Gastrin1) where is it produced and by what cells?2) what is secretion stimulated by3) what inhibits secretion4) target cells5) response to hormone6) How does Omeprazole (PPIs) work
1) G cells in stomach ANTRUM2) amino acids, vagal input (acetylcholine), calcium, ETOH, antral distention, pH>3.03) pH
Somatostatin1) where is it produced and by what cells?2) what is secretion stimulated by3) target cells4) response to hormone5) How does Octreotide work and when to use
1) produced by D (somatostatin) cells in the stomach ANTRUM2) acid in duodenum3) many, it is the great inhibitor!4) inhibits gastrin and HCl release; inhibits release of insulin, glucagon, secretin and motilin. Decreases pancreatic and biliary output5) Somatostatin analogue. Can be used to decrease pancreatic fistula output
CCK1) where is it produced and by what cells?2) what is secretion stimulated by3) response to hormone
1) produced by I cells of the DUODENUM2) amino acids and fatty acid chains3) gallbladder contraction, relaxation of sphincter of Oddi, increases pancreatic enzyme secretion
Secretin1) where is it produced and by what cells?2) what is secretion stimulated by3) what inhibits secretion4) response to hormone
1) S cells of DUODENUM2) fat, bile, pH4.0, gastrin4) increased pancreatic HCO3- release, inhibits gastrin release (this is reversed in pts with gastrinoma), and inhibits HCl release-high pancreatic duct output-> increased HCO3-, decreased Cl–slow pancreatic duct output-> increased Cl-, decreased HCO3- (carbonic anhydrase in duct exchanges HCO3- for Cl-
Vasoactive intestinal peptide1) where is it produced and by what cells?2) what is secretion stimulated by3) response to hormone
1) produced by cells in gut and pancreas2) fat, acetylcholine3) increased intestinal secretion (water and electrolytes) and motility
Glucagon1) where is it produced and by what cells?2) what is secretion stimulated by3) what inhibits secretion4) response to hormone
1) mainly alpha cells of pancreas2) stimulated by decreased glucose, increased aa’s, acetylcholine3) inhibited by increased glucose, increased insulin, somatostatin4) glycogenolysis, gluconeogenesis, lipolysis, ketogenesis, decreased gastric acid secretion, decreased GI motility, relaxes sphincter of Oddi.
Insulin1) where is it produced and by what cells?2) what is secretion stimulated by3) what inhibits secretion4) response to hormone
1) beta cells of the pancreas2) glucose, glucagons, CCK3) somatostatin4) cellular glucose uptake, promotes protein synthesis
pancreatic polypeptide1) secreted by what cells?2) secretion stimulated by?3) response to hormone
1) islet cells in pancreas2) food, vagal stimulation, other GI hormones3) decreased pancreatic and gallbladder secretion
Motilin1) where is it produced and by what cells?2) what is secretion stimulated by3) what inhibits secretion4) response to hormone and what drug acts on it’s receptor to stimulate motility
1) intestinal cells of gut2) duodenal acid, food, vagus input3) somatostatin, secretin, pancreatic polypeptide, duodenal fat4) increased intestinal motility (small bowel, phase III peristalsis)-> erythromycin acts on this receptor
1) Bombesin (Gastrin-releasing peptide) actions2) Peptide YY- where is it released from and actions3) what organ mediates anorexia4) what is the order/timeframe of bowel recovery from surgery
1) increases intestinal motor activity, increases pancreatic enzyme secretion, increases gastric acid secretion2) released from terminal ileum following fatty meal-> inhibits acid secretion and stomach contraction, inhibits gallbladder contraction and pancreatic secretion3) hypothalamus4) Small bowel fnc returns within 24 hoursstomach in 48 hours and large bowel in 3-5 days
Esophagus anatomy1) layers of the esophageal wall2) muscle ina- upper 1/3 of esophagusb- middle and lower 2/3 of esophagus3) blood supply to cervical esophagus4) blood supply to thoracic esophagus5) blood supply to abdominal esophagus6) venous drainage
1) mucosa (squamous epithelium), submucosa, and muscularis propria (longitudinal muscle layer); NO serosa2) a- striated muscle; b-smooth muscle3) inferior thyroid artery4) vessels directly off the aorta5) left gastric and inferior phrenic arteries6) hemi-azygous and azygous veins in chest
Esophagus anatomy1) where do lymphatics drain2) where do the right and left vagus nerves travel and what do they supply3) where does the thoracic duct travel and insert4) MC site of esophageal perforation (usually with EGD)5) cause of aspiration with brainstem stroke
1) upper 2/3 drain cephalad; lower 1/3 caudad2) -Right vagus- travels on posterior stomach as it exits chest and becomes celiac plexus. Also has criminal nerve of Grassi which can cause persistently high acid levels postop if left undivided after vagotomy-Left vagus- travels on anterior stomach. goes to liver and biliary tree3) Travels from right to left at T4-5 as it ascends in the mediastinum. Inserts into left subclavian vein4) cricopharyngeus muscle5) failure of cricopharyngeus muscle to relax
Upper esophageal sphincter1) distance from incisors2) muscle3) nerve innervation4) normal EUS pressure at rest5) normal EUS pressure with food bolus
1) 15cm2) cricopharyngeus muscle (circular muscle, prevents air swallowing)3) recurrent laryngeal nerve4) 60 mmHg5) 15mmHg
Lower esophageal sphincter1) distance from incisors2) what is the resting state3) nl LES pressure at rest4) nl LES pressure with food bolus
1) 40cm2) normally contracted at resting state (prevents reflux). relaxation mediated by inhibitory neurons. Anatomic zone of high pressure but NOT an anatomic sphincter3) 15mmHg4) 0 mmHg
Anatomic areas of esophageal narrowing
at cricopharyngeus muscle, compression by the left mainstem bronchus at aortic arch, and diaphragm
Stages of swallowing1) what initiates it2) primary peristalsis- what initiates3) secondary peristalsis- what initiates4) Tertiary peristalsis5) resting state of UES and LES bw meals
1) CNS2) occurs with food bolus and swallow initiation3) occurs with incomplete emptying and esophageal distention, propagating waves4) non-propagating, non-peristalsing (dysfunctional)5) contracted
Swallowing mechanism
soft palate occludes nasopharynx, larynx rises and airway opening is blocked by epiglottis, cricopharyngeus relazes, pharyngeal traction moves food into esophagus.LES relaxes soon after initiation of swallow (vagus mediated)
Which side should you approach from in surgery for repair of1) cervical esphagus2) upper 2/3 thoracic esophagus3) lower 1/3 thoracic esophagus
1) left2) right (avoids aorta)3) left (left-sided course in this region)
Hiccoughs1) causes2) what nerves are part of the reflex arc
1) gastric distention, temperature changes, ETOH, tobacco2) vagus, phrenic, sympathetic chain T6-12
Esophageal dysfunction1) primary causes2) secondary causes3) best test for heartburn4) best test for dysphagia or odynophagia5) best test for meat impaction
1) achalasia, diffuse esophageal spasm, nutcracker esophagus2) GERD (most common), scleroderma3) endoscopy (can visualize esophagitis)4) barium swallow (better at picking up masses)5) endoscopy (dx and rx)
Pharyngoesophageal disorders1) In what part of swallowing is the prbm?2) causes3) T/F- liquids are worse than solids for these disorders4) Plummer-Vinson syndrome- components of syndrome and rx
1) trouble in transferring food from mouth to esophagus2) MC neuromuscular disease- myasthenia gravis, muscular dystrophy, stroke3) True4) upper esophageal web, Fe-deficient anemiarx- dilation, Fe; screen for oral CA
Esophageal Diverticula1) Zenker’s Diverticuluma- what causes itb- is it true or false diverticulumc- locationd-symptomse-dxf-rx
1) a) increased pressure during swallowing 2/2 failure of cricopharyngeus to relaxb) false diverticulum located posteriorlyc- between the pharyngeal constrictors and cricopharyngeusd- upper esophageal dysphagia, choking, halitosise- barium swallow studies, manometry, risk for perf with EGD and Zenker’sf-cricopharyngeal myotomy, Zenker’s itself can either be resected or suspended. L cervical incision-L cervical incision, leave drains in, get esophogram on POD#1
Esophageal Traction Diverticulum1) True or False diverticulum2) cause3) location4) sx5) rx
1) true diverticulum2) inflammation, granulomatous disease, tumor 3) usually in mid-esophagus and lies lateral4) regurgitation of undigested food, dysphagia5) excision and primary closure if symptomatic, may need palliative therapy (ie- XRT) if due to invasive CA. if asx, leave alone
Esophageal Epiphrenic diverticulum1) what disorders are associated2) location3) sx4) dx5) rx
1) esophageal motility disorders (ie-achalasia)2) in distal 10cm of esophagus3) most are asx. can have dysphagea and regurgitation4) esophagram and esophageal manometry5) rx- diverticulectomy and esophageal myotomy on the side opposite the diverticulum if sx
Achalasia1) sx2) cause/pathophys3) manometry findings4) barium swallow findings5) rx6) what infection can produce similar symptoms
1)dysphagia, regurg, weight loss, respiratory symptoms2) failure of LES to relax and lack of peristalsis after food bolus 2/2 neuronal degeneration in muscle wall3) Increased LES pressure, incomplete LES relaxation. NO peristalsis4) birds beak. tortuous dilated esophagus and epiphrenic diverticula5) balloon dilatation of LES-> effective in 80%. Nitrates, Ca-channel blockers.-If above fails do Heller myotomy (left thoracotomy, myotomy of LOWER esophagus ONLY) plus partial Nissen funduplication6) T. cruzi parasite
Diffuse esophageal Spasm1) sx2) manometry findings3) rx
1) Chest Pain!, dysphagia, psychiatric history2) strong non-peristaltic unorganized contractions; LES relaxes normally3) Ca-channel blockers, nitrates. Heller Myotomy (myotomy of upper and lower esophagus) if meds fail but less effective than for acholasia
Nutcracker esophagus1) sx2) Manometry findings3) rx
1) Chest Pain!, dysphagia2) high-amplitude peristaltic contractions; LES relaxes normally3) Ca-channel blocker, nitrates. Heller myotomy if those fail of upper and lower esophagus, but less effective than for acholasia
Scleroderma leading to dysphagea1) pathophysiology2) rx
1) fibrous replacement of esophageal smooth muscle->dysphagia and loss of LES tone with MASSIVE REFLUX and STRICTURES2) esophagectomy usual if severe
GERD1) what is normal anatomic protection from GERD2) pathophys of GERD3) sx4) empiric rx5) diagnostic studies6) surgical indications7) Nissena- steps of operationb-what is the paraesophageal membrane and extension ofc- key maneuver for wrap is identification of?d-complications8) approach for Belsey procedure9) Collis gastroplasty- when to use it and how it is done
1) need LES competence, normal esophageal body, normal gastric reservoir2) increased acid exposure to esophagus from loss of gastroesophageal barrier3) heartburn sx 30-60min after meal, worse lying down, asthma symptoms (cough), choking, aspiration4) empiric PPI (omeprazole 99% effective) for 3-4 weeks. If fails do diagnostic studies.5) pH probe (best test), endoscopy, histology, manometry (resting LES esophagus (neo-esophagus)
Hiatal Hernia1) Describe type I-IV2) which type usually needs repair 2/2 high risk of incarceration3) how to repair4) Hernia associated with Schatzki’s ring and treatment
1) Type I- sliding hernia from dilation of hiatus (MC); often associated with GERDType II- paraesophageal. hole in diaphragm beside esophagus, normal GE jnction. sx- CP, early satiety, dysphageiaType III- combined I and IIType IV- stomach in chest + another organ (colon/spleen)2) Type II paraesophageal3) Nissen + resect hernia4) ring of tissue in lower esophagus-> esophageal narroing. Associated with sliding hiatal hernia (Type I), rx-dilation of the ring and PPI usually sufficient. Do not resects
Barrett’s Esophagus1) cellular change that occurs2) cause3) how much does its presence increase CA risk4) what is indication for esophagectomy5) treatment and followup
1) squamous metaplasia to columnar epithelium2) long-standing exposure to gastric reflux3) increases cancer risk by 50 times (adenocarcinoma)4) Severe Barret;s dysplasia is indication for esophagectomy5) Treat uncomplicated like GERD (PPI or Nissen). Surgery will decrease esophagitis and further metaplasia but will not prevent malignancy or cause regression of the columnar lining.-Need careful f/u with EGD for lifetime. Even after Nissen
Esophageal Cancer1) T/F: esophageal tumors are almost always malignant but with late invasion of nodes2) How does it spread3) risk factors4) diagnosis5) best test for determining resectability and what factors prevent resection6) MC type of cancer overall-where is adenoCA usually located and where does it met-what about squamous cell cancer7) MC benign esophageal tumor
1) False, almost always malignant with early nodal invasion2) submucosal lymphatic spread3) ETOH, smoking, achalasia, caustic injury, nitrosamines4) Esophagram (best test for dysphagia)5) CT chest and abdomen-unresectable if hoarseness (RLN invasion), Horner’s syndrome (brachial plexus invasion), phrenic nerve invasion, malignant pleural effusion, malignant fistula, airway invasion, vertebral invasion, nodal disease outside the area of resection (ie-supraclavicular or celiac nodes (M1 dz))6) Adenocarcinoma is #1. Found in lower 1/3 of esophagus, mets to liver MC-Squamous cell CA usually in upper 2/3 of esophagus, lung mets MC7) Leiomyoma
Esophageal CA treatment1) role of pre-op Chemo-XRT2) What Chemo agents are used3) Esophagectomya-mortality and cure ratesb- what is primary blood supply to stomach after replacing esophagusc-Describe the diff bw the Transhiatal approach, Ivor Lewis and 3-Hole esophagectomy techniquesd-what additional procedure do you need with all of the above4) when is colonic interposition a good choice and what blood supply does it depend on5) what is needed after esophagectomy to r/o leak and when to do it6) Rx of postop strictures7) Malignant fistulas- how to rx and prognosis
1) can downstage tumors and make resectable2) 5-FU and Cisplatin (for node + disease or use pre-op to shrink tumors)3) a-5% mortality from surgery. 20% cure rateb-Right gastroepiploic artery (have to divide the left gastric and short gastricsc-Transhiatal- abdominal and neck incisions. bluntly dissect thoracic esophagus (has dec mortality from leaks with cervical anastamosis)-Ivor Lewis- Abd incision and R thoracotomy.-> exposes all of intrathoracic esophagus-> intrathoracic anastamosis-3-Hole: abdominal, thoracic and cervical incisionsd- pyloromyotomy4)choice in young pts when you want to preserve gastric function. need 3 anastamoses. blood supply depends on colon marginal vessels5) contrast study on POD76) dilate7) can palliate with stent, most die within 3 mo from aspiration
Leiomyoma1) where is it located2) dx3) Biopsy technique4) rxEsophageal polyps5) how common6) location7) rx
1) in muscularis propria, usually in lower 2/3 of esophagus (smooth muscle cells)2) esophagram #1, EUS, CT scan (to r/o CA)3) Do NOT biopsy bc can for scar and make later resection difficult4) rx if >5cm or symptomatic with excision (enucleation) via thoracotomy5) 2nd MC benign lesion after leiomyoma6) usually cervical esophagus7) if small- resect with endoscopy; if larger-cervical incision
Caustic esophageal injury1) role of NG tube, induced vomiting and drinking water to flush it out in treatment2) Diff in necrosis from alkali and acid injury and which is worse/most likely to cause CA3) How to determine severity/follow injury4) Treatment ifa- Primary burn (hyperemia)b- secondary burn (ulcerations, exudate and sloughing)c-tertiary burn (deep ulcers, charring and lumen narrowing)d- caustic esophageal perforation
1) DON’T do any of these-NO NGT, NO vomiting, NOTHING to drink2)Alkali-> deep liquifaction necrosis (Worse injury and more likely to cause CA). Ie-DranoAcid-> coagulation necrosis, mostly gastric injury3) Do endoscopy to assess lesion except if suspected perforation. Do NOT go past a site of severe injury. Follow with serial exams and plain films4) a-obseve and conservative therapy (IVFs, spitting, abx, po intake after 3-4days, may need future serial dilation for strictures (usually cervical). b-prolonged observation and conservative therapy. Unless Esophagectomy indicated (Sepsis, peritonitis, mediastinits, free air, mediastinal or stomach wall air, crepitance, contrast extravasation, pneumothorax, large effusion)c- same as seconday burn. Most need esophagectomy. Don’t restore alimentary tract until pt recovers from caustic injuryd-esophagectomy (NOT repaired 2/2 extensive damage)
Esophageal Perforation1) MCC2) MC location3) sx4) Dx5) Criteria for nonsurgical management and what does conservative therapy consist of6) Repair of Non-contained perforationsa- if diagnosed in
1) endoscopy2) at cricopharyngeaus muscle in cervical esoph3) dysphagia, tachycardia, pain4) CXR initially for free air. Then Gastrografin swallow followed by barrium swallow5) contained perforation by contrast. self-draining. no systemic effects6) a- primary repair with drains via longitudinal myotomy to see full extent of injury. Consider intercostal muscle flaps to cover repairb- If in Neck- Just place drains (no esophagectomy)-If in Chest: need 1) resection (esophagectomy or cervical esophagectomy) or 2) exclusion and diversion (cervical esophagectomy, staple across distal esophagus, washout mediastinum, place chest tubes and do late esophagectomy at time of gastric replacement=when pt fully recovers)7) pts with severe intrinsic dz (burned out esophagus from achalasia or esophageal CA)
Boerhaave’s syndrome1) classic presentation2) MC site of perforation3) what is Hartmann’s sign4) Dx5) Tx6) prognosis
1) forceful vomiting then chest pain.2) in Left lateral wall of esophagus, 3-5cm above GE junction3) mediastinal crunching on auscultation4) Gastrografin swallow5) same as for esophageal perforation6) highest mortality of all perforations- survival improves with early dx and rx
Stomach1) Stomach transit time2) where does peristalsis occur3) what nerves sense gastroduodenal pain4) Blood supply and branchesa- branches of celiac trunkb- supply to greater curvaturec-supply to lesser curvatured- supply to pylorus
1) 3-4 hours2) distally in antrum only3) afferent sympathetic fibers of T5-104) a- splenic (left gastroepiploic and short gastric are branches, Common hepatic (gastroduodenal and Right gastric are branches) and Left gastricb- right (branch of gastroduodenal) and left gastroepiploics and short gastricsc- right and left gastricsd-gastroduodenal artery
Stomach1) what cells line mucosa2) what do cardia glands secrete3) what do chief cells release and role in digestion4) what do parietal cells release5) what stimulates H+ release6) inhibitors of parietal cells7) role of intrinsic factor
1) simple columnar epithelium2) mucus3) pepsinogen (1st enzyme in proteolysis)4) H+ and intrinsic factor5) Acetylcholine (Vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells)6) somatostatin, prostaglandins (PGE1), secretin, CCK7) binds B12 and complex is reabsorbed in the terminal ileum
H+ release- describe the pathway leading to release for1) Acetylcholine2) Gastrin3) Histamine4) final common pathway5) at what part of the pathway do PPIs work like Omeprazole
1 and 2) Activate phospholipase leasing to inc Ca-> Ca-calmodulin activates phosphorylase kinase-> inc H+ release3) activates adenylate cyclase-> cAMP-> protein Kinase A-> H+ release4) Phosphorylase kinase and Protein Kinase A phosphorylate H+/K+ ATPase channels to increase H+ secretion and K+ absorption5) block H+/K+ ATPase channels
Stomach1) Antrum and pylorus glandsa- name the secreting cells found here and what they releaseb- name the 2 other types of secreting glands here and their function2) what inhibits G-cells3) what stimulates G-cells4) where are Brunner’s glands and what do they secrete5) when are somatostatin, CCK and secretin released
1) a- G cells-> gastrin release (why antrectomy is helpful for ulcer disease) and D-cells- secrete somatostatin. inhibit gastrin and acid releaseb- Mucus and HCO3- secreting glands- protect stomach from acid2) H+ in duodenum3) amino acids, acetylcholine4) In duodenum, secrete alkaline mucus5) with antral and duodenal acidification
Stomach1) causes of rapid gastric emptying2) causes of delayed gastric emptying3) What are Trichobezoars made of and Tx4) what are Phytobezoars made of and Tx5) What is a Dieulafoy’s ulcer6) what is Menetrier’s disease
1) previous surgery (#1), ulcers2) diabetes, opiates, anticholinergics, hypothyroidism3) made of hair. hard to pull out. Rx- EGD generally inadequate so likely need gastrostomy and removal4) made of fiber (seen in DM with poor gastric emptying). rx- enzymes, EGD, diet changes5) vascular malformation (can bleed)6) mucous cell hyperplasia (inc rugal folds)
Gastric Volvulus1) what hernia is it associated with2) type of volvulus3) rx
1) type II (paraesophageal) hernia2) usually organoaxial volvulus3) reduction and Nissen
Mallory-Weiss Tear1) cause and presentation2) Dx/rx (and MC location)
1) 2/2 forceful vomiting-> hematemesis-> bleeding stops spontaneously2) EGD with hemo-clips. tear is usually on lesser curvature, near GE jnc. If continued bleeding may need gastrostomy and oversewing of the vessel
Vagotomies1) Effect of Truncal and Proximal Vagotomies on gastric emptying of solids and liquids2) what about if you add a pyloroplasty to truncal vagotomy3) Other effects of truncal vagotomya- gastric effectsb-nongastric effects4) MC problem after vagotomy and cause
1) Both-> increase liquid emptying (vagally-mediated receptive relaxation is removed-> increased gastric pressure-> inc liquid emptyingFor Solids-Truncal vagotomy divides vagal trunks at level of esophagus-> dec emptying of solids-Proximal Vagotomy (aka- Highly Selective)-> divides individual fibers that supply the gastric fundus only-> nl emptying of solids2) then you will have increased solid emptying3) a- decreases acid output by 90%, inc gastrin, gastrin cell hyperplasiab- decreases exocrine pancreas fnc (digestive), dec postprandial bile flow, inc gallbladder volumes, dec release of vagally-mediated hormones4) diarrhea (40% get) 2/2 sustained MMCs (migrating motor complexes) that force bile acids into the colon
Upper GI bleed1) risk factors2) Dx/Rx3) what test to get if slow bleeding and hard to localize4) biggest risk factor for rebleed at time of EGD5) highest risk factor for mortality with non-variceal UGI bleed6) Cause and Rx in pt with liver failure
1) previous UGI bleed, PUD, NSAIDs, smoking, liver disease, esophageal varices, splenic vein thrombosis, sepsis, burn injuries, trauma, severe vomiting2) EGD, potential rx with hemo-clips, epi-injection or cautery. If ulcer get bx for H. Pylori-> rx with omeprazole and abx3) tagged RBC scan4) #1- spurtung blood vessel (60% chance), #2 visible blood vessel (40% chance), #3 diffuse oozing (30% chance)5) continued or re-bleeding6) MC esophageal varices. Do EGD with variceal bands or sclerotherapy. TIPS if that fails
Duodenal ulcers1) T/F: MC peptic ulcer2) what sex is it MC in3) MC location- which ulcers perforate and which bleed (from what artery)4) sx5) dx6) rx7) what does H. pylori triple therapy consist of
1) True; 2) male;3) 1st part of duodenum, usually anterior. Anterior ulcers perforate; posterior ulcers bleed from the gastroduodenal artery4) epigastric pain radiating to back, abates with eating but recurs 30min later5) EGD6) PPI, triple therapy for H. pylori7) Omeprazole, clarithromycin and amoxicillin. +/- Bismuth salts
Duodenal Ulcers1) what is Zollinger-Ellison syndrome components2) Surgical indications for rx3) Surgical optons and how to reconstruct after antrectomy- which has the lowest ulcer recurrence-which has the lowest mortality
1) gastic acid hypersecretion, peptic ulcers and gastrinoma2) Perforation, protracted bleeding after EGD therapy), Obstruction, Intractability despite medical therapy, inability to rule out cancer (ulcer remains despite treatment)3) a)Proximal vagotomy- lowest complications, no need for antral or pylorus procedure, 10-15% ulcer recurrence, lowest mortality (0.1%)b)Truncal vagotomy and pyloroplasty- 5-10% ulcer recurrence, 1% mortalityc) Truncal vagotomy and antrectomy-1-2% ulcer recurrence (lowest rate), 2% mortalityRECONSTRUCTION: Roux-en-Y gastro-jejunostomy is best bc less dumping syndrome and relfux gastritis compared to Billroth I (gastroduodenal anastomosis) and Billroth II (gastrojejunal anastamosis)
Duodenal Ulcers- complications1) MC complication2) what constitutes major bleeding3) Rx of duodenal bleed4) rx of duodenal obstruction 2/2 ulcer5) rx of perforation6) Intractability with escalating doses of PPI- next step
1) bleed2) >6units in 24 hours or pt remains hypotensive despite transfusion3) EGD- clips, epi, cauterize. If fails-> OR-> duodenotomy and GDA ligation (avoid hitting common bile duct posteriorly); if pt has been on PPI also need acid-reducing surgery4) PPI and serial dilation 1st. If fails-> antrectomy and truncal vagotomy (best), also get bx to r/o CA5) Graham patch (omentum over perf) + acid-reducing surgery if pt has been on PPI6) >3mo PPI without relief based on EGD mucosal findings (not sx)-> acid reducing therapy
GASTRIC ULCERS1) risk factors2) MC location3) T/F: hemorrhage is associated with higher mortality than with duodenal ulcers4) Best test for H. Pylori5) describe the location and whether it is due to high acid secretion vs. decreased mucosal protection for Type I-V peptic ulcers6) surgical treatment if indicated
1) older male, tobacco, ETOH, NSAIDs, H. pylori, uremia, stress (burns, sepsis and trauma), steroids, chemotherapy2) 80% on lesser curvature of the stomach3) true4) biopsy with histo examination from antrum. CLO test (rapid urease test)- detects urease released from H. Pylori5) type I- lesser curve, low along stomach body (decreased mucosal protection)type II- 2 ulcers (lesser curve and duodenal)- high acid secretion (like duodenal ulcers)type III- pre-pyloric ulcer- high acid secretiontype IV- lesser curve, high along cardia. decreased mucosal protection. Type V- ulcer 2/2 NSAIDS6) truncal vagotomy and antrectomy best (try to include ulcer with resection=extended antrectomy) otherwise separate ulcer excision bc of high risk of gastric CA. omental patch and ligation of bleeding vessels poor options 2/2 high recurrence of sx and risk of gastric CA in ulcer
Stress gastritis1) timeframe for occurance2) rxChronic gastritis3) location of Type A and B4) which type is associated with pernicious anemia and autoimmune disease5) which type is associated with H. pylori6) rx
1) 3-10d after event, lesions appear in fundus first2) PPI3) Type A is fundus, Type B is antral4) type A5) Type B6) PPI
Gastric CA1) MC location2) sx3) risk factors4) risk of CA with adenomatous polyps and rx5) what is krukenberg tumor6) what is Virchow’s nodes
1) antrum has 40%2) pain unrelieved by eating, weight loss3) adenomatous polyps, tobacco, previous gastric operations, intestinal metaplasia, atrophic gastritis, pernicious anemia, type A blood, nitrosamines4) 15% risk. Tx- endoscopic resection5) mets to ovaries6) mets to supraclavicular node
Gastric CA1) Intestinal-type gastric CA- who gets it and surgical rx2) diffuse gastric cancer (linitis plastica)-a- who is at riskb- spreadc-prognosis compared to intestinal-type gastric CAd- surgical rx3) use of chemo and what drugs4) what is c/i for resection5) palliative option
1) high-risk populations, older men, japan (rare in US). surgical rx- subtotal gastrectomy (need 10-cm margins)2) a- low-risk populations, women, MC type in USb- diffuse lymphatic invasion, no glandsc- less favorable prognosis (25% 5-yr survival)d- total gastrectomy bc of diffuse nature3) poor response but can try 5-fu, doxorubicin, mitomycin C4) metastatic dz outside of area of resection5) if obstructed-> stent proximal lesions, bypass distal lesions with gastrojejunostomyif low/moderate bleeding/pain-> XRTif above fail can consider palliative gastrectomy
Gastrointestinal Stromal Tumors (GIST)1) benign or malignant?2) US findings3) Dx- what stain?4) indications of malignancy5) rx
1) MC benign gastric neoplasm, although can be malignant2) hypoechoic with smooth edges3) bx- C-Kit positive4) malignant if >5cm or >5mitoses/50HPF5) rx- resection with 1-cm margins; chemo with imatinib (Gleevec, tyrosine kinase inhibitor) if malignant
Mucosa-Associated Lymphoid Tissue Lymphoma (MALT lymphoma)1) what is it cause by2) rx3) MC location
1) H. pylori infection, usually regress after rx2) H. pylori triple therapy (clarithromycin, amoxicillin and PPI) and surveillance. If doesn’t regress, do XRT3) stomach MC location
Gastric Lymphomas1) MC type2) Dx3) rx4) when is surgery indicated5) overall 5-yr survival
1) non-Hodgkin’s lymphoma (B cell). Stomach is MC location for extranodal lymphoma2) EGD with bx3) chemo and XRT.4) surgery for complications, possibly indicated for stage I disease (tumor confined to stomach mucosa) and then only partial resection is indicated5) 50%
Morbid Obesity1) what 4 criteria must be met for bariatric surgery2) bariatric surgery operative mortality3) what comorbidities get better after surgery
1) -BMI> 40 or >35 with coexisting comorbidities-failure of nonsurgical methods of weight reduction-Psychological stability-Absence of drug and alcohol abuse.2) 1%3) DM, HLD, sleep apnea, HTN, urinary incontinence, GERD, venous stasis ulcers, pseudotumor cerebri, joint pain, migrains, depression, polycystic ovarian syndrome, nonalcoholic fatty liver disease
Roux-en-Y gastric bypass1) compare to gastric banding2) risk factors3) what other surgery should you consider performing during the operation4) failure rate due to high carbohydrate snacking5) Leak: a) signs, b) MC cause, c) dx, d) rx6) Marginal ulcers a)how many get b) rx7) rx of stenosis
1) better weight loss2) marginal ulcers, leak, necrosis, B12 deficiency (intrinsic factor needs acidic environment to bind B12), iron-def anemia (bypasses duodenum where Fe absorbed), gallstones (from rapid weight loss)3) cholecystectomy if stones present.4) 10%5) a) inc RR and HR, abd pain, fever, inc WBC; b) ischemia; c) UGI; d)if early leak (not contained)-> re-op. if late leek (likely contained)-> perc drain, abx6) 10%. rx with PPI7) serial dilation
Roux en Y gastric bypass complications1) dilation of excluded stomach postopa) symptomsb) dxc) rx2) SBO rx3) Jejunoilial bypass pts- why don’t we do these operations anymore and what should you do if a pt has one
1) a) hiccoughs, large stomach bubbleb) AXR; c) G-tube2) surgical emergency in these pts 2/2 high risk of small bowel herniation, strangulation, infarction and necrosis. rx- surgical exploration3) associated with liver cirrhosis, kidney stones and osteoporosis (dec Ca). convert to roux-en-y gastric bypass
Postgastrectomy complications1) Dumping syndromea) when does it occurb) causec) describe the 2 phasesd) rx
1) a) after gastrectomy or vagotomy and pyloroplastyb) rapid entering of carbohydrates into small bowelc) phase 1: hyperosmotic load-> fluid shift into bowel (hypotension, diarrhea, dizziness)Phase 2: hypoglycemia from reactive inc in insulin and dec in glucose (rarely occurs)d) 90% resolve with medical rx and diet changes- small, low-fat, low-carb, high protein meals. no liquids with meals, no lying down after meals, octreotide-if need surgery can convert Billroth to roux-en-y or inc gastric reservoir (jejunal pouch) or inc emptying time (reversed jejunal loop)
Post Gastrectomy complications: Alkaline reflux gastritis1) sx2) dx3) rx including surgical option
1) postprandial epigastric pain associated with N/V. pain not relived with vomiting.2) evidence of bile reflux into stomach, histo evidence of gastritis3) PPI, chloestyramine, metoclopramide. surgical options (rarely needed) include conversion of billroth to roux-en-y gastrojejunostomy
Postgastrectomy complications: Chronic gastric Atony= Delayed gastric emptyinga) sxb) dxc) rx including surgical options
a) N/V, pain, early satietyb) gastric emptying studyc) metoclopramide (Reglan), prokinetics (erythromycin)Surgical option is near total gastrectomy with roux en-Y
Effect of small gastric remnant1) sx2) dx3) rx including surgical option
1) early satiety (actually want this for gastric bypass patients)2) EGD3) small meals or jejunal pouch construction
Post Gastrectomy complication: blind loop syndrome1) what surgeries do you get it with?2) symptoms3) cause4) dx5) rx
1) Billroth II or Roux-en-Y2) pain, steatorrhea (bacterial deconjugation of bile), B12 deficiency (bacteria use it up), malabsorption3) poor motility -> stasis in afferent limb-> bacterial overgrowth (E. Coli, GNRs)4) EGD of afferent limb with aspirate and culture for organsims5) tetracycline and flagyl, metoclopramide to improve motility. surgical option: reanastamosis with shorter (40-cm) afferent limb
Post Gastrectomy Complication: afferent-loop obstruction1) what surgeries do you get it with?2) symptoms3) cause and which limb is the afferent4) dx5) rx
1) Billroth II or Roux-en-Y2) RUQ pain, steatorrhea, nonbilious vomiting, pain relieved with bilious emesis3) caused by mechanichal obstruction of afferent limb (the one . risk factors include long afferent limb with billroth II or Roux-en-Y: the limb that carries the bile towards the anastamosis= stomach remnant limb or Y limb of roux en Y)4) CT scan5) balloon dilation may be possible. surgical options are reanastomosis with shorter (40cm) afferent limb to relieve obstruction.
Post Gastrectomy efferent-loop obstruction1) which limb is the efferent-limb2) sx3) dx4) rx
1) efferent= exit (limb from the gastrojejunostomy to the jejunojejunostomy anastomosis)2) N/V/abd pain3) UGI, EGD4) balloon dilation. or surgery to identify site of obstruction and relieve it
Post-vagotomy diarrhea1) mechanism2) rx
1) 2/2 non-conjucated bile salts in the colon-> osmotic diarrhea. Caused by sustained postprandial organized MMCs2)cholestyramine, octreotide. Or reverses interposition jejunal graft
1) treatment of duodenal stump blowout2) PEG complications
1) place lateral duodenostomy tube and drains2) PEG- insert into liver or colon
Liver1) Hepatic artery variants for a- Right hepatic arteryb- Left hepatic artery2) falciform ligament- where is it, what embryologic remnant does it carry3) ligamentum teres location4) what line separates R and L liver lobes
1) a- right hepatic artery off SMA (#1 variant) courses behind pancreas, posterolateral to CBDb-left hepatic artery off left gastric artery (~20%)- found in gastrohepatic ligament medially2) separates medial and lateral segments of the left lobe. attaches to anterior abdominal wall, extends to umbilicus and carries remnant of umbilical vein3) carries the obliterated umbilical vein to the undersurface of the liver, extends from the falciform ligament4) draw line from middle of gallbladder fossa to IVC (portal fissure or Cantlie’s line)
1) What is Glisson’s capsule?2) where is Bare area on liver that doesn’t have capsule?3) where does the portal triad enter the liver4) under which segments does the gallbladder lie
1) peritoneum that covers liver2) posterior-superior surface3 and 4) Segments IV and V
1) What are Kupffer cells2) What makes up the portal triad and where do they lie in relation to each other (ie- posterior, lateral, etc)? What do they come together into3) what is the Pringle maneuver and what type of bleeding doesn’t it stop4) Foramen of winslow is the entrance into what space? Define the anterior posterior inferior and superior boundaries
1) liver macrophages2) Common Bile duct (lateral), portal vein (posterior) and proper hepatic artery (medial) all come together in the hepatoduodenal ligament (porta hepatis)3) porta hepatis clamping. doesn’t stop hepatic vein bleeding4) entrance into lesser sac. -Anterior-Portal triad-Posterior- IVC-Inferior- duodenum-superior-liver
1) what 2 veins make up the portal vein2) how many portal veins are in the liver? how much (%) of blood flow does it provide to the liver?3) segments supplied by left vs right protal vein4) what is the arterial blood supply to the liver?5) where does the middle hepatic artery MC a branch of?6) what are most primary and secondary liver tumors supplied by?7)what are the hepatic veins and where do they drain?
1)superior mesenteric vein joins splenic vein (no valves) and inferior mesenteric vein enters splenic vein2) 2 in liver. provides 2/3 of hepatic blood flow3) Left- seg II, III, IV; Right- seg V, VI, VII, VIII4) right, left and middle hepatic arteries, follows the hepatic vein system below. 5) left hepatic artery6) hepatic artery7) left hepatic vein (seg II, III, superior IV), middle hep vein (seg V and inferior IV), right (VI, VII, VIII)
1) what does the middle hepatic vein branch off of?2) what does the accessory right hepatic vein drain3) where do the inferior phrenic veins drain4) caudate lobe arterial and venous supply
1) comes off left hepatic vein in 80% before going into IVC, other 20% goes directly into IVC2) medial aspect of right lobe directly to IVC3) directly into IVC4) receives separate right and left portal and arterial blood flow. drains directly into IVC via separate hepatic veins
1) where is alkaline phosphatase located2) where does nutrient uptake occur in the liver3) what is the usual energy source for the liver and how is it obtained4) where is glucose stored and in what form? what happens to excess glucose5) where is urea synthesized
1) canicular membrane2) sinusoidal membrane3) ketones4) it is converted to glycogen and stored in the liver. excess converted to fat5) liver
1) what transcription factors are not made in the liver2) what types of vitamins does the liver store3) what are the MC problems associated with hepatic resection4) which hepatocytes are most sensitive to ischemia5) how much of liver can you safely resect
1) vWF and VIII (made in endothelium)2) fat-soluble vitamins. B12 is the only water-soluble vitamin stored in the liver3) bleeding and bile leak4) central lobular (acinar zone III)5) 75%
Bilirubin1) breakdown product of? (chain of breakdown to it)2) what is it conjugated to in the liver and effect of conjugation3) where does breakdown of conjugated bilirubin occur? and what breaks it down?4) what happens to free bilirubin in the intestine?5) what turns urine dark like cocacola?
1) hemoglobin (Hgb-> heme-> biliverdin-> bilirubin)2) glucuronic acid (glucuronyl transferase)-> improves water solubility-> actively secreted into bile3) broken down in terminal ileum by bacteria4) reabsorbed, converted to urobilinogen and released into urine as urobilin (yellow color)5) excess urobilinogen
Bile1) what comprises bile?2) what are bile salts/acids made of?3) what are bile salts conjugated to?4) a) primary bile acids (salts)b) secondary bile acids (salts)5) what is main biliary phospholipid6) role of Bile
1) bile salts (85%), proteins, phospholipids (lecithin), cholesterol, and bilirubin2) cholesterol3) taurine or glycine (improves water solubility)4) a- cholic and chenodeoxycholicb-deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)5) lecithin6) solubilizes cholesterol and emulsifies fats in the intestine, forming micelles which enter enterocytes by fusing with membrane
Jaundice1) at what level of bili does it occur2) first place it is evidence3) maximum bilirubin is 30 unless patient has what?4) causes of elevated un-conjugated bili5) causes of elevated
1) >2.52) under tongue3) underlying renal disease, hemolysis or bile duct-hepatic vein fistula4) prehepatic causes (hemolysis, hepatic deficiencies of uptake or conjugation5) secretion defects into bile ducts, excretion defects into GI tract (stones, strictures, tumor
Hyperbilirubinemia Syndromes- what is the defect and have type of bili is high in the following:1) Gilbert’s disease2) Crigler-Najjar disease3) Physiologic jaundice of newborn4) Rotor’s syndrome5) Dubin-Johnson Syndrome
1) high unconjugated bili. Defect in glycuronyl transferase2) high unconjugated bili. inability to conjugate 2/2 severe deficiency of glucuronyl transferase (Life-threatening dz)3) high unconjugated bili. immature glucuronyl transferase4) high conjugated bili (deficiency in storage ability)5) high conjugated bili. Deficiency in secretion ability
Viral hepatitis1) which hepatitis viral agents can cause acute hepatitis2) which types can cause fulminant hepatic failure3) which types can cause chronic hepatitis and hepatoma (HCC)4) which type rarely has serious consequences5) which type is not an RNA virus6) which type is a cofactor for hepatitis B/worsens prognosis?7) which type causes fulminant hepatic failure in pregnancy8) which can have long incubation period and is MC viral cause for liver txpt9) FOr hep B- what Ab is elevated in first 6 months? then what takes over?10) what are the antibody profiles fora) pt with HBV vaccination, never infectedb) pt with h/o HBV infection, recovery and subsequent immunity
1) all2) Hep B, D, and E more common3) HBV and HCV and Hep D4) Hep A5) HBV (DNA)6) Hep D7) Hep E8) HCV9) Anti-HBcore-IgM. then IgG takes over10) a-Pt will have Anti-HBsurface-IgG onlyb- Anti-HBcore-IgG, Anti-HBsurface IgG. No HB surface antigens
Liver failure1) MCC2) best indicator of synthetic fnc in pt with cirrhosis3) mortality and rx of acute liver failure
1) cirrhosis (palpable liver, jaundice, ascites)2) prothrombin time (PT)3) 80% mortality. consider urgent liver txplt if King’s College criteria met
What are King’s College Criteria of Poor Prognostic Indicators for1) Acetaninophen-Induced ALF (acute liver failure)a-pHb-INRc-Creatinined-encephalopathy grade2) Non-Acetaminophen-Induced ALFa-INRb-or 3 of which other factors
1) a- Arterial pH6.5, Cr>3.4 mg/dL, grade III/IV encephalopathy2) a-INR>6.5 or and 3 of the following:b- age 40, drug toxicity or undetermined etiology, jaundice>7 days before encephalopathy, INR>3.5 bili>17mg/dL
Hepatic encephalopathy1) mechanism of liver failure as a cause2) other causes3) treatment4) what type of food should you limit5) role of abx6) role of Neomycin and rifaximine
1) lier can’t metabolize-> build up of ammonia, mercantanes and false neurotransmitters2) GI bleed, infection (SBP), electrolyte imbalance3) lactulose- cathartic that gets rid of bacteria in gut and acidifies colon (preventing NH3 uptake by converting it to ammonium). titrate to 2-3BM/day4) limit protein intake. Branched-chain amino acids are metabolized by skeletal muscle and may help5) only give if infectious source6) get rid of ammonia-producing bacteria from gut
Mechanism of cirrhosis
hepatocyte destruction-> fibrosis and scarring of liver-> increased hepatic pressure-> portal venous congestion-> lymphatic overload-> leaking of splanchnic and hepatic lymph into peritoneum-> ascites
Ascites treatment1) conservative treatment2) paracentesis for ascites- what should you replace with and ratio for replacement3) surgical treatment
1) water restriction 1.5-1L/day, decreased NaCl intake, diuretics (spironolactone counteracts hyperaldosteronism seen with liver failure)2) replace with albumin 1g for every 100cc removed3) TIPS
Sontaneous Bacterial Peritonitis1) when to use prophylactic abx to prevent2) what abx for ppx3) symptoms and lab findings4) MC pathogens5) risk factors6) treatment
1) if previous SBP or current UGI bleed2) norfloxacin3) fever, abd pain, PMNs> 250 in fluid, positive cultures4) E.Coli (#1), pneumococci, streptococci. MC monoorganism. if not, worry about bowel perf5) prior SBP, UGI bleed (Variceal hemorrhage), low-protein ascites6) 3rd gen cephalosporin. pt’s usually respond within 48 hours
Why is aldosterone elevated with liver failure
2/2 impaired hepatic metabolism and impaired GFR
Hepatorenal syndrome1) lab findings2) treatment
1) same lab findings as prerenal azotemia (progressive renal failure)2) no good therapy other than liver txplt. Stop diuretics, give volume.
what is asterixis
neuro change in liver failure, sign that liver failure is progressing
Postpartum liver failure with ascites1) cause2) dx3) rx
1) from hepatic vein thrombosis, has an infectious component2) SMA arteriogram with venous phase contrast3) heparin and abx
Esophageal varices1) treatment of bleed2) role of propranolol3) treatment of refractory variceal bleeding
1) banding and sclerotherapy (95% effective), Vasopressin (splanchnic artery constriction) and octreotide (decreased portal pressure by decreased blood flow) can be used to temporize2) can help prevent re-bleed. no role in acute bleed3) TIPS
Portal HTN1) causes of presinusoidal obstruction2) causes of sinusoidal obstruction3) causes of post-sinusoidal obstruction4) normal portal vein pressure5) what veins serve as collaterals bw the portal vein and the systemic venous system of the lower esophagus (azygous vein)
1) schistosomiasis, congential hepatic fibrosis, portal vein thrombosis (50% of portal HTN in children)2) cirrhosis3) Budd-CHiari syndrome (hepatic vein occlusive dz), constrictive pericarditis, CHF4) 12 mmHg5) coronary veins
TIPS 1) indications2) end-result3) mechanism of procedure4) complications
1) protracted bleeding, progression of coagulopathy, visceral hypoperfusion or refractory ascites2) allows anterograde flow3) catheter passed into hepatic vein via jugular vein and expandable metal stent placed from hepatic vein through the liver tissue into a major portal vein branch4) dev’t of encephalopathy
Plenorenal shunt1) when can you use it/indications2) contraindications3) what veins do you ligate4) risks and benefits
1) Child’s A Cirrhotics who present with just bleeding (rarely used anymore). Childs B and C must get TIPS.2) pts with refractory ascites (can worsen ascites)3) left adrenal, left gonadal, inferior mesenteric and coronary veins and pancreatic branches of splenic vein4) less risk of encephalopathy but worsens ascites
Child-Pugh Score in Liver failure1) what does it correlate with?2) components and how to determine class
1) mortality after open shunt placement. A=2% mortality; b=10% mortality with shunt, c= 50% mortality2) Albumin, Bilirubin, encephalopathy, ascites, INR (1-3 pts for each). A is 5-6 pts. B is 7-9 pts, C is 10+ pts
Portal HTN in kids1) MCC2) T/F: it is the MCC of massive hematemesis in children
1) extra-hepatic portal vein thrombosis2) true
Budd-Chiari syndrome1) what is occluded?2) symptoms3) dx4) rx
1) hepatic veins or IVC2) RUQ pain, hepatosplenomegaly, ascites, fulminant hepatic failure, muscle wasting and variceal bleeding.3) angiogram with venous phase, CT angio; liver bx shows sinusoidal dilatation, congestion and centrilobular congestion4) porta-caval sunt (needs to connect to IVC above obstruction
Splenic Vein thrombosis1) type of varices seen2) MCC3) tx
1) isolated gastric varices without elevation of pressure in the rest of the portal system2) pancreatitis3) if bleed-> do splenectomy
Liver Abscesses1) Amebica-where is primary infection and how does it get to liverb- signs of liver infection (sx and labs)c- risk factorsd-MC associated infectione- abscess culture resultsf-dxg-rx
1) a-colon (amebic colitis)-> reaches liver via portal veinb-F/C/RUQ pain/jaundice/increase in R lobe of liver, inc LFTs, inc WBCsc-travel to mexico, ETOH, fecal-oral transmissiond-Entamoeba histolytica (90% have infection)e- often sterile, only peripheral rim has protozoaf- CT characteristicsg- Flagyl. Aspirate only if refractory; surgery only if free rupture.
Liver abscesses2)Hydatid cysta-infectious agentb- who are carriers, who exposes humansc- when should you aspirate itd- CT findingse- other diagnostic testsf- when do you need pre-op ERCPg-treatment
1)a-Echinococcusb-sheep are carriers, dogs expose humansc- never! can leak and cause anaphylactic shockd- ectocyst (calcified) and endocyst (double-walled)e- Positive Casoni skin test, positive Echinococcus serologyf- jaundice, inc LFTs or cholangitis to check for communication with the biliary systemg- pre-op albendazole for 2 weeks then surgical removal (intra-op can inject cyst with alcohol to kill organisms and then aspirate out), need to remove all of cyst wall and don’t spill contents!
Liver Abscesses1) Schistosomiasisa) signs/sxb- site of primary infectionc- rx
1) a-maculopapular rash, inc eosinophils, can cause variceal bleeding, petechiae, ulcers and fine granulation tissue in sigmoid colon (primary infection site=b)c-Praziquantel and control of variceal bleeding
Liver abscesses1) Pyogenic abscessa- T/F: 2nd most common abscessb- sxc- #1 organism/caused- dxe- rx
1) False. MC (80% of all abscesses)b-F/C/weight loss, RUQ pain, inc LFTs, Inc WBCs, sepsis, inc in R lobec- E. Coli, MC 2/2 to contiguous infection from biliary tract. Can occur following bacteremia from diverticulitis or appendicitisd- aspiratione-CT-guided drainage and abx. Surgeical drainage if unstable and cont signs of sepsis
Liver Tumors1) Hepatic adnomasa- risk factorsb- sx/risksc- malignant or benignd- MC side of livere- sxf-dxg-rx
1) a- women, steroid use, OCPsb- 20% risk of significant bleed, 80% of symptomatic.c- Benign but Can become malignantd- Righte- pain, inc LFTs, dec BP (from rupture), palpable massf-no Kupffer cells in adenomas-> no uptake on sulfur colloid scan (cold)g- if asx- stop OCPs. if no regression, need surgeryif sx- tumore resection for bleeding and malignancy risk. embolization if multiple and unresectable
Liver TUmors2) Focal nodular hyperplasiaa- characteristic appearanceb- malignant or benignc-dxd-rx
2) a- central stellate scarb- benign, no malig potentialc- abdominal CT. Has kupffer cells so will take up sulfur colloid on liver scar. MRI/CT show hypervascular tumord- no resection. conservative
Liver TUmor1) MC benign hepatic tumor2) MC malignant hepatic tumor3) MC cancer world-wide
1) hemangioma2) mets 20:1 primary3) hepatocellular CA
Liver tumor1) Hemangimaa- MC sexb- dxc-rxd- rare complication
1) a- femalesb- MRI and CT show peripheral to central enhancementc- conservative unless symptomatic, then surgery + or - preop embolizationd- consumptive coagulopathy (Kasabach-Merritt syndrome) and CHF. usually seen in kids
Liver Tumors1) solitary cystsa- who gets them and whereb- rx
1) a- congenital, women, right lobe, walls have charactersitic thickened blue hughb- nothing
Hepatocellular CA (hepatoma)1) risk factors2) T/F: Pt’s with primary biliary cirrhosis and Wilson’s disease are at higher risk of getting HCC3) what 3 types have the best prognosis4) what hormone level do you check for5) 5-year survival with resection
1) #1 is Hep B, Hep C, ETOH, hemochromatosis, alpha-1-antitrypsin deficiency, primary sclerosing cholangitis, aflatoxins, hepatic adenoma, steroids, pesticides2) FALSE- they aren’t risk factors3) Clear cell, lymphocyte infiltrative and fibrolamellar types4) AFP, correlates with tumor size5) 30%
1) risk factors for Hepatic Sarcoma and prognosis2) tx of isolated colon CA mets to liver3) diff in vascularity of primary vs metastatic liver tumors
1) PVC, Thorotrast, arsenic-> rapidly fatal2) resect if can leave enough liver for the patient to survive. 35% 5-year survival rate after resection for cure.3) primary tumors are hypervascular. Mets are hypovascular
Biliary system1) triangle of Calot- borders and what is found inside2) arterial supply to hepatic and common bile duct and their location for consideration in ERCP3) where do cystic veins drain4) where are lymphatics located5) where do parasympathetic fibers come from?6) sympathetic fibers?
1) lateral- cystic duct, medial CBD, superior-liver. cystic artery (branches off R hepatic) is found here2) RIght hepatic (lateral) and retroduodenal branches of gastroduodenal artery (medial) at 9- and 3-o’clock position so make ERCP spincterotomy at 11-o’clock.3) right branch of portal vein4) right side of CBD5) left (anterior) trunk of vagus6) T7-T10 *splanchnic and celiac ganglions
Biliary system1) type of cells in gallbladder mucosa2) type of cells in gallbladder submucosa3) T/F: CBD and common hepatic duct have no peristalsis4) How does gallbladder fill?a- what contracts sphincterb-what relaxes it?
1) columnar epithelium2) none- no submucosa3) true4) contraction of sphincter of oddi at the ampulla of Vatera- morphineb- Glucagon
Normal size of1) Common bile duct b4 and after chole2) Gallbladder wall3) pancreatic duct
1) b4: <4mm
1) effect of cholecystectomy on total bile salt pools2) where are highest [ ] of CCK and secretin cells3) What are Rokitansky-Aschoff sinuses4) where are ducts of luschka
1) decreased total bile salt pools2) duodenum3) epithelial invaginations in the gallbladder wall, formed from increased gallbladder pressure4) in gallbladder fossa, can leak after cholecystectomy
1) Bile excretion:a- what increases excretionb- what decreases excretion2) What causes gallbladder contraction3) what are the essential functions of bile4) function of gallbladder
1) a- CCK, secretin, and vagal inputb- somatostatin, sympathetic stimulation2) CCK causes constant, steady, tonic contraction3) fat soluble vitamin absorption, essential fat absorption, bilirubin and cholesterol excretion4) forms concentrated bile by active resorption of NaCl and water
1) Where does active resorption of conjugated bile salts occur2) where does passive resorption of nonconjugated bile salts occur3) when is postprandial gallbladder emptying maximum4) what cells secrete bile5) what is responisble for the color of bile6) what is the breakdown product of conjugated bili in gut that gives stool brown color?7) what gives urine its yellow color?
1) terminal ileum (50%)2) small intestine (45%) and colon (5%)3) at 2 hours (80%)4) hepatocytes and bile canalicular cells5) 2/2 conjugated bili6) stercobilin7) urobilinogen (coverted form of resorbed conjugated bili breakdown products)
1) what is the rate limiting step in cholesterol synthesis and what is the chain of events for bile salt synthesis2) what % of gallstones are radiopaque3) what % of the population has stones
1) HMG CoA resuctase is RLS in cholesterol synth;HMG CoA-> (HMG CoA reductase)-> cholesterol-> 7-alpha-hydroxylase)-> bile salts (acids)2) 10%3) 10%
1) what type of stones are most common worldwide2) what is MC type of stone in US3)a- what are nonpigmented stones made ofb- causes of nonpigmented stonesc-where they are found4) 3 types of pigmented stones
1) pigmented stones2) nonpigmented (cholesterol) stones3) a-cholesterol; b- stasis, calcium nucleation and increased water reabsorpiton from GB, also caused by decreased lecithin and bile salts; c- almost exclusively in GB4) calcium bilirubinate stones, black stones (hemolysis, cirrhosis), brown stones (primary CBD stones)
Pigmented stones1) Calcium bilirubinate stones- cause2) Black stonesa-causeb- factors for develpmentc-where they formd- rx3) Brown stonesa- who gets them and whereb- cause (MC)c- what else should you check for in patients with these stonesd- rx
1) caused by solubilization of unconjugated bilirubin with precipitation2) a-hemolytic d/o, cirrhosis, ileal resection (loss of bile salts)b- increased bili load, decreased hepatic function, and bile stasis-> get calcium bilirubinate stonesc-gallbladderd-chole if sx3)a-Asians, primary CBD stones, formed in ductsb- Infection (E. Coli) produces beta-glucuronidase which deconjugates bili-> formation of calcium bilirubinatec-ampullary stenosis, duodenal diverticula, abnl sphincter of oddid- biliary drainage procedure (ie- sphincteroplasty)
Cholecystitis1) etiology2) what labs are elevated3) def of suppurative cholecystitis4) MC organsim5) US findings6) what can you get if US unclear to further dilineate7) HIDA results that indicate cholecystectomy after CCK-CS test
1) obstruction of cystic duct by a gallstone2) Alk phos and WBCs3) frank purulence in the gallbladder-> can be associated with sepsis and shock4) E. Coli (#1), Klebsiella, Enterococcus5) stones- hyperechoic focus, posterior shadowing, movement of focus with change in posn. acute cholecystitis- gallstones, gallbladder wall thickening >4mm, pericholecystic fluid6) HIDA- technetium taken up by liver and excreted in biliary tract. can use CCK choleschintigraphy with it to detect cholecystitis (shows contraction)7) gallbladder not seen (stone in cystic duct), takes >60 minutes to empty (chronic cholecysitis), EF
1) risk factors for gallstones2) best initial evaluation test for jaundice or RUQ pain3) Indications for immediate ERCP4) indications for pre-op ERCP5) what % of pts underging cholecystectomy will have a retained CBD stone
1) Age >40, female, obese, pregnant, rapid weight loss, vagotomy, TPN and ileal resection (pigmented stones)2) Ultrasound3) signs that CBD stone is present- jaundice, cholangitis, US shows stone in CBD.4) if any of the following are persistently high for >24hours- AST or ALT >200, bilirubin>4, or amylase or lipase >10005)
1) rx for cholecystitisa- in otherwise healthy ptb- in pt who are v ill and can’t tolerate surgery2) best rx for late common bile duct stone3) ERCP risks
1) a-cholecystectomyb- cholecystostomy tube2) ERCP with sphincterotomy3) bleeding, pancreatitis, perforation
1) causes of air in biliary system2) MC route for bacterial infection of bile3) highest incidence of positive bile cx occurs with what?
1) previous ERCP and sphincterotomy (MC), cholangitis or erosion of the biliary system into the duodenum (ie-gallstone ileus)2) dissemination from portal system (NOT retrograde through sphincter of oddi)3) postop strictures (usually E. coli, polymicrobial)
Acalculous cholecystis1) MC precipitating event2) primary pathology3) US findings4) HIDA findings5) rx
1) after severe burns, prolonged TPN, trauma or major surgery2) bile stasis (narcotics, fasting), leading to distention and ischemia. Also have inc viscosity 2/2 dehydration, ileus and transfusion3) sludge, GB wall thickening, and pericholecystic fluid4) positive HIDA5) cholecystectomy, perc drainage if too unstable
Emphysematous gallbladder disease1) MC infectious source2) what comorbidity increases risk3) sx4) rx
1) clostridia perfringens2) DM3) severe, rapid-onset abdominal pain, nausea, vomiting and sepsis. Can see gas in GB wall on XR4) emergent cholecystectomy or perc drainage if pt too unstable
Gallstone Ileus1) pathophysiology2) XR findings3) MC site of obstruction4) rx
1) fistula bw GB and duodenum that releases stone, causing small bowel obstruction. seen in elderly2) air in biliary system- pneumobilia3) terminal ileum4) remove stone through enterotomy proximal to obstruction. cholecystectomy and fistula resection if pt can tolerate (if old and frail, leave fistula)
CBD injury- intraop injury-type of repair based on size of injury
if <50% can likely do primary repair. if more will need hepaticojejunostomy or choledochojejunostomy
Workup of persistent N/V or jaundice following lap chole-management of bile leak
get US to look for fluid collection. -if present, may be bile leak-> perc drain into collection. If bilious, get ERCP-> sphincterotomy and stent if 2/2 cystic duct remnant leak, small injuries to hepatic or CBD or duct of luschka. larger lesions need hepaticojejunostomy or choledochojejunostomy-if not present and hepatic ducts dilated-> complete CBD transection-> initial manatement with PTC tube, then: -hepaticojejunostomy for lesions with early sx 7d
Management of sepsis following lap chole
fluid resusctation and stabilize. Get US to look for dilated intrahepatic ducts or fluid collections. May be 2/2 complete transection of the CBP and cholangitis
Management of anastamotic leak following transplantation or hepaticojejunostomy for bile leak
perc drainage of fluid collection followed by ERCP with temporary stent (leak will heal)
Bile duct strictures1) MC cause2) other causes3) sx4) Dx5) rx
1) Ischemia following lap chole2) chronic pancreatitis, gallbladder CA, bile duct CA3) sepsis, cholangitis, jaundice4) MRCP (magnetic resonance cholangiopancreatography) defines anatomy and looks for mass-> if CA not ruled out need ERCP with brush biopsies5) if 2/2 ischemia or chronic pancreatitis-> choledochojejunostomyif CA- appropriate wu for CA
hemobilia1) cause2) sx/presentation3) dx4) rx
1) MC with trauma or percutaneous instrumentation to liver (ie- PTC tube) -> fistula bw bile duct and hepatic arterial system (MC)2) UGI bleed, jaundice and RUQ pain3) angiogram4) angioembolization, operation if that fails
1) MC CA of biliary tract
1) gallbladder CA
Gallbladder adenocarcinoma1) MC site of mets2) porcelain gallbladder rx3) 1st nodes for spread4) 1st areas for direct spread5) sx6) rx7) prognosis
1) liver2) cholecystectomy bc 15% CA3) cystic duct nodes (right side)4) liver seg IV and V5) jaundice 1st (bile duct invasion with obstruction) then RUQ pain6) If no muscle involved-> cholecystectomyif in muscle but not beyond-> wedge resection of seg IVb and Vif beyond muscle but resectable-> formal resection of seg IVb and V*laparoscopic approach contraindicated for GB CA7) 5% overall 5-yr survival
Cholangiocarcinoma (bile duct CA)1) risk factors2) sx3) labs4) Dx5) rxa-c) 3 types/areas and rx for each6) prognosis
1) elderly, males, C. Sinensis infection, ulcerative colitis, choledochal cysts, primary sclerosing cholangitis, chronic bile duct infection2) early- painless jaundice; late- weight loss, pruritis3) inc bili and alk phos4) MRCP to define anatomy and look for mass5) consider surgery if no distant mets and tumor resectable.a- upper 1/3 (Klatskin tumor)- MC, worse prognosis, usually unresetable but can try lobectomy and stenting of c/l bile duct if localized to 1 lobeb- middle 1/3=> hepaticojejunostomyc- lower 1/3=> whipple6) 20% 5-yr survival
Choledochal cysts1) who gets them2) what % are extrahepatic3) CA risk4) symptoms5) cause6) MC type7) rx8) where are type IV cysts? what about type V?
1) asian, females2) 90%3) 15% cholangiocarcinoma risk4) older pts- episodic pain, fever, jaundice, cholangitis. infants- biliary atresia like sx5) abnormal reflux of pancreatic enzymes during uterine development6) type I- fusiform or saccular dilatation of extrahepatic ducts (v. dilated)7) cyst excision with hepatico jejunostomy and cholecystectomy usual8) Type IV- partially intrahepatic. V-totally intrahepatic. (need partial liver resection or TXP)
Primary Sclerosing Cholangitis1) who gets it2) associated diseases3) sx4) pathophysiology5) complications6) rx7) does it get better after colon rsxn in Crohn’s pts?
1) Men in 4th-5th decade2) ulcerative colitis, pancreatitis, DM3) jaundice, fatigue, pruritis (from bile acids), weight loss, RUQ pain4) get multiple strictures in hepatic ducts-> portal HTN and hepatic failure 2/2 progressive fibrosis of intrahepatic and extrahepatic ducts5) cirrhosis, cholangiocarcinoma6) liver TXP long term, PTC tube drainage, choledochojejunostomy or balloon dilatation of dominant strictures may relieve sx. Cholestyramine can decrease pruritis (dec bile acids). UDCA (ursodeoxycholic acid) can dec sx (dec bile acids) and improve liver enzymes.7) no, doesn’t get better
Primary Biliary Cirrhosis1) who gets it2) pathophysiology3) symptoms4) what lab test should you check for (Ab test)5) CA risk6) rx
1) women, medium-sized hepatic ducts2) cholestasis-> cirrhosis-> portal HTN3) jaundice, fatigue, pruritus, xanthomas4) antimicrobial Ab5) no CA risk6) liver TXP
Cholangitis1) cause2_ Charcot’s triad3) Reynold’s pentad4) MC organisms5) At what pressure does colovenous reflux occur and what is the result?6) Dx7) late complications of cholangitis8) rx
1) obstruction of bile duct: stone, indwelling tube, stricture, neoplasm, choledochal cysts, duodenal diverticula2) fever, RUQ pain, Jaundice3) Charcot’s + AMS and shock (suggests sepsis)4) E. Coli #1, and Klebsiella5) >200mmHg-> systemic bacteremia6) inc AST/ALT/bili/Alk Phos and WBCs. US-dilated CBD if 2/2 obstruction7) stricture and hepatic abscess. renal failure is #1 erious complication related to sepsis8) IVF and abx initially. Emergent ERCP with sphincterotomy and stone extraction. If this fails, place PTC tube to decompress the biliary system-if due to infected PTC tube, change the PTC tube.
Causes of shock following lap chole1) within 1st 24hrs2) after 1st 24hrs
1) hemorrhagic shock from clip that fell off cystic artery2) septic shock from accidental clip on CBD with subsequent cholangitis
adenomyomatosis1) what is it2) rx
1) thickened nodule of mucosa and muscle associated with Rokitansky-Aschoff sinus. Not premalignant. Doesn’t cause stones, can cause RUQ pain2) cholecystectomy
Granular cell myoblastoma1) benign or malignant2) sx3) rx
1) benign neurectoderm tumor of gallbladder2) can occur in biliary tract with signs of cholecystitis3) cholecystectomy
1) Cholesterolosis- what is it2) Gallbladder polyps- which are concerning for malignancy and rx3) effect of ceftriaxone on GB4) what is delta bilirubin’s t1/2
1) speckled cholesterol deposits on GB2) >1cm concerning for malignancy. Also more likely to be malignant in pts>60yo. rx-chole3) can cause GB sludging and cholestatic jaundice4) bound to albumin covalently, T1/2 18days, may take a while to clear after long-standing jaundice
1) Mirizzi Syndrome- what is it, causes and treatment2) indications for asymptomatic cholecystectomy
1) compression of the common hepatic duct by 1) a stone in the gallbladder infundibulum or 2) inflammation from GB or cystic duct extending to the contiguous hepatic duct-> hepatic duct stricture. rx- cholecystectomy. may need hepaticojejunostomy if stricture2) liver TXP or gastric bypass (if stones are present)
1) relation of superior mesenteric vein and superior mesenteric artery2) what is the kocher maneuver?3) where is the uncinate process of the pancreas4) where do the SMV and SMA lay in relation to the pancreas5) where does the portal vein run in relation to the pancreas
1) SMV is anterior to SMA2) Mobilization of the duodenum to expose head of the pancreas over IVC over Aorta3) rests on aorta, behind SMV4) behind the neck of the pancreas5)forms from the SMV and splenic vein behind the neck of the pancreas
Pancreatic Blood Supply1) to the head of pancreas2) to body of pancreas3) to tail of pancreas
1) superior (off GDA) and inferior (off SMA) pancreaticoduodenal arteries (anterior and posterior branches for each)2) great, inferior and caudal pancreatic arteries off of the splenic artery3) splenic, gastroepiploic and dorsal pancreatic arteries
Pancreas1) venous drainage to where?2) what nodes does the lymph drain to?3) what do pancreatic ductal cells secrete?4) what do pancreatic acinar cells secrete?
1) portal system2) celiac and SMA nodes3) secrete HCO3- solution (have carbonic anhydrase)4) secrete digestive enzymes
Exocrine function of the pancreas1) what enzymes are secreted2) what is the only pancreatic enzyme secreted in active form
1) amylase, lipase, trypsinogen, chymotrypsinogen, carboxypeptidase, HCO3-2) amylase- hydrolyzes alpha 1-4 linkages of glucose chains
Endocrine function of the pancreas1) what cells produce:a- glucagonb-insulinc-somatostatind- pancreatic polypeptidee- vasoactive intestinal peptide (VIP) and serotonin2) which cells receive the majority of blood supply related to size
1) a- Alpha cellsb- Beta cells (at center of islets)c- Delta cellsd- PP or F cellse- Islet cells2) islet cells, then goes to acinar cells
1) Enterokinasea- where is it releasedb- action2) action of Trypsin3) action of secretin (and where is it released)4) of CCK (and where is it released)5) of acetylcholine6) of somatostatin7) of glucagons
1) a- duodenumb- activates trypsinogen to trypsin2) activates other pancreatic enzymes including trypsinogen3) inc HCO3- mostly (duodenum)4) inc pancreatic enzymes mostly (duodenum)5) inc HCO- and enzymes6,7) inhibits exocrine fnc
Embryology of Pancreas1) Ventral pancreatic buda- what duct is it connected tob- path of migrationc- what parts of pancreas does it form2) Dorsal pancreatic buda- what parts of pancreas does it formb- what duct does it contain3) Duct of wirsung- what does it merge with4) Duct of santorini- what does it drain into
1) a- duct of wirsungb- migrates posteriorly to the right and clockwise to fuse with dorsal budc- uncinate and inferior portion of the head2) a- body, tail and superior aspect of the pancreatic headb- duct of Santorini3) merges with CBD before draining into duodenum4) small accessory pancreatic duct that drains directly into the duodenum
Annular pancreas1) embryologic abnormality2) appearance on XR3) symptoms4) associated syndrome5) treatment
1) forms from the ventral pancreatic bud from failure of clockwise rotation-> 2nd portion of duodenum trapped in pancreatic band2) double-bubble on AXR3) pancreatic obstruction- N/V, abd pain4) duodenojejunostomy or duodenoduodenostomy, possible sphincteroplasty (Don’t resect the pancreas!)
Pancreas Divisum1) embryologic abnormality2) sx3) Dx4) rx
1, 2) failed fusion of the pancreatic ducts-> can get pancreatitis from duct of Santorini (accessory duct) stenosis3) ERCP- minor papilla will show long and large duct of santorini; major papilla will show short duct of wirsung4) ERCP with sphincteroplasty. open sphincterotomy if that fails
Heterotopic pancreas1) MC location2) sx3) rx
1) in duodenum2) usually asx3) only if sx, resect
Pancreatitis1)causes2) mortality for a- pancreatitis; b- hemorrhagic pancreatitis3) Diagnostic workup required4) rx5) what pain medication to avoid and why
1) ETOH and gallstones (MC); others- ERCP, trauma, hyperlipidemia, hypercalcemia, viral infection, meds (azathiprine, furosemide, steroids, cimetidine, lamivudine)gallstones obstruct ampula-> impaired extrusion of zymogen granules and activation of degraded enzymes-> pancreatic autodigestionETOH-> auto-activation of enzymes while still in pancreas2) a-10%, b- 50%3) RUQ US to check for stones and CBD dilation, and abdominal CT to check for complications (necrotic pancreas doesn’t take up contrast)4) NPO, IVF, ERCP if retained CBD stone with sphincterotomy and stone extraction, chole once recovered on same admission- can give abx for stones, severe pancreatitis, failure to improve or suspected infection.5) Morphine- can contract sphincter of oddi and worsen attack
Signs of hemorrhagic Pancreatitis, describe:1) Grey Turner sign2) Cullen’s sign3) Fox’s sign
1) flank ecchymosis2) periumbilical ecchymosis3) inguinal ecchymosis
Pancreatic necrosis1) what % become necrotic2) what to do if sterile necrosis3) rx for infected necrosis4) rx of pancreatic abscesses5) rx if gas in necrotic pancreas
1) 15%2) leave it alone!3) if fever, sepsis, positive blood cx-> cx pancreatic fluid to diagnose. Rx- surgical debridement4) surgical debridement5) open debridement (infected necrosis or abscess)
Pancreatitis1) Leading cause of death2) when to operate 3) Most imp risk factor for necrotizing pancreatitis4) Cause of ARDS in pancreatitis5) Cause of Coagulopathy6) cause of Pancreatic fat necrosis7) what are other things that can cause mild inc in amylase and lipase
1) infection (usually GNR)2) if infection or abscess3) obesity4) related to release of phospholipases5) related to release of proteases6) related to release of phospholipases7) cholecystitis, perfed ulcer, sialoadenitis, small bowel obstruction and intestinal infarction
Pancreatic Pseudocyst1) MC in patients with what type of pancreatitis2) what should you worry about in a pt with cyst not associated with pancreatitis3) sx4) location (MC)5) rx
1) chronic pancreatitis2) r/o CA (mucinous cystadenocarcinoma)3) pain, fever, weight loss, bowel obstruction from compression4) head of pancreas (non-epithelialized sac= PSEUDO- cyst)5) most resolve spontaneously, esp if rx with expectent management for 3 months (allows pseudocyst to mature if cystogastrostomy required)- Surgery only for continued symptoms (cystogastrostomy, open or percutaneous)-or for growing pseudocyst (resection to r/o CA)
Pancreatic Pseudocyst1) complications2) rx of incidental cysts not associated with pancreatitis3) what type of cysts have extremely low malignancy risk and can be followed
1) infection of cyst, portal or splenic vein thrombosis2) resect 2/2 concern for intraductal papillary-mucinous neoplasms (IPMNs) or mucinous cystadenocarcinoma) unless cyst is purely serous and non-complex3) non-complex, purely serous cystadenomas
Pancreatic Fistulas1) rxa- medical managementb- what inc chance of spontaneous closurec- what if medical management fails
1) most close spontaenously (esp if low output <200cc/day) . allow drainage, NPO, TPN, octreotide-if failure to resolve with medical management can try ERCP, sphincterotomy and pancreatic stent placement (fistula will usually close, then remove stent)
Pancreatitis- Associated pleural effusion (or Ascites)1) cause2) rx3) dx
1) retroperitoneal leakage of pancreatic fluid from the pancreatic duct or pseudocyst (not a pancreatic-pleural fistula). 2) majority close on their own,. Do thoracentesis (or paracentesis) followed by conservative Rx (NPO, TPN and octreotide- follow pancreatic fistula pathway… ie ERCP if not resolving.3) elevated amylase in the fluid
Chronic pancreatitis1) pathology of cells2) MC causes3) MC sx4) Are endocrine or exocrine functions preserved?5) complication and rx6) Dx7) rx
1) irreversible parenchymal fibrosis2) ETOH (MC), then idiopathic3) pain, anorexia, weight loss, malabsorption, steatorrhea, recurrent acute pancreatitis4) endocrine function preserved (Islet cells preserved). Exocrine fnc decreased-> give pancrelipase5) can cause malabsorption of fat-soluble viatmins- rx c pancrelipase6) Abd CT- shrunken pancreas c calcificationsUS- pancreatic ducts >4mm, cysts, atrophy; or ERCP (very sensitive)
1) what does a chain of lake appearance of pancreatic duct suggest2) rx of chronic pancreatitis3) surgical indications
1) advanced disease (alt seg of dilation and stenosis in duct)2) supportive incl pain control and nutritional support (pancrelipase)3) pain interferes with quality of life, nutrition abnormalities, addiction to narcotics, failure to ro CA, biliary obstruction
Surgical options for chronic pancreatitis1) Puestow procedure- describe procedure and who it works for2) Distal pancreatic resection- when to do3) when to do a Whipple4) Beger-Frey- describe procedure and when to do it5) when to do bilateral thoracoscopic splanchnicectomy or celiac ganglionectomy6) rx if common bile duct stricture causing CBD dilation
1) pancreaticojejunostomy, for enlarged ducts>8mm. open along main pancreatic durct and drain into the jejunum2) if normal or small ducts and only distal portion of gland affected3) if only head is affected with small or normal ducts4) Duodenal preserving head “core out”- for normal or mall ducts with isolated pancreatic head enlargement5) for pain relief6)hepaticojejunostomy or choledochojejunostomy for pain, jaundice, progressive cirrhosis or cholangitis (make sure stricture isn’t CA)
Spleniv vein thrombosis1) MCC2) common complication3) rx
1) chronic pancreatitis2) can get bleeding from isolated gastric varices that form as collaterals3) splenectomy if isolated bleeding gastric varices
Pancreatic insufficiency1) causes2) which function is insufficeint, exocrine or endocrine3) sx4) dx5) rx
1) chronic pancreatitis or after total pancreatectomy (over 90% of function must be lost)2) exocrine function3) malabsorption, steatorrhea4) fecal fat testing5) high-carbohydrate, high-protein, low-fat diet. Pancreatic enzymes (Pancrease)
Workup for Jaundice1) 1st test2) test if CBD stones and no mass3) test if no CBD stones and no mass4) test if mass
1) Ultrasound2) ERCP-> allows for stone extraction3) MRCP4) MRCP
Pancreatic adenocarcinoma1) who gets it/risk factors2) sx3) prognosis4) serum marker for pancreatic CA5) MC mutation, what type of gene is it and function6) what type of spread occurs first
1) Males, 6th-7th decades of life2) weight loss (MC), jaundice, pain3) 20% 5-year survival with resection4) CA 19-95) p16 mutation (tumor suppressor)- binds cyclin complexes6) lymphatic
Pancreatic Adenocarcinoma1) MC location2) what mets indicate unresectable disease3) what type has most cures4) other more favorable prognosis CA of the pancreatic duct5) when to get a bx
1) ductal adenoCA (90%), head (70%)2) invasion of portal vein, SMV or retroperitoneum at time of diagnosis, mets to peritoneum, liver, or omentum or celiac of SMA noral system (nodal systems outside area of resection) 3) pts with pancreatic head disease4) papillary or mucinous cyst-adenocarcinoma5) only if pt appears to have mets to confirm dx. if resectable and no mets in pancreas, will take out regardless so don’t need bx.
1) best test for differentiating dilated ducts 2/2 chronic pancreatitis vs CA2) what sign might you see on CT
1) MRCP- signs of CA= duct with irregular narrowing, displacement, destruction, vessel involvement2) double duct sign for pancreatic head tumors (dilation of both the pancreatic duct and CBD
1) rx for uncresectable pancreatic CA2) complications from Whipple and rx3) rx of bleeding after whipple or other pancreatic surgery4) postop chemo-XRT after whipple for pancreatic CA- when to use it and what chemo agent5) what is non-met pancreatic CA prognosis related to
1) palliation with biliary stents of hepaticojejunostomy (for biliary obstruction) gastrojejunostomy (for duodenal obstruction) and celiac plexus ablation (for pain)2) delayed gastric emptying #1 (tx- metoclopramide), fistula (rx-conservative), leak (rx- drains and rx like fistula), marginal ulceration (rx- PPI)3) angio for embolization4) All post op patients should get it. Gemcitabine5) nodal invasion and ability to get a clear margin
Non-functional endocrine tumors1) what % are malignant2) course compared to pancreatic adenoCA3) rx4) MC site of mets
1) 90% malignant. Non-functional are 1/3 of pancreatic endocrine neoplasms2) more indolent and protracted course3) resect. mets preclude resection. 5-FU and streptozocin may be effective.4) liver
Functional Endocrine pancreatic tumors1) when to use octreotide2) MC tumors in pancreatic head3) 1st site of mets4) MC islet cell tumor of the pancreas5) MC islet cell tumor in MEN-1 patients
1) effective for insulinoma, glucagonoma, gastrinoma, VIPoma2) gastrinoma and somatostatinoma3) liver4) insulinoma5) gastrinoma (Zollinger-Ellison syndrome)
Insulinoma1) Whipple’s triad of symptoms2) malignant or benign?3) Dx4) rx
1) fasting hypoglycemia (0.4 after fasting; increased C peptide and proinsulin (if not elevated suspect Munchausen’s syndrome)4) enucleate if 2cm. If mets- 5-FU and streptozocin. Octreotide.
Gastrinoma1) % malignant? %multiple?2) % spontaneous?3) MC location4) sx5) dx6) rx7) what to do if you can’t find the tumor in the OR8) single-best test for localizing tumor
1) 50%, 50%2) 75%, 25% MEN-13) gastrinoma triangle: CBD, neck of pancreas and 3rd portion of duodenum4) refractory or complicated ulcer disease and diarrhea (improved with PPI)5) serum gastrin >200, 1,000s is diagnostic. Secretin stimulation test for ZES patients: increased gastrin (>200); normal patients: decreased gastrin6) enucleation if 2cm-if malignant disease-> excise suspicious nodes-Duodenal tumor- resect with primary closure, may need whipple if extensive-Debulking can improve sx7)if can’t find tumor-> duodenostomy and look inside duodenum (15% of microgastrinomas are there8) octreotide scan
Glucagonoma1) sx2) dx3) benign or malignant4) MC location5) how to treat skin rash
1) DM, stomatitis, dermatitis (rash- necrolytic migratory erythema), weight loss2) fasting glucagon level3) most are malignant4) distal pancreas5) zinc, amino acids or fatty acids
VIPoma (Verner-Morrison syndrome)1) sx2) dx3) benign or malignant4) MC location5) rx
1) very rare- cause DM, gallstones, steatorrhea, hypochlorhydria2) fasting somatostatin level3) most are malignant4) head of pancreas5) cholecystectomy with resection.
Spleen Anatomy and Physiology1) location of splenic vein in relation to splenic artery2) function of spleen3) % that is read pulp and fnca- what is pittingb-what is cullingc- what are howell-jolly bodiesd- what are heinz bodies4) % that is white pulp and fnc
1) splenic vein is posterior and inferior to the splenic artery2) antigen-processing center for macrophages and largest producer of IgM3) 85% red pulp- acts as filter for aged or damaged RBCsa-removal of abnormalities in RBC membraneb- removal of less deformable RBCsc- nuclear remnantsd- hemoglobin4) 15% white pulp- immunologic function, contains lymphocytes and macs. Major site of bacterial clearance that lacks preexisting Abs, site of removal of poorly opsonized bacteria, particles and cellular debris. Ag processing occurs with interaction bw macs and helper T cells
function of the following1) Tuftsin2) Properdin3) Hematopoeisis- where/when does it occur4) T/F: Spleen is a reservoir for platelets5) MC location of accessory spleen
1) an opsonin, facilitates phagocytosis and is produced in Spleen2) activates alternate complement pathway & produced in spleen3) occurs in spleen before birth and in conditions such as myloid dysplasia4) true5) 20% of ppl have it. MC at splenic hilum
1) indications for splenectomy2) MC non-traumatic condition requiring splenectomy3) vaccines needed before splenectomy (or after if emergent)
1) idiopathic thrombocytopenic purpura (ITP) far greater than for thrombotic thrombocytopenic purpura (TTP), trauma with significant bleed2) idiopathic thrombocytopenic purpura (ITP)3) Pneumovax, H. Flu, Meningococcus
Idiopathic thombocytopenic purpura (ITP)1) etiologies2) cause/pathophysiology3) sx4) T/F: spleen is abnormal in these patients5) who should you avoid splenectomy in?6) rx7) indications for splenectomy and how soon before surgery to give platelets
1) drugs, viruses, etc2) caused by anti-platelet Ab (IgG)-> bind platelets-> decreased platelets3) petechiae, gingival bleeding, bruising, soft tissue ecchymosis4) false- spleen is normal5) in children removes IgG production and source of phagocytosis. 80% cure rate. give platelets 1hour before surgery.
Thrombotic thrombocytopenic purpura (TTP)1) etiologies2) pathophysiology3) sx4) rx5) MCC of death
1)medical reactions, infections, inflammation, autoimmune disease2) loss of platelet inhibition-> thrombosis and infarction-> profound thombocytopenia3) purpura, fever, mental status changes, renal dysfunction, hematuria, hemolytic anemia4) 80% respond to medical therapy- plasmapherisis 1st. If doesn’t work, try immunosuppression. splenectomy rarely indicated5) intracerebral hemorrhage or acute renal failure
Post-Splenectomy Sepsis syndrome1) % risk after splenctomy and who has increased risk2) causative bugs3) pathophysiology4) how to prevent5) time frame for when it occurs
1) 0.1% risk. higher in children and pt with splenectomy for hemolytic disorders or malignancy2) S. pneumonia is #1; H. flu, N. meningitidis3) 2/2 to specific lac of immunity (IgM) to capsulated bacteria4) pre-splenectomy vaccinations, try to wait until at least 5yo for children to allow Ab formation and so child can get fully immunized. Children <10yo should be given ppx abx for 6months (controversial)5) MC within 2 years postop
Definition of hypersplenism: 3 required components
1) Decrease in circulating cell count of RBC, plt and or leukocytes2) normal compensatory hematopoietic responses present in bone marrow3) correction of cytopenia by splenectomy*with or without splenomegaly
Hemolytic Anemias1) types with membrane protein defects and the associated defecit2) types without membrane protein defects3) MC congenital hemolytic anemia requiring splenectomy
1) Spherocytosis- spectrin deficit-> deforms RBCs and leads to splenic sequestration (hypersplenism)Elliptocytosis- spectrin and protein 4.1 deficit2) Pyruvate kinase deficiency, G6PD deficiency, Warm-Ab-type acquired immune hemolytic anemia, sickle cell anemia, Betal thalassemia3) Spherocytosis
Hemolytic anemias1) Spherocytosisa- defectb-complications/sxc-rx2) G6PD deficiencya- precipitatorsb- rx3) rx of warm Ab- type acquired immune hemolytic anemia4) Sickle cella) pathophysiologyb-effect on spleen5) a- Beta Thalassemia (MC thalasemia)a- pathophysb- 2 typesc- sxd- rx and prognosis
1) a- spectrin deficit (membrane protein)b- pigmented stones, anemia, reticulocytosis, jaundice, splenomegalyc- splenectomy and cholecystectomy, curative. try to give immunizations first and do after age 5yo.2) a- infection, certain drugs (ie-sulfa), fava beansb- splenectomy usually not required. 3) splenectomy4) a-HgbA is replaced with HgbS-> spleen usually autoinfarcts and splenectomy not required5) a-2/2 persistent HgbFb- Major- both chains affected, minor- 1 chain, asxc- pallor, retarded body growth, head enlargementd) medical rx: blood transfusions and iron chelators (deferoxamine, deferiprone). Splenectomy if splenomegaly may dec hemolysis and sx. Most die in teens 2/2 hemolysis
Hodgkins disease1) difference between type A and type B2) What cell type do you see on pathology3) which type has best and worst prognosis4) MC type5) rx6) MCC of chylous ascites
1) type A= asx; B= sx (fever, night sweats, weight loss)-> unfavorable prognosis2) Reed-Sternberg cells3) Lymphocyte predominant= best prog; lymphocyte depleted= worst prog4) Nodular sclerosing5) chemo6) lymphoma
Describe Stage I-IV of Hodgkin’s disease
I= 1area or 2 contigous areas on same side of diaphragmII= 2 non-contiguous areas on same sideIII= involved on each side of diaphragmIV= liver, bone, lung or any other non-lymphoid tissue except spleen
Non-Hodgkin’s lymphoma1) prognosis related to Hodgkins2) MC type3) rx
1) worse prog2) 90% are B cell lymphomas3) chemo (generally systemic at time of dx)
Other conditions affecting spleen1) Rx of hairy cell leukemia2) causes of spontaneous splenic rupture3) Cause of splenosis4) cells seen in hyposplenism5) MCC of splenic artery or vein thrombosis
1) rarely need splenectomy2) mononucleosis, malaria, sepsis, sarcoid, leukemia, polycythemia vera3) trauma-> splenic implants4) howell-jolly bodies5) pancreatitis
Other conditions affecting spleen1) Post splenectomy changes in RBC, WBC, Platelets.2) post splenectomy rx of platelets >1 x10^63) #1 splenic tumor and benign splenic tumor4) rx of hemangioma5) #1 malignant splenic tumor
1) all increased2) ASA3) hemangioma4) if sx-> splenectomy5) non-hodgkin’s lymphoma
Other conditions affecting spleen1) rx of splenic cysts2) Sarcoidosis of spleena- labsb- rx3) what is felty’s syndrome and rx4) rx of splenic abscess5) rx of echinococcal splenic cyst
1) surgery if sx or >10cm2) a-anemia, dec plateletsb- splenectomy for symptomatic splenomegaly3) rheumatoid arthritis, hepatomegaly, splenomegaly. rx- splenectomy for symptomatic splenomegaly4) splenectomy bc bleeding risk with percutaneous drainage)5) spelenctomy
Post splenectomy blood smear1) erythrocyte products seen and what from2) platelet product seen3) leukocyte product seen
1) howell-Jolly bodies (nuclear fragments), Heinz bodies (Hgb deposits), Pappenheimer bodies (iron deposits), Target cells, Spur cells (acanthocytes2) transient thrombocytosis3) transient leukocytosis, persistent lymphocytosis, and monocytosis
Guidelines for prevention of postsplenic sepsis1) when to vaccinate2) who gets abx prophylaxis3) T/F: early abx treatment for signs of infection is one.4) what should all post splenectomy patients wear
1) 10-14 days prior at least for pneumococcal vaccine. if urgent, wait until POD14 or later. High risk pts get meningococal and H. flu vaccines as well (immunosuppresed and kids
