Final Material

•

•

•

•

•

o o o o o o o o o o o o o o o o o o o o o o o o o o

• • • •

• • o

• • •

•

•• •• •• •

• •• ••

• • •• • • •

• • • • • •

o  o o o  o o

o o o o • o o o   o o o o  

o o o o o o o o

o o    o



o

  o 

 • • •  • 

• o

• o o • • • • • • • • •

• • o • • •

• • o o o o • o o o o o o • o • o

o • o • o

•

o • o

o • • • • •

o o o o o o o o

o o • o o o o • o

o • o

o •

• • • • •

•

o o o o o o o o o o o

o • • •

o o o o o

• • o o o o o o o • o o o o •

• • o

• • • • • o o o o

• • •

• • •

o

•

o o

•

o o o • •

o • • • • • •

o o o o o o o o o

•

•

•

•

•

•

o o o o o o o o o o o o o o o o o o o o o o o o o o o o o o o

•

o o o o o

• • • • • • • • • • • • • • • • o o •

•

o o  o

•

o

• • • •

• • • •

•

• • • • • • • • •

•

•

o o o o o o o o o o o o o o

• • • • • • •

• • •

o

o o o o

• •

• • • •

• •

o o o

o o

o • • • •

o o o

• o o o o

•

o o

• o o o o o o o • •

•

o

• •

o

• o

• • • • • o o

•

o o

•

•

o o o o o o o o

o o o o o o o

GI Bleeding • Upper GI vs Lower GI • Divided by ligament of Treitz o AKA – suspensory Ligament of duodenum o At duodenojejunal junction o Helps maintain C-shape Upper GI S/SX • Hematemesis o Acute ↑ GI bleed above stomach o Massive GI bleed into stomach o M/c cause → esophageal disease, m/c esophageal varices  Coffee ground emesis • in gastric acids for some hours

• • • • • • •

• •

Can also B cause by esophageal varices Very common in alcoholics

Prostatitis PID – Pelvic Inflammatory DZ Endometriosis Esophageal CA o Known for coffee ground emesis usually if any emesis Esophagitis o Mechanical → eg. Swallowing o Infection PUD → usually Coffee ground

Swallowed hemoptysis o Can be from pulmonary disease • GI bleed scan o Can see location of bleeds Lower GI S/SX • Hematochezia – bright red blood/rectum (BRBPR) o 95% are from the colon down o usually not small bowel o m/c cause hemorrhoids o Blood streaked stool  Suggests that something within the bowel is bleeding and as the stool passes by it becomes streaked. (e.g. polyp) • Melena – black, tar-like stool o Enzymes in GI turn blood black o Chronic ↑ GI bleed – melena (or upper portion of ↓ GI) o Must have a lot of bleeding • Blood streaked stools - ↓ GI only o Bleeding in lumen • Occult blood in stools o Only seen from a hemoccult, Guiac test o Suggest bleeding higher up o Reagent turns blue → + for blood o Must have 3 tests to determine N or blood presence o Associated with occult cancer Lower GI Causes • Meckel’s diverticulum o Remnant of vitelline or omphalomesenteric duct • Diverticulitis → m/c to cause pain & bleeding than diverticulosis

•

o o o  o o o o o o

• o o o o o o o o • • •

• •

• •

• • •

• • • • • • • • •

o o o

• • • • • • • • • • • • •

o o

• • o o o o o o o o o

Herpesviridae

• • •

• •

o • • • • • •

•

• •

o o o o o o o

• • • • • • • • • • • •

o o o o

o • • •

• •

• • • • • • o  o    o o o • o o o

•

•

•

•

o o o o o FF o o o o o o o o o o o

•

• •

• • • • • •

• o   o   o o o o • o   o o o • o

•

o

•

• •

o o

• • • • • •

• • • •

• • • • • • • • • • • •

• • • • • • •

• •

• • •

• o

• • • • • • • • • • • • • • •

o

• • • • • • • •

o o

• •

o o

•

• • • • • • • •

• o

•

• o o •

• •

• • •

• • •

• o   o 

 o   o o o o •

• •

o o •

• • •

• • •

• • • • •

• • • •

o o

• • • • •

o

• • • • • • • o o •

o o o o

• • •

• • • • • • • • • • • •

o

• • • • • • • • o o o o

• • • •

o o o o

•

o o o o

• •

o o

o o o o

•

•

o o o o o o o o o o o

o o

o • o

o o

Test Two Start Now EXAM II ESOPHAGUS Propel food from the oral pharynx [not mouth] to the stomach No real digestive functions Can swallow standing on your head because of peristalsis Lower 2/3 smooth involuntary muscle, Upper 1/3 striated voluntary muscle (only voluntary smooth mm. In body)

Epiglottis keeps food from going into trachea Primary Peristalsis (Reflex-initiated by swallowing) o Initiated by swallowing o Propels food Secondary Peristalsis (peristalsis in lower 2/3) o Not initiated by swallowing, done so by the food which is already in the esophagus o Propels food through lower esophagus Tertiary Peristalsis (Curling phenomenon; Cork screw appearance) o Seen in the elderly o No propulsion  Fibrillation of the esophagus; doesn’t cause any movement; is due to aging and breakdown of myenteric plexus/ usually seen in elderly

ESOPHAGEAL TUMORS - 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) a. When the aorta uncoils due to aging and atherosclerotic Disease 4. Left Atrium 5. Cardiac Sphincter (lower esophageal) Patients can usually with great accuracy point to the location where the bolus is “stuck”

ESOPHAGEAL NEOPLASMS Malignant tumors are most common (85-95%) Leiomyoma is the most common benign tumor of the esophagus(Fibroid in the uterus) o Sessile  broad, wide base o Pedunculated  has a stalk o Most are sessile o Most in lower esophagus (because of reflux) Most tumors occur in the lower esophagus o Due to reflux Squamous cell carcinoma is most common, squamous cells line the esophagus 7.6/100,000 cases in USA 130/100,000 cases in China o Because their diet is high of nitrites, smoked foods M:F  3:1 Most patients greater than 60 years of age Most are asymptomatic because there is NO expansion in the lumen, NO bleeding, not much pain, hematemesis or melena

Dysphagia is a late symptom o 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 9 out of 10 esophageal tumors are malignant o Esophageal tumors present very late

ESOPHAGEAL CANCER - Causes obstruction of the hollow lumen Etiology o Alcohol abuse associated with 80-90% of cases  Cirrhosis  Portal HTN  Esophageal Varices  CA  Higher incidence of reflux (irritating to epithelium)  Alcoholics are usually smokers  Alcohol also irritates the esophagus itself o Cigarette Smoking  Cigarettes  swallow nitrites [via salvia and swallowing air]CA o Nitrate Ingestion o Chronic Achalasia, poor relaxation of the proximal end  Esophageal spasm (stenosis)  Proximal end dilates; food gets stuck & irritates and ferments • Common sign is very bad breath especially when they belch  Swallow  dysphagia  regurgitation o Chronic GERD/Barrett’s Esophagus o CA obstruction of hollow organregurgitation Differential Diagnosis o Achalasia o Diffuse Esophageal Spasm (DES)  Like the cold ice cream chest pain that is never ending and 10x worse

 Pain lasts min to hours o Esophageal Rings  Fibrocartilaginous ring that narrow the esophagus  Schatzki’s  Upper esophageal ring  Lower ring o Scleroderma (Progressive Systemic Sclerosis, newest term)  Connective tissue disease  Hardening of the interstitial tissues  narrowing and lack of peristalsis  dysphagia

ESOPHAGEAL CANCER Physical Findings o Dysphagia  mc symptom  usually asymptomatic until late stages of CA  motor problem – dysphagia with both solids & liquids  obstruction – dysphagia with solids early & progresses to dysphagia with fluids  CA cachexia occurs/wt loss  just skin & fat o Weight Loss, suggestive that CA has metastasized o Cervical Adenopathy  Virchow’s nodes • Enlargement of supraclavicular lymph node • Common with GI malignancy • Many times is first sign o Hematemesis – vomiting of blood / Hemoptysis – spitting up blood o Hoarseness  Due to compression or destruction of recurrent laryngeal in the mediastinum o Cough with clear sputum o Mets to liver, pleura, lungs with associated signs and symptoms  Mc presentation if mets to lung is asymptomatic Diagnostic Imaging o Double contrast esophagram o (With a barium swallow the “shoulder” sign is key  90° cutoff  now use endoscopy instead  get lung & ab CT/MRI to check for mets o Esophagoscopy o Chest/abdominal CT o Abdominal MRI  Mediastinum lymph nodes would be involved with esophageal cancer if metastasis has occurred Laboratory Tests

Done also to check for mets CBC Blood Chemistries Liver Enzymes, again looking metastasis, liver is a common area for the metastasis to occur Treatment o Resection if no mets  En bloc Resection  during surgery to see if they get all out  Take out CA with normal tissue around it  Lab makes sure clean tissue is found around CA to ensure complete removal  Only done if no mets o Stomach/colon used for replacement o o o o

o Radiation Therapy  Targets rapidly changing/high turnover cells • CA cells • Hair • Gonads • Bone marrow  Some divide too fast or too slow and are unaffected • Ex; renal cell CA outpaces chemo/radiation  Radiation not very effective with this cancer o Chemotherapy Prognosis o Surgery  20-50% (all based on 5 year survival rate) o Radiation  6-20%  Have a node  Not very effective again, due to surrounding organs and tissues o Chemotherapy  15-80%  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

BENIGN ESOPHAGEAL TUMORS Tumor Types o Leiomyoma is most common  Tumor in smooth muscle  Found most commonly in the uterus o Papilloma o Fibrovascular Polyps  hamartoma  Hamartoma  overgrowth of normal tissue, made up of normal and fibrous tissue Very Rare ESOPHAGEAL INFLAMMATION

ESOPHAGITIS Reflux Esophagitis Acute Ulcerative Esophagitis Esophageal PUD Crohn’s esophagitis Infectious Esophagitis o More commonly in immune suppressed patients Chemical Esophagitis

REFLUX ESOPHAGITIS Reflux of gastric contents with damage o Contents reflux up through cardiac sphincter with force and through the lower esophageal sphincter o Causing linear and nonlinear erosions of the esophageal lining Progression of GERD Incompetent LES Often associated with hiatus hernia o Protrusion of the stomach through the hiatus 30-60’ (minutes) post-prandial/reclining heartburn NOT GERD  GERD damage is reversible o Is “GERD” gone wild o Permanent damage to esophagus o More severe thus causes strictures TX with Nexium o GERD  tx: Prilosec & Prevacid o Due to incompetent lower esophageal sphincter

ACUTE ULCERATIVE ESOPHAGITIS Seen in patients with PUD Associated with frequent vomiting o Alcoholics, chemotherapy patients, bulimics, etc. o Eventually leading to strictures, thus dysphagia sets in depending on level of dysphagia as to weather solids and or liquids are involved o Regurgitation is often involved  Can lead to laryngitis Contracted fibrotic lower esophagus results

INFECTIOUS ESOPHAGITIS

Immunosuppressed patients o AIDS o Malignancies o Diabetes o Burn patients o Transplant  (Long term corticosteroid treatment) Organisms o Herpes Simplex o Candida Albicans  Typically found in the vaginal region of females and faces of children  Pic: Candida Esophagitis, occurs especially with immunocompromised patients o CMV (Cytomegalovirus), causes encephalitis in kids Dysphagia, Odynophagia (Painful swallowing), Chest Pain – more of a burning sensation instead of a crushing pain Treated with Antibodies

MECHANICAL ESOPHAGITIS Swallowed object becomes lodged Lodge at narrowed portions o Laryngopharynx o Aorta o Gastroesophageal junction o Left Atrium (not very often unless preexisting CHF) Objects include coins, pills, bone pieces o 3 main groups that do this: Elderly, children, and insane Leads to ulceration, maybe perforation o Which can lead to mediastinitis Treated with an EGD, scope with surgical attachments on the end.

ESOPHAGEAL VARICES Varicose veins of the esophagus o Alcohol is the most common cause  portal hypertension (pressure increased in portal venous system, blood backs up)

Lower 1/3 submucosal veins involved 1/3 of patients bleed o Alcohol  Cirrhosis  Esophageal Varices  Bleeding out Caused by portal HTN by hepatic cirrhosis Highest mortality of any UGI bleed o Peptic Ulcer Disease most common reason for UGI bleed Coffee ground emesis, hematemesis o Time depends on which you will see Treated with sclerotherapy, compression o Compression Bougie  balloon down the lower esophagus and the balloon flattens out the varices o Sclerotherapy  inject hardening agent that hardens (sclerosis) the walls so they can no longer extend  also used in peripheral vascular disease S/Sx o Pt has some pain and dysphagia o Symptoms are not extreme

ESOPHAGEAL DIVERTICULA Usually acquired (congenital forms are rare) Two Types: o 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 • Most common in middle esophagus. o Because most lymph nodes are in mediastinum their enlargement can cause them to become adherent to the esophagus o 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 Most common lower/upper esophagus.

Occur anywhere in esophagus o Middle esophageal are traction o Upper/lower are pulsion  Lower just above the diaphragm  Epiphrenic diverticula (just above diaphragm)

ZENKER’S DIVERTICULUM Pulsion Type Occurs at pharyngoesophageal junction o Can be very large in size Loss of upper esophageal sphincter laxity Retains food Signs/Symptoms o Halitosis o Spontaneous Regurgitation  “Verp” – ½ vomit/ ½ burp o Nocturnal choking  The position they are in  Recommended not to eat within a few hours  Neck mass  Can sometimes see peristalsis in the mass 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)

MISCELLANEOUS DIVERTICULA Epiphrenic Diverticulum o Occur in lower esophagus o Normally asymptomatic Middle Esophageal Diverticulum o Usually traction o From mediastinal lymphadenitis G.E.R.D.

GERD  reflux esophagitis  Barrett’s esophagus.  Esophageal. CA  always rule out cardiac Disease first Cough & bronchospasm or laryngitis from aspiration Early satiety GERD  get “full” quickly Chocolate  fat & caffeine contents cause GERD episode Tobacco  when chemicals are swallowed Commonly assoc. with hiatal hernia (>70%) Nitroglycerin  will make anginal chest pain better o Makes GERD chest pain worse Gastroesophageal Reflux Disease Reflux of gastric contents into lower esophagus

Incompetent lower esophageal sphincter o Stuff from your stomach comes back up into the lower esophagus because the esophageal sphincter is not functioning correctly o Believes because of aging o Reflux Esophagitis  Barrett’s Esophagus  Squamous cell carcinoma o Heavier a person is the more chance they can have because increase in intra-abdominal pressure Incidence o 60% of adults have heartburn o 80% of pregnant women have GERD S/Sx o Heartburn (pyrosis) o Dysphagia o Regurgitation o Sour taste in the mouth o Can be confused with angina pectoris o Chronic cough o Bronchospasm, due to irritation of the bronchi airway o Laryngitis o Early Satiety (Getting full fast) o Belching/Bloating Contributing Factors o Chocolate (caffeine and fat), Yellow Onions, Peppermint, Garlic o Tobacco (nicotine and causes sphincter to relax), Alcohol (fat and causes sphincter to relax), Caffeine o 70% of GERD suffers have a hiatal hernia o Beta Blockers (control BP and angina), Ca++ Channel Blockers, nitroglycerin  Causes dilation of lower esophageal sphincter o Gastric Acid Hypersecretion Diagnosis o 24 esophageal pH monitoring o E.G.D. – final dx for GERD o U.G.I o Manometry, to rule out diffuse esophageal spasms Treatment

Avoid triggers (diet modification) Proton pump inhibitors H2-blockers (cimetidine – Prilosec ) Antacids Fundoplication  Reserved for pts with daily reflux  Stomach is wrapped around esophagus  Three types • Nissen (complete) • Posterior (partial) • Anterior (partial) o Drink excessive amount of water, water helps to dilute the acid and provide weight to the stomach to pull the hiatal hernia down. o o o o o

BARRETT’S ESOPHAGUS Pre-malignant Associated with chronic reflux (5-10% incidence) Stratified squamous manifests to columnar epithelium, a pre cancer action Increased risk of adenocarcinoma o 30-50 times increased risk to develop adenocarcinoma of the esophagus o 500/100,000 people with Barrett’s esophagus who have GERD Dx o EGD, biopsy almost always accompanies an EGD o Biopsy Rx o Laser Ablation o Fundoplication o Surgical Resection (En Bloc if area is large enough)

ESOPHAGEAL MOTOR DISORDERS Achalasia Scleroderma Diffuse Esophageal Spasms

ESOPHAGEAL ACHALASIA Spasm (shut tight)of lower esophagus with pre-stenotic dilation which makes peristalsis ineffective Chest pain  can occur when peristalsis is attempted o Pain usually colicky Functional esophageal obstruction Inadequate relaxation of the LES Ineffective Peristalsis 1/100,000 incidence; 30-50 y/o S/Sx o Solid/liquid dysphagia, patient indicates they can feel the food sticking usually in the lower chest o Chest pain o Vomiting of undigested food o Aspiration, can develop pneumonia and die o May be confused with angina o Colicky type pain  Crescendo/decrescendo type pain  Stone, Ureters Etiology o Degeneration of myenteric plexus  Viral • Herpes Zoster • Measles Virus  Autoimmune o Not completely understood, true etiology not known

Diagnosis o EGD with manometry o UGI o Tests to rule out other causes (eg: EKG)  Especially with age group one wants to rule out MI Treatment o Medical  Smooth muscle relaxants (70% effective) • Nitrates • Calcium channel blockers • Botulinum toxins injection  mechanical dilation (90& effective) • Bouginage  mechanical dilation  Esophagomyotomy (90% effective), incise into the muscle (sphincter – draw back, reflux) Prognosis o Excellent with appropriate RX o Long standing Disease increases risk of CA

SCLERODERMA Aka: progressive systemic sclerosis (PSS) Means hardening of the skin o Primarily effects the skin, but is not limited to the skin o Tissue thickens and hardens o Severe hardening of lips to point must be tube feed Sometimes must replace the esophagus o Parastasis is affected, thus difficulty in swallowing, reflux Kidneys are often affected as well Vessels become calcified, thickened and hardened Female>Male Early teens to 20’s Smooth mm relaxants used if esophagus does not need replacing, patient receives temporary relief, usually do not work Multisystem disorder often affecting the esophagus o Lose ability to have peristalsis o Becomes very narrow and can develop strictures o EGD used to diagnose 75% have esophageal involvement

Fibrosis and inelasticity results Signs & Symptoms o Dysphagia o Esophageal reflux/regurgitation o S/Sx associated with scleroderma Diagnosis o EGD o UGI Reaction with smooth muscle relaxants Etiology - unknown

DIFFUSE ESOPHAGEAL SPASM Ice cream eating too fast is the same pain, “brain freeze” Pain lasts minutes to hours Usually end up in the ER thinking they are having a cardiac problem Diffuse sustained contraction (spasm) of esophagus Etiology unknown Can be confused with angina pectoris S/sx o Substernal chest pain o Dysphagia with pain, worsened by swallowing, key differentiating feature o Regurgitation Dx o EGD (Esophagogastroduodenoscopy) o UGI o With barium swallow on x-ray appears as a cork screw o Reaction with Ca++ channel blockers/nitrates  Causes patient to have reflux

DISEASES OF THE STOMACH Gastric Tamponade (fluid around the heart  ventricles and atria can’t contract) o A pressure equilibrium develops outside the heart as inside o Blood in the stomach from pills o Can lose 3-5 cc of blood per aspirin or other NSAID

o Coated so that it will pass the stomach and be absorbed in the small bowel

GASTRIC ANATOMY - Stomach  B12 absorption (intrinsic factor), storage, mixing, mineral absorption - Rugae  increases surface area inside the stomach for production of HCl and pepsin GE Junction o Gastroesophageal Reflux Disease Fundus o Usually holds gas  Magenblase  air in the stomach Antrum Pylorus o Narrowed portion of the distal most aspect of the stomach o Pyloric Sphincter  b/w stomach and duodenum  help prevent outflow of gastric juices that could lead to PUD o Pyloric stenosis  prevents outflow, causes regurgitation Curvatures o Lesser curvature o Greater curvature  More metabolically active (because of where food sits) Estimated that 3 – 5 cc of blood is lost with each aspirin taken that is not buffered

EGD ANATTOMY Normal antrum and pylorus (pictures) GASTRIC PERISTALSIS GASTRIC TUMORS

GASTRIC CANCER Occurs anywhere in the stomach o With a greater occurrence in the greater curvature of the stomach due to the gravity of material to this area of greater metabolism

Incidence of proximal CA is increasing 2 - 4X more common in 1st degree relatives Male : Female 1.6:1 > 55 y/o 7/100,000/year Most common in blood group A No symptom complex presented early in the Disease Pic: Linitis Plastica, an invasive form of gastric carcinoma , not a single tumor mass, the tumor cells spread throughout the entire stomach without causing a single tumor. o Aggressive, Infiltrated carcinoma  invades entire organ and cause thickening of entire organ - rarely found before stage 3 or 4 o S/SX  Cramps  Loss of appetite  Very low bleeding  No ulceration  Poor intrinsic factor production Risk factors o Diet rich in additives (smoked, pickled) o Atrophic gastritis  Inflammatory disease of the stomach where there is atrophy of the rugae  Sequela : B12 deficiency  pernicious anemia o Pernicious anemia o Tobacco use o Hispanic, Japanese o Polyps  Growth into lumen  Sessile and pedunculated  Usually premalignant mass (some benign) o H. pylori infection (PUD associated with H. pylori) o Barrett’s Esophagus DX o Stool guaiac test  test for blood o Any male > 40 with anemia, has GI malignancy until proven otherwise

GASTRIC CANCER S/SX Adenocarcinoma tends to mets to bone and organs 18% survival o but 50% survival if caught in stage 1 o but usually not caught in stage 1 because there are not s/sx Chronic non-colicky (colicky pain crescendo decrescendo) epigastric pain Anorexia Pain unrelieved by antiacids o Helps to differentiate from ulcers or reflux, both of which are often relieved by the use of antiacids Pain exacerbated by food Pain relieved by fasting Dysphagia o With this tumor is near proximal stomach Nausea and Vomiting Constipation Early Satiety  feeling full comes from hypothalamus [Picture] Ulcer mass greater than 1 cm in width, thus increasing the risk for gastric cancer dramatically When a tumor out grows it’s own blood supply the area becomes ischemic and ulcerates

GASTRIC CANCER DIAGNOSIS Positive stool guaiac (blood to stool content) FOB, fecal occult blood test o Will have black tarry stool if blood occurs in the stool Hemoglobin <12g/dl Hematocrit <35 EGD UGI (not done very often anymore) CT/MRI for nodes mets o Any male over the age 40 who is anemic has a GI malignancy until proven otherwise (blood loss from the malignancy)

GASTRIC CA PATHOLOGY Adenocarcinoma 90%, due to the abundance of glandular tissue, {adeno-, glandular}

Lymphoma 6%, malignancy of lymphocytes {mediastinum area is the most common area for a lymphoma} Gastric Sarcoma < 4% Leiomyosarcoma < 1 % GASTRIC CA TREATMENT surgical resection, quit often an en bloc gastrectomy (resect until healthy tissue is found) node resection (when larger then 1cm) radiation non-beneficial (tumors are non-sensitivity to radiation) Chemotherapy non beneficial, research has shown this treatment has very low benefit for gastric cancer. Chemotherapy is designed to “attack” fast growing tissue.

GASTRIC CA PROGNOSIS 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 18% 5 year survival rate o 57% with local Disease (stage I) o 19% with regional spread (stage II) o 2% with distal mets (staged III)

BENIGN GASTRIC TUMORS Leiomyoma – fibroid tissue usually found in the uterus, benign tumor of smooth muscle o Common tumor o Rarely symptomatic o Only with obstruction Adenoma – benign tumor of glandular tissue, aka polyps o Polyps o 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) o Most remain benign o Can obstruct o Over 2cm, have malignant potential

GASTRITIS Erythema – reddening (aka injected) Hemorrhage Erosions types o erosive o non-erosive, non-specific o specific s/sx o post-prandial (after eating) indigestion/pain o Nausea and vomiting o bloating 50% have H. pylori (spiral shaped bacteria)

EROSIVE GASTRITIS Etiology o NSAID’s o Alcohol(ism), portal HTN – venous congestion decreases the removal of waste from the stomach blood supply. o Stress from major illness (burns) Hemorrhage also common with this Disease Usually asymptomatic Can produce pain, hematemesis, n/v Diagnosed with EGD

NON EROSIVE, NON SPECIFIC (Common from over eating) H. pylori gastritis o Spiral gram (-) rod o Causes acute superficial mucosal Disease o S/sx  Nausea and vomiting  Pain Atrophic gastritis

o Associated with pernicious anemia – not producing enough intrinsic factor o Autoimmune, achlorhydria (absence or reduction of HCl in stomach) o Glandular hypertrophy and metaplasia o 3x increase gastric adenocarcinoma over the general population

SPECIFIC GASTRITIS Ménétrier’s Disease o Giant fold gastritis (the rugae become very large) o Enlarged thickened gastric rugae  Get hypoproteinemia due to enlarged rugae • Cause’s edema, pleural effusions, etc. o Severe protein loss  Proteins are metabolized in stomach o Hypoproteinemia o idiopathic Granulomatous gastritis o 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) o Treat specific disorder Phlegmonous gastritis o Phlegmon – aggressive large abscess o Abscess from fungal, bacterial, parasitic infection o Emergent gastrectomy and IV antibiotics Treatment is the removal of the stomach. Common among aids patients (immunosuppressed)

PEPTIC ULCER DISEASE Def: Ulceration of the stomach or duodenum  “Ulcer Crater” ulcer  a crater that penetrates the lining o typically < 1 cm o larger than 2 cm  malignant potential Go through at least the mucosal layer Malignant ulcer  malignant tissue with an ulcer inside of it

Normal acid production with lowered protection  ulcers Normal protection with overproduction of acid  ulcers

Epidemiology (study of the incidence of the disease) Imbalance between protection and damage, a decrease in the protective mechanism or an increase in the amount of HCl being produced – either case will lead to ulcerations of the stomach mucosa Gastric chemical secretion o Helps digest proteins, damaging to lining with good protection  Hydrochloric acid  Pepsin o Stimulated by acetylcholine (acetylcholine production is increased with stress as is the HCl thus a double negative), gastrin, histamine Other ulcerogenic substances o Bile acids, reflux of bile into the stomach, thus the reason for their being found in the pyloric bulb o Pancreatic enzymes Normal Protection o Good blood flow, helps clear chemicals out and helps with healthy cell turnover  Diabetics do not  prone to ulcers o Normal cell renewal  Diabetics do not  prone to ulcers  Chemo patients 500,000/year Duodenal : Gastric  2:1 Predisposing factors o High stress  Increase histamine  cause ↑ acid production  Activates sympathetics and shunt blood away from stomach o Cigarette Smoking  Swallowed chemicals o NSAID use  Irritating to the gastric mucosa – COX inhibitors stop prostaglandin production which stops blood flow to the stomach and inhibits protection to lining o Delayed gastric emptying  Food stays in stomach & irritates • Diabetics o Decreased bowel function, high incident of PUD

H. pylori (produces urease) there is a inferred or coincidental correlation between H. pylori existence and ulcers o Increases gastric acid secretion o 75% of patients are infected with H. pylori o 75% have recurrence in 1 year without antibiotics o 20% with recurrence with antibiotics NSAID use o Cause decrease bicarbonate the base which counter acts stomach acid and pepsin, mucus and blood flow o 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 o 40x increased risk of PUD (photo) Blood is very irritating to the stomach, thus bleeding in the stomach Signs and Symptoms Epigastric Pain o Burning o Gnawing o Cramping Relieved by foods and or antacids (short term - pt. can become addicted) o Gastric ulcers - eating makes it better o Duodenal ulcers - eating makes it worse Pain is clustered (days-weeks) Long symptom free periods (weeks-months-years) Changes in pain o If relapse and pain is worse this time  May mean CA  May mean ulcer may perforate

Differential Diagnosis GERD Reflux Esophagitis, most common condition confused with PUD Gastric CA, particularly if there is a change in the pain pattern

Gastritis Pancreatitis Cholecystitis Cardiac disease Diagnostic Workup Endoscopy o Esophagogastroduodenoscopy (EGD), almost universally the means of diagnosis o 95% accurate (5% due to human error) o Biopsy ALL lesions o Cancer / benign cannot be differentially diagnosed by sight o Also biopsy for H. pylori Upper GI o BaSO4 o Not as reliable as EGD o No biopsy capabilities

LARGE GASTRIC ULCER PERFORATED DUODENAL ULCER TREATMENT Antibiotic therapy (clarithromycin – which is harsh on the stomach lining) Omeprazole H+ pump inhibitors Stop Smoking Stop NSAID use Diet Changes o Bland Diet Stress Reduction o Because of sympathetic reaction o Valium (classic drug prescribed) Manipulation in conjunction with medical therapy has been proven beneficial to the patient o 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 COMPLICATIONS GI Hemorrhage o Most common (50% of all UGI bleeding) o 10-20% is bleeding clinically significant  Cause sx and problems o 80% stop bleeding spontaneously o Mortality rate is 6-10% of the 20% who do not stop bleeding spontaneously  Occult blood  don’t know it’s there o Anemia o Cancer Perforation o 5% incidence o Usually on anterior wall  Because it’s thinner o Zollinger-Ellison should be considered Gastric Outlet Obstruction o At pylorus or duodenal bulb o 2% Incidence o From tissue obstruction  scar tissue (fibrosis)  obstruction Zollinger-Ellison Syndrome o Uncommon cause for PUD

o Occur because of Gastrin secreting tumors (gastrinoma) o Cause multiple peptic ulcers o Perforation is relatively common  Bleed outs common o 2/3 of gastrinomas are malignant  Will metastasize  Can lead to death o Hard to manage these cases due to the continuous production of gastrin from the tumor

HIATUS HERNIAS Herniation of a portion of the stomach into the thoracic cavity (mediastinum) through diaphragmatic hiatus EPIDEMIOLOGY 50% of patients over 50 Female: Male  4:1 Often associated with GERD 90% with EGD esophagitis have a hernia Etiology unknown, age most likely culprit due to weakening of the sphincteric May be congenital or post-traumatic Bowel and stomach in the middle of the chest compressing the lungs and heart is termed a Bochdalek

TYPES OF HERNIAS Sliding (most common) Paraesophageal (AKA: Rolling Esophageal Hernia) Short Esophagus Intrathoracic Stomach SIGNS AND SYMPTOMS (same as reflux with the exception of the addition of borborygmi Heartburn o Because also have GERD Dysphagia Regurgitation Chest Pain (burning) Postprandial fullness o After eating GI Bleeding

Dyspnea Hoarseness o Irritation of larynx from GERD Cough o Irritation and to keep stuff from going into the trachea Wheezing

SLIDING HIATUS HERNIA Most common – the esophagus pull the fundus of the stomach up through the hiatus AKA: Axial or Concentric Hernia GE Junction/upper stomach herniates Usually asymptomatic Symptoms o Reflux o Burning Chest Pain o Regurgitation with recumbency /fatty meals o Episodic Gas bubble above the diaphragm on x-ray (magenblase)

PARAESOPHAGEAL HERNIA Second most common AKA: Rolling Hiatus Hernia GE junction in normal position Fundus herniates through diaphragm Usually asymptomatic Should be surgically reduced May become strangulated o Lead to ischemia (loss of blood supply)

MISCELLANEOUS HERNIAS Short Esophagus Type o Variation of sliding o Uncommon o Congenitally short esophagus Intrathoracic Stomach o Very rare o Entire stomach in chest o Incompatible with life

DIAGNOSTIC WORKUP Exclude other more serious conditions EGD UGI Blood tests non-specific Will find rugae above the hemidiaphragm DIFFERENTIAL DIAGNOSIS PUD Angina Esophagitis GERD DES (Diffuse Esophageal Spasm) Achalasia Diverticulum Esophageal Cancer TREATMENT Diet changes o Avoid caffeine, chocolate, mint, etc.… o Avoid drugs (Ca++ channel blockers) Weight loss Small meals Sleep with head elevated Manipulation Antacids, H+ pump inhibitors, etc.… Surgery for refractive disease COMPLICATIONS Erosive esophagitis Ulcerative esophagitis Barrett’s esophagitis Stricture GI hemorrhage

Colon o 

• •

INFLAMMATORY BOWEL DISEASE Irritable bowel syndrome Crohn’s Disease UC Antibiotic Associated Colitis Bacterial Colitis (Food Poisoning) Appendicitis

IRRITABLE BOWEL SYNDROME aka: Mucous colitis, spastic colon Alteration in normal bowel habits – constipation, diarrhea or a combination of the two Functional disorder o With minimal mucus production associated with 20% of general population affected (2 out of 10 are affected) F:M = 2:1 Begins in late teens/early adulthood 50% pts have psych problems (30% have an anxiety disorder) or are hyperactive etiology unknown, but strong association with stress commonly associated with stress S/SX o Crampy abdominal pain, low grade through the day up to the point that defecation is imminent, at which time the pain increases o Diarrhea  Up to 30 BM/day  Water/mucous in the stool o Bloating/abdominal distention, increased gas o Abdominal tenderness o Pain often relieved (temporarily) by BM o No blood in stool, important differential feature from Crohn’s and or ulcerative colitis o Sign and symptoms present for 3 months before dx o Hyperactive bowel sounds Major concern with this condition is maintaining the patients hydration level due to the condition being in the colon D/DX (other diseases which cause cramp type pain and diarrhea) o Crohn’s Disease o UC

o o o o o

Diverticulitis Colon CA PUD Chronic pancreatitis Biliary Disease

TX o High fiber diet – helps bulk up the stool and helps retain fluid o Fiber supplementation (psyllium) o Anti-spasmodics  Imodium  Lonotil  Bentyl o Eliminate stress o > 60% respond to RX within 1 year

CROHN’S DISEASE chronic granulomatous inflammatory Disease regional enteritis (aka for Crohn’s) debilitating, often requiring surgery 1:1000 population Caucasians, Jews Unknown etiology Affects young people Pathophysiology o Location  33% involve terminal ileum  50% involve distal ileum/proximal colon  20% involve colon only  Can involve any portion of GI tract  o Transmural DISEASE  Inflammation (granulation tissue)  Ulceration  Stricture  Fistula  abscess S/SX o Abdominal distention/bloating o Mass suggests abscess formation o Crampy abdominal pain (RLQ) o Hyperactive Bowel Sounds

o Non-bloody/bloody diarrhea o Perianal fissures/fistulas o Bowel obstruction o Crohn’s arthropathy o Low grade fever, pallor o Weight loss, fatigue Diagnostic Evaluation o CBC  Anemia  Decreased H&H o Electrolyte imbalance o Vitamin B12 deficiency o Endoscopy o UGI o LGI Presentation Patterns o Chronic inflammatory Disease (mc) o Intestinal obstruction from stricture abscess o Fistula formation o Perianal disease o Extraintestinal D/DX o o o o o o o TX o o o o

UC IBS Infectious colitis (yersinia, TB, Salmonella) Parasitic infection (amoebiasis) Ischemic colitis Diverticulitis Colon CA

Nutritional supplementation Low residue diet withobstruction High fiber diet with diarrhea Medications  Sulfasalazine  Corticosteroids  Immunosuppressive drugs o Monitor vitamin levels o Surgery for obstruction, fistulae, etc. Complications o Obstruction o Abscess formation o Fistula formation (inter-organ, skin)

o Perianal fissures o Colon carcinoma o Hemorrhage/shock o Malabsorption o UC Epidemiology o Chronic superficial inflammation o Unknown etiology o Aka-idiopathic proctolitis o 100/100,000 incidence o mc 14 – 38 years o 15-20 % of pts require colectomy Presentation patterns o 70 % relapsing o 20 % chronic continuous o 10 % fulminate (toxic megacolon) S/SX o Abdominal distention o Abdominal pain/tenderness (LLQ, LUQ) o Blood diarrhea o Fevers o Dehydration o Extraintestinal  Liver Disease  Sclerosing cholangitis  Arthritis  Ocular Disease (uveitis, iritis) DX workup o Comprehensive H&P o Laboratory studies  CBC (anemia, elevated ESR)  SMAC (electrolytes, LFTs)  UA (dehydration) o Sigmoidoscopy o Double-contrast BE D/DX o Crohn’s Disease o Bacterial infection o IBS o Protozoal infection o Colon CA o Diverticulitis o Ischemic Bowel DISEASE TX

Correct nutritional deficiencies May need “bowel rest” with TPN Folate supplementation (decrease CA Risk) Low roughage diet during exacerbation Meds  Sulfasalazme  corticosteroids o ? o o o o o

Crohn’s Disease         

(narrowing)

   o o o o o o  o o    (loose fatty CT that connect the bowel, organs)    Perianal disease(other presentation of Crohn’s)  Extraintestinal manifestations   

 Complications        

APPENDICITIS Inflammation of appendix secondary to obstruction Clinical symptom complex o Periumbilical/diffuse pain o RLQ pain  12-244 hrs later  Sign of regional peritonitis  Rebound tenderness  High fever o Can rupture o May cause diffuse peritonitis o May result in abscess formation

DIVERTICULAR DISEASE Epidemiology o Herniation of mucosa and submucosa through muscularis from low fiber diet o Occur at vasa recta (weakened area) o Diverticulosis is asymptomatic o Diverticulitis is symptomatic o Most respond well to antibiotics o Up to 30% require surgery S/SX o Diverticulosis exam is normal o LLQ pain mc o Pain relieved with BM o Abdominal guarding o Rebound tenderness suggests peritonitis o +/- small amount of blood in stool

DIVERTICULAR BLEEDING 70% occurs in right colon bleeding is painless resolves spontaneously in 60% erosion of vessels from fecalith 15 – 20 % re-bleed within 5 yrs

Diagnostic workup o CBC (elevated WBC with diverticulitis) o Microcytic anemia o BE o Sigmoidoscopy o Abdominal CT for abscess formation D/DX o IBS o Crohn’s DISEASE o UC o Colon CA o Ischemic Colitis o Infectious Colitis TX o Increased dietary fiber o Regular exercise o Broad spectrum antibiotics o IV Antibiotics in severe cases o Surgical resection/re-anastomosis Colorectal Cancer Missing first slide Risk Factors • Hereditary polyposis syndromes o Familial polyposis, teens to 30's, pts have thousands of polyps o Gardner’s Syndrome • Inflammatory bowel diseases • History of previous colorectal CA • 1st degree relative with colorectal CA • Age >40 • High fat, low fiber diet • 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] Clinical Presentation • Normally unremarkable • DRE finds 50% of tumors

• • • •

Palpable abdominal mass (mets most likely not the colon cancer itself) Abdominal tenderness alternating constipation / diarrhea Hepatomegaly (mets)

• • • • • • •

• Rectal bleeding • Hematochezia • Melena • Blood streaked stool • Occult blood [blood mixed in with the stool] Abdominal distension o Obstruction o Initial symptom in 15% of patients Pencil thin stools Intusseception Volvulus Weight loss, suggest stage 3 or 4 carcinoma Anorexia Malaise

Clinical Investigation • Anemia (microcytic) [Any male patient over 40 with rectal bleeding is to be considered positive for colon cancer] • Positive FOB test • Elevated CEA (used for Rx response) • Elevated LETS • Colonoscopy • Double contrast BE • CT for staging • CAR (chest is a common place for mets of colon cancer) • 25% have mets at presentation, they are in stage four of the cancer Differential Diagnosis • Diverticular disease • bowel stricture • inflammatory bowel diseases • adhesions • mets • extraluminal masses (ovarian mass) • AVMs

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) Treatment • Surgica resection o 70% are resectable at presentation o 45% cured by primary resection • Radiation therapy (stages B & C) • Chemotherapy (stages B & C)a o 5-fluoroucacil o Levamisole • FOB q 6 months • Colonoscopy q year x 2 years, then q 3 years • CEA levels (Carcinoma Embryonic antigen) Prognosis • Duke A >80% • Duke B 60% • Duke C 20% • Duke D 03% Overall 5 year survival rate 50%

Colon Polyps 50% patients have polyps o hyperplastic o adenomas o lipomas o leiomyomas Sessile / pedunculated 25% patients with colon cancer have polyps Signs / Symptoms most are asymptomatic rectal bleeding most common cramps abdominal pain obstruction anal polyps may prolapse

Diagnosis DRE Endoscopy Double contrast BE Treatment Careful observation (hyperplastic, lipoma) endoscopic surgery open laparotomy

SIGMOID DIVERTICULITIS TX ↑ dietary fiber Broad spectrum antibiotics Reg. Exercise IV antibiotics in severe cases Surgical resection/re-anastomosis TUMORS OF THE COLON Colorectal CA o 2nd leading cause of CA deaths in US 1. lung CA 2. colorectal CA 3. Breast CA o Most common CA is skin CA o 135,000 new cases/year o 50,000 deaths/yr. o 15% of all cancers (except skin cancers) o peak incidence in the 7th decade o Location  Lower colon – 40%  rectosigmoid - 30 %  cecum / ascending – 25 %  transverse – 10% 2 types of CA can occur o adenocarcinoma o squamous cell CA – Most common with HPV (condylomata) Risk factors o Hereditary polyposis syndromes  Familial polyposis  Gardner’s syndrome

• Polyposis & osteoma in skull o Inflammatory bowel Disease o H/o previous colorectal CA o 1st degree relative with colorectal CA o age > 40 o high fat, low fiber diet o regional radiation therapy Clinical presentation o Normally unremarkable o DRE finds 50% of tumors o Palpable abdominal mass (mets) o Abdominal tenderness o Alternating constipation/diarrhea o Hepatomegaly (mets)  Mets usually to liver (stage 4 colorectal Ca) • Liver drains all of GI o Rectal bleeding  Hematochezia  Melena  Blood streaked stool o Abdominal distention  Obstruction  Initial sx in 15% o Pencil thin stools o Intussusceptions o Volvulus o Wt loss o Anorexia o Malaise o Colon CA can cause lumbar & sacral back pain Clinical investigation o Anemia (microcytic) o Positive FOB test o Elevated CEA (used for RX response) o Elevated LFTs o Colonoscopy o Double contrast o CT for staging o CXR o 25% have mets at presentation D/DX o Diverticular Disease

o Bowel stricture o Inflammatory bowel Disease o Adhesions o Mets o Extraluminal masses (ovarian) o AVMs (Arterial venous malformations) Cancerous staging o Duke Classification system  A – confined to the mucosa – submucosa  B – Invasion of muscularis  C – local node involvement  D – Distant mets TX o Surgical resection  70% are respectable at presentation  45% cured by primary resection o radiation therapy (Stages B & C) o chemotherapy (stages B & C )  5-flourouracil  levamisole

o FOB (fecal occult blood) every 6 months  Guaiac test  finds occult blood in feces o Colonoscopy every year x 2 years, then every 3 years o CEA level  Carcinogenic embryonic antigen Prognosis o Duke A – 80 % o Duke B – 60% o Duke C – 20 % o Duke D – 3 % o Overall 5 yr. survival rate – 50 % COLON POLYPS Most non-inflammatory CA arise from polyps 50 % patients have polyps o Hyperplastic o Adenomas o Lipomas o leiomyomas sessile/pedunculated 25% pts with colon CA have polyps S/SX o Most are asymptomatic o Rectal bleeding mc o Cramps o Abdominal pain o Obstruction o Anal polyps may prolapse DX o DRE o Endoscopy  Complicated with severe inflammation disease  May perforate bowel  Do BE instead o Double contrast BE TX o Careful observation (hyperplastic, lipoma) o Endoscopic surgery o Open laparotomy

Test Three and Final Internal DX Test # 3 Notes (In class notes)

3/24/03 Small Bowel Diseases - Usually result in some form of malabsorption CELIAC SPRUE aka: Gluten enteropathy non-tropical sprue Gliadin protein fraction in gluten o Wheat o Rye o Barley o oats Gluten intolerance 50-500/100,000 people incidence ↑ during 1-36 months F>M o Mc to find in a child Clinical Presentation o May B normal presentation o WT ↓ o Dyspepsia (indigestion) o FTT in children (failure to thrive) o Bloating o Diarrhea o Pallor/fatigue (anemia) o Angular cheilosis o Osteomalacia o dermatitis Lab tests o Iron ↓ anemia o Folic acid ↓ o B 12 ↓ o Antigliadin IgA/IgG ↑ o Small bowel biopsy  Show villi atrophy  Signs of inflammation D/DX o IBS (mc d/dx)  More mucous in IBS stools  Age 20 - 40

o Laxative abuse o Intestinal Parasites o Tropical Sprue o Lymphoma TX/PX o Gluten Free Diet o Iron supplementation o Folate supplementation WHIPPLES DISEASE Cz by bacteria Men 30 - 60 Multisystem Disease Tropheryma whippelii (gram +) Aka: intestinal lipodystrophy Uncommon disease 30-60 yr. olds M>F Clinical Presentation o Malabsorption  Diarrhea  Bloating/cramps  Anorexia  Wt ↓ / fatigue  anemia o Extra intestinal  Arthritis • Can be peripheral or sero-negative  Pleuritic chest pain (localized pain)  Pericarditis  osteomalacia Pathology o Bacteria never cultured o No human 2 human transmit ion o Response 2 antibiotics confirms dx D/DX o Celiac sprue o Lymphoma o Crohn’s disease o Short bowel syndrome  Take portion of bowel out  Get malabsorption o Pancreatic insufficiency  Fatty stools

o Lactose intolerance TX/PX o Antibiotics LACTOSE INTOLERANCE Can have a transient form in people that are ill 1 in 6 pts have it Have malabsorption symptoms o But vitamin deficiencies are usually not as bad Insufficient concentration of lactase Results in fermentation of lactose Aka: milk intolerance 50 million R affected > 85% Asian American affected > 60 % African American affected < 25% Caucasians affected Clinical presentation o May B normal o Bloating o Diarrhea o Cramping o ABD pain o Flatulence DX work ↑ o Hydrogen Breath test  Ingest 50 gm of lactose  ↑ in breath hydrogen > 20 ppm in 90 min o exclude other disease o imaging studies not indicated D/DX o IBS o IBD o Pancreatic insufficiency o Sprue TX/PX o Lactose free diet  Milk  Bread  Candies  Cold cuts  Commercial sauces o Read labels o LactAid tablets o Ca ++ supplementation

o Excellent prognosis MECKEL’S DIVERTICULUM Remnant of vitelline (omphalomesenteric) duct Mc misdiagnosed as appendicitis Congenital lesion o 2 % of Population o failure of obliteration of vitelli intestinal o duct connecting interesting 2 yolk sac o mc anomaly of SI Found w/in 3 ft of IC valve ↓ 12 cm in length Complications o bleeding o obstruction o diverticulitis (contains gastric mucosa) perforation RX w/diverticutomy MESENTERIC ISCHEMIA Most painful condition in medicine More proximal obstruction of artery → higher mortality Occurs as a result of either superior mesenteric arterial or venous occlusion Affects the bowel from 2nd part of duodenum 2 transverse colon 50% embolic, 25% atheromatous, 10% venous occlusion Overall mortality is approx. 90% DX features o Nothing highly suggestive o Central abd pain out of proportion o KUB may B normal

3/25/03 GENITOURINARY DISEASES URINARY TRACT INFECTIONS Can present w/ back pain Female UT in close proximity to bacteria From anus Normal urinary tract is sterile M/c bacterial infection in humans o Upper Respiratory Tract Infections m/c viral infection

Women more prone to infections o Shorter tract  Bacteria doesn’t have to travel as far o Hygiene  Wiping A to P NOT P to A Lower UTI o Urethritis o Cystitis  Infection of urinary bladder Upper UTI o Pyelonephritis  Kidney Infections (Pyelo = pelvis)

PATHOPHYSIOLOGY 100,000/ml is threshold o B/w 10,000 – 100,000 is contaminated Must have a certain amount of bacteria in a certain volume of urine to dx a UTI o 10,000 – 100,000 ml = contaminated specimen o > 100,000/ml = UTI → become symptomatic Some patients are symptomatic with less Neonates- m/c in boys from anomalies o 30 days old or less Preschool- m/c in girls from hygiene Adults- m/c in women from hygiene Four pathways o Ascending form urethra o Lymphatic spread o Hematogenous spread o Direct extension  Pelvic abscess from ovary or uterus Diabetics have sugar in urine that bacteria can feed off of and therefore are more prone to UTI’s (Infra somatic cystitis  air in wall of bladder from aerobic bacteria) Pregnancy → higher risk d/t incomplete emptying or obstructed ureters Risk factors o Neurologic disease o Diabetes o Renal failure o Pregnancy Pathogens o E. Coli

o Proteus Mirabilis Defense Mechanisms o Low pH o Normal Micturition  Detrusor mm contracts  Trigone muscle relaxes o High Osmolarity

LOWER UTI Presentation inconsistent o Some asymptomatic, some just have urgency, some have extreme pain testing Urinary frequency, with minimal quantity Dysuria Urgency Urge incontinence Suprapubic pain Hematuria (menstruation most common caused, bladder infection most common pathogenic cause) o Gross  Patient will see in toilet o Microscopic  If the infection is mild to moderate

PYELONEPHRITIS More common in the immunocompromised population (diabetic) Usually secondary to a UTI Patient will be positive for a kidney punch Fever, more prevalent then with a UTI CVA pain Radiating pain into groin o Anterior and inner thighs, males will refer to the ipsilateral testicle Chills o Fever, night sweats Malaise o Fatigue Vomiting Diarrhea CLINICAL TESTING Clean catch UA o Wipe w/alcohol pad → start urination → stop → catch → mid-steam urine → stop before urination is complete Urine Culture & Sensitivity, by culturing you are able to determine the type of bug and degree of activity level and then the sensitivity to antibodies so as to determine treatment plan CBC

o Elevated WBC, anemia (mild) KUB (kidney, ureter, bladder) (a plain film of the abdomen) Ultrasound IVP (Intravenous Pyelogram) o Outlines renal substance CT scan o For tumors or abscess Cystoscopy Retrograde pyelography (obstruction) o Dye from urethra up and stops where infection is o 2 check for stones

Non-gonococcal Urethritis NGU is most common STD NGU twice as common as gonorrhea (the clap) Chlamydia is most common bug Often asymptomatic(~25%) especially in women Symptoms o dysuria o whitish discharge o meatal edema • Treatment w/ antibiotics

Gonorrhea Neisseria Gonorrhoeae Urethra is mc sight of infection Contraction rates(single intercourse) • 20% for males • 80% for females, will tear up the cervix and cause sterility if not aggressively treated Symptoms • dysuria • urethral discharge • urethral itching Treatment w/ antibiotics

Herpes Simplex - HSV II infection affecting ~20% of adults - spread through direct contact - causes blisters/ulcers around genitals blisters release clear fluid which contains high levels of the infected agent - may also infect the eye, skin, other organs - no cure, only symptom control

Genital Warts -

Condylomata acuminata Cause by form of HPV represents 1/3 of cases of STDs, 20 million people most people are exposed at some point in life treated with antiviral creams, cryotherapy, laser will reoccur

Urolithiasis (Kidney stones) calculus in the urinary tract aka- renal colic, when in the active state types of stones o calcium(70%) o uric acid(8%) o struvite(15%) o cystine(3%) 250k-750K /year M:F 4:1 Incidence is highest in summer(dehydrate) Signs/symptoms o acute colicky CVA/flank pain o n/v (nausea and vomiting) o referred pain to testes/vulva/groin o FCNS suggests infection Diagnostic work-up o UA(hematuria) o plain film radiography o renal US o IVP (intra venous pyelogram)

DDx o o o o Rx o

pyelonephritis cystitis diverticulitis PID

increased fluid intake, low calcium diet (contraindicated if an obstruction exists) o uteroscopic stone removal o extracorporeal shockwave lithotripsy 50% pass within 48 hrs 50% recurrence rate without Rx

Glomerulonephritis autoimmune inflammation of glomerulus synonyms o post-infectious GN o acute nephritic syndrome epidemiology o 50% affect < 13 y/o o Most common cause of chronic renal failure (~25%), these individuals wind up on dialysis o post group A beta strep infection mc o collagen vascular disease(SLE) o idiopathic

Proteinuria normal adult excretes ~150 mg/day short and long chain proteins (0 - +2 on a UA dipstick) o 3.5% prevalence in normal adults o perform 3 separate tests o You must not assume that finding protein equates the “normal” amounts excreted. You must rule out all possible causes. positive again-follow up negative-dx transient functional proteinuria Causes o IDDM

o o o o o

Nephrotic syndrome Amyloid Lymphoma NSAID use Orthostatic proteinuria (only when upright)

Nephritic Syndrome secondary to GN signs/symptoms o edema(periorbital, scrotal), due to loss of protein o HTN, damage to kidneys which help regulate HTN o hematuria o proteinuria Nephrotic Syndrome Most common cause is membranous GN signs/symptoms o peripheral edema, protein loss o ascites o HTN, o pleural effusion o hypoalbuminemia o hyperlipidemia / hypercholesterolemia o 1/3 of pts have DM, SLE, amyloidosis Many of these patients end up on dialysis. These patients are placed very low on the transplant list due to DM, they are poor surgical candidates and the DM is not reversible, thus damage to the new organ is inevitable

Acute Renal Failure sudden decrease in renal function inability to maintain fluid/electrolyte balance inability to eliminate wastes signs/symptoms obnoxious bouts of nausea and vomiting oliguria/anuria (very important to monitor intake and output of fluids)

altered sensation, electrolyte influenced laboratory findings elevated BUN/creatinine (creatinine levels are very specific for renal function) electrolyte imbalance anemia, platelet dysfunction Pre-renal failure(most common cause ) o inadequate renal perfusion  hypovolemia  CHF  Strokes  sepsis Intrinsic renal failure o renal disease  GN, drug toxicity, ATN Post-renal(least common) o outlet obstruction, outflow obstruction is going to cause pressure build up in the renal system  Benign Prostatic Hyperplasia (most common cause), prostate CA  ureteral stones  bilateral renal vein occlusion

Chronic Renal Failure progressive decrease in renal function >250,000 dialysis pts/year signs/symptoms o pallor, ecchymosis o edema o HTN o depression o fatigue o n/v o pruritus, urea makes the patient itch Etiology o DM(37%) [also the most common reason for dialysis in the US] o HTN(30%) o GN(12%) o polycystic kidney disease

o drug toxicity o obstructive uropathy o renal artery stenosis Laboratory findings o elevated BUN/creatinine o proteinuria, RBC casts o electrolyte imbalances

Renal Cysts fluid-filled epithelium-lined cavities found on 50% of autopsies rarely symptomatic simple cysts are ~70% of all renal masses Polycystic renal disease o mc hereditary disease in the USA o 50% have renal failure by age 60 o repeated UTIs, large kidneys, flank pain o 50% pts also have liver, pancreas cysts

Renal Cell Carcinoma adenocarcinoma Malignant transformation of renal tubular cells aka-hypernephroma (name no longer used because the name does not suggest malignancy) 1:10,000 people/yr 50-70 y/o male : female 2:1 etiology o familial o smoking, obesity, diuretics, Tylenol {chronic long term use} signs/symptoms {often the tumor is very asymptomatic for long periods prior to its discovery} o Hematuria (50-60%) o abdominal mass(25-45%), found on individuals who are relatively thin or found rather incidentally o Anemia (20-40%) o flank pain(35-40%) - there is no major distention of the capsule thus no pain

o HTN (20-40%) – sudden hypertensive changes are a red flag o Weight loss (30-35%) Classic Triad (5-10%) o hematuria {differentiate runners who classically suffer fro hematuria} o flank pain o abdominal mass Treatment o Nephrectomy – complete removal of the kidney o Radiotherapy o Chemotherapy (5% response rate) Prognosis o Stage I ~90% o Stage II ~75%  Good prognosis in stage I and II but because the tumor is typically asymptomatic during this stage it is not found during these stages o Stage III ~20% o Stage IV ~5%

Prostate Diseases prostatitis benign prostatic hyperplasia prostate carcinoma Prostate specific antigen o normal 0-4 ng/ml (nanograms) o elevated in:  BPH  prostate CA (not 100% accurate)  post-rectal examination  prostate trauma

Prostatitis Men over 50

may be aseptic or septic (infectious or noninfectious) Signs/symptoms o Dysuria (painful urination and in the case the pain is deep inside the pelvis) o Polyuria (because they don’t want to urinate thus they urinate a little at a time) o pelvic/ back pain o urethral discharge o fever - Dx made by culture and stain of prostate secretions - Anti-biotics if infectious

Benign Prostatic Hyperplasia Benign overgrowth of the prostate Generally begins in periureteral area 80% of men by age 80 medical /surgical intervention in 20% men by age 75 TURP (TransUrethral recession prostatotomy) is the 10th mc surgical in USA(>400k/yr) 10-30% w/ BPH have an occult CA Clinical presentation o enlarged prostate on DRE (loss of sulcus) o poor correlation between size and symptoms o hesitancy, decreased caliber and force of stream o double voiding, post-void dribbling o nocturia DDx prostatitis prostate CA urethral stricture - Dx workup PSA protease secreted by epithelial cells elevated in ~40% pts w/ BPH UA Ultrasound to ensure to hidden masses - Treatment avoid caffeine avoid medications (cold and allergy drugs) medications TURP

stents laser coils - Prognosis is good(>70%)

Prostate Cancer has surpassed lung CA as most common cause of CA in men 100,000 new cases/yr; 30,000 deaths Uncommon <50; 80% new cases >65 y/o Average age at dx is 72 Black males(1 in 9) mc pop. in world Clinical presentation o Generally asymptomatic o bone pain/fx may be initial presentation o outflow obstruction o mass on DRE(10% have normal DRE) DDx BPH prostatitis prostate stones Diagnosis elevated PSA (may be normal in 20%) elevated acid phos (extracapsular extension) biopsy Treatment (chemo, rad, prostatectomy) Px depends on stage (~90% w/ stage I)

Testicular Torsion Twisting of spermatic cord Leads to testicular ischemia / infarct 1:4000 incidence 70% occur between 1 – 18 y/o DDX o Testicular tumors o Epididymitis o Incarcerated hernia o Orchitis – caused by mumps virus

o Hydrocele – an obstructive disease where there is enlargement of the epididymis

Testicular Torsion Clinical Findings o Sudden hemi scrotal pain (10% are painless) o Swelling o Nausea and vomiting o Afebrile – no fever o 30% patients report previous episode of pain Dx based on H and P Surgical derotation with suture fixation Epididymitis Septic/traumatic inflammation of epididymis >600k visits per year occurs in sexually active men DDX o Orchitis o Testicular torsion o Hydrocele / varicocele Agents o N. gonorrhoeae o C. trachomatis Clinical presentation o Tender scrotal swelling o Erythema o Dysuria o Urethral discharge o Fever RX o Ice packs with scrotal elevation o Analgesics o Antibiotics Px o Usually self limited Hydrocele fluid collection in the scrotal space if congenital, associated with inguinal hernia in adults o infection o tumor

o trauma Clinical presentation o Scrotal enlargement / pain / radiating to back o Transillumination Rx o None if asymptomatic

Orchitis infection of the testicle usually viral (mumps/coxsackie B virus) occurs in post-pubertal males Clinical presentation o testicular pain / swelling o may be bilateral o inguinal lymphadenopathy, especially in a relatively young male o history of mumps o Rx- observation if viral o may lead to sterility Testicular Cancer seminoma(most common), teratoma, choriocarcinoma 2-3/100k/yr mc in young adults(30-40) Clinical presentation o scrotal mass o does not illuminate o not painful (even less than normal testicle) o pain from mets is more common Workup (70% have elevated hCG/AFP) Rx o surgical resection, chemo, radiation Px o 70-85% for early stages

Bladder Cancer range from low-grade to high-grade cell types o Transitional cell (93%)

o Squamous cell (6%) o Adenocarcinoma (1%) 54,000 new cases/yr; 12,000 deaths 4(F)-10(M)% of all cancers mc over age 60 25% result from occupational exposure o dye, textile, rubber tire, petroleum workers 15-65% associated w/ smoking Clinical presentation o gross painless hematuria o painless microscopic hematuria o frequency, urgency – due to bladder becoming filled with the mass o mets causes pain in distant organ (eg, back pain) Diagnosis o H&P History and physical examination o UA, cystoscopy – and endoscopic procedure for the bladder Rx- chemo, radiations, TURP, cystectomy Px- dependent on cell type and grade

Liver Function Anatomy o four lobes – right, left, caudate and quadrate o Weighs – 3 lbs Blood Supply o hepatic artery (oxygenated blood) (20%) o hepatic portal vein (nutrients) 80% o hepatic veins (drain liver) o holds 1 pint of blood Only organ that can regenerate 75% damaged before failure over 500 functions produces bile produces plasma proteins produces cholesterol converts glucose to glycogen stores iron converts ammonia to urea (one of the reasons that BUN levels can be elevated in the liver as well as the kidney clears drugs blood clotting

normal portal venous pressure=5-10 mm Hg (a relatively low pressure system)

Hepatitis liver inflammation types o viral (A, B, C, D, E, X?) o alcoholic hepatitis o drug-induced hepatitis o toxic hepatitis(carbon tetrachloride, benzene) o leptospirosis o toxoplasmosis o EBV, CMV, HIV, HIV

Hepatitis A caused by HAV (RNA virus) fecal-oral route, close family contacts 9-45/100,000/yr o institutionalized children o day care centers o male homosexuals o exposure to imported apes o undercooked mussels, clams, oysters highly contagious represents 33% of viral hepatitides in USA mc in 2-5 y/o(day care) and age >50 infants may be non-jaundiced neonates have subclinical infection incubation 15-45 days (aka Short incubation Hepatitis) rarely causes fulminant hepatitis rarely transmitted thru infected blood DDx o other hepatitides o viral illness w/ liver involvement(CMV, EBV) o non-viral hepatitides Clinical presentation o often asymptomatic(25% adults, 90% <2 y/o) o anorexia, malaise

o hepatomegaly (87%), RUQ tenderness o splenomegaly rare (9%) o jaundice o dark urine(bilirubinuria) o fever variable (precedes jaundice) Workup o LFTs (Liver Function Test) o HAV antibody Laboratory tests o ALT/AST(often > 8x normal) o Bilirubin (usually 5-15x normal) o Alkaline phosphatase (1-3x normal) o albumin, prothrombin normal o WBC most often normal o hepatitis A IgM imaging studies not normally useful no such thing as chronic hepatitis A it is an acute disease whose course rarely exceeds 8 weeks acute disease lasting < 6 wks rarely prolonged(3-5 mos), no carrier state - Treatment o o o o o Px o o o

avoid hepatically metabolized drugs IV fluid replacement for vomiting (rare) steroids not normally helpful follow-up as outpatient Overall do not over tax the liver, no alcohol <0.1% fatality rate 60% w/ fulminant recover evidence of previous disease in 40% of adults

Hepatitis B acute viral hepatitis(aka serum hepatitis) uncommon chronic form(5-10%) 4000-5000 deaths/yr from chronic HBV incubation 30-180 days DNA virus 200-300k new acute cases/yr(300 deaths) at risk populations(blood transmission) o IV drug users o homosexual males

o hemodialysis and hemophilic pts o health care workers o neonates/infants mc in 20-45 y/o DDx o other viral hepatitides o other viral illness w/ liver involvement o non-viral hepatitides Clinical presentation of acute disease o most often anicteric and asymptomatic o anorexia, malaise, n/v o serum sickness(hives, rash, arthralgia) o hepatomegaly, splenomegaly(uncommon) o jaundice, bilirubinuria, +/- fever Clinical presentation of chronic disease(1-2%) o similar to acute HBV o asymptomatic chronic active carrier (have active virus in the system, patient is asymptomatic and contagious) o hepatic decompensation o cirrhosis o hepatocellular CA Laboratory tests o HBsAg o elevated ALT/AST o hyperbilirubinemia o elevated alk. phos. Treatment o IV fluids for dehydration (increased vomiting over Hep A) o treat for hepatic failure, if present o avoid hepatically metabolized drugs (including alcohol) o steroids not helpful o interferon for chronic cases o antiviral agents famciclovir lamivudine o liver transplant prevention o avoid high-risk behaviors

o testing blood supply o hepatitis B vaccine high risk groups(90% effective) childhood vaccination HBV hyperimmune globulin o given after needle stick o given after birth w/ infected mom o given after sexual exposure

Hepatitis C viral infection of the liver with HCV non-A, non-B RNA virus intermediate incubation(15-150 days) Most common cause of non-alcoholic liver disease in US(40%) epidemiology o transfused hemophiliacs o IV drug users o occupational needle sticks o hemodialysis male=female 18-39 y/o mc Clinical presentation gradual symptom onset milder that HAV/HBV RUQ tenderness hepatomegaly jaundice dark urine(bilirubinuria) many are anicteric asymptomatic (75%) male=female 18-39 y/o mc Clinical presentation o gradual symptom onset o milder that HAV/HBV o RUQ tenderness o hepatomegaly o jaundice o dark urine(bilirubinuria) o many are anicteric asymptomatic(75%) immunity after infection is incomplete fulminant acute disease is rare (0.1%)

persistent infection is common(50-70%) results in chronic hepatitis cirrhosis develops in 20-50% hepatocellular CA develops in 50% DDx(other inflammation hepatic diseases) Diagnostic workup o acute hepatitis c antibody o LFTs o biopsy for complications Rx o avoid meds metabolized by liver o otherwise acute Rx is non-specific o follow-up for complications o Interferon may be helpful in relapses acute disease lasts <6 wks no vaccine immune globulin injections are not helpful

Alcoholic Hepatitis -

Most common form of hepatitis most common cause of cirrhosis SSx similar to other hepatitis x flu-like Sx hepatomegaly splenomegaly more common than viral ascites

Hepatic Cirrhosis caused by hepatocellular injury results in fibrosis ad nodular regeneration micronodular, macronodular, mixed forms 9 deaths/100k people/yr in us(#11 death) most common causes o alcoholism o viral hepatitis(especially HBV and HCV) other causes o drugs(Tylenol), chronic CHF, hemochromatosis, amyloidosis Clinical Presentation

o early weakness, fatigability, disturbed sleep muscle cramps, weight loss advanced o anorexia, weight loss o n/v, hematemesis, due to esophageal varices o jaundice o hepatomegaly, ascites o amenorrhea, due to cholesterol production interference o impotence in men Skin lesions o spider nevi o palmar erythema(alcohol abuse) o glossitis, cheilitis o ecchymosis CNS damage o Asterixis (intermittent lapse of body position) o tremor o delirium o dysarthria, slurred speech o coma Laboratory findings o macrocytic anemia o abnormal LFTs o decreased albumin o leukopenia Rx o avoid hepatotoxic meds o treat disease that caused cirrhosis o treat complications(ascites, varices, CHF))

Primary Biliary Cirrhosis autoimmune disease destruction of intrahepatic bile ducts mc in females(95%) 40-60 y/o age group associated w/ PSS, SLE, Sjögren’s Synd., RA, and other connective tissue arthropathies SSx

o o o o

Fatigue (extreme fatigue) pruritus ~50% are asymptomatic hepatosplenomegaly, jaundice later

on

Laboratory tests o anti-mitochondrial antibodies (98% specific), almost pathognomonic for this disease o abnormal LFTs Rx o Methotrexate, a commonly used chemotherapy agent, which helps control the over growth of cell in the bile duct o colchicine o ursodiol o liver transplant Pxo asymptomatic- 10-16 yrs from time of diagnosis o symptomatic- 7 yrs from time of diagnosis

Hepatic Tumors Benign o Hemangioma Most common benign liver tumor Vascular tumor Asymptomatic Found incidentally o Adenoma Rare solitary or multiple tumor Usually asymptomatic Found in steroid abusers, OCA users Malignant o Hepatocellular Carcinoma (old term Hepatomas) o Cholangiocarcinoma o Metastasis (Most common cause liver malignancy), colon cancer is the most common malignancy which mets to the liver

Hepatocellular CA malignant tumor of hepatocytes

associated with: o chronic liver disease o cirrhosis o HBV, HCV o hepatotoxins(ETOH, steroids) Clinical presentation o weight loss, anorexia o ascites o hepatomegaly o 33% are asymptomatic Diagnostic evaluation o elevated AFP in ~90% (alpha-fetoprotein – this protein non-specific) o elevated LFTs o MRI o Ultra Sound/CT-guided biopsy Treatment o dependent on size of lesion/mets o resection o chemotherapy Px is 20-30% following resection

Cholangiocarcinoma Intrahepatic bile duct malignancy Rare in USA and Europe – more common in Asia Presents as a liver mass Associated with liver fluke infestation – more common in Asian culture Slow progression to metastasis Gallbladder Diseases

Cholelithiasis Gallstones affects 20,000,000 Americans Predisposing factors (Female, forty, fat, flatulence, fair skin) o fair skin o female o obesity o ~40 y/o

o OCA use o DM ~20% chance of developing biliary colic, passage of gallstones pts are asymptomatic unless passing a stone S/Sx o colicky RUQ pain o night pain o refers to right shoulder o lasts mins to hours depends on the amount of time is takes for the gallbladder to push the stone through 75% of stones contain cholesterol Ultrasound is imaging procedure of choice Rx-cholecystectomy, ESWL, dissolution (substances which will dissolve gallstones) Px-good

Cholecystitis (inflammation of the gallbladder) acute and chronic forms 95% associated with gallstones mc in same groups as cholelithiasis Clinical presentation o RUQ pain/tenderness o pain radiating to right shoulder o Murphy's sign o Fever (~33%) o Jaundice (25-50%) o fever, chills, n/v Diagnostic workup o Ultrasound o MRI/CT to rule out more ominous causes Treatment o laparoscopic cholecystectomy (lap chole) o open cholecystectomy o broad-spectrum antibiotics Prognosis o Excellent o 1% complication rate with lap chole

Cholangitis inflammation of bile ducts complication of cholelithiasis(~1%) occurs during 7th decade and older Clinical presentation o Charcot's Triad fever/chills RUQ pain jaundice o bilirubinuria all S/Sx present in 50-85% of pts Diagnostic workup o Ultrasound o ERCP endoscopic retro( if US is inconclusive) Treatment o biliary decompression ERCP(maybe w/ stent placement) percutaneous transhepatic biliary drainage o broad-spectrum antibiotics Prognosis is excellent Chronic disease associated w/ porcelain gallbladder, a premalignant condition Primary Sclerosing Cholangitis diffuse inflammation leading to stricture most common in males age 20 – 40 commonly associated with UC Assoc o Clinical is progress jaundice, indigestion o Malaise, purity, anorexia Poor Px o Most require liver transplant within 10 years Think Walter Patton Gallbladder Cancer Adenocarcinoma most common asymptomatic unless disease is advanced usually found during surgery for stones weight loss, anorexia

palpable gallbladder, RUQ pain associated with stones in 80% porcelain GB also assoc. poor prognosis

Pancreatic Disease Acute pancreatitis Chronic pancreatitis Pancreatic Cancer

Acute Pancreatitis most often secondary to biliary disease enzymes released into pancreas S/Sx o severe abdominal/back pain o fetal position o n/v o mild jaundice o shock – as a reaction to the pain lipase and amylase levels increased CT/MRI for Dx Treatment o IV hydration o NPO o NG suction o pain control o treat complications Prognosis o 5-10% mortality associated with the shock o worse in older, sicker patients

Chronic Pancreatitis recurrent pancreatitis male : female 5:1 S/Sx o recurrent epigastric/back pain o abdominal tenderness/guarding o weight loss

o foul-smelling stools, that are chalky white in color and float associated with alcoholism/biliary disease major DDx is pancreatic CA KUB may reveal calcifications 50% pts die w/in 10 yrs(malignancy)

Pancreatic Carcinoma adenocarcinoma 2nd mc tumor of GI system (colon cancer is #1) m : f 2:1 mc in head of pancreas, carcinoma in the tail will not cause jaundice, because it does not block the duct. S/Sx o jaundice o abdominal pain o weight loss, anorexia, nausea o biliary obstruction S/Sx(head tumor) - CT/MRI are best imaging procedures - Poor Px from early mets