GI- upper GI Flashcards
Gastrin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) target cells
5) response to hormone
6) How does Omeprazole (PPIs) work
1) G cells in stomach ANTRUM
2) amino acids, vagal input (acetylcholine), calcium, ETOH, antral distention, pH>3.0
3) pH
Somatostatin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) target cells
4) response to hormone
5) How does Octreotide work and when to use
1) produced by D (somatostatin) cells in the stomach ANTRUM
2) acid in duodenum
3) many, it is the great inhibitor!
4) inhibits gastrin and HCl release; inhibits release of insulin, glucagon, secretin and motilin. Decreases pancreatic and biliary output
5) Somatostatin analogue. Can be used to decrease pancreatic fistula output
CCK
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) response to hormone
1) produced by I cells of the DUODENUM
2) amino acids and fatty acid chains
3) gallbladder contraction, relaxation of sphincter of Oddi, increases pancreatic enzyme secretion
Secretin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone
1) S cells of DUODENUM
2) fat, bile, pH4.0, gastrin
4) 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 peptide
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) response to hormone
1) produced by cells in gut and pancreas
2) fat, acetylcholine
3) increased intestinal secretion (water and electrolytes) and motility
Glucagon
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone
1) mainly alpha cells of pancreas
2) stimulated by decreased glucose, increased aa’s, acetylcholine
3) inhibited by increased glucose, increased insulin, somatostatin
4) glycogenolysis, gluconeogenesis, lipolysis, ketogenesis, decreased gastric acid secretion, decreased GI motility, relaxes sphincter of Oddi.
Insulin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone
1) beta cells of the pancreas
2) glucose, glucagons, CCK
3) somatostatin
4) cellular glucose uptake, promotes protein synthesis
pancreatic polypeptide
1) secreted by what cells?
2) secretion stimulated by?
3) response to hormone
1) islet cells in pancreas
2) food, vagal stimulation, other GI hormones
3) decreased pancreatic and gallbladder secretion
Motilin
1) where is it produced and by what cells?
2) what is secretion stimulated by
3) what inhibits secretion
4) response to hormone and what drug acts on it’s receptor to stimulate motility
1) intestinal cells of gut
2) duodenal acid, food, vagus input
3) somatostatin, secretin, pancreatic polypeptide, duodenal fat
4) increased intestinal motility (small bowel, phase III peristalsis)-> erythromycin acts on this receptor
1) Bombesin (Gastrin-releasing peptide) actions
2) Peptide YY- where is it released from and actions
3) what organ mediates anorexia
4) what is the order/timeframe of bowel recovery from surgery
1) increases intestinal motor activity, increases pancreatic enzyme secretion, increases gastric acid secretion
2) released from terminal ileum following fatty meal-> inhibits acid secretion and stomach contraction, inhibits gallbladder contraction and pancreatic secretion
3) hypothalamus
4) Small bowel fnc returns within 24 hours
stomach in 48 hours and large bowel in 3-5 days
Esophagus anatomy 1) layers of the esophageal wall 2) muscle in a- upper 1/3 of esophagus b- middle and lower 2/3 of esophagus 3) blood supply to cervical esophagus 4) blood supply to thoracic esophagus 5) blood supply to abdominal esophagus 6) venous drainage
1) mucosa (squamous epithelium), submucosa, and muscularis propria (longitudinal muscle layer); NO serosa
2) a- striated muscle; b-smooth muscle
3) inferior thyroid artery
4) vessels directly off the aorta
5) left gastric and inferior phrenic arteries
6) hemi-azygous and azygous veins in chest
Esophagus anatomy
1) where do lymphatics drain
2) where do the right and left vagus nerves travel and what do they supply
3) where does the thoracic duct travel and insert
4) MC site of esophageal perforation (usually with EGD)
5) cause of aspiration with brainstem stroke
1) upper 2/3 drain cephalad; lower 1/3 caudad
2) -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 tree
3) Travels from right to left at T4-5 as it ascends in the mediastinum. Inserts into left subclavian vein
4) cricopharyngeus muscle
5) failure of cricopharyngeus muscle to relax
Upper esophageal sphincter
1) distance from incisors
2) muscle
3) nerve innervation
4) normal EUS pressure at rest
5) normal EUS pressure with food bolus
1) 15cm
2) cricopharyngeus muscle (circular muscle, prevents air swallowing)
3) recurrent laryngeal nerve
4) 60 mmHg
5) 15mmHg
Lower esophageal sphincter
1) distance from incisors
2) what is the resting state
3) nl LES pressure at rest
4) nl LES pressure with food bolus
1) 40cm
2) normally contracted at resting state (prevents reflux). relaxation mediated by inhibitory neurons. Anatomic zone of high pressure but NOT an anatomic sphincter
3) 15mmHg
4) 0 mmHg
Anatomic areas of esophageal narrowing
at cricopharyngeus muscle, compression by the left mainstem bronchus at aortic arch, and diaphragm
Stages of swallowing
1) what initiates it
2) primary peristalsis- what initiates
3) secondary peristalsis- what initiates
4) Tertiary peristalsis
5) resting state of UES and LES bw meals
1) CNS
2) occurs with food bolus and swallow initiation
3) occurs with incomplete emptying and esophageal distention, propagating waves
4) 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 of
1) cervical esphagus
2) upper 2/3 thoracic esophagus
3) lower 1/3 thoracic esophagus
1) left
2) right (avoids aorta)
3) left (left-sided course in this region)
Hiccoughs
1) causes
2) what nerves are part of the reflex arc
1) gastric distention, temperature changes, ETOH, tobacco
2) vagus, phrenic, sympathetic chain T6-12
Esophageal dysfunction
1) primary causes
2) secondary causes
3) best test for heartburn
4) best test for dysphagia or odynophagia
5) best test for meat impaction
1) achalasia, diffuse esophageal spasm, nutcracker esophagus
2) GERD (most common), scleroderma
3) endoscopy (can visualize esophagitis)
4) barium swallow (better at picking up masses)
5) endoscopy (dx and rx)
Pharyngoesophageal disorders
1) In what part of swallowing is the prbm?
2) causes
3) T/F- liquids are worse than solids for these disorders
4) Plummer-Vinson syndrome- components of syndrome and rx
1) trouble in transferring food from mouth to esophagus
2) MC neuromuscular disease- myasthenia gravis, muscular dystrophy, stroke
3) True
4) upper esophageal web, Fe-deficient anemia
rx- dilation, Fe; screen for oral CA
Esophageal Diverticula 1) Zenker's Diverticulum a- what causes it b- is it true or false diverticulum c- location d-symptoms e-dx f-rx
1) a) increased pressure during swallowing 2/2 failure of cricopharyngeus to relax
b) false diverticulum located posteriorly
c- between the pharyngeal constrictors and cricopharyngeus
d- upper esophageal dysphagia, choking, halitosis
e- barium swallow studies, manometry, risk for perf with EGD and Zenker’s
f-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 Diverticulum
1) True or False diverticulum
2) cause
3) location
4) sx
5) rx
1) true diverticulum
2) inflammation, granulomatous disease, tumor
3) usually in mid-esophagus and lies lateral
4) regurgitation of undigested food, dysphagia
5) excision and primary closure if symptomatic, may need palliative therapy (ie- XRT) if due to invasive CA. if asx, leave alone
Esophageal Epiphrenic diverticulum
1) what disorders are associated
2) location
3) sx
4) dx
5) rx
1) esophageal motility disorders (ie-achalasia)
2) in distal 10cm of esophagus
3) most are asx. can have dysphagea and regurgitation
4) esophagram and esophageal manometry
5) rx- diverticulectomy and esophageal myotomy on the side opposite the diverticulum if sx
Achalasia
1) sx
2) cause/pathophys
3) manometry findings
4) barium swallow findings
5) rx
6) what infection can produce similar symptoms
1) dysphagia, regurg, weight loss, respiratory symptoms
2) failure of LES to relax and lack of peristalsis after food bolus 2/2 neuronal degeneration in muscle wall
3) Increased LES pressure, incomplete LES relaxation. NO peristalsis
4) birds beak. tortuous dilated esophagus and epiphrenic diverticula
5) 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 funduplication
6) T. cruzi parasite
Diffuse esophageal Spasm
1) sx
2) manometry findings
3) rx
1) Chest Pain!, dysphagia, psychiatric history
2) strong non-peristaltic unorganized contractions; LES relaxes normally
3) Ca-channel blockers, nitrates. Heller Myotomy (myotomy of upper and lower esophagus) if meds fail but less effective than for acholasia
Nutcracker esophagus
1) sx
2) Manometry findings
3) rx
1) Chest Pain!, dysphagia
2) high-amplitude peristaltic contractions; LES relaxes normally
3) Ca-channel blocker, nitrates. Heller myotomy if those fail of upper and lower esophagus, but less effective than for acholasia
Scleroderma leading to dysphagea
1) pathophysiology
2) rx
1) fibrous replacement of esophageal smooth muscle->dysphagia and loss of LES tone with MASSIVE REFLUX and STRICTURES
2) esophagectomy usual if severe
GERD
1) what is normal anatomic protection from GERD
2) pathophys of GERD
3) sx
4) empiric rx
5) diagnostic studies
6) surgical indications
7) Nissen
a- steps of operation
b-what is the paraesophageal membrane and extension of
c- key maneuver for wrap is identification of?
d-complications
8) approach for Belsey procedure
9) Collis gastroplasty- when to use it and how it is done
1) need LES competence, normal esophageal body, normal gastric reservoir
2) increased acid exposure to esophagus from loss of gastroesophageal barrier
3) heartburn sx 30-60min after meal, worse lying down, asthma symptoms (cough), choking, aspiration
4) 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 Hernia
1) Describe type I-IV
2) which type usually needs repair 2/2 high risk of incarceration
3) how to repair
4) Hernia associated with Schatzki’s ring and treatment
1) Type I- sliding hernia from dilation of hiatus (MC); often associated with GERD
Type II- paraesophageal. hole in diaphragm beside esophagus, normal GE jnction. sx- CP, early satiety, dysphageia
Type III- combined I and II
Type IV- stomach in chest + another organ (colon/spleen)
2) Type II paraesophageal
3) Nissen + resect hernia
4) 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 Esophagus
1) cellular change that occurs
2) cause
3) how much does its presence increase CA risk
4) what is indication for esophagectomy
5) treatment and followup
1) squamous metaplasia to columnar epithelium
2) long-standing exposure to gastric reflux
3) increases cancer risk by 50 times (adenocarcinoma)
4) Severe Barret;s dysplasia is indication for esophagectomy
5) 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 Cancer
1) T/F: esophageal tumors are almost always malignant but with late invasion of nodes
2) How does it spread
3) risk factors
4) diagnosis
5) best test for determining resectability and what factors prevent resection
6) MC type of cancer overall
- where is adenoCA usually located and where does it met
- what about squamous cell cancer
7) MC benign esophageal tumor
1) False, almost always malignant with early nodal invasion
2) submucosal lymphatic spread
3) ETOH, smoking, achalasia, caustic injury, nitrosamines
4) 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 MC
7) Leiomyoma
Esophageal CA treatment
1) role of pre-op Chemo-XRT
2) What Chemo agents are used
3) Esophagectomy
a-mortality and cure rates
b- what is primary blood supply to stomach after replacing esophagus
c-Describe the diff bw the Transhiatal approach, Ivor Lewis and 3-Hole esophagectomy techniques
d-what additional procedure do you need with all of the above
4) when is colonic interposition a good choice and what blood supply does it depend on
5) what is needed after esophagectomy to r/o leak and when to do it
6) Rx of postop strictures
7) Malignant fistulas- how to rx and prognosis
1) can downstage tumors and make resectable
2) 5-FU and Cisplatin (for node + disease or use pre-op to shrink tumors)
3) a-5% mortality from surgery. 20% cure rate
b-Right gastroepiploic artery (have to divide the left gastric and short gastrics
c-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 incisions
d- pyloromyotomy
4)choice in young pts when you want to preserve gastric function. need 3 anastamoses. blood supply depends on colon marginal vessels
5) contrast study on POD7
6) dilate
7) can palliate with stent, most die within 3 mo from aspiration
Leiomyoma 1) where is it located 2) dx 3) Biopsy technique 4) rx Esophageal polyps 5) how common 6) location 7) 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 difficult
4) rx if >5cm or symptomatic with excision (enucleation) via thoracotomy
5) 2nd MC benign lesion after leiomyoma
6) usually cervical esophagus
7) if small- resect with endoscopy; if larger-cervical incision
Caustic esophageal injury
1) role of NG tube, induced vomiting and drinking water to flush it out in treatment
2) Diff in necrosis from alkali and acid injury and which is worse/most likely to cause CA
3) How to determine severity/follow injury
4) Treatment if
a- 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 drink
2)Alkali-> deep liquifaction necrosis (Worse injury and more likely to cause CA). Ie-Drano
Acid-> coagulation necrosis, mostly gastric injury
3) Do endoscopy to assess lesion except if suspected perforation. Do NOT go past a site of severe injury. Follow with serial exams and plain films
4) 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 injury
d-esophagectomy (NOT repaired 2/2 extensive damage)
Esophageal Perforation 1) MCC 2) MC location 3) sx 4) Dx 5) Criteria for nonsurgical management and what does conservative therapy consist of 6) Repair of Non-contained perforations a- if diagnosed in
1) endoscopy
2) at cricopharyngeaus muscle in cervical esoph
3) dysphagia, tachycardia, pain
4) CXR initially for free air. Then Gastrografin swallow followed by barrium swallow
5) contained perforation by contrast. self-draining. no systemic effects
6) a- primary repair with drains via longitudinal myotomy to see full extent of injury. Consider intercostal muscle flaps to cover repair
b- 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 syndrome
1) classic presentation
2) MC site of perforation
3) what is Hartmann’s sign
4) Dx
5) Tx
6) prognosis
1) forceful vomiting then chest pain.
2) in Left lateral wall of esophagus, 3-5cm above GE junction
3) mediastinal crunching on auscultation
4) Gastrografin swallow
5) same as for esophageal perforation
6) highest mortality of all perforations- survival improves with early dx and rx
Stomach 1) Stomach transit time 2) where does peristalsis occur 3) what nerves sense gastroduodenal pain 4) Blood supply and branches a- branches of celiac trunk b- supply to greater curvature c-supply to lesser curvature d- supply to pylorus
1) 3-4 hours
2) distally in antrum only
3) afferent sympathetic fibers of T5-10
4) a- splenic (left gastroepiploic and short gastric are branches, Common hepatic (gastroduodenal and Right gastric are branches) and Left gastric
b- right (branch of gastroduodenal) and left gastroepiploics and short gastrics
c- right and left gastrics
d-gastroduodenal artery
Stomach
1) what cells line mucosa
2) what do cardia glands secrete
3) what do chief cells release and role in digestion
4) what do parietal cells release
5) what stimulates H+ release
6) inhibitors of parietal cells
7) role of intrinsic factor
1) simple columnar epithelium
2) mucus
3) pepsinogen (1st enzyme in proteolysis)
4) H+ and intrinsic factor
5) Acetylcholine (Vagus nerve), gastrin (from G cells in antrum), and histamine (from mast cells)
6) somatostatin, prostaglandins (PGE1), secretin, CCK
7) binds B12 and complex is reabsorbed in the terminal ileum
H+ release- describe the pathway leading to release for
1) Acetylcholine
2) Gastrin
3) Histamine
4) final common pathway
5) 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+ release
3) activates adenylate cyclase-> cAMP-> protein Kinase A-> H+ release
4) Phosphorylase kinase and Protein Kinase A phosphorylate H+/K+ ATPase channels to increase H+ secretion and K+ absorption
5) block H+/K+ ATPase channels
Stomach
1) Antrum and pylorus glands
a- name the secreting cells found here and what they release
b- name the 2 other types of secreting glands here and their function
2) what inhibits G-cells
3) what stimulates G-cells
4) where are Brunner’s glands and what do they secrete
5) 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 release
b- Mucus and HCO3- secreting glands- protect stomach from acid
2) H+ in duodenum
3) amino acids, acetylcholine
4) In duodenum, secrete alkaline mucus
5) with antral and duodenal acidification
Stomach
1) causes of rapid gastric emptying
2) causes of delayed gastric emptying
3) What are Trichobezoars made of and Tx
4) what are Phytobezoars made of and Tx
5) What is a Dieulafoy’s ulcer
6) what is Menetrier’s disease
1) previous surgery (#1), ulcers
2) diabetes, opiates, anticholinergics, hypothyroidism
3) made of hair. hard to pull out. Rx- EGD generally inadequate so likely need gastrostomy and removal
4) made of fiber (seen in DM with poor gastric emptying). rx- enzymes, EGD, diet changes
5) vascular malformation (can bleed)
6) mucous cell hyperplasia (inc rugal folds)
Gastric Volvulus
1) what hernia is it associated with
2) type of volvulus
3) rx
1) type II (paraesophageal) hernia
2) usually organoaxial volvulus
3) reduction and Nissen
Mallory-Weiss Tear
1) cause and presentation
2) Dx/rx (and MC location)
1) 2/2 forceful vomiting-> hematemesis-> bleeding stops spontaneously
2) EGD with hemo-clips. tear is usually on lesser curvature, near GE jnc. If continued bleeding may need gastrostomy and oversewing of the vessel
Vagotomies
1) Effect of Truncal and Proximal Vagotomies on gastric emptying of solids and liquids
2) what about if you add a pyloroplasty to truncal vagotomy
3) Other effects of truncal vagotomy
a- gastric effects
b-nongastric effects
4) MC problem after vagotomy and cause
1) Both-> increase liquid emptying (vagally-mediated receptive relaxation is removed-> increased gastric pressure-> inc liquid emptying
For 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 solids
2) then you will have increased solid emptying
3) a- decreases acid output by 90%, inc gastrin, gastrin cell hyperplasia
b- decreases exocrine pancreas fnc (digestive), dec postprandial bile flow, inc gallbladder volumes, dec release of vagally-mediated hormones
4) diarrhea (40% get) 2/2 sustained MMCs (migrating motor complexes) that force bile acids into the colon
Upper GI bleed
1) risk factors
2) Dx/Rx
3) what test to get if slow bleeding and hard to localize
4) biggest risk factor for rebleed at time of EGD
5) highest risk factor for mortality with non-variceal UGI bleed
6) 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 vomiting
2) EGD, potential rx with hemo-clips, epi-injection or cautery. If ulcer get bx for H. Pylori-> rx with omeprazole and abx
3) tagged RBC scan
4) #1- spurtung blood vessel (60% chance), #2 visible blood vessel (40% chance), #3 diffuse oozing (30% chance)
5) continued or re-bleeding
6) MC esophageal varices. Do EGD with variceal bands or sclerotherapy. TIPS if that fails
Duodenal ulcers
1) T/F: MC peptic ulcer
2) what sex is it MC in
3) MC location- which ulcers perforate and which bleed (from what artery)
4) sx
5) dx
6) rx
7) 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 artery
4) epigastric pain radiating to back, abates with eating but recurs 30min later
5) EGD
6) PPI, triple therapy for H. pylori
7) Omeprazole, clarithromycin and amoxicillin. +/- Bismuth salts
Duodenal Ulcers
1) what is Zollinger-Ellison syndrome components
2) Surgical indications for rx
3) 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 gastrinoma
2) 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% mortality
c) Truncal vagotomy and antrectomy-1-2% ulcer recurrence (lowest rate), 2% mortality
RECONSTRUCTION: 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- complications
1) MC complication
2) what constitutes major bleeding
3) Rx of duodenal bleed
4) rx of duodenal obstruction 2/2 ulcer
5) rx of perforation
6) Intractability with escalating doses of PPI- next step
1) bleed
2) >6units in 24 hours or pt remains hypotensive despite transfusion
3) 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 surgery
4) PPI and serial dilation 1st. If fails-> antrectomy and truncal vagotomy (best), also get bx to r/o CA
5) Graham patch (omentum over perf) + acid-reducing surgery if pt has been on PPI
6) >3mo PPI without relief based on EGD mucosal findings (not sx)-> acid reducing therapy
GASTRIC ULCERS
1) risk factors
2) MC location
3) T/F: hemorrhage is associated with higher mortality than with duodenal ulcers
4) Best test for H. Pylori
5) describe the location and whether it is due to high acid secretion vs. decreased mucosal protection for Type I-V peptic ulcers
6) surgical treatment if indicated
1) older male, tobacco, ETOH, NSAIDs, H. pylori, uremia, stress (burns, sepsis and trauma), steroids, chemotherapy
2) 80% on lesser curvature of the stomach
3) true
4) biopsy with histo examination from antrum. CLO test (rapid urease test)- detects urease released from H. Pylori
5) 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 secretion
type IV- lesser curve, high along cardia. decreased mucosal protection.
Type V- ulcer 2/2 NSAIDS
6) 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 gastritis 1) timeframe for occurance 2) rx Chronic gastritis 3) location of Type A and B 4) which type is associated with pernicious anemia and autoimmune disease 5) which type is associated with H. pylori 6) rx
1) 3-10d after event, lesions appear in fundus first
2) PPI
3) Type A is fundus, Type B is antral
4) type A
5) Type B
6) PPI
Gastric CA
1) MC location
2) sx
3) risk factors
4) risk of CA with adenomatous polyps and rx
5) what is krukenberg tumor
6) what is Virchow’s nodes
1) antrum has 40%
2) pain unrelieved by eating, weight loss
3) adenomatous polyps, tobacco, previous gastric operations, intestinal metaplasia, atrophic gastritis, pernicious anemia, type A blood, nitrosamines
4) 15% risk. Tx- endoscopic resection
5) mets to ovaries
6) mets to supraclavicular node
Gastric CA
1) Intestinal-type gastric CA- who gets it and surgical rx
2) diffuse gastric cancer (linitis plastica)-
a- who is at risk
b- spread
c-prognosis compared to intestinal-type gastric CA
d- surgical rx
3) use of chemo and what drugs
4) what is c/i for resection
5) 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 US
b- diffuse lymphatic invasion, no glands
c- less favorable prognosis (25% 5-yr survival)
d- total gastrectomy bc of diffuse nature
3) poor response but can try 5-fu, doxorubicin, mitomycin C
4) metastatic dz outside of area of resection
5) if obstructed-> stent proximal lesions, bypass distal lesions with gastrojejunostomy
if low/moderate bleeding/pain-> XRT
if above fail can consider palliative gastrectomy
Gastrointestinal Stromal Tumors (GIST)
1) benign or malignant?
2) US findings
3) Dx- what stain?
4) indications of malignancy
5) rx
1) MC benign gastric neoplasm, although can be malignant
2) hypoechoic with smooth edges
3) bx- C-Kit positive
4) malignant if >5cm or >5mitoses/50HPF
5) 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 by
2) rx
3) MC location
1) H. pylori infection, usually regress after rx
2) H. pylori triple therapy (clarithromycin, amoxicillin and PPI) and surveillance. If doesn’t regress, do XRT
3) stomach MC location
Gastric Lymphomas
1) MC type
2) Dx
3) rx
4) when is surgery indicated
5) overall 5-yr survival
1) non-Hodgkin’s lymphoma (B cell). Stomach is MC location for extranodal lymphoma
2) EGD with bx
3) chemo and XRT.
4) surgery for complications, possibly indicated for stage I disease (tumor confined to stomach mucosa) and then only partial resection is indicated
5) 50%
Morbid Obesity
1) what 4 criteria must be met for bariatric surgery
2) bariatric surgery operative mortality
3) 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 bypass
1) compare to gastric banding
2) risk factors
3) what other surgery should you consider performing during the operation
4) failure rate due to high carbohydrate snacking
5) Leak: a) signs, b) MC cause, c) dx, d) rx
6) Marginal ulcers a)how many get b) rx
7) rx of stenosis
1) better weight loss
2) 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, abx
6) 10%. rx with PPI
7) serial dilation
Roux en Y gastric bypass complications
1) dilation of excluded stomach postop
a) symptoms
b) dx
c) rx
2) SBO rx
3) 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 bubble
b) AXR; c) G-tube
2) surgical emergency in these pts 2/2 high risk of small bowel herniation, strangulation, infarction and necrosis. rx- surgical exploration
3) associated with liver cirrhosis, kidney stones and osteoporosis (dec Ca). convert to roux-en-y gastric bypass
Postgastrectomy complications
1) Dumping syndrome
a) when does it occur
b) cause
c) describe the 2 phases
d) rx
1) a) after gastrectomy or vagotomy and pyloroplasty
b) rapid entering of carbohydrates into small bowel
c) 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 gastritis
1) sx
2) dx
3) 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 gastritis
3) PPI, chloestyramine, metoclopramide. surgical options (rarely needed) include conversion of billroth to roux-en-y gastrojejunostomy
Postgastrectomy complications: Chronic gastric Atony= Delayed gastric emptying
a) sx
b) dx
c) rx including surgical options
a) N/V, pain, early satiety
b) gastric emptying study
c) metoclopramide (Reglan), prokinetics (erythromycin)
Surgical option is near total gastrectomy with roux en-Y
Effect of small gastric remnant
1) sx
2) dx
3) rx including surgical option
1) early satiety (actually want this for gastric bypass patients)
2) EGD
3) small meals or jejunal pouch construction
Post Gastrectomy complication: blind loop syndrome
1) what surgeries do you get it with?
2) symptoms
3) cause
4) dx
5) rx
1) Billroth II or Roux-en-Y
2) pain, steatorrhea (bacterial deconjugation of bile), B12 deficiency (bacteria use it up), malabsorption
3) poor motility -> stasis in afferent limb-> bacterial overgrowth (E. Coli, GNRs)
4) EGD of afferent limb with aspirate and culture for organsims
5) tetracycline and flagyl, metoclopramide to improve motility. surgical option: reanastamosis with shorter (40-cm) afferent limb
Post Gastrectomy Complication: afferent-loop obstruction
1) what surgeries do you get it with?
2) symptoms
3) cause and which limb is the afferent
4) dx
5) rx
1) Billroth II or Roux-en-Y
2) RUQ pain, steatorrhea, nonbilious vomiting, pain relieved with bilious emesis
3) 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 scan
5) balloon dilation may be possible. surgical options are reanastomosis with shorter (40cm) afferent limb to relieve obstruction.
Post Gastrectomy efferent-loop obstruction
1) which limb is the efferent-limb
2) sx
3) dx
4) rx
1) efferent= exit (limb from the gastrojejunostomy to the jejunojejunostomy anastomosis)
2) N/V/abd pain
3) UGI, EGD
4) balloon dilation. or surgery to identify site of obstruction and relieve it
Post-vagotomy diarrhea
1) mechanism
2) rx
1) 2/2 non-conjucated bile salts in the colon-> osmotic diarrhea. Caused by sustained postprandial organized MMCs
2) cholestyramine, octreotide. Or reverses interposition jejunal graft
1) treatment of duodenal stump blowout
2) PEG complications
1) place lateral duodenostomy tube and drains
2) PEG- insert into liver or colon
Liver
1) Hepatic artery variants for
a- Right hepatic artery
b- Left hepatic artery
2) falciform ligament- where is it, what embryologic remnant does it carry
3) ligamentum teres location
4) what line separates R and L liver lobes
1) a- right hepatic artery off SMA (#1 variant) courses behind pancreas, posterolateral to CBD
b-left hepatic artery off left gastric artery (~20%)- found in gastrohepatic ligament medially
2) separates medial and lateral segments of the left lobe. attaches to anterior abdominal wall, extends to umbilicus and carries remnant of umbilical vein
3) carries the obliterated umbilical vein to the undersurface of the liver, extends from the falciform ligament
4) 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 liver
4) under which segments does the gallbladder lie
1) peritoneum that covers liver
2) posterior-superior surface
3 and 4) Segments IV and V
1) What are Kupffer cells
2) 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 into
3) what is the Pringle maneuver and what type of bleeding doesn’t it stop
4) Foramen of winslow is the entrance into what space? Define the anterior posterior inferior and superior boundaries
1) liver macrophages
2) 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 bleeding
4) entrance into lesser sac.
- Anterior-Portal triad
- Posterior- IVC
- Inferior- duodenum
- superior-liver
1) what 2 veins make up the portal vein
2) 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 vein
4) 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 vein
2) 2 in liver. provides 2/3 of hepatic blood flow
3) Left- seg II, III, IV; Right- seg V, VI, VII, VIII
4) right, left and middle hepatic arteries, follows the hepatic vein system below.
5) left hepatic artery
6) hepatic artery
7) 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 drain
3) where do the inferior phrenic veins drain
4) caudate lobe arterial and venous supply
1) comes off left hepatic vein in 80% before going into IVC, other 20% goes directly into IVC
2) medial aspect of right lobe directly to IVC
3) directly into IVC
4) receives separate right and left portal and arterial blood flow. drains directly into IVC via separate hepatic veins
1) where is alkaline phosphatase located
2) where does nutrient uptake occur in the liver
3) what is the usual energy source for the liver and how is it obtained
4) where is glucose stored and in what form? what happens to excess glucose
5) where is urea synthesized
1) canicular membrane
2) sinusoidal membrane
3) ketones
4) it is converted to glycogen and stored in the liver. excess converted to fat
5) liver
1) what transcription factors are not made in the liver
2) what types of vitamins does the liver store
3) what are the MC problems associated with hepatic resection
4) which hepatocytes are most sensitive to ischemia
5) 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 liver
3) bleeding and bile leak
4) central lobular (acinar zone III)
5) 75%
Bilirubin
1) breakdown product of? (chain of breakdown to it)
2) what is it conjugated to in the liver and effect of conjugation
3) 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 bile
3) broken down in terminal ileum by bacteria
4) reabsorbed, converted to urobilinogen and released into urine as urobilin (yellow color)
5) excess urobilinogen
Bile
1) 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 phospholipid
6) role of Bile
1) bile salts (85%), proteins, phospholipids (lecithin), cholesterol, and bilirubin
2) cholesterol
3) taurine or glycine (improves water solubility)
4) a- cholic and chenodeoxycholic
b-deoxycholic and lithocholic (dehydroxylated primary bile acids by bacteria in gut)
5) lecithin
6) solubilizes cholesterol and emulsifies fats in the intestine, forming micelles which enter enterocytes by fusing with membrane
