ࡱ> ` jbjbj PBaS^^^^^^^dfffffx Hhhhhhh~i,iǗɗɗɗɗɗɗ$hf^ihhii^^hhDsDsDsi,^h^hDsiǗDsDsR!^^hh p =Lfk͔0Hl<^ DsiiirXiiiHiiiix x x [fx x x f^^^^^^ Abdominal Pain Patterns Retroperitoneal More superficial (typically palpable, and mobile) Can pinpoint where it hurts Referred pain patterns More they can localize Diagnosing tools Plain film ( MAS Called an abdominal series Also known as KUBureter is not typically seen Look at kidney contour Look at calcification of the ureters and kidneys Size of the stomachobstruction Chest film can be used for esophageal lesions Both KUB and Chest filmused in pancreatic disease US Can detect masses Can tell if patients mass is fluid or solid Bowel gas can disrupt the sound beam CT Better than MR (CT- still the diagnostic tool of choice) Density window change is important MR Hard to get good images due to organ movement Radionuclide studies Used to determine secretion of various enzymes to judge secretions Watching WBCs congregate. Air Contrast Esophagography Technique Upright LPO (RPO) 1 swallow high density barium 1tsp effervescent granules/10cc water drink down 3-4 oz barium rapidly spot radiographs Proposed Risk Factors for Esophageal Cancer Cigarette smoking Alcoholism Nutritional Deficiencies Carcinogens (mercury, carbontetrachloride, inhaled gases other than smoke) Endemic microorganisms Regional practices Soil salinity Squamous cell carcinoma Achalasia Celiac sprue Ley stricture Plummer-Vinson syndrome Head and neck cancer Tylosis Esophageal Webs and Rings Web- mucosa A ring- muscular ( B ring (Schatzki)- mucosal Squamo-columnar junction (between the B ring) Patient Hx. Pain (site, duration, type, palliative factors) Retroperitoneal Intraperitoneal Nature of pain Right scapular pain in gallbladder- pain that is referred is often not reproducible Referral pain to either shoulder can be bronchogenic carcinoma that has broken from its capsule Epigastric pain Aortic aneurysm may produce pain, surface or lateral Males- testicular pain Females- vulvar pain Distention- pain came on quickly and went away quickly Rupture- gets worse and worse and worse, then tissue fails and the tissue decompresses and they feel better Insidious onset- Cant remember when the pain/process started. Cancer can progress this way. Irritation/inflammation- long spurts of pain Progressive pain, no comfort, difficult to sleep, weight loss- cancer, cancer, cancer Eat, go to bed, and cant make it through the night (people automatically think GERD) Upper GI (UGI) Mouth Esophagus Stomach First 10cm of proximal duodenum By including the proximal duodenum have 95% of all duodenal problems Have to add more contrast and time to include the duodenumhave to have contrast pass through the Iliocecal valve before the test is endedsmall bowel abnormalities Do not like to use contrast above an obstruction Use water soluble contrast instead so the GU system can clear Ultrasound Widely available Inexpensive Low risk to pt Gas destroys the quality of US Homogenous acoustic Liver providesupper and middle right quadrants Bladderpelvis Left middle complaint will not give the best results CT Helical/spiraldata acquisition is continuous MRI Up and coming w/in our practice life time Angiography Very limited use Major vessel dilation MRA can do this today Has trouble w/cascadescopious collateral circulation Abdominal angina Endoscopy Increasing uses Very flexible fiber optics Not many places w/in the GI system that they cannot see Can even use this to treat in some cases Associated with DISH and Scleroderma Difficulty swallowing Odinophagia Painful swallowing *patient can have one or the other, or both Progressive Dysphagia Used to be only trouble with large things, then went to having trouble with smaller things Moved next to small pieces of food Now thicker liquids have trouble Slowly getting worse Fixed Dysphagia Liquids do not cause problem Small pieces of food and well chewed pieces are not a problem Large pieces get stuck and go down with liquid Total dysphagia Cant swallow liquids or solids Stroke Pre-Esophageal Dysphagia @ level of C5 is where esophagus starts we look above this varicosities- alcoholics, portal HTN pharyngeal or laryngeal cancer Esophageal Zancres diverticulum Difficulty swallowing around clavicular area Abnormal nails When the patient is in bed it decompresses, might get a mouthful of vomit in their mouth. (mixed meals appearance, obstruction of sequestration) Achalasia- spasmodic closure of the sphincter Tx.- catheterization, close the defect Cancer Varicosities Motor disorders- Scleroderma Barretts epithelium Metaplasiachange in tissue (esophageal into gastric) Chronic reflex 80% of the time this is useful 20% of the time is turns into adenocarcinoma Barrett's is the intermediate stage Cardiogenic dysphagia- cardiac hypertrophy that pushes on the esophagus- barium w/ displacement of the contrast Plummer-Vinson Syndrome- have iron deficiency anemia, get web like structures throughout the esophagus Present with c/c that solids don't make it through Network of webs at distal end of pharynxconsequence of the iron deficiency What does the tongue look likebright redglottis Handsabnormal fingernails (spoon nail, coylonchia) Barium studymisses web on plain film study Stomachdenuded surface on the stomach Atrophic gastritis Loss of rugaeappear smooth Look at CBC No or low stored or serum iron High TIBC Iron supplements Recheck 4-6 wks down the road AnemiaMicrocytic Hypochromic Balloon dilatation will break up the webs Will come back if do not supplement w/iron Will go away over time w/just iron supplement Factors and conditions w/esophageal CA Smoking-smoke mixes w/saliva and is swallowed Keep in mind that the esophagus starts in the neck and goes into the chest Chest films may be required to see the esophagus all the way down Alcoholirritative; the immune system is compromised by something in the alcohol; keep in mind varices Head and neck CA Corrosive Esophagitisfailed suicide attempt in adults, children eating things that they should not Achalasiano openingsection later Tylosis (palmer and plantar)not responsible for Plummer-Vinson syndromeolder populationprofound iron deficiency anemia Raynauds Event Recognition of what the patient was doing at time of painful spasm Hiatal Hernia- paraesophageal/rolling hernia The stomach rolls up in the esophageal hiatus Produces an inability to dilate or a fixed dysphagia Scleroderma Tight thin skin Truncated distal finger Acroosteolysis Muscle ache Dysphagia Fibrotic deposition in myoneural junction No peristaltic wave Pulsion Epephrenic diverticulum Incoordination of esophageal peristalsis and distal sphincter opening and closing Lower esophagus Around the sphincter Have a blockage Pyloric stenosis Asymptomatic Achalasia Loss of ganglion cells Degeneration of dorsal motor nucleus Degeneration of vagal fibers Chalasiaopening Thereforeno opening Gastroesophageal opening Neurogenic lesion Vomit of multiple meals in several different stages of digestions Normal peristalsis of the esophagus allows the sphincter to relax 3 phases Incomplete relaxation Aperistalsis LES hypertension CCK Octapeptide Test (Cholecystis kinase) 2 positive effects in normal Smooth muscleelevate tone Inhibitory signals to the muscle to relaxmuch stronger effect Reduced lower esophageal pressure Achalasia Nerve does not respond Minor effect on smooth muscle of esophagus Increase lower esophageal pressure Sx Dysphagia to solids90% Dysphagia to liquids80% Difficulty belching100% Chest Pain--<50% Nocturnal Regurgitation--<50% Aspiration pneumonitis--<25% (think CA of the lung first) Loss of heartburn--<25% Lack of GERD Tx Meds have been tried but due not work all that well Drugs Nitrates Ca2+ channels blockers Botulinm toxin injections Procedure has to be repeated After the 3rd time, have to try something else Body can fight off the botulinum toxin Pneumatic dilation, balloon Myotomyradial slices in muscle (endoscopic guided) Removal of the esophagus, cinching off the stomach Reflux-dysfunction of anti-reflux mechanisms Caustic Material- acid, pepsin, bile, pancreatic enzymes Sufficient Duration of contact-inadequate clearance mechanisms **above three leave to an overwhenming mucosal resistance Barretts Esophagus can turn into carcinoma 800 cancers per 100 patients 1 cancer to 125 patients GERD Indications for ambulatory esophageal pH monitoring patients with normal endoscopy and: typical GERD symptoms unresponsive to anti-reflux therapy atypical chest pain extra-esophageal disorders possibly related to GERD patients with endoscopic esophagitis unresponsive to anti-reflux therapy patients considered for anti-reflux surgery Management Elevate head of bed Lose excess weight Eliminate: tobacco, alcohol, bedtime snacks, certain drugs, fatty foods, chocolate, peppermint, others Achalasia- little or no opening between the stomach and the esophagus Nerve death and degeneration of vagal fibers is one of the main causes of the disease CCK- has an excitatory effect on the nerve body, the nerve body has an inhibitory effect on the sphincter. Normal people have decreased LES in presence of CCK. In patients with achalasia, their LES will elevate in presence of CCK. Mallory Weis Syndrome Painful swallowing Lose amounts of blood that can cause anemia Men tend to get discovered a little sooner Vomiting of bright red blood, something close to the mouth, the more mixed it is, the farther up the GI tract the lesion is A tear that is often the consequence of violent wretching. Quite often an alcoholic. The patient will continue to vomit long after the stomach is empty. Has more direct effect on the stomach- wretching Dx. Of tear- flexofiberoptics, allows us to visualize the dripping blood, angiogram. Does not pass through the esophageal area. Tx. Switched to a liquid diet, or intravenously Slowly switching to solids Presbyesophagus Upper 1/3- controls lower 2/3, composed of striated musculature. When the upper contracts, the lower automatically contract. Lower 2/3- Patients present with: lose the voluntary function of swallowing cant eat without a full glass of water. Jerking their head to have to swallow. Unlinking of the primary vs. secondary swallowing events. Uncomfortable swallowing due to transient distention Almost like the esophagus is working against himself Can also look like the diabetic neuropathy of the esophagus Loss of master-servant relationship Separated by when they got their dx. Of diabetes. They must have recognized their diabetes typically as a juvenile. It takes that long to mount a primary contraction event of the esophagus. Treatment Small bites Chew thoroughly Have water handy to wash it down *curling phenomenon, barber pole, corkscrew appearance- multiple contraction happening at the same time. Alternating bands of white/black. Diffuse Esophageal Spasm Strong vagal stimulation produces an environment where we have a more global contraction instead of happening in sequence. Can be very painful. Spontaneously resolve. Usually get lots of testing to rule out cardiac disease. Osteopaths have said that spinal manipulation can help with the problem. VOGTs Classification system of esophageal atresia Type I- mouth ends in a blind sac, no entrance to the stomach, incompatible with life Type II- thick wall of tissue plugging up the opening, ends up being a surgical fix, a bridgeable gap, or membrane that needs to be perforated. well tolerated by the child. 2nd most common 10% Type III- fistula. Abnormal communication between the trachea and esophagus (lower 1/3) When the patient is not eating there is potential for gas to escape from the trachea to the esophagus through the fistula. When food or liquid goes from the esophagus into the trachea through the fistula. Most common 80-90%. Foreign body aspiration. Type IV- Duplex Esophagus- 2 parallel tubes that can pass food and liquids into the stomach. poorly developed typically has more trouble Congenital Extra chambers in the stomach. There is a partition that rarely goes all the way up to the top. Food has to work its way over the partition. They typically have a mixed meal vomit, due to the portioning. Dextro-rotation of the stomach can occur. The valves are all reversed. Complete flip of all organs. (citisinvertus) Pyloric Stenosis (what Simon had) Congenital- baby, projectile vomiting. A pyloric valve that has received high levels of contraction signal. Can get twice as big as the typical pyloric valve, and does not allow full opening of the stomach. Tx. Balloon dilation. Acquired- adult patients, most common cause is peptic ulcer disease. If the ulcer is near the pyloric valve it can reduce the threshold and causes it to be in spasm. The ulcer can also repair fibrotically, and that can shrink causing pyloric stenosis. Tx. Balloon dilation. Sliding Hernia or axial A portion of the stomach comes above the diaphragm Most common complaint is GERD Can present w/air/fluid level above the diaphragm on plain film Reducing the hernia Press in below the diaphragm on the L and then ask the pt to breath out and pull down Incarcerationthe stomach has become trapped and presents w/bowel sounds above the diaphragmif the blood supply is cut off then this hernia can become strangulated Endoscopy can help to id this lesion common complaints: GERD Advise about the reducible hernia Carcinoma Incompetent of the hiatus of the diaphragm Seat belt injury Obesity Lifting injury Straining while sitting Sx Substernal filling Reflex Air in the esophagus Peri-esophageal Hernia (Rolling) Less common More complications Type of hiatial hernia Dysphagiahiatus is not big enough for food to go through and the part of the stomach and GERD Substernal filling Reflex Air in the esophagus Harder to reduce manually Valvulus- the stomach twisted. Can occur from over-expansion of the stomach. Gastric-diverticula- herniation of mucosal tissue through the muscular tissue. An area of defect in stomach wall that allows an out-pocket Gastritis most secure way to dx. Gastritis is by doing a biopsy. The distal part of the stomach is more prone to gastritis than other parts, also it is closest to reflux from the sphincter. Biopsy shows- Cellular injury, inflammation, WBCs NEVER identified on a radiographic study Risk Factors for Gastritis Alcohol intake NSAIDs- make mucosal tissue weak 15% is associated with helobacterpylori infection pyloric reflux can lead to erosion or ulcer smoking occupational sources- chemicals that can mix with saliva. By contact can produce irritation of gastric wall chemotherapy patients patients with chronic renal failure, elevated BUN Signs and Symptoms Stomach pain- typically in R. Upper Quadrant chronic gastritis- there has to be documented repair stomach capacity- 10L Crohns- inflammatory bowel disease, distal small intestines. But can be found everywhere from mouth to anus. Complications Neoplasias, since the mucosal lining is already so damaged Diverticuli3 types Zenker'supper esophageal Food collecting in the out pocketing of the esophagus Killian's dehiscence Sx Heartburn Halitosis Regurgitation of food when lay down Dysphagia Neck mass which is compressible Aspiration of foodbronchitis Not sure of the cause Pharyngeal/esophageal junction Typically at C5/C6 Weakness of the cricopharyngeus muscles Barium swallow w/x-ray Traction Middle esophagus Inflammation w/granulomatous Enlarged lymph nodes Asymptomatic Gastroesophageal reflux ds Refluxdysfxn of anti-reflux mechanisms Caustic materialacid, pepsin, bile, pancreatic enzymes Sufficient duration of contactinadequate clearance mechanism These overwhelm mucosal resistance Hiatial herniacorrection done on expiration Barrett esophagusneoplasm from long standing reflux 5-10% carcinoma potential Long stricture Metaplasia Retrosternal pain Dyspepsia Reflux w/occasional dysphagia 8-10% adenocarcinoma Tx Antacids, stop smoking Squamous to columnar cells Peptic ulcer disease Classified by location Then by gastric and duodenal ulcers Smokers have a higher incidence of ulcers, more recurrences, more frequent complications, and greater ulcer-related mortality Barrier disruption, followed by erosion, then ulceration Tx. options An ulcer needs rest to heal Bland diet Smaller meals Stay away from spicy foods and alcohol Antibiotic Gastric Ulcer Normal or low secretory output If you eat and feel better right away is indicative of a gastric ulcer Helicobacter Pylori Best way to diagnose is by a endoscopic biopsy test Helicobacter pylori infection can be detected by various methods Duodenal Increased secretory output (hypersecretion) Parietal and chief cells seem to be larger and more productive Decreased HCO3 secretion Increased nocturnal H+ secretion Increased duodenal acid load Made to resist alkaline loads If you eat and feel better 45 min to an hour later, is indicative of a duodenal ulcer Diagnosis 70% epigastric pain BAO = PAO, but PAO is normal Zollinger-Ellison Syndrome is a clinical triad consisting of: 1. Gastric acid hypersecretion 2. Severe peptic ulcer disease 3. Non-beta islet cell tumors of the pancreas The tumors produce gastrin (G17 & G34); referred to as gastrinomas Tumors localized usually to head of pancreas, duodenal wall or regional lymph nodes Bout one-half of gastrinomas are multiple and two-thirds malignant About one-fourth have multiple endocrine neoplasias syndrome (MEN I)- tumors of parathyroid, pituitary, and pancreatic islets There are clinical features that can distinguish ZE syndrome from DU features diarrhea weight loss/steatorrhea large gastric folds large amounts of gastric secretions family hx. of endocrine tumor, increase for cancer intractable or post-surgical recurrences of ulcer disease mechanism(s) increase gastric acid secretion decrease duodenal/jejunal pH inactivation of lipase mucosal inflammation trophic effect of gastrin secretory effect of gastrin MEN I- parathyroid tumor/hyperplasia Acid hypersecretion due to gastrin-secreting tumor Fasting Secretin stimulated(^ >110) N <150 - DU <150 - H2 antagonist <150-500 - Antral G Cell 150-500 - Post-vagotomy 150-1000 - Gastric atrophy 150-10,000 - ZE syndrome 150-100,000 + Tx. of ZE Syndrome is based upon clinical findings: If isolated duodenal wall tumor is present on CT and/or visceral angiography, surgical resection followed by measurement of gastric acid secretion If no evidence of tumor or evidence of Metastatic tumor, H+/K+ ATPase inhibitor or H2 receptor antagonist therapy in a dose determined individually to suppress fasting acid output to <10 mmol/h. Drug efficacy checked at 3 month intervals Total gastrectomy is generally obsolete. An Ulcer extends through the muscularis mucosa. Erosion is superficial to the muscularis mucosa. Gastric Ulcer- ulcer nitch (collection of contrast) can be seen on X-ray. Gastric Cancer Esophagus Herpes simples Tablet induces (tetracycline, KCl, others) Cytomegalovirus Duodenum Crohns disease Pancreatic carcinoma Stomach Carcinoma Kaposis lymphoma Pancreatic rest Syphilis Candida Prevalence Pt. seen by physicians 3-4 million Pt. self medicating 3-4 million Total pt. visits to physicians 12-14 million Hospitalizations >400,000 Total days ~4 million Deaths ~ 9,000 Operations >130,000 Peptic Ulcer is a Common Disease The annual incidence of active ulcer in the us is about 1.85 500,000 new cases per year In addition there are approximately 4 million ulcer recurrences yearly Hospitalizations for bleeding upper GI lesions are increasing with increased NSAID use Decrease in DU GU flat-lined and increase with an increase use of NSAIDs Prescriptions for NSAIDs tripled from 1975-1985 GD Mucosal Integrity is Determined by Protective (defensive) and Damaging (aggressive) Factors: Protective HCO3 Mucus Blood flow Growth factors cell renewal Prostaglandins Damaging H- Pepsins Smoking Ethanol Bile acids Ischemia NSAIDs Hypoxia Helicobacter pylori The Ingestion of NSAIDs daily is Major Factor in Ulcer Pathogenesis, Complications and Deaths: ~3 x 10 6th people in the us take NSAIDs daily about 1 in 10 pt. taking NSAOD daily have an acute ulcer 2-4% of NSAID users have GI complications each year >3000 deaths/yr and >25,000 hospitalizations/yr are attributable to NSAID induced GI complications compared to the general population NSAIDs increase the risk of GI complication ~2 to 10 fold. NSAIDs are Associated with an Increased Incidence of Bleeding Ulcers Gastric Ulcers- increased 10=20x DU- increase 5-15x Increased risk proportional to daily dose of NSAID NSAID ingestion causes both acute and chronic Gastroduodenal Injury All NSAIDs produce mucosal damage Ulcer risk is dose-related Acute mucosal response does not predict subsequent ulcer risk Acid Output tests Basal Peak Pentagastrin Decreased with: Pernicious Anemia 0-1 0-5 Gastric Atrophy 0-2 0-10 Gastric Ulcer 1-2 2-20 Gastric Cancer 0-5 0-30 Increased with: Duodenal Ulcer 1-15 12-60 Gastrinoma (ZE synd.) 5-80 20-110 Duodenal Ulcer is a Disease of Multiple Etiologies: Gastric acid and pepsin secretion are required Antral gastritis is present and almost universally assoc. with H. pylori Proximal duodenal mucosal bicarbonate secretion is frequently (~70%) impaired Nocturnal acid secretion and duodenal acid load are frequently increased Maximal acid Outputs are greater in DUs compared with Normals About 70% of DUs fall int eh normal range DU rarely occurs with a MAO <10 mmol/h H. Pylori has high urease activity High molecular weight pI isoelectric point) 5.9 20x more activity than proteus vulgaris (produces urea) high affinity for urea urease reaction is the basis of the diagnostic C14/C13 breath tests the presence of ammonia raises the local pH H. Pylori Infection can be Detected by Various Methods SensitivitySpecificityEndoscopic biopsy tests Culture60-90%100% Histologic exam95%98% Rapid urease test90%95%-100%Non-invasive tests (should be done 1st) Serologic (IgG antibodies to H. pylori)80-95%80-95% Urea Breath test (13C or 14C urea ( *CO295%95% Genetic Factors Influence Ulcer Incidence Risk Ratio Identical Twins ~5x First-Degree Relatives ~3x DU and GU cluster independently Certain Diseases are Assoc. with an Increased Prevalence of Ulcer COPD 3-5x Hepatic Cirrhosis 5-8x Chronic Renal Failure 1.5-3x The Effects of Smoking on Ulcers: Smokers have: a higher incidence of ulcers More ulcer recurrences More frequent complications Greater ulcer-related mortality A portion of this effect can be attributed to smoking-induced COPD Cigarette smoking also decreases pancreatic bicarbonate production Myths on Causes and Tx. of ulcers: Causes: Spicy foods, not a generator, just an aggravator Alcohol Psychological stress Tx. Ulcer is an executives disease A bland diet heals ulcers tricobesors- hair and insoluble Gastric Cancers (#2 cause of death) Metastatic( melanoma (most frequent visitor to the GI system) Anything that can move through the vascular three Benign Adenoma polyps-broad based, narrow at the top sessile or pedunculated 40% malignant degeneration rate, adenoma to adenocarcinoma. the bulk is in the lumen itself, and hangs off the wall. Can take up room. Esophageal dysphagia is often a complaint. There is a higher chance for malignancy if it is easier to bleed. Liomyoma within the walls of benign tumors (intramural lesion), by GE junction can give them GERD, by pyloric valve it can be compromised, can cause obstruction, can cause achalasia with proper motor function. Aggressive Malignant adenocarcinoma 90-95% of the primary malignancies to the stomach 3% lymphoma 2% lyomyosarcoma Etiologies that predispose us to Gastric Cancers Diet needs to be at the top of our list, coal mining industry, smoking, dusty environments, smoky environments. Patient Presentation 90% present with weight loss 80-90% dysphagia 50% blood in the stool RED FLAGS Vomiting of blood Blood in the stool      PAGE 2 of  NUMPAGES 24 Abdominal Pain Patterns  CREATEDATE 11/13/05 3:21 PM  PAGE 1 of  NUMPAGES 24 Dysphagia  CREATEDATE 11/13/05 3:21 PM Achalasia  CREATEDATE 11/13/05 3:21 PM Hernia  CREATEDATE 11/13/05 3:21 PM Peptic Ulcers  CREATEDATE 11/13/05 3:21 PM  CREATEDATE 11/13/05 3:21 PM ! " 3 4 > ? 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W(f4D HjT4D 1\4D 4{4D 6V85D jQU5D 2Nl)AA5D &S6D rh6D 6D זbX50                                                                                           ,\        O'WX XXX1X2X3X4X@XGXLXMXaXeXiXjXXXXXXXXXXXXX"Y&Y*Y+Yb_WNSectionTitle88D_WNSectionTitle_2l8D_WNSectionTitle_38D_WNSectionTitle_48D_WNSectionTitle_58D_WNSectionTitle_68D_WNSectionTitle_78DEnableWordNotes8DAbdominal Pain Patterns Dysphagia AchalasiaHernia Gastritis Peptic UlcersCancer0@66+66b@@UnknownGz Times New Roman5Symbol3& z Arial;Wingdings7&  VerdanaK1   MS Gothic-3 0000?5 z Courier New hq&&kR1R1!h4aa@Pc>? 3.KpG䀊WɬʓʨJ9c Steve Baker<         Oh+'0D+$0@ T`    Abdominal Pain PatternsP乩歫椠䱡畳椀㸲㻸ꔿ㌋䬮ꍰ䞮誀圇짗꾬钒붤鏊꣊㥊揤鞁Normal Steve Baker4Microsoft Office Word@NZ@ H@@H|=LRGl)VT$m] U  ."Systemp9# -j@"Verdana- .2 Abdominal Pain Patternsg]][*_Z*5YZ*_5ZZ;;Y@_N 2  @"Verdana-#2 11/13/05 3:21 PM@@-@@-?@#@-@@#<T- 2 * ^'@Times New Roman- 2 h 122   of 2!2  2422 2   -'- @ !X--.2 UXAbdominal Pain PatternsD>>=a?<$<<@#<<((<+?4 2 U$ @'-"2 XRetroperitonealF<'+=>;+'=?<< 2 ^ @'@Symbol- 2 .@"Arial- 2  h-U2 1More superficial (typically palpable, and mobile)T=+<#4?><+#4<$-'<>4<;#?<>=><$#=@>#a=><- 2   A'- 2 .- 2  h-42 Can pinpoint where it hurtsuF<?#>@>=@'#R?<+<#'#@?+'4 2 x  A'- 2 .- 2  h-,2 Referred pain patternsF<#<*+<>#><?#><('<+?4 2  @'- 2 C.- 2 C h-,2 CMore they can localizeT=+<#'?<;#4<?#=4<5< 2 Cx ?'- 2 X @'-#2 oXDiagnosing toolsM<>?=4?>$'==4 2 o A'-2 X Plain film<<?##a 2 $ A'- 2 .- 2  h- 2 <-2 V MAS#TDD 2 U A'- 2 1.- 2 1 h-22 1Called an abdominal seriesF<<>#<?#=>>=a?<#4<+<4 2 1`  @'- 2 .- 2  h-%2 Also known as KUBaD4=#;?=R?#<5#EIF 2 d2 D ureter is no?+<'<+#4#?=#2  t typically seen'#'<>5<;#4<<? 2   A'@1Courier New- 2 ] o<- 2 ]  Z-,2 ] FLook at kidney contour8==;#<'#;>?<;#4=@(=?+ 2 ]  @'- 2 o<- 2  Z-S2 F0Look at calcification of the ureters and kidneys8==;#<'#4<4$4<(=@#=##'?<#?+<'<+4#<?>$;>?<;4 2 v A'- 2 o<- 2  Z-(2 FSize of the stomachoD5<#=##'?<#4'=a<4@ 2 * d2 obstruction =>4'+?4'=@# 2  A'- 2  .- 2   h-O2  -Chest film can be used for esophageal lesionseF?<4'##a#4<?$><#@4<>##=+#<4=>?<><<#<4=?4 2    @'- 2 .- 2  h-.2 Both KUB and Chest filmE='?#EIE#<?>#F?<4(##a 2 e22 V used in pancreatic disease?4<>#?#><@4+<<'4#?4<<4< 2  @'- 2 K .- 2 K  h-2 K USID 2 K  A'- 2 o<- 2  Z-%2 FCan detect massesF<?#><'<4'#a<44<4 2  A'- 2 w o<- 2 w  Z-#2 w FCan tell if patiF<?#'<$##?<'52 w ents mass is fluid or solid<@'4$a<44#4$#@>#=+#4=> 2 w !  @'- 2 o<- 2  Z-A2 F$Bowel gas can disrupt the sound beamE=R<#><4#4<?#>4+@>'#(?<#4=??>#><<a 2   A'- 2 .- 2  h-2 CTF> 2  ?'- 2 9o<- 2 9 Z-&2 9FBetter than MR (CTE<''<+#'?<?#TF#-F> 2 9 -.C2 9? % still the diagnostic tool of choice)#4'$'?<#>=>?=4(4#(==#=##4?=4<- 2 9 A'- 2 o<- 2  Z->2 F"Density window change is importantM<?4';#S?>=R#4?=?><#4#a>=+'<@' 2 j  A'- 2 e.- 2 e h-2 eMRTF 2 e @'- 2 o<- 2  Z-O2 F-Hard to get good images due to organ movementeK<+>#'=#><'#>==>$b<><4#>?<#'=#=+><?$a=;<a<?' 2  @'- 2 .- 2  h-)2 Radionuclide studiesF<>=??4><#4'@>=4 2  @'- 2 'o<- 2 ' Z-12 'FUsed to determine secretilI4<>#'=#><'<+a?<#5<4+<':2 'W on of various enzymes to judge =?#=##;<+=?4$<?5;a<4#'=#"?>><$'2 F secretions4<4+<'=?4 2 C @'- 2 So<- 2 S Z-22 SFWatching WBCs congregate.c<'4?@>#cEF4#4=?>+<><'<$ 2 S  A'- 2 X @'-C2 X%Air Contrast Esophagography TechniqueD+#F=?'+<4'$?4=>?=>=>+<>?;#><4??>?< 2 :  @'- 2 .- 2  h-%2 Upright LPO (RPO)iI>+>@'#8<O#-F<O- 2  A'- 2 .- 2  h-72 1 swallow high density bariume@#4R<=R#???#><?5';$><+?a 2   A'- 2 A.- 2 A h-C2 A%1tsp effervescent granules/10cc water@'4>#<##<+;<44<?'#>+<??<4-@@44#R<'<+ 2 A  @'- 2 .- 2  h-2  drink down 3>+?;#>=R?#@ 2 --(2 4 oz barium rapidlys@#=5#?<+?a#+<>>; 2   A'- 2 m.- 2 m h-#2 mspot radiographs4>='#+<>=>+<??4 2 mg A'- 2 X @'-                    ՜.+,0 hp   { P獫票楧栮捯洀鉭曮㞱Û뜰⠲쎔딁烊皭〼፥ᙼ䕸忤઱1a eAbdominal Pain PatternsAbdominal Pain PatternsRetroperitoneal6 More superficial (typically palpable, and mobile) Can pinpoint where it hurts Referred pain patterns More they can localizeDiagnosing tools Plain film ( MAS Called an abdominal series5 Also known as KUB—ureter is not typically seen Look at kidney contour9 Look at calcification of the ureters and kidneys+ Size of the stomach—obstruction 2 Chest film can be used for esophageal lesions9 Both KUB and Chest film—used in pancreatic disease US Can detect masses7 Can tell if patient’s mass is fluid or solid- Bowel gas can disrupt the sound beam CTA Better than MR (CT- still the diagnostic tool of choice)+ Density window change is important MR6 Hard to get good images due to organ movement Radionuclide studiesK Used to determine secretion of various enzymes to judge secretions% Watching WBC’s congregate.&Air Contrast Esophagography Technique Upright LPO (RPO)" 1 swallow high density barium* 1tsp effervescent granules/10cc water% drink down 3-4 oz barium rapidly spot radiographs,Proposed Risk Factors for Esophageal CancerCigarette smoking AlcoholismNutritional DeficienciesKCarcinogens (mercury, carbontetrachloride, inhaled gases other than smoke)Endemic microorganismsRegional practicesSoil salinitySquamous cell carcinoma Achalasia Celiac sprue Ley stricture Plummer-Vinson syndrome Head and neck cancer TylosisEsophageal Webs and Rings Web- mucosaA ring- muscular (B ring (Schatzki)- mucosal.Squamo-columnar junction (between the B ring) Patient Hx. 4 Pain (site, duration, type, palliative factors) Retroperitoneal Intraperitoneal Nature of painUpper GI (UGI) Mouth Esophagus Stomach$ First 10cm of proximal duodenumI By including the proximal duodenum have 95% of all duodenal problemsW Have to add more contrast and time to include the duodenum—have to have contrast5 Do not like to use contrast above an obstructionF Use water soluble contrast instead so the GU system can clear Ultrasound Widely available Inexpensive Low risk to pt# Gas destroys the quality of US Homogenous acoustic : Liver provides—upper and middle right quadrants Bladder—pelvis= Left middle complaint will not give the best resultsCT4 Helical/spiral—data acquisition is continuousMRI. 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