football field.
  5. Small bowel ischemia assoc w/global atherosclerosis.
  6. Ampulla is in the second portion of the duodenum.
  7. Ligament of Trietz is in the 3rd portion of duodenum.
  8. B12 is absorbed in the distal ilium.
 


 Colon

  1. 5 - 7 ft in length
  2. simple columna epithelium
  3. layer of mucous secreting cells
 

Lymphocytic Colitis
- Related to previous viral illness.


 Diverticulosis Diverticulitis   Ischemic Colitis
  1. BLEEDING
  2. older pts sometimes on ASA and Plavix
  1. NO BLEEDING
  2. "L. sided appendiciits" 
  3. abdominal pain
  4. change in bowel habits
  5. Fever
  6. Increased WBC
  7. CT - wall thickening

  1. Common, occurs in all age groups.
  2. 70-90% get better with conservative treatment.
  3. Mucos and Submucosa
  4. Presents like diverticulosis + diverticulitis combined. 
  5. Often segmental.
  6. Rectal ischemia doesn't occur b/c of its dual blood supply from the IMA (branch of iliac a., and ___ artery ?.
  7. Always work up IC. Often people on antihypertensives who contacts a gastric virus will then develop ischemia, often at the splenic flexure.
  8. Usually IC isn't occlusive.
  9. Dysentery is in the DDX (salmonella, shigella, enteroinvasive e. coli.). These patients are sick as snot.
  10. Whitish bands on colonoscopy are signs of healed ischemic colitis.


  • Note - inflammatory bowel ds (IBD) can also present with bleeding, pain, microcytic anemia.
  • There is a 20% miss rate for polyps on colonoscopy.
 Next week - reflux, GERD pathology, Eosinophilic Esophagitis, Clarifying non-acid reflux.

Medstudy GI 33 - Free air under the diaphragm is unlikely in the absence of rebound.
Medstudy GI 34 - Doxycycline is a common cause of pill esophagitis.
Medstudy GI 35 - Macrocytic anemia can be due to distal small bowel disease (B12) deficiency.
Medstudy GI 36 - Anyone with 1st degree relative with CRC needs 5-yr screening exams.
Medstudy GI 38 - Hemachromatosis - damage to liver, adrenal and testicular tissue.
Medstudy GI 43 - Dermatitis herpetiformis responds to dapsone.
Medstudy GI 44 - Upper endoscopy doesn't pick up GERD b/c only 2% GERD pts have esophagitis.



Dysphagia - occurs to liquids, to solids and to both at the same time.
- Due to benign esophageal or peptic stricture 70% of the time.
- DDX - Peptic stricture (10% of those with GERD), Eosinophilic Esophagitis, Malignancy, Schotski ring.
- is never psychogenic and major complaint is that "food just won't go down", or "it gets hung up".
- Ask - to solids , to liquids, both, is it progressing ?
- Most difficult foods to swallow are grilled meats and untoasted bread

Acid Reflux Treatment
- Start with OTC Omeprazole PPI first thing in the AM on an empty stomach 30 min before meals.
- The 30 minutes allows time to irreversibly and covalently bind active proton pump.
- Omeprazole t1/2 is 12 - 14 hours.
- Parietal cell proton pumps become active with eating.
- If it isn't working:
  1. raise head of bed.
  2. decrease night meals.
  3. take a dietary history.
  4. switch to another PPI
  5. make sure pt is taking it correctly
  6. BID - prilosec 20 mg BID is more efficacious than prilosec 40 mg QD
  7. may next need to add a pro kinetic, like Domperidone, Reglan or Cytotec.
  8. Weight loss is (even a gain of 10 lb can cause GERD) is most effective tx.
  9. Long term PPI risks: anemia, hypocalcemia, eldery - hip fx and pna.
  10. PPI decrease total acid secretion so no increase in cancer or other SE.
  11. Surgery: young, severe ds, those who won't take meds, 90% glad they did it at 5 years.
  12. GERD can be alkaline reflux so if it turns out to be IBS try Elavil.
  13. H2 blocker problem is pt gets used to them and tachyphylaxis occurs.
  14. H2 blockers ok PRN or for nocturnal symptoms, carafate doesn't' work.

Barrett's Esophagus
- incidence is 10-15% of those who already have GERD
- gastric metaplasia of eso that looks like stomach b/c has mucous layer and pH gradient
- metaplasia occurs whether lining of esophagus or duodenum is exposed to acid
- <1% chance per year of becoming adenocarcinoma
- Dr. F. has seen only 1 eso ca.
- Has had several patients with high grade dyplasia
- EGD Q 2,3,5 mo if no dysplasia then check Q6 months.
- If there is high grade dysplasia then perform RF ablation - Barrett's does not return.
- In Barrett's always put pt on PPI.  Best day in a Barrett's pt's life is when his endoscopist dies.

GERD -> stricture -> swallowing is improved but then GERD returns.
- non-progressive (say 10 years)
- they don't lose weight
- takes longer to eat - last one at the table
- often won't eat steak or go out to dinner

Shotski ring
- thin membranous ring @ GE junction
- usu present with impaction in the esophagus
- TX - put down largest dilator you can and snap the ring

Eosinophilic Esophagitis
- If a person < 30 presents with food impaction in the esophagus it's EE.
- hx is often that a young pt was hurrying at lunch eating meat.
- Most will say it's higher in the throat b/c C3-5 innervates the myotome from above.
- If the patient states that it's higher, then fallow the somatic NS.
- Fagels sign - raising chin to swallow.
- The patient usu have a history of allergy
- Diagnose with biopsy.
- Treat with flonase, would also want to tx any associate reflux
- Dilate gently with 40 vs 52, as it is very easy to tear.

Esophageal Cancer
- only 6,000 cases /year.
- is usually identified late.
- GERD -> Barretts's esophagus -> adenocarcinoma.
- Squamous cell CA is usu 2/2 smoking and drinking
- Natural history of both are the same (20% survival at 5 years).
- progressive dysphagia over a time frame like 6 months, starts with solids, wt loss
- dysphagia to solids is 2/2 impingement

---------------------
Not sure of the association for the following notes:
- use due to neuromuscular pathology - there are 19 sets of mm use in swallowing. ?
- liquids - usu gagging after L-sided MCA infarct
- must take PEG out in 2-3 months
- stroke, dementia, ALS, MS, myopathy
- mm dystrophy - usu do better w/ solids b/c liquids seep into lungs
---------------------

Dilation therapy:
- does not help in malignancy
- Peptic Stricture - does help
- Schotski ring - tx is to to aggressively dilate until the ring breaks
- Eosinophilic esophagitis - very gentle dilation therapy helps

Achalasia 
- Incomplete relaxation of the LES. 1/100,000, a case Q 2-3 years.
- CP, dysphasia to solids & liquids, wt loss, no cancer
- DX - manometry & barium swallow
- TX - botox, balloon dilation (3% chance of perf), myotomy.
- Dilate - w/ 3 cm balloon to tear sphincter until it stays open.
- Surgery more effective than manometry.

Esophageal spasm 
- The "IBS" of the esophagus.
- Abnormal manometry but there is no correlation between manometry findings and sx.
- Bravo pH will show no signs of GERD
- irregular dysphagia to solids and liquids
- TX Nitrates and Nifedipine decreases manometry abnormalities but not symptoms.
- TX Elavil helps sx, Salzman prefers nifedipine.
- Elavil SEs are dry mouth and drowsiness, 1-2 wks to kick, start at 10mg then to 25 mg in 2 wks.
- Elavil is a great intervention if pt is also having difficulties with sleep.


- In both achalasia and eso spasm there is dysphasia to solids and liquids.

Atypical CP - if related to eating it's a GI problem 60% of the time.

Odynophagia - pill esophagitis vs infectious: Herpes, CMV, Candidal.
Herpes - inclusions on bx, mouth sores.
Candida - ABX, immunosuppression, steroids, DMII

Pill esophagitis presents as CP in the middle of the night. Always ask pt if it hurts to eat.  
- Vitamin C, Chromium, Fe, NSAIDS, minocycline, doxycycline.
- Put patient on a PPI BID
- Sometimes have strictures or other problems.
- Take pills while sitting upright.
- Eso and heart shares neural afferents.
- 75% of acid dripped into the esophagus causes CP and ST changes.

Atypical CP - always include pill esophagitis (esp minocycline & doxycycline).
Recall the sign of Levine if you do CP for your talk.
Mike Guenther performs Whipples at UC.

Dr. Barne's GI Cocktail:
Bentyl - cramping
Visitoril (hydroxyzine) - itching / agitation
Clonidine - BP, sedative.


DDX for dysphagia with regurgitation of undigested food:
- Zenker diverticulum
- Achalasia
- Pseudo achalasia (esophageal carcinoma)


Flatulence (which fits under the umbrella of IBS)

- There are 5 gases in the bowel: O2, N, CO2, Methane or Hydrogen
- These gases are 99% of all bowel gas, and they are odorless.
- Sulfur-forming bacteria create 1% of bowel gas and create the odor.
- The human nasal mucosa picks up 1 pt / bln of sulfur - so farts rarely escape unnoticed.
- 1/3 of people have Methane and their stools float.
- 2/3 of people have Hydrogen and theirs stools sink.
- Methane and Hydrogen carriers are family-based and are inherited in early childhood.
- There is 1-200 ml gas in the bowel at any one time - confirmed by dilution technique.
- 200 ml to 2L gas passed daily depending on diet.
- The average person passes gas 8-13 X / day +/- 5. Confirmed by med students wearing pantaloons.
- H producers make more gas because there are 2 mols / molecule.
- M requires 5 moles to make a module so volume is less.
- M producers have a higher incidence of colon cancer.
- Mammalian cells can't make H2 or Methane.
- Stomach has 79% H2 and 21% O2, just like air.
- All stomach gas is swallowed air.
- The average person swallows 1X / minute.
- People swallow saliva and 1 tsp air.
- There are about 1000 swallows / d resulting in 1 liter swallowed, but actually 2-5 L air swallowed / day.
- Of the 5 L 1/2 L goes to GI tract and 4.5 L comes back up.
- After Nisson Fundoplication air cannot track back up.
- Factoid break - Serrated sessile adenomas are under the radar.
                        - Colonoscopy has reduced colon CA in the left colon but not in the right colon.
                        - If find 1 poly in the colon must increase vigilance, repeat in 1 year.
- H2 has been responsible for fatal explosions in the presents of mannitol prep - increases sugar ferm.
- There are 3 syndromes:
 1. increased burping 2/2 increased air swallowing
 2. increased flatus - which is assoc w / increased gas, unlike the others.
 3. bloating.
- Sometimes people swallow air and belch to relieve bloating. 
- Burping - Treatment is all about education.
- Incr burping cx by chewing gum, eating too fast, smoking, eating hard candy (incr saliva and swallowing)
- Tx burping by making someone hold a pencil in their mouths betw teeth.
- If hanging pictures you start to pool saliva.
- But if a person is spitting with esophageal impaction that must be treated immediately.
- Factoid break - In UC only the mucosa is inflamed - no fistulas or deep fissures formed.
                       - Crohn's (Crohn, Crohns) have same risk of cancer development in the long run.
                       - 1/4 small bowel involvement, 1/4 colon, 1/2 both.
                       - There are 3 presentations of Crohn's disease for 1 of UC.
- Burping - 1/3 realize and move on, 1/3 respond to pencil but take it out, 1/3 get a new doc.
- 200 - 400 ml of air moves into the small bowel.
- Flatus - excess flatus is associated with increased intestinal gas.
- We pass gas (fart) in our sleep but we don't burp.
- IBS does not wake people up.
- Crohn's disease, UC (ulcerative colitis) and infectious colitis do wake from sleep.
- Simethicone and GasX just make little bubbles out of big bubbles. Charcoal helps a little. 
- Michael Levitt treated a pt passing gas 36X / day. In lab he drank and passed gas 174X.
- NEJM - 70x/4hr is pending as an entry in the Guinness Book of WRs.
- Flatus results from the fermentation of undigested carbohydrates - CO2 and methane or H2.
- Flatus is produced predominantly in the colon.
- There are 1 trillion bacteria / ml colonic flora.
- Anaerobes & aerobes - some bacteria produce gas some consume. ABX can change the ratio.
- A clean out will sometimes favorably change the organisms or substrate.
- Rice is 99% digested and the undigested portion ferments into gas.
- Flatus can be altered by changing what a person eats and when they eat it.
- If they say GasX works then that's fine.
- Bloating - swollen belly. This is subjective, no objective.
- Several studies demonstrated no difference in the amt of gas between bloated and non-bloated persons.
- SO, bloating is actually relaxation of the abdominal wall. IBS people are actually just hypersensitive.
- It's a subset of IBS - visceral hypersensitivity after eating related to increased motor activity.
- Treatment of flatus: (try each step and proceed to next if it fails).
1. Clean out (8 glasses miralax and start fiber the next day).
2. fiber & miralax, diet and bowel habits
3. low gas form diet. Synthetic fiber (benefiber, fibercon) are better than natural.
4. Linsess - helpful in constipation predominan IBS. NNT = 6-7 patients.
5. Amatiza.
6. If pain predominant try low dose elavil.
7. Reassurance
8. Probiotics

- At that is the end of this - 9.20.13 Friday 16:53

Relevant material from the AAFP and other sources

What is the most common cause of recurrent abdominal pain in children 4–16 years of age. REF

Barrett's eso converts to adenocarcinoma in 1/200 pts annually. REF

Most bleeding in Meckel’s diverticulum is secondary to heterotrophic gastric mucosa, causing acid-induced ileal ulceration. REF

The Hatfield NG tube unclogging solution:
- Sodium Bicarbonate 650 mg tablet
- Any pancreatic enzyme
- 10 ml of warm water
Let it sit for 15 minutes and then flush.

Prevalence of celiac disease in the US is 1:13 (which seems wrong to me) REF

Chronic calculous cholecystitis is assoc with a 20% incidence of GB ca. REF

Hepatitis C (HCV) screening is indicated for recipients of a transfusion prior to July 1992, patients with needlestick or mucosal exposure to HCV, and children born to mothers with HCV infection. REF
Think of BuN Peg (92) and Hep C.

Screening should begin at 40 or 10 yrs b4 the age at dx of the youngest 1st deg relative. REF

How does HRT affect the risk of colon cancer ? REF

UC is associated with colon cancer, Crohn's ds is not. REF

IBS - constipation, diarrhea, pain and mixed predominant & tx - GI question #2 MedStudy.com

Which virus causes 90% of non-bacterial gastroenteritis ? (REF)

What is the most common inherited disorder of bilirubin metabolism ? (REF)

What is the most common function disorder of the GI tract ? (REF)

Symptoms of colicky RUQ pain radiating to the right shoulder makes you think of what ds ? (REF)

Half of the person with this enteropathy present with anemia or osteoporosis and no GI SX (REF)

The celiac triad - abdominal distention, anorexia, dermatitis (dermatitis herpetiformis).
- Half the pts in America present with anemia and osteoporosis with no bowel complaints.
-- DX - antiendomysial antibodies and small bowel biopsy (must have bx to confirm).

I don't get the point of this question - if pt is Hep B&C why US if it's NFLD ? REF


UWCases


206. A 40-year-old businessman has recently been diagnosed with irritable bowel syndrome after extensive testing by his gastroenterologist. His predominant symptoms are diarrhea and pain. 
Which one of the following has been shown to be helpful in controlled trials? 
A) Probiotics such as yogurt and buttermilk 
B) Insoluble fiber such as wheat bran, corn bran, and defatted flaxseed 
C) Soluble fiber such as psyllium (ispaghula) 
D) Turmeric 
E) Peppermint oil 
Item 206 
ANSWER: E 
Studies suggest that in 25% of patients, irritable bowel syndrome may be caused or aggravated by one or 
more dietary components. Restriction of fermentable, poorly absorbed carbohydrates is beneficial, 
including fructan (found in wheat and onions), sorbitol, and other such alcohols. Further studies are 
needed, however. Despite its popularity, fiber is marginally beneficial and insoluble fiber may worsen 
symptoms in patients with diarrhea. Probiotics in the form of foods such as buttermilk and live-culture 
yogurt have thus far not been established as useful. Daily use of peppermint oil has been shown to relieve 
symptoms. 
Ref: Heizer WD, Southern S, McGovern S: The role of diet in symptoms of irritable bowel syndrome in adults: A narrative 
review. J Am Diet Assoc 2009;109(7):1204-1214. 2) Graham L: Practice guidelines. ACG releases recommendations on 
the management of irritable bowel syndrome. Am Fam Physician 2009;79(12):1108-1117.

84. Which one of the following is found most consistently in patients diagnosed with irritable bowel 
syndrome? 
A) Passage of blood per rectum 
B) Passage of mucus per rectum 
C) Abdominal pain 
D) Constipation 
E) Diarrhea 
Item 84 
ANSWER: C 
A large review of multiple studies identified abdominal pain as the most consistent feature found in irritable 
bowel syndrome (IBS), and its absence * makes the diagnosis less likely. Of the symptoms listed, passage 
of blood is least likely with IBS, and passage of mucus, constipation, and diarrhea are less consistent than 
abdominal pain (SOR A). 
Ref: Ford AC, Talley NJ, Veldhuyzen van Zanten SJ, et al: Will the history and physical examination help establish that irritable 
bowel syndrome is causing this patient’s lower gastrointestinal tract symptoms? JAMA 2008;300(15):1793-1805.






Amitriptyline worsens constipation.
tag: side effects / drug interactions / TCA / constipation

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