Download GI-GU Exam III Notes

Friday, February 13, 1998:
GI Starts Today
ANATOMY REVIEW:
 Retroperitoneal give more of a referred pain pattern.
 Duodenum is considered retroperitoneal except for duodenal bulb
 Duodenal bulb is site for peptic ulcer disease and points right toward the surface.
 Ascending colon, descending colon and pancreas are retroperitoneal.
 Stomach is divided into cardiac portion, Gastresophageal junction (poor sphincter), and fundus
and finally the Antrum distally. Most of the complaints involve antrum.
 Gastroesophageal junction is poorly developed valve
 Pyloric valve is a good valve that is a specialized large muscle. Under neurologic control and
endocrine control
 Ileocecal valve is also a good valve
 Anal sphincter (internal and external) are under voluntary and involuntary control
 Esophagus upper 1/3 is striated (voluntary control). Lower 2/3 are smooth muscle and are
involved in neurologic cascade. They are linked together via neurologic cascade that leads to
passage of food via peristaltic wave.
 Meisners and aurbachs plexus are in the intestines.
 Peristaltic wave produces relaxed sphincter but tone must return after food passes. Many patients
have leaky sphincters that reflux.
 Liver is multifunctional operation
 Gall bladder is a storage mechanism for bile produced in the liver.
 Pancreatic duct transports pancreatic enzyme that denatures proteins and emulsifies fats.
 Difference in presentation: referred pain in retroperitoneal organs. They are non-palpable unless
they are huge. Masses are not mobile
 Intraperitoneal are palpable and project straight to surface. Masses tend to be more mobile
IMAGING AVAILABLE:
 KUB: key benefits are view abnormal calcifications, visualize organ location, organomegaly,
wasting of organs. Can visualize tumors that are calcified (renal tubular carcinoma). Obstruction
may be visualized due to packed in fecal material (mass effect) or obstruction producing air/fluid
levels. Aneurysm may be visualized with patient with flank pain. Ascites visualized while patient
is lying down (obliteration of the psoas silhouette). FREE AIR can also be seen, This is a cardinal
finding to make.
 Most abdominal imaging starts with KUB. If there is an obstruction, you do not want to
image with barium. KUB may tell you what to do next, or in this situation, what not to do.
Do not put barium above a high grade obstruction.
 Barium Exams:
 Esophagram: material passes through mouth and esophagus and watch down to stomach.
Don’t watch it much past stomach. Use video-fluoroscopy to view peristalsis
 Upper GI: watch it empty into stomach and roll patient to coat stomach. Put fizzies in
stomach to blow up the stomach and give double contrast with barium and extra air in
stomach. Watch until some of barium leaks through sphincter and goes 10 mm into
duodenum
 Lower GI is same as barium enema. Add canulica into rectum. Easily go through entire
colon and even watch material go through illeo-cecal valve. It is hard to get enough pressure
to do this. After you coat the colon, you pump them up with an air foot bag to get the double
contrast. This is usually uncomfortable for the patient, the more uncomfortable the study is
the more likely it is there is something there. Cannot declare test over until you get contrast to
ileocecal valve. (some take 15 minutes, some take hours)
 If there is a leak in the intestine, you do not want to use barium because you may cause
peritonitis when the barium gets into the peritoneal space.
 Ultrasound: Cannot use in some areas because gas obstructs signal. Works good in RUQ because
liver is good acoustic window. Stomach is good acoustic window when it is full. US is not
universal for the abdomen but it is excellent in some areas. There is no known risk to the patient.
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Radionucleid Imaging: phosphor labeled technicium goes into bone and shows up as a hot spot.
Galium, thalium are also used. Main difference is half life. You want it short as possible with a
reasonable azuasition time. Can do liver scans, spleen scans by tagging materials that collect in
tissue that you want to examine. Look for hypoactivity and hyperactivity in tissue scans.
Hypoactivity means there is no tissue there or that there is no blood going to the tissue.
 Can tag white blood cells because they go to every infection in the body. Very good way to
detect early stages of infection. This is used for leakage in the abdomen and peritoneal
reactions. This is usually indicative of abscess.
 Flexible fiber optics:
 Abdominal CT: useful but not as clear and crisp as one would like.
 Cutaneous studies: sticking needles through skin to find vessel to do arteriogram. Find vellesls ot
liver and other organs. Can run retrograde collangio pancreatopophy? Can do selective back
filling and unified back filling.
Differentiate high grade from low grade obstruction in clinical setting is by what is coming out!
People may vary so compare to what is considered normal.
High grade obstruction is no fecal material getting through. Do not add barium to this it makes it
worse. It can happen in small and large intestine. Retrograde exams may be indicated (barium enema)
Should observe fecal bulk declining and interval between movements lengthens. Increased mass in
abdomen with presentation of colicky pain pattern. This is due to unfulfilled contractions. May run
risk of ischemia due to stretching veins so small and thin (can loose large sections of the colon in this
condition)
Monday, February 16, 1998:
No School: Presidents Day
Tuesday, February 17, 1998:
Skipped Class
Friday, February 20, 1998:
Exam II hour before lunch.
First hour after lunch: Start by going over Exam II.
Dysphagia
Odenophaygia
They can both appear separately or together.
Classification:
 Pre-esophageal
 Stroke patients have lost voluntarily control of upper 1/3
 Pummer vincent syndrome: look in library for 2 page article
 Profound iron deficiency anemia commonly seen in older patients who do not eat a proper
diet. Can also see in youngsters who are fed formula too long without iron supplementation.
 This is pre-esophageal because it produces a network of webs that cross over pharnys and
prevent food from getting into esophagus. If you are on a liquid diet you wouldn’t notice. If
you heat whole food you are in trouble. May also be in trouble if taking large tablets of meds.
 Diagnose by differentiating problems with liquid vs solid food. If they have problems with
only whole food, it is probably pmmmer vincent. If they have problem with both it is
probably due to stroke.
 Spoon nail is also another sign. Spoon nail is when your finger nail can hold a drop of water.
See red smooth swollen tongue (glossitis)
 Esophagram may help if webs are thick enough that they can hold the contrast. The
esophagram may also be of no help.
 Fiber optics is the most useful exam. Esophascope or laryngoscope may also let you see it.
 Blood work would show decreased MCV and MCH due to the lack of iron.
 Test pH of the stomach. It may be high (achlorhydria or hypochlorhydria)
 SSX may be vomiting, problems only with solids
 TX: supplement iron, this will take a few months (3-4) to kick in.
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Esophageal dysphagia
 Schotsky rings: some think it is a normal variant, some think it is the junction between gastric
and esophageal tissue. Some think it is normal, some think it is a true stricture. There is no
consensus for this point.
 Barium swallow would show this better than endoscopy because you can only see it when the
esophagus is open.
 Obstructive
 Carcinoma
 Will allow fluids to get by but solid food will have difficulty getting by
 Middle 1/3 is target site of esophageal carcinomas.
 There is a bad prognosis because these is not very much elasticity.
 Tumors can get large before they get obstructive. When you cut out tumor, nerves are
disrupted and this produces a patient management problem.
 Gastric orignin of esophageal carcinoma would have to be so big it would close up tube.
 Motor disorders are for liquids and solids.
 Achalasia means “no opening”: esophageal spasm. High grade spasm you can collect 2-3
liters in the esophagus.
 Scleroderma is an invasive process here. When in esophagus it produces motor
dysfunction by messing with nerves. SCLERODERMA CAN ONLY BE
CATEGORIZED AS A MOTOR DISORDER.
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 Strictures
 Produced by fibrotic repair as see in Gastresophageal Reflux disease
 Schotskys ring
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Barrats Esophagus AKA Barrats Epithelium: this is when gastric juice routinely gets into esophagus.
 Defined as metaplasia of esophageal tissue into gastric tissue.
 Barium swallow is useful to detect area of retention around fibrotic repair
 Esophagoscopy is useful
 Biopsy is best way to diagnose.
 Problem with Barrats is that it goes through anaplasia or neoplasia and it is a very aggressive
malignant cancer. Occurs in 1/5 of Barrats patients.
 Other complications (benign) are related to fibrotic repair and retraction of fibrotic tissue.
 The better the reflux is managed, the better this problem is fixed.
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Cardiogenic Dysphasia
 Broad based intrusion likely to be missed on endoscopy
 Unlikely to be missed on barium swallow
 Looking for a extrinsic pressure change on back side of esophagus. Will be able to visualize on
oblique films.
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Foreign body Dysphasia:
 Usually kids. This is an example of child swallowing bottle cap.
 Dentures can also be a culprit. An old man swallowed his wives dentures by drinking the water
too fast where her dentures were sitting.
 Mental patients, stroke patients

Raynauds Phenomenon
 Cold triggers Aperistalsis in 80% of affected patients
Simple Raynauds
Syndrome of Raynauds
 Crests disease; similar to scleroderma but skin lesions are not as pronounced. Get calcinosis cutis
and can affect esophagus. Esophageal atresia (underdevelopment) sclerodactaly and telengatasia
make up the rest of the pneumonic.
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Scleroderma:
 90% of patients have dysphasia at some point in their history due to neuro-muscular compromise.
 Missed some other things on scleroderma
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Hiatial Hernia:
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Diverticulum:
 Zankers diverticulm
 Most predictable
 Forms outpocketing of tissue in upper 1/3 and is always posterior because of defective
cricopharyngeal muscle defect.
 Normal swallowing can cause herniation of tissue.
 Can be as small as a pea and as big as a golf ball. Smaller they are the less likely they will be
to produce dysphagia. As they get bigger they always produce dysphagia.
 Pt. Reports hard time swallowing. (dysphagia) have them do barium swallow and you will
see it.
 SSx: after using cervical pillow wake up with foul smelling bad tasting stuff in mouth. If
they can have them collect it and see if it is what they have eaten most recently. “small
amounts of regurgitate, mixed meals and various stages of degradation” this is the trigger
word.
 Third way to determine is when person gets recurrent pneumonia after sitting up while
sleeping. As they sleep the zanker seeps contents into lungs.
 Tx: decompress zanker and put stitches over opening so nothing else goes in and over time
potential space will eventually self seal. In past more vigorous methods did not work as well.
 Traction diverticulum
 Found in mid-esophageal area
 Para-esophageal lymph node inflammation that instituted fibrotic repair that is in contact with
esophagus. Over time, fibrous tissue shrinks and it tenses the esophagus and it can now
herniate under high pressure conditions.
 This is an aquired condition.
 Theses never get as big a zankers and are usually an incidental finding. Can be treated as
incidental finding (ignore it)
 Not likely to produce obstruction
 Pogen Diverticulum
 Lower esophagus
 Constructed weakness (built wrong)
 Often an accompanying problem such as achlasia
 Don’t have coordinated peristaltic activity.
 Rarely symptomatic
 Not likely to produce obstruction
 Incidental diagnosis and finding.
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Odenophasia (painful swallowing)
 Globus estarigus is the sensation of patient that they are having trouble swallowing.
 Lump in the throat with stress.
 This is unlikely to benefit with work up because it is mental.
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Monday, February 23, 1998:
Dr. Kuhn is a no show!
Assignment: Article on Hernias and Ulcers.
Tuesday, February 24, 1998:
Dysphagia, intrinsic and extrinsic
Diverticulum: 3 main types
Globus Hystericus: sensation of trouble swallowing.
General symptoms of esophageal disorders
 Dysphagia, Retrosternal pain burning pain, Tyrosis is heartburn pain due to bad sphincter. Dyspepsia
or gas symptoms may be sign of incompetent valve.
 Dysphagia may be present but does not have to be present
 Complications are baratts esophagus (esophagus into gastric tissue),
Tests that will be utilized:
 Hemccult
 Vomiting blood demands more work up. Coughing up blood (hemoptysis), vomiting blood are two
very different things.
 Barium study; Esophagram or upper GI. Do Upper GI with burning pain. Worst case for patient is
standing reflux. Reclined, supine and inverted are least levels of incompetent sphincters in that order.
 Identify a person who has reflux, do minometric pressures. Put ballons in upper esophagus and lower.
 Endoscopy is another method of evaluation.
 24 hour pH monitor through nose to back of throat. Put it in place with flouroscopy and get a
continuous recording of pH.
Tx for achalasia:
 Blow balloon up across GE Junction: turn patient into obligatory refluxor.
 Surgeons dilate manually and cut it to undergo fibrotic repair. Cannot help but reflux
 Botulism injection to neurogenically inhibit sphincter. This is just a possible treatment that has had
some favorable review in the media lately.
 Drug therapies such as calcium channel blockers.
 Substernal bypass: more serious treatment. Put other tissue above obstruction and lead it into the
stomach. This could create a leakage site to produce coliforms. This produces peritonitis.
Reflux Esophagitis Introduction:
 This can be a cause of dysphagia
 If enough reflux comes back to produce irritation, this is esophagitis.
 Most often there is lower esophageal sphinctor incompetence
 There may also be too much content in the stomach.
 Eat a good meal and lay down may cause a short bout of reflex esophagitis
SSx:
 Substernal pain described as heartburn
 They usually point to and area and give up and down or circular motion
 Crushing substernal pain is usually shown as a fist. This indicates MI or Angina pain.
 Pain referral to mid thoracic region ocassionally.
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Friday, February 27, 1998:
Reflux esophagitis:
Different grades
 Bad if refluxing contrast while standing up. Theses are most common to produce esophagitis.
 Most serious will have most frequent bouts of signs and symptoms. Leading to fibrotic repair and can
turn to metaplasia. Barrats does not mean carcinoma. 80% of the time it is a useful adaptation. 20%
of the time it turns to cancer.
Conditions:
 Foods that delay emptying of the stomach: Red meat that are more fatty, caffeine is a secretagog, it
has ability to stimulate gastric response. Alcohol is also a secretagog. Dairy will also stimulate due to
the fat.
 In summary secretagogs are fat, alcohol and caffeine.
 Cannot see reflux on x-ray
 Might be good to do KUB in case of hiatal hernia, may show movement or absence of gas bubble
under diaphragm.. May be good to do chest to see fundal gas bubble up above diaphragm.
 May see double density due to food.
ACHALASIA
No opening
Lower sphinctor spasm
Patient complains of pain that is episotic and intermittent.
Friday, February 27, 1998:
Afternoon class, missed the first half.
Mallory-weiss syndrome
Chalasia:
 Mostly in context of the young children
 Simply means opening and in neonates and infants. They leak or vomit.
 Projectile vomiting is a more serious sign and is not what we are talking about her. What we are
talking about is leaking, vomit coming up with burps.
 Make sure the baby is still thriving, don’t worry about these kids.
 Worry about kids who get worse and are failing to thrive.
 Self resolving condition. Burp baby several times during meals
 Chalasia may require workup under certain conditions such as: weight loss, blood present,
dehydration, mailase, skin tests, decreased urinay output, strong smelling urine is sign of dehydration.
Curling Phenomenon:
 Found commonly with presbyesophagus
 Considered aging phenomenon associated with decreasing motility of primary peristaltic wave.
 Get incoordination between primary and secondary peristaltic waves. Don’t get wave phenomenon.
 Rapid wave of secondary peristalsis
 We have control of upper 1/3
 No control of lower 2/3. This is a wave of depolarization that leads t
Diffuse Esophageal spasm:
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Diabetic neuropathy of esophagus
 Unknown etiology
 Seen more often in patients with juvenile diabetes
 Seen much less often with adult onset diabetics.
 Looks like presbyesophagus because primary wave is decreased but there is no uncoupling of
secondary peristaltic wave.
 CAN GIVE US CASE STUDY AND IMPORTANT PART IS WHAT HAPPENS IN THE SECOND
AND THIRD WAVE. THIS WOULD BE PRESBYESOPHAGUS.
Esophageal Atresia
 Young kid vomits enough to get to failure to thrive
 Possibilites are atresia (incomplete developments)
 Use Vogts classification system.
 Type 1 is complete absence: easiset to recognize. Oropharnyx ends in blind sack. There is not
even a potential pathway to stomach. This is incompatable with life. Not very common.
 Type II is second most common type (less than 10%): near communication of upper and lower
segments of esophagus. Sometimes sever cm of tissue missing. There are two blind pouches, one
from above and one from below. The farther apart they are the more difficult to connect
 Type III: Most common is a fistula between airway and esophagus
 Type IIIa. Fistula between esophagus and trachea
 Type IIIB: Most common: Lower trachea and esophagus. (85%)
 Type IIIC: Upper airway. Bronchio and esophagus. Not very common
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How would you recognize type III esophageal atresia?
Duplication of the esophagus: there is a well developed and a poorly developed esophagus. The poorly
developed esophagus is the one that will give you trouble.
Stomach:
Congenital abnormalities
Dextrposition: stomach is just flipped over from left to right.
Hiatal hernias:
 Sliding hernia or axial hernia: cardiac portion and GE junction are above diaphragm. Most common
type and typically reducible.
 Incarceration of hiatal hernia: where we grab onto it. And example is diaphragmatic spasm or enough
stomach above diaphragm to cause constriction during muscle contraction. Incarcerated hernia needs
to be monitored closely in your office, the MD’s office or the ER.
 Strangulated Hiatal Hernia: patient can loose small to large sections of stomach due to ischemic
necrosis. Leads to peritonitis.
How to differentiate incarceration VS strangulation:
 Degree of pain is greater in strangulation. Vascular compromise may cause more pain along with
stronger contractions.
 Strangulated: we will not hear gastric sounds above strangulated hernia.
Sliding hernia is the most common type and can be easily reduced.
Most rare and most dangerous is the intrathoracic stomach. This is a grossly incompetent hiatus. It is very
large. It is not abrupt failure, it is due to recurrent trauma.
The great risk is it can fold over on itself (valvulus) this is a high grade occulsion and causes avascular
necrosis.
This is most rapidly serious complication of a hernia.
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Short esophagus syndrome:
 Form of atresia, may be congenital.
 Can see this in failed suicide attempts related to multiple chemical burns of the esophagus. Draino
contained Lye and was used for suicide.
 Fire victims may get this due to swallowing super heated gasses and the fibrotic repair may pull up the
stomach. Not associated with cigarette smoking because it is not a super heated gas.
Monday, March 02, 1998:
Valvulus: hopefuly in action notes
Telescoping
Gastric Diverticula:
 Outpocketings usually formed as a result of high pressure events
 Incidental findings while using contrast medias
 Usually rare
 Can be site of food stuff retention that usually does not cause problem
Dilitation
 Stomach, expansion to near physiologic limits
 Causes are organic, peptic ulcer disease near pyloric channel to cause pyloric spasm and causes
swelling.
 Ulceration’s can occur in the pyloric channel
 Inflammatory bowel disease, stricture
 Can see lesser degrees of dilatation in adynamic ileus (atonic small intestine). Have interrupted
neurologic (motor) function of sometimes small or sometimes large portions of bowel are
compromised. We get no contractions and there is a problem emptying stomach contents and produces
backup all the way into the stomach. Stomach has to work against a gradient and will need to be fuller
to move the food forward.
 In general, between organic and functional causes, organic obstructions will be more high grade.
 Stomach can hold 10-15 liters (esophagus can hold 2-3 liters). Stomach may get so large it pushes
poles of kidneys outward, sometimes can reduce diaphragmatic excursion.
 There is no gas bubble in the stomach because there is no room for it.
 Sometimes rupture can occur in the stomach. Peritonitis is prominent.
 Must worry about bleeding with rupture. This is an immediate problem
 Rupture may also occur from trauma.
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Gastritis:
 DDx: in the past it was just an upset stomach with no finding of an ulcer. Today DDx is more specific
 Today Biopsy is most diagnostic procedure.
 Chief complaint can range from transient minor complaints to very sever complaints
 DDx without biopsy is going to be by process of exclusion. When problem progresses, may get biopsy
 Upper GI for patients will be non-illuminating, same for the KUB. It will reveal nothing for gastritis.
 Will not see free air under diaphragm. This only gets you closer because you have ruled out other
diseases.
 Contrast exams are not sensitive enough to be useful. It will probably be done to rule out peptic ulcer
disease
 Endoscope may find nothing. If thre is positive finding it relates to an irritation. (hyperemia)
 Endoscopy with biopsy is useful after symptoms have been very persistent.
 Angioagrophy will do nothing because patient does not leak enough to show up.
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Acute Gastritis:
 Acute transient inflammatory where superficial tissue is primary target.
 Chronic aspirin use a cause or risk factor. Change to buffered type or drink more water
 Heavy smoking and excess alcohol intake. Smoking has to do with mixing of saliva and
chemical constituents, contact time produces the most trouble. Pyloric reflux is also a
problem for cigarette smokers. Can progress from gastritis to ulceration.
 Excess alcohol (secretagogic substance). Can overwhelm normal mucosa and produce
gastritis. Fatty foods and alcohol is even worse. Fatty foods slows down stomach and
increases contact time in the stomach.
 Food poisioning.
 Viral gastritis (flu)
 Chemotherapy: try to kill tumor quicker than host. Nausea and vomiting may lead to gastritis
 Uremia: azotemia. Makes mucousa tissue less protective.
 Infections: local
 Stress: may increase release of acids.
 Shock, hypovolemic:
 Cytomegalo virus: particular virus that makes superficial infection like gastritis
 Helobacter Pylorii: found in numerous patints with ulcers. Patients pass through gastritis to
get to ulcers.
 Two scenarios:
 Abnormal mucosa allows problems
 Normal mucosa that is overwhelmed.
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Chronic Gastritis:
 Persistent acute gastritis becomes more routinely symptomatic
 Evidence of fibrotic repair that is permanent.
 Drugs: NSAIDS, Aspirin, Chemotherapy.
 Inflammatory bowel disease (Chrone’s) will associate with gastritis
 Viral infections that go untreated
 Idiopathic disease.
 Three categories based on anatomy
 Superficial gastritis: looks more like acute with hyperemia
 Atrophic gstritis: mucosal atrophy. Bare areas with no protective mechanism.
Develop achlorhydria
 Gastric Atrophy: full thickness of stomach wall undergoes fibrotic repair and
undergoes retraction. Replace secretory crypts with fibrotic tissue. Malabsorption is
typically seen.
 10% of time turns to gastric carcinoma
 Autoantibodies are formed against body and produce pernicious anemia as a result.
 Patient may have period of no symptoms. May have symptoms of acute gastritis.
 Once you had fibrotic repair you are classified as chronic gastritis.
 May slow progression but unlikely to get much repair. Try to coat stomach lining.
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Other signs and symptoms:
 Anorexia: if they don’t eat it wont hurt.
 Feeling of pressure, nausea and vomitins and delayed gastric emptying which produces
artificial satiety.
 Vomit may have blood or may have HEMOCCULT.
 Most frequent is tenderness in abdomen.
Treatment:
 Stop aspirin in older patient. Then move to buffered aspirin. May take pills with milk, if they take
with whole milk it will slow gastric emptying due to fat.
 7-10 days will feel better.
Acute Vs. Chronic symptomatically will have similar complaints. Chrone’s and fibrosis is chronic.
Tuesday, March 03, 1998:
Giant hypertrophic Gastritis (Menintiers Disease) know both names:
 Variant of gastritis with very thick rugal folds in stomach. Has effect of filling in the valleys.
 No known etiology
 Male predomination in 4th and 5th decade
 Early feeling of fullness. Dispensability of stomach is decreased.
 May have a burning feeling
 Usuallly have a great decrease in secratory function. Pepsin and HCL is less. This will cause
incomplete breakdown in stomach and it cannot be absorbed as easily. Pepsin breaks down proteins so
we will have incompletely broken down proteins.
 Even broken down proteins are very large so they are probably over 100,000 daltons.
 Patients will loose weight due to getting full easily and malabsorbing proteins.
 Muscle wasting because of decreased protein intake. Body need protein so it takes it from muscle
 Will lead to hypoalbunemia
 Get dependent edema because osmotic pressure will loose ability to keep fluid in vascular tree. Goes
along with hypoalbunemia and protein deficiency.
Complications
 Metaplase and adenocarcinoma arises in 10% of these patients.
 Which of the following is most dangerous complication? Metaplasia and adenocarcinoma
 Most common complication: hypoalbunemia.
Zoellinger Ellison syndroms: AKA gastronemia
 Characterized by ectopic gastric secratory cells.
 This means anywhere outside stomach including pancreas, duodenum, mechels diverticulum
 Gastrin is stimulus of release of gastric enzymes
 Patients demonstrate enlarged rugae du to overwork. This is a form of stress hypertrophy.
 Hypertrophic changes are a response to a persistant demand of gastrin
 Patients will commonly describe pain like peptic ulcer and there may be ulceration in patients due to
high amounts of gastric secretions.
 Elevated serum gastrin because the feedback loop is destroyed because there are no receptors in
ectopic secratory cells.
 Find hypoalbuminemia because we have extra gastrin secrtetion and excess stimulates bleeding out of
protenatious material (including blood).
 KEY TEST TO DIAGNOSE: Checking Acid Output.
 1. Check BAO (basal Acid Output) Acid at rest.
 2. Histamine Challenge: after injecting histimine (strong gastric release) recheck BAO. In
normal patient BAO is less than PAO (peak Acid Output). With ectopic gastric tumor, the
histamine challenge will not make a difference because they are already maxed out. The PAO =
BAO. We know there is a hypersecratory state.
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Leads to severe ulcer disease
Diarrhea, elevated serum gastrin, hypoalbunemia.
Treatment:
 Find and remove gastrinoma. Find it with radionucleotide tagging.
 Can do spec scanning, sequental postron and something else.
 More narrowly or specific directions are to endoscopus, the higher yield of return and better prognosis.
There are some similarities between menintuares and zoellinger ellison. They both have hyperalbunimia
but for different reasons.
Peptic Ulcers: (Today and Friday)
 Ulcerations of mucous membranes that penetrates through muscular layer and mucousa
 Duodenal ulcers and Gastric ulcers. They can occur anywhere acid is.
 Decreased tissue resistance is one way these can develop. Can develop in meniniers and
zoellinger elison syndrome. Expect it more in zoeller.
 Patients with chronic renal disease with high levels of uremia or azotemia. This can decrease
resistance.
 NSAID and aspirin can overwhelm mucousa.
 Have abnormally high stress that overwhealms normal tissue or abnormal tissue that cannot hold
up to normal stress.
 Massive burns can lead to ulcers do to massive amounts of stress and redirection of body
resources. Proteins are not available to do normal rejuvenation processes.
 30% or more of tissue involvement (not sure about %) are when you have to start worrying about
this.
 Steroid therapy may be precipitating factor
 Smoking is two-fold: contact time of irritants mixing with saliva and going down GI tract.
Gastric ulcer patients demonstrate reflux. As smoking habit develops, reflux increases. If they
stop smoking reflux slows down. This produces a temporary acidic environment that can lead to
ulceration’s
 Selye: maladaptive responses by body. Patient subject to stressor and body can adapt. If stress
maintains or is overwhelming and patient cannot adapt, this is called disease or dis-ease of
adaptation. This is an etiologic factor for ulceration
 COPD is associated with 30% incidence of ulceration that can lead to perforation. This produces a
mortality rate of 5 times greater.
 Hyperparathyroidsm. 10% will deveolp ulcerations
 Cirrhosis have 10x general risk and 5x mortality rate
 Helocobactor Pylorii: some can progress to peptic ulcer disease. 90% of peptic ulcer patients
have H. Pylorii. 70% of duodoneal ulcers have H. Pylorii. 100% of patients with persistent ulcers
have H. Pylorii.
 Spinal cord injury can lead to this
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Friday, March 06, 1998:
Today is the last day for test III Material:
Tuesday went over peptic ulcer disease:
 Duodenal and gastric and differences.
 24 hour pH monitor tests acidity of stomach.
 BAO vs PAO Tests the secretory function of the stomach. (don’t need to know numbers but know
concept)
 Histimine challenge was talked about in last class period.
 Hypersecratory people have an equal BAO and PAO.
 Hyposecratory conditions such as atrophic gastritis when secretory tissue turns to fibrotic tissue. May
have BAO = PAO but low values for both.
Duodenal Ulcers:
 Fun facts!
 Relatively common (1 in 10 have some level of gastric distress)
 25 – 50% of duodenal ulcer patients typically have a positive family history. There may be some
genetic suseptablity or connection with environment.
 More and more are secondary to Helobacter Pylorii. There may be some genetic susceptibility to
Helobacter Pylorii.
 Blood type O has a 35% suseptability. This could be genetic
 50% of patients have increase of pepsinogen I cell levels. This correlates to an increased gastric
output
 Chronic renal failure have 53% increased risk. Uremia and Azotemia break down membranes and
cannot support normal mucosal protection.
SSx epigastric distress:
 40-60 minutes after meals. This may not mean a whole bunch because of differences in food, time to
eat, different transport rates ect. just be aware of these.
 Gastric ulcer pain are relieved by eating.
 Burning and dull ache are descriptors. They push and probe in the stomach area.
 Hemocult positivity in male and female when there is no good reason. Look for proximal loss of blood
in the gastric and duodenum.
 Histamine response is BAO = PAO. BAO value will be high.
DDx:
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Contrast exams may be used.
Major patterns of barium collection of ulcers.
 Benign ulcer: collection of barium Is below lumen but within the expected confines or
thickness of the wall.
 Tumors (malignant ulcer): a growth or neovascularization is more fragile than normal. The
growth rate is higher. Tumor may outgrow the blood supply. Ulceration may take place and
collection of barium gets stuck on ulcer nitch. Barium collection is ABOVE the lumen.
 Gastric Diverticulum herniation of mucousal tissue through defect of musculature of stomach.
Described as a collection of barium or nitch that extends outside confines of the gastric wall.
Likely a benign ulcer.
Once there is an ulcer nitch Kuhn like to send the endoscapous in (person who does endoscopy).
In malignant ulcer they need a biopsy. In other ulcers they can see exactly what the problem is.
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Types of Ulcers:
 Post bulbar location is the duodenal bulb. These are uncommon and notoriously difficult to treat
with the old methods. These bleed regularly, almost always a positive hemacult. May lead to
anemia.
 Bulbar is the most common type.
 Pyloric channel ulcer. Pyloric valve stays closed. When it dialates and acid mixed food passes
through, the pressure exerted forces acid food stuff into ulcer. Once food passes through the pain
goes away.
 IN general peptic ulcer disease is the most common cause of gastric obstruction. Pyloric channel
produces a lot of the obstruction by itself. It causes obstruction by fibrotic tissue and also by
spasticity during acute phases.
Gastric ulcers can be located in antral area before pyloric valve and can lead to delayed gastric emptying
due to contraction of valve.
Complications of duodenal ulcers
 Delayed gastric emptying
 Bleeding in the stomach an vomiting blood.
 Perforation is very serious sign and symptom. After rupture pain decreased due to decreased
pressure but eventually they will get very sick due to peritonitis.
 Will See: rigid abdomen, spreading tenderness. KUB will show free air (uncontained air) patient
will be upright and there will be free air on the right near the liver and diaphragm. This is a
required surgical consult.
 This injury will also produce adynamic ilius. Reduced activity in the abdomen. Rebound
tenderness seen. Increase in body temperature. Worried about complication of peritonitis
Treatment: duodenal ulcers
 Coating agents may produce some relief.
 HCL blockers
 Decrease acid outputs.
 Significant percentage of patients have bacterial infections. Which comes first? If bacteria is
erradicated, it goes away and stays away much longer than in the past. 10% or less have recurrences.
 80% of tagament users had recurrent symptoms
Friday, March 06, 1998:
Missed notes the first half of class after lunch.
GI Cancer is the 6th leading cause of death in the U.S.
Male predominated but females are catching up.
Low socioeconomic classes, metal workers, coal workers or smoky environments.
Background of irradioateion, arophich gastrities leaadint to pernicious anemia. See action notes 28.
Location of neoplasm in the stomach. DO NOT WORRY ABOUT THIS.
Cancers:
 Type I: Polyploid. Adenoma. It intrudes and is most likely to asymptomatic and an incidental
finding.
 Type II: Diffuse or Inflitrative. Leather bottom stomach or linitus Plasticus. Develop macrocytic,
normochromic anemia. Look for it based on symptom of anemia, grossly increased fecal bulk.
Lyeomyoma is classic. Dampened peristaltic wave.
 Type III: Ulcerative: SSx are like peptic lucer. This is most likely to bleed in hemocult or vomit.
Type II and III call attention to themselves
 Type IV: Fungating or protruding. Has effect of producing space occupation. Have early fullness
feeling as in type II. Contrast study would show up nicely. Repeat gastric activity with muscular
contractions. Restless stomach, constantly churning trying to rest itself.
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Staging of tumors
 Upon diagnosis 50% will have reached lymph nodes
 80% of patients have some metastasis. Either local or distant lymph nodes.
SSx.
 Most frequent symptom at time of diagnosis is weight loss. 80-90%
 Next most frequent symptom of gastric carcinoma is dysphagia. Explanation is GE junction is not
normal tissue any more.
 Pain in general is demonstrated by 50-70% of patients. It is ulcer and chest pain.
 Anemia, achlorhdria, vomiting,
Studies:
 Hemoccult is good study
 Upper GI contrast study is good
 Endoscopy with ability to sample and possibly do something is good.
 Mass biopsy determine benign from malignant
Treatment
 Surgery is option even though 80% are not resectable.
 Chemotherapy can be done.
 Best hope for patient is early detection and diagnosis.
 Patients with significant meatstasis usually do not make it more than 3 years
LOOK AT PAPER IN LIBRARY
Class cut short today.
END EXAM III MATERIAL.
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