Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
Gastrointestinal
FA complete review
| Question | Answer |
|---|---|
| What are common Histamine-2 blockers? | Cimetidine, Ranitidine, Famotidine, and Nizatidine |
| What does the blockage of H-2 receptor by histamine-2 blockers cause? | Decrease H+ secretion by parietal cells |
| What are the most comon uses of Hitamine-2 receptor blockers? | Peptic ulcer disease and mild esophageal reflux |
| What is an important adverse effect of Cimetidine? | Potent inhibitor of cytochrome P-450 |
| What are the common antiandrogenic effcts of Cimetidine? | Prolactin release, gynecomastia, impotence, and decreased libido |
| Which histamine-2 receptor blcoker is the one with the most adverse effects? | Cimetidine |
| What is a common adverse effect of Cimetidine and Ranitidine? | Decrease renal excretion of creatine |
| List of common Proton pump inhibitors: | Omeprazole, Lansoprazole, Esomeprazole, pantoprazole, and dexlansoprazole. |
| Irreversibly inhibit H+/K+ ATP in stomach parietal cells. | Mechanism of action of PPIs |
| What is the mechanism of action so Histamine-2 receptor blockers? | Reversible block of H-2 receptor |
| Common pathologies treated with PPIs? | PUD, gastritis, esophageal reflux, Zollinger-Ellison syndrome, component of therapy for H. pylori, and stress ulcer prophylaxis |
| What are common infections seen with use of PPIs? | C. difficile infection, pneumonia, and acute interstitial nephritis |
| What cation (electrolyte) is severely decreased by chronic use of PPIs? | Serum Mg2+ |
| Why is an elder person at increase risk of bone fracture in case of long term treatment with PPIs? | Due to decreased Mg2+ and decreased Calcium absorption. |
| In the parietal cell of stomach, which drug inhibits Ach action to the M3 receptor? | Atropine |
| What electrolyte imbalance is seen with all antacids? | Hypokalemia |
| What adverdse effets with Aluminum hydroxide? | -Constipation and hypophosphatemia - Proximal muscle weakness, osteodystrophy, and seizures |
| What is the featured adverse effect of Calcium carbonate? | Milk-alkali syndrome (hypercalcemia), and rebound acid. |
| Antiacid able to chelate and decreased effectiveness of drugs? | Calcium carbonate |
| What are the associated adversse effects of Magnesium hydroxide? | Diarrhea, hyperreflexia, hypotension, cardiac arrest |
| MOA of Bismuth and/or sucralfate: | Bind to ulcer base, providing physical protection and allowing HCO3- secretion to reestablish pH gradient in the mucous layer. |
| What kind of enviroment is required in Bismuth? | Acidic |
| What medications are not given with Bismuth? | PPIs and H2 blockers |
| Common PGE2 analog | Misoprostol |
| Misoprostol is a __________________. | PGE1 analog |
| What is the mode of action of misoprostol? | Increase production and secretion of gastric mucous barreir, and decresa acid prodiction |
| Abortifacient PGE1 analog | Misoprostol |
| What is the main use for Misoprostol? | Prevention of NSAID-induced pepti ulcers |
| What is the off-label use of Misoprostol? | Induction of labor (abortive) |
| Why is Misoprostol used to induce abortion? | Ripens the cervix |
| Long-acting somatostatin analog | Octreotide |
| MOA of Octreotide: | Inhibits secretion of various splanchnic vasodilatory hormones |
| What are common uses for Octreotide? | Acute varicieal bleeds, acromegaly, VIPoma, and carcinoid tumors |
| Why is the use of Octreotide associated with develpment of Cholelithiasis? | Due to CCK inhibition |
| What is the mechanism of action of Sulfasalazine? | Combination of Sulfapyridine and 5-aminosalicylitic acid; activated by colonic bacteria |
| What are the most common uses for Sulfasalazine? | Ulcerative colitis, and Crohn disease |
| Severe adverse effects of Sulfasalazine? | Sulfonamide toxicity and reversible oligospermia |
| Agonist a u-opioid receptors. | Loperamide |
| What GI medication is known to slow gut motility? | Loperamide |
| What is the most common condition for using Loperamide? | Diarrhea |
| Ondansetron is an _________ antagonist. | 5-HT3 |
| Powerful central-acting antiemetic. | Ondansetron |
| Which antiemetic is known to decrease vagal stimulation? | Ondansetron |
| What is the clinical use for Ondansetron? | Control vomiting postoperatively and in patients undergoing cancer chemotherapy |
| What are the most serious adverse effects seen with Ondansetron? | 1. QT interval prolongation 2. Serotonin syndrome |
| Metoclopramiede is an: | D2 receptor antagonist |
| MOA of Metoclopramide | Increase resting tone, contractility, LES tone, motily, promoteis gastric empyting. |
| What is the effect of Metoclopramide on conlon transport time? | None |
| Which are the MC uses for Metoclopramide? | 1. Diabetic and postsurgery gastroparesis 2. Antiemetic 3. Persistent GERD |
| Which GI drug is seen iwht development of parkinsonian effects? | Metoclopramide |
| Metoclopramide may have an drug interaaciotn with what other drugs? | Digoxin and diabetic agents |
| Which patients should not be treated with Metoclopramide? | - Small bowel obstruction patiens - Parkison disease patients |
| Why are Parkinson patient patients not treated with Metoclopramide? | Due to D2-receptor blockade. |
| A patient just after a surgery is seen with tardive dyskinesia. Which is the most likely drug causing such adverse effect? | Metoclopramide |
| What is the mode of action of Orlistat? | Inhibits gastric and pancreatic lipase leading to the breakdonw and absorption of dietary fats |
| What are the main types (categories) of laxatives? | 1. Bulk-forming laxatives 2. Osmotic laxatives 3. Stimulants 4. Emollients |
| Examples of Bulk-forming laxatives: | Psyllium, and methylcellulose |
| What are some Osmotic laxatives? | Magnesium hydoxide, magnesium citrate, polyethylene glycol, and lactulose. |
| Most common stimulant laxative | Senna |
| Emollient example? | Docusate |
| Soluble fibers draw water into gut lumen, foring a viscous liquid that promotes peristalsis | Mechanism of action Bulk-forming laxatives |
| What category or type of laxatives may be abused by bulimics? | Osmotic laxatives |
| What is a rare and unique side effect of Stimulant laxatives? | Melanosis coli |
| What is melanosis coli? | Harmless condition in which the lining of the colon turns a shade of black or brown |
| What is the mode of action of Senna? | Enteric nerve stimulation leading to colonic contraction |
| Promotes incorporaton of water and fat into stool. | Mode of action of Emollients |
| What kind of laxatives work by providing osmotic load to draw water into GI lumen? | Osmotic laxatives |
| Substance P antagonist | Aprepitant |
| What medication or GI drug opposes the actions of Substance P? | Aprepitant |
| Which receptors are blocked by Aprepitant? | NK1 receptors in the brain |
| Which medication is used to block the actions by neurokinin-1 receptors in the brain? | Aprepitant |
| What is the use of Aprepitant? | Antiemetic for chemotherapy-induced nausea and vomiting |
| What are colonic polyps? | Growths of tissue within the colon |
| Gross description of colonic polyps | Flat, sessile, or pedunculated on the basis of protrusion into colonic lumen |
| List of Non-neoplastic colonic polyps: | 1. Hamartomatous polyps 2. Mucosal polyps 3. Inflammatory pseudopolyps 4. Submucosal polyps 5. Hyperplastic polyps |
| What conditions are associated with Hamartomatous polyps? | Peutz-Jeghers syndrome and Juvenile polyposis |
| Growths of normal colonic tissue with distorted architecture. | Hamartomatous polyps |
| Solitary colonic lesions/polyps that do not have significant risk of transformation. | Hamartomatous polyps |
| What kind of polyps are seen in Inflammatory bowel disease? | Inflammatory pseudopolyps |
| What is included as Submucosal polyps? | Lipomas, leiomyomas, and fibromas, among others. |
| What kind of polyp is a lipoma considered? | Submucosal polyp |
| What are the most common non-neoplastic polyps? | Hyperplastic polyps |
| Hyperplastic polyps: | Most common; Smaller and predominantly located in the rectosigmoid region |
| Where are most hyperplastic polyps located? | Rectosigmoid region |
| What are the two main types of Malignant polyps? | Adenomatous polyps and Serrated polyps |
| What gene mutations are associated with adenomatous polyps? | APC and KRAS |
| What neoplastic polyps are due to chromosomal instability pathway with mutations in APC and KRAS? | Adenomatous polyps |
| What are the three types of adenomatous polyps? | Tubular, Tubulovillous, and Villous adenomatous polyps |
| Which type of adenomatous polyps has the less potential for malignancy? | Tubular adenomatous polyps |
| Which type of adenomatous polyps is the most prone for malignancy? | Villous adenomatous polyps |
| Tubular < Tubulovillous < Villous | Increasing potential of adenomatous polyp malignancy |
| What is the most relevant symptom of Adenomatous polyposis? | Occult bleeding |
| Premalignant polyps? | Serrated polyps |
| CpG island methylator phenotype. Associated with: | Serrated polyps |
| What is CIMP? | Cytosine base followed by guanine, linked by a phosphodiester bond |
| CIMP is associated with ________________ polyposis. | Serrated |
| MMR gene mutation. Dx? | Serrated polyposis |
| What is the genetic result of silence MMR gene mutation? | Microsatellite instability and mutations in BRAF ---> Serrated polyps |
| Featured finding in biopsy of Serrated polyps? | "Saw-tooth" pattern of crypts |
| What is the cause for Familial adenomatous polyposis? | AD mutation of APC tumor suppressor gene on chromosome 5q21. |
| Mode of inheritance of FAP? | Autosomal dominant |
| What tumor suppressor gene mutation is involved in FAP development? | APC |
| On which chromosome is the APC gene mutated in FAP? | 5q21 |
| What polyposis syndrome is associated with a 2-hit hypothesis? | Familial adenomatous polyposis |
| What is the most significant complication of untreated FAP? | 100% progress to CRC (colorectal cancer) |
| What are some features of FAP? | 1. Thousands of polyps arise starting after puberty 2. Pancolonic 3. Always involves rectum |
| FAP + osseous and soft tissue tumors. Dx? | Gardner syndrome |
| What is Gardner syndrome? | FAP + osseous and soft tissue tumors, congenital hypertrophy of retinal pigment epithelium, impacted/supernumerary teeth. |
| FAP and malignant CNS tumor. Dx? | Turcot syndrome |
| What other type of tumor is associated in Turcot syndrome, along with FAP? | Malignant CNS tumor |
| What are the types of associated CNS tumors in Turcot syndrome? | Medulloblastoma and Glioma |
| What is Peutz-Jeghers syndrome? | AD syndrome featuring numerous hamartomas throughout GI tract, along with hyperpigmented mouth, lips, hands, and genitalia. |
| What type of polyps are associated with Peutz-Jeghers syndrome? | Hamartomatous polyps |
| What are associated risk of Peutz-Jeghers syndrome? | Breast and GI cancers |
| Mode of inheritance of Peutz-Jeghers syndrome? | Autosomal dominant |
| A patient with colonic polyps and hyperpigmented mouth, lips, hands, and genitalia. Dx? | Peutz-Jeghers syndrome |
| A 3 year old with multiple hamartomatous polyps in colon, stomach, small bowel. Dx? | Juvenile polyposis syndrome |
| Juvenile polyposis syndrome is associated with increased risk of _________. | CRC (colorectal cancer) |
| What is the old name of Lynch syndrome? | Hereditary nonpolyposis colorectal cancer (HNPCC). |
| AD mutations of DNA mismatch repair genes with subsequent microsatellite instability. Associated colon pathology? | Lynch syndrome |
| Which part is always involved in Lynch syndrome? | Proximal colon |
| What are the associated cancers of Lynch syndrome? | Endometrial, ovarian, and skin cancers. |
| Approximate percent of Lynch syndrome cases progress to CRC? | 80% |
| What are risk factors of Colorectal cancer? | - Adenomatous and serrated polyposis - Familial cancer syndromes - IBD - Tobacco use - Diet of processed meat with low fiber |
| Presentation of Ascending Colorectal cancer? | Exophytic mass, iron deficiency anemia, and weight loss |
| What is the clinical presentation of Descending CRC? | Infiltrating mass, partial obstruction, colicky pain, and hematochezia. |
| Right sided CRC ---> | Bleeds |
| Left sided CRC ---> | Obstructs |
| Why do Left-sided CRC tend to obstruct more than right sided CRC? | Narrower lumen in the left sided |
| What is the typical finding of CRC by barium enema? | "Apple core" lesion |
| What is a good CRC tumor maker? | CEA |
| At what age should low-risk patients should start screening for CRC? | 50 years old |
| What hematologic condition should raise suspicion of CRC in men over 50 years old and postmenopausal women? | Iron deficiency anemia |
| A person with a first degree relative with Hx of CRC, should start monitoring at what age? | 40 years old, or at least 10 year prior to their relative's presentation. |
| At what age should the brother of a CRC patient, start monitoring, if the sibling presented CRC at age 45? | 35 years old |
| Most mutations of APC cause ---> | FAP |
| Sporadic mutations APC cause _____________. | Colorectal cancer (CRC) |
| What are the two pathways that may be involved in the development of CRC? | 1. Chromosomal instability Pathway 2. Microsatellite instability Pathway |
| What conditions are associated with the Chromosomal instability pathway? | 1. Mutations of APC --> APC 2. Sporadic CRC |
| What mutations are involved in the Microsatellite instability pathway? | Mutations or methylation of mismatch repair gentes (MLH1) |
| Sporadic CRC due to chromosomal instability pathway is caused via: | Adenoma-carcinoma sequence |
| Sporadic CRC due to Microsatellite instability pathway is caused via: | Serrated polyp pathway |
| What conditions are associated with the Microsatellite instability pathway? | Lynch syndrome and some sporadic CRC |
| What cancer has been linked or associated with overexpression of COX-2? | Colorectal cancer (CRC) |
| Which analgesics may used as chemopreventive in CRC? | NSAIDs |
| Why are NSAIDs chemopreventive of CRC? | Inhibits the overexpression of COX-2 |
| Mnemonic used to remember order of events causing CRC via the Chromosomal instability pathway? | AK-53 |
| What does the "AK-53" stand for? | Chromosomal instability pathway order of events: 1. Loss of APC gene 2. KRAS mutation 3. Loss of tumor suppressor genes (p53, DCC) |
| Which are the tumor suppressor genes involved in CRC development via the Chromosomal instability pathway? | p53 and DCC |
| What is caused by the loss of APC gene? | - Decreased intercellular adhesion - Increased proliferation of colon cells |
| What does a KRAS mutation cause in development of CRC? | Unregulated intracellular signaling |
| Increased tumorigenesis is seen at what point of CRC development? | At loss of tumor suppressor gene (p53, DCC) |
| What is cirrhosis? | Diffuse bridging fibrosis and regenerative nodules disrupt normal architecture of liver. |
| Cirrhosis increases the risks of developing which malignancy? | Hepatocellular carcinoma |
| What are the common etiologies for Cirrhosis? | Alcohol, non-alcoholic steatohepatitis, chronic viral hepatitis, autoimmune hepatitis, biliary disease, genetic/metabolic disorders. |
| Portal Hypertension definition: | Increase pressure in portal venous system |
| What are common etiologies of Portal hypertension? | Cirrhosis, vascular obstruction, and schistosomiasis |
| What is the MCC of portal hypertension in the western countries? | Cirrhosis |
| Common examples of vascular obstruction causing portal hypertension? | Portal vein thrombosis, Budd-Chiari syndrome |
| What are the effects of Portal hypertension? | 1. Esophageal varices ---> hematemesis 2. Gastric varices ---> Melena |
| What are common Integumentary manifestation of cirrhosis and portal HTN? | Jaundice, Spider angiomas, Palmar erythema, Purpura, and Petechiae |
| Neurologic symptoms in liver disease? | 1. Hepatic encephalopathy 2. Asterix |
| What is another way to refer to asterix? | "flapping tremor" |
| What are effects in the reproductive system of an indicitula with cirrhosis? | Testicular atrophy (if male), Gynecomastia (maes), and amenorrhea (female) |
| How is Spontaneous bacterial peritonitis also known as? | Primary bacterial peritonitis |
| What is a possible fatal bacterial infection in patients with cirrhosis and ascites? | Primary bacterial peritonitis |
| What are the most common organism that cause Primary Bacterial peritonitis? | Gram (-) organism (E. coli, Klebsiella), and less commonly gram (+) Streptococcus |
| Paracentesis with ascitic fluid absolute neutrophil count (ANC) > 250 cell/mm3. Dx? | Primary Bacterial peritonitis |
| What is the most common treatment for Spontaneous (primary) bacterial peritonitis? | 3rd generation cephalosporin (Cefotaxime) |
| How are serum markers of liver pathology categorized? | 1. Enzymes released in liver damage 2. Functional liver makers |
| Which are the enzymes released in liver damage? | 1. Aspartate aminotransferase and Alanine aminotransferase 2. Alkaline phosphatase 3. g-glutamyl transpeptidase |
| Examples of function liver markers: | Bilirubin, Albumin, Prothrombin time, and Platelets |
| ALT and AST levels in most liver disease? | ALT > AST |
| Which enzyme is more elevated, ALT or AST, in alcoholic liver disease? | AST |
| A higher level of AST than ALT in non-alcoholic liver disease indicates? | Progression to advanced fibrosis or cirrhosis |
| Which conditions have ALP (alkaline phosphatase) elevated? | 1. Cholestasis 2. Infiltrative disorders 3. Bone disease |
| Which enzyme is elevated with ALP in most cases except in bone disease? | g-glutamyl transpeptidase |
| Increased or Decreased. Bilirubin in liver disease? | Increased |
| How are the levels of Albumin altered in liver disease? | Decreased |
| Decreased levels of albumin indicate? | Advanced liver disease |
| Which functional serum markers are elevated in liver disease? | Bilirubin and Prothrombin time |
| Which functional serum markers are decreased in liver disease? | Albumin and Platelets |
| What does a decrease in platelets indicate about the liver? | Advanced liver disease and/or Portal hypertension |
| What is Reye syndrome? | Rare, and often fatal childhood hepatic encephalopathy. |
| What viral infections are often associated with Reye syndrome? | VZV and influenza virus treated with Aspirin. |
| What are findings of Reye syndrome? | - Mitochondrial abnormalities - Fatty liver (microvesicular fatty changes), - Hypoglycemia - Vomiting - Hepatomegaly - Coma |
| What medication intoxication causes Reye syndrome? | Aspirin |
| Result of treating fever or viral infections to children with aspirins? | Reye syndrome |
| How does aspirin cause Reye syndrome? | Decrease B-oxidation by reversible inhibition of mitochondrial enzymes. |
| List of Alcoholic-related liver diseases: | 1. Hepatic steatosis 2. Alcoholic hepatitis 3. Alcoholic cirrhosis 4. Nonalcoholic fatty liver disease 5. Hepatic encephalopathy |
| Macrovesicular fatty liver change that may be reversible with alcohol cessation. Dx? | Hepatic steatosis |
| What is the approximate AST to ALT level in Alcoholic hepatitis? | AST 2:1 ALT |
| What are the histological findings and changes in Alcoholic hepatitis? | - Swollen and necrotic hepatocytes with neutrophilic infiltration - Mallory bodies |
| What liver disease is seen with (+) Mallory bodies? | Alcoholic hepatitis |
| What is the key histologic fining in alcoholic hepatitis? | Mallory bodies |
| What are Mallory bodies? | Intracytoplasmic eosinophilic inclusions of damaged keratin filaments. |
| Final and usually irreversible form of lliver disaase/damage. Dx? | Alcoholic cirrhosis |
| What is a histological feature in early Alcoholic cirrhosis? | Sclerosis around central vein |
| What are the final results/consequences of Alcoholic cirrhosis? | Portal hypertension and End-stage liver disease |
| Which liver disease is due to a metabolic syndrome? | Non-alcoholic fatty liver disease |
| Pathogenesis of Nonalcoholic fatty liver disease | Metabolic syndrome (insulin resistance) --> Obesity --> Fatty infiltration of hepatocytes --> cellular "ballooning" and eventual necrosis. |
| Which, AST or ALT, is higher in Nonalcoholic fatty liver disease? | ALT |
| Non-alcoholic fatty liver disease is _______________ of alcohol use. | Independent |
| What substance is in excess (or decreased secretion) in Hepatic encephalopathy? | NH3 |
| What is the pathogenesis of Hepatic encephalopathy? | Cirrhosis --> portosystemic shunts --> decreased NH3 metabolism which leads to neuropsychiatric dysfunction. |
| What are the Hepatic encephalopathy triggers? | 1. Increased NH3 production and absorption 2. Decreased removal of NH3 |
| What conditions lead to increased NH3 production and absorption? | Due to GI bleed, constipation, and infection. |
| What are conditions that decrease NH3 removal from body, leading to Hepatic encephalopathy? | Renal failure, diuretics, bypassed hepatic blood flow post-TIPS |
| What are the 2 medications used to treat Hepatic encephalopathy? | 1. Lactulose 2. Rifaximin |
| What is the mode of action of Lactulose? | Increase NH4+ generation |
| Mechanism of action of Rifaximin? | Decrease NH3-producing gut bacteria |
| What condition is treated with Lactulose and Rifaximin? | Hepatic encephalopathy |
| What is the MC primary malignant tumor of liver in adults? | Hepatocellular carcinoma (HCC) |
| What is the most common hepatitis virus associated with HCC development? | HBV |
| What are some common conditions leading to Hepatocellular carcinoma? | HCV, HBV, alcoholic and nonalcoholic fatty liver disease, autoimmune disease, hemochromatosis, Wilson disease, and alpha 1- antitrypsin deficiency |
| What are specific carcinogens leading to hepatocellular carcinoma? | Aflatoxin from Aspergillus |
| What is a common condition caused by HCC? | Budd-Chiari syndrome |
| What are some key findings of HCC? | Jaundice, hepatomegaly, ascites, polycythemia, and anorexia. |
| Which protein is elevated in HCC and is used as a diagnostic tool? | Increased alpha-fetoprotein (AFP) |
| Liver angiosarcoma is associated with exposure of which substances? | Arsenic, and vinyl chloride |
| Malignant liver tumor of endothelial origin. Associated with arsenic and vinyl chloride exposure? | Angiosarcoma |
| What is a Cavernous hemangioma? | Most common benign liver tumor |
| Benign liver tumor due to venous malformation in a 40 year old patient. Dx? | Cavernous hemangioma |
| Rare, benign liver tumor, often related to oral contraceptive or anabolic use. Dx? | Hepatic adenoma |
| What substance uses/therapies are associated with Hepatic adenoma development? | Oral contraceptive use and Anabolic use |
| What are the 3 main types of metastasis to liver? | GI malignancies, breast and lung cancer |
| Thrombosis or compression of hepatic veins with centrilobular congestion and necrosis. Dx? | Budd-Chiari syndrome |
| What veins are compressed or obstructed in Budd-Chiari syndrome? | Hepatic veins |
| Key physical finding in Budd-Chiari syndrome? | Absence of JVD |
| No JVD + Ascites, varices, abdominal pain and liver failure + Hx of DVT. Dx? | Budd-Chiari syndrome |
| What liver syndrome is associated with Nutmeg liver? | Budd-Chiari syndrome |
| What are some conditions associated with Buu-Chiari syndrome development? | Hypercoagulable states, polycythemia vera, postpartum state, and HCC. |
| Mottled liver appearance, is termed _______________ ____________. | Nutmeg liver. |
| What causes a1-antitrypsin deficiency? | Misfolded gene product protein aggregates n hepatocellular ER leading to cirrhosis with PAS (+) globules in liver |
| Which two organs are affected by alpha 1- antitrypsin deficiency? | Lungs and liver |
| What does alpha 1-antitrypsin (ATT) deficiency cause in the lungs? | Uninhibited elastase in alveoli which causes decreased elastic tissue causing Panacinar emphysema |
| Which enzyme deficiency leads to liver cirrhosis with PAS (+) globules? | Alpha 1- antitrypsin (ATT) |
| What is jaundice? | Abnormal yellowing of the skin and/or sclera due to bilirubin deposition |
| What are the most common conditions/pathologies that cause increased bilirubin levels? | Hemolysis, Obstruction, Tumor, and Liver disease |
| What are the main conditions leading to increased levels of Conjugated (direct) bilirubin? | 1. Biliary tract obstruction 2. Biliary tract disease 3. Excretion defects |
| What are common biliary tract obstructions that cause Conjugated hyperbilirubinemia? | Gallstones, Cholangiocarcinoma, pancreatic or liver cancer, liver fluke. |
| Which are the MC biliary tract diseases that increment conjugated bilirubin? | 1. Primary Sclerosing Cholangitis 2. Primary Biliary Cholangitis |
| What are common excretion defects leading to Conjugated (direct) hyperbilirubinemia? | Dubin-Johnson syndrome and Rotor syndrome |
| Crigler-Najjar disease causes _________ hyperbilirubinemia. | Unconjugated (indirect) |
| What conditions are associated with development of Unconjugated (indirect) hyperbilirubinemia? | Hemolytic, physiologic (newborns), Crigler-Najjar, and Gilbert syndrome. |
| What conditions lead to Mixed (direct and indirect) hyperbilirubinemia? | Hepatitis, and cirrhosis |
| What is the MC reason for pediatric liver transplantation? | Biliary atresia |
| What is the most common cause of physiologic neonatal jaundice? | Immature UDP-glucuronosyltransferase --> unconjugated hyperbilirubinemia --> jaundice/kernicterus. |
| When is physiologic neonatal jaundice first noticed? | After the first 24 hours of life, and resolves in 1-2 weeks |
| Treatment for Physiologic neonatal jaundice? | Phototherapy (non-UV) isomerizes unconjugated bilirium to water-soluble bilirubin |
| What kind of bilirubin, direct or indicred, is accumulated in Physiologic Neonatal jaundice? | Unconjugated (indirect) bilirubin |
| What are the common signs and sympotso that indicate possible Biliary atresia? | Persistent jaundice after 2 weeks of life, darkening urine, acholic stools, and hepatomegaly |
| What are the labs found in Biliary atresia? | Increased direct bilirubin (conjugated hyperbilirubinemia) and increased GGT. |
| Mode of inheritance of all Hereditary hyperbilirubinemia? | Autosomal recessive |
| Which hyperbilirubinemias have excess Unconjugated bilirubin? | Gilbert syndrome and Crigler-Najjar syndrome |
| Which two known hyperbilirubinemias have excess Conjugated bilirubin? | Dubin-Johnson syndrome and Rotor syndrome |
| What is the reason for Gilbert syndrome development? | Mildly decreased UDP-glucuronosyltransferase conjugation and impaired bilirubin uptake. |
| What enzyme is decresed in Gilbert syndrome? | UDP-glucuronosyltransferase |
| Which is a benign Unconjugated hyperbilirubinemia syndrome? | Gilbert syndrome |
| What type of triggers or events lead to jaundice in Gilbert syndrome? | Stress, illness, or fasting. |
| Absent UDP-glucuronosyltransferase. Dx? | Crigler-Najjar syndrome |
| Which Crigler-Najjar type is more severe? | Type 1 |
| Crigler-Najjar type 2 responds well to ____________________, which increase liver enzyme synthesis. | Phenobarbital |
| If a patient with Crigler-Najjar syndrome responds well to Phenobarbital, it indicates that it is type _____. | 2 |
| What are the findings associated with Crigler-Najjar syndrome? | Jaundce, Kernicterus, and UNCONJUGATED hyperbilirubinemia |
| Bilirubin deposition in the brain. | Kernicterus |
| How does Phenobarbital has proven to work in Type II Crigler-Najjar syndrome? | Increases liver enzyme (UDP-glucuronosyltransferase). |
| What are the two types of Conjugated hyperbilirubinemia? | Dubin-Johnson syndrome and Rotor syndrome |
| What is the most common cause of Dubin-Johnson syndrome? | Conjugated hyperbilirubinemia due to defective liver excretion |
| Rotor syndrome is due to : | Impaired hepatic uptake and excretion by the liver. |
| Gross view of Dubin-Johnson syndrome? | Black (dark) liver |
| Which is most severe, Dubin-Johnson or Rotor syndrome? | Dubin-Johnson syndrome |
| What is the cause of Wilson disease? | Autosomal recessive mutations in hepatocyte copper-transporting ATPase |
| What does the mutation causing Wilson disease results in? | Decreased copper incorporation into apoceruloplasmin and excretion into bile leading to decreased serum ceruloplasmin. |
| Which metal is accumulated in Wilson disease? | Copper |
| Which gene and chromosome suffer mutations in Wilson disease? | ATP7B gene; chromosome 13 |
| Which organs get copper accumulated in Wilson disease? | Liver, brain, cornea, and kidneys |
| Copper in urine. Dx? | Wilson disease |
| What key finding in Wilson disease? | Kayser-Fleisher rings |
| What are Kayser-Fleischer rings? | Deposits in Descemet membrane of cornea |
| What are complications of Wilson disease? | 1. Liver disease (failure, cirrhosis) 2. Neurologic disease (dysarthria, dystonia, tremor, Parkinsonism) 3. Psychiatric disease 4. Kayser-Fleischer rings 5 Hemolytic anemia 6. Renal disease (Fanconi syndrome) |
| What are the Liver complications of Wilson disease? | Hepatitis, liver failure, and cirrhosis |
| What is the treatment of Wilson disease? | Chelation with penicillamine or trientine, and oral zinc |
| Penicillamine is used to treat __________ ____________. | Wilson disease |
| What type of anemia is seen in Wilson disease? | Hemolytic anemia |
| Gene mutated in Hemochromatosis? | HFE |
| HFE gene is located in which chromosome? | Chromosome 6 |
| HLA associated with Hemochromatosis? | HLA-A3 |
| What are the most common mutations in Hemochromatosis? | C282Y mutation > H63D mutation in HFE gene, located in chromosome 6 |
| Abnormal iron sensing and increased intestinal absorption. Dx? | Hemochromatosis |
| What is a common secondary cause of Hemochromatosis? | Chronic transfusion therapy (B-thalassemia) |
| Which organs accumulate/deposited most iron in Hemochromatosis? | Liver, pancreas, skin, heart, pituitary, and joints |
| Modes to identify Hemosiderin? | MRI or Biopsy with Prussian blue stain |
| Why is a young healthy woman with a slow Hemochromatosis progression? | Iron loss through menstruation |
| What metal is accumulated or deposited in organs in Hemochromatosis? | Iron |
| What is the classic triad of Hemochromatosis? | Cirrhosis, Diabete mellitus, and skin pigmentation |
| "bronze diabetes" . Dx? | Hemochromatosis |
| What are secondary complications or symptoms of Hemochromatosis? | - Restrictive and/or Dilated cardiomyopathy - Hypogonadism - Arthropathy |
| Arthropathy in Hemochromatosis? | Calcium pyrophosphate deposition; especially in metacarpophalangeal joints. |
| What is a common cause of death in Hemochromatosis? | Hepatocellular carcinoma |
| What is the treatment for Hemochromatosis? | 1. Repeated phlebotomy 2. Chelation with deferoxamine 3. Chelation with oral deferiprone |
| Deferasisox, Deferoxamine, and deferiprone are: | Iron chelating agents used in Hemochromatosis treatment |
| At what level is Iron overload considered relevant for Hemochromatosis diagnosis? | Total body iron > 20 grams |
| What is the classic type of cardiomyopathy seen as a complication of Hemochromatosis? | Restrictive |
| What are the shared signs and symptoms of all biliary tract diseases? | Pruritus, jaundice, dark urine, light-colored stool, and hepatosplenomegaly. |
| What are the LFTs in Biliary tract diseases? | - Increased conjugated bilirubin, - Increased cholesterol - Increased ALP |
| What are some common biliary diseases? | 1. Primary Sclerosing Cholangitis 2. Primary Biliary cholangitis 3. Secondary Biliary cholangitis |
| Unknown cause of concentric "onion skin" bile duct fibrosis leading to alternating strictures and dilation with "beading" of intra- and extrahepatic bile ducts on ERCP, magnetic resonance cholangiopancreatography (MRCP) | Pathology of Primary Sclerosing Cholangitis |
| Epidemiology of Primary sclerosing cholangitis | Classically in middle-aged men with IBD |
| What are the key features of intra and extrahepatic ducts in PCS? | Alternating structures and dilation with "beading" |
| What condition is seen with concentric "onion skin" bile duct fibrosis? | Primary sclerosing Cholangitis |
| Which biliary tract disease is (+) p-ANCA? | Primary sclerosing Cholangitis |
| What is a biliary conditions caused by Primary Sclerosing Cholangitis? | Secondary biliary cholangitis |
| What IBD is associated strongly with primary sclerosing cholangitis? | Ulcerative colitis (UC) |
| What malignancies are at risk of development in patient with Primary Sclerosing cholangitis? | Cholangiocarcinoma and gallbladder cancer |
| What is the MC Biliary tract disease is most commonly seen in middle-aged women? | Primary biliary cholangitis |
| What is the pathology of Primary Biliary cholangitis? | Autoimmune reaction --> lymphocytic infiltrate + granulomas --> destruction of lobular bile ducts |
| Biliary disease seen with destruction of lobular bile ducts due to lymphocytic infiltrate and granulomas? | Primary Biliary cholangitis |
| Primary biliary cholangitis is (+) ___________________________ antibody. | Antimitochondrial antibody |
| Increased IgM is seen which Biliary tract diseases? | Primary sclerosing cholangitis and Primary biliary cholangitis |
| What are autoimmune disorders associated with Primary Biliary cholangitis? | Sjogren syndrome, Hashimoto thyroiditis, CREST , rheumatoid arthritis, and celiac disease |
| How is Secondary biliary cholangitis complicated? | Development of Ascending cholangitis |
| What is the initial problem in Secondary biliary cholangitis? | Extrahepatic biliary obstruction leading to increased pressure in intrahepatic ducts |
| A patient with gallstone, or any other obstructive lesion, is more susceptible to develop which biliary tract disease? | Secondary biliary cholangitis |
| What are the most common causes of Gallstones? | 1. Increased cholesterol and/or bilirubin, 2. Decreased bile salts 3. Gallbladder stasis |
| Common term of Cholelithiasis? | Gallstones |
| What are the two types of Gallstones? | 1. Cholesterol stones 2. Pigment stones |
| What are common associations for cholesterol gallstones synthesis? | Obesity, Crohn disease, advance age, estrogen therapy, multiparity, and rapid weight loss, and Native American origin. |
| 80% of cholesterol gallstones are __________________. | Radiolucent |
| What causes the opacity of cholesterol gallstones? | Calcifications |
| What are the main risk factors for Gallstones? | Female Fat Fertile (multiparity) Forty (40s year old) |
| What is the most common complication of Gallstones? | Cholecystitis |
| Black pigment gallstones are due to: | Calcium bilirubinate and hemolysis |
| Which pigment gallstone type is radiolucent? | Brown; due to infection |
| Dark pigment gallstone is _____________. | Radiopaque |
| What pathologies or conditions associated of Pigment gallstones? | Crohn disease, chronic hemolysis, alcoholic cirrhosis, advanced age, biliary infections, and total parental nutrition. |
| Neurohormonal activation triggers contraction of gallbladder, forcing stone into cystic duct. | Biliary colic |
| What is a common neurohormonal activation for a biliary colic? | CCK after a fatty meal |
| Presence of gallstone in the common bile duct. Dx? | Choledocholithiasis |
| What is the MC type of Cholecystitis? | Calculous cholecystitis |
| Calculous cholecystitis is due to: | Gallstone impaction in the cystic duct resulting in inflammation and gallbladder wall thickening |
| What are the major causes of Acalculous cholecystitis? | Gallbladder stasis, hypoperfusion, or infection (CMV) |
| What is the Murphy sign? | Inspiratory arrest on RUQ palpation due to pain |
| What sign is associated with Cholecystitis? | Murphy sign |
| Where does pain radiate in a person with (+) Murphy sign? | Right shoulder |
| What is Gallstone ileus? | Fistula between gallbladder and GI tract --> stone enters GI lumen which leads obstructs at ileocecal valve |
| Where is the MC place were a fistula will produce gallstone ileus? | Ileocecal valve |
| Calcified gallbladder due to chronic cholecystitis. Dx? | Porcelain gallbladder |
| What is the common treatment of Porcelain gallbladder? | Prophylactic cholecystectomy due to high rates of gallbladder cancer |
| What is Ascending cholangitis? | Infection of biliary tree usually due to obstruction that leads to stasis/bacterial overgrowth. |
| What is the Charcot triad of cholangitis? | Jaundice, fever, and RUQ pain |
| What is Reynolds pentad? | Charcot triad plus altered mental status and shock (hypotension) |
| Charcot triad + Altered mental status + Shock = | Reynolds pentad |
| Autodigestion of pancreas by pancreatic enzymes surrounded by edema. Dx? | Acute pancreatitis |
| What are the causes of acute pancreatitis? | I GET SMASHED: Idiopathic Gallstones Ethanol Steroids Mumps Autoimmune disease Scorpion sting Hypercalcemia/Hypertriglyceremia ERCP Drugs |
| What are common drugs that are linked to development of acute pancreatitis? | Sulfa drugs, NRTIs, and Protease inhibitors |
| Complete 3 item list for diagnose of Acute pancreatitis: | 1. Acute epigastric pain often radiating to the back 2. Increased serum amylase or lipase to 3x upper limit 3. Characteristic imaging findings |
| Which serum level is more specific when diagnosis acute pancreatitis? | Lipase |
| What are some common complications of acute pancreatitis? | 1. Pseudocyt 2. Abscess 3. Necrosis 4. Hemorrhage, infection and organ failure 5. Hypocalcemia |
| What is characteristic of a pseudocyst due to acute pancreatitis? | Lined by granulation tissue, not epithelium |
| What lines the pseudocyst due to acute pancreatitis? | Granulation tissue |
| How does acute pancreatitis cause hypocalcemia? | Due to precipitation of Ca2+ soaps |
| Pathology of chronic pancreatitis? | Chronic inflammation, atrophy, and calcification of the pancreas |
| Which are the two major causes of chronic pancreatitis? | Alcohol abuse and genetic predisposition |
| What condition poses a genetic predisposition to the development of chronic pancreatitis? | Cystic fibrosis |
| Complications of chronic pancreatitis? | Pancreatic insufficiency and Pseudocysts |
| How is Pancreatic insufficeny clinically presented? | Steatorrhea, fat-soluble vitamin deficiency, and diabetes mellitus |
| Which, acute or chronic pancreatitis, always have elevated amylase and lipase serum levels? | Acute pancreatitis |
| Where does Pancreatic adenocarcinoma arise from? | Pancreatic ducts |
| Which part of the pancreas are tumor likely to be located? | Head of Pancreas |
| What is the result of tumors in the head of pancreas? | Obstructive jaundice |
| What is the most specific tumor serum marker of Pancreatic adenocarcinoma? | CA 19-9 |
| (+) CA 19-9. Dx? | Pancreatic adenocarcinoma |
| WHat are common risk factors of Pacreatic adenomcarcinoma? | Tobacco use, Chronic pancreatitis Diabetes Age > 50 years Jewish and African-American males |
| What are the most significant clinical features of Pancreatic adenocarcinoma? | - Abdominal pain radiating to the back, - Weight loss - Migratory thrombophlebitis |
| What is another term used for Migratory thrombophlebitis seen in Pancreatic adenocarcinoma? | Trousseau syndrome |
| Redness and tenderness on palpation of extremities | Trousseau syndrome |
| What are the two signs/syndromes that are present in Pancreatic adenocarcinoma? | Trousseau syndrome and Courvoisier sign |
| What is Courvoisier sign? | Obstructive jaundice with palpable, non-tender gallbladder |
| What is the treatment (s) for Pancreatic adenocarcinoma? | 1. Whipple procedure 2. Chemotherapy 3. Radiation therapy |
| What is the Whipple procedure? | Complex operation to remove the head of the pancreas, the first part of the small intestine (duodenum), the gallbladder and the bile duct. |
| What part of the pancreas is often removed by the Whipple procedure? | Head of Pancreas |
| What is Sialolithiasis? | Stones in salivary gland duct |
| Which are the major salivary glands in which stones can appear? | Paratid, Submandibular, and sublingual. |
| What duct is the most common salivary duct in which stones may appear? | Wharton duct |
| What is the typical presentation of sialolithiasis? | Recurrent pre/periprandial pain and swelling in affected gland. |
| What are the most common causes of sialolithiasis? | Dehydration and trauma |
| What is the treatment for salivary stones? | NSAIDS, gland massage, warm compresses and sour candies |
| Why are sour candies used in treating Sialolithiasis? | To promote salivary flow |
| What is Sialadenitis? | Inflammation of salivary gland due to obstruction, infection, or immune-mediated mechanisms. |
| Which gland is most commonly affected by salivary gland tumor? | Parotid gland |
| Tumors in smaller salivary glands ---> | More likely malignant |
| If salivary gland tumor present with facial pain or paralysis, it most likely suggest involvement of: | CN VII |
| What are the 3 most common Salivary gland tumors? | 1. Pleomorphic adenoma 2. Mucoepidermoid carcinoma 3. Warthin tumor |
| Benign mixed tumor of the salivary gland | Pleomorphic adenoma |
| What is the most common salivary gland tumor? | Pleomorphic adenoma |
| What is the composition of Salivary gland Pleomorphic gland tumor? | Chondromyxoid stroma and epithelium |
| What is the most common malignant tumor of the salivary glands? | Mucoepidermoid carcinoma |
| Which salivary tumor has mucinous and squamous components? | Mucoepidermoid carcinoma |
| What is anther name for Warthin tumor? | Papillary cystadenoma lymphomatosum |
| Which salivary gland tumor often present with Germinal centers? | Warthin tumor |
| Benign cystic tumor with germinal centers of salivary gland origin? | Warthin tumor |
| Which population is often seen with Warthin tumor development? | Smokers |
| Failure of LES to relax due to loss of myenteric (Auerbach) plexus due to loss of postganglionic inhibitory neurons. Dx? | Achalasia |
| What does the postganglionic inhibitory neurons involved in Achalasia, contain? | NO and VIP |
| Which GI sphincter fails to relax leading to Achalasia? | Lower Esophageal Sphincter (LES) |
| Which is another name for the Myenteric plexus loss in Achalasia? | Auerbach |
| What are the manometric findings of Achalasia? | - Uncoordinated or absent peristalsis with high LES resting pressure ---> progressive dysphagia to solids and liquids |
| "bird's beak" | Achalasia |
| What causes the common "bird's beak" in Achalasia? | Barium swallow shows dilated esophagus with an area of distal stenosis |
| Dilated esophagus with an area of distal stenosis. This causes with typical sign? | "bird's beak" in Barium swallow |
| Achalasia is associated with increased risk of _______________________. | Esophageal cancer |
| What common condition leads to development of secondary achalasia? | Chagas disease |
| T. cruzi infection is common cause of: | Chagas disease which can cause Achalasia subsequently. |
| Extraesophageal malignancies that cause mass effect of paraneoplastic effects, are known possible causes of: | Secondary achalasia |
| Transmural, usually distal esophageal rupture with pneumomediastinum due to violent retching. Dx? | Boerhaave syndrome |
| What is Boerhaave syndrome? | Transmural, esophageal distal ruputure due to viiolent/inetense retching. |
| What is an accompanying symptoms or condition of Boerhaave syndrome? | Pneumomediastinum |
| What is pneumomediastinum? | Rare situation in which air leaks into the mediastinum |
| Air in the mediastinum? | Pneumomediastinum |
| Why is there subcutaneous emphysema in a patient with Boerhaave syndrome? | Due to dissecting air |
| Crepitus felt in the neck region or chest wall. Possible diagnosis? | Boerhaave syndrome with Pneumomediastinum which lead to Subcutaneous emphysema. |
| Infiltration of eosinophils in the esophagus often in atopic patients. | Eosinophilic esophagitis |
| What are the endoscopy findings of Eosinophilic esophagitis? | Esophageal rings and linear furrows |
| What condition is often caused by food allergens, and leads to dysphagia and food impaction? | Eosinophilic esophagitis |
| Associations of Esophageal strictures? | Caustic ingestion and acid reflux |
| Dilated submucosal veins in lower 1/3 of esophagus, secondary to portal hypertension. Dx? | Esophageal varices |
| Which patients are often seen with Esophageal varices? | Cirrhotics |
| Candida -induced esophagitis? | White pseudomembrane |
| How are the ulcers caused by esophagitis concurrent HSV-1 and CMV caused? | HSV-1 ---> punched-out ulcers CMV ---> linear ulcers |
| Esophagitis is associated by: | Reflux, immunocompromised, caustic ingestion, or pill esophagitis. |
| What are common medication (pills) are associated with development of Esophagitis? | Bisphosphonates, tetracyclines, NSAIDs, iron, and potassium chloride. |
| What are the most common signs of GERD? | Heartburn, regurgitation, and dysphagia. |
| What are some possible symptoms seen with GERD? | Hoarseness and chronic cough |
| Which obstructive lung disease is often associated with GERD? | Asthma |
| Partial-thickness mucosal laceration at gastroesophageal junction due to severe vomiting. Dx? | Mallory-Weiss syndrome |
| Which two populations are most often presented with Mallory-Weiss syndrome? | Alcoholics and bulimics |
| How does the laceration caused by Mallory-Weiss syndrome differs from the Boerhaave syndrome lacerations? | MWS it is partially mucosal laceration at the Gastroesophageal junction. BS laceration : transmural; distal esophageal |
| What is the triad of Plummer-Vinson syndrome? | 1. Dysphagia 2. Iron deficiency anemia 3. Esophageal webs |
| What is a common associated condition/symptoms seen with Plummer-Vinson syndrome? | Glossitis |
| Plummer-Vinson syndrome increases risk of developing | Esophageal squamous cell carcinoma |
| Dysphagia, Iron deficiency anemia, and Esophageal webs. Dx? | Plummer-Vinson syndrome |
| What is the esophageal condition part of CREST syndrome? | Scleroderma esophageal dysmotility |
| Pathogenesis of Scleroderma esophageal dysmotility? | Esophageal smooth muscle atrophy leads to a decreased LES pressure and dysmotility -------> Acid reflux and dysphagia ---> stricture, Barrett esophagus, and aspiration |
| What is Barrett esophagus? | Specialized intestinal metaplasia of nonkeratinized stratified squamous epithelium with intestinal epithelium in distal esophagus. |
| Barrett esophagus increases the risk of what type of esophageal cancer? | Esophageal adenocarcinoma |
| Replacement of normal esophageal epithelium by intestinal epithelium. Dx? | Barrett esophagus |
| What is the normal type of epithelium found in the esophagus (specially the distal part)? | Nonkeratinized stratified squamous epithelium |
| What is the kind of epithelium that replaces normal epithelium in the esophagus of a Barrett esophagus patient? | Non-ciliated columnar with goblet cells |
| Esophageal histologic view shows nonciliated columnar epithelium with goblet cells. Dx? | Barrett esophagus |
| Which part of the esophagus is most affected by Squamous cell carcinoma? | Upper 2/3 |
| What type of esophageal cancer is seen in the lower 1/3 of the esophagus? | Adenocarcinoma |
| List of risk factors that increase risk of Esophageal squamous cell carcinoma. | Alcohol Hot liquids Caustic strictures Smoking Achalasia |
| Which type of esophageal cancer is more common worldwide? | Squamous cell carcinoma of the esophagus |
| Which type of esophageal cancer is more common in the USA? | Adenocarcinoma of the esophagus |
| Which are the risk factors that increase probability of esophageal adenocarcinoma? | - Chronic GERD - Barrett esophagus - Obesity - Smoking - Achalasia |
| If the cancer cells are found in the upper 2/3 of esophagus. Most likely type of esophageal cancer is? | Squamous cell carcinoma |
| What are the most common causes of acute gastritis? | 1. NSAIDS 2. Burns (Curling ulcer) 3. Brain injury (Cushing ulcer) |
| How doe NSAIDS cause gastritis? | Decrease PGE2 which leads to a decrease in gastric mucosa protection |
| Which population is most prone to develop acute gastritis? | Alcoholics and those taking daily NSAIDs |
| A Curling ulcer refers to a _____________. | Burn |
| A Cushing ulcer refers to a _______________ ______________. | Brain injury |
| What is the result of a Curling ulcer? | Hypovolemia which leads to mucosal ischemia |
| How does a Cushing ulcer lead to acute gastritis? | Increase in vagal tone causes increase ACh which causes an elevation in H+ production. |
| Increase vagal tone leads to ---------------> | Increase in ACh |
| Increased levels of ACh in the stomach will cause --> | Increase in H+ production |
| What are the possible consequences of chronic gastritis? | 1. Atrophy (hypochlorhydria --> hypergastrinemia) 2. Intestinal metaplasia |
| What is the most common cause of gastritis? | H. pylori infection |
| What conditions are often associated as result of H. pylori-induced gastritis? | Peptic ulcer disease and MALT lymphoma |
| Which part of the stomach is most affected by H. pylori infection? | Antrum |
| Antibodies to parietal cells and intrinsic factor. Increase risk of anemia. Dx? | Autoimmune gastritis |
| Which part of the stomach is most affected the autoimmune gastritis? | Body/fundus of stomach |
| What is the MCC of antrum localized gastritis? | H. pylori infection |
| If the gastritis is known to be in the body of the stomach. Most likely etiology? | Autoimmune gastritis |
| Hyperplasia of gastric mucosa causing a hypertrophied rugae. Dx? | Menetrier disease |
| What is the result of Menetrier disease? | Excess mucus production with resultant protein loss and parietal cell atrophy with decreased acid production |
| What gastric disease is considered precancerous? | Menetrier disease |
| Why Menetrier disease presented with edema? | Due to protein loss |
| What is the MC gastric cancer? | Gastric adenocarcinoma |
| What blood type is often associated with development of gastric cancer? | Blood type A |
| What is the most common clinical presentation of Gastric cancer? | Late, weight loss, abdominal pain, early satiety, and sometimes Acanthosis nigricans or Leser-Trelat sign |
| What are some rare features of Gastric cancer? | Acanthosis nigricans, and Leser-Trélat sign. |
| What are the two types of gastric adenocarcinoma? | Intestinal and Diffuse gastric cancer |
| Which type of gastric cancer is associated with H. pylori infection? | Intestinal type |
| What are some common associations/risk factors for Intestinal gastric cancer? | 1. H. pylori infection 2. Dietarary nitrosaminies (smoked foods) 3. Tobacco smoking 4. Achlorhydria 5. Chronic gastritis |
| Which gastric cancer is often seen at the lesser curvature of the stomach? | Intestinal type |
| Which type of gastric cancer presents like an ulcer with raised margins? | Intestinal type |
| Signet ring cells are seen with: | Diffuse gastric carcinoma |
| Which gastric cancer type is not associated with H. pylori infection? | Diffuse type |
| What are Signet ring cells? | Mucin-filled cells with peripheral nuclei |
| What are some features of Diffuse gastric cancer? | 1. Signet ring cells 2. Stomach wall grossly thickened and leathery |
| Linitis plastica | Diffuse gastric carcinoma |
| Common nodes/sites of gastric cancer metastases? | 1. Virchow node 2. Krukenberg tumor 3. Sister Mary Joseph nodule |
| Involvement of left supraclavicular node by metastasis form the stomach. | Virchow node |
| What is Krukenberg tumor? | Bilateral metastasis to ovaries form stomach cancer. |
| What type of cells are often abundant in Krukenberg tumor? | Mucin-secreting, signet ring cells |
| Name of nodule. Subcutaneous periumbilical metástasis. | Sister Mary Joseph nodule |
| Most common location of gastric cancer metastases to the periumbilical region | Sister Mary Joseph nodule |
| If the gastric cancer is known to come from another organ. Which are the most common sites of metastases to stomach? | Lymph node and liver |
| What are the two types of ulcers seen with PUD? | Gastric and Duodenal ulcers |
| Which ulcer is greater with meals? | Gastric ulcer |
| What is the mechanism of action in which gastric ulcers cause disease? | Decrease mucosal protection against gastric acid |
| Which type of ulcer is associated with increased risk of carcinoma? | Gastric ulcer |
| Biopsy margins to rule out malignancy. Association? | Gastric ulcer |
| Decreases pain with meals. Ulcer type? | Duodenal ulcer |
| Which ulcer type is associated with weight loss? | Gastric ulcer |
| Person with _______________ ulcer tends to gain weight. | Duodenal |
| How do duodenal ulcers cause disease? | 1. Decrease mucosal porteiction, or, 2. Increase gastric acid secretion |
| Which type of PUD ulcer is not associated with increased risk of carcinoma? | Duodenal ulcer |
| Ulcer seen with hypertrophy of Brunner glands. | Duodenal ulcer |
| What are the 3 MC complication of ulcers? | Hemorrhage, Obstruction, and Perforation |
| What is the most common complication of ulcers? | Hemorrhage |
| Which duodenal ulcer location is most susceptible for hemorrhage? | Posterior |
| Which arterial body bleeds in a gastric ulcer on the lesser curvature of stomach? | Left gastric artery |
| Which artery bleeds in a hemorrhage-complicated ulcer in the posterior doudenum? | Gastroduodenal artery |
| Which is the MC artery that bleeds in a hemorrhagic gastric ulcer? | Left gastric artery |
| Which artery is most common to bleed/hemorrhage in a duodenal ulcer? | Gastroduodenal artery |
| What is a common imaging sign of a perforated duodenal ulcer? | Free air under diaphragm |
| What is an important accompanying symptoms of perforated Duodenal ulcer? | Referred pain to the shoulder via irrigation of phrenic nerve |
| Which nerve conducts referred shoulder pain from an perforated duodenal ulcer? | Phrenic nerve |
| Free air under diaphragm. Dx? | Perforated duodenal ulcer |
| What stain is used to identify fecal fat? | Sudan stain |
| What symptoms seen with all malabsorption syndromes? | Diarrhea, steatorrhea, weight loss, weakness, vitamin and mineral deficiencies. |
| Gluten-sensitive enteropathy | Celiac disease |
| What is Celiac disease? | Autoimmune-mediated intolerance of gliadin |
| To which protein is a Celiac disease patient sensitive to? | Gliadin |
| What is Gliadin? | Gluten protein found in wheat |
| What are some common associations to Celiac disease? | 1. HLA-DQ2 and HLA-DQ8 2. Northern European descent 3. Dermatitis herpetiformis 4. Decreased bone density |
| Associated cutaneous condition of Celiac disease? | Dermatitis herpetiformis |
| What are the autoantibodies of Celiac disease? | - IgA anti-tissue transglutaminase (IgAtTG) - anti-endomysial - anti-deamidated gliadin peptide |
| What histological findings of Celiac disease? | Villous atrophy, crypt hyperplasia, and intraepithelial lymphocytosis |
| What areas of small intestine is affected in Celiac disease? | Distal duodenum and/or proximal jejunum |
| (+) D-xylose test. Which a possible malabsorption disease? | Celiac disease |
| Normal-appearing villi + lactase deficiency? | Lactose intolerance |
| What are clinical signs of Lactose intolerance? | Osmotic diarrhea with decreased stool pH |
| Test for aid in diagnosis of Lactose intolerance? | Lactose hydrogen breath test |
| What are causes of Pancreatic deficiency? | Chronic pancreatitis, cystic fibrosis, and obstructing cancer. |
| What are some consequences of Pancreatic insufficiency? | Malabsorption of fat, fat-soluble vitamins (including B12). |
| What are some changes caused by Pancreatic insufficiency? | Decrease duodenal pH Decrease fecal elastase |
| Similar symptology of Celiac sprue but responds to antibiotics. | Tropical sprue |
| What are some associated conditions of Tropical sprue? | Folate and Vitamin B12 deficiency ---> megaloblastic anemia |
| Infection with Tropheryma whipplei. Dx? | Whipple disease |
| PAS (+) foamy macrophages in intestinal lamina propria, mesenteric nodes. Dx? | Whipple disease |
| What are the most significant clinical symptoms of Whipple disease? | Cardiac symptoms, Arthralgias, and Neurologic |
| Which are the two most common Inflammatory bowel disease? | Crohn disease and Ulcerative colitis |
| Where does Crohn disease occurs? | Any portion of the GI tract; most commonly the terminal ileum and colon |
| Skip lesions, and rectal sparing, are characteristics of: | Crohn disease |
| Location of Ulcerative colitis | Continuous colonic lesions, always with rectal involvement |
| Which inflammatory bowel disease always involves the rectum? | Ulcerative colitis |
| Which inflammatory bowel disease spares the rectal area? | Crohn disease |
| Gross morphology of Crohn disease | Transmural inflammation --> fistulas - Cobblestone mucosa, creeping fat, bowel wall thickening, linear ulcers, and fissures |
| Cobblestone mucosa | Crohn disease |
| The gross inspection of a terminal ileum specimen shows creeping fat, thick wall of bowel, and linar ulcers as well as fissures. Dx? | Crohn disease |
| Which IBD shows transmural inflammation? | Crohn disease |
| IBD with fÃstulas formation? | Crohn disease |
| What is the typical sign on Barium swallow of a patient with Crohn disease? | "string sign" |
| Inflammation in UC (ulcerative colitis)? | Mucosal and submucosal inflammation only |
| What is the typical or featured sign in UC? | "lead pipe" due to loss of haustra |
| What gives UC colon the "lead pipe" look? | Los of Haustra |
| Friable mucosa with superficial and/or deep ulcerations. Dx? | Ulcerative colitis |
| IBD with linear ulcerations. MC Dx? | Crohn disease |
| IBD with deep ulcerations. MC Dx? | Ulcerative colitis |
| Noncaseating granulomas and lymphoid aggregates. | Microscopic morphology of Crohn disease |
| Which are the helper T-cells are involved in Crohn's disease immune mediation? | TH1 |
| What is the microscopic morphology of Ulcerative colitis? | Crypt abscesses and ulcers, bleeding, no granulomas. |
| TH2 mediates the immune response of which IB-disease? | Ulcerative colitis |
| UC is ________ mediated. | TH2 |
| Crohn disease is _________- mediated. | TH1 |
| IBD with noncaseating granulomas. Dx? | Crohn disease |
| NO granulomas. MC IBD? | Ulcerative colitis |
| __________ _______________ does not have granuloma formation. | Ulcerative colitis |
| Which are the main complications seen in both, UC and Crohn disease? | Malabsorption/malnutrition, colorectal cancer (increased risk of pancolitis) |
| What are the main complications seen with Ulcerative colitis? | - Fulminant colitis - Toxic megacolon - Perforation |
| Toxic megacolon is a common complication of which IBD? | Ulcerative colitis |
| Fistulas, phlegmon/abscess, structures, and perianal disease, are the main complications of ______________ ______________. | Crohn disease |
| What is a subsequential compilation of enterovesical fistula, seen in Crohn disease? | Recurrent UTI and pneumaturia |
| Perianal disease is a common complication of _______ ___________. | Crohn disease |
| Which IBD is always seen with bloody diarrhea? | Ulcerative colitis |
| What are extraintestinal manifestations of both, UC and Crohn disease? | 1. Rash (pyoderma gangrenosum, erythema nodosum) 2. Eye inflammation (episcleritis, uveitis) 3. Oral ulcerations (aphthous stomatitis) 4. Arthritis (peripheral, spondylitis) |
| What are extraintestinal manifestations are exclusive of Crohn disease? | Kidney stones (calcium oxalate), gallstones, and may be (+) for anti-Saccharomyces cerevisiae antibodies (ASCA) |
| (+) ASCA | Extraintestinal manifestation of Crohn's disease |
| What is the main extraintestinal manifestation of Ulcerative colitis? | Primary Sclerosing cholangitis |
| List of common treatment options for Crohn disease. | Corticosteroids Azathioprine Antibiotics Infliximab Adalimumab |
| What are treatment options of Ulcerative colitis? | 5-aminosalicylic preparations (mesalamine), 6-MP, infliximab, and colectomy. |
| Skip lesions | Crohn disease |
| Cobblestone mucosa | Crohn disease |
| Calcium oxalate kidney stones + cholesterol gallstones + ASCA (+) | Crohn disease |
| Always rectal involvement | Ulcerative colitis |
| IBD with Primary sclerosing cholangitis (PSC) | Ulcerative colitis |
| Which monoclonal antibody (drug) is used in both, Crohn disease and Ulcerative colitis? | Infliximab |
| Which are the criteria added to recurrent abdominal pain in order to diagnose Irritable bowel syndrome? | 1. Related to defecation 2. Change in stool frequency 3. Change in consistency of stool |
| Mixed diarrhea/constipation episodes in a middle aged woman. Dx? | Irritable bowel syndrome |
| What is the most common cause of Appendicitis in children? | Lymphoid hyperplasia |
| What is the MCC of appendicitis in adults? | Obstruction by fecalith |
| Initial diffuse periumbilical pain migrates to McBurney point. | Pain migration seen in appendicitis |
| Perforated appendicitis leads to development of __________. | Peritonitis |
| What are common signs in clinically of appendicitis? | Pain in RLQ after it migrated from periumbilical region. Psoas, Obturator, and Rovsing signs (+) Guarding and rebound tenderness on exam |
| Pain in McBurney point. Dx? | Appendicitis |
| Location of McBurney point? | 1/3 the distance from right anterior superior iliac spine to umbilicus |
| Blind pouch protruding from the alimentary tract that communicates with the lumen of the gut. Dx? | Diverticulum |
| Most diverticula are ____________ diverticula. | False |
| What is a "true" diverticulum? | All gut walls layers outpouch |
| What is an common example of a true diverticulum? | Meckel |
| Only mucosa and submucosa output. Dx? | False diverticulum |
| Where is a common place for a False diverticulum? | At vasa recta perforate muscularis externa |
| What is diverticulosis? | Many false diverticula of the colon, commonly the sigmoid. |
| What is the cause of diverticulosis? | Increased intraluminal pressure and focal weakness in colonic wall. |
| What are some associated causes of diverticulosis? | Obesity and diets low in fiber, high in total fat/red meat |
| What is diverticulitis? | Inflammation of diveticula with wall thickineing, classically causes LLQ pain, fever, and leukocytosis |
| Which type of GI tract diverticula condition lead to LLQ pain and leukocytosis? | Diverticulitis |
| What are the most common complications of Diverticulitis? | Abscess, fistula, obstruction, and perforation |
| What is the most common fistula formed in Diverticulitis? | Colovesical fistula leading to pneumaturia |
| Pharyngoesophageal false diverticulum. | Zenker diverticulum |
| What is the cause of Zenker diverticulum? | Esophageal dysmotility causes herniation of mucosal tissue at Killian triangle between the thyropharyngeus and cricopharyngeus parts of the inferior pharyngeal constrictor |
| What are the most common symptom of Zenker diverticulum? | Dysphagia, obstruction, gurgling, aspiration, foul breath, and neck mass |
| What is Meckel diverticulum? | True diverticulum; Persistance of the Vitelline (omphalomesenteric) duct. |
| What is contained in a Meckel diverticulum? | Ectopic acid-secreting gastric mucosa and/or pancreatic tissue. |
| What is the most common congenital anomaly of GI tract? | Meckel diverticulum |
| How is Meckel diagnosis made? | Pertechnetate study for uptake by heterotopic gastric mucosa |
| What are some possible accompanying conditions of Meckel diverticulum? | Hematochezia/melena, RLQ pain, intussusception, volvulus, or obstruction near terminal ileum. |
| 2 feet from the ileocecal valve | Meckel diverticulum |
| Killian triangle. Dx? | Zenker diverticulum |
| What pathology presents as true diverticulum and contains pancreatic/gastric mucosa? | Meckel diverticulum |
| Congenital megacolon characterized by lack of ganglion cells/enteric nervous plexus (Auerbach and Meissner) in distal segment of colon. | Hirschsprung disease |
| What is the cause of Hirschsprung disease? | Failure of neural crest cell migration |
| Hirschsprung disease associated mutations: | RET mutations |
| What trisomy is associated with Hirschsprung disease? | Down syndrome |
| What is the "squirt sign"? | Explosive expulsion of feces |
| Absence of ganglionic cells on rectal suction biopsy. Dx? | Hirschsprung disease |
| What is the clinical presentation of Hirschsprung disease? | Bilious emesis, abdominal distension, and failure to pass meconium within 48 hours --> chronic constipation |
| What conditions is seen with a "transition zone"? | Hirschsprung disease |
| What causes the "transition zone" in Hirschsprung disease? | The change in the colon from normal colon innervation to aganglionic portion of colon. |
| What is the "transition zone" caused in Hirschsprung disease? | Normal portion of colon proximal to the aganglionic segment is dilated. |
| Anomaly of midgut rotation during fetal development. Dx? | Malrotation |
| Neonate has not pass meconium in the first 2 das of life. Dx? | Hirschsprung disease |
| What does the abnormal rotation of the midgut during fetal development causes? | 1. Improper positioning of bowel and, 2. Formation of fibrous bands (Ladd bands) |
| What bands are formed in Malrotation? | Ladd bands |
| What are Ladd bands? | Fibrous bands formed by malrotation |
| What are possible serious complications of Malrotation? | Volvulus and duodenal obstruction |
| Where is the bowel improperly positioned in Malrotation? | Small bowed clumped in the right side |
| What is Volvulus? | Twisting of portion of bowel around its mesentery |
| What is the possible result of volvulus? | Obstruction and infarction of the area |
| Which population is most common to develop Midgut volvulus | Children and infants |
| What volvulus is seen in children/infants? | Midgut volvulus |
| The elderly develop _____________ volvulus, more often. | Sigmoid |
| What type of volvulus is seen in a 75 year old man? | Sigmoid volvulus |
| X-ray -- Coffee bean sign | Sigmoid volvulus |
| Intestine in volvulus, twist around its ____________________. | Mesentery |
| Telescoping of proximal bowel segment into a distal segment. Dx? | Intussusception |
| What is the MC location of Intussusception | Ileocecal junction |
| The compromised blood supply seen in Intussusception causes --> | Intermittent abdominal pain often with "currant jelly" stools |
| What is a common action taken by patients with intussusception to ease the pain? | Draw legs to the chest |
| Physical exam: (+) sausage-shaped mass. Dx? | Intussusception |
| What is the sign seen in Ultrasound of a patient with intussusception? | "Target sign" |
| What is the most common cause of Intussusception? | Lead point |
| What is a Lead Point? | A piece of intestinal tissue that protrudes into the bowel lumen |
| What is the most common pathology associated or due to a lead point? | Meckel diverticulum |
| What are some possible associative causes of Intussusception? | Rotavirus vaccine Henoch-Schonlein purpura Recent viral infection (adenovirus) |
| What is a possible complication of Peyer patch hypertrophy? | Intussusception |
| What is Acute mesenteric ischemia? | Critical blockage of intestinal blood flow |
| What is a key feature during the physical examination of patient with acute mesenteric ischemia? | Abdominal pain out of proportion to physical findings |
| Stool careachreics in acute mesenteric ischemia? | red "currant jelly" stools |
| Intestinal angina = | Chronic mesenteric ischemia |
| Which artery is most common to be occluded in acute mesenteric ischemia? | SMA |
| Atherosclerosis of celiac artery, SMA, or IMA. Dx? | Chronic mesenteric ischemia |
| What are some clinical characteristics or features of chronic mesenteric ischemia? | Postprandial pain caused by intestinal hypoperfusion, which leads to food aversion and weight loss |
| Which areas are most susceptible for Colonic ischemia? | Watershed areas |
| What are the most common watershed areas affected by colonic ischemia? | Splenic flexure and distal colon |
| What is the common sign on imaging of Colonic ischemia? | Thumbprint sign due to mucosal edema/hemorrhage |
| Tortuous dilation of vessels ---> hematochezia. | Angiodysplasia |
| Which side of colon is most affected by angiodysplasia? | Right side |
| What are common associated conditions of Angiodysplasia? | Aortic stenosis and von Willebrand disease |
| What is an Adhesion? | Fibrous band of scar tissue; commonly after a surgery |
| What is the most common cause of Small Bowel obstruction? | Adhesions |
| How are adhesions diagnosed? | Multiple dilated small bowel loops on X-ray |
| What is shown in x-ray of patient with Adhesions? | Multiple dilated small bowel loops |
| Intestinal hypomotility without obstruction leading to constipation and decreased flatus. Dx? | Ileus |
| What are symptoms seen with Ileus? | Constipation, decreased flatus, distended/tympanic abdomen with decreased bowel sounds |
| Common associations of Ileus: | Abdominal surgeries, opiates, hypokalemia, and sepsis |
| What electrolyte imbalance is often associated with development of ileus? | Hypokalemia |
| What is the purpose of cholinergic drugs to treat ileus? | Stimulate intestinal motility |
| What condition is often seen with Meconium ileus? | Cystic fibrosis |
| A neonate with CF, often aslos develops: | Meconium ileus |
| Meconium plug obstructs intestine in neonate. Dx? | Meconium ileus |
| What population is often seen with Necrotizing enterocolitis? | Premature, formula-fed infants with immature immune system. |
| What are consequences of Necrotizing enterocolitis? | Necrosis of intestinal mucosa with possible perforation, leading to pneumatosis intestinalis, free air in abdomen, and portal venous gas. |
| Severe consequences of Necrotizing enterocolitis? | Perforation leading to: 1. Pneumatosis intestinalis 2. Free air in abdomen 3. Portal venous gas |
| What cells produce Gastrin? | G cells |
| Where are G cells located? | Antrum of Stomach and Duodenum |
| What actions are performed by Gastrin? | Increase in: - Gastric H+ secretion - Growth of gastric mucosa - Gastric motility |
| Chronic use of PPI can cause an increase in secretion of which GI regulatory substance? | Gastrin |
| What regulatory substance is seen in increased levels by chronic atrophic gastritis (H. pylori)? | Gastrin |
| Gastrinomas produce elevated levels of ______________. | Gastrin |
| What change in pH would cause an decrease in Gastrin production? | pH < 1.5 |
| What conditions lead to the increase release of Gastric? | Increase by stomach distension/ alkalinization, amino acids, peptides, vagal stimulation via gastrin-releasing peptide (GRP) |
| What substance is secreted by D cells? | Somatostatin |
| Where are found D cells? | Pancreatic islets, and GI mucosa |
| Which cells secrete somatostatin? | D cells |
| What is the main role of Somatostatin? | Inhibits secretion of various hormones |
| Analog of Somatostatin? | Octreotide |
| What is the main use for Octreotide? | Acromegaly |
| What drug is often used for treatment of Acromegaly? | Octreotide |
| What are conditions often treated with Octreotide? | Acromegaly, Carcinoid syndrome, and variceal bleeding |
| List of actions of Somatostatin: | Decrease release of: 1. Gastric acid and pepsinogen secretion 2. Pancreatic and small intestine fluid secretion 3. Gallbladder contraction 4. Insulin and glucagon release |
| What substance decreases the release of insulin and glucagon? | Somatostatin |
| What does the increase the release of Somatostatin? | Acid |
| Vagal stimulation has what effect on Somatostatin? | Decrease release of Somatostatin |
| What cells secrete Cholecystokinin? | I cells |
| Which GI structures have I cells? | Duodenum and Jejunum |
| I cells secrete | Cholecystokinin (CCK) |
| What compounds increase the release of CCK? | Fatty acids and amino acids |
| What actions are increased/ speed up by the release of CCK? | Pancreatic secretion and Gallbladder contraction, and Sphincter of Oddi relaxation. |
| On which pathways does CCK act on to cause pancreatic secretions? | Neural muscarinic pathways |
| What is the effect of CCK on gastric emptying? | Decreases |
| S cell secrete ______________. | Secretin |
| Which part of small intestine have S cells? | Duodenum |
| What Pancreatic substance secretion is increased by Secretin? | HCO3- |
| What is the role of the increasing amount to HCO3- in the duodenum? | Neutralize gastric acid, allowing pancreatic enzymes to function |
| Which regulatory GI substance is secreted by K cells in the duodenum and Jejunum? | Glucose-dependent insulinotropic peptide |
| What is another name for Glucose-dependent insulinotropic peptide? | GIP |
| What conditions lead to an increase release of GIP? | - Fatty acids - Amino acids - Oral glucose |
| What is the exocrine function of GIP? | Decreased gastric H+ secretion |
| What is the Endocrine function of GIP? | Increase insulin release |
| Motilin is secreted by the _______ _____________. | Small intestine |
| What is the role or function of Motilin? | Produces migrating motor complexes (MMCs) |
| What condition increases the production/release/secretion of Motilin? | Fasting state |
| What is a common Motilin receptor agonist? | Erythromycin |
| What is the MC use for Motilin receptor agonists? | Stimulate intestinal peristalsis |
| What substance produces MMCs? | Motilin |
| What GI structures produce VIP? | 1. Parasympathetic ganglia in sphincters 2. Gallbladder 3. Small intestine |
| Known VIP tumor? | VIPoma |
| non-a, non-B islet cell pancreatic tumor that secretes VIP? | VIPoma |
| What are the known features caused by a VIPoma? | Watery diarrhea, Hypokalemia, and Achlorhydria |
| WDHA | Mnemonic for VIPoma signs and symptoms |
| What are the two actions or roles of VIP? | 1. Increase intestinal water and electrolyte secretion 2. Increase relaxation of intestinal smooth muscle and sphincters |
| Which conditions lead to the increase secretion of VIP? | Distention and vagal stimulation |
| What are the GI functions of Nitric oxide? | Increase smooth muscle relaxation, including the lower esophageal sphincter (LES) |
| Which GI substance deficiency or loss is associated with the development of Achalasia? | Nitric oxide |
| Achalasia can be partially due to the loss of _______________. | Nitric oxide |
| Why is the deficiency of NO associated with Achalasia? | NO serves to relax the SM of LES |
| Which GI structure/organ secretes Ghrelin? | Stomach |
| GI relulator substnce responsable for incrased appetite? | Ghrelin |
| What decreases the secretion of Ghrelin by the stomach? | Food |
| In a fasting state, the release of Ghrelin is increased or decreased? | Increased |
| Which congenital condition is characterized by elevated levels of Ghrelin? | Prader-Willi syndrome |
| A decrease in Ghrelin secretion is seen with: | Gastric bypass surgery |
| Which cells are known to secrete Intrinsic factor? | Parietal cells of the stomach |
| What is the role or function of the Intrinsic factor (IF)? | Required for B12 uptake in the terminal ileum |
| Vitamin B12-binding protein. | Intrinsic factor (IF) |
| What is the result of the autoimmune destruction of parietal cells of the stomach? | Chronic gastritis and pernicious anemia (lack of IF) |
| Which two GI secretory products are known to be secreted by Parietal cells of the stomach? | Intrinsic factor and Gastric acid |
| Which substance decrease the stomach pH? | Gastric acid |
| What actions/ substances produce an increase release of Gastric acid? | 1. Histamine 2. Vagal stimulation (ACh) 3. Gastrin |
| Gastric acid is inhibited by: | 1. Somatostatin 2. GIP 3. Prostaglandin 4. Secretin |
| Chief cell of the stomach secrete? | Pepsin |
| Where are the Chief cells that secrete pepsin? | Stomach |
| What is the main responsibility of Pepsin? | Protein digestion |
| Protein digestion is done by: | Pepsin secreted by stomach Chief cells |
| What is the inactive form of pepsin? | Pepsinogen |
| What is pepsinogen? | Inactive form of pepsin |
| How is Pepsinogen converted into pepsin? | Presence of H+ |
| What would be the effect on Pepsin/Pepsinogen in a environment lacking of H+? | No conversion of pepsinogen into pepsin (active) |
| What are 2 know actions that increase release of Pepsin? | 1. Vagal stimulation (ACh) 2. Local acid |
| Vagal stimulation causes ____________________. | Increased concentration of ACh |
| Which are the sources of Bicarbonate? | 1. Mucosal cells 2. Brunner glands |
| Mucosal cells of which organs secrete bicarbonate, or a source of bicarbonate? | Stomach, doudenum, salivary glands, and pancreas |
| Brunner glands are in the _________________. | Duodenum |
| Which GI regulatory substance neutralizes acid? | Bicarbonate |
| What causes an increase release of Bicarbonate? | Pancreatic and biliary secretion with secretin |
| What is trapped in mucus that covers the gastric epithelium? | Bicarbonate |
| What are three important cells located in the Duodenum? | I cells, S cells, and K cells. |
| Which part of the stomach holds most of the mucous cells and D cells? | Antrum |
| What cells are often found in the Body of the stomach? | Chief cells and Parietal cells |
| What is the main effect of the Enterochromaffin-like cells? | Increased gastrin levels |
| What substance is release by ECL cells? | Histamine |
| What is the effect of Histamine on Parietal cells? | Increase secretion of IF and HCl |
| What is the main role of a-amylase? | Starch digestion |
| What is the role of Lipases? | Fat digestion |
| What is the main role of Proteases? | Protein digestion |
| Pancreatic proteases main role is to digest ______________. | Protein |
| What are common Pancreatic secretions? | a-amylase, lipases, proteases, and trypsinogen |
| What enzyme converts Trypsinogen into is active form (trypsin)? | Enterokinase/enteropeptidase |
| Brush-border enzyme on duodenal and jejunal mucosa that converts trypsinogen into trypsin? | Enterokinase/enteropeptidase |
| What are some common Proteases? | Trypsin, Chymotrypsin, elastase, carboxypeptidases |
| What is another name for proenzymes? | Zymogens |
| Which kind of sugars are the only ones absorbed by enterocytes? | Monosaccharides |
| What are some common monosaccharides? | Glucose, galactose, and fructose |
| Which monosaccharides are taken up by the cell through SGLT1? | Glucose and Galactose |
| Which protein channel is used by Galactose and glucose for their uptake into the enterocyte? | SGLT1 |
| SGLT is _______ dependent. | Na+ |
| How is Fructose taken up by the enterocyte? | Via facilitated diffusion by GLUT5 |
| Which GLUT is used by Fructose? | GLUT5 |
| Which GLUT is used by all monosaccharides to be transported to the blood? | GLUT2 |
| What is the D-xylose absorption test? | Simple sugar that requires intact mucosa for absorption, but does not require digetive enzymes |
| What is one important use for the D-xylose test? | Distinguish GI mucosal damage from other causes of malabsorption |
| Where is Iron absorbed? | Duodenum |
| What important water soluble vitamin is absorbed in the small bowel? | Folate |
| Where is Vitamin B12 absorbed? | Terminal ileum |
| What is required for Vitamin B12 to be absorbed by the terminal ileum? | Intrinsic factor |
| What else is absorbed along terminal ileum with cobalamin? | Bile salts |
| Iron Fist, Bro? | Mnemonic to recall absorption of Fe (iron- duodenum), Fist (folate- small bowel), Bro (Vit B12 -- terminal ileum |
| Unencapsulated lymphoid tissue found in lamina propria and submucosa of ileum. | Peyer patches |
| What structure contain specialized M cells that sample and present antigens to immune cells? | Peyer patches |
| What are the antigen presenting specialized cells found in Peyer patches? | M cells |
| What does the differentiation of germinal center B cells of Peyer patches convert into? | IgA-secreting plasma cells |
| What is the purpose for IgA-secreting plasma cells in Peyer patches to travel to the lamina propria? | To receive protective secretory component |
| How is Bile composed? | Bile salts + phospholipids + cholesterol + bilirubin + water + ions |
| What properties of bile make it water soluble? | Bile salts (bile acids conjugated to glycine or taurine. |
| What is the end result of bile acids conjugation with glycine or taurine? | Makes bile water soluble |
| What enzyme catalyzes rate-limiting step of bile acid synthesis? | Cholesterol 7a-hydroxylase |
| What are the 3 main functions of bile? | 1. Digestion and absorption of lipids and fat-soluble vitamins 2. Cholesterol excretion 3. Antimicrobial activity |
| What conditions are associated with a decreased absorption of bile acids in the ileum? | Short bowel syndrome and Crohn disease |
| Why is a patient with Crohn disease seen with abnormal fat absorption? | Due to decrease absorption of enteric bile salts in the distal ileum |
| What kind of kidney stones are seen with abnormal bile absorption? | Calcium Oxalate kidney stones |
| Increased levels of fat, due to decreased bile absorption in the distal ileum can produce ---> | Calcium Oxalate kidney stones |
| What enzyme converts Heme ito biliverdin? | Heme oxygenase |
| What is the reduced form of Biliverdin? | Bilirubin |
| Direct bilirubin: | - Conjugated with Glucuronic acid -Water soluble |
| Indirect bilirubin: | Unconjugated and water insoluble |
| Direct bilirubin is conjugated with _________________________. | Glucuronate |
| Which bilirubin state is water soluble? | Direct bilirubin |
| Which organs removes unconjugated bilirubin? | Liver |
| Conjugated bilirubin is removed/excreted from the body by ___________ or __________. | Urine or feces |
| What is the enzyme involved in the conversion of Unconjugated bilirubin to Conjugated bilirubin? | UDP-glucuronosyltransferase |
| Where is unconjugated bilirubin formed? | Macrophages |
| At which point is albumin added to unconjugated bilirubin? | In the bloodstream |
| At what organ is Direct (conjugated) bilirubin formed? | Liver |
| What compound gives urine its yellow color and feces its brownish color? | Bile |
| Most (80%) of bilirubin is excreted in the form of? | Stercobilin |
| The foregut is extended from the_________________ to the ___. | Esophagus to the Upper duodenum |
| What is covered by the Midgut? | Lower Duodenum to proximal 2/3 of transverse colon |
| What is the extent of the hindgut? | Distal 1/3 of transverse colon to anal canal above the pectinate line. |
| Esophagus -----> Upper duodenum | Foregut |
| Lower Duodenum----> Proximal 1/3 of transverse colon | Midgut |
| What structure covers the distal 1/2 of transverse colon to to anal canal above pectinate line? | Hindgut |
| In respect to the Midgut development in embryo, what occurs at the 6th week of gestation? | Physiologic midgut herniates through umbilical ring |
| What ring (structure) is used by embryological midgut to herniate during early gestational development? | Umbilical ring |
| What happens to midgut at the 10th week of development? | Midgut returns to abdominal cavity + rotates around superior mesenteric artery (SMA) total 270 degrees counterclockwise |
| Embryological midgut develops around which vessel? | Superior Mesenteric Artery (SMA) |
| What direction does the developing midgut rotate? | 270 degrees counterclockwise around the SMA |
| What are Ventral wall defects due? | Developmental defects due to failure of rostral fold closure, lateral fold closure, or caudal fold closure. |
| What are the example condition of rostral fold closure failure? | Sternal defects (ectopia cordis) |
| What is defective in embryogenesis for development of Ectopia cordis? | Failure of rostral fold closure |
| What are examples of conditions due to lateral fold closure during embryogenesis? | Omphalocele and Gastroschisis |
| Omphalocele and Gastroschisis are due to? | Failure of lateral fold closure during gestation |
| What kind of embryological developmental failure lead to bladder exstrophy? | Failure of caudal fold closure |
| Etiology of Gastroschisis | Extrusion of abdominal contents through abdominal folds (typical right of umbilicus) |
| Which ventral wall defect is characterized by abdominal contents outside of body without coverage by peritoneum or amnion? | Gastroschisis |
| What is Omphalocele etiology? | Failure of lateral walls to migrate at umbilical ring leading to persistent midline herniation of abundant contents into umbilical cord. |
| Which condition has its abdominal contents outside body and covered by peritoneum? | Omphalocele |
| Which are important associations of Omphalocele? | 1. Congenital abnormalities (trisonomies 13 and 18, Beckwith-Wiedemann syndrome) 2. Structural abnormalities (cardiac, GU, and neural tube) |
| Abdominal contents covered by peritoneum newborn. Dx? | Omphalocele |
| Which fold failed to close during GI development in Gastroschisis and Omphalocele? | Lateral fold |
| What is Congenital umbilical hernia due to? | Failure of umbilical ring to close after physiologic herniation of the intestines |
| Failure of umbilical ring to close after the intestines herniated. Dx? | Congenital umbilical hernia |
| What are the Tracheoesophageal anomalies? | 1. Esophageal atresia (EA), and, 2 Tracheoesophageal fistula (TEF) |
| What is the most common Tracheoesophageal anomaly? | EA with distal TEF |
| Esophageal atresia with distal Tracheoesophageal fistula is the | Most common Tracheoesophageal anomaly. |
| What is often presented with EA with distal TEF? | Polyhydramnios in utero. |
| What is the reason of the polyhydramnios in utero of a neonate with EA with distal TEF? | Due to inability to fetus to swallow amniotic fluid |
| What are the most common clinical signs of a neotan with a Tracheoesophageal anomalies? | Drool, choke, and vomit with first feeding. |
| Which tracheoesophageal anomaly allows for air to enter the stomach? | Tracheoesophageal fistula |
| What is the clinical test to diagnose Tracheoesophageal anomalies? | Failure to pass nasogastric tube into stomach |
| Why is Pure TEF also called H-type? | The fistural conecting the esophagus to the trachea creates a form the remembles the letter "H" |
| What is the typical clinical presentation of Intestinal atresia? | Bilious vomiting and abdominal distension within the first 1-2 days of life. |
| Duodenal atresia is due to: | Failure to recanalize |
| What are associations of Duodenal atresia? | 1. "Double bubble" on X-ray 2. Down syndrome |
| Jejunal and ieald atresia sure due to: | Disruption of mesenteric vessels leading to ischemic necrosis and segmental resorption |
| What is another way to describe segmental resorption in Jejunal and Ileal atresia? | Bowel discontinuity or "apple peel" |
| Apple peel intestines refer to: | Jejunal and ileal atresias |
| What causes ileal and jejunal atresia to develop "apple peel" appearance? | Ischemic necrosis leading to segmental resorption |
| Hypertrophic pyloric stenosis is the MCC of: | Gastric outlet obstruction in infants |
| What are some key features of Pyloric stenosis ? | 1. Palpable olive-shaped mass in epigastric region 2. Visible peristaltic waves 3. Nonbilious projectile vomiting at ~2-6 weeks old |
| What antibiotic exposure increases the risk of developing hypertrophic pyloric stenosis? | Macrolides |
| What is the electrolyte imbalance seen in Pyloric stenosis? | Hypokalemic Hypochloremic Metabolic Alkalosis |
| Why is the reason for the Hypokalemic hypochloremic metabolic alkalosis in Pyloric stenosis? | Secondary to vomiting of gastric acid and subsequent volume contraction. |
| What are the findings of US in Pyloric stenosis? | Thickened and lengthened pylorus |
| The pancreas is derived from the _______________. | Foregut |
| What do the ventral pancreatic buds contribute for? | Uncinate process and main pancreatic duct |
| What is to become of the dorsal pancreatic bud? | Body, tail, isthmus, and accessory pancreatic duct |
| Which pancreatic bud(s) contribute to development of Pancreatic head? | Both, the ventral and dorsal buds. |
| What is Annular pancreas? | Abnormal rotation of ventral pancreatic bud forms a ring of pancreatic tissue around the second part of the duodenum. |
| What are some possible symptoms of Annular pancreas? | Duodenal narrowing and vomiting |
| What fails in order to develop Pancreas divisum? | Ventral and dorsal parts fail to fuse at 8 weeks |
| Where does the spleen arises from? | Mesentery of stomach but has foregut supply (celiac trunk --> splenic artery). |
| What is included in retroperitoneal structures? | GI structures that lack a mesentery and non-GI structures |
| Injuries to the retroperitoneal structures cause: | Blood or gas accumulation in retroperitoneal space |
| Mnemonic used to remember Retroperitoneal structures | SAD PUCKER |
| What does SAD PUCKER stand for? | Retroperitoneal structures: Suprarenal (adrenal) glands Aorta and IVC Duodenum (2nd to 4th parts) Pancreas (except tail) Ureters Colon (descending and ascending) Kidneys Esophagus (thoracic portion) Rectum (partially) |
| What part of the doudenum is in the retroperitoneal space? | 2nd to 4th parts |
| Which parts of the colon are retroperitoneal structures? | Descending and ascending colon |
| Which part of the Pancreas is NOT found in the retroperitoneal space? | Tail |
| Which glands are retroperitoneal? | Suprarrenal or Adrenal glands |
| What is connected by the Falciform ligament? | Liver to anterior abdominal wall |
| What ligament connects the liver to the anterior abdominal wall? | Falciform ligament |
| What structures are found/contained by the Falciform ligament? | 1. Ligamentum teres hepatis 2. Patent paraumbilical veins |
| Which ligament is known to be derivative of Ventral mesentery? | Falciform ligament |
| The hepatoduodenal ligament connects the: | Liver to duodenum |
| Which GI ligament is known to connect the liver and the doudenum? | Hepatoduodenal ligament |
| Which ligament contains the Portal triad? | Hepatoduodenal ligament |
| What are the components of the Portal triad contained by the Hepatoduodenal ligament? | Proper hepatic artery, Portal vein, and common bile duct |
| What is the Pringle manuever? | It is when the Hepatoduodenal ligament is compressed between thumb and index finger placed in omental foramen to control bleeding. |
| Which foramen is bordered by the Hepatoduodenal ligament? | Omental foramen |
| Which is a common maneuver used to stop bleeding by pressing on the Hepatoduodenal ligament? | Pringle manuever |
| The liver to lesser curvature of stomach is connected by the: | Gastrohepatic ligament |
| Which structures are contained by the Gastrohepatic ligament? | Gastric vessels |
| What ligament separates the greater and lesser sacs of the right? | Gastrohepatic ligament |
| Which structures are connected by the Gastrocolic ligament? | Greater curvatures and transverse colon |
| Which ligament contains the Gastroepiploic arteries? | Gastrocolic ligament |
| The _________________ ligament connects the Greater curvature to the spleen. | Gastrosplenic |
| Which structures are contained by the Gastrosplenic ligament? | Short gastric, left gastroepiploic vessels |
| Which ligament connects the Spleen to the posterior abdominal wall? | Splenorenal ligament |
| What structures are contained by the Splenorenal ligament? | Splenic artery and vein, and tail of pancreas. |
| What are the 4 layers of the gut wall? | 1. Mucosa 2. Submucosa 3. Muscularis externa 4. Serosa |
| What is the deepest layer of the gut wall? | Mucosa |
| What is the outermost layer of the gut wall? | Serosa |
| Which layer of the gut wall are the Meissner plexuses? | Submucosa |
| Which layer of the gut wall secretes fluid? | Submucosa |
| What nerve plexus are found in the Muscularis externa layer of the gut wall? | Myenteric nerve plexus (Auerbach) |
| Another name for Myenteric nerve plexus? | Auerbach plexus |
| What layer of the gut wall is in charge of Motility? | Muscularis externa |
| What is the name given to the serosa if it is retroperitoneal? | Adventitia |
| If the outermost layer is referred as Adventitia, then it is safe to assume that is indicating? | Retroperitoneal structure/space |
| What is the extent of a possible ulcer in relation to the gut layers? | Submucosa, inner or outer muscular layer |
| How far (deeply) does an erosion extend in relation to gut layers? | Mucosa only |
| Which has a greater degree of extend into the layers of the gut wall, erosions or ulcers? | Ulcers |
| What are the slow waves? | Frequencies of basal electrical rhythm |
| What is the frequency of waves of the Stomach? | 3 waves/ minute |
| How many slow waves per minute are seen in the Duodenum? | 12 waves/ minute |
| Which structure has an approximate 8-9 waves/min? | Ileum |
| Which is the GI structure with the slowest basal electrical rhythm? | Stomach (3 waves/min) |
| What are the three structures that compose the Mucosa layer of the gut wall? | Epithelium, Lamina propia, and Muscularis mucosa |
| Submucosal nerve plexus = | Meissner |
| Which gut layer contains the Inner circular layer? | Muscularis |
| Myenteric nerve plexus = | Auerbach |
| Which is deeper into the gut wall, Auerbachs or Meissner? | Meissner |
| What is the outermost sublayer of the Muscularis externa layer? | Outer longitudinal layer |
| Epithelium of the esophagus? | Nonkeratinized stratified squamous epithelium |
| Is the esophagus epithelium, keratinized or nonkeratinized? | Nonkeratinized |
| Which GI structure has nonkeratinized stratified squamous epithelium? | Esophagus |
| What is the role of the Villi and microvilli of the doudenum? | Increase absorptive surface |
| Where in the GI tract are the Brunner glands found? | Duodenum |
| The doudenum is the location of which particular HCO3- secreting glands? | Brunner glands |
| What are two featured histologic findings in the Duodenum? | 1. Brunner glands 2. Crypts of Lieberkühn |
| HCO3- secreting glands of the duodenal mucosa? | Brunner glands |
| What is contained in the crypts of Lieberkuhn? | Stem cells that replace enterocytes/goblet cells and Paneth cells that secrete defensins, lysozyme, and TNF. |
| Where are the Paneth cells found? | Inside the crypts of Lieberkühn of the doudenum |
| What is secreted by the Paneth cells? | Defensins, lysozyme, and TNF |
| Histological findings/features of the Jejunum | 1. Plicae circulates and, 2. crypts of Lieberkühn |
| Which part of the small intestine are the Peyer patches mostly found? | Ileum |
| What are the Peyer patches? | Lymphoid aggregates in lamina propria, and submucosa of the ileum |
| Which ileal layers contain Peyer patches? | Lamina propria and submucosa |
| What are the 3 key histological findings of the ileum? | 1. Peyer patches 2. Plicae circulares 3. Crypts of Lieberkühn |
| Which digestive tract section/structure is with Crypts of Lieberkuhn but not with villi, and with abundant goblet cells? | Colon |
| Crypts of Lieberkühn are found in: | Duodenum, Jejunum, Ileum, and colon |
| Which part of the digestive tract is abundant with goblet cells? | Colon and Ileum |
| What part of the small intestine has the largest number of Goblet cells? | Ileum |
| Which part of the digestive tract has more Goblet cells, Ileum or Colon? | Ileum |
| At what level does the abdominal aorta starts? | T12 |
| What arteries branch off the aorta at T12? | - Inferior phrenic - Superior and Middle suprarenal |
| At which level of the abdominal aorta does the Superior Mesenteric artery branches off? | At mid-L1 |
| Which imporatnt artery branches off the abodimian aorta at L3 level? | Inferior Mesenteric artery |
| At what level does the Right and Left common iliac arteries begin? | L5 |
| How do arteries that supply GI structures branch off the abdominal aorta? | These are single and branch ANTERIORLY |
| If a artery is single and branches anteriorly form abdominal aorta, it is to supply _______________ structures. | Gastrointestinal |
| Arteries supplying non-GI structures that branch from abdominal aorta. | Paired and branch LATERALLY and POSTERIORLY |
| Which are three main branches of the abdominal aorta that branch off anteriorly? | Celiac, SMA, and IMA |
| Since SMA, IMA, and Celiac arteries branch off anteriorly --> | They are single and will supply GI structures |
| What is the Superior mesenteric syndrome? | Condition in which the SMA and aorta compress transverse (third) of doudenum |
| What is the clinical features of Superior Mesenteric artery syndrome? | Intermittent intestinal obstruction symptoms (primarily postprandial) |
| Malnutrition patient complains of episodic abdominal pain, especially after eating. Dx? | Superior Mesenteric artery syndrome |
| Which areas are most susceptible to colonic ischemia? | "Watershed regions" |
| What are the two "watershed regions" of the colon? | 1. Splenic flexure 2. Rectosigmoid junction |
| What dual blood supply create the Splenic flexure? | SMA and IMA |
| The junction of the SMA and IMA | Splenic flexure |
| What arterial bodies form the Rectosigmoid junction? | Last sigmod arterial branch from the IMA and Superior rectal artery |
| At what point approximately do the Gonadal arteries branch off (laterally) from the abdominal aorta? | At the superior part of L2 |
| Which paired vessel branches off the abdominal aorta exactly at the the junction of L1 and L2? | Renal arteries |
| What artery supplies the Foregut? | Celiac |
| What artery supplies the Midgut? | SMA |
| What artery supplies the Hindgut? | IMA |
| Which embryonic gut region(s) are Parasympathetically innervated by the Vagus nerve? | Foregut and Midgut |
| The Hindgut is innervated by the _____________ nerve. | Pelvic |
| Which nerve innervates the Pharynx? | Vagus |
| What are the branches of the Celiac trunk? | 1. Common hepatic artery 2. Splenic artery 3. Left Gastric artery |
| What arterial bodies constitute the main blood supply to of the stomach? | The branches of the Celiac trunk |
| At the Celiac trunk and stomach levels, which are some strong anastomoses that exist? | 1. Left and right gastroepiploic 2. Left and right gastrics |
| What artery is penetrated by posterior duodenal ulcers? | Gastroduodenal artery |
| Which artery is perforated by anterior duodenal ulcers? | Anterior abdominal cavity, potentially leading to pneumoperitoneum |
| Antrum of stomach is mostly irrigated by _________________. | Common hepatic artery |
| Which vessels form the anastomosis in the esophagus? | Left gastric <---> Azygos |
| Caput medusae appears at the region of the _______________. | Umbilicus |
| What arterial and venous bodies create the anastomosis that lead to Caput medusae? | Paraumbilical <---> Small epigastric veins the anterior abdominal wall. |
| Which type of varices are seen in Portal hypertension? | Esophageal varices, Caput medusae, and anorectal varices. |
| What is a common invasive treatment for Portal hypertension? | TIPS |
| TIPS can precipitate _________. | Hepatic encephalopathy |
| What is TIPS? | Treatment with a transjugular intrahepatic portosystemic shunt (TIPS) between the portal vein and hepatic vein relieves portal hypertension by shunting blood to the sytemic circuation bypassin the liver. |
| Where is the Pectinate line? | Formed where endoderm (hindgut) meets ectoderm |
| What is another name for Pectinate? | Dentate |
| Innervation above the pectinate line? | Visceral innervation |
| Arterial supply above the pectinate line? | Superior Rectal artery (branch of IMA) |
| Where does lymph form above the pectinate line drains into? | Internal iliac lymph node |
| What type of hemorrhoids are developed above the pectinate line? | Internal hemorrhoids |
| What type of malignancy is associated with tissue above the pectinate line? | Adenocarcinoma |
| Not painful hemorrhoids | Internal hemorrhoids |
| Non-painful hemorrhoids must be _____________ pectinate line. | Above |
| External hemorrhoids appear ________ the pectinate line. | Below |
| What are some pathologies/malignancies that are seen below the pectinate line? | 1. External hemorrhoids 2. Anal fissures 3. Squamous cell carcinoma |
| Painful hemorrhoids appear ________________ the dentate line. | Below |
| What is an anal fissure? | Tear in the anal mucosa below the Pectinate line. |
| What are associated conditions that accompany anal fissures? | Low-fiber diets and constipation |
| Why do anal fissures tend to appear posteriorly? | It is a poorly perfused area |
| Which type of hemorrhoids receive Somatic innervation? | External hemorrhoids |
| Which artery supplies below the pectinate line? | Inferior rectal artery (branch of the Internal Pudendal artery) |
| Where does lymph below the pectinate line drain to? | Superficial inguinal Lymph node |
| The inferior rectal artery is a branch of the: | Internal pudendal artery |
| Inferior rectal vein --> internal pudendal vein --> internal iliac vein --> Common iliac vein -----> IVC | Venous drainage below the pectinate line |
| Superior rectal vein ---> Inferior mesenteric vein ---> Splenic vein ---> portal vein | Venous drainage above the pectinate line |
| Venous blood below the pectinate line ultimately drains into what major venous body? | IVC |
| Which is the vein that receives venous blood from areas above the pectinate line? | Portal vein |
| Description of liver architecture | Hexagonally arranged lobules surrounding the central vein with portal triads on edges . |
| What are the portal triads in liver architecture, composed of? | Portal vein, Hepatic artery, bile ducts, as well lymphatics |
| Which surface of the hepatocytes faces the canaliculi? | Apical surface |
| The basolateral surface of the hepatocytes faces the ______________________. | Sinusoids |
| What are Kupffer cells? | Specialized macrophages of the liver, located ate the sinusoids. |
| What is the name of liver macrophages? | Kupffer cells |
| Where in the liver architecture are the Kupffer cells located? | Sinusoids |
| What is the abbreviation used for Hepatic stellate cells? | Ito |
| Where are the Hepatic stellate (Ito) cells located? | Space of Disse |
| What do Hepatic stellate cells store? | Vitamin A |
| What do hepatic stellate cells produce when activated? | Extracellular matrix |
| Which cells are responsible for hepatic fibrosis? | Ito cells (hepatic stellate cells) |
| What is the name of the Liver Zone 1? | Periportal zone |
| Which zone of the liver is first affected by viral hepatitis? | Zone I |
| Ingested toxins such as cocaine affect which zone of the liver? | Zone I |
| Name of Zone II of the liver? | Intermediate zone |
| Which is the known pathology to affect zone II of the liver? | Yellow fever |
| Yellow fever will cause liver damage by affecting the Zone _____. | II |
| Different forms to refer to Zone III of the liver? | - Pericentral vein zone or, - Centrilobular zone |
| Which zone of the liver is 1st affected by ischemia? | Zone III |
| Which zone, I, II, or III, has the highest cytochrome P-450 concentration in the liver? | Zone III |
| Which is the site of alcoholic hepatitis? | Zone III |
| Which zone of the liver is the most sensitive to metabolic toxins? | Zone III |
| What are some common metabolic toxins that affect the zone III of liver? | Ethanol. CCl4, halothane, and rifampin |
| Which cells in the liver store vitamin A? | Stellate cells in space of Disse |
| Gallstones that get lodged in the ampulla of Vater cause: | - Blockage of both: 1. Common bile duct ----> Cholangitis 2. Pancreatic ducts ----> Pancreatitis |
| What is the most common type of tumor seen at the head of the pancreas? | Ductal adenocarcinoma |
| What is the Courvoisier sign? | Enlarged bladder with painless jaundice |
| What is a consequence of a tumor at the head of the pancreas? | Obstruction of common bile duct ---> enlarged bladder with painless jaundice |
| How do a cholangiography help to visualize gallbladder problems? | Shows filling defects in gallbladder and cystic duct |
| What is the organization of the femoral region in respect of structures passing through? | Arranged for lateral to medial: Nerve-Artery-Vein-Lymphatics |
| Which is the most lateral structure of the femoral region? | Nerve |
| Mnemonic used to describe the order and organization of structures in the femoral region | NAVeL |
| What structures are contained by the Femoral triangle? | Femoral nerve, artery, and vein |
| What structures are contained by the Femoral sheath? | Femoral artery, vein, and canal, but NOT the femoral nerve |
| Facial tube 3-4 cm below inguinal ligament? | Femoral sheath |
| What is in the canal covered by the Femoral sheath? | Deep inguinal lymph nodes |
| Where is the site of protrusion of a direct inguinal hernia? | Abdominal wall |
| What is the site of protrusion of an indirect inguinal hernia? | Deep (internal) inguinal ring |
| What is a hernia? | Protrusion of peritoneum through an opening, usually at site of weakness. |
| What are two significant concerns or complications of all hernias? | 1. Incarceration (not reducible back into abdomen/pelvis) 2. Strangulation( ischemia and necrosis) |
| When a hernia is said be incarcerated, it means? | Hernia cannot be reducible back into the abdomen or pelvis |
| Complicated hernias present with: | Tenderness, erythema, and fever |
| Abdominal structures enter the thorax. Dx? | Diaphragmatic hernia |
| Which side is more prone to develop a diaphragmatic hernia? | Left side due to relative protection of right hemidiaphragm by liver. |
| Which is the most common type of diaphragmatic hernia? | Hiatal hernia |
| What is a hiatal hernia? | Stomach herniates upward through the esophageal hiatus of the diaphragm |
| Stomach protrudes upward through the diaphragm | Hiatal hernia |
| What are the two most common types of hiatal hernias? | 1. Sliding hiatal hernia 2. Paraesophageal hiatal hernia |
| Gastroesophageal junction is displaced upward as gastric cardia slides into hiatus | Sliding hiatal hernia |
| Which condition is described with "hourglass stomach" | Sliding hiatal hernia |
| Which is the MC type of hiatal hernia? | Sliding hiatal hernia |
| What is a Paraesophageal hiatal hernia? | Gastroesophageal junction is usually normal but gastric fundus protudes into thorax. |
| Which part of the stomach is protruded/herniated upward in a Sliding hiatal hernia? | Gastric cardia |
| Which hiatal hernia has the gastric fundus protrading/herniating upward into the thorax? | Paraesophageal hiatal hernia |
| Which type of inguinal hernia goes THROUGH the internal (deep) inguinal ring? | Indirect inguinal hernia |
| Which inguinal hernia goes into the scrotum? | Indirect inguinal hernia |
| Protrusion of peritoneum goes through the deep inguinal ring --> external inguinal ring, and finally into scrotum. Dx? | Indirect inguinal hernia |
| Anatomically, how does an indirect inguinal hernia enter the internal inguinal ring? | Lateral to inferior epigastric vessels |
| What is the cause of Internal inguinal hernias? | Failure of processus vaginalis to close |
| What is developed in a person that suffered of failure of processus vaginalis to close? | Indirect inguinal hernia |
| Besides an indirect inguinal hernia, what other condition may be developed due to failure of processus vaginalis to close? | Hydrocele |
| Which population is seen with Indirect inguinal hernias most commonly? | Infants; especially males |
| What path is followed by an indirect inguinal hernia? | Path of descent of testes; covered by all 3 layers of spermatic fascia. |
| During a hernia repair, the surgeon notices the hernia is covered by all 3 layer of the spermatic fascia. Dx? | Indirect inguinal hernia |
| What is the featured structure by which a direct inguinal hernia goes through? | Hesselbach triangle |
| Bulges directly through parietal peritoneum medial to the inferior epigastric vessels but lateral to the rectus abdominis. | Direct inguinal hernia |
| Which type of inguinal hernia is only covered by the external spermatic fascia? | Direct inguinal hernia |
| What type of inguinal hernia is mostly seen in older men? | Direct inguinal hernia |
| Weakness in the transversalis fascia leads to the development of: | Direct inguinal hernia |
| Hesselbach triangle is associated with: | Direct inguinal hernia |
| Medial to inferior epigastric vessels ---> | Direct inguinal hernia |
| Lateral to the Inferior Epigastric vessels------> | Indirect inguinal hernia |
| Which population is more affected by Direct inguinal hernia development? | Older men |
| Through which ring does a Direct inguinal hernia passes? | External (superficial) inguinal ring only |
| If the inguinal hernia only passes through one inguinal ring. Dx? | Direct inguinal hernia |
| Femoral hernia pathogenesis: | Protrudes below inguinal ligament through femoral canal below and lateral to pubic tubercle |
| What gender is most commonly affected by Femoral hernias? | Female |
| Which type of hernia, inguinal or femoral, are more prone to present with incarceration or strangulation? | Femoral hernia |
| Which hernia is found to protrude below the inguinal ligament? | Femoral hernia |
| If the hernia is said to be lateral to pubic tubercle. Most likely Dx? | Femoral hernia |
| What are the bordering structures of the Hesselbach triangle? | - Inferior Epigastric vessels - Lateral border of rectus abdominis - Inguinal ligament |
| What is the INFERIOR border of the Hesselbach triangle? | Inguinal ligament |
| What is the MEDIAL border of the Hesselbach triangle? | Lateral border of the Rectus abdominis |
| What is the SUPEROLATERAL border of the Hesselbach triangle? | Inferior epigastric vessels |
Created by:
rakomi
Popular USMLE sets