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198 Cards in this Set
- Front
- Back
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What does the parasympathetic innervation of the vagus nerve control in the Enteric Nervous System? |
dorsal motor nucleus of the vagus controls primarily the motility of the esophagus and stomach |
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Where does the parasympathetic innervation of the colon and rectum come from? |
Sacral parasympathetic nucleus contributes to control of motility of the distal colon and rectum |
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Where does the sympathetic innervation of the gut come from? What does it do? |
The prevertebral sympathetic ganglia mediate peripheral reflexes that inhibit motility of the gut. |
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Where is Auerbach's plexus located? |
Between the outer longitudinal and the inner circular muscle layers |
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Where is Meissner's plexus of the ENS located? |
Located between the circular muscle and the muscularis mucosae |
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What is the interaction between the enteric nervous system and parasympathetic nervous system? |
The ENS controls intestinal motility and secretion largely independently of extrinsic parasympathetic and sympathetic innervation, although these extrinsic influences have a modulatory role on ENS activity |
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What does Auerbach's and Meissner's plexus do respectively? |
Neurons of the myenteric plexus control the activity of the smooth muscle of the gut whereas those in the submucosal plexus also regulate mucosal secretion and blood flow. |
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How does the afferent limb of the enteric nervous system get activated? |
Stimuli arising from the mucosa (distention) activate primary afferent neurons (IPANs) in part via release of serotonin from enterochromaffin cells; serotonin activates terminals of IPANs via 5-HT3 receptors. |
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How does the ascending excitatory reflex work in peristalsis? |
Primary afferent neurons (IPANs) detect serotonin release from enterochromaffin cells, triggered by distention and stretch. Then IPANs trigger the ascending excitatory reflex involves myenteric motor neurons that utilize ACh and substance P and elicit contraction of the smooth muscle located orally to the site of stimulation. |
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How does the descending inhibitory reflex of peristalsis work? |
The descending inhibitory reflex involves inhibitory motor neurons that utilize NO, VIP, ATP, and NPY, in various combinations, and elicit relaxation of the smooth muscle located anally to the site of stimulation. |
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During peristalsis of the GI tract, what cells are the intermediary between efferent motor neurons and smooth muscle cells? |
The excitatory and inhibitory influences of motor neurons are relayed to the intestinal smooth muscle cells via the interstitial cells of Cajal, which are pacemaker cells of the gastrointestinal tract |
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What is MINGE syndrome? What are its clinic manifestations? |
Mitochondrial neurogastrointestinal encephalomyopathy is a rare autosomal recessive disorder caused by mutations of the gene encoding thymidine phosphorylase. The main manifestations are external ophthalmoplegia, gastrointestinal dysmotility and pain, cachexia, peripheral neuropathy, and leukoencephalopathy. |
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What is the treatment of MINGE syndrome? |
Treatment with peritoneal dialysis may improve the gastrointestinal manifestation without affecting plasma nucleoside levels. |
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What is Allgrove Syndrome? What are its manifestations? |
Allgrove or triple A syndrome is a rare autosomal recessive disorder that can be variably associated with autonomic and neurologic features. These include progressive bulbospinal amyotrophy, hyperreflexia, orthostatic hypotension, urinary retention, excessive sweating, and optic atrophy. This disorder is due to mutations of the AAS gene encoding for a protein called ALADIN that localize to nuclear pore complexes. In some cases, this disorder may mimic familial dysautonomia |
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What is Hirschsprungs disease? What are its manifestations? |
Hirschsprung disease is a developmental disorder of the ENS resulting in absence of ganglion cells in Auerbach and Meissner plexuses, most |
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What is the inheritance pattern of Hirschsprungs disease? |
Although most causes are sporadic, there are also familial cases. |
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What is the genetic mutation in Hirschsprungs disease? |
Hirschsprung disease is a polygenic disorder that has been linked to mutations in the RET proto-oncogene and its ligands, endothelin-3 and endothelin receptors, and the transcription factors, Sox 10 and SMADIP1. |
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What stomach cell produces gastrin? |
Gastrins are physiologically produced primarily by antral G cells and endocrine cells of the gut. |
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What is a normal fasting gastrin level? How does it vary normally? |
Normal fasting gastrinemia is in the range of 30-50 pmol/L, and it increases to 100-150 pmole/L in response to a meal. |
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What is the relationship between gastrin and carcinoid formation? |
Gastrin has a trophic effect on normal and tumoral cells equipped with its target CCK2R (the Cholecystokinin receptor-2). Indeed, in rodents receiving PPIs for a long period, hypergastrinemia leads to the development of gastric carcinoids. |
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Describe briefly the results of the STAMPEDE trial? |
A three tiered randomized trial of gastric bypass vs sleeve gastrectomy vs medical therapy in diabetes that were overweight. At three years, soft measures of cardiovascular and diabetic disease such as A1C, BMI, and LDL were much greater improved in the gastric bypass and sleeve group over the medical therapy group. Dumping syndrome and ulcers were the most common complications of surgery. |
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How much fecal fat needs to be present in order for diarrhea to be classified as pancreatic or biliary insufficiency? |
pancreatic and biliary diarrheas typically do not affect fluid and electrolyte absorption, and so the unabsorbed fat is disbursed in a smaller stool volume. A fecal fat concentration greater than 9.5 g / 100 g strongly suggests the presence of pancreatic or biliary steatorrhea. |
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What are the Rome III diagnostic criteria for irritable bowel syndrome? |
Recurrent abdominal pain or discomfort at least 3 days per month in the last 3 months with 2 or more of the following: |
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A patient comes to you with the complaint of chronic diarrhea. What finding on history of nocturnal symptoms lowers the probability of IBS? |
Any nocturnal diarrhea makes the patient unlikely to have IBS. Think about IBD. |
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Is blood mixed with stool associated with IBS? |
No, IBS should never be bloody. Always think colitis such as ischemic colitis if you find this on history. |
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You find out that a patient with chronic abdominal pain has been treated many times in the past with antibiotics. What should you evaluate for? |
SIBO - small intestinal bacterial overgrowth. |
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Patients with the NOD2 gene mutation are thought to have predisposition to what disease? |
Ileal-predominant Crohn's disease. |
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Ulcerative colitis affects which two anatomical structures? |
Colon and rectum only. Rectum universally involved. |
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Crohns disease affects which part of the GI tract? |
Any part of the GI tract. 10% rectal involvement. |
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Describe the pattern of extension characteristic of Crohns disease and ulcerative colitis respectively. |
Crohns disease - skip lesions |
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What is the difference in clinical characteristics between Crohns disease and Ulcerative colitis? |
Crohns - smoldering onset, weight loss, abdominal pain |
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Will CRP be elevated in all patients with Ulcerative Colitis flares? |
No. Because UC is mucosal affecting disease, not all patients with UC flares will have elevated CRP. |
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When do you consider Vedolizumab for UC patients? |
Patients who cannot get off of steroids or patients who cannot tolerate or use a TNF inhibitor |
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In patients with HBV, what is the pattern of AST/ALT? What happens during Cirrhosis? |
Usually, ALT levels are higher than those of AST. However, when the disease pro- gresses to cirrhosis, the ratio may be reversed. |
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What happens to albumin, protein, PT, platelets when cirrhosis develops? |
A progressive decline in serum albumin concentrations and/or increase of globulins and prolongation of the prothrombin time, often accompanied by declining platelet counts, are characteristically observed after cirrhosis has developed. |
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Normal esophagus. Close-up of esophagogastric junction on the right. Note transition in color from silver-red squamous mucosa to red columnar epithelium. |
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Esophago-Gastric junction. View of squamocolumnar junction from the retroflexed position. |
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Inlet patch. Salmon-colored patch of mucosa found in the proximal esophagus, just below the upper esophageal sphincter. This represents an island of heterotopic gastric mucosa, and appears distinct from the surrounding squamous mucosa, which has a silvery color. |
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Inlet patch. Salmon-colored patch of mucosa found in the proximal esophagus, just below the upper esophageal sphincter. This represents an island of heterotopic gastric mucosa, and appears distinct from the surrounding squamous mucosa, which has a silvery color. |
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Esophageal web. Asymptomatic ring incidentally found in the proximal esophagus of a 40 year-old man. |
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Esophageal web. Asymptomatic, nonobstructing partial web found in the midesophagus of a 74 year-old woman. |
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Zencker's diverticulum in an 86 year-old woman undergoing gastrostomy tube placement. View of the pharynx showing the circular orifice of the diverticulum, to the right of which is the triangular opening of the trachea formed by the vocal cords. Entry into the diverticulum revealed this smooth, blind ending of the pouch. |
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Zencker's diverticulum in an 80 year-old woman undergoing endoscopy for evaluation of dysphagia. The mouth of the diverticulum is open; the upper esophageal sphincter is contracted (arrow). |
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Diverticulum in the mid-esophagus in a 78 year woman. |
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Hiatal hernia. Gastric mucosa with longitudinal folds can be seen through the esophagogastric junction. The caliber of the lumen then becomes narrow at the level of the impingement of the diaphragm, signifying the lower edge of the hernia. |
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Mild, nonobstructing Schatzki ring at the esophagogastric junction, below which the longitudinal gastric folds of the hiatal hernia are visible. Further downward, the lumen becomes narrow where the diaphragm compresses the stomach, at the lower edge of the hernia. |
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"Sliding" type: The upper portion of the stomach has herniated upward through the diaphragm, and into the thorax. Endoscopically best seen by retroflexing the instrument and viewing from below. The lumen becomes narrow where the diaphragm presses against the stomach. The sliding type of hiatal hernia is in-line with the path of the endoscope. |
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Paraesophageal type: This retroflexed view shows a portion of the stomach herniating upward through the diaphragm. The path of this type of hernia is adjacent to that of the endoscope. |
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Combined types: Retroflexed view showing a large sliding type hernia (surrounding the shaft of the endoscope), as well as a second tract (at lower left) which lead upward to a large paraesophageal hernia. |
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Schatzki ring. Smooth, concentric narrowing of the lumen at the esophagogastric junction. 82 year-old woman with nausea refractory to therapy; endoscopy also demonstrated gastritis and duodenitis. |
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Schatzki ring is often seen in the setting of reflux esophagitis, as seen here with linear, longitudinal esophageal ulcers. 53 year-old man with pyrosis (heartburn) and dyspepsia (indigestion). |
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A linear mucosal laceration caused by the force of vomiting, generally at or just below the esophagogastric junction, resulting in bleeding. Seen here is an elliptical-shaped mucosal tear which has stopped bleeding, from the forward view (on the left) and from the retroflexed position (on the right). |
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Mallory Weiss tear. 44 year-old man with hematemesis. endoscopy revealed a thin, linear tear beginning just above the squamocolumnar junction and extending proximally, from which there was active bleeding. |
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42 year-old woman presenting with hematemesis. Endoscopy demonstrated a linear ulcer (see arrows at right), at the distal (lower) end of which was an adherent "sentinel" clot, denoting the site of recent bleeding. The lesion spans the junction of squamous and columnar mucosa at the esophagagastric junction; the clot resides on the gastric side. |
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Esophageal fistula. 69 year-old man with esophageal carcinoma, with a fistula tract (arrow) leading into the left bronchial tree. Placement of a coated wire-mesh stent successfully covered the fistula. |
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34 year-old woman with AIDS who presented with dysphagia and odynophagia. Endoscopy revealed a fistula, which proved on barium study to be intramural. Endoscopic biopsies were negative for pathogens and for neoplasia. |
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Achalasia. Retained content with an air-fluid level in the esophagus of an 87 year-old man with difficulty swallowing. |
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Achalasia. View of lower esophageal sphincter zone, which never relaxed more than a few millimeters. |
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Fundoplication. Retroflexed views of the eosphagogastric junction in two patients. The gastric mucosa appears to have been tightly wrapped around the endoscope as it passes into the stomach. |
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Failed fundoplication. The mucosal wrap appears loose rather than tight, rendering the esophagogastric junction incompetent. |
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Phlebectasia. Focally dilated venous structures in the proximal esophagus of a 94 year old woman undergoing percutaneous endoscopic gastrostomy placement. She had no history of liver disease, and there were no typical varices either in the remainder of the esophagus or in the stomach. |
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Mucosal inflammation caused by reflux of gastric acid into the esophagus. With increasing severity, may be associated with erosions, ulceration and stricture formation. |
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Mucosal inflammation caused by reflux of gastric acid into the esophagus. With increasing severity, may be associated with erosions, ulceration and stricture formation. |
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What are the nucleoside analogues for HBV treatment? |
lamivudine, telbivudine, emtricitabine, entecavir |
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What are the nucleotide analogues for HBV treatment? |
Adefovir and tenofovir |
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Endoscopy demonstrated severe inflammation of the esophageal mucosa, with diffuse oozing of blood. Biopsies were benign, and were negative for infectious agents. |
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What is the rate of HBe seroconversion from treatment with PEG-IFN-2A? |
Anti-HBe seroconversion rates were of the order of 30% with PEG-IFN and approximately 20% with NAs. Liaw YF, etal Hepatology 2011;54:1591–1599. |
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Can you dose PEG-IFN for 6 mos effectively as opposed to 12 mos? |
A 6-month course of PEG-IFN-2a and/or a lower dose are inferior to the recommended 12-month course Liaw YF, etal Hepatology 2011;54:1591–1599. |
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Which of the following therapies is associated with the greatest HbSAg loss: PEGIFN, lamivudine, adefovir, entecavir, telbivudine, tenofovir? |
Rates of HBsAg loss following 12 months of treatment were 3– 7% with PEG-IFN, 1% with lamivudine, 0% with adefovir, 2% with entecavir, 0.5% with telbivudine, and 3% with tenofovir |
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In HBeAg-positive CHB, what are predictors of anti-HBe seroconversion are: HBV DNA? ALT level? HBV genotype? activity score on biopsy? |
Low viral load (HBV DNA below 2 108 IU/ml), high serum ALT levels (above 2–5 times ULN), HBV genotype A& B, and high activity scores on liver biopsy (at least A2) |
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In HBeAg-negative CHB, what are pre-treatment predictors of virological response? |
In HBeAg-negative CHB, there are no strong pre-treatment predictors of virological response. |
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What are your treatment goals early on in HBeAg+ patients? Does HBeAg status matter? |
In HBeAg-positive CHB, a HBV DNA decrease to <20,000 IU/ ml at 12 weeks is associated with a 50% chance of anti-HBe seroconversion. In HBeAg-negative pts, HBV DNA decrease to <20,000 IU/ ml at 12 weeks has been reported to be associated with a 50% chance of sustained off-treatment response |
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Candida. Whitish yeast colonies which may become confluent, and which may be associated with ulceration. |
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Candida. 52 year-old woman receiving corticosteroids for lung disease, presenting with dysphagia. more severe inflammation and ulceration shown |
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37 year-old man with HIV undergoing endoscopy for abdominal pain. Endoscopy revealed Candida esophagitis. |
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Candida. dense exudate extending to the squamocolumnar junction |
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Herpes esophagitis. multiple superficial ulcerations. Cytologic exam of mucosal brushings demonstrated evidence of herpesvirus. |
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Herpetic ulcers in the esophagus of a 31 year old man with AIDS who presented with odynophagia and dysphagia. |
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Herpes. Ulcerated inflammatory process in a patient on chronic steroids. |
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What factors are predictive of response in patients treated with Nucleotide Analogues for HBV? |
Low viral load (HBV DNA below 2 x 10^8 IU/ml), high serum ALT levels, high activity scores on liver biopsy |
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Is genotype predictive of response in patients treated with Nucleotide Analogues for HBV? |
HBV genotype does not influence the virological response to any NA |
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What is the marker for a sustained response to a nucleotide analogue in treatment for HBV? |
During treatment Virological response (undetectable HBV DNA) at 24 weeks during treatment with lamivudine or telbivudine and at 48 weeks during treatment with adefovir is associated with a lower incidence of resistance, i.e. an improved chance of maintained virological response, in both HBeAg-positive and HBeAg-negative patients and with a higher chance of anti-HBe seroconversion in HBeAg-positive patients |
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In what patients is PEG-IFN contraindicated during treatment for HBV? |
PEG-)IFN is contraindicated in patients with decompensated HBV-related cirrhosis or autoimmune dis- ease, in patients with uncontrolled severe depression or psycho- sis, and in female patients during pregnancy |
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What are the first line nucleotide analogues in treatment for HBV? |
Entecavir and tenofovir are potent HBV inhibitors with a high barrier to resistance . Thus, they can be confidently used as first-line mono therapies. Lamivudine - high resistance Adefovir - higher resistance Telbivudine - low barrier of resistance |
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When would it be best to use Telbivudine as a nucleotide analogue for HBV? |
resistance rates to telbivudine are relatively low in patients with low baseline viremia (<2 x 10^8 IU/ml for HBeAg-positive and <2 x 10^6 IU/ml for HBeAg-negative patients) who achieve undetectable HBV DNA at 6 months of therapy |
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CMV and Herpes. 34 year-old man with AIDS who presented with a complaint of odynophagia (painful swallowing). Endoscopy demonstrated inflammation with multiple ulcerations. Biopsies demonstrated both cellular CMV inclusions and intranuclear Herpes inclusions. |
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Irradiation Esophagitis. 77 year-old man with dysphagia (difficulty in swallowing), who had previously undergone radiation therapy for carcinoma of the lung. Endoscopy revealed esophageal inflammation, with vascular hyperplasia. |
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Irradiation esophagitis. 60 year-old woman with dysphagia, who had undergone radiation therapy for carcinoma of the lung several years earlier. Endoscopy revealed a segment of severe inflammation confined to the proximal third of the esophagus, severe inflammation with exudation (CENTER) |
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Why are the combinations of PEG-IFN with lamivudine or telbivudine are not recommended for HBV treatment? |
PEG-IFN + lamivudine = higher on-treatment virological response but no sustained off-treatment virological or serological response [
PEG-IFN + telbivudine = high risk of severe polyneuropathy |
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A patient achieves anti-HBe seroconversion during NA administration, treatment is prolonged for an additional 12 months, what are his chances of persistent response? |
a durable off-treatment response (per- sistence of anti-HBe seroconversion) can be expected in 40–80% of these patients |
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A patient with moderate C.diff infection does not respond to Metronidazole after 5 days of therapy, whats the next step? |
Switch to PO Vancomycin. |
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Which treatment strategy for HBV is preferred in Cirrhotics regardless of serologic status? |
Indefinite Nucleos(t)ide analogue therapy |
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HIV Ulcer. 38 year-old man who presented with severe odynophagia and dysphagia to both solids and liquids. Multiple biopsies and brushings, obtained at two separate endoscopies, showed no cytologic, histologic or culture evidence for any pathogens or for neoplasia. |
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Bile esophagitis. 74 year-old woman with several days of bilious vomiting. Endoscopy revealed severe esophagitis, with reflux of bile. She was ultimately diagnosed as having partial small bowel obstruction. |
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Sarcoidosis. 64 year-old woman with sarcoidosis undergoing endoscopy for evaluation of dyspepsia and pyrosis. Focal inflammation was present in the distal esophagus, and biopsies revealed noncaseating granulomas consistent with sarcoidosis. Biopsies from the stomach were also consistent with gastric sarcoidosis. |
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You find no polyps on colonoscopy in a 51 yo woman with average risk. What is your surveillance interval? |
10 years |
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You find a 9mm hyperplastic polyps in rectum. What is your surveillance interval? |
10 years for Small (<10 mm) hyperplastic polyps in rectum or sigmoid |
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You find a 9mm tubular adenoma in the sigmoid. What is your surveillance interval? |
5-10 years for 1–2 small (<10 mm) tubular adenomas |
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You find four tubular adenomas on colonoscopy. What is your surveillance interval? |
3 years for 3–10 tubular adenomas |
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You find a total of 15 polyps on colonoscopy. What is your surveillance interval? |
<3 years for >10 adenomas |
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You find an 11mm tubular adenoma in the rectum. What is your surveillance interval? |
3 years for one or more tubular adenomas ≥10 mm |
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You find a villous adenoma. What is your screening interval? |
Every three years for one or more villous adenomas |
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You find an adenoma in the sigmoid that comes back high grade dysplasia. What is your surveillance interval? |
Every three years for adenoma with HGD |
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You find a sessile polyp that comes back serrated pathology. No dysplasia. It measured 7mm. What is your surveillance interval? |
5 years for sessile serrated polyp(s) <10 mm with no dysplasia |
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You find a sessile polyp that comes back serrated pathology. No dysplasia. It measured 17mm. What is your surveillance interval? |
3 years for sessile serrated polyp(s) ≥10 mm |
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You find a sessile polyp that comes back serrated pathology. Some mild dysplasia is present. It measured 5mm. What is your surveillance interval? |
3 years for sessile serrated polyp with dysplasia |
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What are the three criteria of the serrated polyposis syndrome? What is the surveillance interval? |
(1) at least 5 serrated polyps proximal to sigmoid, with 2 or more ≥10 mm; (2) any serrated polyps proximal to sigmoid with family history of serrated polyposis syndrome; and (3) >20 serrated polyps of any size throughout the colon. Screen them every year |
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Which patient do you use Rifaximin in SIBO on? What is the dose? |
Hydrogen producers: Rifaximin 1600 mg for 10 to 14 days |
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Which patients do you use Rifaximin + Neomycin on in SIBO? Whats the dose? |
Hydrogen and Methane producers: Rifaximin 1600 mg per day + neomycin 1000mg per day for 10 days -OR- Rifaximin 1600 mg day + Metronidazole 750 mg per day for 10 days |
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What are the natural antibiotics? |
Allicin from garlic Oregano Berberrine Neem Cinnamon |
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Esophageal squamous papilloma. 5 mm polypoid lesion in the proximal esophagus of a 37 year-old man. Close-up at right. |
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Esophageal squamous papilloma. Small benign-appearing polyp just above the squamocolumnar junction in a 66 year-old woman. |
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Why does HDV occur only in patients with HBV? |
HDV uses the HbsAg as its envelope protein. |
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Is there greater liver inflammation with with greater HDV viremia? |
No. |
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Esophageal lyomyoma. 63 year-old woman with dysphagia (difficulty swallowing) and a history of an esophageal polyp. |
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Granular cell tumor. 29 year-old woman with gastroesophageal reflux symptoms. Endoscopy revealed changes of Barrett's disease, and this 1 cm raised, firm, yellow lesion in the mid-esophagus. On biopsy, this proved to be a granular cell tumor. |
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Hyperplastic polyp. Bland, barely elevated polypoid lesion in the mid-esophagus of a 63 year-old woman with chronic gastroesophageal reflux and short-segment Barrett's disease. |
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Hyperplastic polyp. Distal esophageal polypoid lesion in a 64 year-old woman. Histology was benign, ulcerative acute esophagitis with granulation tissue. No neoplasm, fungi, viral inclusions or intestinal metaplasia were seen. |
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Squamous Cell Carcinoma of Esophagus. 72 year-old man with progressive dysphagia (difficulty swallowing) to solids, who was found to have this firm, midesophageal mass causing high-grade obstruction of the esophageal lumen. Much of the remaining lumen consisted of the groove in the tumor caused by the longitudinal ulcer. |
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Multifocal Squamous Cell Carcinoma of Esophagus. 74 year-old woman with dysphagia (difficulty swallowing) to solids. Endoscopy revealed a complex array of squamous cell carcinoma. An ulcerated mass was present in the lower third of the esophagus (LEFT), with small satellite lesions extending upward towards the midesophagus (RIGHT). |
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Adenocarcinoma of esophagus. 77 year-old man with dysphagia, found to have an ulcerated, constricting tumor of the distal esophagus. Located several centimeters above the esophagogastric junction, this is consistent with an adenocarcinoma arising in a segment of Barrett's esophagus. |
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Kaposis Sarcoma. Raised, slightly violet colored lesions in the midesophagus of a year-old man with the acquired immune deficiency syndrome. Kaposi lesions were also seen in the colon. |
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Pyloric stenosis |
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Pyloric stenosis associated with ulcer disease. You see balloon dilatation on the right. |
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Post-gastrectomy. These images show a patent gastrojejunostomy, with a typical degree of inflammation at the anastomosis. Both jejunal limbs of the end-to-side anastomosis can be seen in the distance: the afferent limb up and to the right, and the efferent limb down and to the left. |
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Name the operation
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Bilroth II, Gastrojejunostomy |
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Osler-Weber-Rendu. 80 year-old woman with occult gastrointestinal bleeding. The small red mucosal lesions shown here are typical vascular ectasias of the Osler-Weber-Rendu Syndrome. Shown on the left is the tip of the heater probe, preparing to eradicate the lesion located to the right. |
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Findings on CT of acute pancreatitis? |
CT findings of acute pan- creatitis can range from isolated diffuse or focal enlarge- ment of the gland to peripancreatic stranding and peripancreatic fluid collections and, at its most severe, pancreatic gland necrosis. |
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Is abdominal MRI okay for acute pancreatitis? |
Yes CT and MRI are equally effective. |
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NG Tube Injury. Multiple small circular and oval erythematous mucosal markings, often arranged linearly, induced acutely by nasogastric suction. With long-standing nasogastric suction, the lesions may also show evidence of associated inflammation, suggesting more significant mucosal trauma. |
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NG Tube Injury. Mucosal fold has been disengaged from the suction tube, revealing the raised erythematous mucosal bleb caused by the suction injury. |
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Idiopathic Thrombocytopenic Purpura View of gastric mucosal lesions in an 81 year-old man with ITP undergoing endoscopy for evaluation of gastrointestinal bleeding. |
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What is the benefit of CT with contrast than without in acute pancreatitis? |
CT with contrast can quantify the degree of pancreatic necrosis. |
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Gastric Xanthelasma. Pale mucosal elevation found in the gastric antrum in a 76 year-old woman undergoing endoscopy for evaluation of bleeding. Biopsies revealed moderate chronic inflammation and increased numbers of foamy, lipid-laden histiocytes, consistent with a diagnosis of gastric xanthelasma (xanthoma). No Helicobacter pylori were seen. |
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Gastric Xanthelasma. Yellow mucosal plaque seen in the gastric antrum of a 53 year-old woman with acid-peptic symptoms that failed to respond to therapy. Biopsies revealed moderate to severe acute and chronic inflammation with numerous Helicobacter pylori, and collections of foamy macrophages underneath the surface epithelium, consistent with xanthelasma (xanthoma) of the stomach. |
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Gastric Xanthelasma. Small polypoid xanthoma, with a pattern of fine pale granularity; an incidental finding at the time of percutaneous endoscopic gastrostomy placement in an 89 year-old woman with inability to swallow |
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Gastric Xanthelasma. Small polypoid xanthoma, with a pattern of fine pale granularity; an incidental finding at the time of percutaneous endoscopic gastrostomy placement in an 89 year-old woman with inability to swallow. |
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Gastric Fundic Diverticulum. Diverticulum in the fundus of the stomach, seen at retroflexion (the shaft of the endoscope is seen descending through the esophagogastric junction at the 12 o'clock position). The diverticulum was an incidental finding in an 83 year-old woman undergoing endoscopy. |
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Two air fluid levels on an abdominal XR. Dx? |
Gastric volvulus. |
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"Watermelon" Stomach 70 year-old man, with no history of gastrointestinal bleeding, undergoing endoscopy for evaluation of abdominal pain. Numerous vascular ectatic lesions were found in the gastric antrum. |
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"Watermelon" Stomach 78 year-old woman undergoing evaluation of asymptomatic occult gastrointestinal bleeding with anemia. Endoscopy revealed antral vascular ectasia without active bleeding. |
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Gastric Angiodysplasia 73 year-old woman with hematemesis (vomiting blood), melena (black, tarry stools) and severe anemia (hemoglobin 5.7g). Endoscopy revealed this vascular ectasia in the proximal gastric body, which was not actively bleeding. No other lesions of any kind were present. |
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Gastric Angiodysplasia 46 year-old woman with history of recurrent iron deficiency anemia and positive stool tests for occult blood. Retroflexed view on the left; forward view on the right. |
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Hyperplastic Gastric Polyp. These polypoid lesions occur multiply or singly, and have smooth overlying mucosa resembling that of normal stomach. |
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Hyperplastic Gastric Polyp. Rarely cause symptoms in the absence of inflammation, and have no malignant potential. They cannot, however, be reliably distinguished from adenomatous polyps on the basis of gross appearance |
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Stomach |
Inflammatory Gastric Polyp 69 year-old man with protracted nausea and vomiting. Endoscopy revealed small and large polyps which grossly appeared adenomatous, but which microscopically proved to be inflammatory pseudopolyps. These inflammatory lesions may be the source of bleeding from the stomach, but are not true polyps and do not have a potential for malignant transformation. |
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Stomach |
Inflammatory Gastric Polyp Coincidental finding in the antrum of a 76 year-old woman with adenocarcinoma in the proximal stomach. |
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Stomach |
Smooth, benign-appearing gastric polyp grossly indistinguishable from hyperplastic polyps, this lesion surprisingly proved to be a tubular adenoma with high-grade dysplasia on biopsy, and was therefore subsequently excised. |
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Stomach |
(Spindle Tumor of Uncertain Malignant Potential) 51 year-old woman with an episode of hematemesis (vomiting blood). Endoscopy revealed this large, focally ulcerated polypoid lesion in the proximal gastric body. The lesion grossly resembled a leiomyoma. Biopsies demonstrated a spindle cell tumor, with few mitotic figures. Examination of the resected specimen confirmed the benign nature of the lesion. |
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Antrum |
Pancreatic Rest. Prominent raised antral mucosal lesion with a central umbilication in a 46 year-old man with abdominal pain and dyspepsia. Biopsy revealed heterotopic pancreatic tissue. |
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Antrum. |
Pancreatic Rest. Slightly raised polypoid mucosal lesion in the gastric antrum (shown here retracted into view using a biopsy forceps). The lesion had a small central umbilication. Biopsy revealed ectopic pancreatic tissue. |
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What laboratory test do you send if you suspect ischemic hepatitis? |
LDH. For ischemic hepatitis: ALT/LDH ratio of 0.87+/-0.70 AST/LDH ratio of 0.81+/-0.34 APAP and Viral etiologies have higher ratios (1.46 to 4.65 respectively) Cassidy WM, et. al. J Clin Gastro 1994; 19(2):118-21 |
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Stomach |
Acute Gastritis. 82 year-old woman with protracted nausea, and occult gastrointestinal bleeding. Endoscopy revealed gastritis involving the gastric fundus (left) |
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Stomach |
Chronic Gastritis. 86 year-old woman with occult gastrointestinal bleeding and abdominal pain. Endoscopy demonstrated diffuse chronic gastritis. |
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Stomach |
NSAID Gastritis 74 year-old man with recent hematemesis (vomiting blood), who had been taking NSAIDS and drinking alcohol. Endoscopy demonstrated antral gastritis with multiple small, superficial ulcers. |
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Stomach |
NSAID Gastritis 75 year-old woman with upper abdominal pain and blood in the stool, who had been taking NSAIDS for arthritis. Endoscopy revealed patchy gastritis in the gastric fundus and in the antrum (shown here). Biopsies were negative for Helicobacter pylori. |
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Stomach |
Lymphoid Nodularity Lymphoid nodularity associated with Helicobacter pylori gastritis, seen here in a 29 year-old woman with acid-peptic symptoms. |
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Stomach |
Lymphoid Nodularity Nodularity of the gastric mucosa in a 63 year-old woman with dyspepsia. |
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Stomach |
Gastric Candida 90 year-old woman undergoing percutaneous endoscopic gastrostomy tube insertion. Whitish mucosal macules in the distal gastric body and antrum were positive for Candida. Other than malnutrition, she was not known to be immunocompromised. |
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Stomach |
CMV Gastritis 34 year-old man, infected with the AIDS virus, with erythematous lesions in the gastric body; biopsy revealed cytomegalovirus inclusions. |
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Duodenum |
MAI Duodenitis 37 year old man with HIV undergoing upper endoscopy for abdominal pain. At endoscopy the duodenal villi appeared edematous, without other gross features of inflammation. Histology revealed numerous macrophages containing abundant Mycobacterium avium intracellulare (MAI). |
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Post-transplant HCV patient presents with elevated LFTs. What features make you think of cholestatic hepatitis? What test has the greatest negative predictive value? |
5% of post-transplant patients transplant occurred in last 6 mos. Very high HCV RNA levels Bilirubin >6mg/dl Elevated ALP GGT levels elevated. no known risk factors or pathophys HCV RNA <10 million, makes this dx unlikely Taga SA, Washington MK, Terrault N, Cholestatic hepatitis C in liver allografts. Liver Transplant Surg 1998;4:304–10. |
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Liver biopsy: Dx and important features: |
Cholestatic hepatitis characterized byextensive swelling and degeneration of hepatocytes, accumulation of bile in tissue (cholestasis) and spotty hepatocyte necrosis. |
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Post-transplant HCV patient presents with worsening liver function in setting of interferon therapy. ANA is up. What's the dx and management? |
The plasma-cell variant of HCV recurrence is described in patients who are transitioning from acuteto chronic infection and in the context of interferon therapy. Autoimmune markers, such asantinuclear antibodies and IgG levels, may be elevated but are not universal. Some patients manifestother autoimmune diseases. The prognosis of this disease is worse than patients with typical recurrentHCV disease, with a substantial proportion of patients progressing to graft loss. Thus, early interventionshould be considered. Optimizing immunosuppression and discontinuation of interferon (if applicable)are recommended |
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Endscopy: |
Ampulla. Spatial relationship between the major ampulla (white arrow) and the more proximal minor ampulla (black arrow). |
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Your patient gets a transplant for HCV Cirrhosis. You want to know if his virus will recur and cause a recurrence in cirrhosis. What can you do to prognosticate? |
Liver biopsies showing stage 2 fibrosis(scale of 4) and hepatic venous pressure gradient greater than 6 mmHg at 12 months are predictive ofclinical decompensation in the future. With hepatic elastography, a liver stiffness value of >9.0 kPa at 6 months post-transplant had 70% positive predictive value and 80%negative predictive value for fibrosis stage 2 or more (scale of 4) at 1 year post-LT Blasco A,et al. Hepatic venous pressure gradient identifiespatients at risk of severe hepatitis C recurrence after liver transplantation. Hepatology 2006;43:492–9. |
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Your HCV patient undergoes transplant. You consider the benefit of early vs late HCV therapy. What is the benefit? |
There is no evidence that preemptive therapy offers any advantage over delayedtherapy Bzowej N, et al. PHOENIX: a randomized controlled trial ofpeginterferon alfa-2a plus ribavirin as a prophylactic treatment after liver transplantation for hepatitis C virus. LiverTransplant 2011;17:528–38. |
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VCE |
Normal appearance of fundic mucosal folds. During capsule endoscopy, organs are not distended as they would be during conventional fiberoptic endoscopy. |
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VCE |
Gastric body and antral mucosal folds during contractions. Folds can briefly have a polypoid appearance. |
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VCE |
Capsule views of a normal pylorus. |
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VCE |
Normal Antral prepyloric folds. |
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VCE |
Normal jejunal mucosal folds. Unlike conventional endoscopy, the lumen is not distended during capsule studies, and the folds are seen in various states of contraction. The white mucosal lines may represent lymphatic channels. The shaggy appearance of folds, as seen in the center image, represents mucosal villi. |
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VCE |
Normal duodenal bulbar mucosa. Unless transit is delayed, the view of the duodenal bulb is brief. The bulb is distinguished from postbulbar duodenum by its relatively smoother appearance, relative absence of folds and less prominent villi. |
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VCE |
Normal colonic mucosa as seen by the capsule endoscope. |
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At what platelets count is it safe to perform a biopsy? |
>20,000 VanOs, E.C., etal. Gastrointest. Endosc. 50, 536–543 (1999). |
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What are the risk factors for perforation on EGD? |
cervical osteophytosis Zenker’sdiverticulum pharyngeal pouches malignant orbenign strictures Eosinophilic esophagitis PEM CEZ. mnemonic |
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MRCP on left and ERCP on right |
Main duct IPMN. Arrow is pointing to a mural nodule. Notice how the PD is very dilated. |
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MRCP on left and ERCP on right |
Branched duct IPMN. Arrows are pointing to a narrow pancreatic duct. Notice how it communicates with the pancreatic duct. |
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MRCP on left and ERCP on right |
Mixed type IPMN. Has features of both branched and main duct IPMN |
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What are the four phases of a normal swallow? |
oral preparatory, oral propulsive, pharyngeal andoesophageal |
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What is involved in the oral prepatory phase of swallow? |
Placing a fluid or solid food bolus on the anterior tongue with a tight seal of the tongue against the roof of the pharynx behind it |
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What is involved in the oral propulsive phase of swallow? What muscle is primarily involved? |
The oral propulsive phase involves transfer of the bolusfrom the mouth through the pharynx to the oesophagus and is mainly caused by the squeezing action of the tongueagainst the palate, providing driving forces to propel swal‐lowed material across the UES with minimal resistance. |
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Oropharyngeal dysphagia with dry mouth and poor gag reflex. Which nerve is affected? |
Cranial nerve 9, glossopharyngeal nerve. |
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Which cranial nerves work together to open the pharynx and UES for swallowing? |
Cranial nerve 5, 9, and 10. |
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Which neurotransmitters mediate LES relaxation? |
The main neurotrans‐mitter mediating up to 75% of human LES relaxationin in vitro studies is nitric oxide, with a minor role forpurines (through P2Y1 receptors) and vasoactive intes‐tinal peptide |
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What is the prevalence of FAP? |
2-3 cases per 100,000 individuals |
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Are men or women affected more commonly in FAP? |
men andwomen being affected equally |
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Capsule, Stomach |
Inflamed gastric mucosal folds. Consistent with gastritis |
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Capsule, Duodenum |
Villous edema and mucosal erythema in the duodenal bulb. Consistent with Duodenitis |
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Capsule, Duodenum |
Duodenal ulcer with flat vessel |
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What are the signs of impending colonic perforation? |
Persistent dilation Fever and anorexia |
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Operative indications in fulminant colitis |
Failure to progress on medical therapy in 72 hours |
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What are the three medications that cause intrinsic (not Cyp mediated) liver damage? |
Acetaminophen INH Amanita Mushrooms |
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What is Hy's law? |
In a patient who develops elevated AST/ALT in setting of drug (DILI)... Serum ALT <3 X ULN: not associated with liver injury, does not typically lead to liver injury 3-5X ULN: 10% risk of developing acute liver failure if patient becomes jaundiced >5X ULN: Up to 50% risk of liver failure with jaundice |
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You have a patient with DILI, when is it appropriate for liver biopsy? |
1) When it is necessary to continue the suspected medication 2) Whenever the etiology of the liver injury is in question. ANA or other immune serologies positive. Metabolic syndrome. 3) Prolonged duration of elevated liver chemistries without improvement. Suggests this may be another form of chronic liver injury and not DILI. |
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Histopathology of PJ polyp. |
Their histology is characterized by extensive smooth muscle arborization throughout the polyp. |
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Mode of inheritance for Juvenile Polyposis syndrome? |
autosomal dominant fashion and has been associated with mutations in either the SMAD4 or BMPR1A gene |
