ࡱ> Q Xbjbj >8X22WWWWWkkkkok:N:P:P:P:P:P:P:$<U?ft:Wrrrt:WW:333rnWWN:3rN:33:9,9 k1:9 :::0:D9R?b2f?99?W93 vt:t:3:rrrr?2 ; Patients history Chronological sequence of events Pain then N/V= appendicitis N/V then Pain= gastroenteritis Sudden or gradual onset of pain Character of pain Autonomic nerves innervate the viscera Visceral pain- dull, cramp like, insidious Somatic nerves innervate parietal peritoneum Somatic pain- localized sharp constant Duration of pain Pain for hours to days is often more severe than pain lasting for weeks Location of pain May not be specific Referred pain diaphragmatic irritation- kehr's sign Periumbilical going to the right lower quadrant- appendicitis Changes in location marker of progression Palliation Use of heat or ice- musculoskeletal origin Medications: ASA, ibuprofen Relation to food- duodenal ulcer- pain 2 hours after meals relieved by eating Relation to food- worse with eating- gastric ulcer Movement- peritonitis, fatty food- billiary colic comes with cholithiasis Severity of pain scale 1/10 Single rating is not much clinical help Serial determinants of pain severity- useful Temporal nature of pain Awaken patients at night? Post prandial- cholelithias or gastric ulcer Randomly through day vs at a certain time Fever chills- infection Nausea, vomiting, diarrhea, constipation History of severe retching/vomiting- mallory-weiss (tear) or boerhaave's syndrome (triad- vomiting, subcutaneous emphysema and LLQ pain) Urinary and bowel habits- change in caliber of stool- cancer makes it pencil thin Last menstrual period, sexual and pregnancy hx Upper resp tract symptoms- lower lobe pneumonia as cause of abdominal pain Family social medical history Cardiac history-atypical acute MI- stomach pain in women or silent MI in elderly and diabetics a-fib-abdominal vascular infarction- mesenteric ischemia test is mesenteric angiography FOB is positive Exposure history- corrosive esophagitis Caustic chemicals, lead Alcohol or narcotic withdrawal Mushrooms ticks (deer tick) spiders (black widow) Travel Appearance Pain constant (parietal, lying still) vs. crampy (gall bladder, cant sit still)- still vs. writhing Diaphoresis- acute MI sepsis or shock Pallor anemia shock Vital signs Orthostatics- 3rd spacing or volume depletion- acute pancreatitis Heent and neck Sclera icterus (jaundice greater than 2.5) Fundoscopic signs of emboli (A-Fib) Carotid bruits Chest Crackles and wheezes at bases Consolidation, pulmonary edema Heart murmurs Pleural rubs Hard stool- constipation/impaction may have diarrhea Pelvic genital and rectal exam on every patients with severe abdominal pain Cervical motion tenderness PID- Shandeliar Sign Adnex mases of the testicular portion can also present as abdominal pain **adhesions ms cause of acute bowel obstruction with surgery Abdomen palpate from area of least pain to areas with most pain Inspection: scars (adhesions, rash (herpes zoster), visible pulsatile masses AAA **Adhesions are the most common cause for acute small bowel obstructions in patients without virgin abdomens MCC of SBO without surgeries is hernia Auscultation: bowel sounds- least revealing! Abdominal bruits Percussion: identify ascites- shifting dullness to percussion Palpation Obtaining rebound tenderness is most often unnecessary and unkind to the patient pain with cough has similar specificity and sensitivity CBC with diff: inflammation like IBD which would be UC and Crohns or infection Serum electrolytes BUN and Creatin, urinalysis (UTI), UCG (pregnancy) Metabolic causes, dehydration, UTI, pregnancy Liver function tests: AST (alcohol), ALT (viral) Pancreatic enzymes- amylase, lipase (more specific) Cardiac enzymes- CKMB, troponin Elderly patients: pain presentation is often atypical in location and severity; may not mount febrile response. We may see hypothermia or nothing at all. Immunosuppressed patients; steroids may mask pain and decrease inflammation, immunosuppression leads to opportunistic infections and may cause the following diseases: CMV, lymphoma In an obese patients organs are not in place where you think they are there is overall abdominal distortion Patients on medication: some medications may change the perception of pain or cause constipation Pregnancy: distorted abdomen may be difficult to examine, variable organ location. Symptoms of preg my mimic those of some gasteroenteritis i.e. N/V, electrolyte disturbances and dehydration Imaging studies: Upright supine Intraperitoneal free air obstruction Air fluid levels and dilated loops of bowels specific for bowel obstruction Colon cutoff sign is acute pancreatitis Abdominal pelvic ultrasound- modality of choice for RUQ pain and Gyn disease CT scan- evaluates intrabdominal infections vasculature inflammation and solid organs Diagnostic test of choice Appendicitis, diverticulitis, pancreatitis Not good for gall bladder and pelvic organs MRI scan- not much use in diagnostic workup of abdominal pain EKG- rule out ischemia and mi Diseases of esophagus GERD Recurrent reflux of gastric contents due to Weak or incompetent lower esophageal sphincter Decreased resting pressure of LES Prolonged or transient relaxation of LES Conditions pregnancy scleroderma Drugs: anticholinergics, b-adrenergic, CCB Substances: nicotine alcohol Foods: chocolate, peppermint, and nitrates. All Aggravate the lower esophageal sphincter pressure and promotes reflux Delayed gastric emptying in gastroporesis in diabetics Esophageal will begin to occur in a pH less than 4 Clinical manifestations Heartburn- MC Regurgitation Anemia Cough hiccups Dysphagia to solids- because you have mucosal damage Recurrent laryngitis Reflux induced asthma Diagnosis Barium swallow upper gi series Endoscopy with biopsy Esophageal manometery: evaluates LES pressure- motility disorders Esophageal 24 hour pH monitoring- diagnostic test of choice Treatment: lifestyle changes Avoid eating prior to sleep weight loss Avoid aggravating acidic foods Avoid tight fitting clothes Antacids: calcium, mg, bicarbonate. Taken before meals and at bedtime H2 receptor antagonists: cimetidine, pepsid *Proton pump inhibitor: omeprazole. Most potent* Promotility agents: metoclorpramide Surgery: nissen fundoplication. Indicated in Barretts esophagus when PPI doesnt work or when we have extra esophageal signs of GERD Complications: stage one is hyperemia, stage two is linear non-confluent lesions, and stage three is circular confluent erosions (Barretts Esophagus) persistent reflux can produce cycle of mucosal damage that causes hyperemia edema and erosion to surface leading to strictures PUD gi bleed Barretts esophagus Normal squamous mucosa replaced by columnar epithelium Premalignant state Dx: endoscopy with biopsy Tx: same as Gerd, serial biopsies for high grade dysplasia Corrosive esophatitis Chemical burn to upper gi mucosa due to ingestion of alakaline or acidic substances, bleach or detergents, assc. with suicide attempts Clinical manifestations Burning oropharyngealk and or retrosternal pain Poropharyngeal erythema burns erosions ulcers. Even if you dont see burns in the mouth does not mean that they dont exist further down in the esophagus Excessive gagging dysphagia odynophagia, drooling hematemesis, melena Diagnosis clinically established. Within 24 hours make sure you do an upper endoscopy to check for grade of damage Treatment supportive (IV fluids) no inducing emesis Steroids and broad spectrum antibiotics initially Steroids given to prevent stricture Surgery esophagogastrectomy, colon interposition Complications stricture, formation cancer risk Esophageal cancer There are 2 types; in the past SCC accoutered for more than 90% of cases Squamous cell carcinoma Incidence higher in African men MC location upper and mid thoracic esophageous Risk factors Alcohol and tobacco use HPV **achlasia** plumner vinson syndrome (esophageal web, iron deficiency anemia, and glossitis) Caustic ingestion, nasopharyngeal carcinoma Adenocarcinoma Incidence higher in white men Mc location distal 1/3 esophagus gastroesohpageal junction Risk factor Gerd, barretts Alcohol and tobacco Prognosis is very poor Clinical features Dysphagia (difficulty): mc symptoms; initially solids and then liquids Anorexia wieght loss- 2nd MCC Odynophagia (painful) late finding Suggests mediastinum invasion Hematemsis chest pain Hoarseness Aspiration pneumonia and resp symptoms once the cancer has spread to the tracheal bronchial tree Diagnosis Barium swallow- outline a diverticula Upper endoscopy with biopsy: definitive dx*** Full metastic workup Ct scan of chest and ab Treatment Palliation is goal Surgery; esophagetctomy may be curative Chemotherapy and radiation before surgery Mallory-Weiss syndrome Inadequate relaxation of the esophageal sphincter during vomiting with subsequent mucosa tearing of the gastroesphageal junction Hematemesis status post retching episode Amount may vary- from blood streaked to massive frank blood Risk factors: alcoholics bulimics Diagnosis: upper endoscopy but may not be necessary because 90% self resolve If not, then you will do endoscopy: local injection, sclerotherapy or cautery or surgery if we need to repair the tear Boerhaves syndrome Complete full thickness longitudinal rupture of distal esophagus usually above gastroesohpageal junction- stomach contents empty into the peritoneal Triad: vomiting, chest pain, subcu emphysema Homans Crunch Risk factors: sudden increase in intra abodminal pressure caused by retching vomiting heavy lifting childbirth Dyspnea diaphoresis DX: upright CXR- air in mediastinum, esophagram- usually dont do because pt is not stable Tx: surgical repair broad spectrium antibiotics Benign esophageal stricture Sequelae of prolonged reflux esophagitis s/s heart burn solid food dysphagia Dx: barium swallow endoscopy Tx: balloon dilation catheters Esophageal web: plummer vinsons syndrome Located in upper 1/3 of esophagus Higher risk factor for squamous cell carcinoma (10% will develop into oral and esophageal carcinoma) Causes: dysphagia, iron deficiency anemia, atrophic oral mucosa, coroenichia (spoon shaped finger nails) Treatment esophageal dilation that will break the web and iron supplements Esophageal rings: schatzki rings A circumferential ring in the lower esophagus, usually accompanied by a sliding hiatial hernia MC occurs at the squamous columnar junction Usually asymptomatic Mild to moderate dysphagia and reflux can occur if you have that hernia If there is no reflux all you have to do is dilate the esophagus. If theres reflux you have to dilate the esophagus and Anti-reflux surgery which is the Nissan fundopigation Esophageal diverticula Three types: traction, zenkers, and epiphrenic Most esophageal diverticula are saved by an underlying motility disorder Zenker's diverticulum: (pulsation, failure of the cricopharengeal muscles to relax during swallowing) mc esophageal diverticula Mucosal herniation found in upper 1/3 of esophagus S/S: dysphagia regurge (solid food) halitosis weight loss cough Tx: surgery. Be careful with endoscopy because you dont want to perforate Traction diverticulum (traction, being pulled on by lymphadenopathy) asymptomatic no treatment Located at mid-point of esophagus near tracheal bifurcation Traction from continuous mediastinal inflammation and adenopathy causing retraction of esophagus pulmonary TB or sarcoidosis Epiphrenic diverticulum (pulsation) often asymptomatic Mucosal herniation found in lower 1/3 of esophagus Assc with spastic dysmotlity or **achlasia** Dx: barium swallow Tx: surgery Achlasia Acquired disorder of esophageal smooth muscle LES fails to completely relax with swallowing Abnormal peristalsis of the esophageal body in the lower third because the neuroplexus is missing Causes: idiopathic, assc. with gastric cancer Ss: dysphagia odynophagia CP weight loss nocturnal cough recurrent bronchitis or pneumonia Equal difficulty in swallowing solids and liquids Wash food with lots of water, twist their necks to help the food to go down Diagnosis Barium swallow: birds beak narrowed distal esophagus with large dilated proximal esophagus Endoscopy required to exclude malignancy because achlasia is risk factor Esophageal manometry confirms Dx. Because manometry is the best test for motility disorders Treatment adaptive measures: chew food better, dont eat before bed medical therapy includes CCB, sublingual nitroglycerin, and injection of botulism into the LES, dilation to the LES ring and surgery Diffuse esophageal spasm Non peristaltic spontaneous contraction of esophageal body Several segments contract simultaneously preventing appropriate advancement of food bolus Complain of both chest pain and dysphagia Nutcracker esophagus more complaint on chest pain** because the spasm is of higher amplitude In contrast to achlasia LES function is normal. Food will go to stomach Ss non cardiac chest pain that mimic angina, dysphagia is common, regurgitation of food is uncommon Diagnosis esophageal manometry: simultaneous repetitive contraction that occur after swallowing with normal LES response Barium swallow cork screw: multiple spontaneous contractions Treatment nitroglycerin CCB TCA Hiatal hernias Sliding account for greater 90 of cases Both gastroesophageal junction and portion of the stomach herniate into the thorax through the esophageal hiatus Les is above the diaphragm Medical- antacids, small meals, elevation of trunk 10% require nissen's Presents with a several month history of intermittent dysphagia foods such as steak seem to get stuck He is able to clear these foods by drinking extra liquids symptoms are not getting worse: lower esophageal ring shitakes ring A 65 y/r male. Trouble swallowing for 5 weeks. At first only meat stuck in his through now trouble with soft foods. No hx of similar problems or of any gi problems. He is a moderately heavy drinker and has smoked 1 pack per day for 40 years Esophageal cancer Presents sp having dry heaves after drinking- mallory weiss Acute gastiritis Diffuse or localized inflammation of gastric mucosa Etiology Aspirin nsaids alcohol smoking H. pylori infection, severe illness/stress Ss: epigastric burning and pain n/v gi bleed Diagnosis: endoscopy with or without biopsy Gastric mucosa may appear congested friable with superficial ulcerations or petechia Treatment remove offending agent Antacids h2 receptors antagonist PPI Antibiotics for h. pylori Chronic gastritis Autoimmune gastritis assc with Parietal and gastric cell antibodies pernicious anemia Low chloride levels Etiology Helicobacter pylori infection Diag: endoscopy with biopsy Tx: h. pylori, irradication PUD Areas of discrete GI tissue destruction occurring mostly in the proximal duodenum and stomach More common in men MCC: h. pylori and nsaids Acid hypersecretion states: zolinger elisson syndrome Caused by combination of impaired mucous defense and acid gastric contents Clinical manifestation Epigastric pain Duodenal ulcers: caused by increase in offensive 70-90 of patients low very rare, younger patients, nsaids, eating relieves pain Gastric: older patients, smoking, more complications higher recurrence Diagnosis: endoscopy most accurate Barium swallow: less reliable Upright x-ray for perforation Lab tests for h. pylori infection Treatment: supportive alter all risk factors Acid suppression Eradicate h. pylori infestation Cytoprotection Misoprostol Surgery required for complications Gastric cancer Rare in the us MC: adenocarcinoma Risk factor severe atrophic gastritis gastric dysplasia Gastric polyps H. pylori infection Pernicious anemia Clinical manifestation Abdominal pain, unexplained weight loss Early satiety* N/v, anemia, melena Diag: endoscopy with multiple biopsies most accurate Gastric lymphoma Type of non hogdkins lymphoma Stomach is the most common extra nodal site Similar to adenocarcinoma Zolinger ellison syndrome Pancreatic gastric secreting islet cell tumor Causes: refractory PUD Clinical manifestiontion: similar to PUD but worse Secretin injection test Elevated fasting gastrin level Elevated basal acid output Remove tumor Vomiting anorexia weight loss abdominal pain worsened by foods- gastric ulcer Chronic GERD progressive dysphagia weight loss x6 months diagnostic method- endoscopy and biopsy What are two causes of PUD? H pylori, nsaids Treatment: Misoprostal Acute pancreatitis Inflammation of the pancreas resulting from prematurely activated digestive enzymes Invokes pancreatic tissue auto digestion Causes Alcohol abuse (40%) Gallstones (40%) Bluntabdominal trauma: MCC in children Post- ERCP, pancreatic cancer Viral infections: mumps, coxsackie Scorpion bite Clinical manifestations Epigastric abdominal pain radiates to back Nausea vomiting anorexia Fever tachycardia hypotension Decreased or absent bowel sounds Hemorrhagic pancreatic: grey turners, Cullen, fox Diagnosis: Serum amylase and lipase LFTs Hyperglycemia, leukocytosis Abdominal x-ray: calcifications- chronic disease Sentinel loop Colon cut-off sign Abdominal ultrasound CT scan or MRI Ransons's criteria- determine prognosis and mortality Tx: bowel rest NG tube, IV fluids pain control Complications: pancreatic necrosis pseudocyst or absecess Chronic pancreatis Persistent continual p\pancreatic inflammation Fibrotic tissue replaces pancreatic parenchyma Alteration ort stricture of pancreatic ducts Altered endocrine and exocrine functions Causes: chronic alcholism (>80) hereditary pancreatitis, idopathic chronic pancreatitits Severe epigastric pain recurrent or persistent Often accompanied by NV Pain radiates to the back Aggravated by drinking episodes or by eating Steatorhea and weight loss due to malabsorption Anemia and signs of alcohol abuse DM due to endocrine dysfunction CT scan initial study of choice Calcifications Abdominal x ray ERCP gold standard Serum amylase and lipase levels Non operative Narcotic analgesics Operative Pancreaticjejunostomy: most common Pancreatic duct drainage; ductal decompression Pancreatic resection: whipples procedure Pancreatic cancer Most common in elderly patients 75% of patients over 60 Rare before 40 More common among African Americans Anatomic locations: pancreatic head, body, tail Smokings most established risk Chronic pancreatitis heave alcohol Diabetes Jaundice more common with head involvement Abdominal pain ERCP is most sensitive test Also differentiates pancreatic head cancer from tumors of CBD CT scan is preferred test for diagnosis and assessment of disease spread Tumor markers CA19-9 CEA- used for monitoring and test for reoccurrence of colon cancer Treatment: surgical resection: whipple's procedure only hope for cure Acute pancreatitis is most commonly associated? Alcoholic gall stones Suspected of having pancreatic disease. Ultrasound is inconclusive. Which test would be the next most appropriate? ERCP Viral hep A clinical syndrome with lab evidence of liver cell necrosis preceded or accompanied by malaise fever and jaundice All types of viral hep produce clinically similar No virus directly cytopathic to hepatocytes Acute liver injury is caused by immunologic response of the host cytotoxic t cells recognize and destroy host cells Panlobar inflitration loss of lobar pattern asymptomatic infection only serological markers acute hepatitis Fulminatent hep massive liver cell necrosis MC with B, D, E viruses Rapidly shrinking liver size and rising bilirubin level Tx. Liver transplant Chronic hep Persistent minimal cell necrosis Active gradual cell necrosis leading to failure Clinical manifestation Onset abrupt or gradual URI symptoms Myalgias and arthalgias Malaise, fatigue Anorexia n/v Fever and chills Epigastric, RUQ pain Jaundice, pruritis, dark urine Tender hepatomegaly, averison to smoking Risk factors: Travel Inmates Homos Overcrowding Poor sanitation Contaminated foods Infected blood Daycare Hep B Window period- no HBsAg, no HBsAb ,+HBcAb Resolving infection- +HBsAb, +HcAb, +HBeAb Infectivity- high= +HBeAg, Low= +HBeAb Hep C May diagnose with PCR serology RIBA ELISA Assays for HCV RNA are most sensitive- gold standard In addition to serological markers CBC- wbc normal or decreased Urinalysis- + bilirubin Liver function tests= elevations of LFTs does not correlate with severity AST and ALT increase 10-1,000 times normal level Lower enzymes elevation in chronic hepatitis Alkaline phosphate= mild elevation Conjugated bilibruin- moderately elevation Liver biopsy Acute illness resolves over 2-3 weeks 5-10% if cases have a protracted course Avoid hepatotoxic agents Supportive therapy Chronic hep B- interferon Hep D- treat hep b Alcoholic hep Chronic and excessive alcohol ingestion Fatty liver steatois Alcoholic hep: precurorsor to cirrhosis Hepatocyte injury and necrosis fibrosis Potentially reversible with cessation of drinking Clinical manifestation Hepatomegaly RUQ pain Anorexia NV Fatique fever and chills Jaundice Spider nevi Ascitis CBC- macrocytic anemia leukoctrosis Impaired liver function High bilirubin High alakaline phosphates Diag: Liver function tests Bilirubin elevated Liver biopsy- confirms diagnosis Treatment: complete abstinence from alcohol Nutritional and psychological Portal hypertension Normal pressure in portal vein is low because vascular resistance in hepatic cells is minimal Portal HTN results from increase resistance to blood flow System lacks valves- portal HTN leads to retrograde transmission of pressure Splanchnic vasodilation, portal systemic collateral formation Major sites of collateral formation involves veins at: Cardioesophageal junction- esophageal varices Rectum- hemorrhoids Abdominal wall- caput medusa Occurs at 3 levels relative to hepatic cells: Pre sinusoidal: proximal to cells so liver si not exposed to elevated pressure commonly portal veins Sinusoidal: cirrohisis Post sinusoidal Clincal manifesetation Hepatomegaly splenomegaly ascities varicies CBC: anemia leukopenia thrombyocytopenia Diag: markers of hepatic dysfunction Portal venous pressure may be measured by percutaneous transhepatic catheterization Fiberoptic endoscopy- esophageal varices MRI or CT scan to detect collateral circulation Tx: reduce pressure in portal venous system Tips: transjugular intrahepatic partosystemic shunt B-blockers: cause vasocontstriction splanchnic arterease decrease cardiac output Liver transplantation Cirrhosis Irreversible chronic injury to hepatic parenchyma fibrosis in assc. with regenerative nodules Disruption of liver architecture decreased blood flow through liver and hepatic dysfunction/failure Clinical manifestations Malaise fatigue Anorexia weight loss jaundice pruritis hepatic nodularity Abd pain Edema ascitis hypotension Coagulopathy Splenomegaly Spider elangiectasias Palmar erythema Portal HTN Gynecomastia Testicular atrophy Types of cirrhosis Alcohol: MC type in US Post hepatic: MCC chronic hepatitis infection Bilary: MCC injury or prolonged obstruction of biliary ducts Cardiac: MMCC by prolonged severe right heart failure Metabolic/ drug: ehemochromtosis, wilson's disease tylenol, methotrexate Diag: liver biopsy Treatment: treat underlying cause Ascites: sodium restriction diuretic paracentesis Coagulopathy: vitamin K injections Liver transplantiation- only care Complications: hepatic encephalopathy Acute reversible chronic irreversible mental status changes Affects behavior intellect neuromuscular function and LOC Caused by liver dysfunction and shunting of portal blood into systemic circulation so liver is bypassed Various toxic metabolites ** ammonia are absorbed Hepatic encephalopathy Clinical man: all those cirrhosis plus Decreased mental status confusion coma Asterexis: flapping tremor Fetor hepaticus: musty breath Reflexes symmetrically hyperactive rigidity Diag: Elevated ammonia levels markers of hepatic insufficiency Distinction EEG changes Spontaneous bacterial peritonitis Occurs in pts with ascities caused by chronic liver disease Clinical manifestation: abd pain rebound tendernes fever vom Diag: paracentesis with ascites fluid analysis increase WBC increase PMN Treatment emperic antibiotics Hepatocellular carcinoma primary malignant tumor of liver arising from the hepatocyte or blood vessels within the liver Excludes: gall bladder and biliary passages Signs and symptoms of cirrhoisis Unexplained deterioration in stable cirrhosis Diag: abd liver function tests Alpha fetoprotein screening and diagnosis of HCC Ultra sound best test to diagnoses HCC when AFP is normal Liver biopsy req for definitive diagnosis Ct scan determine extrahepatic spread of disease Tx: Curative conditions: no metastasis, 3 or fewer nodules, each nodule less than 5 cm Ablation with x ray radiation chemotherapy Embolization of supplying artery Surgical resection of nodules with 2cm Hemochromatosis Idiopathic autosomal recessive disorder where small intestine absorbs excessive iron Stored in glands and busmcels Excess hemosiderin deposition affects primarily Liver pancreases heart joints skin thyroid gonads hypothalamus Must be differentiated from iron overload Clinical manifestations Weakness ascites peripheral edema DOE cardiac arrhythmias Hepatomegaly cirrhosis fibrosis jaundice splenomegaly DM symptoms abdominal pain Artharalgia increased skin pigmentation Gynecomastia loss of libido amenorrhea loss of body hair Diagnosis: liver biospy with iron concentration gold standard Increased LFTs hyperglycemia Transferrin staturation over 70% Decreased TIBC Increased serum ferritin and iron Decreased FSH LH testosterone Treatment: removal of excess iron: repeated phlebotomy 1-2x weekly Lifelong phlebotmomy to keep iron stores at normal levels Iron chelating agent: deferoxamine Lisons disease Idiopathic autosomal recessive defect in copper transport Toxic accumulation in brin leiver skin kidney and bones Normally copper excreted billiary system Defect in chromosome 13: low ceruloplasmin Hep dis: hep portal HTN Diagnosis: liver biopsy hepatic copper measurement- goldstandard Low levels of serum ceruloplplasmin Elevated urinary copper levels Coppor chelation- d penicillamine Zinc therapy Vaccine for Hep B was successufl? HBsAb Poor prog sing in alcoholic hep Tumor marker for primary liver cell carc: alpha Evaluation of jaundice RBC breakdown Heme- heme oxygenase- biliverdin Biliverdin- biliverdin reductase- bilirubin Unconjugated indirect insoluble Bound to albumin- liver Indirect bilirubin- glucuronosyltransferase- conjugated bilirubin Conjugated, direct, soluble Bile channels- ATP pump Excreted via feces and urine Overproduction of bilirubin Impaired uptake or Prehepatic increase heme production Spherocytosis sickle cell anemia G6PD deficiency Hemolytic uremic syndrome increase marrow production Hepatic decrease liver uptake or conj Drug induced: Tylenol INH probenecid Gilbert syndrome- mild unconj Hyperbilirubenemia Dubin johnsons syndrome- mutated ATP pump Rotors syndrome- impaired hepatic storage Impaired excretion of conjugates Understanding lab LFTs' ast and ALT Alt is more sensitive and specific for liver damage In cirrhosis and chronic liver disease may be normal Alkaline phosphate Not specific to liver also found in bone GI Elevated in obstruction to bile flow Albumin Decreased in chronic liver disease, nephritic Cholestasis Blockage of bile flow Increased conjugated Jaundice gray stools dark urine Pruritis bile salt deposit in skin Elevated serum alkaline phosphatase Elevated serum cholesterol cant excrete Skin xanathomos Conjugated bilirubin- extrahepatic biliary obstruction Unconjugated hyper bilirubinemia (pre hepatic jaundice) casued by- hemolytic anemia Gallbladder disease Cholelithiasis- galls stones Three types Cholesterol stones Pigment stones Mixed Clinical manifestiations: biliary colic Diagnosis: RUQ ultrasound, CT or MRI as alternatives Treatment Non if asymptomatic Elective cholecystectomy for patients with recurrent episodes of bilary colic Acute cholecystitis Prolonged obstruction of the cystic duct with gall bladder wall inflammation Happens in absence of infection Epigastric RUQ abd pain and tenderness Radiates to the right shoudler or scapulat Diagnosis: RUQ ultrasound best of choice RUQ CT scan HIDA scan If gall bladder not visual after 4 hours confirmed Acalculous cholecystitis Acute cholecystitis without stones obstruction the cystic duct Usually idiopathic assc. with severe illness Same clinical manifestation Choledocholoithiasis Gallstones in the common bile duct Asymptomatic jaundice epigastric RUQ pain Total and direct hyper bilirubinemia Elevated alkaline phosphates RUQ ultrasound initially ERCP gold standard Diagnositic and therapeutic Sphincterectomy with stone extraction Acute cholangitis Life threatening infection of the biliary tract due to obstruction Leads to biliary stasis bacterial overgrowth Caused by choleducholitiasis in 60% of canes Clinical manifestation Charcot's triad: RUQ pain, jaundice and fever Reynolds pentad: plus septic shock and AMS RUQ ultra sound: initial study Hyperbilirubinemia Leukocytosis, mild elevation LFTs Cholangiography: ERCP Gall bladder carcinoma Most are adenocarcinoma Most in elderly Risk factors: gallstones, porcelain gallbladder Clinical manifestation Non-specific suggest bile duct obstruction Jaundice biliary colic weight loss Palpable gall bladder- sign of advanced disease Typical manifest nation of acute cholecystitis: murphy's Small bowel obstruction Partial vs. complete obstruction Partial: able to pass gas or have bowel movements Complete: any gas or bowel movement is residual from a Point distal to the obstruction Closed loop vs. open loop obstruction Closed loop: bowel is occluded at 2 points by adhesive ban or hernia ring comprising blood supply Proximal vs. distal obstruction Distal: distention of proximal bowel, late vomiting Proximal: early vomiting and minimal distention Pathophysiology- intestinal distention causes: reflex vomiting increase intestinal secretion proximal to obstruction decreased absorption Etiology: adhesions from abdominal surgery MCC adults Incarcerated hernia: second MCC Malignancy Intrasusception Inflammatory bowel disease Clinical features: Abdominal pain: cramping severe continuous Nauseas and vomiting, abdominal distension Altered bowel sounds, obstipation Diagnosis plain abdominal x ray Dilated loops of bowel, air fluid levels Barium enema- identifies site of obstruction Upper GI series Treatment Nonoperative if SBO is incomplete without fever tachycardia leukocytosis peritoneal signs Iv fluids ng tube antibiotics Surgery for complete obstruction Paralytic ileus Peristalsis is decreased or absent Without the presence of mechanical obstruction Causes: post operative state shock hypokalemia, medications spinal cord injury Diagnosis: abdominal xray; uniform distribution of gas in bowel colon and rectum Barium enema failure to pass contrast beyond a fixed point is diagnostic Treatment IV fluids NPO correction of electrolytes Celliac sprue Hypersensitivity to gluten (wheat products) Clinical manifestations: Weight loss abdominal distension Bloating, diarrhea Diagnosis: Biopsy: flattening of the villi, malabsorption Treatment Strict adherence to gluten-free diet IBD Inflammation of GI tract subsequent tissue damage More common in white and jews Mean age of onset 15-35 Chron's disease Chronic transmural inflammatory disease Affects any part of the GI tract MC small bowel Terminal illeum and cecum most common Pathology: Terminal ileum is hallmark location Transmural thickening and inflammatoun** Skip lesions- discontinuous involvement Fistula luminal strictures non casseating granulomas Clinical manifestation Diarrhea malabsorption RLQ abd pain NVF weight loss Extra intestinal manifestation Arthritis MC extra intestinal manifestation anklyosing sspondylitis sacrolitis Hyper coagulablility Diag: endosocophy with typical findings: Apthous ulcers Cobblestone appearance, skip lesions Barium enema Treat: surgery- reserved for complications Antidiarrheal agents Sulfasalazine- blocks prostaglandin reduces inflammation Metronidazole- if no response to sulfasalizine Systemic steroids- for acute exacerbations Immunosuppressants: azathiprine Complications Fistula formation Anorectal disease Small Bowel Obstruction- MC indication for surgery Maligancy- risk for colon cancer UC>>crohn's disease Cholelithiasis Nephrolithiasis Aphtous ulcers Narcotic abuse Ulcerative colitis Chronic inflammation disease of colon or rectal mucosa Dist: involves rectum in all cases Path- uninterrupted involvement, inflammation limited to mucous and submucosa, PMNs accumulate in colon crypts Clinical feat: Hematochezia, bloody diarrhea, tenesums Abd pain Diagnosis: stool cultures: R/O- c. dificile ova and parasites Fecal leukocytes Appear in UC ischemic colitis infectious diarrhea Colonoscopy Treat: surgery can be curative Systemic steroids- for acute exacerbations Sulfaslalazine- mainstay of treatment Immunosuppressants- azathiprine Complications Iron deficiency anemia Hemorrhage Malignancy Strictures Sclerosing cholangitis Cholangiocarcinoma Electrolyte disturbance, dehydration IBS Idiopathic functional disorder MC presents in teenage years females??males 50% have comorbid psychiatric disorders Depression anxiety high stress occupation Abd pain irregular bowel Discontinous involvement- crohns Acute appendicitis Obstruction of the appendix lumen caused by: Hyperplasia of lymphoid Fecalith Foreign body, tumor or parasite Leads to stasis, bacterial growth and inflammation; distension may compromise blood supply Necrosis may result in appendix perforation and ultimately peritonitis Peak incidence; teenager to mid 20s Rarely lasts greater than 72 hrs Abd pain periubmilical to RLQ pain Anorexia Nausea and vomiting Low grade fever RLQ tenderness; mcburnery Rebound tenderness Rovsings sign Psoas sign Obturator sign Diagnosis: Mild leukocytosis CT scan abd ultrasound Treatment: appendectomy Colorectal cancer 3rd most common cancer in US Virtually all tumors arise from adenomas Risk factors Age greater than 50 family history Adenomatous polyps History colorectal cancer polyps Screening: fecal occult blood digital rectal examination Colonoscopy most sensitive and specific test Diagnosis study of choice for positive FOB test CEA tumor marker baseline and recurrence Pattern of spread: direct extension, hematogenous- to liver, lymphatic-regional spread, transperitoneal Clinical manifestiation may be asymptomatic Abd pain- MC presenting symptom MCC of large bowel obstruction in adults Weight loss blood in stools Colonic perforation Left sided- smaller lumen diameter hematochezia more common Obstruction constipation Narrow stool Right sided- larger lumen diameter Fecal occult blood, melena Iron deficiency anemia Triad- anemia, weakness, RLQ mass Treatment Surgical resection of tumor and regional lymphatics Post operative chemotherapy Stool guiac test Annual ct abdomen and pelvis x ct for five years Diverticulosis Due to increase intraluminal pressure inner layer of colon bulges through focal area of weakness in colon wall MC location- sigmoid colon Risk factors: age, low fiber diet, constipation, family history Clinical features: Usually asymptomatic and discovered incidentally on barium enema or colonoscopy Vague LLQ pain, bloating constipation 10-20 symptomatic Diag: barium enema is best of choice Treat: high fiber foods, psyllium Complications Painless rectal bleeding- usually clinically insignificant and stops spontaneously no Tx Bleeding may be sever in 5 of cases Diverticulitis- feces become impacted in diverticulum leading to erosion and microperforation Ss: fever LLQ pain leukocytosis Dx: ct scan is test of choice barium enema and colonscopy are contraindicated in acute disease Tx: iv antibiotics no low residue diet iv fluids surgery Complications Abscess formation Colovescicual fistula Bowel obstruction Colonic perforation with peritonitis Recurrence: diverticulitis Angiodysplaisia of the colon Torturous dilated veins in submucosa of colon Common cause of lower GI bleed in patient>60 Low grade bleeding, unless veins rupture In 90% patients, bleeding stops spontaneously Dx: colonoscopy Tx: colonoscopy coagulation, right hemicolectomy LLQ pain, fever leukocytosis- diverticulitis Upper GI bleed refers to source of bleeding proximal to the duodenal ligament of Treitz Lower GI bleed refers to source of bleeding distal to the duodenal ligament of treitz Types of bleeding Hematomeis Coffee ground Upper GI bleed- PUD, Gerd, esophageal varices, gastric varices, mallor weiss tear, av malformation, endoplasm Lower GI bled- diverticulosis, angiodysplasia, IBD, colorectal carcinoma   (7<PQSX F G 6 7 R S T l p д޴޴Уބs„ hhwh%lCJOJPJQJaJhE9CJOJPJQJaJ hhwhhwCJOJPJQJaJ hL)hhwCJOJPJQJaJh%lCJOJPJQJaJhL)CJOJPJQJaJhhwCJOJPJQJaJ hL)h%lCJOJPJQJaJ hL)hL)CJOJPJQJaJ-3On G X 7 b m  & Fd@&gdE9 & Fd@&gdhw & Fd@&gdhw & Fd@&gdL) & Fd@&gdL) d@&gdL)  5   # P z { E 0Kd@&`KgdL) & Fd@&gdL) & Fd@&gdL)   J ` ~ # . : ? 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