GI - First Aid Flashcards

1
Q

A new mother gives birth to triplets. One child has a TE fistula. The second has omphalocele. The third has an a ganglionic descending colon. What anatomical sections of the GI tract are affected in each child?

A

TE fistula is in the foregut (pharynx -> duodenum). Omphalocele is in the midgut (duodenum -> transverse colon). Descending colon is n the hindgut (distal transverse colon -> rectum).

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2
Q

A new mother of a Down Syndrome child is very concerned 3 days after birth when the child still has not had a bowel movement. The child also throws up after feeding. What developmental abnormality associated with trisomy 21 may this child have?

A

Duodenal atresia caused by failure to recanalize during development.

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3
Q

A pregnant mother goes to the doctor because she feels like there is a lot more fluid in her belly lately. Ultrasonography reveals bowel that has an “apple peel” spiral appearance. What likely caused this?

A

Occlusion of the SMA during fetal development can cause jejunal, ileal and colonic atresia.

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4
Q

What other birth defect can happen instead of the condition shown below?

A

Failure of the lateral folds to close during development can result in gastroschisis (intestine not covered by peritoneum) or omphalocele (persistent herniation of intestines through umbilical cord covered by peritoneum) as shown in the image.

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5
Q

When during fetal development is your child at risk for developing omphalocele and when does the risk go away?

A

6th week: midgut herniates through umbilical ring. 10th week: midgut returns to abdominal cavity with rotation around SMA.

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6
Q

A mother gives birth to a 7 lb baby girl. During her first feeding, the baby chokes and vomits the breast milk. Chest x-ray reveals air in the child’s stomach. The next day the child becomes cyanotic. What are the different causes of this baby’s condition?

A

This child has esophageal atresia with distal tracheoesophageal fistula, the most common form. Kids can also present with pure esophageal atresia and H-type pure TEF.

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7
Q

A first-time mother brings in her 2 week old boy complaining of vomiting right after feeding. She says the vomit is the same color as the breast milk. Physical exam reveals a palpable olive mass in the epigastric region. What is causing this child’s condition and how do you fix him?

A

Pyloric stenosis from hypertrophy of the pylorus. This is treated by surgical myotomy.

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8
Q

What embryological origin do pancreatic carcinomas in the head of the pancreas have?

A

The ventral pancreatic bud contributes to the main pancreatic head and duct. It also forms the entire uncinate process. The dorsal pancreatic bud becomes everything else.

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9
Q

A pregnant woman presents with excess amniotic fluid in her final weeks. The child is born and has bilious vomiting immediately after feeding. How could the child’s pancreas be causing this?

A

Annular pancreas. The head of the pancreas wraps around the duodenum, causing fetal polyhydramnios and bilious vomiting in the newborn.

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10
Q

A 15 year old girl presents with periumbilical boaring abdominal pain, nausea and vomiting. This happens to her multiple times each year. What congenital abnormality could be causing her condition?

A

Pancreas divisum. This is due to failure of the ventral and dorsal pancreatic buds to fuse at 8 weeks, resulting in absence of the main pancreatic duct. Pancreatic enzymes are secretes through the minor duct, get backed up and cause chronic pancreatitis.

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11
Q

Does the pancreas arise from the foregut, midgut or hindgut?

A

Foregut

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12
Q

What organ arises from mesoderm but is supplied by the foregut artery?

A

The spleen. It rises from the mesentery and is supplied by there celiac artery.

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13
Q

What are the retroperitoneal structures?

A

“SAD PUCKER”: Suprarenal gland, Aorta/IVC, Duodenum (2 & 3), Pancreas (not tail), Ureters, Colon (descending & ascending), Kidneys, Esophagus, Rectum

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14
Q

What is the neonatal and postnatal function of the ligamentum teres hepatis?

A

Neonatal: fetal umbilical vein. Adult: falciform ligament connects liver to abdominal wall

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15
Q

After a car accident the driver has internal bleeding from the liver. He is rushed to the hospital and opened up. What abdominal ligament can you compress to control bleeding?

A

Hepatoduodenal. This contains the portal triad. Placing your fingers in the omental foramen to compress it is called the Pringle maneuver.

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16
Q

What arteries are likely to be ligated when a surgeon needs to access the lesser sac on the right side?

A

Gastric arteries. These are contained in the gastrohepatic ligament and separates the greater from the lesser sac on the right.

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17
Q

What ligament contains the gastroepiploic arteries?

A

Gastrocolic ligament. It connects the greater curvature and the transverse colon.

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18
Q

What arteries may be ligated when a surgeon needs to access the lesser sac on the left side?

A

Short gastrics and left gastroepiploic vessels. These are contained in the gastrosplenic ligament, which connects the greater curvature of the stomach to the spleen.

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19
Q

What ligament contains the splenic artery, vein and tail of the pancreas?

A

Splenorenal ligament.

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20
Q

What is the difference between a GI ulcer and erosion?

A

Erosions are only in the mucosa. Ulcers can go all the way through to the outer muscular layer

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21
Q

When does the GI tract have serosa vs. adventitia?

A

Serosa = intraperitoneal. Adventitia = retroperitoneal.

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22
Q

Which layer of the GI tract is responsible for mucosal motility?

A

Muscularis mucosa

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23
Q

Which layer of the GI tract is responsible for control of secretory activity?

A

Submucosal plexus

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24
Q

Which layer of the GI tract is responsible for control of GI muscle contraction?

A

Myenteric plexus

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25
Q

What region of the GI tract has the fastest basal electrical rhythm (slow waves)?

A

Duodenum: 12 waves/min. Ileum: 8 waves/min. Stomach: 3 waves/min.

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26
Q

What region of the GI tract is this section from?

A

Esophagus. Note the nonkeratinized stratified squamous epithelium.

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27
Q

What region of the GI tract is this section from?

A

Stomach. Note the gastric glands and pits.

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28
Q

What region of the GI tract is this section from?

A

Gastroduodenal junction. Note the gastric glands and pits on the right indicating stomach. Note the villi, submucosal Brunner’s glands and crypts of Lieberkuhn, indicating duodenum.

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29
Q

What region of the GI tract is this section from?

A

Jejunum. Note the plicae circulares and crypts of Lieberkuhn and absence of Brunner’s glands and Peyer’s patches.

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30
Q

What region of the GI tract is this section from?

A

Ileum. Note the Peyer’s patches in the lamina propria and submucosa, plicae circulares, crypts of Lieberkuhn, and largest amount of goblet cells in the small intestine.

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31
Q

What region of the GI tract was this section from?

A

Colon. Note that there are crypts w/o villi and numerous goblet cells.

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32
Q

What is the blood supply and innervation from the stomach to proximal duodenum, to include the liver, gallbladder, spleen and pancreas?

A

The foregut is supplied by the celiac artery and vagus nerve.

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33
Q

What is the blood supply and innervation from the distal duodenum to the proximal 2/3 of the transverse colon?

A

The midgut is supplied by the SMA and the vagus nerve.

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34
Q

What is the blood supply and innervation from the distal 1/3 of the transverse colon to the upper portion of the rectum?

A

The hindgut is supplied by the IMA and pelvic splanchnic nerves.

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35
Q

What is the watershed region of the gut?

A

Splenic flexure, this is where SMA supply transfers to IMA supply.

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36
Q

What are the branches that come off of the celiac trunk?

A

Left: splenic artery and left gastric artery. Right: common hepatic (which gives off the right gastric, gastroduodenal and hepatic proper arteries)

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37
Q

A 60 year old man with a history of hepatitis C presents with liver cirrhosis. What veins would you expect to be dilated in this patient as his liver gets more and more cirrhotic?

A

Varices of the gut, butt and caput are seen with portal hypertension. This is because blood flowing from the left gastric vein backs up in the liver and anastomosis w/systemic esophageal veins = esophageal varices. Blood flowing from the paraumbilical vein backs up and anastomosis w/systemic epigastric veins = Caput Medusa. Blood flowing from the superior rectal vein backs up in the liver and anastomosis w/systemic middle & inferior rectal veins = Hemorrhoids.

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38
Q

A 60 year old man with a history of hepatitis C presents with liver cirrhosis. Physical exam reveals Caput Medusa, esophageal varices and hemorrhoids. What can you do to treat these symptoms of portal hypertension?

A

TIPS (transjugular intrahepatic portosystemic shunt) links the portal vein with the hepatic vein to shunt extra blood to the systemic circulation.

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39
Q

What type of hemorrhoids present with painless bleeding? Where does the blood come from?

A

Those above the pectinate line. This area is derived from the endoderm, receives blood supply from the IMA superior rectal branch and drains blood to the portal system via the superior rectal vein.

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40
Q

What type of hemorrhoids present with painful bleeding? Where does the blood come from?

A

Those below the pectinate line. This are is derived from the ectoderm, receives blood supply from the pudendal artery via the inferior rectal artery and drains blood to the IVC via the rectal vein.

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41
Q

Rectal cancer with painless bleeding

A

Adenocarcinoma typically occurs above the pectinate line

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42
Q

Rectal cancer with painful bleeding

A

Squamous cell carcinoma typically occurs below the pectinate line.

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43
Q

Where does lymphatic drainage flow in the liver?

A

Space of Disse. This is the space between the hepatocyte and the sinusoids.

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44
Q

What is the function of the cell indicated below?

A

Kupffer cells are the macrophages in the liver, located in the sinusoids.

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45
Q

What region is the apical part of the hepatocyte?

A

Apical surface faces the bile canaliculi. The basolateral surface faces the sinusoids.

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46
Q

What region of the liver is affected 1st by viral hepatitis?

A

Zone I: periportal zone

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47
Q

What region of the liver is affected 1st by ischemia and toxic injury (to include alcoholic hepatitis)?

A

Zone III: pericentral vein zone. This zone is furthest away from fresh blood and nutrients and gets injured 1st.

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48
Q

What region of the liver contains the P-450 system?

A

Zone III: pericentral vein zone

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49
Q

A patient presents with a boaring periumbilical pain radiating through to the back. What are the two most common causes of this pain?

A

Pancreatitis is most commonly caused by gallstones blocking the ampulla of Vater and alcohol causing contraction of the sphincter of Oddi around the ampulla of Vater.

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50
Q

What is a hernia?

A

Typically it is a protrusion of peritoneum through a site of weakness

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51
Q

What type of hernia is seen in newborns and causes pulmonary hypoplasia?

A

Diaphragmatic hernia. Failure of the pleuroperitoneal membrane to develop allow bowel to go into the thorax.

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52
Q

What is the most common type of hernia?

A

Sliding hiatal hernia, note the hourglass stomach.

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53
Q

Hernia characterize by protrusion of the fundus into the thorax

A

Paraesophageal hernia

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54
Q

What type of hernia follows the path of the descent of the testes in infants?

A

Indirect inguinal hernia. This follows the path of the testes through the deep inguinal ring, lateral to the inferior epigastric artery, through the external inguinal ring and into the scrotum. Note that it will be covered by all 3 layers of spermatic fascia.

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55
Q

What type of hernia usually happens in older men?

A

Direct inguinal hernia. This bulges through the inguinal triangle medial to the inferior epigastric artery and goes through the external inguinal ring only. Note that this will only be covered by external spermatic fascia.

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56
Q

What type of hernia is more common in women and is the leading cause of bowel incarceration?

A

Femoral hernia

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57
Q

A 30 year old woman presents with recurrent peptic ulcers in her duodenum. Endoscopy reveals rugal thickening of the stomach and a mass in the duodenum. What is causing her recurrent ulcers?

A

She has Zollinger-Ellison syndrome, ulcers from a gastrin-secreting tumor in the duodenum. Upregulation of gastrin secretion by G-cells also happens with chronic PPI use.

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58
Q

What is the effect of gastrin secreted by the G-cells in the antrum of the stomach?

A

Increased H+ secretion, increased growth of gastric mucosa and increased gastric motility.

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59
Q

How are G-cells regulated?

A

Increased activity: distention, alkalization, AAs (especially Phe & Trp), vagal stimulation. Decreased activity: stomach pH < 1.5

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60
Q

What is the effect of cholecystokinin secreted by the I-cells in the duodenum and jejunum?

A

Gallbladder contraction, decreased gastric emptying, relaxation of sphincter of Oddi and activation of muscarinic-mediated pancreatic enzyme secretion.

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61
Q

How are I-cells regulated?

A

Secretion of CCK is increased by fatty acids and amino acids

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62
Q

What is the effect of secretin secreted by the S-cells in the duodenum?

A

HCO3 secretion to neutralize gastric acid in duodenum & activate pancreatic enzymes, increase bile secretion and decrease gastric acid secretion.

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63
Q

How are S-cells regulated?

A

Secretion of secretin is increased by acid and fatty acids in the lumen of the duodenum.

64
Q

What is the effect of somatostatin secreted by D-cells in the pancreatic islets and GI mucosa?

A

Decrease secretion of gastric acid, pepsinogen, pancreatic fluid, small intestine fluid, decreased gallbladder contraction and decreased glucagon/insulin release. Basically it is an antigrowth and inhibitory hormone, stopping digestion and absorption of nutrients.

65
Q

How are D-cells regulated?

A

Vagal stimulation decreases secretion of somatostatin and acid increases somatostatin secretion.

66
Q

What is the effect of glucose-dependent insulinotropic peptide (gastric inhibitory peptide, i.e. GIP) secreted by K-cells in the duodenum and jejunum?

A

Decreased gastric H+ secretion and increased insulin release.

67
Q

How are K-cells regulated?

A

GIP secretion by K-cells is increased as fatty acids, amino acids and oral glucose levels increase.

68
Q

What is the effect of vasoactive intestinal polypeptide (VIP) secreted by parasympathetic ganglia in sphincters, the gallbladder and the small intestine?

A

Increase in secretion of water and electrolytes from intestinal mucosa and relaxation of intestinal smooth muscle and sphincters.

69
Q

How is VIP secretion regulated?

A

Secretion is increased by distention and vagal stimulation. It is decreased by adrenergic input.

70
Q

A patient presents with copious amounts of water diarrhea, hypokalemia and achlorhydria. What tumor could be causing the patient’s condition?

A

A VIPoma is a non-alpha/beta pancreatic islet cell tumor that secretes VIP. This results in chronic release of fluid and electrolytes from the intestine into the lumen and causes the symptoms seen in this patient.

71
Q

A patient presents with halitosis and non-bilious vomiting. Upper GI series reveals a bird beak stopping at the LES. Decreased secretion of what compound could be causing these symptoms?

A

Achalasia is caused by decreased secretion of NO, resulting in increased LES tone and loss of esophageal relaxation.

72
Q

What GI hormone causes those massive rumbling sounds in your gut while you are fasting?

A

Motilin. It produces the migrating motor complexes (MMCs).

73
Q

What stomach pathology results in chronic gastritis and pernicious anemia?

A

Autoimmune destruction of parietal cells in the body of the stomach. These cells secrete intrinsic factor that binds B12 in the terminal ileum.

74
Q

A 40 year old man presents with chronic epigastric pain. Endoscopy reveals a tumor in the stomach and stomach analysis reveals a very low pH. What things could you give the patient to antagonize the effects of this tumor? What would you not want to give?

A

The patient has a gastrinoma. Gastrin promotes secretion of gastric acid by parietal cells directly and by stimulating ECL secretion of histamine which also stimulates secretion of gastric acid by parietal cells. You could give somatostatin, GIP, prostaglandin or secretin to reduce gastric acid secreted by parietal cells and counter the effects of the gastrinoma. Also note that ACh increases gastric acid secretion by parietal cells and would be something you don’t want to give the patient.

75
Q

What cells in the stomach are key in initiation of protein digestion?

A

Chief cells. Vagal stimulation and local acid stimulates release of pepsinogen. Local H+ converts it to pepsin which chops up the protein into oligopeptides.

76
Q

What cells are H. pylori’s best friend in the stomach, duodenum, pancreas and salivary glands?

A

Mucosal cells (stomach, duodenum, pancreas, salivary glands) and Brunner’s gland (duodenum). These cells release HCO3- into the mucus that govern the gastric and intestinal epithelium, neutralizing acid and making the area more habitable for H. pylori.

77
Q

What increases secretion of HCO3- by mucosal cells and Brunner’s glands?

A

When fatty acids and acid enters the lumen of the duodenum, S-cells secrete secretin. Secretin turns on these cells.

78
Q

What happens to the composition of saliva and you approach that piece of pizza?

A

Normally saliva is hypotonic because of absorption of water. When saliva flow rates increase, there is less time for reabsorption of water and it becomes more isotonic.

79
Q

Name 5 receptors present on the gastric parietal cell that allow for modulation of gastric acid secretion.

A

1) ACh -> M3 receptor -> Gq -> IP3/Ca2+ -> + H/K ATPase. 2) Gastrin -> CCK receptor -> Gq -> IP3/Ca2+ -> + H/K ATPase 3) Histamine -> H2 receptor -> increase cAMP -> + H/K ATPase 4) Prostaglandins/Misoprostol -> receptor -> Gi -> decreases cAMP -> - H/K ATPase 5) Somatostatin -> receptor -> Gi -> decreases cAMP -> - H/K ATPase

80
Q

Why do we experience a metabolic alkalosis for 2 hours after eating a meal?

A

The parietal cell needs to secrete gastric acid (HCl). It gets H+ by carbonic anhydrase conversion of CO2 + H2O to HCO3- and H+. It gets Cl- by pumping HCO3- out the basolateral aspect into the blood and taking Cl- into the cell and pumping it into the lumen of the stomach.

81
Q

A 35 year old male presents with recurrent epigastric pain. Tums seemed to work for a few years, but not anymore. Labs reveal a positive stool antigen for H. pylori. What would you expect to see on histological analysis of this patient’s duodenal submucosa?

A

Hypertrophied Brunner’s glands. These secrete alkaline mucus to try to protect the stomach from peptic ulcer disease.

82
Q

How does the composition of pancreatic fluid change from low flow to high flow?

A

During high flow, the CFTR is exchanging Cl- for HCO3- and fluid becomes more heavy in HCO3-. In low flow states, Cl- is in higher concentration.

83
Q

When does the workday start for the pancreatic enzymes? When does it end?

A

As fatty acids and amino acids enter the duodenum, I-cells release CCK, triggering release of enzymes from the pancreas, and S-cells secrete secretin, increasing pancreatic HCO3- secretion. 1st, enteropeptidase converts trypsinogen to trypsin. Trypsin then activates the other proenzymes (chymotrypsinogen, proelastase and procarboxypeptidase) and cleaves more trypsinogen to trypsin. The lipases (collapse, lipase and phospholipase A) and alpha-amylases are active upon secretion. Pancreatic secretions stop when somatostatin is release by D-cells in response to decreased vagal stimulation and increased acid.

84
Q

What enzymes are key in breaking down carbohydrates to disaccharides?

A

Salivary amylase (hydrolyzes alpha-1,4 linkages to yield maltos and alpha-dextrins) and pancreatic amylase

85
Q

What enzyme is the rate limiting stamp in carbohydrate digestion?

A

Oligosaccharide hydrolases. They sit at the intestinal brush border and produce monosaccharides from oligo and disaccharides

86
Q

How are carbohydrates taken up by the enterocytes?

A

It can only take up monosaccharides. Glucose and galactose are taken up by SGLT1 (Co-transport w/Na+) and fructose is taken by by facilitated diffusion by GLUT-5. All carbohydrates are transported to the blood via GLUT-2 transporters.

87
Q

A patient with IBD presents with Fe deficiency anemia. What location of the GI tract is likely affected?

A

Duodenum

88
Q

A patient with IBD presents with folate deficiency. What location of the GI tract is likely affected?

A

Jejunum

89
Q

A patient with IBD presents with B12 deficiency. What location of the GI traction is likely affected?

A

Terminal ileum. Intrinsic factor is required for reabsorption, note that bile acids are also taken up here.

90
Q

Where does antibody used to defend pathogens in the lumen of the gut come from?

A

Unencapsulated lymphoid tissue in the lamina propria and submucosa of the ileum (Peyer’s patches). Antigen are caught by M cells in these patches. M cells present the antigen to B cells in the germinal centers of the Peyer’s patch. The B cells differentiate into plasma cells and migrate to the lamina propria where they secrete IgA across the enterocytes into the lumen.

91
Q

What final step in bile salt production makes them water soluble?

A

Conjugation with glycine or taurine.

92
Q

What makes up bile?

A

Bile salts, phospholipids, cholesterol, bilirubin, water and ions.

93
Q

What enzyme catalyzes the rate limiting step in production of bile?

A

Cholesterol 7alpha-hydroxylase

94
Q

How does urine become yellow and stool become brown?

A

Macrophages breakdown old RBCs to heme and then to unconjugated bilirubin. The unconjugated bilirubin binds albumin and heads to the liver. In the liver unconjugated bilirubin is conjugated with glucuronate by the enzyme UDP-glucuronosyl transferase. Conjugated bilirubin is secreted as bile into the gut where it meets gut bacteria. Gut bacteria convert the conjugated bilirubin to urobilinogen. 80% is secreted in the feces as stercobilin, giving stool a brown color; 10% is secreted as urobilin in urine, giving it a yellow color and the last 10% goes back to the liver via enterohepatic circulation.

95
Q

Why do liver problems cause jaundice?

A

Inability to conjugate bilirubin = insoluble bilirubin = not excreted and causes jaundice.

96
Q

What part of the body is this slice taken from?

A

Note the light-staining mucus-secreting cells and the dark-staining serous-secreting cells. This is the submandibular salivary gland.

97
Q

What kind of exocrine glands do you find in the pancreas?

A

Almost all serous-secreting cells.

98
Q

How does the ductwork proceed from the acini in salivary glands?

A

Acini -> Intercalated ducts -> Striated ducts (mitochondrial striations at base of ductal cells)

99
Q

Why are there so many mitochondria in the striated ducts of the salivary glands?

A

In order to move fluid you need to pump ions which requires energy

100
Q

What areas of the brain coordinate the swallowing reflex?

A

Nucleus ambiguus and DMX in the medulla

101
Q

What is there response of the esophagus to a bolus of food entering after a swallow?

A

Initial voluntary swallow -> Tongue forces food bolus down into esophagus -> relaxation of UES -> peristalsis -> relaxation of LES

102
Q

What does the esophagus do if you get a chicken bone stuck in the esophagus?

A

Secondary peristalsis

103
Q

What foods decrease LES pressure?

A

Fats, alcohol, chocolate, protein and coffee. This is why these are high risk foods for GERD.

104
Q

What hormone and NT are released in response to gastric distention?

A

Gastrin & ACh. Gastrin stimulates parietal cells to secrete HCl directly and indirectly by stimulating ECL secretion of histamine. Histamine then stimulates HCl secretion by parietal cells.

105
Q

What do parietal cells secrete at the basal rate?

A

Na and Cl

106
Q

What happens in the upper stomach when food enters?

A

Receptive relaxation causes an increase in stomach volume without increasing pressure.

107
Q

What substance is secreted by parietal cells in addition to protons?

A

Intrinsic factor, helps for absorption of cobalamin (B12).

108
Q

What factors increase gastric emptying into the duodenum?

A

Increased food volume and gastrin.

109
Q

What area of the GI tract absorbs the greatest amount of water?

A

Duodenum and jejunum. Most water has been absorbed by the time you get to the ileum and colon.

110
Q

How much liter is secreted by the GI tract in a day?

A

8-9L. You also absorb about this much.

111
Q

What type of food causes the greatest delay in gastric emptying?

A

Fat, digestion does not start until the small bowel bile solubilizes it. Amino acids stimulate G-cell secretion of gastrin, which causes relaxation of the pyloric sphincter, encouraging speeding up of digestion process.

112
Q

What nutrient undergoes extensive post-absorption processing by intracellular enzymes in the enterocyte?

A

Lipid. Triglycerides emulsified into micelles by bile -> fatty acids are taken up by enterocyte -> re-esterified as TAGs w/apolipoprotein -> sent into lymph as chylomicrons -> systemic circulation

113
Q

What are 2 major routes of sodium absorption following a meal?

A

Passive absorption secondary to H2O transport and active co-transport

114
Q

3 factors that control the net direction of water movement in the gut

A

Location in bowel (more water moved in proximal small bowel), luminal osmolality (milk of magnesia) and rate of active solute transport

115
Q

When does the osmolality of a meal become isotonic?

A

Duodenum, this is largely due to H2O secretion

116
Q

What percentage of Na entering the small bowel is absorbed by the small bowel?

A

85-95%

117
Q

What product is made by bacterial metabolism of some carbs in the colon and is reabsorbed and used as a fuel by the colonocytes?

A

Short chain fatty acids are a bacterial byproduct.

118
Q

What is the response to cholera toxin and mediated by an increase in cAMP?

A

Increased pumping of Cl- into the lumen increases H2O leaving into the lumen.

119
Q

Why would you rehydrate with Gatorade?

A

Addition of Na and Gluc to water enhances H2O co-transport into the enterocytes and on into the circulation.

120
Q

What marks the intestinal phase of pancreatic secretion?

A

Entrance of chyme into the duodenum

121
Q

What agent stimulates pancreatic enzyme secretion from the acinar cells in the intestinal phase?

A

CCK. Secretin stimulates HCO3- release from ductal cells during the intestinal phase.

122
Q

What agent stimulates pancreatic bicarbonate secretion in the cephalic phase?

A

VIP stimulates early on

123
Q

What are the primary bile acids converted to by bacteria in the distal ileum, cecum and colon?

A

Primary bile acids go to secondary bile acids (Cholic acids -> deoxycholic acid)

124
Q

What part of the body was this section taken from?

A

Pancreas. Note the serous-secreting acini w/centroacinar cells. Pancreatic serous cell is shown below.

125
Q

What cell of the pancreas is indicated below?

A

Centroacinar cell.

126
Q

How would cutting the vagus affect digestion in the stomach?

A

Inhibits receptive relaxation. This is why diabetics can feel full too soon, neuropathy of the vagus.

127
Q

What controls ileocecal sphincter tone?

A

Sympathetics and hormones

128
Q

The colon lacks what motor pattern?

A

Phase III, migrating motility complex (MMC). It has phase I, basal phase and phase II, peristaltic phase.

129
Q

Following a meal, what causes movement of feces into the rectum?

A

Mass movement.

130
Q

What reflex increases the motility of the colon and increases the frequency of mass movement in response to the presence of food in the stomach?

A

Gastrocolic reflex

131
Q

An increase in the concentration of what ion in the stomach inhibits gastrin release and stimulates the secretion of somatostatin?

A

H+

132
Q

What portion of the stomach has no BER and acts as a reservoir?

A

Fundus

133
Q

Where is the most effective place to inhibit acid secretion in the stomach?

A

H/K ATPase. Blocking H2 receptors was originally the most effective way.

134
Q

Elevated plasma levels of what agent are associated with phase III contractions of the MMC?

A

Motilin

135
Q

What organ is this slice from?

A

Liver, this is the portal tract (note you will find lymphatics and nerves in addition to the bile duct and blood vessels)

136
Q

What is the major reason for de novo synthesis of bile acids by the hepatocyte?

A

Make up for the 5% lost in the stool

137
Q

What agents increase the flow of bile?

A

Choleretic. There are bile-dependent and bile-independent bile secretions. Chleretics increase bile-dependent secretions

138
Q

What part of bile is poorly recovered?

A

Bilirubin (bile pigment)

139
Q

Most common GI diagnosis?

A

IBS

140
Q

Gastroenteritis from preformed toxin

A

S. aureus, b. cereus, botulism, c. perfringens

141
Q

Gastroenteritis from tissue invasion

A

Shigella, salmonella, EIEC, Yersinia, Campylobacter

142
Q

Gastroenteritis from intoxication in gut

A

Cholera, ETEC, STEC/ECHEC, infant botulism

143
Q

Presence of lactoferrin in fecal sample

A

Inflammatory diarrhea: Shigella, salmonella, campylobacter, yersinia

144
Q

No WBCs or blood in fecal sample

A

Secretory diarrhea: ETEC, Cholera, staph and viral

145
Q

Heat labile toxin

A

ETEC (also makes ST) and cholera

146
Q

Grown at special temp and causes Guillain-Barre

A

Campylobacter

147
Q

Bacteria that mimics appendicitis

A

Yersinia

148
Q

Identical to shigella but does not produce shiga toxin

A

EIEC

149
Q

E. Coli w/shiga toxin

A

EHEC

150
Q

Human specific bacterial gastroenteritis

A

Salmonella typhi and shigella

151
Q

Old lady dies from food poisoning sepsis

A

Salmonella enterica

152
Q

Where should you culture if you suspect typhoid fever?

A

Blood 1st, stool 2nd

153
Q

Gastroenteritis with low infectious dose

A

EHEC, shigella, norovirus, rotavirus

154
Q

Gastroenteritis with high infectious dose

A

Salmonella, campylobacter

155
Q

How enteroviruses get to their target tissue

A

Viremia

156
Q

Entamoeba path to infection

A

Cecum -> breaks through GI wall -> cyst in liver

157
Q

Ancylostoma and Necator

A

Hookworm