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ID2 test 2

I. Esophagus:
A. Normal:
i. Function: Propel food from the oral pharynx [not mouth] to the stomach, lined with epithelia
a. No real digestive functions
b. Can swallow standing on your head because of peristalsis
c. Lower 2/3 smooth involuntary muscle
. d. Upper 1/3 striated voluntary muscle (only voluntary smooth mm. In body), gravity helps
e. Epiglottis keeps food from going into trachea
B. Primary Peristalsis (bolus propelled thru hollow viscera): voluntary most powerful
i. Initiated by swallowing (reflex)
ii. Propels food: less strength
C. Secondary Peristalsis (peristalsis in lower 2/3):
i. Not initiated by swallowing, done so by the food which is already in the esophagus
ii. Propels food through lower esophagus:
D. Tertiary Peristalsis (Curling phenomenon; Cork screw appearance)
i. Seen in the elderly - common
ii. No propulsion
a. Fibrillation of the esophagus; doesn’t cause any movement; is due to aging and breakdown of
myenteric plexus/ usually seen in elderly
E. Tumors: Malignant m/c- 90%
i. Leiomyoma is the most common benign tumor of the esophagus (Fibroid in the uterus)
ii. Sessile  broad, wide base, no stalk: most common
iii. Pedunculated  has a stalk
iv. Most in lower esophagus (because of reflux) (Barrett’s carcinoma/adenocarcinoma)
v. Squamous cell carcinoma is most common, squamous cells line the esophagus
vi. 7.6/100,000 cases in USA (per year): 130/100,000 cases in China
a. Because their diet is high of nitrites, smoked foods, preservatives
vii. M: F  3:1: Adenocarcinoma/Barrett’s carcinoma
a. Most patients greater than 60 years of age
viii. Most are asymptomatic because there is NO expansion in the lumen, No bleeding, not much pain,
hematemesis or melena.
F. Esophageal carcinoma:
i. Etiology:
a. Alcohol abuse (long-term) associated with 80-90% of cases: Cirrhosis  Portal HTN 
Esophageal Varices  CA
1. Higher incidence of reflux (irritating to epithelium)
2. Alcoholics are usually smokers
3. Alcohol also irritates the esophagus itself
b. Cigarette Smoking:  swallow nitrites [via salvia and swallowing air]CA
1. Nitrate Ingestion in lungs
2. Chronic Achalasia, poor relaxation of the proximal end caused by destruction: prestenotic
dilation reflux neoplasm: poor reflux sphincter
3. Esophageal spasm (stenosis):
a. Proximal end dilates; food gets stuck & irritates and ferments
b. Common sign is very bad breath especially when they belch
c. Swallow  dysphagia  regurgitation: Chronic GERD/Barrett’s Esophagus, CA 
obstruction of hollow organregurgitation
c. Where food gets stuck
1. Thoracic inlet
2. Pharyngeal Esophageal Sphincter (Larynx)
3. Aortic Knob (because of aorta uncoiling leaves an indentation in the esophagus)
4. When the aorta uncoils due to aging and atherosclerotic Disease
5. Left Atrium
6. Cardiac Sphincter (lower esophageal)
7. Patients can usually with great accuracy point to the location where the bolus is
ii. S&S:
a. Dysphagia is a late symptom: Leads to these being unknown until metastasis
Patients don’t know they have usually until they become malignant
Adenomas, lipomas, angiomas all possible in the GI tract. Think of the structures in the GI tract and
the types of tumors associated with that type of tissue
b. 9 out of 10 esophageal tumors are malignant
iii. Physical Findings
a. Dysphagia mc symptom: usually asymptomatic until late stages of CA: vomiting frequent
b. motor problem – dysphagia with both solids 1st & then liquids
c. obstruction – dysphagia with solids early & progresses to dysphagia with fluids
d. CA cachexia occurs/wt loss  just skin & fat (chronic disease wasting)
e. Weight Loss, suggestive that CA has metastasized: stage 3 or 4 usually
f. Cervical Adenopathy: Lymph nodes
g. Virchow’s nodes: Enlargement of supraclavicular lymph node: Common with GI malignancy-
Many times is first sign.
h. Hematemesis – vomiting of blood / Hemoptysis – spitting up blood (red or coffee grounds)
1. Direct extension into trachea or fistula- communicating tract  aspiration pneumonia
a. Shouldering with barium swallow: squared off line across esophagus
i. Hoarseness: Due to compression or destruction of recurrent laryngeal in the mediastinum
j. Cough with clear sputum
k. Mets to liver m/c, pleura, lungs with associated signs and symptoms
l. Mc presentation if mets to lung is asymptomatic, depends on site
iv. Diagnostic Imaging
a. Double contrast esophagram: CO2 & Barium (barium swallow- “shoulder” sign- key  90° cutoff
Now we use endoscopy instead
b. Get lung & ab CT/MRI to check for mets
c. Esophagoscopy: EGD
d. Chest/abdominal CT: looking for mets
e. Abdominal MRI:
f. Mediastinum lymph nodes would be involved with esophageal cancer if metastasis has occurred
v. Laboratory Tests
a. Done also to check for mets
b. CBC, (WBC up, RBC down maybe), Blood Chemistries
1. Anemic male over 40 has GI cancer, unless proven otherwise
c. Liver Enzymes, metastasis to the liver is common
vi.. Differential Diagnosis
a. Achalasia: failure of sphincter to relax
b. Diffuse Esophageal Spasm (DES): cold ice cream chest pain that is never ending and 10x worse
Pain lasts min to hours
c. Esophageal Rings- (congenital): Fibrocartilaginous ring that narrow the esophagus
1. Schatzki’s  Upper esophageal ring
2. Lower ring
d. Scleroderma (Progressive Systemic Sclerosis, newest term): Connective tissue disease: Hardening
of the interstitial tissues  narrowing and lack of peristalsis  dysphagia
vii. Treatment
a. Resection if no mets: En bloc Resection  during surgery to see if they get all out
1. Take out CA in pieces till normal tissue seen in pathology & anastamose ends
2. Lab makes sure clean tissue is found around CA to ensure complete removal
3. Only done if no mets
4. Stomach/colon used for replacement of gut removed
5. Radiation Therapy: Targets rapidly changing/high turnover cells: CA cells, Hair, Gonads,
Bone marrow. Some divide too fast or too slow and are unaffected- renal cell = CA outpaces
chemo/radiation - Radiation not very effective with this cancer
6. Chemotherapy
viii. Prognosis: depends on stage at diagnosis: with -
a. Surgery  20-50% (all based on 5 year survival rate): stage 1 or 2 only usually
b. Radiation  6-20% (stage 2-3 usually)
1. Have a node involved (3-4)
2. Not very effective again, due to surrounding organs and tissues (4)
3. Squamos cell not radio-sensitive
c. Chemotherapy  15-80%: stage 1 best cure rate
1. Kills cells that are in the S1 phase (immature cells) that are rapidly dividing
Hair, gonads, bone marrow are all affected because they turn over very rapidly
G. Benign Tumors:
1. Tumor Types
a. Leiomyoma is most common: Found most commonly in the uterus
a. Broad based, smooth muscle & fibroid  obstruction
b. Younger age than malignant: biopsy for diagnosis
b. Papilloma: unusual
c. Fibrovascular Polyps  hamartoma - overgrowth of normal tissue, made up of normal and
fibrous tissue: Rare: can have occult blood- rare to bleed
H. Esophagitis: types
1. Reflux: Reflux of gastric contents with damage- stricture- Barrett’s = metaplasia
a. Contents reflux up through cardiac sphincter with force and through the lower esophageal
sphincter. Causing linear and nonlinear erosions of the esophageal lining
b. Progression of GERD
c. Incompetent LES (Lower esophageal sphincter)
d. Often associated with hiatus hernia: Protrusion of the stomach through the hiatus
e. 30-60’ (minutes) post-prandial/reclining heartburn
f. NOT GERD  GERD damage is reversible: Is “GERD” gone wild:
g. More severe thus causes strictures
h. TX with Nexium
i. GERD  tx: Prilosec & Prevacid
2. Acute Ulcerative:
a. Seen in patients with PUD: precursor
b. Associated with frequent vomiting: leads to inflammation of lower to mid-esophagus 
ulceration if chronic  contracted, inflexible lower esophagus,or can perforate into
mediastinum (heart-pericardial dilation leaks fluid around heart, trachea, great vessels)
c. Alcoholics, chemotherapy patients, bulimics, etc.
d. Eventually leading to strictures, thus dysphagia sets in depending on level of dysphagia as
to weather solids and or liquids are involved
e. Can lead to laryngitis
f. Contracted fibrotic lower esophagus results
3. Infective:
a. Infection of the esophagus is rather unusual
b. Immunosuppressed patient: not seen in healthy usually
1. AIDS most common group, cancer, DM, transplant
c. Long term corticosteroid treatment
d. Organisms: Herpes Simplex, Candida Albicans-Typically found in the vaginal region of
females and faces of children
e. Pic: Candida Esophagitis, occurs especially with immunocompromised patients
f. CMV (Cytomegalovirus), causes encephalitis in kids
g. S & S: Dysphagia, Odynophagia (Painful swallowing), Chest Pain – more of a burning
sensation instead of a crushing pain
h. Treated with Antibodies
4. Mechanical:
a. Swallowed object becomes lodged at narrowed portions
1. Laryngopharynx, Aorta, Gastroesophageal junction, Left Atrium (not very often
unless preexisting CHF)
b. Objects include coins, pills, bone pieces
c. 3 main groups that do this: Elderly, children, and insane
d. Leads to ulceration, maybe perforation- Which can lead to mediastinitis
e. Treated with an EGD, scope with surgical attachments on the end.
5. Esophageal Varicies: Enlarged tortuous veins in the esophagus, typically occurring in the lower 1/3
of the esophagus: Varicose veins of the esophagus
a. Alcohol is the most common cause  portal hypertension (pressure increased in portal
venous system, blood backs up cirrhosis)
b. Lower 1/3 submucosal veins involved
c. 1/3 of patients bleed: Alcohol  Cirrhosis  Esophageal Varices  Bleeding out
d. Highest mortality of any UGI bleed
1. Peptic Ulcer Disease most common reason for UGI bleed
e. Coffee ground emesis, hematemesis: Time depends on which you will see
f. Treated with sclerotherapy & Compression Bougie  balloon down the lower esophagus
and the balloon flattens out the varices
g. Sclerotherapy  inject hardening agent that hardens (sclerosis) the walls so they can no
longer extend  also used in peripheral vascular disease
h. S/Sx : Pt has some pain and dysphagia: Symptoms are not extreme
6. Esophageal Diverticula: Localized outpouching of tubular viscus
a. Usually acquired (congenital forms are rare)
b. Two Types:
1. Traction (extraesophageal) : Mediastinal mass (inflamed lymph node next to
esophagus)that as it grows attaches to the esophagus  as patient swallows and
breaths it pulls on the wall  months to years  creates a weak spot that allows the
outpouching: Something pulls on esophagus from the outside-Eg; an attached
neoplasm
a. Most common in middle esophagus. Adhesions outside tract
b. Because most lymph nodes are in mediastinum their enlargement can cause
them to become adherent to the esophagus
2. Pulsion: Weakness in the esophageal wall (where the vessels enter a lot of time)
that eventually becomes weak and forms a diverticula occurs from a pushing out of a
weak area of the esophageal wall where the small micro vascularity occurs to supply
blood to the esophagus
a. Most common lower/upper esophagus.
b. Occur anywhere in esophagus
c. Lower just above the diaphragm  Epiphrenic diverticula (just above
diaphragm)
7. Zenker’s diverticulum: pulsion type:
a. Occurs at pharyngoesophageal junction
b. Can be very large in size
c. Loss of upper esophageal sphincter laxity
d. Retains food
e. Signs/Symptoms
1. Halitosis – bad breath
2. Spontaneous Regurgitation
3. “Verp” – ½ vomit/ ½ burp
4. Nocturnal choking – position- elevate head of bed
5. Recommended not to eat within a few hours
6. Neck mass: pain & dysphagia
7. Can sometimes see peristalsis in the mass
f. Complications – Aspiration (inhaling something that wasn’t there  Aspiration pneumonia
– which has a high mortality rate), abscess (walled off chronic infection), bronchiectasis
(chronic obstruction of the air flow that results in fluid build up  infection; 3 layered
mucous, foul smelling sputum),
1. Aspiration, abscess, bronchiectasis – dilation = easier for bacteria
2. AM coughing: spit layered: surfactant, serous, pus
8. Epiphrenic diverticulum: weakened area in lower esophagus: usually asymptomatic & small
9. Middle esophageal diverticulum: usually traction type
a. From mediastinal lymphadenitis: lymphadenopathy
I. GERD reflux esophagitisBarrett’s esophagusEsophageal. CA always rule out cardiac Disease 1st
1. Cough & bronchospasm or laryngitis from aspiration
2. Early satiety GERD  get “full” quickly
3. Chocolate  fat & caffeine contents cause GERD episode
4. Tobacco  when chemicals are swallowed
5. Commonly assoc. with hiatal hernia (>70%)
6. Nitroglycerin  will make anginal chest pain better & Makes GERD chest pain worse
7. Gastroesophageal Reflux Disease: Reflux of gastric contents into lower esophagus
8. Incompetent lower esophageal sphincter: Stuff from your stomach comes back up into the lower
esophagus because the esophageal sphincter is not functioning correctly-Believes because of aging
9. Reflux Esophagitis  Barrett’s Esophagus  Squamous cell carcinoma
10. Heavier a person is the more chance they can have because increase in intra-abdominal pressure
11. Incidence: 60% of adults have heartburn: 80% of pregnant women have GERD
12. S/Sx: Heartburn (pyrosis) most common, Dysphagia, Regurgitation, Sour taste in the mouth
a. Can be confused with angina pectoris
b. Chronic cough- Bronchospasm, due to irritation of the bronchi airway
c. Laryngitis
d. Early Satiety (Getting full fast)
e. Belching/Bloating
13. Contributing Factors:
1. Chocolate (caffeine and fat), Yellow Onions, Peppermint, Garlic
2. Tobacco (nicotine and causes sphincter to relax), Alcohol (fat and causes sphincter to
relax), 3. Caffeine
4. 70% of GERD suffers have a hiatal hernia
5. Beta Blockers (control BP and angina), Ca++ Channel Blockers, nitroglycerin  Causes
dilation of lower esophageal sphincter
6. Gastric Acid Hypersecretion
14. Diagnosis: 24 esophageal pH monitoring
a. E.G.D. – final dx for GERD
b. U.G.I (upper GI series, with barium swallowed)
c. Manometry, to rule out diffuse esophageal spasms (pressure test)
15. Treatment
a. Avoid triggers (diet modification)
b. Proton pump inhibitors
c. H2-blockers (cimetidine – Prilosec )
d. Antacids
e. Fundoplication: fundus of stomach wrapped around esophagus
1. Reserved for pts with daily reflux
2. Three types
a. Nissen (complete)
b. Posterior (partial)
c. Anterior (partial)
f. Drink excessive amount of water, water helps to dilute the acid and provide weight to the
stomach to pull the hiatal hernia down.
J. Barrett’s: usually asymptomatic
1. Pre-malignant
2. Associated with chronic reflux (5-10% incidence)
3. Stratified squamous manifests to columnar epithelium, a pre cancer action
4. Increased risk of adenocarcinoma
a. 30-50 times increased risk to develop adenocarcinoma of the esophagus
b. 500/100,000 people with Barrett’s esophagus who have GERD
5. Dx: EGD, biopsy almost always accompanies an EGD
6. Treatment:
1. Laser Ablation
2. Fundoplication
3. Surgical Resection (En Bloc if area is large enough)
K. Esophageal Achalasia:
1. Spasm (shut tight) of lower esophagus sphincter with pre-stenotic dilation which makes peristalsis
ineffective
2. Chest pain  can occur when peristalsis is attempted: Pain usually colicky
3. Functional esophageal obstruction
4. Inadequate relaxation of the LES
5. Ineffective Peristalsis
6. 1/100,000 incidence; 30-50 y/o
7. S/Sx: Both Solid/liquid dysphagia-immediately, patient indicates they can feel the food sticking
usually in the lower chest = Chest pain- May be confused with angina (after meals)
a. Vomiting of undigested food with lying down- Aspiration, can develop pneumonia and die
b. Crescendo/decrescendo type pain like Stone in Ureter
c. Progressive dysphagia with classic “beck: at junction with stomach
8. Etiology
a. Degeneration of myenteric plexus
b. Viral
1. Herpes Zoster, Measles Virus
c. Autoimmune
d. Not completely understood, true etiology not know
9. Diagnosis: EGD with manometry, UGI
a. Tests to rule out other causes (eg: EKG), Especially with age group one wants to R/O MI
10. Treatment
a. Medical: Smooth muscle relaxants (70% effective)
1. Nitrates
2. Calcium channel blockers: relax LES
3. Botulinum toxins injection
4. mechanical dilation (90& effective): Bouginage: some GERD after
5. Esophagomyotomy (90% effective), incise into the muscle (sphincter – draw back,
reflux)
b. Prognosis: Excellent with appropriate RX
1. Long standing Disease increases risk of CA
L. Scleroderma: (PSS-) non-inflammatory arthritis
1. Aka: progressive systemic sclerosis (PSS): Means hardening of the skin
2. Primarily effects the skin, but is not limited to the skin: Tissue thickens and hardens
3. Severe hardening of lips to point must be tube feed: Sometimes must replace the esophagus
4. Parastasis is affected, thus difficulty in swallowing, reflux
5. Kidneys are often affected as well
6. Vessels become calcified, thickened and hardened
7. Female>Male Early teens to 20’s
8. Smooth mm relaxants used if esophagus does not need replacing, patient receives temporary relief,
usually do not work
9. Multisystem disorder often affecting the esophagus
10. Lose ability to have peristalsis
11. Become very narrow and can develop strictures
12. EGD used to diagnose
13. 75% have esophageal involvement
14. Fibrosis and inelasticity results
15. Signs & Symptoms
a. Dysphagia
b. Esophageal reflux/regurgitation
16. Diagnosis: EGD, UGI
17. Reaction with smooth muscle relaxants
18. Etiology – unknown
M. Diffuse Esophageal Spasm:
1. Ice cream eating too fast is the same pain, “brain freeze”
2. Pain lasts minutes to hours
3. Usually end up in the ER thinking they are having a cardiac problem
4. Diffuse sustained contraction (spasm) of esophagus
5. Etiology unknown
6. Can be confused with angina pectoris: vaso-vagal reaction
7. S/sx:
a. Substernal chest pain
b. Dysphagia with pain, worsened by swallowing, key differentiating feature
c. Regurgitation
8. Dx:
a. EGD (Esophagogastroduodenoscopy) & mamometer- pressure balloon
b. UGI: With barium swallow on x-ray appears as a cork screw
c. Reaction with Ca++ channel blockers/nitrates- muscle relaxant: Causes reflux
II. Stomach Diseases:
A. Anatomy:
1. Stomach  B12 absorption (intrinsic factor), storage, mixing, mineral absorption
a. Decreased intrinsic factor low B12 pernious anemia malabsorption neuropathy -
hematopoetic
- 2. Rugae  increases surface area inside the stomach for production of HCl and pepsin
3. GE Junction
4. Gastroesophageal Reflux Disease
5. Fundus- Usually holds gas
6. Magenblase  air in the stomach
7. Antrum
8. Pylorus -Narrowed portion of the distal most aspect of the stomach
9. Pyloric Sphincter  b/w stomach and duodenum  help prevent outflow of gastric juices that
could lead to PUD
10. Pyloric stenosis  prevents outflow, causes regurgitation
11. Curvatures: Lesser (top) & Greater curvature (bottom) - More metabolically active (because of
where food sits)
12. Estimated that 3 – 5 cc of blood is lost with each aspirin taken that is not buffered
B. Gastric digestion is mostly protein
1. HCL & pepsin secreted
2. HCO3- buffer
3. G astrin – stimulates muscle to “churn” food
C. Tampanade: fluid build up around organ: Heart – cannot work: Gastric = plug at sphincter
D. Cancer: occurs anywhere in stomach
1. Incidence is increasing in proximal CA (in Asia): Body & fundus
2. 2 - 4X more common in 1st degree relatives (mom, dad, siblings)
3. Male: Female 1.6:1: > 55 y/o: 7/100,000/year
4. Most common in blood group A
5. No symptom complex presented early in the Disease
6. Aggressive, Infiltrated carcinoma  invades entire organ and cause thickening of entire organ -
rarely found before stage 3 or 4
7. S/SX: Cramps (colicky pain) unrelieved by antacids: S&S of ulcer
a. Loss of appetite- food may make pain worse: better with fasting: early satiety = not ulcer
b. Very low bleeding, No ulceration, Poor intrinsic factor production
c. Dysphasia: High in GES; n/v, constipation
8. Risk factors: Diet rich in additives (smoked, pickled); Atrophic gastritis
a. Inflammatory disease of the stomach where there is atrophy of the rugae Sequela : B12
deficiency  pernicious anemia
b. Tobacco use: decreases blood flow & swallows air & tar
c. Hispanic, Japanese
d. Polyps - Growth into lumen Sessile and pedunculated. Usually premalignant mass (some
benign)
e. H. pylori infection (PUD associated wipatith H. pylori)
f. Barrett’s Esophagus
9. DX: Stool guaiac test  test for blood
a. Any male > 40 with anemia, has GI malignancy until proven otherwise
b. Positive stool guaiac (blood to stool content): FOB, fecal occult blood test
c. Will have black tarry stool if blood occurs in the stool
d. Hemoglobin <12g/dl: Hematocrit <35
e. EGD: UGI (not done very often anymore): CT/MRI for nodes mets
f. Adenocarcinoma 90%, due to the abundance of glandular tissue, {adeno-, glandular}
g. Lymphoma 6%, malignancy of lymphocytes {mediastinum area is the most common area
for a lymphoma}
h. Gastric Sarcoma < 4%
i. Leiomyosarcoma < 1 %
10. Treatment: surgical resection, quit often an en bloc gastrectomy (resect until healthy tissue is
found)
a. node resection (when larger then 1cm)
b. radiation non-beneficial (tumors are non-sensitivity to radiation)
c. Chemotherapy non beneficial, research has shown this treatment has very low benefit for
gastric cancer. Chemotherapy is designed to “attack” fast growing tissue.
11. GASTRIC CA PROGNOSIS
a. No s/sx until late in course, primarily due to the size of the hollow organ. It takes a rather
large amount before it interferes with the function of the stomach
b.18% 5 year survival rate
c. 57% with local Disease (stage I)
d. 19% with regional spread (stage II)
e. 2% with distal mets (staged III)
12. BENIGN GASTRIC TUMORS
a. Leiomyoma – fibroid tissue usually found in the uterus, of smooth muscle
1. Common tumor
2. Rarely symptomatic- Only with obstruction

b. Adenoma – benign tumor of glandular tissue, aka polyps


1. Most of the stomach are hyperplastic (an adenoma with an increase in the number
of cells – a reaction to chronic gastritis – a reaction to chronic inflammation)
2. Most remain benign
3. Can obstruct
4. Over 2cm, have malignant potential
E. Gastritis: Causes/leads to
1. Erythema – reddening (aka injected)
2. Hemorrhage Atrophic gastritis – associated with
3. Erosions anemia
4. Types-3
a. Erosive
b. Non-erosive, non-specific cause
c. Specific – bacterial, etc.
5. S/sx: post-prandial (after eating) indigestion/pain LUQ
a. Nausea and vomiting
b. Bloating
c.50% has H. pylori (spiral shaped bacteria)
6. Erosive Gastritis: Etiology:
a. NSAID’s: m/c (3-5cc blood/tablet)
b. Alcohol(ism), portal HTN – venous congestion decreases the removal of waste from the
stomach blood supply. Leads to cirrhosis
c. Stress from major illness (burns): m/c in cancer
d. Hemorrhage also common with this Disease
e. Usually asymptomatic
f. Can produce pain, hematemesis, n/v
g. Diagnosed with EGD
7. Non-erosive/non-specific
a. H. pylori gastritis: Spiral gram (-) rod
1. Causes acute superficial mucosal Disease
2. S/sx: Nausea and vomiting, Pain LUQ
b. Atrophic gastritis
1. Associated with pernicious anemia – not producing enough intrinsic factor for B12
2. Autoimmune, achlorhydria (absence or reduction of HCl in stomach)
3. Glandular hypertrophy and metaplasia = increased risk of cancer
4. 3x increase gastric adenocarcinoma over the general population: loss of rugae 
less intrinsic factor
8. Specific:
a. Ménétrier’s Disease: malabsorption of protein, due to poor digestion in stomach
1. Giant fold gastritis (the rugae become very large)
2. Enlarged thickened gastric rugae
3. Get hypoproteinemia due to enlarged rugae
4. Cause’s edema, pleural effusions, etc.
5. Severe protein loss: pt very sick (cannot breakdown)
6. Proteins are metabolized in stomach? Denatured?
7. Hypoproteinemia: Ascites, kidney & heart problems, 3rd spacing fluid
8. Idiopathic
b. Granulomatous gastritis
1. Crohn’s Disease (a chronic inflammatory granulomatous bowel Disease), TB,
sarcoidosis (idiopathic autoimmune disease that normally affects the lymph nodes of
the chest, found primarily in young black males, non-infective? Granuloma that starts
in chest at mediastinal lymph nodes: “Potato nodes”, brain, GI, joints & is fatal
sometimes)
2. Treat specific disorder
c. Phlegmonous gastritis
1. Phlegmon – aggressive large abscess perforate  peritonitis
2. Abscess from fungal, bacterial, parasitic infection
3. Emergent gastrectomy and IV antibiotics
4. Treatment is the removal of the stomach.
5. Common among aids patients (immunosuppressed)
d. Others: Mechanical, chemical, ate too much
III. Peptic Ulcer disease: acid/base imbalance between protection & damage
1. Ulceration of the stomach or duodenum  “Ulcer Crater”  a crater that penetrates mucosa of hollow
viscera: H. pylori m/c: tx with antibiotics
a. typically < 1 cm
b. larger than 2 cm  malignant potential
c. Go through at least the mucosal layer
2. Malignant ulcer  malignant tissue with an ulcer inside of it
3. Normal acid production with lowered protection  ulcers
4. Normal protection with overproduction of acid  ulcers
5. Gastric chemical secretion helps digest proteins, damaging to lining with good protection
a. Hydrochloric acid
b. Pepsin
c. Stimulated by acetylcholine (acetylcholine production is increased with stress as is the HCl thus a
double negative), gastrin, histamine
6. Other ulcerogenic substances: Bile acids, reflux of bile into the stomach, thus the reason for their being
found in the pyloric bulb
a. Pancreatic enzymes
7. Normal Protection:
a. Good blood flow, helps clear chemicals out and helps with healthy cell turnover: Diabetics do not
 prone to ulcers
b. Normal cell renewal: Diabetics do not  prone to ulcers: Chemo patients
c.500,000/year Duodenal: gastric 2:1
8. Predisposing factors:
a. High stress: Increase histamine  cause ↑ acid production: Activates sympathetics and shunt
blood away from stomach
b. Cigarette Smoking: Swallowed chemicals
c. NSAID- chronic: Irritating to the gastric mucosa – COX inhibitors stop prostaglandin production
which stops blood flow to the stomach and inhibits protection to lining
d. Delayed gastric emptying: Food stays in stomach & irritates
e. Diabetics: Decreased bowel function, high incident of PUD
9. H. pylori (produces urease) there is an inferred or coincidental correlation between H. pylori & ulcers
a. Increases gastric acid secretion: overwhelms mucosa
b.75% of patients are infected with H. pylori
c.75% have recurrence in 1 year without antibiotics
d.20% with recurrence with antibiotics
10. NSAID use cause decrease bicarbonate the base which counter acts stomach acid and pepsin, mucus and
blood flow
a. Aspirin is most ulcerogenic, buffered aspirin helps protect stomach but still begins to break down
in the duodenum thus the increase in ulcers in this area
b. 40x increased risk of PUD: Blood is very irritating to the stomach: perpetuates self
11. Signs and Symptoms
a. Epigastric Pain: Burning, Gnawing, Cramping
b. Relieved by foods and or antacids (short term - pt. can become addicted)
1. Gastric ulcers - eating makes it better
2. Duodenal ulcers - eating makes it worse
c. Pain is clustered (days-weeks)
d. Long symptom free periods (weeks-months-years)
e. Changes in pain may mean cancer perforation: pattern usually consistent with ulcer exacerbations
12. Differential Diagnosis:
a. GERD: damage not permanent
b. Reflux Esophagitis, most common condition confused with PUD: permanent damage
c. Gastric CA, particularly if there is a change in the pain pattern
d. Gastritis: epigastric pain
e. Pancreatitis: umbilical pain: fetal position for comfort
f. Cholecystitis- RUQ
g. Cardiac (always R/O 1st+)
13. Diagnostic Workup: Esophagogastroduodenoscopy (EGD), almost universally the means of diagnosis
95% accurate (5% due to human error)
a. Biopsy ALL lesions: Cancer / benign cannot be differentially diagnosed by sight
Also biopsy for H. pylori
b. Upper GI: BaSO4: Not as reliable as EGD: no biopsy capabilities
14. Treatment:
a. Antibiotic therapy (clarithromycin – which is harsh on the stomach lining)
b. Omeprazole
c. H+ pump inhibitors - Tagamet
d. Stop Smoking; Stop NSAID use
e. Diet Changes: Bland Diet
f. Stress Reduction: Because of sympathetic reaction: Valium (classic drug prescribed)
g. Manipulation in conjunction with medical therapy has been proven beneficial to the patient
h. Don’t use milk anymore because the sugar in it can help feed the bacterial and can actually make
the ulcer work in the long run
15. Complications:
a. GI Hemorrhage: Most common (50% of all UGI bleeding is from ulcers), only 10-20% of bleeding
is clinically significant. Cause sx and problems: 80% stop bleeding spontaneously
Mortality rate is 6-10% of the 20% who do not stop bleeding spontaneously
1. Occult blood  don’t know it’s there
b. Anemia
c. Cancer
d. Perforation: 5% incidence: Usually on anterior wall -Because it’s thinner
Zollinger-Ellison should be considered
e. Gastric Outlet Obstruction At pylorus or duodenal bulb: 2% Incidence
From tissue obstruction  scar tissue (fibrosis)  obstruction
` 16. Zollinger-Ellison Syndrome: Uncommon cause for PUD
a. Occur because of Gastrin secreting tumors (gastrinoma)
b. Cause multiple peptic ulcers
c. Perforation is relatively common
d. Bleed outs common
e. 2/3 of gastrinomas are malignant & will metastasize: Can lead to death
f. Hard to manage these cases due to the continuous production of gastrin from the tumor
IV. Hiatus Hernias: Herniation of a portion of the stomach into the thoracic cavity (mediastinum) through
diaphragmatic hiatus
1. EPIDEMIOLOGY: 50% of patients over 50: Female: Male  4:1: Often associated with GERD
90% with EGD esophagitis have a hernia
2. Etiology unknown, age most likely culprit due to weakening of the sphincteric. May be congenital or
post-traumatic
3. Bowel and stomach in the middle of the chest compressing the lungs and heart is termed a Bochdalek
4. TYPES OF HERNIAS (4)
a. Sliding (most common)
b. Paraesophageal (AKA: Rolling Esophageal Hernia)
c. Short Esophagus
d. Intrathoracic Stomach
5. SIGNS AND SYMPTOMS (same as reflux with the exception of the addition of borborygmi
a. Heartburn-Because also have GERD
b. Dysphagia
c. Regurgitation
d. Chest Pain (burning)
e. Postprandial fullness (After eating)
f. GI Bleeding
g. Dyspnea
h. Hoarseness- Irritation of larynx from GERD
i. Cough- Irritation and to keep stuff from going into the trachea
j. Wheezing
6. SLIDING HIATUS HERNIA
a. Most common – the esophagus pulls the fundus of the stomach up through the hiatus
b. AKA: Axial or Concentric Hernia
c. GE Junction/upper stomach herniates
d. Usually asymptomatic
e. Symptoms: Reflux, Burning Chest Pain, Regurgitation with recumbency /fatty meals
f. Episodic (no clue- wk, hours, Gas bubble above the diaphragm on x-ray (magenblase)
7. PARAESOPHAGEAL HERNIA: Second most common: AKA: Rolling Hiatus Hernia
a. GE junction in normal position
b. Fundus herniates through diaphragm
c. Usually asymptomatic
d. Should be surgically reduced- May become strangulated- Lead to ischemia (loss of blood supply)
8. MISCELLANEOUS HERNIA
a. Short Esophagus Type: Variation of sliding: Uncommon: Congenitally short esophagus
b. Intrathoracic Stomach: Very rare: Entire stomach in chest: Incompatible with life
9. DIAGNOSTIC WORKUP: Exclude other more serious conditions: EGD; UGI; Blood tests non-specific
*Will find rugae above the hemidiaphragm
10. DIFFERENTIAL DIAGNOSIS: PUD, Angina, Esophagitis, GERD, DES (Diffuse Esophageal Spasm),
Achalasia; Diverticulum; Esophageal Cancer
11. TREATMENT: Diet changes- Avoid caffeine, chocolate, mint: eat small meals
a. Avoid drugs (Ca++ channel blockers)
b. Weight loss
c. Sleep with head elevated
d. Manipulation
e. Antacids, H+ pump inhibitors, etc.…
f. Surgery for refractive disease
12. COMPLICATIONS: Reflux; Erosive esophagitis; Ulcerative esophagitis; Barrett’s esophagitis; Stricture
GI hemorrhage
V. Colon: 4 layers:
1. Review normal anatomy and structure of the colon:
a. Proximal absorption right colon- functional part
b. Electrolyte balance left colon: storage & transport
c. Veins near anus straining variscosities hemorrhoids
d. Methane m/c gas: from fermentation process of bacteria
e. Ilio-cecal valve: to decrease reflux to small bowel
f. No vili: has crypts
g. Circular muscular ring Hoffstrae for peristalsis
h. Longitudinal band: Tinnea coli: pull accordion fashion, like a snake
i. Ependices
j. Smoother inside as you go down tube
k. 2 spinchters:
1. Internal: involuntary, stimulated by:
a. eating: gastro-colic reflex
b. Bowel Hygiene: hold to long: increase water & fiber & go every day
2. External: voluntary (HNP may affect)
2. Review blood supply to colon: Both Superior & Inferior Mesenteric arteries branch off aorta
3. Blood supply interruption: Life threatening; acute abdomen: necrosis & perforation
a. Mesenteric Thrombosis ischemia necrosis inflammation distention perforation
b. Diabetics M/C: smokers: poor circulation
c. Trauma causing vasocompression
4. Colonoscopes used to view the colon
5. Tapeworm –S/SX abdominal pain, weight loss
6. INFLAMMATORY BOWEL DISEASE: Bubos – plaque`
a. Irritable bowel syndrome
b. Crohn’s Disease
c. UC
d. Antibiotic Associated Colitis
e. Bacterial Colitis (Food Poisoning)
f. Appendicitis
7. IRRITABLE BOWEL SYNDROME: aka: Mucous colitis, spastic colon
a. Alteration in normal bowel habits – constipation, diarrhea or a combination of the two
b. Functional disorder: (alternating patterns are pathological usually)
c. With minimal mucus production associated? (Not my note)
d. 20% of general population affected (2 out of 10 are affected)
e. F:M = 2:1
f. Begins in late teens/early adulthood: life altering disease
g. 50% pts have psych problems (30% have an anxiety disorder) or are hyperactive
h. etiology unknown
g. commonly associated with stress
h. S/SX: Crampy abdominal pain, low grade through the day up to the point that defecation is
imminent, at which time the pain increases
1. Diarrhea: Up to 30 BM/day: Water/mucous in the stool
2. Bloating/abdominal distention, increased gas
3. Abdominal tenderness: LLQ m/c (more peristalsis)
4. Pain often relieved (temporarily) by BM
5. No blood in stool, important differential feature from Crohn’s and or ulcerative colitis
6. Sign and symptoms present for 3 months before dx
7. Hyperactive bowel sounds
i. Major concern with this condition is maintaining the patient’s hydration level
j. D/DX (other diseases which cause cramp type pain and diarrhea): Crohn’s Disease, UC,
Diverticulitis (LLQ), Colon CA (alternating), PUD, Chronic Pancreatitis (less fat digestion), Biliary
Disease: less emulsifying of fat (6 Fs: fat, forty, fertile, etc)
k. TX:
1. High fiber diet – helps bulk up the stool and helps retain fluid
2. Fiber supplementation (psyllium)
3. Anti-spasmodics: Imodium, Lonotil, Bentyl
4. Eliminate stress
5. > 60% respond to RX within 1 year
11. CROHN’S DISEASE: aka- chronic granulomatous inflammatory Disease: regional enteritis- skip lesions
a. debilitating, often requiring surgery
b. 1:1000 population: Caucasians, Jews
c. Unknown etiology:
d. Affects young people:
e. Pathophysiology
1. Location
a. 33% involve terminal ileum
b. 50% involve distal ileum/proximal colon (ileocecal)
c. 20% involve colon only
d. Can involve any portion of GI tract: uveula deviation
2. Transmural DISEASE (across wall): Inflammation (granulation tissue), Ulceration,
Stricture, Fistula –connection between organs or skin, abscess – cause obstruction, perotinitis;
f. S/SX:
1. Abdominal distention/bloating
2. Mass suggests abscess formation
3. Crampy abdominal pain: ileocecal (RLQ): Hyperactive Bowel Sounds
4. Non-bloody/bloody diarrhea: small amounts (more blood from UC)
5. Perianal fissures/fistulas
6. Bowel obstruction: from fissures/fistulas, abcesses
7. Crohn’s arthropathy: Seronegative arthridities- bilateral, asymmetrical, SI joints
(inflammatory ankylosing spondylitis before S &S of Crohn’s)
8. Low grade fever, pallor
9. Weight loss, fatigue
g. Diagnostic Evaluation: CBC, SMAC, & UA
1. CBC: Anemia, Decreased H&H, Electrolyte imbalance, Vitamin B12 deficiency (stomach
& ileum)
2. Endoscopy
3. UGI
4. LGI
h. Presentation Patterns:
1. Chronic inflammatory Disease (mc)
2. Intestinal obstruction from stricture abscess = acute abdomen
3. Fistula formation: between bowel & bladder (ishio-ileo?)
4. Perianal disease
5. Extraintestinal:
i. D/DX: UC (superficial only), IBS (no true inflammation), Infectious colitis (yersinia, TB,
Salmonella), Parasitic infection (amoebiasis), Ischemic colitis, Diverticulitis (older pt), Colon CA-
alternating constipation & diarrhea.
j. TX:
1. Nutritional supplementation: (TPN m/c in UC than Crohn’s)
2. Low residue diet with obstruction
3. High fiber diet with diarrhea
4. Medications: Sulfasalazine, Corticosteroids, Immunosuppressive drugs (no real effect)
5. Monitor vitamin levels
6. Surgery for obstruction, fistulae, etc.
k. Complications: Obstruction, Abscess formation, Fistula formation (inter-organ, skin), Perianal
fissures, Colon carcinoma (small risk, more with UC), Hemorrhage/shock, Malabsorption, UC
r. Crohn’s Disease
1. One-third of the cases involve only the distal small bowel (ileitis)
2. Half the cases involve the distal small bowel and proximal colon (ileocolitis)
3. In 20% of the cases only the colon is involved
4. Crohn’s disease is a transmural process that can result in:
a. Inflammation, Ulceration, Stricturing (narrowing), Fistula formation, Abscess
formation
5. Crohn’s disease presents with a wide variety of signs and symptoms because its
involvement is variable in both location and severity of inflammation
6. Most commonly, there is one or a combination of the following clinical presentations:
a. Chronic inflammatory disease: This is the most common presentation: Often seen in
patients with ileitis or ileocolitis
b. Patients report low-grade fever, malaise, weight loss, and loss of energy
c. There may be diarrhea which is non-bloody and intermittent
d. Cramping or steady pain in the right lower quadrant or periumbilical area
e. Examination reveals focal tenderness in the right lower quadrant
f. Intestinal obstruction: Narrowing of the small bowel may occur as a result of
inflammation of fibrotic stenosis
g. Patients report postprandial bloating, cramping pains, and loud borborygmi
h. Fistulization with or without infection: Some patients develop sinus tracts that
penetrate through the bowel and form fistulas to other areas:
1. Fistulas to the mesentery are usually asymptomatic (loose fatty CT that
connect the bowel, organs)
2. Fistulas from the colon to the small intestine or stomach car result in
bacterial overgrowth with diarrhea, weight loss and malnutrition
3. Fistulas to the bladder or vagina produce recurrent infections
i. Extraintestinal manifestations: Oral aphthous ulcers
1. Increased prevalence of gallstones due to malabsorption of bile salts
2. Nephrolithiasis with urate or calcium oxalate stones
10. Complications: Abscess, Obstruction, Fistulas, Perianal disease,
a. Carcinoma – Patient’s with colonic disease are a t a greater risk of developing
colonic carcinoma
b. Hemorrhage – unusual in Crohn’s disease (except for Crohn’s colitis)
c. Malabsorption – from bacterial over-growth in patients with fistulas
11. No specific treatment exists for Crohn’s disease, treatment is directed toward
symptomatic improvement and controlling the disease process: steroids
12. Ulcerative Colitis (UC): aka- idiopathic proctocolitis: chronic superficial inflammation: LLQ (descending)
& rectum M/C site: unknown etiology: 100/100,000; 20% require colectomy- partial or complete
a. 14-38 year old m/c
b. Presentation: 70% relapsing, 20% chronic continuous, 10% fulminant (toxic Megacolon) –
abdominal distention & rupture: Hertz-Sprung Dz- poor myenteric plexus- VERY YOUNG
c. S&S: Adominal distention
1. Pain LLQ, LUQ
2. Bloody diarrhea: Hematochazia & electrolyte imbalance
3. Extraintestinal: Liver inflammation, sclerosing cholangitis, arthritis, uveitis, irisitis
4. .DX workup: Comprehensive H&P: Laboratory studies
a. CBC (anemia-m/c, elevated ESR)
b. SMAC (electrolytes, LFTs- liver function)
c. UA (dehydration): oliguria & high Specific gravity
d. Sigmoidoscopy: can perforate bowel
e. Double-contrast BE
5. D/DX: Crohn’s Disease, Bacterial infection, IBS, Protozoal infection, Colon CA,
Diverticulitis, Ischemic Bowel DISEASE
6. TX: Correct nutritional deficiencies
a. May need “bowel rest” with TPN
b. Folate supplementation (decrease CA Risk)
c. Low roughage diet during exacerbation
d. Meds: Sulfasalazme, corticosteroids
e. Colectomy/colsotomy
13. APPENDICITIS
a. Inflammation of appendix secondary to obstruction
b. Clinical symptom complex
1. Periumbilical/diffuse pain first
2. RLQ pain: 12-244 hrs later
3. Sign of regional peritonitis: Rebound tenderness, High fever (Robertson’s sign- push LQ =
pain on right
4. Can rupture: May cause diffuse peritonitis: sudden decrease in pain
5. May result in abscess formation
6. TX: Surgery: “Button Hole”
14. DIVERTICULAR DISEASE
a. Epidemiology: Older pt with poor bowel hygiene- very common: 30% >40y/o: 50% >70
1. Herniation of mucosa and submucosa through muscularis from low fiber diet
a. Occur at vasa recta (weakened area, where vessels pierce wall of GIT)
2. Diverticulosis is asymptomatic – pressure feelings only
3. Diverticulitis is symptomatic- if obstructed
4. Most respond well to antibiotics
5. Up to 30% require surgery
b. S/SX: Diverticulosis exam is normal
1. LLQ pain mc = itis
2. Pain relieved with BM
3. Abdominal guarding
4. Rebound tenderness suggests peritonitis
5. +/- small amount of blood in stool: Interluminar/extraluminar
c. DIVERTICULAR BLEEDING: 70% occurs in right colon
1. Bleeding is painless: the more diffuse the more blood
2. Resolves spontaneously in 60%
3. Erosion of vessels from fecalith
4. 15 – 20 % re-bleed within 5 yrs
d. Diagnostic workup
1. CBC (elevated WBC with diverticulitis): Microcytic anemia wit bleeding
2. BE, Sigmoidoscopy-best
3. Abdominal CT for abscess formation
e. D/DX: IBS, Crohn’s, UC, Colon CA, Ischemic Colitis, Infectious Colitis
f. TX:
1. Increased dietary fiber
2. Regular exercise & good bowel hygiene
3. Broad spectrum antibiotics
4. IV Antibiotics in severe cases
5. Surgical resection/re-anastomosis: If re-occur or if diffuse
15. 1Colorectal Cancer: clover-leaf appearance to polyp (slide)
1. 2nd leading cause of CA deaths in USA: 135,000 new/year: 50,000 deaths
a. 15% of all cancers (except skin cancers)
b. Peak incidence in 7th decade
c. Location: 40% Left colon; 30% rectosigmoid; 25% cecum/ascending; 10% transverse
(more aggressive- goes up to right lymph drainage to vena cava
2. Risk Factors
a. Hereditary polyposis syndromes
b. Familial polyposis, teens to 30's, pts have thousands of polyps
c. Gardner’s Syndrome: familial adenomatous polyposis malignant if untreated- osteoma
d. Inflammatory bowel diseases
e. History of previous colorectal CA
f. 1st degree relative with colorectal CA
g. Age >40, High fat, low fiber diet
h. Regional radiation therapy (eg. Female receives radiation for ovarian cancer - if the colon
is in the port, the fast turnover of the epitheal cells makes them prone to damage from the
radiation, due to the effect of radiation on fast growing tissue) [brain tumors can be treated
with sterotactic radiation]
3. Clinical Presentation: Normally unremarkable
a. DRE finds 50% of tumors
b. Palpable abdominal mass (mets most likely not the colon cancer itself)
c. Abdominal tenderness
d. alternating constipation / diarrhea
e. Hepatomegaly (mets)
f. Rectal bleeding: Hematochezia, Melena, Blood streaked stool, Occult blood [scant]
g. Abdominal distension
1. Obstruction
2. Initial symptom in 15% of patients
h. Pencil thin stools
i. Intusseception
j. Volvulus
k. Weight loss; suggest stage 3 or 4 carcinoma
l. Anorexia
m. Malaise
4. Clinical Investigation
a. Anemia (microcytic) [Any male patient over 40 with rectal bleeding is to be considered
positive for colon cancer]
b. Positive FOB test
c. Elevated CEA (used for Rx response)
d. Elevated LFTS (liver)
e. Colonoscopy, Double contrast BE
f. CT for staging
g. CXR (chest is a common place for mets of colon cancer)
h. 25% have mets at presentation; they are in stage four of the cancer
5. Differential Diagnosis: Diverticular disease, bowel stricture, inflammatory bowel diseases,
adhesions, mets, extraluminal masses (ovarian mass) AVMs
6. Cancer Staging: Duke Classification System
A - Confined to the mucosa-submucosa
B - Invasion of muscularis
C - Local node involvement
D - Distant mets (liver, lung, brain)
7. Treatment: Surgical resection- 70% are resectable at presentation: 45% cured by primary resection
a. Radiation therapy (stages B & C)
b. Chemotherapy (stages B & C) a 5-fluoroucacil, Levamisole
c. FOB q 6 months
d. Colonoscopy q year x 2 years, then q 3 years
e. CEA levels (Carcinoma Embryonic antigen)
8. Prognosis
a. Duke A >80%
b. Duke B 60%
c. Duke C 20%
d. Duke D 03%
e. Overall 5 year survival rate 50%
16. Colon Polyps: 50% patients have polyps
a. hyperplastic
b. adenomas
c. lipomas
d. Leiomyoma: Sessile / pedunculated
e. 25% patients with colon cancer have polyps
f. Signs / Symptoms: most are asymptomatic
1. Rectal bleeding most common
2. Cramps
3. Abdominal pain
4. Obstruction
5. Anal polyps may prolapse
g. Diagnosis: DRE, Endoscopy, Double contrast BE
h. Treatment: Careful observation (hyperplastic, lipomas)
1. Endoscopic surgery
2. Open laparotomy
i. SIGMOID DIVERTICULITIS TX
1. ↑ dietary fiber
2. Broad spectrum antibiotics
3. Reg. Exercise
4. IV antibiotics in severe cases
5. Surgical resection/re-anastomosis
17. TUMORS OF THE COLON
a. Colorectal CA: 2nd leading cause of CA deaths in US
lung CA, colorectal CA, Breast CA, Most common CA is skin CA
b. 135,000 new cases/year: 50,000 deaths/yr.
c. 15% of all cancers (except skin cancers)
d. peak incidence in the 7th decade
e. Location
1. Lower colon – 40%
2. rectosigmoid - 30 %
3. cecum / ascending – 25 %
4. transverse – 10%
f. 2 types of CA can occur
1. adenocarcinoma
2. Squamous cell CA – Most common with HPV (condylomata)
g. Risk factors
1. Hereditary polyposis syndromes: rare
2. Familial polyposis: bad dz: thousands of polps- resect colon before cancer occurs
3. Gardner’s syndrome: associated with colon cancer
4. Polyposis & osteoma in skull & sinuses
5. Inflammatory bowel Disease: UC m/c to cancer
6. H/o previous colorectal CA
7. 1st degree relative with colorectal CA
8. age > 40: M>F: high fat, low fiber diet:
9. Regional radiation therapy involving colon (uterus, ovary): GI 2nd most sensitive tissue
due to increased activity of cells. Malabsorption, diarrhea, etc.
h. Clinical presentation: Normally unremarkable: asymptomatic, incidental finding or chasing RUQ-
liver m/c mets
1. DRE finds 50% of tumors
2. Palpable abdominal mass (mets)
3. Abdominal tenderness: sigmoid down
4. Alternating constipation/diarrhea classic
5. Hepatomegaly (mets): Mets usually to liver (stage 4 colorectal Ca): Liver drains all of GI
6. Rectal bleeding: Hematochezia, Melena, Blood streaked stool, Occult blood- need 3 to dx
7. Abdominal distention
8. Obstruction
9. Initial sx in 15% Pencil thin stools: rectal-anus region
10. Intussusceptions or Volvulus
11. Wt loss: stage 3 or 4, Anorexia, Malaise
12. Colon CA can cause lumbar & sacral back pain
i. Clinical investigation
1. Anemia (microcytic): blood loss
2. Positive FOB test: occult blood
3. Elevated CEA (used for therapy response): not specific: tumor marker
4. Elevated LFTs: ominous sign
5. Colonoscopy, Double contrast BE, CT for staging & mets: better than MRI for air
6. CXR: mediastinal lymphadenopathy
7. 25% have mets at presentation
j. D/DX: Diverticular Disease: left colon m/c (like cancer); Bowel stricture: 15% obstruction;
Inflammatory bowel Disease(s): diarrhea alternate with constipation; Adhesions: obstructed s&s
Mets
k. Extraluminal masses (ovarian)
l. AVMs (Arterial venous malformations): obstructive s&s: tumor-like mass of vessels
m. Cancerous staging: Duke Classification system: 1-4 based on local or distant m/c
1. A – confined to the mucosa – submucosa: best prognosis
2. B – Invasion of muscularis: line for serious dz
3. C – local node involvement:
4. D – Distant mets: liver to lungs & bone
n. TX:
1. Surgical resection: 70% are respectable at presentation: (with A, no mets, vessels, nerves
involved): 45% cured by primary resection: 30% overall
2. radiation therapy (Stages B & C):
3. chemotherapy (stages B & C ): 5-flourouracil, levamisole
4. FOB (fecal occult blood) every 6 months: Guaiac test  finds occult blood in feces
5. Colonoscopy every year x 2 years, then every 3 years
6. CEA level: Carcinogenic embryonic antigen
o. Prognosis:
1. Duke A – 80 % (chance of survival) usually asymptomatic (polyp)
2. Duke B – 60% (cut off for cure)
3. Duke C – 20 %
4. Duke D – 3 %
5. Overall 5 yr. survival rate – 50 %
18. COLON POLYPS: Most non-inflammatory CA arise from polyps: 50 % patients have polyps
a. Hyperplastic: inflammation
b. Adenomas: gland
c. Lipomas: must watch
d. leiomyomas: sessile/pedunculated
e. 25% pts with colon CA have polyps (polypoid cancer m/c start as polyp)
f. S/SX: Most are asymptomatic: must screen for: Rectal bleeding mc brings into MD
Cramps, Abdominal pain, Obstruction, Anal polyps may prolapse
g. DX: DRE ; Endoscopy;
1. Complicated with severe inflammation disease
2. May perforate bowel
3. Do BE instead: Double contrast BE
h. TX: Careful observation (hyperplastic, lipoma)
1. Endoscopic surgery: (adeno)
2. Open laparotomy: for large FAP
VI. Small Bowel Diseases:
1. Celiac Sprue: also known as gluten enteropathy or celiac disease: gluten intolerance
a. This condition is thought to be a genetically predisposed sensitivity to gliadin fraction of gluten:
Wheat, rye, barley, oats
b. The gluten incites a humoral or cell-mediated inflammatory response that results in mucosal
inflammation and destruction leading to a malabsorption of most nutrients -hypoproteinemia
c. Signs & Symptoms of diagnosis are: Weight loss, dyspepsia, Distention, flatulence, greasy stools-
Steatorrhea, Diarrhea, Abnormal bowel biopsy: Bloating is classic sign of small bowel disease.
d. Failure to thrive (FTT) in children, pallor, fatigue, angular chelitis (B12), dermatitis, ricketts
e.. Clinical improvement on a gluten-free diet: M/C 1-36 months old & F > M
f. May be anemic (folic acid, iron, B12), bruise easily due to Vitamin K deficiency,
g. Have hyperkeratosis (thick skin) due to Vitamin A deficiency, and bone pain due to osteomalacia
h.. 10% of patient with celiac sprue have a skin condition called dermatitis herpetiformis.
i. DX: Biopsy shows inflamed vili: Hypoprotienemia:
1. Iron deficiency anemia
2. Folic acid deficiency
3. B12 deficiency
4. Antigliadin IgA/IgG antibodies elevated: specific for this disease
j. TX: Products containing wheat, rye, and barley must be eliminated from the patient’s diet.
Products and flours made from rice, soybean, potato and corn are safe.
1. Gluten free diet: good prognosis if follow diet
2. Iron supplement
3. Folate & B12 supplement
k. DDX: IBS m/c: laxative abuse; intestinal parasites; tropical sprue; lymphoma- malignancy m/c
chest or small bowel Peyer’s Patches, inguinal, posterior tibia.
2. Whipples Disease: multiple system disease: uncommon: 30-60 y/o: M>F: Trophyrema whipelli (gram+)
never cultured: aka-Intestinal lipodystrophy.
a. Clinical Presentation: Inflamed bowel
1. Malabsorption: diarrhea, bloating/cramping; anorexia; wt loss; fatigue, anemia
2. Extraintestinal findings: arthritis- may migrate; pleuritic chest pain; pericarditis;
osteomalacia- adult rickets.
3. Weight loss
4. Non-gastrointestinal symptoms may include low-grade fever, chronic cough,
lymphadenopathy (because of infection), and arthralgias. Other systems that could be
involved include cardiac, ocular, and central nervous system
5. TX: Antibiotic therapy – respond well = DX
6. If untreated, the disease is fatal. Respond well to antibiotics
7. No human to human transmission
b. DDX: Celiac sprue, lymphoma, Crohn’s (malabsorption); short bowel; pancreatic insufficiency;
lactose intolerance- milk gives S & S (Bread, candy, sauses)
c. TX: antibiotics: Trimethoprim, sulfamethoxazole: vitamins, iron
3. Lactose Intolerance: Lactase Deficiency: Lactase is a brush border enzyme that hydrolyzes the
disaccharide lactose into glucose and galactose: aka milk intolerance
a. Results from fermentation of lactace  gas
b. 50 million affect: 85% Asian; 60% African; 23% Caucasians
c. Lactase deficiency is common in premature infants of less than 30 weeks’ gestation
d. Lactase levels are high at birth but decline steadily in non-Europeans during childhood,
adolescence, and into adulthood.
e. S&S: With mild to moderate amounts of lactose malabsorption, patients may experience bloating,
abdominal cramps, and flatulence. In more severe cases, diarrhea may result
f. TX: Lactase supplementation or a limited lactose diet are the choices of treatment
1. Patients on a lactose-free diet should add calcium supplementation to prevent osteoporosis
2. Read labels
3. Lactaid tablets
4. Calcium supplement
g. Excellent prognosis

4. Merckel’s diverticulum: Congenital lesion: an appendix in small bowel- RLQ: 2% of population:


a. Failure of closure of vitello-intestinal duct connecting intestine to yolk sac
b. M/C anomaly of small intestine
c. Found within 3 feet if ileocecal valve
d. Less than 12 cm long
e. Complications: bleeding (ulcerated); obstruction (rare); diverticulitis (contain gastric mucosa);
perforation
f. Central umbilicus, Merckel’s scan
g. TX: diverticulectomy
5. Mesenteric Ischemia: Superior mesenteric artery or venous occlusion (back flow)
a. Affects second part of bowel from duodenum to transverse colon
b. 50% embolic (severe pain), 25% atheromatous, 10% venous occlusion
c. Mortality 90%
d. DX: Nothing suggestive usually
1. Central abdominal pain – out of proportion
2. KUB may be normal
3. Severe pain suggests rupture  peritonitis
e. Risk factors: ETOH, DM, high cholesterol
6. Short Bowel Syndrome
a. This syndrome is a malabsorptive condition that arises secondary to the removal of significant
segments of small intestine
b. The most common causes in adults are
c. DDX: Crohn’s disease, Mesenteric infarction (supposedly most painful condition in humans),
Radiation enteritis (cancer patient on radiation), Trauma
d. The type and degree of malabsorption depend upon the length and site of the resection and the
degree of adaptation of the remaining bowel.