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Surgery Review 7
SR 7: GI tract (esophagus, stomach, small bowel, colorectal, anus)
| Question | Answer |
|---|---|
| What are the effects of gastrin? | Increase HCl, instrinsic factor, and pepsinogen secretion |
| What are the effects of cholecystokinin (CCK)? | Stimulates gallbladder contraction and pancreatic enzyme secretion, and relaxes sphincter of Oddi |
| Where is cholecystokinin (CCK) produced? | I cells of duodenum and jejunum |
| What are the effects of secretin? | Stimulates flow and alkalinity of bile and pancreatic secretions while inhibiting gastric acid secretion and gastrin release |
| What is the primary stimulus of pancreatic bicarb secretion? | Secretin |
| What effects the amount of bicarbonate in pancreatic secretions? | Flow rate: high flow = high bicarb and low Cl. Slow flow allows more HCO3/Cl exchange |
| What are the effects of somatostatin? | Universal “off” switch – inhibits release of GI and pancreatic hormones and gastric acid |
| Where is somatostatin produced in the GI tract? | D cells in antrum |
| What stimulates somatostatin secretion? | acid in duodenum |
| What are the effects of gastrin-releasing peptide (Bombesin)? | Universal “on” switch – stimulates release of all GI hormones except secretin and increases GI motility |
| What is the effect of motilin? | stimulates GI tract motility |
| What drug stimulates motilin receptors? | Erythromycin |
| What are the effects of vasoactive intestinal peptide? | potent vasodilator, stimulates pancreatic and intestinal secretion and motility, inhibits gastric acid secretion |
| What are the effects of gastric inhibitory peptide? | inhibit gastric acid secretion and stimulate insulin release |
| What is the effect of peptide YY? | Inhibits pancreatic and gastric secretion and gallbladder contraction, "ileal break" |
| Where is peptide YY secreted? | terminal ileum |
| Where is gastric inhibitory peptide produced? | K cells in duodenum |
| What is the effect of omeprazole? | Blocks H/K ATPase of parietal cell (final pathway for H+ release) |
| What is the effect of pancreatic polypeptide? | deceased pancreatic and gallbladder secretion |
| What is the order of bowel recovery after surgery? | Small bowel 24 hours, stomach 48 hours, large bowel 3-5 days |
| What are the layers of the esophagus? | Squamous epithelium, circular inner muscle layer, outer longitudinal muscle layer; no serosa. Upper esophagus – striated muscle; lower esophagus – smooth muscle |
| What is the blood supply to the esophagus? | Cervical – inferior thyroid artery; thoracic – directly off aorta; abdominal – left gastric and inferior phrenic arteries |
| What is normal LES tone and length? | 15-25 mm Hg, 4cm long, 40cm from incisors |
| What is primary, secondary, and tertiary peristalsis? | Primary - CNS initiates swallow, occurs with food bolus; Secondary - occurs with esophageal distention (propagating waves); Tertiary - non-propagating/dysfunctional |
| What is the most common site of esophageal perforation? | Cricopharyngeus muscle (usually after EGD) |
| What are the 3 anatomical areas of narrowing of the esophagus? | Cricopharyngeus muscle, compression by left mainstem bronchus and aortic arch, and diaphragm |
| What is the surgical approach to the esophagus? | Cervical – left; upper 2/3 thoracic – right (avoids aorta); lower 1/3 thoracic – left |
| What is Killian's triangle? | A potentially weak spot where a pharyngoesophageal diverticulum (Zenker's) is more likely to occur. Posterior triangular area in the pharynx between the inferior constrictor and the cricopharyngeus muscle |
| What are the types of esophageal diverticula? | Traction (true) and pulsion (false, Zenker’s, epiphrenic) |
| What is the treatment for a Zenker’s diverticulum? | cricopharyngeal myotomy (removal of diverticula not necessary) |
| What is the cause of a traction diverticulum? | granulomatous inflammation (TB or fungal disease) or tumor |
| What is an epiphrenic diverticulum? Treatment? | Acquired pulsion diverticula in distal 10 cm of the esophagus usually associated with esophageal motor disorders (achalasia, DES); Tx: diverticulectomy and long esophageal myotomy on side opposite of diverticulectomy |
| What is the pathophysiology of achalasia? | Decreased ganglion cells in Auerbach's plexus, absence of peristalsis and esophageal dilation. High LES pressures |
| What does manometry showing normal LES tone but strong unorganized contractions suggest? | Diffuse esophageal spasm |
| What does manometry showing increased LES pressure, incomplete relaxation, and no peristalsis suggest? | Achalasia |
| What is the treatment of diffuse esophageal spasm? | calcium channel blockers, nitrates, Heller myotomy (transect circular layer of upper and lower esophagus). Surgery better at resolving dysphagia than pain |
| What is the treatment for achalasia? | Calcium channel blockers, dilation effective in 60%. Heller myotomy with transection of circular layer of lower esophagus only and partial Nissen fundoplication if failed medical treatment) |
| What is the key maneuver in a Nissen fundoplication? | identification of left crura |
| What is the most common cause of dysphagia after a Nissen fundoplication? | wrap is too tight |
| What are the types of hiatal hernia? | Type I – sliding hernia from dilation of hiatus; II – paraesophageal, normal GE junction; III – combined I+II; IV – entire stomach plus another organ in chest |
| What is the treatment of a type II hiatal hernia? | Repair of diaphragm and Nissen fundoplication (diaphragm repair can affect LES, also helps anchor stomach) |
| What is the indication for esophagectomy in Barrett’s esophagus? | severe dysplasia or a diagnosis of adenocarcinoma |
| What is the effect of a Nissen fundoplication on Barrett’s esophagus? | Surgery will decrease esophagitis and progression of metaplasia, but will not induce regression or prevent malignancy. Still need close follow-up for lifetime |
| What suggests unresectability of esophageal cancer? | hoarseness (RLN), Horner’s syndrome, phrenic nerve involvement, malignant pleural effusion, malignant fistula, airway invasion, or vertebral invasion |
| What is main arterial supply to stomach when used to replace esophagus? | right gastroepiploic artery |
| What is the standard chemotherapy regimen for esophageal cancer? | 5-FU and cisplatin |
| What is the treatment of esophageal leiomyoma? | If symptomatic or >5cm excise by enucleation via thoracotomy. Do not biopsy on EGD |
| What type of caustic esophageal injury causes deep liquefaction necrosis? | alkali |
| What type of caustic esophageal injury causes coagulation necrosis? | acid |
| What is the workup and treatment for caustic esophageal injuries? | CXR for free air, then EGD if no perforation. Conservative treatment of NPO, IVF, spitting, ABx. NO nasogastric tube |
| What is the initial treatment of GI bleeding in Mallory-Weiss syndrome? | Observation - most cases stop with nonoperative management |
| Describe the anatomy of the vagus innervation of the stomach | Left vagus (anterior) gives hepatic branch, Right (posterior) gives celiac branch and "criminal nerve of Grassi" |
| Which cells produce pepsinogen? | Chief cells |
| Which cells produce intrinsic factor? | Parietal cells |
| What are the main stimuli for H+ production in the stomach? | Gastrin, acetylcholine, and histamine |
| What are the 3 phases of gastric acid stimulation? | Cephalic (30%) – anticipation of eating signaling through vagus; Gastric (50%) – stimulated by stomach distention and amino acids; Intestinal (10-20%) – small bowel distention and amino acids |
| What is the treatment for gastric volvulus? | Reduction and Nissen |
| How does vagotomy affect gastic empyting? | All forms increase liquid emptying – vagally mediated receptive relaxation is removed resulting in increased gastric pressure accelerating liquid emptying. Complete (truncal or selective) causes decreased emptying of solids |
| What is the most common symptom post-vagotomy? | Diarrhea (30-50%) caused by sustained MMC forcing bile acids into colon |
| What are the risk factors for rebleeding of an UGIB at time of EGD? | 1 – spurting blood vessel (60% chance of rebleed), 2 – visible blood vessel (40%), 3 – diffuse oozing (30%) |
| What is the treatment for an UGIB in a patient with liver failure? | EGD with sclerotherapy or TIPS, not OR as patient is likely bleeding from esophageal varices |
| What are the types of gastric ulcers? | I – lesser curvature, II – 2 ulcers (lesser curve and duodenal), III – prepyloric, IV – along cardia of stomach, V – NSAID use |
| What types of gastric ulcers are due to high acid secretion? What types are due to decreased mucosal protection? | Types I and IV – decreased mucosal protection; types II and III – high acid secretion |
| What is the mechanism of ulcer formation with chronic NSAID use? | Inhibits prostaglandin synthesis, causing decreased mucus and bicarb secretion and increased acid production |
| What blood types are associated with gastric ulcers? | Type A blood – type I ulcers; type O blood – type II-IV ulcers |
| What is the most common benign gastric neoplasm? | gastric leiomyoma (GIST tumor). Most are C-KIT positive |
| What is the cells of origin for GIST tumors? | interstitial cells of Cajal |
| What is the treatment of a GIST? | Resection with 1-cm margins, +/- chemotherapy -> Gleevec (tyrosine kinase inhibitor) |
| What is the treatment for gastric lymphoma? | chemotherapy and XRT, surgery for complications |
| What is MALT a precursor to? | gastric lymphoma - regresses with H. pylori treatment |
| What is the treatment for MALT (mucosa-associated lymphoproliferative tissue)? | triple therapy antibiotics for H. pylori, as most are associated with H. pylori and regress after treatment. Chemotherapy (CHOP) if does not regress |
| What are some specific complications of roux-en-Y gastric bypass? | marginal ulcers, leak, necrosis, B12 deficiency (losses acidic environment needed to bind B12), iron deficiency anemia (bypasses duodenum), gallstones |
| What are the specific complications of jejunoileal bypass? | increased liver cirrhosis and kidney (stones) problems, osteoporosis (decreased calcium) |
| What is the cause of early (15-30 min) dumping syndrome? | Hyperosmotic load, fluid shift causes neuroendocrine response, peripheral and splanchnic vasodilation |
| What is the cause of late (2-3 hrs) dumping syndrome? | Increased insulin with decreased glucose |
| What is the treatment of dumping syndrome? | Dietary changes resolve 90% - small, low-fat, low-carbohydrate, high-protein meals with no liquid and no lying down after meals. Octreotide may be effective. Conversion of billroth I or II to roux-en-Y is rarely needed |
| What is the cause after gastrectomy of postprandial epigastric pain associated with N/V, but not relieved after vomiting? Treatment? | alkaline reflux gastritis. Tx: H2 blockers, cholestyramine, metoclopramide, or possible conversion of billroth to roux-en-Y |
| What is the treatment of roux stasis? | metoclopramide, prokinetics, possible shortening of roux limb to 40 cm |
| What causes blind-loop syndrome? | bacterial (E. coli, GNR) overgrowth and stasis in afferent limb, therefore treat with antibiotics (tetracycline, flagyl) |
| What is the most common site of GI lymphoma? | stomach |
| What margins are necessary for gastric cancer resection? | 5-6cm due to intramural microscopic spread and extensive lymphatics around stomach |
| Describe the phases of the migratory motor complex | Phase I - quiescence; Phase II - acceleration, gallbladder contraction; Phase III - peristalsis; Phase IV - subsiding electric activity; occurs in 90 min cycles |
| What is the key stimulatory hormone of the MMC? | motilin |
| How are bile salts reabsorbed? | 50% passive absorption (45% ileum, 5% colon), 50% active resorption in terminal ileum |
| What test can assist with the diagnosis of short gut syndrome? | Schilling test – checks for B12 absorption (radiolabeled B12 in urine) |
| What are the causes of a non-healing fistula? | FRIENDS – foreign body, radiation, IBD, epithelialization, neoplasm, distal obstruction, and sepsis |
| What is able to induce remission and fistula closure with small bowel Crohn’s disease? | TPN |
| What is the pathology of Crohn’s disease? | transmural involvement, cobblestoning, skip lesions (segmental disease), fistulas, perianal disease |
| What is the surgical treatment for a crohn's patient with multiple strictures? | Do not resect (to avoid short gut), do stricturoplasties |
| What are the side effects of terminal ileum resection? | bile salt diarrhea, cholelithiasis, megaloblastic anemia, nephrolithiasis |
| What are the cells of origin of gastrointestinal carcinoid tumors? | Kulchitsky cells (enterochromaffin or argentaffin) at the base of the crypts of Lieberkuhn |
| What are the most common sites of carcinoid tumors? | AIR – appendix, ileum, and rectum; 10% arise in bronchus or lung |
| What are the symptoms of carcinoid syndrome? | flushing, diarrhea, asthma, R sided heart valve dz |
| What is the test for carcinoid syndrome? | urinalysis for 5-HTP (secreted by foregut), 5-HIAA, and serotonin |
| What chemotherapy agents are used for carcinoid tumors? | Steptozocin, doxorubicin, 5 FU |
| What % of patients with carcinoid tumors get carcinoid syndrome? | 9% - mostly those with extensive mets to the liver |
| What is the most reliable tumor marker for carcinoid? | serum chromagranin A |
| What is the most common second malignancy seen in a patient who has a midgut carcinoid? | another midgut carcinoid (50% of the time) |
| What pressor is most useful in GIB? | Vasopressin: reduces splanchnic blood floow, portal flow ~40%. Give with B-blocker to avoid angina |
| What agent is able to significantly decrease nausea and vomiting in a patient with malignant bowel obstruction? | Octreotide |
| What is the treatment for diversion colitis of a Hartmann’s pouch? | short-chain fatty acid enemas |
| What is the most common stomal infection? | Candida |
| What is the treatment of mucocele of the appendix? | appendectomy; right hemicolectomy if malignant. Avoid rupture – can result in pseudomyxoma peritonei |
| What is the preferred fuel of the colon? | Short chain fatty acids - butyric acid |
| What electrolytes are actively secreted by the colon? | K and HCO3 |
| What is the treatment of lymphocytic colitis? | sulfasalazine |
| What is the most common type of colon polyp? | hyperplastic – no cancer risk |
| What is the most common type of intestinal neoplastic polyp? | tubular adenoma |
| When is polypectomy adequate treatment for invasive carcinoma? | >2mm margin, well differentiated, and no lymphovascular invasion |
| When is the next colonoscopy after removal of a polyp? | If <1cm and single – 5 years, if >1cm or high risk – 3 years, if resection needed – 1 year |
| What infection is colon cancer associated with? | Clostridium septicum |
| What is the most common presenting symptom of colorectal carcinoma in patients under 40? | Rectal bleeding |
| What are the most common genetic mutations in colon cancer? | p53 (85%), DCC (70%), ras (50%) |
| What is the treatment for a low T2 rectal carcinoma? | APR or LAR (need 2cm margin from levator muscles for LAR) |
| What is the extent of a T2 colorectal cancer? | Into muscularis propria |
| What is the main purpose of colonoscopy after colectomy for cancer? | Detect new colon cancers (metachronous) – 5% |
| When is XRT indicated for rectal CA? | T3 tumors (into serosa) or positive nodes |
| What gene is FAP associated with? | APC gene on chromosome 5 (but 20% of FAP are spontaneous) |
| What is the most common cause of death following colectomy in patients with FAP? | periampullary tumors of duodenum |
| Amsterdam criteria | ”3, 2, 1” - 3 first degree relatives, over 2 generations, 1 diagnosed before age 50 |
| What is Lynch syndrome associated with? | DNA mismatch repair gene; Lynch 1 – just colon CA; Lynch II – colon, ovarian, endometrial, bladder, and stomach CA |
| Gardner's syndrome | colon CA and desmoid tumors |
| Turcot's syndrome | colon CA and brain tumors |
| Peutz Jeghers | polyposis and mucocutaneous pigmentation; increased risk of GI, gonadal, breast cancers |
| What is the treatment of sigmoid volvulus? | Colonoscopic decompression (80% reduce, 50% will recur), bowel prep, then sigmoid colectomy during admission |
| What is the pathology of ulcerative coloitis? | Rectal involvement in 90%, but spares anus, contiguous involvement, involves mucosa and submucosa, rectal bleeding |
| What is the most common site of perforation in Crohn’s disease? UC? | Crohn’s – terminal ileum, UC – transverse colon |
| What gene is associated with sacroiliitis in IBD? | HLA B27 |
| What is the most common extraintestinal manisfestation requiring total colectomy in UC? | failure to thrive in children |
| Which extraintestinal manisfestations of UC do not improve after colectomy? | Primary sclerosing cholangitis and ankylosing spondylitis |
| What is pyoderma gangrenosum? What is the treatment? | Painful raised pustules on skin with necrotic center which progress to spreading ulceration - a/w IBD; Rx - local wound care, steroids, dapsone |
| What is the treatment of low rectal carcinoid tumors? | <2cm – wide local excision with negative margins; >2cm or invasion of muscularis propria – APR |
| What is the law of LaPlace? | tension = pressure x radius |
| What are the indications for surgery in diverticulitis? | emergent complications, recurrent disease, or inability to exclude cancer |
| What demonstrates cyanotic edematous mucosa covered with exudates on colonoscopy? | Ischemic colitis |
| What is a key finding in pseudomembranous colitis? | PMN inflammation of mucosa and submucosa |
| What marks the transition between the anal canal and the rectum? | Levator ani |
| What marks the anatomic transition between the anal canal and the anal verge? | Anal canal is above dentate line, anal verge is below it |
| Describe the blood supply of the rectum | Superior rectal artery off IMA Middle off internal iliac Inferior off internal pudendal (off internal iliac) |
| What is the arterial supply to the anus? | inferior rectal artery |
| What are the two types of fascia surrounding the rectum? | Denonvilliers (anterior – rectovesicular/rectovaginal fascia) and Waldeyer’s (posterior – rectosacral fascia) |
| What is the grading of internal hemorrhoids? | 1 – slides below dentate with strain, 2 – prolapse that reduces spontaneously, 3 – prolapse with manual reduction, 4 – unable to reduce |
| What are the surgical indications for hemorrhoids? | recurrent disease (bleeding), thrombosis, large external component |
| What is the cause of rectal prolapse? | pudendal neuropathy and laxity of anal sphincters |
| What is the treatment for rectal prolapse? | High fiber initially; LAR is definitive surgery, but may perform rectosigmoid resection (Altmier) if older and frail or simply rectopexy in the absence of large redundant colon or constipation symptoms |
| Where are most anal fissures located? | posterior midline, 10% are anterior in women |
| What are the causes of anal fissures which are lateral or recurrent? | IBD, TB, or syphilis |
| What is Goodsall’s rule? | anterior fitulas contact with rectum in a straight line, whereas posterior fistulas go toward midline internal opening in rectum |
| What are the most common types of anal canal tumors? | Squamous cell (AKA epidermal, basaloid, cloacogenic, transitional), Adenocarcinoma, and melanoma |
| What is APR indicated in squamous cell CA of the anal canal? | Only with persistent or recurrent cancer (after treatment with Nigro protocol) |
| What is Nigro protocol? | 5FU, mitomycin, and XRT |
| What is the treatment for adenocarcinoma of the anal canal? | APR; WLE if <3cm, <1/3 circumference, T1, well differentiated, and no lymphovascular invasion |
| What is intraepidermal apocrine gland CA of the anal margin that stains PAS positive? Treatment? | Paget’s disease, tx – WLE, groin dissection for positive nodes |
| What is intraepidermal squamous cell CA of the anal margin (squamous cell carcinoma in situ)? Treatment? | Bowen’s disease, tx – WLE, check for other malignancies |
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jclanton82
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