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GI -Episode 185 – Step 1, Step 2CK, Step 3Vignette: 45-year-old male has hypercalcemia and severe episodes of epigastric pain that does not radiate to the back. What other findings in this person? Hyperprolactinemia – MEN1 syndrome: triad of Para-Pan-Pit causing peptic ulcer disease. Two possibilities: Hyperparathyroidism causing hypercalcemia causing peptic ulcer disease. Hypercalcemia increases the release of gastrin resulting in increased gastric acid release. Two, pancreatic neuroendocrine tumor of gastrinoma causing peptic ulcer. Parathyroid hyperplasia (primary hyperparathyroidism), pituitary adenoma, pancreatic neuroendocrine tumor (gastrinoma most common – tumor that releases gastrin).How is gastric acid secreted?Parietal cells in the stomach secrete: (HY)H+ ions (H+/K+ ATPase antitransporter) ATP is required as K+ is being brought into the cell against the concentration gradient. (Primary pump!!)Intrinsic factor which is needed to reabsorb B12 at the terminal ileum.Vagus nerve releases gastrin releasing peptide (GRP) and this acts on G cells in the antrum of the stomach. G cells makes gastrin and this gastrin activates parietal cells to make acid. Gastrin also activate enterochromaffin-like cells (ECL) to release histamine. Histamine binds to H2 receptors (Gs GPCR) on parietal cells to promote acid secretion. (VHY) To decrease acid secreting, give H2 receptor blocker such as famotidine, cimetidine (CYP 450 inhibitor), ranitidine. Vagus nerve can also activate M3 receptors on parietal cells. M3 receptors can increase release of acid. Parietal cells also have prostaglandin receptors. These are Gi GPCR and decrease AC. This results in decreased release of stomach acid. This is why taking NSAIDs can lead to peptic ulcer disease. NSAIDs bind to COX and inhibit production of prostaglandins. Low PGE leads to increased acid production.Knowing all this, how does pernicious anemia develop?Antibodies can develop against:H+/K+ ATPase antitransporterEntire parietal cellsIntrinsic factorProton pump inhibitorsEnd with “prazole”These will inhibit the H+/K+ ATPase antitransporterHigh stomach pH decreases intrinsic factor releaseHow does a gastrinoma affect the acid production in the stomach? (HY)Known as Zollinger-Ellison syndromePresents as: peptic ulcers in the jejunum or distal duodenum (very far from stomach)Treat with: PPIs and remove gastrinoma tumorTreat with: octreotide (somatostatin analog).Stops G cellsStops parietal cells from making acidWhat stimulates the G cells to make gastrin? (HY)Vagus nerve releases Gastrin Releasing Peptide (GRP)GRP acts on G cells to release gastrinThough Vagus nerve as part of the PNS would usually secrete Ach, do NOT pick Ach as the answer. What else is happening in the stomach?Chief cells are making a zymogen called pepsinogen. Low stomach pH will cleave pepsinogen to pepsinPepsin digests protein and so, protein breakdown starts in the stomachMucosal cells make bicarbBicarb protects the stomach lining from the very acidic environment (pH:2)Stomach is made of simple, columnar epithelium (HY)What does B12 deficiency lead to?Pernicious anemiaPeripheral neuropathyIncreased homocysteineMethylmalonyl CoA requires B12 as a co-factor to work. Without B12, no succinyl CoA is made from methylmalonic acid. Megaloblastic anemia – hyper-segmented neutrophils seen classicallySubacute combined degeneration of the spinal cord – LCST screwed up – UMN issues. Dorsal column, medial lemniscus screwed up – fine touch, proprioception messed up.Blood supply (Draw it out)GI tract is divided into:Foregut – stomach, duodenum (up to ligament of trites or Ampulla of Vater), gallbladder, spleen, liver, esophagus;Blood supply: celiac arteryBranches of the celiac arteryComes off thoracic aortaLeft gastric arterySplenic artery → left gastroepiploic arteryCommon hepatic artery → right gastric artery (anastomoses along lesser curvature of the stomach (VHY))Hepatic artery proper Right hepatic artery → cystic artery (gallbladder)Left hepatic arteryGastroduodenal artery (GDA)Right gastroepiploic artery (greater curvature of stomach anastomosis (VHY))Anterior superior pancreaticoduodenal artery (anastomosis with anterior inferior pancreaticoduodenal artery (VHY))Midgut – duodenum to proximal 2/3 of the transverse column:Blood supply: superior mesenteric arteryHindgut – sigmoid colon, descending colon, splenic flexure to upper 1/3rd of rectum (ends at the pectinate line)Blood supply: inferior mesenteric artery (VHY) and portal veinMucosa below the pectinate line: internal iliac artery and IVCEsophagusThe esophagus is divided into three parts:Upper third (purely skeletal muscle)Middle third (mixture of skeletal and smooth)Lower third (purely smooth muscle)Esophageal sphinctersUpper sphincterLower sphincterMyenteric plexus or Auerbach plexus missing will mean no relaxation. Diagnosis: achalasia.Barium swallow shows bird’s peak signTreat with: Esophageal myectomyLower sphincter tone increasedEsophageal motility is abnormal (HY)Chagas disease (HY) – Trypanosoma cruzeiAchalasiaDilated cardiomyopathyDilated bowel – Hirschsprung diseaseCREST scleroderma: associated with anti-centromere antibodies (HY)CalcinosisRaynaud’s phenomenon (most common presentation of CREST)Esophageal dysmotility – can have very bad GERD from lower esophagus issueSclerodactylyTelangiectasias Vignette: person presents with trouble swallowing, smooth tongue, Hgb = 8, MCV = 67Think: Iron deficiency anemia (microcytic anemia) with dysphagia (esophageal web) and smooth tongueDiagnosis: Plummer Vinson syndromeVignette: alcoholic for 40 years, severe hematemesis, severe volume depletionDiagnosis: Esophageal varices from portal hypertensionBleeding varices leads to deathTreatment: endoscopy therapy – banding of varix, sclerotherapy, TIPS procedure (shunt between portal and hepatic vein – bypass liver – this can cause hyperammonemia), IV octereotide therapy (1st line for acute phase), reduce portal pressure by giving beta blocker like propranolol, or give spironolactone, or give fluroquinolones.Vignette – painful vomiting with blood, very febrile, very hypotensive, rice crispy crackles sensation on skin, image shows air along aorta (pneumomediastinum). Diagnosis: Boerhaave syndrome (very very bad). For diagnostic testing – DO NOT pick Barium swallow (will cause mediastinitis). Pick gastrografin enema (water soluble contrast enema) for diagnostic testing. Immediate surgical issue with high mortality.Vignette: laceration or perforation of GI junction with small volume of hematemesis – Diagnosis: Mallory Weiss tearVignette: patient lost 20 lb. in a month, dysphagia to solids, 20-year history of GERDDiagnosis: Esophageal adenocarcinoma. Starts as intestinal metaplasia → Barrett’s esophagus → cancerBiggest risk factor for adenocarcinoma: Barrett’s esophagus is the answer when given; NOT GERD (it is not the closest or the most direct relationship to carcinoma)Normal histology: non-keratinized stratified squamous epithelium → (chronic acid load leads to metaplasia) → non-ciliated (simple) columnar epithelium with goblet cells or intestinal metaplasia → esophageal adenocarcinomaMost common esophageal cancer in America - adenocarcinoma.Terrible prognosis. Esophageal squamous cell cancer (most common worldwide) Any other risk factor other than Barrett’s could result in SCC. So, if asked what does Barrett’s lead to, pick adenocarcinoma. If asked what does smoking lead to, pick SCC.Ingestion of lye or DrainoVignette: person drinks lye and has dysphagia a few weeks later. Diagnosis: esophageal strictures.Aside: If person has GERD for prolonged period and develops dysphagia, think esophageal strictures as reason for dysphagia.AchalasiaPlummer Vinson syndromeVignette: 65-year-old person has bad breath and regurgitates undigested food.Diagnosis: Zenker’s diverticulum (upper 3rd of esophagus)Zenker’s arises from weakness at the Kilian triangle because of atrophy or denudement of cricopharyngeal musclesDiagnosis: Do Barium swallow to see outpouchingTreat: excise the diverticulumContraindication: EGD – Esophagogastroduodenoscopy – microscopic look at esophagus, stomach and duodenum. EGD can cause perforation of esophagus.Aside: Traction diverticulum (mid esophagus), epiphrenic diverticulum (lower 3rd of esophagus)Differentiate between true diverticulum and false diverticulum:True diverticulum contains all four layers (mucosa, submucosa, muscularis propria and serosa) – Traction diverticulumFalse diverticulum only contains mucosa and submucosa – Zenker’s diverticulumVignette: Person with CD4 = 40 has odynophagia (painful swallowing) for 2 weeks and white membrane on tongue. Diagnosis: candida esophagitis.Aside: Esophagitis can occur from CMV or HSVPick candida over the other two as it is more common if NO specific symptoms or signs are givenTreat Candida: nystatin or clotrimazole lozengesTreat HSV: Acyclovir. If doesn’t work: Foscarnet (pyrophosphate analog)Treat CMV: Ganciclovir. If not an answer choice, resistance from UL-97 mutation: FoscarnetHistology or biopsy:Candida – hyphaeCMV – perinuclear halo or intranuclear inclusion bodiesHSV – intranuclear inclusion with chromatin pushed to the side and NO perinuclear halo (VHY)[HIGH YIELD FACTOIDS ABOUT THE ESOPHAGUS]Esophagus does not have a serosa. So esophageal cancer can easily metastasize to other nearby structures.Esophagus traverses’ diaphragm at T10 (Mnemonic: I 8 10 Eggs aT 12) (HY)IVC traverses’ diaphragm at T8Thoracic aorta traverses’ diaphragm at T12Glands of the mouth:Parotid gland: serous secretionsLow chance of tumor being malignantSublingual gland: mixed secretions of water and mucusHigh chance of tumor being malignantSubmandibular: mixed secretions of water and mucusMixture between high and low chance of being malignantAll these glands make secretions that contains alpha amylase which breaks down carbohydrates. (HY)Saliva also contains lysozymes and defensins that are antibacterial.IgA is primary immunoglobulin of saliva (HY)Parasympathetic innervation of salivary gland: watery mucus because this is better for digestionSympathetic innervation of salivary gland: thick mucus productionPleiomorphic adenoma – most common benign tumor found in the parotid gland. CN IX innervates parotid VII passes through parotid gland. So, an adenoma in the parotid gland can compress CN VII and cause Bell’s palsy or facial nerve palsy. (HY)Mucoepidermoid carcinoma – second most common tumor and most common malignant carcinoma. Warthin tumor – not malignant. Second most common benign tumor of the salivary glands. Sjogren’s syndrome – Autoimmune disease of exocrine glands. Problem producing saliva – dry mouth (xerostomia), dental caries (no saliva to kill bacteria).Antibodies: anti-Ro (SS-A) and anti-La (SS-B) antibodies.These antibodies can cross the placenta, damage the conducting system, and cause a 3rd degree heart block in the fetus. (VHY)Sialolithiasis – stones obstructing the glands. Can be painful. Sialadenitis - infection (S. aureus or S. viridans) behind the stone obstruction. What can cause sialadenitis?MumpsExcessive dehydrationSjogren’s syndromeIntubationTreatment for sialadenitis: give gum or sour candy to produce saliva and flush stone out.TongueAnterior 2/3rd:General taste sensation – pin prick, pain – V3 – mandibular nerveSpecial taste sensation – CN7 – facial nervePosterior 1/3rd:General and special sensation – CN IX (mostly) and CN X (a little bit at the very back)Motor activity – Hypoglossal CN XIIAll intrinsic muscles are CN XII except palatoglossus – innervated by CN XHypoglossal injury is tongue deviates towards side of injury (lick the wound) ................
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