GI&HB Week Three

  1. A form of liver disease observed in middle-aged patients with abnormal liver biochemical test results and histologic evidence of alcoholic hepatitis but no history of alcohol abuse
    Nonalcoholic Steatohepatitis (NASH)
  2. The causes of NAFLD may be divided into two main categories. What are they?
    • Drugs & Toxins
    • Metabolic Abnormalities (aquired or congenital)
  3. What condition is most often reported associated with NAFLD?
  4. In regard to obesity-related NAFLD development, which is more important, the distribution of body fat or the total adipose tissue mass in the patient?
    Distribution of Body Fat (intraabdominal or viceral fat may be an important predictor of NAFLD)
  5. What is the hallmark histologic feature of NAFLD?
    Hepatic Steatosis
  6. What are the two primary pathogenic factors in steatosis in most patients with NAFLD?
    • Insulin Resistance
    • Hyperinsulinemia
  7. How does NAFLD usually present?
    It is usually discovered incidentally bc of elevated liver biochemical test levels or hepatomegaly noted during an evaluation for an unrelated medical condition. Most patients are asymptomatic
  8. What is the advanced form of NAFLD?
  9. In contrast to NAFLD, this is a localized or patchy process that stimulates a space-occupying lesion in the liver on imaging studies
    Focal Fatty Liver
  10. What is the main contributer to the amino acid pool?
    Dietary Protein
  11. In a mature adult, the Nitrogen Balance should be....?
    • 0
    • Anabolism = Catabolism
  12. In what situations should there be a positive nitrogen balance (nitrogen intake > nitrogen excretion)?
    • Growing animal
    • Pregnancy
    • Recovery from starvation or a wasting disease
    • Any circumstance where building up muscle tissue
  13. In what situations should a negative nitrogen balance (nitrogen intake < nitrogen excretion) exist?
    • Starving animal
    • Acute injury or infection
    • Senescent animal
    • Deficiency of one or more essential amino acids in diet
  14. What are the essential amino acids?
    • Phenylalanine
    • Valine
    • Threonine

    • Tryptophan
    • Isoleucin
    • Methionine

    • Histidine
    • Arginine
    • Leucine
    • Lysine
  15. What are the nonessential amino acids?
    • Proline
    • Tyrosine
    • Alanine
    • Aspartate
    • Asparagine
  16. What are the conditional non-essential acids, and what essential acid are they derived from?
    • Tyr (derived from Phe)
    • Cys (derived from Met)
  17. Where does protein degradation begin, and what is the main protease involved?
    • Stomach
    • Pepsin
  18. What activates the zymogen pepsinogen to form the active pepsin protease?
    The low pH in the stomach (pH 2-3)
  19. For protein degradation in the intestine, what enzyme is responsible for the activation of the zymogen Trypsinogen? Where is this enzyme derived from?
    • Enteropeptidase
    • Intestinal Enzyme
  20. For protein degradation in the intestine, what enzyme is responsible for the activation of the zymogen Chymotrypsinogen? Where is this enzyme derived from?
    • Trypsin
    • Pancreatic Enzyme
  21. For protein degradation in the intestine, what enzyme is responsible for the activation of the zymogen Procarboxypeptidase? Where is this enzyme derived from?
    • Trypsin
    • Pancreatic Enzyme
  22. For protein degradation in the intestine, what enzyme is responsible for the activation of the zymogen Proelastase? Where is this enzyme derived from?
    • Trypsin
    • Pancreatic Enzyme
  23. When trypsin becomes abnormally activated in the pancreas, what molecule is responsible for binding to and inhibiting the active trypsin?
    Pancreatic Trypsin Inhibitor
  24. Where does Trypsin cleave?
    • Arg
    • Lys
  25. Where does Chymotrypsin cleave?
    • Tyr
    • Phe
    • Trp
  26. Where does Elastase cleave?
    Small Amino Acids
  27. Where does Carboxypeptidase A cleave?
    C-terminal Aromatics or Aliphatics
  28. Where does Carboxypeptidase B cleave?
    • C-terminal Arg
    • C-terminal Lys
  29. From what end of the small peptide particle does Aminopeptidase cleave?
    N-terminal End
  30. From what end of the small peptide particle does Carboxypeptidase cleave?
    C-terminal End
  31. What is the most common genetic disease of amino acid transport?
  32. This is an AR disease characterized by a defect in the absorption of basic amino acids in kidneys and liver
  33. What are the symptoms of Cystinuria?
    • Cystine Crystals: form under acidic conditions
    • Cystine Crystals: appearance of ground glass
  34. What is the treatment for Cystinuria?
    • Increased Fluid Intake
    • Alkalinization of the Urine above pH
  35. What are the four basic amino acids deficiently absorbed in Cystinuria?
    • Lysine
    • Arginine
    • Ornithine
    • Cystine
  36. This disorder is an AR disease characterized by a defect in the absorption of neutral amino acids in kidneys and intestine (major mediator of tryptophan uptake)?
    Hartnup Disorder
  37. What are the symptoms of Hartnup Disorder?
    • Pellagra-like Skin Rash (scaly, red rash)
    • Neurologic Symptoms (seeing double, ataxia, etc)
  38. What is the treatment for Hartnup Disorder?
    Nicotinic Acid Supplementation
  39. What cells secrete HCl?
    Parietal Cells
  40. HCl is required for Chief Cells to secrete what?
  41. In the intestine, what absorbs the amino acids?
    Intestinal Mucosa
  42. What can impair the release of HCl into the stomach?
    • Gastric Bypass Surgeries
    • Some Gastric Carcinomas
  43. What can cause a failure of pancreatic zymogen cleavage? What can this cause? How can it be treated?
    • A problem or deficiency in Enteropeptidase
    • Can cause Failure to Thrive due to an inability to absorb amino acids
    • Treat by supplementing diet with time-released pellets of active pancreatic proteases
  44. True or False:
    Statin treatment is safe and can improve liver tests and reduce cardiovascular morbidity in patients with mild-to-moderately abnormal liver tests that are potentially attributable to non-alcoholic fatty liver disease.
  45. What is the most common cause of abnormal liver tests in the developed world?
    NAFLD (non-alcoholic fatty liver disease)
  46. NAFLD and Non-Alcoholic Steatohepatitis (NASH) may be independent risk factors for what type of disease, which is classified as the main cause of death in these patients?
    Cardiovascular Disease
  47. What percentage of patients in developed countries have Fatty Liver or Non-Alcoholic Steatohepatitis (NASH)?
    20% or more
  48. Is ALT testing specific to the liver?
    No; includes liver, heart, muscle, and kidney
  49. What is the most common monosaccharide found in humans?
  50. How are monosaccharides classified?
    According to the most oxidized functional group
  51. Monosaccharides are classified according to the most oxidized functional group. If it is an aldehyde, what is it called?
  52. Monosaccharides are classified according to the most oxidized functional group. If it is a ketone, what is it called?
  53. Monosaccharides that have the same chemical formula, but different structures are called?
  54. A specialized type of isomer in which the structure is varied around a single carbon is called?
  55. If the single carbon that isomers are varied around happens to be the carbonyl carbon, then the two compounds are called?
  56. Anomers of glucose are in equilibrium so that in our bodies, glucose is 2/3 __________ anomer and 1/3 _________ anomer
    • Beta
    • Alpha
  57. Monosaccharides that are mirror images of each other are called?
  58. An example of glucose enantiomers is D-glucose and L-glucose. Our cells can use __________ in metabolic pathways, but cannot use ________
    • D-glucose
    • L-glucose
  59. What are monosaccharides linked by?
    Glycosidic Bonds
  60. True or False:
    All monosaccharides are reducing agents
    True, because the carbonyl carbon can be further oxidized to a carboxyl carbon
  61. True or False:
    All dissaccharides are reducing agents
    False; they can be reducing sugars as long as the carbonyl carbon of one of the monosaccharides is not in a glycosidic linkage
  62. What is an example of a reducing dissacharide?
  63. What is an example of a non-reducing dissarcharide?
  64. Where does digestion of carbohydrates begin?
    Oral Cavity
  65. What enzyme begins digesting plant starches and animal glycogen in the oral cavity?
    Salivary Alpha-Amylase
  66. What are the major dietary complex carbohydrates?
    • Starch
    • Glycogen
  67. What stops salivary alpha-amylase activity when it reaches the stomach?
    Low pH; salivary alpha-amylase works at neutral pH
  68. When the stomach contents enter the small intestine, the pH is neutralized by the secretion of what from what organ?
    • Bicarbonate
    • Pancreas
  69. What enzyme is secreted into the small intestine to further digest the oligosaccharides?
    Pancreatic Amylase
  70. What does pancreatic amylase in the small intestine break the oligosaccharides down into?
  71. The final stage of dissacharide digestion occurs by the action of...?
    Dissacharidases that are associated with the luminal side of the brush border membranes of the intestinal mucosal cells
  72. What are the 5 major dissacharidases?
    • Isomaltase
    • Maltase
    • Lactase
    • Sucrase
    • Trehalase
  73. What results from digestion of the dissacharides by dissacharidases in the intestinal mucosa?
  74. The monosaccharides that result from digestion by the dissarcharidases are absorbed by....?
    Intestinal cells of the duodenum and upper jejunum
  75. What are the two mechanisms by which the monosaccharides that result from digestion of disaccharides in the small intestine absorbed by the intestinal cells of the duodenum and upper jejunum?
    • Active Transport
    • Facilitative Diffusion
  76. What is the active transporter protein responsible in part for the absorption of monosaccharides into the duodenum and upper jejunum? What is it dependent on?
    • SGLT-1
    • Energy- and Sodium-Dependent
  77. How are the monosaccharides absorbed by the small intestine transported during faciliated diffusion?
    Down a concentration gradient
  78. Glucose and Galactose are transported across the brush border in the duodenum and upper jejunum by which transport process?
    Active Transport
  79. Fructose is transported across the brush border in the duodenum and upper jejunum by which transport process?
    Facilitative Diffusion
  80. What is the facilitative diffusion transporter involved in the absorption of monosaccharides into the small intestine?
  81. Abnormalities in the degradation of dissacharides can lead to digestive problems. What results from a deficiency of lactase? What are its symptoms? How can it be treated?
    • Lactose Intolerance
    • Bloating, Diarrhea, Dehydration
    • Treat by dietary change
  82. Abnormalities in the degradation of dissacharides can lead to digestive problems. What deficiency results in an intolerance to sucrose? How can this be treated?
    • Sucrase-maltase deficiency
    • Supplementary digestive products can be given
  83. Triacylglycerol degradation is carried out by ....?
    Pancreatic Lipase
  84. Pancreatic lipase can be inhibited by high concentrations of what?
    Bile Salts
  85. During triacylglycerol degradation, a second protein, _______, helps to anchor the pancreatic lipase to the lipid/aqueous interface facilitating enzymatic activity
  86. Cholesteryl ester degradation is carried out by _______ which removes the free fatty acid from the 3-hydroxyl group
    Cholesteryl ester hydrolase
  87. Cholesterylesterase is activated by the presence of what?
    Bile Salts
  88. Secretion of the digestive enzymes that degrade dietary lipids is under hormonal control. The mucosal cells in the duodenum and jejunum secrete the peptide _________, which is responsible for this digestion
    Cholecystokinin (CCK)
  89. What are the three main functions of CCK?
    • Signals the gallbladder to secrete bile
    • Signals the exocrine portion of the pancreas to secrete the digestive enzymes
    • Slows gastric motility
  90. What hormone signals the liver and pancreas to secrete bicarbonate to neurtralize the gastric contents (chyme)?
  91. This consists of digested lipid products and bile salts to form an amphipathic particle. This particle has a hydrophilic outer surface and a hydrophobic core
    Mixed Micelle
  92. What part of the mixed micelle allows the digested lipid materials to be transported through the unstirred water layer that separates the mucosal membrane from the bulk fluid contents of the intestine?
    The hydrophilic outer surface
  93. What is found in the interior of the mixed micelle?
    • Free Cholesterol (from the diet)
    • Fat-Soluble Vitamins (A, D, & K)
    • Free Fatty Acids
  94. What occurs once the contents of the mixed micelle are taken up by the intestinal cell (enterocyte)?
    Resynthesis of Triacylglycerol and Cholesterol Esters
  95. What is the first step in the resynthesis process of triacylglycerol and cholesterol esters?
    The activation of the long chain fatty acids to form fatty Acyl CoA molecules
  96. What is used for the glycerol backbone for triacylglycerol synthesis?
  97. Malabsorption of lipids leads to increased fat content of fecal material. What is this called, and what can it cause?
    • Steatorrhea
    • Causes: defective secretion of bile salts from the gallbladder, defective secretion of pancreatic enzymes, or a defect in the intestinal mucosal cells
  98. What are complex lipids formed in the enterocytes synthesized into?
  99. Throughout the length of the GI tract, the wall of the gut can be divided into four layers. What are they?
    • Mucosa
    • Submucosa
    • Muscularis Externa
    • Serosa
  100. What is the inner layer of the digestive tract?
  101. The luminal surface of the gut is lined by a layer of epithelium that is moistened by glandular secretions. What lies deep to the epithelium?
    Lamina Propria
  102. This is a layer of loose connective tissue that is rich in blood vessels, nerves, and lymphatic ducts.
    Lamina Propria
  103. In most regions of the GI tract, lying in the outer region of the lamina propria (away from the lumen) is a thin layer of smooth muscle called the ...?
    Muscularis Mucosa
  104. Contractions of the muscularis mucosa affect the folding of the epithelial surface into ridges called ______ (stomach) and _______ (intestines)
    • Rugae
    • Pleicae
  105. What cell type secrete various signaling molecules into the lamina propria where they can: 1) act as hormones by entering the blood stream; 2) activate neural reflexes by acting on nerves in the lamina propria; 3) act as paracrine compounds by acting on nearby cells in the epithelial layer and lamina propria; or 4) have an autocrine action by providing feed-back to each other
    Enteroendocrine Cells
  106. What is the double layer of smooth muscle (inner circular and outer longitudinal) that lies outside the submucosa?
    Muscularis Externa
  107. What are the sheets of smooth muscle of the Muscularis Externa necessary for?
    Mechanical processing and propagation of luminal contents of the bowel
  108. What ganglionated plexus lies between the longitudinal and circular muscle layers of the Muscularis Externa and regulates the actions of the smooth muscle layers?
    Myenteric Plexus (Auerbach's)
  109. What is the ganglionated plexus of nerves located in the Submucosa called?
    Submucosal Plexus (Meissner's)
  110. Within the peritoneal cavity, the structures of the digestive tract are covered with a sheet-like serous membrane comprised of a monolayer of mesothelial cells. What is this known as?
  111. A dense network of collagen fibers, referred to as ________, envelops GI structures that are retroperitoneal, as well as the upper regions of the GI tract from the oral cavity to the esophagus as it passes through the diaphragm. It attaches these regions of the digestive tract to adjacent structures.
  112. What are the muscle layers of the small intestine?
    • Longitudinal Muscle Coat
    • Circular Muscle Layer
    • Muscularis Mucosa
  113. The motor function of the longitudinal and circular muscle layers of the small intestine is coordinated by?
    Myenteric Plexus
  114. The motor function of the muscularis mucosa and epithelial function of the small intestine are regulated via the?
    Submucosal Plexus
  115. What is the primary function of the intestine?
    The absorption of water, electrolyte and nutrient substances
  116. This is most commonly caused by an adverse mucosal response to dietary gluten which is present in wheat- or rye-based foods. It results in a stunting of the villi and a decreased absorptive mucosal surface area.
  117. What is the primary site of nutrient absorption?
  118. What is the primary function of the small intestine?
    Absorption of water, electrolyte, and nutrients
  119. Within the small intestine, what cell type tends to be absorptive?
    Villous Cells
  120. Secretion of fluids and electrolytes occurs in the small intestine. What cell type are responsible for secretion?
    Crypt Cells
  121. What are the two routes of epithelial transport in the small intestine?
    • Intercellular or Paracellular: through tight junctions
    • Intracellular or Transcellular: active or passive transport through the cell (across brush border)
  122. The permeability of tight junctions varies depending on location in the GI tract. Are they tight or loose in the small intestine?
    Relatively loose, or leaky
  123. What are the four methods of sodium transport across enterocytes?
    • Electrogenic Transport: active transport, Na-K pump (basolateral side) rheogenic
    • Substrate-Coupled Transport: rheogenic
    • Electro-neutral Transport: Symport
    • Anti-Porter: with H ions
  124. Water movement in the intestine is passive and relies on what three things?
    • Osmolality of Chyme
    • Rate of Solute Transport
    • Size of the Intercellular Spaces
  125. Describe calcium transport across the enterocyte?
    • Actively absorbed in duodenum and jejunum by a membrane bound carrier, activated by 1,25-dihydroxycholecalciferol.
    • Diffuses into the enterocyte where it is bound to calcium binding protein
    • Is then actively transported across the basolateral membrane
  126. There are at least two methods of Iron uptake, one for __________ and a second for __________
    • Heme Iron
    • Free Iron
  127. Free iron is toxic when it enters the cell, so it binds to _______ to form __________
    • Apo-Ferritin
    • Ferritin
  128. How does absorbed ferritin exit the enterocyte, and where does it go?
    • By the Ferroportin Transport Protein
    • Enters the Plasma
  129. How is chloride secreted from crypt cells in the small and large intestine?
    • Na-K-Cl Triporter
    • Acetylcholine: by increasing intracellular Ca
    • VIP and Prostaglandins by elevating intracellular cAMP
  130. What stimulates anion secretion? What mediates it?
    • Response to neuronal or hormonal influences
    • Bacterial toxins
    • May be mediated by a rise in intracellular cAMP or Ca
  131. What stimulates fluid secretion? Where is this particularly important?
    • High luminal osmolality
    • Proximal duodenum
  132. Increased interstitial hydrostatic pressure, also called secretory filtration, may accompany what?
    Severe luminal distention
  133. The small intestine is involved in the breakdown and assimilation of three important food components. What are they?
    • Carbohydrates
    • Proteins
    • Lipids
  134. Emulsified fat products must first pass through two barriers:
    • The unstirred water layer lying above the brush border
    • The lipid membrane barrier
  135. What are the components of the mixed micelle?
    • Bile Salts
    • Cholesterol
    • Lecithins
    • Monoglyceride
    • Free Fatty Acid
  136. Efficient absorption of fat-soluble vitamins requires what?
    Bile Salts
  137. What happens to the intestine when longitudinal muscle contracts?
    Becomes shorter
  138. What happens to the intestine when circular muscle contracts?
    Becomes occluded
  139. What does postprandial mean?
  140. When do interdigestive patterns occur?
    Between meals (fasting)
  141. What type of contractions promote forward movement of luminal contents in the small intestine?
    Peristaltic Contractions
  142. What type of contractions promote mixing with no net forward movement of luminal contents in the small intestine?
    Segmental Contractions
  143. What provides contact between smooth muscle cells and allows for coordinated contractions?
    Gap Junctions
  144. Circular smooth muscle cells in the small intestine are characterized by rhythmic episodes of spontaneous depolarization of 5-15 mV in amplitude lasting 1-5 sec. These are called what?
    Slow Waves
  145. What happens if slow waves reach threshold?
    They generate action potentials
  146. What are the action potentials or spikes of slow waves due to?
    The inward movement of calcium
  147. Is the strength of contractions in the small intestine determined by the number of spikes or their amplitude?
    The number of spikes
  148. Where do propagating slow waves originate in the small intestine?
    In the Interstitial Cells of Cajal (ICCs)
  149. What are the pacemakers of the gut?
    Interstitial Cells of Cajal (ICCs)
  150. Slow waves do not directly produce contractions and are propagated from cell to cell via _________
    Gap Junctions
  151. What is the primary neurotransmitter released from intrinsic nerves associated with the longitudinal muscle?
  152. What is the primary neurotransmitter associated with circular smooth muscle?
    VIP or NO
  153. A large portion of the increase in intracellular calcium in smooth muscle is derived from an influx of __________ calcium. In contrast, in skeletal muscle calcium is mobilized from _________ stores.
    • Extracellular
    • Intracellular
  154. The contractions of the small intestine serve to:
    • Mix chyme, facilitating its exposure to the absorptive surface
    • Move chyme towards the large intestine
  155. The frequency of slow waves varies along the upper GI tract. What are the frequencies per minute in the stomach, duodenum, and ileum?
    • 3/min Stomach
    • 12/min Duodenum
    • 8/min Ileum
  156. This is a motor phenomenon that occurs in the small intestine during the interdigestive period
    Migrating Motility Complex (Migrating Myoelectic Complex) (MMC)
  157. MMC migration requires what two things?
    • An intact myenteric plexus
    • Motilin (hormone)
  158. What are the three phases of the MMC, and what do they entail?
    • Phase I: period of relative quiescence
    • Phase II: characterized by intermittent motor activity
    • Phase III: is composed of regular, propagating contractile activity
  159. What does phase III activity of the MMC do?
    Clears the lumen of debris (sloughed epithelial cells, etc.)
  160. What terminates the MMC?
  161. These type of contractions displace chyme in an oral and aboral direction. The forces for this are exerted by the circular muscle layer only.
    Segmentation (mixing)
  162. What is the most common type of contraction following a meal?
    Segmentation (mixing)
  163. This says that stimulation (e.g. distention by a bolus) at one locus of the small bowel induces contraction above and relaxation below the point of stimulation
    Law of the Intestine or Peristaltic Reflex
  164. The Law of the Intesine or Peristaltic Reflex is mediated by the?
    Enteric Nervous System
  165. This occurs when distension of one segment of small bowel reflexively inhibits the contractile activity of other segments
    Intestino-Intestinal Reflex
  166. This is a state of no muscle contractility. Electrical slow waves are present but there is little or no spike activity. This results from continuous activity of the intrinsic inhibitory neurons and is caused by peritoneal irritation
  167. This is the opposite of ileus in that there is no activity of the inhibitory neurons. The syncitial properties of the intestinal smooth muscle cells and their inherent contractility then produce maximal contractions
    Spasm of the Circular Muscle
  168. Name the Protozoan:
    Disease: Amebiasis/Amebic Dysentery/Liver Abscesses
    Epidemiology: Worldwide; male homos in US; trop and subtrop climates
    85-90% pts asymptomatic
    2-21 day incubation period
    Variable or chronic intestinal symptoms (GI upsets, including colitis & diarrhea)
    Very Severe Cases: ulcers; ameboma; perforation; hemorrhage; fulminant, bloody diarrhea; intestinal hemorrhages & dysentery; Amebic hepatitis = single abscess in right lobe (RUQ pain, fever, weight loss)

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Entamoeba Histolytica
    • Fecal-oral route through ingestion of cyst stage in contaminated food & water
    • Differential diagnosis: must exclude bacillary dysentery; finding trophozoites in loose stools or the cyst in formed stools; X-ray/US to detect ulcers and abscesses
    • Treatment: Metronidazole plus Iodoquinol
    • Prevention: Avoid contaminated water & food; practice good personal hygiene
  169. What are the differences between Amebic and Bacillary Dysentery?
    • Amebic: gradual onset of symptoms; no fever, chills, or pus; less prostration; chronic course
    • Bacillary: sudden onset; fever, chills, and pus; more prostration; acute course
  170. Identify the Protozoan:
    Epidemiology: Worldwide; common in hikers who drink unfiltered water
    Organism is non-invasive, but destroys epithelial microvilli
    Acute Infections: 2-21 day incubation period; severe diarrhea, but no dysentery; greasy, fatty, foul-smelling stools; abdominal distension w N&V
    Chronic Infections: Low antibody titers; diarrhea, weight loss, and intestinal malabsorption; flatulence

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Giardia Lamblia
    • Tranmission: Fecal-oral route through ingestion of cysts in contaminated water or food; anal sex
    • Diagnosis: Finding trophozoites or cysts in feces
    • Treatment: Metronidazole
    • Prevention: Avoid contaminated water; practice good personal hygiene
  171. Identify the Protozoan:
    Disease: Cryptosporidiosis
    Epidemiology: Worldwide; outbreaks in US due to inadequate water purification
    Symptoms: Abdominal cramping with watery, non-bloody stool
    Opportunistic Infection: chronic diarrhea, severe fluid loss, malnutrition, can be fatal

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Cryptosporidium Parvum
    • Diagnosis: Finding oocytes in feces
    • Treatment: No current drugs or vaccines available; fluid replacement and supportive therapy
    • Prevention: water filtration; boil water that is suspected of contamination
  172. Identify the Protozoans:
    Disease: Coccidiosis
    Epidemiology: Worldwide; outbreaks in US due to inadequate water purification
    Symptoms: Mild to severe diarrhea with varying degrees of abdominal cramping, gas, fever, nausea, and vomiting

    How are they diagnosed, treated, and prevented?
    • Isospora and Cyclospora
    • Diagnosis: ID of oocytes in stool
    • Treatment: Trimethoprim-sulfamethoxazole; hydration
    • Prevention: Boiling and filtering water; washing fruit and veggies
  173. Identify the Helminth:
    Epidemiology: Worldwide, mostly southern US
    Symptoms: Largely asymptomatic; weakness and diarrhea

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Hymenolepis nana (dwarf tapeworm)
    • Transmission: Ingesting beetles containing cysticerci which develop into adult worms in the host's intestine
    • Diagnosis: Identification of eggs in stools
    • Treatment: Prazinquantal
    • Prevention: Hygiene and Sanitation
  174. Identify the Helminth:
    Disease: common tapeworm in pets that can be passed to humans
    Epidemiology: worldwide
    Symptoms: Mostly asymptomatic; diarrhea & pruritis

    How is it transmitted?
    How is it diagnosed and treated?
    • Dipylidium caninum (dog tapeworm)
    • Transmission: Ingesting fleas containing cysticerci which develop into adult worms in the host's intestines
    • Diagnosis: Identification of proglottids (rice-like beads) in stool
    • Treatment: Niclosamide
  175. Identify the Helminth:
    Epidemiology: Worldwide; predominantly tropics; 2.2 mil cases/yr in US
    Symptoms: Mostly asymptomatic; Abdominal pain; Diarrhea; Rectal Prolapse

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Trichuris trichiura (whipworm)
    • Transmission: Digestion of eggs from contaminated soil or food/water
    • Diagnosis: Identification of eggs in stool; Adult worms can sometimes be identified in rectal mucosa by proctoscopy
    • Treatment: Mebendazole
    • Prevention: Proper disposal of feces
  176. Identify the Helminth:
    Epidemiology: Worldwide; most common human helminth infection
    Acute infections are asymptomatic
    Moderate to heavy infections can cause abdominal pain and intestinal obstruction
    Adult worms may cause bile tract obstruction
    Migrating worms can cause pulmonary problems including eosinophilia, pneumonia, and cough
    Malnutrition in children in developing countries

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Ascaris lumbricoides
    • Transmission: Digestion of eggs from contaminated soil, food, or water
    • Diagnosis: Identification of eggs in stool; Occasionally, worms can migrate out of the body via the rectum or mouth
    • Treatment: Mebendazole
    • Prevention: Proper disposal of feces
  177. What is the most common human helminth infection?
    Ascaris lumbricoides
  178. Identify the Helminth:
    Epidemiology: worldwide; tropics, southern US
    Symptoms: 1/3 cases are asymptomatic
    Skin penetration may cause a pruritic papular erythematous rash ("ground itch")
    Pulmonary complications during lung migration (Loffler's syndrome)
    Burning or colicky abdominal pain, diarrhea with passage of mucosa.
    Nausea, vomiting, and weight loss Immunocompromised patients are more likely to suffer from autoinfection.
    Presents with abdominal pain, distension, shock, pulmonary and neurologic complications and septicemia.
    Can be fatal

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Strongyloides stercoralis
    • Transmission: filariform larvae in contaminated soil can penetrate skin; autoinfection
    • Diagnosis: Identification of larvae in stool or duodenal fluid; Larvae may be detected in sputum from patients with disseminated strongyloidiasis
    • Treatment: Ivermectin or Thiabendazole
    • Prevention: Wear shoes and proper disposal of feces
  179. Identify the Helminths:
    Disease: Hookworm disease
    Epidemiology: Africa, Asia, Americas; Americas and Australia
    Skin penetration may cause a pruritic papular erythematous rash ("ground itch")
    Iron deficiency anemia and other nutritional disorders caused by worm attachment to intestine
    Abdominal pain, diarrhea, weight loss due to adults residing in small intestine where they attach and feed on blood
    Pulmonary eosinophilia during lung migration (Loffler's Syndrome)

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Ancylostoma Duodenale; Necator Americanus
    • Transmission: Filariform penetrate skin
    • Diagnosis: Detection of eggs in fecal smear
    • Treatment: Mebendazole; treat severe anemia with ferrous sulfate
    • Prevention: wear shoes and proper disposal of feces
  180. Identify the Helminth:
    Disease: pinworm, seatworm, enterobiasis
    Epidemiology: worldwide; most common helminth infection in US
    Children are most often infected but infection is typically asymptomatic
    Perianal pruritis (nightime) leading to excoriations and bacterial infections.
    Anorexia, irritiability, and abdominal pain
    In rare cases causes peritoneal granulomas and vulvovaginitis (bacterial, Trichomonas, and Candida)

    How is it transmitted?
    How is it diagnosed, treated, and prevented?
    • Enterobius vermicularis (pinworm)
    • Transmission: ingestion of eggs; retroinfection occurs when eggs hatch and juvenile worms crawl back into anus
    • Diagnosis: Eggs detected in perianal region by using Scotch Tape; must be performed in morning before defecation and washing; cannot detect
    • eggs in feces
    • Treatment: Pyrantel pamoate (treat all family members bc of ease of infection
    • Prevention: personal hygiene and washing all bedding and clothes
  181. What are the three primary functions of the large intestine?
    • To store fecal material, which consists of indigestible food products
    • To extract water from the luminal contents
    • To move fecal material towards the rectum
  182. What digestive enzymes are secreted from the colon, and where does nutrient absorption take place in this organ?
    • None, and it doesn't
  183. The longitudinal muscle of the colon is concentrated into three bands. What are these called? Due to this, the circular muscle has the appearance of bulging outwards in sacculations called what?
    • Tenia Coli
    • Haustra
  184. Why is transit time so much slower in the colon than in the small intestine?
    Because it has a storage function
  185. What are the most common motility patterns in the colon, and where do they occur?
    • Mixing Movements
    • Proximal Colon
  186. In the colon, ______ migration results in a net movement of chyme in an aboral direction. In this case slow waves are associated with long bursts of spike activity.
    Haustral Migration
  187. The _______ anal sphincter is composed of smooth muscle which is tonically contracted. Activation of the parasympathetic nerves relaxes it via the release of VIP while activation of sympathetic nerves causes it to contract.
    Internal Anal Sphincter
  188. The ________ anal sphincter is composed of skeletal muscle and receives excitatory innervation from the pudendal nerve. It is under voluntary control.
    External Anal Sphincter
  189. Defecation is initiated by mild distension which activates the __________ reflex which relaxes the internal anal sphincter and elicits the urge to defecate.
    Rectosphincteric Reflex
  190. During defection, mild distension of the rectum induces a reflexive contraction of the external anal sphincter, termed __________.
  191. Defecation is facilitated by voluntary contraction of the abdominal muscles. What is this termed?
    Valsalva Maneuver
  192. The intrinsic innervation of the colon produces a net ________ influence on the muscular layers.
  193. The proximal colon receives extrinsic ________ innervation from both the vagus and the pelvic nerves. _______ stimulation causes segmental contractions; _______ nerve stimulation causes propulsive activity in the distal colon.
    • Parasympathetic
    • Vagal
    • Pelvic
  194. Sympathetic innervation to the proximal colon is via the _______ nerves. In the distal colon it is the _________ colonic nerves, although these fibers are associated with the entire colon.
    • Splanchnic
    • Lumbar
  195. The large intestine absorbs ____, _____, and _______ and secretes _______ and _______.
    • Na
    • Cl
    • Water
    • K
    • HCO3
  196. Are the intercellular spaces smaller or larger in the colon compared to the small intestine?
    Smaller; generates a significant electron gradient
  197. How does the colon absorb Na?
    Against a concentration gradient
  198. Two or more of the following for 3 months or more is classification for what?

    Straining more than 25% of the time
    Hard stools more than 25% of the time
    Incomplete evacuation more than 25% of the time
    Two or fewer bowel movements in one week
  199. What are some of the common constipating drugs (4)?
    • Analgesics/Narcotics
    • Anticholinergics -- Antidepressants, Phenothiazines (for Schizos), Anti-Parkinsonism Drugs
    • Calcium/Aluminum Antacids
    • Calcium Channel Blockers
  200. What is an important aspect of the physical exam for constipation? What other screening methods are used?
    • Digital Rectal Exam
    • Endoscopy & Radiology
  201. What are the treament options for constipation (general)?
    • Increase fiber to 20-40 g/day
    • Increase fluid intake
    • Laxatives
  202. What type of diarrhea persists with fasting and has no osmotic "gap"?
  203. Which type of diarrhea disappears with fasting and is characterized by nonabsorbed ions?
  204. Which diarrhea type is characterized by:

    Stool (Na) > 90 and
    Osmotic Gap of < 50
  205. Which diarrhea type is characterized by:

    Stool (Na) < 60 and
    Osmotic Gap >100
  206. What is the single most common cause of Osmotic Diarrhea? What are some other possible causes?
    • Lactose Malabsorption
    • Antacids
    • Dietetic Foods/Drugs
    • Miscellaneous Drugs
    • Enteral Feeding
  207. What are some common causes of Secretory Diarrhea?
    • Laxatives
    • Medications
    • Toxins
    • Bile Acids
    • Hormone Producing Tumors (rare)
  208. What is the typical duration of an acute diarrhea? Acute diarrheas are usually infectious. What is the most common culprit?
    • Less than 2-3 weeks
    • E. Coli (Rotavirus most common in regard to viral issues)
  209. What are the danger signs associated with acute diarrheas (7)?
    • High Fever (>38.5 or 101.3)
    • Systemic Illness
    • Tenesmus (crampy abdominal pain)
    • Dysentery
    • Prolonged Course (>2 weeks)
    • Dehydration
    • Elderly or Immunocompromised
  210. When treating acute diarrheas with antibiotics for a suspected parasite, we dont typically wait for the culture to come back. Instead, what are the first through 4th lines of treatment often used?
    • Quinolones (Ciprofloxacin, Levofloxacin)
    • Sulfa-Trimethoprim
    • Metronidazole
    • Azithromycin, Clarithromycin, or Erythromycin
  211. What is the first line of defense for C. Diff? Due to resistance, what is the second line of defense that is more costly, but has no known resistance?
    • Metronidazole
    • Vancomycin
  212. How long does it typically take C. Diff patients to respond to antibiotics?
    5-6 days
  213. What is the most common type of Chronic Diarrhea?
    Watery Diarrhea
  214. What are the treatment options for Nonspecific Chronic Diarrhea?
    • Bismuth (peptobismol)
    • Opiates: Diphenoxylate (lomotil); Loperamide (Imodium)
    • Anticholinergics
    • Adsorbents (Kaolin, Kaopectate)
  215. What is the most common cause of severe diarrhea among young children worldwide?
  216. What is the mode of transmission of Rotavirus?
    Feces or Fecal-contaminated Water
  217. What is the diagnosis?
    These are non-enveloped, triple-layer viruses, segmented dsRNA (11 segments), RNA genome. They cause viral gastroenteritis, and typically infect the intestines in children of age 6 months-3 years. The diarrhea results in fluid loss and severe dehydration.

    Associated Symptoms:
    Watery stools and vomiting after a 1-2 day incubation period in young children
    Vomiting is common and may be prolonged
    High, urine-specific gravity and metabolic acidosis
    Usually no blood or fecal leukocytes
  218. True or False:
    Natural rotavirus infection efficiently protects against severe disease associated with re-infection.
  219. These are single stranded, positive sense RNA. Naked.
    Major cause of non-bacterial diarrhea in children (> 2 years) and adults.
    Most common cause of epidemics of viral gastroenteritis
    Associated Symptoms:
    Watery Diarrhea
    Projectile Vomiting

    What is the diagnosis?
    Noroviruses (Caliciviruses): Norwalk and Norwalk-like
  220. What is the most common cause of epidemics of viral gastroenteritis in schools, camps, cruise ships, etc?
    Noroviruses (Caliciviruses): Norwalk
  221. Do noroviruses have long term protection, or is re-infection possible?
    No long term protection
  222. These are ss, + sense RNA viruses, naked, icosahedral capsid.
    Most commonly affect children under 2, but also elderly and immunocompromised.
    Transmission appears to be person to person, fecal-oral.
    Symptoms manifest 2-3 days post-infection
    Disease usually lasts only a few days.
    Symptoms very similar to rotavirus but not as severe.
  223. Crohn's Disease has been associated with polymorphisms in what three genes, which contribute to the function of the innate immune system and the process of autophagy?
    • NOD2
    • ATG16L1
    • IRGM
  224. Patients with Crohn's Disease are more likely to have anitbodies to (3)?
    • ASCA
    • Cbir
    • OmpC,12
  225. 50-80% of Ulcerative Colitis patients have what antibodies?
  226. What is the diagnosis?:

    A chronic, recurrent, usually focal, asymmetric and transmural inflammation of the GI tract, which may effect any portion of tract but most commonly small bowel and colon.
    Symptoms/Complications: diarrhea, pain, weight loss, malabsorption, fistula and strictures, abscesses, and anemia
    Crohn's Disease
  227. If a Crohn's patient has this symptom, it means that the disease will be hard to treat. What is the symptom?
    Perianal Pain
  228. What is the diagnosis?:

    Chronic inflammatory condition of the colon characterized by inflammation of the mucosa resulting in ulceration, characterized by abdominal pain and diarrhea (usually bloody). Proctitis may result in tenesmus, bleeding. Has a contiguous spread.
    Symptoms: bloody diarrhea, abdominal pain, tenesmus, and, in severe disease, tachycardia, fever, and anemia.
    Ulcerative Colitis
  229. What two extraintestinal manifestations of inflammatory bowel disease have a course that follows the course of the disease?
    • Erythema Nodosum
    • Peripheral Arthritis
  230. What extraintestinal manifestation of inflammatory bowel disease, characterized by bile duct inflammation resulting in fibrosis, is associated with an increased risk of colon cancer and choangiocarcinoma?
    Primary Sclerosing Cholangitis
  231. What are the two goals of treatment for inflammatory bowel disease?
    • Induce Remission
    • Maintain Remission
  232. What is the main non-surgical treatment for Ulcerative Colitis?
    Mesalamine (oral and rectal)
  233. What is the best non-surgical treatment for Crohn's Disease?
  234. What is this characteristic of?

    Perceived disturbance in GI function without structural or biochemical abnormalities by objective testing.
    Sensorineural motor dysfunction
    Low level inflammation without end organ damage
    Functional Bowel Disease
  235. What type of probiotics are used for IBS?
    • Lactobacillus
    • Bifidobacterial
    • E. Coli
    • Saccharomyces Boulardii
  236. What is the most common cause of food poisoning in the US?
    Staphylococcal Aureus
  237. What is the diagnosis:
    Gram-positive coccobacillus
    Typically transmitted through food that requires hand preparation
    Virulence factors are several toxins which are produced by the organism that induce projectile vomiting
    Typically occurs within hours of eating contaminated food
    Diarrhea almost never occurs
    Toxins are heat stable and directly cause release of serotonin in the intestine that results in vomiting
    Staphylococcal Aureus
  238. How can Staph Aureus be differentiated from Norwalk virus?
    Norwalk often causes diarrhea, whereas staph aureus doesn't
  239. What is the diagnosis?:

    Gram positive rod
    Two types of food poisoning
    Type I: often a quick onset (2-3hrs), typically after ingesting starchy food. Causes vomiting through a heat-stable toxin
    Type II: caused by ingestion of contaminated meat or veggies and the organism produces a heat-labile toxin that causes diarrhea in 10-12 hours after ingestion

    Virulence factors are several toxins which are produced by the organism that induce vomiting, often projectile.
    Bacillus Cereus
  240. What is the diagnosis?:

    Gram-positive rod
    Causes abdominal cramping and watery diarrhea within 8-12 hours of ingesting infected food
    Produces heat resistant spores that are not killed by cooking.

    Virulence factors is an enterotoxin
    The diagnosis is usually suspected when a local outbreak of the disease has occurred.
    Clostridium Perfringens
  241. What is the diagnosis?:

    Gram-positive rod
    Mostly found in people that have ingested improperly home-canned veggies or sausage
    Very rare
    Causes death in ~30% of infected individuals

    Virulence factor is a toxin that takes 1-2 days after ingestion for symptoms to occur, because the toxin must spread from the intestine to the nerve synapses
    Only food borne disease that takes more than 12 hours from ingestion to symptom onset
    Symptoms are severe and include blurred vision followed by bilateral descending, flaccid paralysis
    Death is typically caused by respiratory failure
    Clostridium Botulinum
  242. What is the only food borne disease that takes more than 12 hours from ingestion to symptom onset?
    Clostridium Botulinum
  243. Which two forms of Escherichia coli cause "traveler's diarrhea"?
    • ETEC
    • EAEC
  244. Which form of Escherichia coli causes a heat-labile and heat-stable toxin which causes watery diarrhea? Disease lasts ~ 24 hours.
  245. Which form of Escherichia coli causes disease by binding the mucosal cells of the intestine and then killing the cells, which leads to watery diarrhea. Disease does not typically resolve for several days.
  246. Which form of Escherichia coli does not produce a toxin, but rather injects proteins into the mucosal epithelial cells that leads to watery diarrhea. This causes a mild form of the disease and seems to be restricted typically to children 6 months of age or less
  247. What is the diagnosis?:

    Typed using O antigen (139 serogroups): serogroup O1 (classical or El Tor; casuses pandemics); Non-O1 (cause less severe disease); recent Bangledesh outbreak (O139 "Bengal")

    Non-inflammatory, enterotoxic disease
    Causes massive efflux of fluid (up to 20 L/day)
    Symptoms are due to dehydration

    Primary virulence factor: 2-component toxin (AB toxin)

    Incubation time: 7-14 days
    Then, sudden onset of massive diarrhea ("rice water stool"); contains large numbers of organisms. Dehydration and shock can follow. Mucosa remains intact, no invasion.
    Vibrio Cholera
  248. What is the diagnosis?:

    Thin, Gram-negative rod; non-motile
    Serogroups: S. flexneri; S. sonnei

    Symptoms: causes bacillary dysentery, invasive (gets into cells of large intestine), abdominal pain

    Route of transmission: fecal-oral

    Most cases are children < 5 yrs; outbreaks are long lasting

    Virulence factor is Shiga Toxin
  249. What is the diagnosis?:

    Causes self-limiting gastroenteritis
    Dysentery type mechanism
    Symptoms last from 2 days to a week and resolve spontaneously
    Can be transferred to humans by reptiles, such as turtles
    Salmonella Enterica
  250. What bacterial agent is motile by peritrichous flagella?
  251. What is the diagnosis?:

    Prototype Enteric Fever
    Typhoid Fever
    Penetrating Disease--can penetrate through intestinal wall

    Humans are sole carriers
    Route of transmission is by ingestion of contaminated food and water
    Incubation time is about 10-14 days

    Symptoms, Week 1: Lethargy, fever, malaise, general aches and pains, constipation
    Symptoms, Week 2: severely ill, sustained temp of 104, Diarrhea, Rose Spots

    Diagnosis requires isolation from blood, two vaccines are available, and antimicrobial therapy is necessary
    Salmonella typhi
  252. What is the diagnosis?:

    Causes acute enteritis
    Common cause of human bacterial gastroenteritis
    Zoonotic disease: most infections are due to ingestion of contaminated food and water, esp. chicken and turkey

    Affects young children
    Causes illness in all ages

    Incubation time: 3-5 days
    Low infective dose
    Severe abdominal pain with fever, can mimic acute appendicitis, dysentery, usually self-limiting

    Incubates at 42 degrees celcius

    Anti-microbial therapy is used for treatment
    Campylobacter Jejuni
  253. EHEC can cause a severe life-threatening illness that most commonly strikes children under 5 and the elderly. It destroys RBCs, causing acute kidney failure. Treatment is blood transfusion. What is the illness?
    Hemolytic Uremic Syndrome (HUS)
  254. Other than HUS, what other life-threatening illness can be caused by E. coli?
    Disease of the CNS: in adults, seizures and coma; after effects, blood clots in brain, death
  255. What form of E. coli can cause severe life-threatening illnesses, such as HUS and CNS problems, as well as the non life-threatening dysentery. This form is linked to the powerful Shiga toxin, causing severe abdominal cramps, dysentery, vomiting, and nausea. However, there is NO FEVER present. Incubation time is 4-8 days, and duration of illness is 5-10 days.
  256. What is the most common cause of pseudomembranous colitis?
    C. diff
  257. What is the diagnosis?:

    Gram-positive rod
    Can survive at low temps, and often transmitted in soft cheeses, processed meats, even when properly refrigerated

    Symptoms include fever, muscle aches, nausea, and diarrhea

    Organism is an intracellular pathogen and can travel to the nervous system where symptoms include HA, stiff neck, loss of balance, confusion, and convulsions

    The bacteria release toxins and other proteins in the intracellular niche they reside and use these invaded cells to help them traffic to other parts of the body.

    Treatable with antibiotics
    Listeria monocytogenes
  258. Jaundice is not usually seen until bilirubin exceeds ___mg/dL
Card Set
GI&HB Week Three