GI-GU EXAM #3 – 10/20/08
*** Missed Both Class Sessions ***
10/21/08
GI SECTION OF THE CLASS
*** Flexible Fiber Optic Study ***
Flexible fiber optics is a tool to check for inflammatory damage or other problems in the GI system. The tool can be used to
investigate biopsy or give interventions in real time. With other tools, you have to schedule the biopsy or provide treatment at
a later time
GI OVERVIEW
History
Does the history separate the condition or is it part of the picture?
Location of Pain -- Examples
Many GI problems do have a pain component associated. Some problems get to the body core (front, side or back). Back pain
can be misinterpreted. The problem will actually be internal and refer to the back. The conditions are often retroperitoneal
based complaints.
1. GERD & Upper GI Pain: The classic pattern of upper GI problem is substernal pain. Pain behind the sternum
may be a direct reflection of the body core. We can’t really test internal complaints with palpation, as we can’t push
through the sternum. We note the location and note how the patient description of pain. A couple of fingers over the
area of the sternum with a burning pain description may indicate reflux phenomenon (there is a strong correlation
between the listed presentation and reflux). There is a 70% association between patients with GERD and patient
presentation of fingertips rubbing up the sternum with stated, burning pain.
2. MI Presentation: MI also has a strong correlation between the way the pain is described and patient presentation of
pain. The typical presentation and patient report list, “something sitting on the chest” with pain behind the chest and
arm radiation. L shoulder is often associated with cardiogenic based pain. Cardiogenic pain can also slip into the R
shoulder and into the jaw based on neurological distributions.
3. Gallbladder or Diaphragm Presentation: Referred pain to the deltoid may be diaphragm or gallbladder disease
(sometimes R or L shoulder).
4. Epigastric/Stomach Pain: Pain in the epigastric area right beneath the xiphoid (epigastric area) that is poke
able/palpable indicates stomach pain. The stomach is intraperitoneal.
5. Mid Back Pain = Pancreas Pain…We also have to worry about the aorta.
6. R scapular pain = Gallbladder or Pancreas (classically is the tip of the scapula).
7. Perimumbilical Pain = The patient describes the pain with fingers circulating around the belly button. In the
differential list are: Appendicitis, and Diverticulitis. These conditions all start with belly rubbing and then localize as
the disease changes/progresses.
Onset of Pain
1. Rapid = Obstruction, or Obstruction Leading to Rupture…These are abrupt events.
2.
Gradual Onset = Inflammation with increasing discomfort and fatigue. Other possibilities include:
Carcinomas, Chemical Irritations, Reflux Irritation. GERD shows gastric secretions impacting the mucosal
tissue.
3.
Short Pain/Colicky Pain = Short, colicky pain is often transient distention. Fibrous bands can narrow the colon.
When the patient eats, small dilation occurs at the proximal tub. The bowel then empties and allows material
through the narrow space. Discomfort doesn’t hit to the next meal when material backs up in restricted areas.
Transient distention, intermittent pain lasting seconds is the typical profile.
4.
Longer Bouts = Irritation and Inflammation…Longer periods of time with discomfort.
5.
Chronic Unrelenting Pain = This is the type of pain caused by cancers, metastasis, or chronic pancreatitis.
6.
Pain for years with Mixed Pattern = Motility disorder, Chronic Bowel Disease, Whipple’s, Crohn’s…The
motility problem can be neurological in nature.
Duration of Pain
Colicky Pain = Unsatisfied Contraction
Ex. Biliary Colic = In biliary colic, the neurological system is in place and recognizes the stretch.. The motor system attempts
to respond to stimulation but can’t fully empty the GI. The patient experiences phases of pain as the material is moved through
the system.
Character of Pain
Burning and Cramping
1. Burning = Causes are either Chemical or Reflux…It is possible that both the pyloric valve and LES are
incompetent. When both valves are incompetent, duodenal content goes back into the stomach. The pH then
becomes more alkaline. Alkaline pH of the stomach by reflux irritates the gastric mucosa. Gastric juices are
force into the esophagus. The esophagus can’t handle the gastric content. The esophagus can be damaged. The 2
valve problems may be iatrogenically induced, disturbing smooth muscles by inducing relaxation of the valves.
2.
Cramping Pain = Motor Problem…Interference with motor work, leads to obstruction. The system can
contract but is not productive (unsatisfied contraction - colic).
DYSPHAGIA
Difficulty swallowing. The patient reports that they feel food gets stuck and they need to wash it down with fluid. People can
have dysphagia without pain.
Odynophagia
Odynophagia is problems swallowing coupled with pain.
Causes of Dysphagia
1. Neurological = Stroke or CNS Problem…We can have neurological compromise leading to Dysphagia.. Stroke
patients can have problems starting swallowing. The middle and lower parts of esophagus will then have problems
triggering the motion of peristalsis.
2.
Obstruction(Inside-Out Problems) = Cancer…We can also have things push from inside out (cancer) creating
obstruction.
3.
DISH (Outside-In Problems) = DISH…About 20% of DISH have dysphagia, as the ALL pushes into the area. Solid
foods would bother the condition more so than liquids, particularly in DISH.
4.
Congenital = Esophageal Atresia…We also have people that never have a normal tube (esophageal atresia) via
congenital under-development.
5.
Other Conditions Linked to Dysphagia = Reflux, Mallory Weis Syndrome, Varicosities – Esophageal Varices
a. Esophageal Varices = Can be seen in people with drug addiction (inducing damage to the liver)
or via portal hypertension (damaging the liver). Venous drainage of the esophagus is part of
portal system and is valveless. 2 way flow through the venous network of the esophagus occurs
with a diseased liver. The condition of portal hypertension can manifest as esophageal varices or
as hemorrhoids.
Elevation of pressure is exhibited throughout the system because of the liver. Webs can form
around the esophagus impacting dilation. The webs cause swallowing of solids to be problematic
and even painful. Venous engorgement can be so severe that contour can change in the lumen
creating webs and varices. On contrast exam, the contrast would pass slowly and show fluid
channels that resist pressure.
*** Upper GI Study -- Varices Present ***
Bag of Worms presentation, as the veins are overfilled to the point where they stiffen the wall of the
esophagus.
Types of Dysphagia
1. Total Dysphagia = Think CNS lesion or Meningioma...Total Dysphagia shows inability to swallow solids and
liquids. Total Dysphagia is often linked with stroke patients or other CNS lesions (brain injuries, SOL). Loss
of motor control of the esophagus occurs.
2.
Progressive Dysphagia= Patient often reports that the condition gets worse over time. They go from trouble with
solids to trouble with semi-solids to trouble with liquids progressing over time.
3.
Fixed Dysphagia = The condition has always been this way. Liquids have never been a problem. Meat and solids
are often a problem. They also report the more they chew the better it is or the smaller the portion they are.
a.
Congenital Webs = A fixed type of Dysphagia that allows passage of smaller items with larger items getting
stuck.
4.
Cardiogenic Dysphagia = Related to chamber enlargement (mostly the LV or RV) and can occur silently.
Chamber enlargement creates an outside in pressure that causes the Dysphagia.
5.
Foreign Body Dysphagia = Dentures, chicken bone, egg shell are examples of items than can be stuck
6.
Scleroderma, SLE and Reynaud’s = These problems all involve connective tissues including tissues of the upper
GI (mouth and esophagus).
a.
b.
7.
Scleroderma = Can be linked with Reynaud’s phenomenon and 80% of the cases have difficulty
swallowing. In. Scleroderma, the myoneuronal junction interferes with conduction of impulse causing lack
of muscular response. Food gets stuck as the muscles become weak.
SLE = Dysphagia is a connective tissue based problem with an active and quiet phase based on active
involvement of the disease. Fibrosis can shrink when the acute autoimmune, inflammatory process goes
down.
Esophageal Cancers= Can create Dysphagia. GI cancers can be benign to very serious. A risk assessment is very
important, particularly in the elderly.
Anatomy of Dysphagia
1. Pre-esophageal = Patient has trouble clearing the pharynx…a). Plummer Vinson Syndrome = Webs that cross the
pharynx 2). Tumor
Plummer Vinson – Example of Pre-Esophageal Dysphagia
The root cause is profound iron deficiency anemia (microcytic, hypochromic anemia).
Some causes of Plummer Vinson induced Dysphagia are:
1. Dietary Iron Deficiency: More commonly seen in the elderly with nutritional
deficiencies.
2. Poor Fitting Dentures: The dentures may cause pain in the gums and mouth during
eating, so they choose not to eat.
3. Thoroughly Cooked Foods: The iron is cooked out of the foods (ex. spinach)
4. Blood Loss in the GI Tract = Leads to anemia
5. Combination = Combination of some of the above reasons
The clinical picture is that liquids pass the web, but solids don’t pass and come back up.
This is a pre-esophageal problem occurring around C5. They cough food up. Glossitiis
(painful tongue) can occur. Red, Swollen, tender tongue is common to Plummer Vinson.
Koilyonchia or spoon nails can develop where the contour of the nail changes as the nails
become brittle.
Long term, the iron deficiency anemia needs to be addressed. A thorough history helps to
find the cause. The webs recede with iron supplementation. Swallowing is restored in
weeks to months after supplementation is started. Another treatment is balloon catheter
dilating/tearing the web. Supplementation must still be enforced before and after the
balloon catheter as the condition can return without supplementation.
2. Esophageal = a). Congenital = A Ring/Schotzke Ring Hypertrophy b). Prior Injury with Fibrotic Repair 3).
Carcinoma
Barrett’s Esophagus & Epithelium – Example of Esophageal Dysphagia
The condition occurs because of long standing GERD. GERD first causes Dysphagia and later shows tissue
transformation. Everyone with various epithelium has GERD, but not everyone with GERD has varous
epithelium. The frequency of acids that travels to the esophagus causes conversion from squamous to
columnar epithelium. We find “gastric tissue” in the esophagus. This is metaplasia to gastric tissue in the
esophagus. As a consequence, the patients have less reflux symptoms, but about 20% converts to carcinoma
(adenocarcinoma).
DIVERTICULUM
Diverticulum can occur throughout the entire GI tract. Sigmoid colon statistically is the most likely site for diverticulum (of
any kind).
1. Esophageal Diverticulum – Zenker’s Diverticulum,
Zenker’s Diverticulum arises from an abnormality with the crico-pharyngeus muscle in the upper 1/3 of
the esophagus. Local defect in the upper 1/3 of the esophagus is the most significant and most risky
of the esophageal based diverticulum.
We initially investigate for Zenker’s because of patient complaint. Failure or disruption to the cricopharygneus
muscle is the root cause. The diverticulum enlarges because of one way valves/check vales. Enlargement allows
content from esophagus into the diverticulum. The tissue stretches and pulls mucosal tissue in. Swallowing causes
the muscle to be forced apart allowing food into the osteum.
*** View on Screen ***
We see an early defect. We then see mucosal tissue within the muscle (cricopharyngeus). Over time the
diverticulum grows.
*** Cervical Spine Film with Diverticulum Sketch Overlay ***
The esophagus starts at about C5. Zenker’s is an upper 1/3 based problem starting at C5 or slightly lower. We
have to go looking for the condition to come up with the diagnosis. The contrast column (white ball) moves into
the diverticulum. Contrast can be “grape sized” or “ping-pong ball sized.”
*** Chest Film ***
72” PA gives us a good representation of relative size. Zenker’s can even be larger than the aortic arch. If the
chest film I taken at 40” AP, the shot gives magnification of Zenker’s. The film on screen demonstrates that the
diverticulum is very big. The patient has trouble clearing the pharynx because the diverticulum takes up space.
The diverticulum is positioned between the trachea and the spine. The diverticulum pushes on the esophagus
anteriorly, but can’t go posteriorly because the spine is rigid. Dysphagia will be the complaint.
Relaxation of the Cricopharygeus During Sleep – Zenker’s Diverticulum
During sleep, relaxation of the criocpharyngeus occurs. The grip is effectively loosened and
progressive Dysphagia occurs. Thick liquids and solids can now be problematic. The muscle
loosens its grip and tissue decompresses forcing the content back to the esophagus. Content
can end up back in the mouth. These food particles are not digested and putrefied causing bitter
tasting vomit.
The patients are in deep sleep and may be at risk for vomiting or swallowing the putrefied material.
Request that the patient spit the food particles out. Have them bring the particle into the office. Check
for mixed meals. Mixed meals means sequestration or obstruction in the esophagus. Ex. Meals over a
couple of days in the diverticulum..
Dysphagia, putrefied vomit at night, mixed meals, screams Zenker’s Diverticulum.
The most serious complication is aspiration pneumonitis. The epiglottis is relaxed during sleep.
Relaxation of the of the epiglottis during sleep can allow food content/foreign body into the lung. The
condition can cause foreign body pneumonitis, leaving scarring in lung tissue or bacteria
infection of the respiratory system.
*** Lateral View – Contrast Exam ***
The collection of material is bigger than the vertebral body.
Treatment of Zenker’s Diverticulum
1. Surgery = Old method of treatment. The complication rate was severe.
2. Endoscopic Cleaning/Lavage/Stitching = Now they wash it with saline and stitch the opening to close it off.
Only in the worst cases, do they buttress the muscle. The procedure is now done endoscopically with
minimal complications.
2. Traction Diverticulum
MID ESOPHAGUS/HIATAL REGION OF THE LUNG (middle lung field) is the area of this diverticulum. The
opening into the diverticulum is big showing free communication. Traction diverticulum are often silent and found
incidentally with contrast exam. Lymph node inflammation triggers scar tissue adherence of the node to the
esophagus. Scar tissue shrinks and pulls apart the outer layers of the esophagus creating a defect in the outer muscular
wall of the esophagus. We don’t have Dysphagia because the diverticulum doesn’t push against any relevant structures.
Often nothing needs to be done about traction diverticulum. See it, explain it and forget about it.
3. Pulsion Diverticulum
Can occur from both congenital and acquired forms. Pulsion diverticulum occurs in the distal 1/3 of the esophagus and
can grow very large. The large size still may not make it noticeable as no pain, no Dysphagia typically occur. The
finding is often accidental. Gravity can hold content in the diverticulum. The diverticulum can be seen on plain film as a
midline mass above the diaphragm
a. Congenital = Esophagus doesn’t form correctly, missing a section of muscular wall coupled with mucosal
hypertrophy
b. Acquired = Acquired by obstruction due to: a). Foreign Body b). Hiatal Hernia.
GU-GU EXAM 10/27/08
GERD
*** Pre-printed slides ***
Reflux: Dysfunction of anti-reflux mechanisms
Caustic Material: Acid, pepsin, bile, pancreatic enzymes (pancreatic enzymes are a 2 valve problem --- LES & Pyloric
Valve)
Sufficient Duration of Contact: Inadequate clearance mechanisms
Most times the caustic material is from the body itself and not exogenous poisons or toxins. In either case, the mucosal
resistance is overwhelmed.
Gastric Secretions
Excess gastric secretions is often not the etiology of the problem. These patients are often prescribed medications for excess
secretions, that aren’t effective because they don’t address the underlying problem (Lower Esophageal Sphincter/GastroEsophageal Junction). The source of the problem is lack of tone and un-coordination of the sphincter.
Pattern of GERD
1. Erythema/Redness = First sign of injury to the distal esophagus is erythema/redness. The tissue is sensitive and
annoyed. There is burning pain. Typically the patient rubs over the sternum.
2.
Erosion = 2nd step is erosion with the defect contained by the mucosal layer.
3.
Ulceration = 3rd Stage of the progression. Mucosal damage occurs with the problem penetrating to the
submucosal layer.
4.
Perforation = 4th Stage that shows rupture through the submucosal layer. Small numbers of people arrive at
stage 4 (perforation).
Sphincter Quality
The LES is not a good sphincter and can be interfered with very easily. Mechanical pressure alone can defeat the LES. The
condition can even be iatrogenically induced as medications can inhibit smooth and skeletal muscle relaxing the sphincters.
Pregnant females in trimesters 2 and e can show GERD with increased IAP and hormones that cause relaxation of tissues and
the LES.
Pressure Change With Inspiration and Expiration
Pressures vary in the LES with inspiration and expiration. Breathing in causes the hiatus to grip the LES a little tighter and
causes increased pressure. Breathing out relaxes the LES as pressure drops about 10 mm. WE see a pressure difference of
about 10 above and below the diaphragm. Pressure changes favor reflux of stomach content back into the esophagus.
Normal Resting Pressures
LES = +25 mm Hg (poor excuse for a sphincter…very easy to interfere with)
Intra-Thoracic = -5 mm Hg
Intra-abdominal = +5 mm Hg
*** Study on Overhead ***
Mannometers: Long string with yellow pellets that is a series of pressure sensors put into the system.
pH Sensors: Can be attached to a string monitoring pH of the area above the GE junction
Examples of GERD
IN a patient with LES weakness, sudden changes in intra-abdominal pressure will show change in LES pressure leading to
symptoms associated with GERD. Breathing in creates better separation between esophagus and stomach. Breathing out may
show acid splash due to pressure changes. Pushing on the patient suddenly causes changes in IAP (intra-abdominal pressure)
and drop pH as acid is forced into the esophagus. When pressure is release (stop pushing on the patient), the pH goes back to
normal. Changes of position, sneezing, coughing, punching or poking the abdomen can mechanically overload the stomach
and LES leading to GERD.
*** Study on Overhead -- Graphs***
Each pressure spike from the pharynx to the esophagus is called advancing peristaltic wave. The condition is normal. The
Upper 1/3 of the esophagus is skeletal muscle (striated). We get obligatory contractions of the middle and lower 1/3. We
can’t consciously control the middle and lower 1/3. The advancing waves propel the material down the esophagus.
Interruptions of the advancing peristaltic waves lead to dysfunction.
The activation of the primary wave shows a pH of near 7. 7 is a normal value. If the LES does its job and isolates the stomach
from the esophagus, the pH is neutral. In GERD, stomach recoil occurs because of changes in pressure and poor LES quality.
Failed Peristalsis
Contractions don’t occur in middle and lower 1/3 of the esophagus. The LES relaxes and acid enters the esophagus. The pH
sensor is triggered in the upper portions of the Esophagus. The gastric acid and gastric secretions must travel a good deal
upwards to trigger the sensors. Prolonged relaxation allows stomach recoil jutting content back into the esophagus.
24 Hour pH Monitor
The test allowed us to discover hormonal, mechanical and other pathological ways (ex. medications) to interfere with the
process.
Hiatal Hernia
Most frequent complaint with a hiatal hernia is GERD. Manual reduction of the hiatal hernia is possible and can help
with both the hernia and GERD. The technique is a low tech way to help the patient.
Peptic Esophagitis(due to GERD) – Signs and Symptoms
Sour Taste: Esophograms show bubbles rising up the esophagus stimulating the taste receptors on the back of the tongue.
Sour tastes can be triggered by carbonated beverages and antacids.
Difficult or painful swallowing; choking: Early symptom is painful swallowing. Fibrotic repair and shrinkage of fibrotic
tissue leads to progressive Dysphagia with limited contraction. Choking is due to more prominent problems like
presbyesophagus.
Chest Pain (r/o cardiac): Tends to be retrosternal pain. Assess the likelihood that heart disease may be the cause with
thorough testing. The DDx can be hiatal hernia or cardiogenic pain.
Back Pain: A common complaint of back pain/parathoracic pain. True referral pain is not reproducible, so separate the
biomechanical (which can be provoked) and the referral (can’t be provoked).
Heartburn
Epigastric pain or distress
Nausea and vomiting
Anemia (blood loss): Long-standing conditions…Check for palor, Low BP, high HR…Do a blood panel to document for
anemia
GERD WITH CHALASIA
*** Picture on Overhead of Young Kid ***
Chalasia is an extreme version of GERD that shows free communication between the stomach and the esophagus via the
LES. We can’t tell whether contrast goes in or contrast goes out as they look alike.
*** Endoscopic Picture on Overhead ***
The first 3 destructive stages of GERD are present: 1).Erythema 2). Erosion 3). Ulcer. The outer rim is red indicating
erythema. The gray rim is erosion. The white rim is the ulceration. Ulceration goes into the submucosal tissue. The
shiny/silvery areas are scar tissue that will shrink over time, restrict the opening and cause Dysphagia.
Drug Management
Patients are sold anti-secretory meds (proton pump inhibitors or H2 blockers). The condition is usually not over acid
production. The condition is weak muscle. Medication to treat the weak muscle of the LES affects every other muscle and
valve in the body. Medication to treat the pH/acidic problem masks the condition improving symptoms while not addressing
the root of the problem. Overall, drugs are not the solution as they can only treat symptoms and not the problem.
GERD With Transition to Barrett’s Esophagus
*** Picture on Overhead ***
Distal Esophagus above the LES shows ulceration with fibrotic repair. This patient has Dysphagia and reflux. The condition
may be driven to metaplasia (Barrett’s Esophagus). Barrett’s occurs when esophagus becomes more gastric in nature.
Reduction of irritation occurs as the esophagus becomes a more gastric environment. 1/5th of the time the condition can
go to adenocarcinoma, a serious tumor of GI tract.
GERD With Hyperplasia and Anemia
Hyperplasia (tissue overgrowth) can also occur. Blood leakage is common. Sometimes the patients throw up blood. Blood
loss can be sufficient to create anemia. Menstruating females with GI bleeds are more likely to be anemic. GI blood loss is
the most common source of iron deficiency anemia in men, and in the top 3 for blood loss iron deficiency anemia in
females. It deserves investigation.
Ulcer vs. Tumor
*** Picture on Overhead ***
A white rim is present where contrast collects. White radiating lines are called Spoke Wheel appearance. The
ulcer is the hub and the spokes are the white lines. Spoke wheel appearance is typically an ulcer.
Tumors can also ulcerate. The most mature center of the tumor outgrows its blood supply as it attempts to push outwards.
The lack of blood supply to the tumor foci causes liquifactive necrosis. The tumor collapses into itself as a crater, cradling
contrast, looking like an ulcer during radiographic exams. The tumor obliterates the ruggal folds. An ulcer crater without
spoke wheel appearance is almost always an aggressive cancer till proven otherwise. Typically, it is comforting to have
ulcer with spoke wheel appearance because that is a benign indication that an ulcer (not a tumor) is present.
3 Patterns of Contrast Collection
1. Benign/Intramural Ulcer = a). Contained b). Non-contained
2. Diverticulum = Increased Sized contrast column in the esophagus, SI, or stomach
3. Intraluminal Collection = Cancerous (contrast collects in the center)…
Heartburn in Pregnancy
Frequency 30-50% in Pregnancy
Mechanisms:
Hormonal: Increased Estrogen and progesterone ---- LES dysfunction
Mechanical: Enlarging Uterus --- Increased Intra-abdominal Pressure
Commonly both hormonal and mechanical causes the sphincter to he incompetent…Middle to late trimesters are more common
Common Therapies: Antacids, Sucralfate, H2 Blockers
Simple Solutions to GERD Management
This is a management problem for chiropractors.
1. Patient education (smaller meals)
2. Do not eat and lay down (it brings fluids and secretions in greater contact)
3. Examine medications
4. Lay R side down = Takes product away from opening and can help reduce discomfort.
5. Eating and staying upright is a good solution.
Hiatal Hernia and GERD
LES Dysfunction– Pressure often low
Gastric Pouch – Intrathoracic Reservoir
Diaphragm – No Esophageal Pinch
*** Axial/Sliding Hernia ***
LES is pulled from esophageal hiatus and we don’t support from diaphragm. The hiatus holds onto the cardiac portion of the
stomach. They have an extra 15 mm of pressure differential causing the reflux. The most common complaint is retrosternal
burning called heartburn/GERD.
Barrett’s Esophagus & GERD
Columnar Epithelium replaces squamous epithelium in the distal esophagus Metaplasia occurs. We need to reduce the GERD
incidence and reduce further conversion of tissue. Watchful waiting is the appropriate response.
1x per year for the next 2-3 years we biopsy/ check for further neoplastic change. They check for 2-3 years in a row, and then
if no problem they then check every 2 years. 8/10 times the change in benign. 2/10 times malignant change can occur.
Surgical methods remove GI tissue. Removal of GI tissue comes with complications as nervous plexi and vascular
channels need to be restored. We also worry about intra-thoracic and peritoneal complications. (peritonitis). Risk to
benefit ratio must favor surgery for it to be performed.
Incidence of Adenocarcinoma – Barrett’s Esophagus
800 cancers per 100,000 patients
1 cancer per 125 patients (.8%)
Indications for ambulatory Esophageal pH Monitoring
Patients with normal endoscopy and:
Typical GERD symptoms unresponsive to anti-reflux therapy
Atypical Chest Pain
Extra-esophageal disorders possibly related to GERD (asthma, chronic cough, chronic hoarseness, posterior
laryngitis, and globus)
Patients with endoscopic escophagitis unresponsive to anti-reflux therapy
Patients considered for anti-reflux surgery: Surgery tightens the hiatus…Lots of risk and expense (including achalasia or
diaphragm risk.)
Recorder Tool and 24 Hour Monitoring
Monitors pH and secretory changes. It may be a better tool than endoscopy and contrast exams. The recorders help explain
that there is more ways to interfere with mechanisms than what we thought. Do not choose a – test result from contrast or
endoscopy over the patient presentation. 24 Hour pH monitoring is the best way to concur or eliminate the GERD diagnosis.
Extra-Esophageal Problems and GERD
Extra-esophageal based problems may be linked with GERD (asthma). The gastric secretions inflame the airway and can
induce swallowing of material (due to bypass of the epiglottis). Swallowing of material/gastric secretions stimulates an
asthmatic attack. Chronic cough and hoarseness are though to be a product of repetitive GERD on the vocal cord with
changing vocal characteristics.
Lifestyle Modifications
Elevate the head of the bed: Little Elevation (2-3 inches)
Lose Excess Weight…10% reduction in weight has a big impact on joint pain and GERD. 10% is do-able.
Eliminate:
Tobacco:
Alcohol:
Bedtime Snacks: Don’t eat and lay down (1-2 hours before bedtime). Food stays near the opening of the stomach
and can create pain. The distress by eating and lying down is related to what they eat. Alcohol and fatty foods can
induce the reflux. Hot sauces can be mucosal irritants further damaging/irritating tissue. The stomach takes longer to
get rid of proteins, fats, and irritating foods.
Certain Drugs: New drugs or changed medication can impact GERD (changes in dosage, changes in drugs)
Fatty Foods
Chocolate
Peppermint
Others: Tight Clothing (increased IAP), Back Belts & SI Belts (Increased IAP), Inversion Tables, Thoracic
Subluxation
10/28/08
*** Missed 1st hour ***
ESOPHAGEAL VARICES & DYSPHAGIA
*** Esophogram on Screen ***
“BAG OF WORM APPEARANCE “ = A contrast term for coiling, linear filling defects of the esophagus. IN this patient,
portal hypertension and esophageal varices are present. As a consequence of alcoholism, damage to liver caused backup and
esophageal varices. This is a management problem.
MALLORY WEIS SYNDROME
Alcoholism, induced vomiting. The vomit causes tearing (vertical/linear) of the esophageal lining. The person may note
blood with vomit that is bright red arterial blood. Angiogram is a better test than contrast exam for this patient. Brisk
bleeding is managed with cauterization via endoscope. Violent retching causes esophageal tears, inducing blood loss.
CHALASIA
Classically, chalasia is opening and puking (free communication between stomach and esophagus facilitates the
vomiting). In children over 3, reliable vomiting requires a contrast study or endocscopic exam. If +, it may require aggressive
management. In newborns and infants, chalasia is normal.
PRESBYESOPHAGUS
There is age related un-coordination between primary and secondary peristaltic waves. In very bad presbyesophagus,
they cant’ swallow properly and must flush the food/bolus down with fluids. The un-coordination can be modest enough
to be occasional problem and severe enough to be every meal. Medication and surgery are not effective options. This is a
management process.
The diagnosis of presbyesophagus is given with testing and diagnosis by exclusion. Doctors rule out diabetic neuropathy of the
esophagus causing Dysphagia.. History helps separate the 2. Presbyesophagus is slowly progressive, adult aged, with
denial of DM. Diabetic neuropathy of esophagus shows the problem as a juvenile, long history with DM problems, and
Dysphagia is the latest complaint.
Upper GI barium swallow test shows a weak to absent upper 1/3 contraction. We show suspension of the barium column
indicated by more than 2.5 contractions to force the food downward. Solid foods tend to produce prominent symptoms and
liquid foods are easier to manage.
Radiographic terms include curling phenomenon/barber pole phenomenon, showing white and black areas. The
problems is a management problem, not a drug or surgery problem. Have the patient drink fluids. Also, remind them to
eat foods that are more liquid/easy to swallow and chew the food more before swallowing.
DIFFUSE ESOPHAGEAL SPASM
The spasm shows significant pain and can be spontaneous or due to cold liquids. The spasm can be mistaken for a heart
attack. They have a normal contrast study. History and exam should be geared towards ruling out DM, SLE, and Scleroderma.
Also, rule out hiatal hernia. This is a diagnosis by exclusion done by testing.
ESOPHAGEAL ATRESIA
Congenital Esophageal Abnormality = A “sheet” across the esophagus that causes blockage.
Classification system
1. Class 1 = Complete Absence of the Esophagus = We won’t see this often. The pharynx ends in a stump and there is
a space where the tube should be. The tube never united. This occurs with other organ mal-development. Class 1 can
be a lethal, congenital abnormality. Regurgitation is a hallmark feature.
2. Class 2 = Membrane Blockage of the Lumen = The motor and nervous system are intact. The parts of the esophagus are there.
Antero-lateral surgery can be done to stitch the parts together. At first, there is a fibrous zone that doesn’t react to stimulation. In children,
stem cell regeneration occurs. Regurgitation is a hallmark feature. In children, regurgitation occurs very quickly.
3. Class 3 = Fistula….Fistulas show abnormal communication/conduit between esophagus and
trachea. Mother’s milk can be trapped in the fistula causing aspiration pneumonitis. The foreign proteins of
milk annoys the lung tissues. The history is a young kid with multiple episodes of pneumonia.
Repeatable episodes make the condition stand out.
Chest film may show consolidation. Contrast exam may show a channel. Endoscopic exam cannot be used unless
the child is over 5 lbs. Repeat pneumonitis will impact quality of life. Fistula induced pneumonia/aspiration
pneumonitis is the most common reason for pneumonia in newborns. Doctors stitch the esophagus
during a minimally invasive procedure. The procedure has excellent long term prognosis.
MISCELLANOUES ANOMALIES & DYSPHAGIA
1. Duplex Esophagus = One good tube and one bad tube.
2. Duplex Pharynx = A Y shaped entry via 2 pharynxes meeting up. Usually the smaller one causes the problem. Duplex
pharynx or esophagus is usually surgically managed if problematic. If not a problem, they will leave it alone.
PLUMMER VINSON -- DYSPHAGIA
Dysphagia with early vomiting are clues to think about Plummer Vinson. Contrast studies are not good to identify the
condition as liquids pass right through the webs. The best study is endoscope or even a mirror on a stick to view the webs.
Profound iron deficiency anemia triggers the webs. Iron deficiency anemia can happen in kids and the elderly with poor
socio-economic status. Another reason can be poor fitting dentures. Poor fitting dentures will make the gums raw. Another
way is via the loss of blood. Webs also keep out foods with iron that further perpetuates the problem.
Treatment for Plummer Vinson
Supplement with Iron.
Iron injections
Balloon Popping of the webs + supplementation…If we pop them too quickly and do not supplement, they will come
back…You typically wait 3-4 weeks after supplementation to pop the webs. Blended foods with iron are preferable prior to
popping of the webs.
CONGENITAL ANOMALY OF STOMACH --- DEXTRO POSITION
Hiatus on the R. Terminal end is on the L in this condition. The duodenum is dragged over as well. This can be a complete
flip (situs inversus where everything is flipped --- all the organs are reversed) or partial flip. The more complete the
reversal, the less chance for problems. Situs inversus may be found by mistake, thinking the marker was placed in the wrong
spot during an X-ray exam.
PYLORIC STENOSIS & GERD
The condition is both congenital or acquired.
A). Congenital = In infants the situation is congenital. The theory goes, in utero, the fetus gets strong stimulus to the pyloric
valve. The valve becomes so massive it is “muscle bound.” The pyloric valve cannot relax or is incompletely relaxed. IN
children, strong stomach contraction and improper opening are linked with weakness in the LES. The baby spits due to healthy
contraction by the stomach (normal in children). Pyloric stenosis patients will spit for great distance (often feet).
B). Acquired Version
Seen in adults with peptic ulcer disease. Peptic ulcers irritate/facilitate or damage/fibrose the tissue. If the ulcer is near the
pyloric channel, it can be facilitated keeping the pyloric valve in spasm. The condition can show fibrotic repair with closure of
he pyloric valve. Stomach contraction forces material through the LES.
The description is, “I’ve thrown up before, but not like this and every time now it happens like this.” Contrast exam is used
and we see delayed gastric emptying. There may be reverse peristalsis present during vomiting. We watch the contrast in
real time and we won’t see dilation of the valve indicating stenosis.
HIATAL HERNIA
Types of Hernias
1. Sliding Hiatal Hernia/Axial Hiatal Hernia = The simplest and most common of the hiatal hernias. The hiatus is
squeezed. The hiatus is pulled or pushed above the diaphragm. The most common complaint is retrosternal burning
from GERD. Reflux with retrosternal burning is the most common complication of hiatal hernia.
Hernia Terminology
A). Incarcerated Hernia = The condition is not reducible. This patient needs to go to the hospital. We need to listen for
bowel sounds above the diaphragm (as evidence that function occurs). Loss of bowel sounds is a bad sign indicating an
immediate emergency
B). Strangulated = Worst Case Scenario…Occurs once the condition goes silent. Venous engorgement increases pressure to
match arterial pressure. When pressure equilibrates, no net flow of blood, nutrients and gases occurs. The GI tract becomes
ischemic. The patient will be in extreme pain. This is an emergency!
C). Double Bubble Sign/Double Density Sign = Thick walled collection of contrast (?) in the GI and biased to the posterior
indicates a hiatal hernia.
D). Reducible = If the grip is not tight, the condition is reducible. The condition is manageable and does not require
surgery (often in sliding hiatal hernia/axial hiatal hernia)
*** X-ray ***
Flat white line is air fluid level. Gas collection that project above the heart = double density sign.
*** X-ray ***
Granulomas are present with increased fibrous tissues on R side of the heart. We think a full hiatal hernia is present
*** Contrast on Same Patient ***
Quite a bit of stomach is above the diaphragm. We see a 9 cm thoracic aortic aneurysm on the film. We take notice at 3 cm, 4
cm is a vascular consult, and at 9 this thing is ready to pop. The study is used to document. In today’s medical world, 9 cm
aneurysms always rupture.
2.
Rolling Hiatal Hernia/Para-esophageal Hernia = Stomach rolls next to the esophagus in the hiatus. Paraesophageal hernia is a greater producer of Dysphagia than sliding hiatal hernia. Limited ability to dilate causes
Dysphagia by not allowing food. through. They point to the area (food is stuck here). Theses patients can get reflux
that is not esophageal reflux, but static secretions in the stomach. Prolonged stomach contact can create irritation
and is a pain generator. They show retrosternal burning due to retention of HCL above the hiatus. It is more
difficult to put food into the esophagus due to the tight fit of the hiatus. .
*** Contrast Study ***
Contrast above and below the diaphragm indicates a paraesophageal hernia.
3.
Intrathoracic Stomach Hernia = The stomach is connected to the pharynx. The stomach is pulled above its
normal alignment because of surgery, tumor, or removal of a tumor. The problem can also be congenital.
The tissue above the diaphragm is not held by ligaments. The tissue can fold and strangle itself. The name is
volvulus (folding of GI tissue). Volvulus and strangulation cuts venous drainage, raises pressure and creates ischemia
Serious problems can develop.
*** The 3 types of hernias can then be further separated into: A). Reducible B). Incarcerated C). Strangulated ***
Reducing a Hiatal Hernia
Heel Drops: quickly drinking a little water and have them rise on their toes and drop down (calf raises) At most, go up 1 step
and 1 step only and jump landing stiff legged to reduce the hernia. If that doesn’t work, call the doctor and get them in. Put
them on a table with about 15 degrees of angulation (bending knees) to soften blow. Breathe in deeply to maximally flatten the
diaphragm. The doctor must poke pretty deep in the middle of the diaphragm. As they blow out, traction down. Do it 3-5
times. This maneuver may reduce the stretch irritation causing less problems.
11/3/08
DIAPHRAGMATIC HERNIAS
Can be acquired or congenital.
1. Bochdalek Hernia = A diaphragmatic hernia, that tends to congenital and posteriorly located. It is incomplete
formation of diaphragm or gap in fibrous tissues. These hernias are usually paired.
*** Pneumonic…Bochdalek = Back ***
2. Morgagni = Defect is 1 side or other (typically L) in the area of the xiphoid (anterior hernia). The dome of
diaphragm is missing and will show the liver above the diaphragm on the R.
3.Hiatal = Most famous of the diaphragmatic hernias.
______________________________________________________________________________________________________
GASTRITIS
Inflammation of the gastric mucosa. The suspected etiology list is long. There are many ways to irritate the mucosa to make
the condition symptomatic. Gastritis is not a specific entity.
ACUTE GASTRITIS
Pink, red and inflamed tissue is present in the mucosa. The condition can progress, but most people stay in this category.
1. Aspirin = Can cause acute gastritis…Older people often take this as a blood thinner to prevent clotting in the arteries.
People are using aspirin with greater frequency for pain control and for anti-coagulant properties. The long use and
abuse increases the risk for gastritis. We try to take the lowest affective dose (about 25 mg – the baby aspirins) to
reduce risk. Inform your patient of this and have them ask their doctor if the dose may be too high.
2. Excess Alcohol = The amount is variable. Generally, drinking so much that your stomach hurts is too much. Alcohol
affects gastric secretions (increasing secretions) and irritates your stomach.
3. Heavy Smoking = 2 Main reasons for inflammation: 1). Vasoconstrictive chemicals in the stomach that don’t allow
normal dilation. Tobacco keeps the vessels narrow limiting blood flow and limiting repair of GI mucosa. GI mucosa
is very metabolically active demanding a lot of blood flow. Decreasing blood flow leads to loss of mixing/mashing
function as well as loss of gastric secretions. 2). Tobacco weakens the control over the pyloric valve and pyloric
reflux develops. Stomach contents return from the duodenum. Mucosa weaken when alkaline products are forced
back into the stomach. Bile salts, pancreatic and liver products come back and attack of gastric mucosa. The stomach
attempts to fight the rise in pH, by increasing the capacity of chief and parietal cells to increase acid load. The end
result is injured tissue that can’ resist alkaline loads that irritates itself by its own acidic productions.
***The key ingredient is choice. We choose to take aspirin, choose to drink and choose to smoke ***
Other Etiologies:
4. Chemotherapy
5. Food Poisoning
6. Uremia
7. Infection
a. Cytomegalovirus
b. B). H. Pylori = Linked with peptic ulcers & duodenal ulcers. 7/10 people with peptic ulcers have H.
Pylori. 15% of people with culturable levels of H. pylori show acute gastritis
8. Stress
Gastritis Complaints
Most complaints are due to contact irritation. Pain is listed as being below the liver, burning pain projecting to the
abdominal wall (not retroperitoneal). The patient’s condition can get bad enough to get the true anorexia. The inflammation
of the gastric mucosa is so great, that edema forms in the wall of the organ triggering the stretch receptors in the satiety center
of the brain causing anorexia.
Gastritis patients live in a persistent state of stretch simulation. The stretch stimulation suppresses the appetite. Other
complaints are fullness, vomiting and general discomfort.
We often miss gastritis with a lot of – studies. Endoscopic analysis increases our findings of erythema (typical of gastritis).
The endoscope allows us to sample tissue. The endoscopic exam with biopsy is the poof + or proof – for gastritis. We find the
irritating substances in the gastric mucosa tissue.
The worst cases of acute gastritis may show slight elevation of body temp. They can even get some shaking and chills. This
tends to be the patient that may transition into chronic gastritis. The worst cases of acute often transition into chronic gastritis.
Treatment
Ask the patient about recent nutrition, smoking, drinking, aspirin use and other habits. You may want to ask them to amend
their habit. Another thing to do is to adjust the mid-thoracic subluxations.
Endoscopy with Biopsy
They have to complain about the case several times to get endoscopy and biopsy done. The first time, the test is usually not
approved. Most of the time, they improve with specific dietary and habit recommendations. If the case continues and the
episodes repeat, you need to address the issue.
CHRONIC GASTRITIS
Histological change in the wall of the stomach with fibrous tissue found on endoscopic exam in the mucosa indicates a change
from acute to chronic . The increase in fibrotic tissue causes loss of function: 1). Loss of muscular activity 2). Decreased
Secretions.
The repair site and tissue continue to get inflamed. The patient tends to worsen/progress with time as more tissue becomes
fibrotic.
Causes of Change from Acute to Chronic
1. Drugs = Specific drugs, including aspirin can lead to the fibrotic change.
2. Inflammatory Bowel Disease = Particularly Crohn’s….Most famously the site is the distal ileum, but it can be
anywhere from mouth to anus. The condition can even affect the stomach.
3. Viral Infections = Can lead to fibrotic change.
4. Idiopathic = We can’t identify truly the source of the insult. We can identify the histological evidence and
diagnosis, but can’t find the etiology.
Our Role
Observe the situation and make available the choices to the patient. AS fibrotic changes increase, secretory levels decrease..
We lose the ability to break down proteins and our poop becomes protein laden. The patients may go after endogenous
proteins and we see “mushy muscle” (muscle is a source of protein storage). WE may see anemia(pernicious anemia).
Patients can have low levels of acid (achlorhydria).
Supplementation is often the best conservative way to treat chronic gastritis.
GIANT HYPERTROPHIC GASTRITIS/MENTRIERE’S DISEASE
*** Upper GI Study on the Screen ***
The hills are too big and the “valleys are too small” as thin contrast streaks in the antrum are present. We see enlargement of
the cells of the rugal folds generating the “high hills.” Gastritis occurs as pain/irritation occurs in the stomach. The
hypertrophied tissue displaces gastric and parietal cells. We lose secretory capacity. We see bulky stools with large
molecular weight proteins. Acid output of stomach declines. The condition is progressive.
The etiology is idiopathic. We are concerned because we cannot tell the difference in contrast between lymphoma and
giant hypertrophic gastritis. Lymphoma is more serious and should be considered with + contrast study.
Stretch receptor stimulation is present that sends message to the cord. The satiety center is stimulated. They show true
anorexia. This is a patient that cannot break down proteins n the stomach. Uptake is not available in the SI. They go after
muscle or endogenous protein sources. Patients lose strength and get “mushy muscles.” They are overly tender
(myomalacia --- softening of the muscle). Hypoalbuminemia can also be present.
*** Menetriere’s Slide = Looks identical to Zoellinger Ellison on Contrast Exam because of impact to ruggal folds ***
ACID OUTPUT TESTING
BAO and PAO Testing – Acid Output Testing
Nasogastric tube is introduced by the nose and worked down to the antrum of the stomach (pre-pyloric area). The
first measurement is the BAO (Basal or Base Acid Output). This is the pre-stimulus measurement or the
measurement at rest. We then do a histamine challenge test. Histamine increases Gastrin. Gastrin is the hormone
responsible for chief and parietal cell secretion. With histamine ---- gastrin ---- chief and parietal cell increase --increased release of HCl ---- PAO (Peak Acid Output).
1. Normal BAO should be less than PAO (drop in pH should occur when going from rest to stimulus to
peak stimulus) (E/N = Essentially Normal for BAO and PAO)
*** Gastritis has normal secretory profile, even with a complaint. BAO is less than PAO, with BAO and PAO normal
in gastritis ***
2. Hypo-secretory patients will have BAO at normal range. Histamine administration shows low PAO.
So in hypo, BAO is less than PAO (but PAO is decreased when compared to normal). This is the Giant
Hypertrophic Gastritis patient. (BAO is essentially normal for Hypo)
*** Menetriere’s/Giant Hypertrophic Gastritis shows less #’s of chief and parietal cells (early hypo-secretory
condition). ***
3. Hypo-Late = We see decreased BAO and very low PAO…Hypo-Late shows BAO less than or equal to
PAO (with decreased BAO)
*** Hypo-Late can show great compromise in the stomach and BAO can equal PAO levels but BAO is very low and
PAO is exceedingly low (due to low BAO levels). The patient is at peak due to loss of cells. ***
4. Hyper Secretory = Increased BAO, yet PAO is essentially normal…BAO is roughly equally to PAO
(PAO is roughly normal). We say that the stomach is living in an maximal secretory environment. We
can’t get the stomach to go beyond maximum...Ex. person running on a treadmill and you force then to
run faster and faster, at a certain point that can’t go faster and they are at peak output. The same occurs in
the stomach where the stomach is at max output and peak demand.
*** Hyper (Zoellinger Ellison or GASTRINOMA where the patient is in a persistent state of hyper secretion (BAO
levels are high, give them histamine, and we see PAO levels in normal range and BAO about equal to PA…So we think
the stomach is in stimulated state because BAO is very high) ***
*** Be able to predict an outcome with information from the chart ***
ZOELLINGER-ELLISION SYNDROME/GASTRINOMA
Gastrin secreting tumor present, that can’t be shut off. They are outside the – feedback loop. The stomach always
produces acid. The duration of peak level production of acid overwhelms the mucosa.
The ruggal folds hypertrophy. Persistent demand of peak output from the body requires reserve capacity. The stomach tries
to be more capable with HCl and Pepsin. The body reacts to the stimulus hypertrophying the ruggal folds.
This patient is in the hyper category on the acid load chart. The cause is tumor. The tumor can be in many locations
including pancreas, stomach, and Meckel’s diverticulum.
Zoellinger Ellison Syndrome Clinical Triad
Gastric Acid Hyper-secretion
Severe Peptic Ulcer Disease
Non-beta islet cell tumors of the pancreas
The tumors produce Gastrin (G17 and G34); referred to as “gastrinomas”
Tumors localized usually to head of pancreas, duodenal wall or regional lymph nodes.
About ½ of gastrinomas are multiple and 2/3 malignant
About ¼ have multiple endocrine impact????
Clinical Features That Can distinguish ZE Syndrome from DU
Diarrhea = Increased gastric acid secretion
Weight Loss/steatorrhea = Decrease duodenal/jejunal pH inactivation of lipase, Mucosal Inflammation
Large Gastric Folds = Trophic Effect of Gastrin
Large amounts of gastric secretions = Secretory effect of gastrin
Family history of endocrine tumor, Increased Calcium= MEN 1 = Parathyroid tumor/hyperplasia
Intractable or Post-surgical recurrence of ulcer disease = Acid Hyper secretion due to ???
Fasting and Stimulated Plasma Gastrin are Sensitive and Specific in the DX of ZE Syndrome
ZE Peak # = 150-100,000 in fasting state
Normal Patient = Less than 150 in fasting state
Treatment of ZE Syndrome is Based Upon Clinical Findings
A). If isolated duodenal wall tumor is present on CT and/or visceral angiography = Surgical resection followed by
measurement of gastric acid secretion
B). If no evidence of primary tumor, or metastatic tumor = H/K ATPase inhibitor or H2 receptor antagonist therapy in
dose determined individually to suppress fasting acid output to less than 10 mmol/h. Drug efficacy check at 3 month intervals
*** Total gastrectomy is generally obsolete. Removing the tumor rather than the stomach will reduce gastric secretions (we
recognize we change gastrin levels by removing the inappropriately secreting tumor ***
Imaging Studies
MRI, PET, Radionucleotide Studies = Tumors signal very differently than surrounding tissue .
ZE looks very similar to Menetriere’s on Contrast Study.
ZE vs. Menetriere’s
ZE hypertrophy shows stimulated capacity to increase (hyper-secretory on acid output testing) vs. Menterieres which shows a
hypo-secretory condition. Mentriere’s treatment is just management. ZE treatment is the hunting and removal of tumors.
11/4/08
PEPTIC ULCER DISEASE
The cause of why people ulcerate may be multi-factorial, including: environmental, what they eat, bad formation of
mucosal tissue, bacteria (H. Pylori), medication (Prilosec, Tagament, Zantac, and Nexium). The medical community
thought too much acid was the problem. In reality, the medical pathomechanical model may be wrong. 90% of duodenal
ulcers are associated with H Pylori and 70% of gastric ulcers are related to H. Pylori.
Research found that you do indeed feel better on the standard medical drugs for ulcer, but when you stop the meds you feel
the same or worse. The patients were experiencing relief of symptoms, but the volume of tissue damaged increased and
greater # of ulcers occurred with traditional drug management. . What they found, was acid bothers ulcers. 8/10 patients
on meds relapsed and got the disease again. He found that 8/10 treated by antibiotics stayed better, 1/10 was about the
same and 1/10 relapsed. This is a complete flip of the response, generated by aggressively treating the cause of ulcers (H.
Pylori) and not the symptoms (acid production). Overproduction occurs in less than 10% of the ulcer conditions. Most drugs
don’t treat the disease, they manage the condition.
Peptic Ulcer disease Remains One of the Most Prevalent and Costly GI Disease
Prevalence
Patients seen by physician….3-4 million (increased more today)
Patients self-medicating…….3-4 million (increased more today)
Total Patient Visits to Physicians…….12-14 million
Hospitalizations…….Grater than 400,000 (down)
Total Days…… About 4 million (down)
Deaths….About 9,000 (down)
Operations….Greater than 130,000
Total Costs (indirect and direct) = Around 7 billion (increased more today)
Peptic Ulcer is a Common Disease
The annual incidence of active ulcer (Gastric Ulcer and Duodenal Ulcer) in the US is about 1.8% - 500,000 new cases per year
In addition there are over 4 million recurrences yearly
Hospitalizations For Bleeding Upper GI Lesions are Increasing Along with Increased NSAID Use
Prescription for NSAID’s tripled from 1975 to 1985. NSAID use today has increased dramatically and so have
complications .
Peptic Ulcers are Caused by Increased Aggressive Factors and/or Decreased Defensive Factors
Increased Aggressive Factors and/or Decreased Defensive Factors…(leads to)…Mucosal Damage…(leads to)…Ulcer
Examples
Ex. Too much alcohol and drugs --- Aggressive chemical attack (increased aggressive factor - drugs) and secondary
decreased defenses of the mucosa lead to damage (decreased defensive factor).
Gastroduodenal Mucosal Integrity is Determined by Protective (“Defensive”) and Damaging (“Aggressive”) Factors
Protective Factors = HCO3, Mucus, Blood Flow, Growth Factors, Cell Renewal, PG
VS.
Destructive Factors = H+, Pepsins, Smoking, Ethanol, Bile Acids, Ischemia, NSAIDs, Hypoxia, H. Pylori…H Pylori and
NSAIDs cause the most damage….H+ should be at the bottom of the list as we’ve found it is not as big a concern…Hypoxia
occurs in smokers’. Smoking impacts valve function and bile acids can reflux back to the stomach. Gastric mucosa is designed
to resist acidic pH. Alkaline load regurgitated back into a acidic environment can destroy tissue.
*** In healthy people = Protective balances Damaging factors ***
The Ingestion of Non-Steroidal Anti-Inflammatory Drugs (NSAIDs) Daily is a Major Factor in Ulcer Pathogenesis,
Complications and Death
3x10 to the 6th power in the US take NSAIDs daily
About 1 in 10 patients taking NSAIDs daily have an acute ulcer
2-4% of NSAID users have GI complications each year
Greater than 3000 deaths/year and Greater than 25,000 hospitalizations/year
NSAID’s Are associated with an Increased Incidence of Bleeding Ulcers
Gastric Ulcers: Risk Ratio (Increased 10-20x)
Duodenal Ulcers: Risk Ratio (Increased 5-15x)
Increased risk proportional to daily dose of NSAID
NSAID Ingestion Causes Both Acute and Chronic Gastroduodenal Injury
All NSAIDs produce mucosal damage
Ulcer risk is dose-related
Acute Mucosal Response does not predict subsequent ulcer risk
Acute Ulcer & Damage (1-2 Weeks): Mucosal Erythema (60-100%), Subepithelial Hemorrhages (60-100%), Erosions
(60-100%), Increased Fecal Blood Loss (60-100%),
Chronic (greater than 1 month): Gastric and duodenal erosions (40-60%), Gastric and duodenal ulcers (10-30%)
11/4/08
Gastric Acid Secretory Rates Are Altered In Patients With Upper GI Diseases
Normal:
Basal = 1-8 mmol
Peak Pentagastrin = 6-40
Decreased with:
Pernicious Anemia = 0-1
0-5
Gastric Atrophy = 0-2
0-10
Gastric Ulcer
= 1-3
2-20
Gastric Cancer = 0-5
0-30
Increased With
Duodenal Ulcer 1-15
12-60
Gastrinoma
5-80
20-110
*** There is extensive overlap between groups ***
Duodenal Ulcer is a Disease of Multiple Etiologies
Gastric acid and pepsin secretion are ???
Antral gastritis is present and almost universally associated with H. Pylori
Proximal Duodenal mucosal Bicarbonate secretion is frequently (about 70% of the time) impaired
Nocturnal acid secretion and duodenal acid load are frequently increased
Secretory Abnormalities in Duodenal Ulcers
Decreased Duodenal HCO3 Secretion
Increased Nocturnal H+ Secretion
Increased duodenal Acid Load
Increased Daytime Acid Secretion
Increased Pentagstrin – stimulated MAO
Increased Sensitivity to Gastrin
Increase Basal Gastrin
Increased Gastric Emptying
Decreased Inhibition of Gastrin Release
Increased Postprandial Gastrin Release
Mean Parietal Cell Number is Increased In DU but not in GU
*** At least 2/3 of DU’s and GU’s fall within the normal range ***
Even tough duodenal ulcers can be hyper-secretory, they typically are not
Maximal Acid Outputs are Greater in DUs Compared with Normals
Gastric Ulcer Disease Involves Loss of Mucosal Defenses in the Presence of Acid
Gastritis involves the antrum and distal corpus
Other contributing factors: NSAIDs, Bile Reflux, Smoking, Alcohol, H. Pylori
H. Pylori has High Urease Activity
High molecular weight (300-500 kDA)
pI (isoelectric point) 5.9
20x more activity than Proteus Vulgaris
High affinity for urea (Km = 0.8 mM)
Urease reaction is the basis for the diagnostic 14 C/13 C breath tests
The presence of ammonia raises local pH
H. Pylori Infection Can be Detected by Various Methods --- Testing Methods
Endoscopic biopsy tests
Sensitivity
Specificity
Culture
60-90%
100%
Histologic examination
95%
98%
Rapid Urease Test
90%
95-100%
Non-Invasive Tests
Serologic (IgG antibodies to H. Pylori)
80-95%
80-95%
Urea Breath Test
13 C or 14 C urea ---- CO2
95%
95%
A complication of biopsy is perforation and peritonitis. We should first do a blood test for antibodies for H. Pylori that
has 80-95% Sensitivity. The urea breath test is another very good test. So, use the less invasive tests for about the same
results. Test and re-test to confirm the diagnosis.
Genetic Factors Influence Ulcer Incidence
Identical Twins = Risk Ratio of about 5x…This is about 5x the normal rate of getting the ulcer
First Degree Relative = Risk Ratio of about 3x…The rate is still 3x the normal rate of getting the ulcer
DU (duodenal ulcer) and GU (gastric ulcer)cluster independently…You should ask about history of ulcers (peptic and
duodenal) in the patient history. If there is family history, suggesting testing and treatment of other family members.
Certain Diseases are Associated with an Increased Prevalence of Ulcer
Chronic Pulmonary Disease = Risk Ratio of 3-5x..Chronic CO2 retainers and chronically hypoxic
Hepatic Cirrhosis = Risk Ratio of 5-8x…this comes from portal hypertension
Chronic Renal Failure = Risk Ratio of 1.5-3x …he patient with chronic renal failure maintaining mucosal integrity. A risk of
chronic renal failure is ulcer.
Cigarette Smoking is Strongly Associated with Ulcer Disease
Smokers have:
A higher incidence of ulcers
More ulcer recurrences
More Frequent complications
Greater Ulcer – Related Mortality
A portion of this effect can be attributed to smoking-induced chronic pulmonary disease
Cigarette smoking also decreases pancreatic bicarbonate production
There Are a Number of Myths Surrounding the Causes and Treatment of Ulcer Diseases
Spicy Foods: The foods are irritants but spices are not ulcerogenic in nature. They can irritate the patient’s symptoms when
they do have an ulcer. You don’t have to give the foods up altogether, but you may have to limit them whey symptoms are
present. You may also have to watch the foods the spice goes on, because the food and not the spice may be an irritant.
Alcohol: Extreme utilization of alcohol may induce the ulcer. Overwhelming of the mucosal tissue by the insult of alcohol can
occur. Loss of mucosal tissue with repetitive insults can causes ulceration.
Psychological Stress: There is little downside to asking the person to reduce their stress levels….Stress may or may not be part
of the generation of the ulcer, but it doesn’t hurt to reduce stress levels (regardless).
Ulcer is an executive’s disease: Not true as all types of people can get ulcers
A bland diet heals ulcers: Not true
The Diagnosis of Ulcer Disease by Symptoms Alone I s Imprecise
We can’t predict the ulcer by onset and duration of symptoms. Ulcers occur without symptoms (10-40%) and ulcer
symptoms occur without ulcer 30-60% of time. Classic pain presentation is substernal pain on R side, including pain
with palpation.
Pilot Study of Chiropractic vs. Medical Care
*** 11 Adult men and women from 18-34 were studied. ½ the group had adjustment and the other half had medical
management (drugs). SMT caused pain relief within 9 days (within 3 days in most subjects) and clinical remission 10 days
earlier than the medical group based on endoscope. The endoscope saw better healing in the chiropractic group than the drug
group. The drug group still showed signs of ulceration and ulcerative damage.***
BEEZOR
*** AP Spine Film ***
A mid-late teenager is studied in the film. The mother thought the child had anorexia. The child was thin and appetite
diminished over time. The mother tried to listen to the child to see if she vomited after meals. The mother took the child to the
chiropractor. The chiropractor shot films and the films show a soft zone of white crossing over the L1-Ll2 vertebral levels.
We don’t see the fundal gas vertebra. This is a gas-less stomach. We don’t see the Meganblaz or Splenic Gas Flexure.
This is worrisome and requires contrast exam.
*** Contrast Exam of Same Patient ***
Contrast is pushed to the periphery. Something has to push the contrast to the periphery. Most contrast is on the pyloric side,
but doesn’t pool. The chiropractor asks a couple of questions.
The patient admits they are losing weight. They are admitting they just aren’t hungry. They do not have anorexia nervosa as
they don’t have disordered body image. The girl has long hair down to the buttock. The child runs the hair through the mouth
as a nervous habit. As a habit, the child would swallow the hair. The condition is called Trichobeezor. The condition is
trapping of substance in the stomach (beezor). Tricho for hair. This is why the child doesn’t have an appetite and also has
stomach based problems. Actually, the girl has OCD and needed counseling. A haircut would have helped, but remember she
had OCD. The child had manual extraction of the hair under anesthesia.
Other beezors are glue or clay which can be swallowed and “stick” to the stomach. The stomach cannot empty itself of
soluble products. Typically all the beezors have to be removed usually by endoscopy.
GASTRIC CANCERS
1. Metastasis: Should be first thought for cancer. The #1 for metastasis is melanoma (most common for both
GU and GI).
2. Benign Primary Cancer: Adnenoma and Lyomyoma are the big 2. They are equally distributed (40% and
41%). Lipoma is a distant 3rd place specific to the stomach (5%). The remaining 14% is spread amongst the
remaining primary cancers.
a. Adenoma: Growth into the stomach. Cessile adenoma = projection into the lumen…Pedunculated
Adenoma or Polyp = Stalk like growth into the area (lumen)…Another key feature is that 40% of
adenomas grow to become adenocarcinomas. There are histologically benign at first and later go onto
malignancy.
b. Lyomyoma: Wall based tumors that infiltrate the walls of the stomach. We see it best by contrast
exam. As the tumor infiltrates stomach wall, motor function is compromised. So there is dampening of
peristaltic wave. This is wall based infiltrative process that presents like lymphoma. If it is wall based
and shows dampening or peristalsis, it should be biopsied to differentiate from lymphoma. If it comes
back lyomyoma, it is good news and watchful waiting should be done. When it is removed, it is
because it is in a bad location more than any other reason.
3. Primary Malignant = #1 Carcinomas account for 90-95% of aggressive cancers. #2 is Lyomyosarcoma
(2%) #3 Lymphoma (Less than 2%). GI carcinomas are on the rise across the US. The #2 cause of death in
this country is cancer death. There are countries with rates 30x greater than ours. The higher rates could be due
to genetics. The counties are Chile, Japan, and Iceland. These are 3 homogenous genetic groups. These are very
costal countries that rely heavily on fish and seafood. Costal pollution goes up and we see a later rise in cancer
Products in water and seafood can cause the metaplasia (mercury). Other risks are diet, metal or coal industry
workers, firemen, tobacco workers or people who work in smoking areas, nitrites. All of these lead to
metaplasia. Grilling meats is another reason for induction of carcinoma as grilling can leave carcinogens on the
meat. If we find the condition earlier, we can treat it more successfully.
Treatment and Identification
1. Unexplained Weight Loss = 85-95% have weight loss unexplained at the time of diagnosis with gastric cancers.
There should not be a good reason to lose weight unexplained (typically about 10 lbs per month or about 3 lbs per
weak)
2. Episodes of Dysphagia = It is hard to force food through a tumor lumen (80-90%).
3. Occult Bleeding = 65% have bleeding. 7 mL will show a + Hemoccult test.
4. Anemia = 50% have GI blood loss. No good reason for a patient to be anemic.
5. Pain = 50-70% claim pain. We can’t reliably use pain.
_______________________________________________End of Test 3 Material___________________________________