GI Anatomy and Physiology Flashcards

Question

*Helicobacter pylori*

Answer 1

* Can colonize the gastric epithelial cells * Can survive in low pH * Have flagella * Secrete urease that produces ammonia * Produce a vacuolating toxin (VacA) that promtoes bacterial survival and causes epithelial injury * Presence of CagA gene

Answer 2

* 90-95% of malignant tumors of the stomach are gastric carinomas * 2 leading cause of cancer related deaths in the world * One of the leading killers among cancers * low 5 year survival rate of less than 20%

Answer 3

* Infection with *H. pylori* * Food additives such as nitrates * High levels can lead to the conversion of carcinogenic nitrosamines in the stomach * High salt intact * Enhances conversion to nitrates * Caustic to stomach * Low intake of fruits and vegetables * Vit C and carotenoids thought to be protective

Answer 4

* Atropic gastritis and intestinal metaplasia are strongly linked to the association with gastric cancer * Leads to insufficent acid production which allows bacteria colonization * Bacteria convert nitrates to nitrosamines * Cause DNA damage to mucosal epithelium * Leads to further damage

Answer 5

* Lactose Intolerance * Malabsorption syndrome * Celiac sprue * Inflammatory bowel disease (IBD) * Diverticulosis/diverticulitis * Bowel Obstruction * Appendicitis * Diarrhea * Irritable Bowel * Colon cancer

Answer 6

* A deficiency in the intestinal mucosal enzyme lactase * Leads to the inability to hydrolyze lactose into glucose and galatose * Undigested and unabsorbed lactose is metablized by bacteria in the colon

Answer 7

* Syndrome implies a common constellation of symptoms arising from multiple causes * Inadequate gastric mixing * Insufficient digestive agents * Improper milieu * Damage to intestinal epithelium * Impaired transport

Answer 8

* Immunological sensitivity to gluten (gliaden peptide) * Low absorptive villi (flattened villi) * Improves when gluten is removed from diet * Large genetic component (HLA-DQ2, HLA-DQ8)

Answer 9

* Gliadin induces epithelial cells to produce IL-15 * IL-15 triggers activation and proliferation of CD8+ intraepithelial lymphocytes that express NKG2D and MIC-A receptor * These CD8+ lymphocytes destroy enterocytes that express MIC-A

Answer 10

* Crohn's disease and ulcerative colitis are chronic relapsing inflammatory disoders of unknown origin * 1 million Americans have IBD * Likely a combination of the following * Inappropriate host interactions with intestional flora * Intestinal epithelial dysfunction * Abnormal mucosal immune response

Answer 11

* 1-Genetics * More apparent in Crohn's Disease * NOD2, ATG16L1, IRGM * 2-Mucosal Immune Response * Immunosuppression therapy improves symptoms * IL-23 receptor * 3-Epithelial barrier defects * Dysfunction of tight junction (Crohn's) * Allow organism to invade and active the immune response * 4-Microbiota * Antibodies against flagella proteins * Probiotics help?

Answer 12

* Transmural inflammation of the GI tract * Generally affects the proximal colon and the terminal ileum * 30% are small bowel only * 50% are small and large bowel * 15-20% are large bowel only * Noncontiguous "skip" lesions * Appears to begin in the intestinal submocsa and spreads to the mucosa and serosa * Obstruction of lymphatics within the GI tract * Inflammatory reaction leads to deep penetrating ulcers in the intestinal wall * Abscesses, fistulas, and microperforations * Pain is often constant with diarrhea and malabsoprtion syndrome * Incidence * 1-10cases/100,000 * Males and females are equally affected * Higher incidence in European ancestry and Ashkenazi jews * Genetic factors * NOD2, ATG16L1, IRGM

Answer 13

* Cortiosteroids, immunosuppresive drugs * Infliximab (monoclonal antibody thta targets TNF-A) and ultimately surgery

Answer 14

* Ulcerative colitis is an inflammatory disease of the mucosa of the colon and rectum. * The inflammation involves the mucosal surface and not the underlying tissue layers * UC presents with abdominal pain, diarrhea and rectal bleeding. * Results in inflammation (neutrophilic/mono-cytic inflitration) and eventual abscess formation * Both B and T cells seems to be involved with large amounts of IgG antibodies produced * Tends to be more chronic relapsing than Crohns * Increased risk of colon/rectal cancer * Assess UC disease severity * Examining the Number of stools per day * Hematocrit * Albumin level

Answer 15

* Small herniations of the mucosal of the mucosal and sub-mucosal layers of the colon wall * Usually occurs in the large intestine due to the structural differences * Occur as a result of increased intraluminal pressure and decrease in luminal diameter * Age * High density low bulk (low fiber) * Straining during defection * An inflamed or infected diverticulum * This inflammation can result in severe abdominal pain, abscess and possible rupture into the peritoneal cavity causing life-threatening peritonitis * Rx: Increase fiber (increase stool weight and decrease intraluminal pressure) and antibiotics

Answer 16

* Small intestine more commonly obstructed * Causes * Tumors * Herniation * Torsion (volvulus) * Intussusception * Adhesion * Paralytic ileus * Neuropathies

Answer 17

* Affects 500 million children throughout the world and is the leading cause of death of children under 4 * About 220,000 Americans children hospitalized for gastroenteritis * Two-types * Large-volume * Small volume

Answer 18

* Osmotic * Non absorbale substance in the intestine draws water into the lumen by osmosis * Secretory * Excessive mucosal secretion or lack of Na+ reabsorption * Motility * Increased motility

Answer 19

* Tend to affect the superificial epithelial of the small intestine leading to destruction of these cells * Repopulation of epithelial cells result in immature enterocytes that leads to a lack of absorption of water and nutrients * Norwalk Virus and Rotavirus are classic examples

Answer 20

* Tend to be more severe than viral forms * Massive fluid lsos, destruction of intestinal mucosa, sepsis and perforation * Can be caused by several mechanism * Ingestion of preformed toxins * Infection by toxigenic organisms that proliferate and produce toxins * Infection be enteroinvasive organism which invade and destroy the epithelial mucosa

Answer 21

* Functional disorder with no identifiable pathology * Fluctuations in stool frequency and consistency * Characterized by a variable combination of chronic and recurrent intestinal symptoms * Hallmark is abdominal pain/bloating alleviated by defecation

Answer 22

1. Abnormal GI motility and secretion 2. Post infectious IBS 3. Overgrowth of Intestinal flora 4. Food allergy or food intolerance 5. Psychoscial factors 6. Hormones It is not IBS, if fever, bloody stools, nocturnal diarrhea, or weight loss are present

Answer 23

* Colon/rectum is host to more primary neoplasms than any other organ in the body * Colorectal carcinoma is the 2 leading cancer in the US * Adenocarcinomas constitute the vast majority of the colorectal cancers

Answer 24

* Make up about 70% of intestinal neoplasms * A polyp is a mass that protrudes into the gut lumen * Begin as benign neoplasms that arise from the mucosal epithelium due to alterations in the replication of the crypt epithelial cells * Maligant risk with adenomatous polyps is correlated with the size of the polyp and the degree of dysplasia * Familial Adenomatous Polyposis (AD) * Mutations in the adenomatous polyposis coli (APC) gene * Develop 500-2500 colonic adenomas * Development of adenocarcinoma is nearly 100% by midlife unless a prophylactic colectomy is performed

Answer 25

* 2nd leading cause of cancer related deaths in US * Risk Factors * Family history * UC * adenomatous polyps * perhaps diet * Aspirin may protect * May be asymptomatic for a long time * Bleeding often first symptom * Believed to be two distinct pathways involved in colorectal carcinogenesis * 1) APC. B-catenin pathway * 2) Mismatch Repair Pathway

Answer 26

1. A-Cancer limited to the mucosa or submucosa. 90% surival 2. B1- Cancer pernetrates into but not through the muscularis propria. 80% surivival 3. B2-Cancer penetrates through the muscularis. 70% 4. C1-Same, as B1, plus lymph node metastases 50% 5. C2-Same as B2, plus lymph node metastases. 50% 6. D-distant metastases are present, x\<30%

Answer 27

* Cholelithiasis * Cholecystitis * Choledocholitiasis * Cholangitis

Answer 28

* A condition in which cholesterol stones form within the gallbladder * The formation of gallstones is the result of bile that is supersaturated with cholesterol * Supersaturation sets the stage for cholesterol crystal formation which leads to "microstones" * Overtime microstones aggregate and grow to form "macrostones" * Several factors * Enzyme defect; increases cholesterol synthesis by hepatocytes * Decreased secretion of bile acids, which normally promote cholesterol solubility * Decreased reabsorption of bile acids from the ileum * Gallbladder smooth muscle hypomotility, stasis

Answer 29

* **_Cholecystitis:_** is an inflammatory disease of the gall bladder * Typically a result of cholelithiasis and obstruction of the cystic duct * If left untreated the gallbladder may perforate and rupture possibly resulting in empyema

Answer 30

* Choledocholithiasis * Blockage and inflammation of the common bile duct * Typically due to a stone * May result in an secondary pancreatitis * Cholangitis * Bacterial infection of the bile duct

Answer 31

* Acute pancreatitis is an inflammatory condition of the pancreas which alters the exocrine and endocrine functions of the pancreas * General precipiating factors * pancreatic duct obstruction (stone, tumor) * edema (leads to ischemic injury) * acinar cell injury (alcohol, drugs, virus)

Answer 32

* Chronic inflammatory lesions within the pancreas along with persistent pancreatic insufficiency over long periods. * Eventually, fibrosis adversely affects the exocrine and endocrine tissue and calcification develops * Almost all cases of chronic pancreatits are associated with alcoholism

Answer 33

* One of the most deadly malignancies with a 5 year survival rate of about 4-5% * Age (50+), smoking, alcohol, chronic pancreatitis and diabetes mellitus * 95% are adenocarcinomas of the ductal epithelium

Answer 34

* Jaundice (symptom) * Hepatitis * Cirrhosis * Toxic liver disorders * Liver tumors

Answer 35

* Jaundice (Icterus) is a yellow pigmentation of the skin caused by hyperbillirubinemia * Can result from * Extrahepatic obstruction to bile flow (gallstones) * Intrahepatic obstruction (hepatitis or cirrhosis) * Excessive production of billrubin (excessive hemolysis of RBCs)

Answer 36

* Hepatitis refers to inflammation of the liver parenchyma. This inflammation may be due to an infectious agent or it may be chemically induced * There are many viruses capable of infecting the liver. The types we conser are Hepatitis A-E

Answer 37

* HAV: RNA virus * Spread by fecal-oral route * Drinking contaminted milk, or water, or eating shellfish from infected waters * 2-7 week incubation period * May be asymptomatic or mild (jaundice variable) * Malaise, aneroxia, nasuea, fever, upper right pain are symptoms * Clinical course usually self limiting * Usually does not result in chronic hepatitis * Vaccine available

Answer 38

* HBV: DNA virus * Prevalent worldwide (5% of population) * Spread by blood/body fluids, sex perinatal * Incubation period: 2-6months * May be silent, mild hepatisis or fulminant * May procedd to chronic hepatits...cirrhosis * Increased risk of liver cancer * Vaccine available (Recombivax)

Answer 39

* HCV: RNA virus * Prevalent worldwide (3% of population) * Most common cause of chronic hepatits * Incubation 15-150 days (Avg 50) * Spread: same as HBV (sex, perinatal less likely) * Acute infection usually asymptomatic * Increased risk of liver cancer * No vaccine available

Answer 40

* Hepatitis Delta virus-defective RNA virus * Two forms * Coinfection with acute Hep B * Super-infection which Hep D is imposed on chronic Hep B * HDV can increase severity of HBV * Transmission is similar to HBV

Answer 41

* Uneveloped, single stranded RNA * Transmitted by fecal oral route * Manifestations similar to Hep A * Does not cause Chronic Hep or carrier state * High mortality rate-20% in preg women * Occurs primarily in developing areas * US cases only from those who traveled to edemic areas

Answer 42

* Chronic persistent or chronic active liver inflammation of more than six months duration. * Progressive and destructive inflammatory disease that involves necrosis of the hepatic lobule * HBV/HCV * Maybe autoimmune in nature * Chief reason for liver transplants

Answer 43

* Cirrhosis of the liver is an irreversible state that represents the end stage of a disease process (e.g. hepatitis, alcoholic liver disease). It is represented by widespread hepatic fibrosis * This fibrosis alters liver blood flow, bile flow and hepatocellular biochemical functions (e.g. protein synthesis, urea synthesis). * The eventual end result is liver failure

Answer 44

* Chronic abuse of alcohol commonly leads to liver disorders such as: fatty liver, hepatitis and cirrhosis. * Fatty liver (steatosis) is an accumulation of triglycerides in the hepatocytes * Decreased ability to metabolize them * Defective transport mechanism. * Results in an enlarged liver and is usually asymptomatic

Answer 45

* Hemochromatosis: iron overload due to an increase in iron absorption in the small intestine. * Iron is deposited in many tissues in excess including the liver. Inherited disorder (AR). * Wilson’s Disease: Copper deposition in the liver as a result mutation in the (ATP7B) gene which there is decreased production of ceruloplasmin, the protein carrier of copper in the blood. (AR)

Answer 46

* Relatively rare – 0.5-2% of all cancers * 5-yr survival – 1%- most die within 6 months * Two main types * Hepatocellular carcinoma – etiologic agents include chronic viral Hep, cirrhosis, arsenic contaminated water, chronic aflatoxin (molds) exposure * Serum alpha-fetoprotein found in 60-70% * Cholangiocarcinoma – * Risk factors include chronic inflammation and injury to bile duct epithelium

GI Anatomy and Physiology Flashcards

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