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Gastro 1.1
UWORLD Gastrointestinal
| Question | Answer |
|---|---|
| What are the two (2) main divisions of the embryologic pancreas? | Dorsal Pancreatic Bud and the Ventral Pancreatic Bud |
| What is formed or derived from the Dorsal Pancreatic Bud? | Majority of pancreatic tissue, including the: Body, Tail, and most of the Head |
| What is formed or derived from the Ventral Pancreatic Bud? | 1. The Uncinate Process 2. Inferior and Posterior portions of the head of Pancreas 3. Major Pancreatic Duct (of Winsung) |
| The failure of ___________________ of the dorsal and ventral pancreatic buds, leads to the development of : | FUSION; leads to Pancreas Divisum |
| Which are the PRO-inflammatory cytokines? | IL-17, INF-gama, TNF-alpha, and IL-2 |
| Which are the the ANTI-inflammatory cytokines? | IL-4, IL-10, and TGF-beta |
| Which TH cells secrete the PRO-inflammatory cytokines? Each induced by? Secretes? | 1. TH-17; induced by IL-1, IL-6, and IL-23; secretes IL-17 2. TH-1; induced by IL-12; secretes INF-gamma, TNF-alpha, IL-2 |
| What are 2 common causes of BLACK pigment stones? | 1. Chronic hemolysis( as seen in Sickle Cell and Spherocytosis) 2. Increased intrahepatic cyclin of bilirubin ( as in iliael disease) |
| What is the main reason of BROWN pigment stones? | Biliary tract infection; commonly seen in E. coli and liver fluke infections |
| In the development of Brown pigment gallstones, after the infection of the biliary tract, there is a release of: | microbial (bacterial or helminthic) B-glucuronisidases |
| The production of pigment stones is described with an: | Increase in UNCONJUGATED bilirubin |
| What is the composition of pigment stones? | Calcium- bilirubinate precipitate |
| Patient with flatulance, crampy abdominal pain, and watery diarrhea after ingestion of dairy products, commonly indicates what disorder? | Lactose Intolerance |
| Lactose intolerace affects the: | mucosal brush border of the small intestine |
| The labs/studies of Lactose Intolerace show: | 1. Increased: a- breath hydrogen content b- stool osmolality (high water content stool) 2. Decreased: a- stool pH |
| What are the two main treatments for Hepatic Encephalopathy? | Lactulose and Rifamixin |
| What is the MOA of Lactulose? | Increases the conversion of ammonia (NH3) into ammonium (NH4) |
| What is the MOA of Rifamixin? | Decreases Intraluminal ammonia (NH3) production |
| What is the classic clinical presentation of Hepatic Encephalopathy? | seen as a complication of liver cirrhosis, as the liver is no longer able to convert NH3 to urea for excretion. The patient is seen with altered mental status (nitrogen byproducts cross BBB) and Asterix. |
| Common causes/precipitating factors for Hepatic Encephalopathy? | GI bleeding (RBC lytic products), high-protein intake, infections, sedatives. |
| In Zollinger-Ellison Syndrome, the most common accompanying gastrin producing tumor is? | Gastrinoma |
| Zollinger-Ellison Syndrome is most often associated with: | MEN type 1 |
| Zollinger- Ellison Syndrome is seen with | Peptic ulcers (commonly beyond the duodenal bulb), abdominal pain/acid reflux, and diarrhea |
| External hemorrhoids are originated ______________________ the dentate line | below |
| External hemmorrhoids are covered by what kind of tissue? | modified squamous epithelium |
| External hemorrhoid innervation is: | Cutaneous (somatic) nervous innervation form the INFERIOR RECTAL NERVE, which is a branch of the PUDENDAL NERVE |
| Are External Hemorrhoids painful? | YES; may present with bleeding while defecating |
| Internal Hemorrhoids originate _________________ dentate line | Above |
| Internal Hemorrhoids are covered in what type of tissue? | Columnar Epithelium |
| How are internal hemorrhoids innervated? | Autonomic innervation from the INFERIOR HYPOGASTRIC PLEXUS |
| The Inferior Hypogastric plexus is only sensitive to? | Only to STRETCH; not sensitive to pain, temperature or touch |
| What are the 3 main causes of GERD? | 1. decreased tone or excessive transient relaxation of the LES 2. Anatomic disruption of GastroEsophageal juntion 3. Increased risk in obesity, pregnancy, smoking, and EtOH intake |
| What is the most common anatomical disruption of the gastroesophageal juntion? | Hiatal Hernia |
| What are some common manifestations of GERD? | Regurgitation of acidic material to the mouth; HEARTBURN; Odynophagia; and extraesophageal symtoms include cough, laryngitis, and wheezing |
| In case of suspected GERD and sudden onset of ODYNOPHAGIA, it is highly indicative of: | Reflux (Erosive) Esophagitis |
| What are the main complications of GERD? | 1. Erosive Esophagitis 2. Strictures 3. Barret's Esophagus --> adenocarcinoma |
| Patient with chronic GERD, ulcers, and new onset odynophagia, indicates: | Erosive Esophagitis |
| Patient with chronic GERD, dysphagia and the sensation of having food stuck in throat, often indicates: | Stricures |
| Barret's Esophagus | Patient with GERD, no increased manifestations, but unexplained weight loss and dysphagia. |
| What is the name for Vitamin B2? | Riboflavin |
| Riboflavin is percursor for: | FMN and FAD |
| What is FAD a component of? What mitochondrial process it is mainly involved? | Component of SUCCINATE DEHYDROGENASE (complex II); involved in Electron Transport Chain (ETC) |
| The FMN is part of the: | complex I in the ETC |
| Riboflavin deficiency is clinically manifested with: | angular stomatitis, chelitis, glossitis, seborrheic dermatitis, eye changes (kerotitis, corneal neovascularization) and anemia; commonly seen in malnourished, alcoholics and homeless. |
| The regulation of Ras is done by: | The balance of ACTIVE ( GTP-bounded) Ras and INACTIVE (GDP-bounded ) Ras proteins |
| A mutated Ras protein leads to an increase expression of the ____________________________ form, leading to development of ____________________________ tumors. | ACTIVE (GTP-bound) Ras protein; MALIGNANT |
| A simpler definition to BILIARY ATRESIA is: | The obstruction of Extra-hepatic bile ducts |
| Biliary Atresia presents with a triad of? symptoms due to? | 1. Jaundice 2. Dark Urine 3. Acholic (pale) stools Symtoms due to UNconjugated HYPERbilirubinemia. |
| At what time in life is Biliary Atresia commonly presented? | during the first 2 months of life |
| A biopsy of the afected hepatic area of in Biliary Atresia will show: | 1. Intrahepatic bile duct proliferation 2. Portal Tract edema 3. fibrosis |
| What are the 2 common large intestine watershed areas? | 1. Splenic Flexure 2. Rectosigmoid juntion |
| By which 2 main arteries is the Splenic Flexure confined? | SMA and IMA |
| By which 2 major arteries is the Rectosigmoid juntion confined? | Sigmoid Artery and the Superior Rectal artery |
| What areas of the intestine are more suceptible to ischemic damage in case of hypovolemic or hypoperfused event? | The "Watersheed areas" |
| The granuloma formation is due to activation of which type of cells? | TH1 and macrophages by antigen. |
| What is a Langhans Giant Cell? | it is a multinucleated cell, made by the fusion of many epitheloid macrophages, during the formation of granuloma. |
| The band surrounding a granuloma is made of what type of cells? | Lymphocytes |
| What are the gastrointestinal symptoms of Celiac Disease? | 1. N/V 2. Abdominal pain 3. Diarrhea (rarely constipation) 4. Flatulance and bloating |
| What are the extraintestinal symptoms of Celiac Disease? | 1. Short STATURE and weight loss 2. Iron deficient anemia 3. Dermatitis Hepatiformis |
| Kid shorter than classmates, that is constantly complaining of stomach pain, and often refuses to eat at home, as the food causes loose stools and abdominal pain. Suspect Diagnosis? | Celiac Disease |
| What are the two main auto antibodies seen in Celiac Disease? | 1. Tissue trans-GLUTAMINASE IgA 2. Anti-endomysial antibody |
| What is the confirmatory test/lab/study for Celiac Disease? | Duodenal Biopsy; it should show intraepithelial lymphocytes and flattened villi. |
| What are the 5 features of CREST Syndrome? | 1. Calcinosis 2. Raynaud phenomenon 3. Esophaeal dysmotility 4. Sclerodactility 5. Telangietsia |
| What is the mophological change seen in ESOPHAGEAL DISMOTILTY, a common feature of Crest syndrome? | It results in ATROPHY and FIBROUS REPLACEMENT of the Muscularis in the Lower Esophagus. |
| What is a common compliation of chronic Raynaud Phenomenon? | Fingertip ulcers |
| What is the common age range for initial presentation of Celiac Disease? | 6-24 months |
| What is shown in Duodenal biopsy? | 1. Crypt hyperplasia 2. Villous atrophy 3. Intraepithelial lymphocytic infiltration |
| What is the main treatment or modification in Celiac Disease? | Gluten-free diet (dietary grain modification) |
| What phases stimulate (increase) gastric acid secretion? | Cephalic and Gastric Phases |
| What phase(s) inhibit or decrease the secretion of gastric acid? | Intestinal influences |
| The GI tract's blood supply is done by which major arterial bodies? | Celiac Trunck, SMA, and the IMA |
| What GI structures are supplied by the __________________ trunk? | Celiac; Stomach, 1st part of duodenum, gallbladder, liver, spleen, and Pancreas. |
| The SMA and IMA form ______________________, for what purpose? | Anastomoses; to 1- provide collateral arterial/blood irrigation, and 2- prevent isquemic damage in case of either been occluded or obstructed. |
| What is the marginal Artery of Drummond? | It is the main ANASTOMOSE of the SMA and IMA |
| What is the name of the inconsistent anastomose of SMA- IMA? | The Arc of Riolan (mesenteric meandering artery) |
| What is the first mutation in the sequence of develpment of Colon cancer? | APC inactivation |
| The APC is responsible for: | the regulation and growth/adhesion of cells |
| APC is a: | tumor suppresor gene |
| The progression of colon cancer after APC mutation is followed by? | Methylation abnormalities and then by COX-2 overexpression |
| The last 3 steps of colon cancer gene mutation development are: | 1. K-ras activation 2. DCC inactivation 3. p53 - inactivation |
| What are the main risk factors for bile (cholesterol) gallstone formation? | increasing age, obesity, excessive bile salt lost (terminal ileum disease), and female (remember 4Fs) |
| What is the prefered treatment for cholethiasis? | Cholecystectomy |
| If the patient refuses surgical treatment of cholesterol gallstone due to fear to surgery, the next best option of treatment would be? MoA? | Hydrophilic bile acids, such as ursodeoxycholic acid; it is used to dissolve the gallstone by: 1. reducing the amount of cholesterol secreted 2. increasing bile acid concentration |
| What is the most common bening hepatic tumor? | Cavernous hemangioma |
| Tumor consitingof cavernous, blood-filled vascular spaces of variable size lined by single epithelial layer, dx? | Cavernous Hemangioma |
| Is a biopsy of a Cavernous Hemangioma a recomended procedure? | Not recommended |
| Why is a bx of a Cavernous Hemangionma contraindicated? | The procedure may cause fatal hemorrhage and produce a low diagnostic yield. |
| Common larvae infection introduced by skin abration from soil. | Strongyloides stercolaris |
| The Strongyloides stercolaris, is intrduced by _________________ _____________________ in the form of _______________________ larvae. | Skin penetration; Filiform |
| The diagnosis of Stronglyloides stercolaris is made by: | Rhabditiform larvae in stool |
| Is the Rhabdiriform presentation of Strongyloides stercolaris infectious or non-infectious? | Non-infectious |
| How is Hyperinfection Syndrome by Strongyloides stercolaris caused? | The transformation of Rhabditiform larvae into Filiform larvae all inside the HOST's body. |
| What is cell immunity is deficient in Hyperinfection Syndrome by Strongyloides stercolaris? what kind of patients are most suceptible? | TH-2 - directed cellular immunity; the immunocompromised and patients infected by HLTV-1. |
| How is the infection with Strongyloides stercolaris clinically presented? | Chronic GI and pulmonary symptoms, Pruritic, erymatous, linear (larva currens) on thighs and buttocks. |
| What is the treatment for Strongyloides stercolaris infection? | Ivermectin |
| What are some common causes of Vitamin A deficiency? | 1. Biliary Disorders (PCB, PBC), 2. Exocrine Pancreatic Insufficiency 3. Intestinal Malabsorption 4. Small Bowel resection (Chron's, Bariatic Sx) |
| What are some common symtoms of Vitamin a deficiency? | 1. Night blindness 2. Hyperkeratosis 3. Growth retardation |
| How is Hyperkeratosis often described on vignette? | Dry and coarse skin |
| What is the most common cause of Fulminant Hepatitis? | The administration of INHALED ANESTHETICS; |
| Which is the most commonly used inhaled anaesthetic worldwide? In the USA? | HALOTHANE; enflurane, isoflurane, desflurane, and sevoflurane |
| How is Fulminant Hepatitis clinically presented? | Fever, anorexia, nausea, myalgias, athralgias and a rash |
| What condition is clinically indistinguishable from acute viral hepatitis? | Fulminant Hepatitis |
| Which are the main lab results elevated in Fulminant Hepatitis? | 1. AST/ALT, due to hepatocellular injury 2. PTT due to failureof hepatic synthetic function |
| Immunoglobulin attachement sites. Where does the Antigen, Complement, and Phagocytic cells attach? | 1. the Antigen attaches at the Fab 2. the Complement attaches at the middle of the structure 3. the Phagocytic cells attaches at the Fc portion, (the one-pointed end) |
| What is the process responsible for fixing single-base DNA defects? | Base Excision Repair |
| What are the sequence of steps in Base Excision Repair? | 1. Glycosylase- removes the defective base 2. Endonucleases - cleave the corresponding empty-sugar phophate 3. Lyase - removes the empty-sugar phosphate 4. DNA pol- replaces the missing nucleotide 5. Ligase - seals the remaining final nick |
| What are the promodomal signs of Acute HAV infection? | fever, malaise, anorexia, N/V, and RUQ pain |
| Following the initial promodomal symptoms of Acute HAV infection, the patient develops sings of? | Cholestasis |
| What are the signs of Cholestasis? | Jaundice, Pruritus, Dark - colored urine, and clay - colored stool |
| What is shown in a histological view of hepatocytes with acute HAV infection? | 1. Spotty Necrosis with balloowing degeneration (hepatocyte swelling with wispy/clear cytoplasm 2. Counsilman bodies 3. Mononuclear Cell infiltrates |
| What are the Phagocytic cells that attach to the Fc segment of Immunoglobulins? | Neutrophils and Macrophages |
| A defect in the Linea Alba, leads to the development of: | Umbilical Hernias |
| An Umbilical hernia most commonly caused by? | Incomplete closedure of the UMBILICAL RING |
| An umbilical hernia is most often associated with: | 1. Down Syndrome, 2. Optional surgical resection at age 5; 3. Nontender bulge; 4. protrusion of sac by increasing abdominal pressure (baby crying, laughing) |
| Chron's Disease may affect which part of the GI tract? is the rectum spared or involved? | Any part of the GI tract, from the mouth to the anus; The rectus is spared |
| Which IBD condition always involves damage to the rectum? | Ulcerative Colitis |
| Cobblestone mucosa, narrowed bowel lumen, creeping fat, are characterisics of? | Chron's Disease |
| Pseudopolyps, Ulcers, PSC, are comonly seen in? | Ulcerative Colitis |
| What are some common complication of Chron's Disease? | Strictures, Fistulas, and Abscesses |
| Strictures in Chron's Disease are due to: | Bowel wall edeman, fibrosis, and thickening of the muscularis mucosae (narrow lumen) |
| Associated with Chron's disease, and due t penetration of ulcers though the intestinal wall | Fistulas |
| Zenker Diverticulum is a _______________________ diverticulum. | FALSE. |
| What is the most common cause of Zenker's Diverticulum? | Crycopharyngeal Motor dysfunction; this creates areas with abnormal peritaltic movement, thus creating areas with decreased pressure to esophageal movement, thus creating a POSTERIOR outpuching. |
| Is Zenker Diverticulium, most commonly, a Posterior, Anterior, or Lateral outpuching? | Posterior |
| What is the common clinical presentation of Zenker's diverticulum? | Oropharyngeal dysphagia, halitosis, Regurgitation, and recurrent aspiration |
| Which enzyme deficiency causes the most severe Galactose metabolism defect? | Galactose-1-phosphate Uridyl Transferase |
| What is the clinical Presentation fo G1PUDT deficiency? | Jaundice, Renal dysfunction (aminoaciduria and hyperchloremic metabolic acidosis), E. coli sepsis, catarats, and hemolytic anemia |
| The deficiency of __________________________ leads to the mild disease of galactose metabolism. Describe its clinical presentation. | Galactokinase; patient presents with Catarats and rarely develops Pseudomotor Cerebri |
| What is the most common GI Emergency of the newborns? | Necrotizing Enterocolitis (NEC) |
| NEC is characterized pathologically by: | Bacterial invasion and ischemic necrosis of the bowel wall |
| NES is associated to: | 1. Prematurity 2. Initiation of enteral feeding |
| What is Pneumtosis intestinalis? to which pathology is it associated? | Air in the bowel wall; it is the dignostic sign for Necrotizing Enterocolitis |
| How is Pneumatosis intestinalis described on abdominal X-ray? | curvilianear lines of LUCENCY parallel to bowel wall lumen |
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