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ID2 test 2I. Esophagus:

A. Normal:i. Function: Propel food from the oral pharynx [not mouth] to the stomach, lined with epithelia

a. No real digestive functionsb. Can swallow standing on your head because of peristalsisc. 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 tracheaB. Primary Peristalsis (bolus propelled thru hollow viscera): voluntary most powerfuli. 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 esophagusii. Propels food through lower esophagus:

D. Tertiary Peristalsis (Curling phenomenon; Cork screw appearance)i. Seen in the elderly - commonii. No propulsion

a. Fibrillation of the esophagus; doesnt 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 commoniii. Pedunculated has a stalk iv. Most in lower esophagus (because of reflux) (Barretts carcinoma/adenocarcinoma)v. Squamous cell carcinoma is most common, squamous cells line the esophagusvi. 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, preservativesvii. M: F 3:1: Adenocarcinoma/Barretts 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 HTNEsophageal Varices CA

1. Higher incidence of reflux (irritating to epithelium)2. Alcoholics are usually smokers3. Alcohol also irritates the esophagus itself

b. Cigarette Smoking: swallow nitrites [via salvia and swallowing air] CA1. Nitrate Ingestion in lungs

2. Chronic Achalasia, poor relaxation of the proximal end caused by destruction: prestenoticdilation 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 belchc. Swallow dysphagia regurgitation: Chronic GERD/Barretts Esophagus, CAobstruction of hollow organ regurgitation

c. Where food gets stuck 1. Thoracic inlet2. Pharyngeal Esophageal Sphincter (Larynx)3. Aortic Knob (because of aorta uncoiling leaves an indentation in the esophagus)

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4. When the aorta uncoils due to aging and atherosclerotic Disease5. Left Atrium6. 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 metastasisPatients dont know they have usually until they become malignantAdenomas, 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 malignantiii. Physical Findings

a. Dysphagia mc symptom: usually asymptomatic until late stages of CA: vomiting frequent b. motor problem dysphagia with both solids 1 st & then liquidsc. obstruction dysphagia with solids early & progresses to dysphagia with fluidsd. CA cachexia occurs/wt loss just skin & fat (chronic disease wasting)e. Weight Loss, suggestive that CA has metastasized: stage 3 or 4 usuallyf. Cervical Adenopathy: Lymph nodesg. Virchows 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 pneumoniaa. 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 sputumk. Mets to liver m/c, pleura, lungs with associated signs and symptomsl. Mc presentation if mets to lung is asymptomatic, depends on site

iv. Diagnostic Imaginga. Double contrast esophagram: CO2 & Barium (barium swallow- shoulder sign- key 90 cuto

Now we use endoscopy instead b. Get lung & ab CT/MRI to check for mets

c. Esophagoscopy: EGDd. Chest/abdominal CT: looking for metse. Abdominal MRI:f. Mediastinum lymph nodes would be involved with esophageal cancer if metastasis has occurred

v. Laboratory Testsa. Done also to check for mets

b. CBC, (WBC up, RBC down maybe), Blood Chemistries1. Anemic male over 40 has GI cancer, unless proven otherwise

c. Liver Enzymes, metastasis to the liver is commonvi.. 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 worsePain lasts min to hoursc. Esophageal Rings- (congenital): Fibrocartilaginous ring that narrow the esophagus

1. Schatzkis Upper esophageal ring2. Lower ring

d. Scleroderma (Progressive Systemic Sclerosis, newest term): Connective tissue disease: Hardeningof the interstitial tissues narrowing and lack of peristalsis dysphagia

vii. Treatmenta. 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 ends2. Lab makes sure clean tissue is found around CA to ensure complete removal

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3. Only done if no mets4. Stomach/colon used for replacement of gut removed

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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 outpaceschemo/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-sensitivec. Chemotherapy 15-80%: stage 1 best cure rate

1. Kills cells that are in the S1 phase (immature cells) that are rapidly dividingHair, 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 uterusa. 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 andfibrous tissue: Rare: can have occult blood- rare to bleed

H. Esophagitis: types1. Reflux: Reflux of gastric contents with damage- stricture- Barretts = metaplasia

a. Contents reflux up through cardiac sphincter with force and through the lower esophagealsphincter. Causing linear and nonlinear erosions of the esophageal lining

b. Progression of GERDc. Incompetent LES (Lower esophageal sphincter)d. Often associated with hiatus hernia: Protrusion of the stomach through the hiatuse. 30-60 (minutes) post-prandial/reclining heartburnf. NOT GERD GERD damage is reversible: Is GERD gone wild:

g. More severe thus causes stricturesh. TX with Nexiumi. 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-esophagusulceration if chronic contracted, inflexible lower esophagus,or can perforate intomediastinum (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 asto weather solids and or liquids are involvede. Can lead to laryngitisf. Contracted fibrotic lower esophagus results

3. Infective:a. Infection of the esophagus is rather unusual

b. Immunosuppressed patient: not seen in healthy usually1. AIDS most common group, cancer, DM, transplant

c. Long term corticosteroid treatmentd. Organisms: Herpes Simplex, Candida Albicans-Typically found in the vaginal region of females and faces of childrene. Pic: Candida Esophagitis, occurs especially with immunocompromised patientsf. CMV (Cytomegalovirus), causes encephalitis in kids

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g. S & S: Dysphagia, Odynophagia (Painful swallowing), Chest Pain more of a burningsensation instead of a crushing painh. Treated with Antibodies

4. Mechanical:a. Swallowed object becomes lodged at narrowed portions

1. Laryngopharynx, Aorta, Gastroesophageal junction, Left Atrium (not very oftenunless preexisting CHF)

b. Objects include coins, pills, bone pieces

c. 3 main groups that do this: Elderly, children, and insaned. Leads to ulceration, maybe perforation- Which can lead to mediastinitise. 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 1/3of the esophagus: Varicose veins of the esophagus

a. Alcohol is the most common cause portal hypertension (pressure increased in portalvenous system, blood backs up cirrhosis)

b. Lower 1/3 submucosal veins involvedc. 1/3 of patients bleed: Alcohol Cirrhosis Esophageal Varices Bleeding outd. 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 seef. Treated with sclerotherapy & Compression Bougie balloon down the lower esophagusand the balloon flattens out the varicesg. Sclerotherapy inject hardening agent that hardens (sclerosis) the walls so they can nolonger extend also used in peripheral vascular diseaseh. S/Sx : Pt has some pain and dysphagia: Symptoms are not extreme

6. Esophageal Diverticula: Localized outpouching of tubular viscusa. Usually acquired (congenital forms are rare)

b. Two Types:1. Traction (extraesophageal) : Mediastinal mass (inflamed lymph node next toesophagus)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 theoutpouching: Something pulls on esophagus from the outside-Eg; an attachedneoplasm

a. Most common in middle esophagus. Adhesions outside tract b. Because most lymph nodes are in mediastinum their enlargement can causethem 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 aweak area of the esophageal wall where the small micro vascularity occurs to supply

blood to the esophagusa. Most common lower/upper esophagus.

b. Occur anywhere in esophagusc. Lower just above the diaphragm Epiphrenic diverticula (just abovediaphragm)

7. Zenkers diverticulum: pulsion type:a. Occurs at pharyngoesophageal junction

b. Can be very large in sizec. Loss of upper esophageal sphincter laxityd. Retains foode. Signs/Symptoms

1. Halitosis bad breath2. Spontaneous Regurgitation

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3. Verp vomit/ burp4. Nocturnal choking position- elevate head of bed5. Recommended not to eat within a few hours6. Neck mass: pain & dysphagia7. Can sometimes see peristalsis in the mass

f. Complications Aspiration (inhaling something that wasnt 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 bacteria2. AM coughing: spit layered: surfactant, serous, pus

8. Epiphrenic diverticulum: weakened area in lower esophagus: usually asymptomatic & small9. Middle esophageal diverticulum: usually traction type

a. From mediastinal lymphadenitis: lymphadenopathyI. GERD reflux esophagitis Barretts esophagus Esophageal. CA always rule out cardiac Disease 1st

1. Cough & bronchospasm or laryngitis from aspiration2. Early satiety GERD get full quickly3. Chocolate fat & caffeine contents cause GERD episode4. Tobacco when chemicals are swallowed

5. Commonly assoc. with hiatal hernia (>70%)6. Nitroglycerin will make anginal chest pain better & Makes GERD chest pain worse7. Gastroesophageal Reflux Disease: Reflux of gastric contents into lower esophagus8. 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 aging9. Reflux Esophagitis Barretts Esophagus Squamous cell carcinoma10. Heavier a person is the more chance they can have because increase in intra-abdominal pressure11. Incidence: 60% of adults have heartburn: 80% of pregnant women have GERD12. 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 airwayc. Laryngitisd. Early Satiety (Getting full fast)e. Belching/Bloating

13. Contributing Factors:1. Chocolate (caffeine and fat), Yellow Onions, Peppermint, Garlic2. Tobacco (nicotine and causes sphincter to relax), Alcohol (fat and causes sphincter torelax), 3. Caffeine4. 70% of GERD suffers have a hiatal hernia5. Beta Blockers (control BP and angina), Ca++ Channel Blockers, nitroglycerin Causesdilation of lower esophageal sphincter 6. Gastric Acid Hypersecretion

14. Diagnosis: 24 esophageal pH monitoringa. 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. Treatmenta. Avoid triggers (diet modification)

b. Proton pump inhibitorsc. H2-blockers (cimetidine Prilosec )d. Antacidse. Fundoplication: fundus of stomach wrapped around esophagus

1. Reserved for pts with daily reflux

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2. Three typesa. Nissen (complete)

b. Posterior (partial)c. Anterior (partial)

f. Drink excessive amount of water, water helps to dilute the acid and provide weight to thestomach to pull the hiatal hernia down.

J. Barretts: usually asymptomatic1. Pre-malignant

2. Associated with chronic reflux (5-10% incidence)3. Stratified squamous manifests to columnar epithelium, a pre cancer action4. Increased risk of adenocarcinoma

a. 30-50 times increased risk to develop adenocarcinoma of the esophagus b. 500/100,000 people with Barretts esophagus who have GERD

5. Dx: EGD, biopsy almost always accompanies an EGD6. Treatment:

1. Laser Ablation2. Fundoplication3. 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 peristalsisineffective2. Chest pain can occur when peristalsis is attempted: Pain usually colicky3. Functional esophageal obstruction4. Inadequate relaxation of the LES5. Ineffective Peristalsis6. 1/100,000 incidence; 30-50 y/o7. S/Sx: Both Solid/liquid dysphagia-immediately, patient indicates they can feel the food stickingusually 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. Etiologya. Degeneration of myenteric plexus

b. Viral1. Herpes Zoster, Measles Virus

c. Autoimmuned. Not completely understood, true etiology not know

9. Diagnosis: EGD with manometry, UGIa. Tests to rule out other causes (eg: EKG), Especially with age group one wants to R/O MI

10. Treatmenta. Medical: Smooth muscle relaxants (70% effective)

1. Nitrates2. Calcium channel blockers: relax LES3. Botulinum toxins injection4. 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 RX1. Long standing Disease increases risk of CA

L. Scleroderma: (PSS-) non-inflammatory arthritis1. Aka: progressive systemic sclerosis (PSS): Means hardening of the skin2. Primarily effects the skin, but is not limited to the skin: Tissue thickens and hardens3. Severe hardening of lips to point must be tube feed: Sometimes must replace the esophagus

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4. Parastasis is affected, thus difficulty in swallowing, reflux5. Kidneys are often affected as well6. Vessels become calcified, thickened and hardened7. Female>Male Early teens to 20s8. Smooth mm relaxants used if esophagus does not need replacing, patient receives temporary relief,usually do not work 9. Multisystem disorder often affecting the esophagus10. Lose ability to have peristalsis

11. Become very narrow and can develop strictures12. EGD used to diagnose13. 75% have esophageal involvement14. Fibrosis and inelasticity results15. Signs & Symptoms

a. Dysphagia b. Esophageal reflux/regurgitation

16. Diagnosis: EGD, UGI17. Reaction with smooth muscle relaxants18. Etiology unknown

M. Diffuse Esophageal Spasm:1. Ice cream eating too fast is the same pain, brain freeze2. Pain lasts minutes to hours3. Usually end up in the ER thinking they are having a cardiac problem4. Diffuse sustained contraction (spasm) of esophagus5. Etiology unknown6. Can be confused with angina pectoris: vaso-vagal reaction7. S/sx:

a. Substernal chest pain b. Dysphagia with pain, worsened by swallowing, key differentiating featurec. Regurgitation

8. Dx:a. EGD (Esophagogastroduodenoscopy) & mamometer- pressure balloon

b. UGI: With barium swallow on x-ray appears as a cork screwc. Reaction with Ca++ channel blockers/nitrates- muscle relaxant: Causes reflux

II. Stomach Diseases:A. Anatomy:

1. Stomach B12 absorption (intrinsic factor), storage, mixing, mineral absorptiona. Decreased intrinsic factor low B12 pernious anemia malabsorption neuropathy -hematopoetic

- 2. Rugae increases surface area inside the stomach for production of HCl and pepsin3. GE Junction4. Gastroesophageal Reflux Disease

5. Fundus- Usually holds gas6. Magenblase air in the stomach7. Antrum8. Pylorus -Narrowed portion of the distal most aspect of the stomach9. Pyloric Sphincter b/w stomach and duodenum help prevent outflow of gastric juices thatcould lead to PUD10. Pyloric stenosis prevents outflow, causes regurgitation11. 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

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1. HCL & pepsin secreted2. 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 & fundus2. 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 A5. No symptom complex presented early in the Disease6. Aggressive, Infiltrated carcinoma invades entire organ and cause thickening of entire organ -rarely found before stage 3 or 47. 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 productionc. Dysphasia: High in GES; n/v, constipation

8. Risk factors: Diet rich in additives (smoked, pickled); Atrophic gastritisa. Inflammatory disease of the stomach where there is atrophy of the rugae Sequela : B12deficiency pernicious anemia

b. Tobacco use: decreases blood flow & swallows air & tar c. Hispanic, Japanesed. Polyps - Growth into lumen Sessile and pedunculated. Usually premalignant mass (some

benign)e. H. pylori infection (PUD associated wipatith H. pylori)f. Barretts Esophagus

9. DX: Stool guaiac test test for blooda. Any male > 40 with anemia, has GI malignancy until proven otherwise

b. Positive stool guaiac (blood to stool content): FOB, fecal occult blood testc. Will have black tarry stool if blood occurs in the stoold. Hemoglobin

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2. Rarely symptomatic- Only with obstruction

b. Adenoma benign tumor of glandular tissue, aka polyps1. 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 obstruct4. Over 2cm, have malignant potentialE. Gastritis: Causes/leads to

1. Erythema reddening (aka injected)2. Hemorrhage3. Erosions4. Types-3

a. Erosive b. Non-erosive, non-specific causec. Specific bacterial, etc.

5. S/sx: post-prandial (after eating) indigestion/pain LUQa. Nausea and vomiting

b. Bloatingc.50% has H. pylori (spiral shaped bacteria)

6. Erosive Gastritis: Etiology:a. NSAIDs: m/c (3-5cc blood/tablet)

b. Alcohol(ism), portal HTN venous congestion decreases the removal of waste from thestomach blood supply. Leads to cirrhosisc. Stress from major illness (burns): m/c in cancer d. Hemorrhage also common with this Diseasee. Usually asymptomaticf. Can produce pain, hematemesis, n/vg. Diagnosed with EGD

7. Non-erosive/non-specifica. H. pylori gastritis: Spiral gram (-) rod

1. Causes acute superficial mucosal Disease2. S/sx: Nausea and vomiting, Pain LUQ

b. Atrophic gastritis1. Associated with pernicious anemia not producing enough intrinsic factor for B122. 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 rugaeless intrinsic factor

8. Specific:a. Mntriers Disease: malabsorption of protein, due to poor digestion in stomach

1. Giant fold gastritis (the rugae become very large)2. Enlarged thickened gastric rugae3. Get hypoproteinemia due to enlarged rugae4. Causes 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, 3 rd spacing fluid8. Idiopathic

b. Granulomatous gastritis

Atrophic gastritis associated withanemia

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1. Crohns 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 startsin chest at mediastinal lymph nodes: Potato nodes, brain, GI, joints & is fatalsometimes)2. Treat specific disorder

c. Phlegmonous gastritis1. Phlegmon aggressive large abscess perforate peritonitis

2. Abscess from fungal, bacterial, parasitic infection3. Emergent gastrectomy and IV antibiotics4. Treatment is the removal of the stomach.5. Common among aids patients (immunosuppressed)

d. Others: Mechanical, chemical, ate too muchIII. Peptic Ulcer disease: acid/base imbalance between protection & damage

1. Ulceration of the stomach or duodenum Ulcer Crater a crater that penetrates mucosa of hollowviscera: H. pylori m/c: tx with antibiotics

a. typically < 1 cm b. larger than 2 cm malignant potentialc. Go through at least the mucosal layer

2. Malignant ulcer malignant tissue with an ulcer inside of it3. Normal acid production with lowered protection ulcers4. Normal protection with overproduction of acid ulcers5. Gastric chemical secretion helps digest proteins, damaging to lining with good protection

a. Hydrochloric acid b. Pepsinc. Stimulated by acetylcholine (acetylcholine production is increased with stress as is the HCl thus adouble negative), gastrin, histamine

6. Other ulcerogenic substances: Bile acids, reflux of bile into the stomach, thus the reason for their beingfound 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 patientsc.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 chemicalsc. NSAID- chronic: Irritating to the gastric mucosa COX inhibitors stop prostaglandin productionwhich stops blood flow to the stomach and inhibits protection to liningd. Delayed gastric emptying: Food stays in stomach & irritatese. Diabetics: Decreased bowel function, high incident of PUD

9. H. pylori (produces urease) there is an inferred or coincidental correlation between H. pylori & ulcersa. Increases gastric acid secretion: overwhelms mucosa

b.75% of patients are infected with H. pyloric.75% have recurrence in 1 year without antibioticsd.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 downin the duodenum thus the increase in ulcers in this area

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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 exacerbations12. Differential Diagnosis:a. GERD: damage not permanentb. Reflux Esophagitis, most common condition confused with PUD: permanent damagec. Gastric CA, particularly if there is a change in the pain patternd. Gastritis: epigastric paine. Pancreatitis: umbilical pain: fetal position for comfortf. Cholecystitis- RUQg. Cardiac (always R/O 1 st+)

13. Diagnostic Workup: Esophagogastroduodenoscopy (EGD), almost universally the means of diagnosis95% accurate (5% due to human error)

a. Biopsy ALL lesions: Cancer / benign cannot be differentially diagnosed by sightAlso biopsy for H. pylori

b. Upper GI: BaSO4: Not as reliable as EGD: no biopsy capabilities14. Treatment:

a. Antibiotic therapy (clarithromycin which is harsh on the stomach lining) b. Omeprazolec. H+ pump inhibitors - Tagametd. Stop Smoking; Stop NSAID usee. Diet Changes: Bland Dietf. Stress Reduction: Because of sympathetic reaction: Valium (classic drug prescribed)g. Manipulation in conjunction with medical therapy has been proven beneficial to the patienth. Dont use milk anymore because the sugar in it can help feed the bacterial and can actually makethe 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 bleedingis clinically significant. Cause sx and problems: 80% stop bleeding spontaneouslyMortality rate is 6-10% of the 20% who do not stop bleeding spontaneously

1. Occult blood dont know its there b. Anemiac. Cancer d. Perforation: 5% incidence: Usually on anterior wall -Because its thinner Zollinger-Ellison should be considerede. Gastric Outlet Obstruction At pylorus or duodenal bulb: 2% IncidenceFrom tissue obstruction scar tissue (fibrosis) obstruction

` 16. Zollinger-Ellison Syndrome: Uncommon cause for PUDa. Occur because of Gastrin secreting tumors (gastrinoma)

b. Cause multiple peptic ulcersc. Perforation is relatively commond. Bleed outs commone. 2/3 of gastrinomas are malignant & will metastasize: Can lead to deathf. 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) throughdiaphragmatic hiatus

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1. EPIDEMIOLOGY: 50% of patients over 50: Female: Male 4:1: Often associated with GERD90% with EGD esophagitis have a hernia2. Etiology unknown, age most likely culprit due to weakening of the sphincteric. May be congenital or

post-traumatic3. 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 Esophagusd. Intrathoracic Stomach5. SIGNS AND SYMPTOMS (same as reflux with the exception of the addition of borborygmi

a. Heartburn-Because also have GERD b. Dysphagiac. Regurgitationd. Chest Pain (burning)e. Postprandial fullness (After eating)f. GI Bleedingg. Dyspneah. Hoarseness- Irritation of larynx from GERD

i. Cough- Irritation and to keep stuff from going into the trachea j. Wheezing6. SLIDING HIATUS HERNIA

a. Most common the esophagus pulls the fundus of the stomach up through the hiatus b. AKA: Axial or Concentric Herniac. GE Junction/upper stomach herniatesd. Usually asymptomatice. Symptoms: Reflux, Burning Chest Pain, Regurgitation with recumbency /fatty mealsf. Episodic (no clue- wk, hours, Gas bubble above the diaphragm on x-ray (magenblase)

7. PARAESOPHAGEAL HERNIA: Second most common: AKA: Rolling Hiatus Herniaa. GE junction in normal position

b. Fundus herniates through diaphragmc. Usually asymptomaticd. Should be surgically reduced- May become strangulated- Lead to ischemia (loss of blood supply)

8. MISCELLANEOUS HERNIAa. Short Esophagus Type: Variation of sliding: Uncommon: Congenitally short esophagusb. 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 hemidiaphragm10. 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 lossc. Sleep with head elevatedd. Manipulatione. Antacids, H+ pump inhibitors, etc.f. Surgery for refractive disease

12. COMPLICATIONS: Reflux; Erosive esophagitis; Ulcerative esophagitis; Barretts esophagitis; StrictureGI 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

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c. Veins near anus straining variscosities hemorrhoidsd. Methane m/c gas: from fermentation process of bacteriae. Ilio-cecal valve: to decrease reflux to small bowelf. No vili: has cryptsg. Circular muscular ring Hoffstrae for peristalsish. Longitudinal band: Tinnea coli: pull accordion fashion, like a snakei. 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 day2. External: voluntary (HNP may affect)

2. Review blood supply to colon: Both Superior & Inferior Mesenteric arteries branch off aorta3. Blood supply interruption: Life threatening; acute abdomen: necrosis & perforation

a. Mesenteric Thrombosis ischemia necrosis inflammation distention perforation b. Diabetics M/C: smokers: poor circulationc. Trauma causing vasocompression

4. Colonoscopes used to view the colon

5. Tapeworm S/SX abdominal pain, weight loss6. INFLAMMATORY BOWEL DISEASE: Bubos plaque`a. Irritable bowel syndrome

b. Crohns Diseasec. UCd. Antibiotic Associated Colitise. Bacterial Colitis (Food Poisoning)f. Appendicitis

7. IRRITABLE BOWEL SYNDROME: aka: Mucous colitis, spastic colona. 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 = 2:1f. Begins in late teens/early adulthood: life altering diseaseg. 50% pts have psych problems (30% have an anxiety disorder) or are hyperactiveh. etiology unknowng. commonly associated with stressh. S/SX: Crampy abdominal pain, low grade through the day up to the point that defecation isimminent, at which time the pain increases

1. Diarrhea: Up to 30 BM/day: Water/mucous in the stool2. Bloating/abdominal distention, increased gas

3. Abdominal tenderness: LLQ m/c (more peristalsis)4. Pain often relieved (temporarily) by BM5. No blood in stool, important differential feature from Crohns and or ulcerative colitis6. Sign and symptoms present for 3 months before dx7. Hyperactive bowel sounds

i. Major concern with this condition is maintaining the patients hydration level j. D/DX (other diseases which cause cramp type pain and diarrhea): Crohns Disease, UC,Diverticulitis (LLQ), Colon CA (alternating), PUD, Chronic Pancreatitis (less fat digestion), BiliaryDisease: 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

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2. Fiber supplementation (psyllium)3. Anti-spasmodics: Imodium, Lonotil, Bentyl4. Eliminate stress5. > 60% respond to RX within 1 year

11. CROHNS DISEASE: aka- chronic granulomatous inflammatory Disease: regional enteritis- skip lesionsa. debilitating, often requiring surgery

b. 1:1000 population: Caucasians, Jewsc. Unknown etiology:

d. Affects young people:e. Pathophysiology1. Location

a. 33% involve terminal ileum b. 50% involve distal ileum/proximal colon (ileocecal)c. 20% involve colon onlyd. Can involve any portion of GI tract: uveula deviation

2. Transmura l DISEASE (across wall): Inflammation (granulation tissue), Ulceration,Stricture, Fistula connection between organs or skin, abscess cause obstruction, perotinitis;

f. S/SX:1. Abdominal distention/bloating2. Mass suggests abscess formation3. Crampy abdominal pain: ileocecal (RLQ): Hyperactive Bowel Sounds4. Non-bloody/bloody diarrhea: small amounts (more blood from UC)5. Perianal fissures/fistulas6. Bowel obstruction: from fissures/fistulas, abcesses7. Crohns arthropathy: Seronegative arthridities- bilateral, asymmetrical, SI joints(inflammatory ankylosing spondylitis before S &S of Crohns)8. Low grade fever, pallor 9. Weight loss, fatigue

g. Diagnostic Evaluation: CBC, SMAC, & UA1. CBC: Anemia, Decreased H&H, Electrolyte imbalance, Vitamin B12 deficiency (stomach& ileum)2. Endoscopy3. UGI4. LGI

h. Presentation Patterns:1. Chronic inflammatory Disease (mc)2. Intestinal obstruction from stricture abscess = acute abdomen3. Fistula formation: between bowel & bladder (ishio-ileo?)4. Perianal disease5. 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 Crohns)2. Low residue diet with obstruction3. High fiber diet with diarrhea4. Medications: Sulfasalazine, Corticosteroids, Immunosuppressive drugs (no real effect)5. Monitor vitamin levels6. Surgery for obstruction, fistulae, etc.

k. Complications: Obstruction, Abscess formation, Fistula formation (inter-organ, skin), Perianalfissures, Colon carcinoma (small risk, more with UC), Hemorrhage/shock, Malabsorption, UCr. Crohns Disease

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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 involved4. Crohns disease is a transmural process that can result in:

a. Inflammation, Ulceration, Stricturing (narrowing), Fistula formation, Abscessformation

5. Crohns disease presents with a wide variety of signs and symptoms because itsinvolvement 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 energyc. There may be diarrhea which is non-bloody and intermittentd. Cramping or steady pain in the right lower quadrant or periumbilical areae. Examination reveals focal tenderness in the right lower quadrantf. Intestinal obstruction: Narrowing of the small bowel may occur as a result of inflammation of fibrotic stenosisg. Patients report postprandial bloating, cramping pains, and loud borborygmih. 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 thatconnect the bowel, organs)2. Fistulas from the colon to the small intestine or stomach car result in

bacterial overgrowth with diarrhea, weight loss and malnutrition3. Fistulas to the bladder or vagina produce recurrent infections

i. Extraintestinal manifestations: Oral aphthous ulcers1. Increased prevalence of gallstones due to malabsorption of bile salts2. Nephrolithiasis with urate or calcium oxalate stones

10. Complications: Abscess, Obstruction, Fistulas, Perianal disease,a. Carcinoma Patients with colonic disease are a t a greater risk of developingcolonic carcinoma

b. Hemorrhage unusual in Crohns disease (except for Crohns colitis)c. Malabsorption from bacterial over-growth in patients with fistulas

11. No specific treatment exists for Crohns disease, treatment is directed towardsymptomatic 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 YOUNGc. S&S: Adominal distention

1. Pain LLQ, LUQ2. Bloody diarrhea: Hematochazia & electrolyte imbalance3. Extraintestinal: Liver inflammation, sclerosing cholangitis, arthritis, uveitis, irisitis4. .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 gravityd. Sigmoidoscopy: can perforate bowele. Double-contrast BE

5. D/DX: Crohns Disease, Bacterial infection, IBS, Protozoal infection, Colon CA,Diverticulitis, Ischemic Bowel DISEASE6. TX: Correct nutritional deficiencies

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a. May need bowel rest with TPN b. Folate supplementation (decrease CA Risk)c. Low roughage diet during exacerbationd. Meds: Sulfasalazme, corticosteroidse. Colectomy/colsotomy

13. APPENDICITISa. Inflammation of appendix secondary to obstruction

b. Clinical symptom complex

1. Periumbilical/diffuse pain first2. RLQ pain: 12-244 hrs later 3. Sign of regional peritonitis: Rebound tenderness, High fever (Robertsons sign- push LQ =

pain on right4. Can rupture: May cause diffuse peritonitis: sudden decrease in pain5. May result in abscess formation6. TX: Surgery: Button Hole

14. DIVERTICULAR DISEASEa. 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 dieta. Occur at vasa recta (weakened area, where vessels pierce wall of GIT)

2. Diverticulosis is asymptomatic pressure feelings only3. Diverticulitis is symptomatic- if obstructed4. Most respond well to antibiotics5. Up to 30% require surgery

b. S/SX: Diverticulosis exam is normal1. LLQ pain mc = itis2. Pain relieved with BM3. Abdominal guarding4. Rebound tenderness suggests peritonitis5. +/- small amount of blood in stool: Interluminar/extraluminar

c. DIVERTICULAR BLEEDING: 70% occurs in right colon1. Bleeding is painless: the more diffuse the more blood2. Resolves spontaneously in 60%3. Erosion of vessels from fecalith4. 15 20 % re-bleed within 5 yrs

d. Diagnostic workup1. CBC (elevated WBC with diverticulitis): Microcytic anemia wit bleeding2. BE, Sigmoidoscopy-best3. Abdominal CT for abscess formation

e. D/DX: IBS, Crohns, UC, Colon CA, Ischemic Colitis, Infectious Colitisf. TX:

1. Increased dietary fiber 2. Regular exercise & good bowel hygiene3. Broad spectrum antibiotics4. IV Antibiotics in severe cases5. Surgical resection/re-anastomosis: If re-occur or if diffuse

15. 1Colorectal Cancer: clover-leaf appearance to polyp (slide)1. 2 nd 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 7 th decadec. Location: 40% Left colon; 30% rectosigmoid; 25% cecum/ascending; 10% transverse(more aggressive- goes up to right lymph drainage to vena cava

2. Risk Factorsa. Hereditary polyposis syndromes

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b. Familial polyposis, teens to 30's, pts have thousands of polypsc. Gardners Syndrome: familial adenomatous polyposis malignant if untreated- osteomad. Inflammatory bowel diseasese. History of previous colorectal CAf. 1st degree relative with colorectal CAg. Age >40, High fat, low fiber dieth. Regional radiation therapy (eg. Female receives radiation for ovarian cancer - if the colonis 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 treatedwith 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 tendernessd. alternating constipation / diarrheae. Hepatomegaly (mets)f. Rectal bleeding: Hematochezia, Melena, Blood streaked stool, Occult blood [scant]g. Abdominal distension

1. Obstruction

2. Initial symptom in 15% of patientsh. Pencil thin stoolsi. Intusseception

j. Volvulusk. Weight loss; suggest stage 3 or 4 carcinomal. Anorexiam. Malaise

4. Clinical Investigationa. Anemia (microcytic) [Any male patient over 40 with rectal bleeding is to be considered

positive for colon cancer] b. Positive FOB testc. Elevated CEA (used for Rx response)d. Elevated LFTS (liver)e. Colonoscopy, Double contrast BEf. CT for stagingg. 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) AVMs6. Cancer Staging: Duke Classification System

A - Confined to the mucosa-submucosaB - Invasion of muscularisC - Local node involvementD - Distant mets (liver, lung, brain)

7. Treatment: Surgical resection- 70% are resectable at presentation: 45% cured by primary resectiona. Radiation therapy (stages B & C)

b. Chemotherapy (stages B & C) a 5-fluoroucacil, Levamisolec. FOB q 6 monthsd. Colonoscopy q year x 2 years, then q 3 yearse. CEA levels (Carcinoma Embryonic antigen)

8. Prognosisa. Duke A >80%

b. Duke B 60%c. Duke C 20%

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d. Duke D 03%e. Overall 5 year survival rate 50%

16. Colon Polyps: 50% patients have polypsa. hyperplastic

b. adenomasc. lipomasd. Leiomyoma: Sessile / pedunculatede. 25% patients with colon cancer have polyps

f. Signs / Symptoms: most are asymptomatic1. Rectal bleeding most common2. Cramps3. Abdominal pain4. Obstruction5. Anal polyps may prolapse

g. Diagnosis: DRE, Endoscopy, Double contrast BEh. Treatment: Careful observation (hyperplastic, lipomas)

1. Endoscopic surgery2. Open laparotomy

i. SIGMOID DIVERTICULITIS TX1. dietary fiber 2. Broad spectrum antibiotics3. Reg. Exercise4. IV antibiotics in severe cases5. Surgical resection/re-anastomosis

17. TUMORS OF THE COLONa. Colorectal CA: 2nd leading cause of CA deaths in USlung 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 decadee. Location

1. Lower colon 40%2. rectosigmoid - 30 %3. cecum / ascending 25 %4. transverse 10%

f. 2 types of CA can occur 1. adenocarcinoma2. Squamous cell CA Most common with HPV (condylomata)

g. Risk factors1. Hereditary polyposis syndromes: rare2. Familial polyposis: bad dz: thousands of polps- resect colon before cancer occurs3. Gardners syndrome: associated with colon cancer 4. Polyposis & osteoma in skull & sinuses5. Inflammatory bowel Disease: UC m/c to cancer 6. H/o previous colorectal CA7. 1st degree relative with colorectal CA8. age > 40: M>F: high fat, low fiber diet:9. Regional radiation therapy involving colon (uterus, ovary): GI 2nd most sensitive tissuedue 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 tumors2. Palpable abdominal mass (mets)

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3. Abdominal tenderness: sigmoid down4. Alternating constipation/diarrhea classic5. Hepatomegaly (mets): Mets usually to liver (stage 4 colorectal Ca): Liver drains all of GI6. Rectal bleeding: Hematochezia, Melena, Blood streaked stool, Occult blood- need 3 to dx7. Abdominal distention8. Obstruction9. Initial sx in 15% Pencil thin stools: rectal-anus region10. Intussusceptions or Volvulus

11. Wt loss: stage 3 or 4, Anorexia, Malaise12. Colon CA can cause lumbar & sacral back paini. Clinical investigation

1. Anemia (microcytic): blood loss2. Positive FOB test: occult blood3. Elevated CEA (used for therapy response): not specific: tumor marker 4. Elevated LFTs: ominous sign5. Colonoscopy, Double contrast BE, CT for staging & mets: better than MRI for air 6. CXR: mediastinal lymphadenopathy7. 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&sMetsk. Extraluminal masses (ovarian)l. AVMs (Arterial venous malformations): obstructive s&s: tumor-like mass of vesselsm. Cancerous staging: Duke Classification system: 1-4 based on local or distant m/c

1. A confined to the mucosa submucosa: best prognosis2. B Invasion of muscularis: line for serious dz3. 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, nervesinvolved): 45% cured by primary resection: 30% overall2. radiation therapy (Stages B & C):3. chemotherapy (stages B & C ): 5-flourouracil, levamisole4. FOB (fecal occult blood) every 6 months: Guaiac test finds occult blood in feces5. Colonoscopy every year x 2 years, then every 3 years6. 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 polypsa. Hyperplastic: inflammation

b. Adenomas: glandc. Lipomas: must watchd. leiomyomas: sessile/pedunculatede. 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 MDCramps, Abdominal pain, Obstruction, Anal polyps may prolapseg. DX: DRE ; Endoscopy;

1. Complicated with severe inflammation disease2. May perforate bowel

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3. Do BE instead: Double contrast BEh. 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 mucosalinflammation and destruction leading to a malabsorption of most nutrients -hypoproteinemiac. 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, rickettse.. Clinical improvement on a gluten-free diet: M/C 1-36 months old & F > Mf. 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 osteomalaciah.. 10% of patient with celiac sprue have a skin condition called dermatitis herpetiformis.i. DX: Biopsy shows inflamed vili: Hypoprotienemia:

1. Iron deficiency anemia2. Folic acid deficiency3. B12 deficiency4. Antigliadin IgA/IgG antibodies elevated: specific for this disease

j. TX: Products containing wheat, rye, and barley must be eliminated from the patients diet.Products and flours made from rice, soybean, potato and corn are safe.

1. Gluten free diet: good prognosis if follow diet2. Iron supplement3. Folate & B12 supplement

k. DDX: IBS m/c: laxative abuse; intestinal parasites; tropical sprue; lymphoma- malignancy m/cchest or small bowel Peyers 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 bowel1. Malabsorption: diarrhea, bloating/cramping; anorexia; wt loss; fatigue, anemia2. Extraintestinal findings: arthritis- may migrate; pleuritic chest pain; pericarditis;osteomalacia- adult rickets.3. Weight loss4. Non-gastrointestinal symptoms may include low-grade fever, chronic cough,lymphadenopathy (because of infection), and arthralgias. Other systems that could beinvolved include cardiac, ocular, and central nervous system5. TX: Antibiotic therapy respond well = DX6. If untreated, the disease is fatal. Respond well to antibiotics7. No human to human transmission

b. DDX: Celiac sprue, lymphoma, Crohns (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 thedisaccharide lactose into glucose and galactose: aka milk intolerance

a. Results from fermentation of lactace gas b. 50 million affect: 85% Asian; 60% African; 23% Caucasiansc. Lactase deficiency is common in premature infants of less than 30 weeks gestationd. Lactase levels are high at birth but decline steadily in non-Europeans during childhood,adolescence, and into adulthood.

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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 resultf. 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 osteoporosis2. Read labels3. Lactaid tablets4. Calcium supplement

g. Excellent prognosis

4. Merckels 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 intestinec. Found within 3 feet if ileocecal valved. Less than 12 cm longe. Complications: bleeding (ulcerated); obstruction (rare); diverticulitis (contain gastric mucosa);

perforationf. Central umbilicus, Merckels scang. 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 occlusionc. Mortality 90%d. DX: Nothing suggestive usually

1. Central abdominal pain out of proportion2. KUB may be normal3. Severe pain suggests rupture peritonitis

e. Risk factors: ETOH, DM, high cholesterol6. Short Bowel Syndrome

a. This syndrome is a malabsorptive condition that arises secondary to the removal of significantsegments of small intestine

b. The most common causes in adults arec. DDX: Crohns disease, Mesenteric infarction (supposedly most painful condition in humans),Radiation enteritis (cancer patient on radiation), Traumad. The type and degree of malabsorption depend upon the length and site of the resection and thedegree of adaptation of the remaining bowel.