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GI Midterm > Histology of the Upper GI Tract: Esophagus and Stomach > Flashcards

Histology of the Upper GI Tract: Esophagus and Stomach Flashcards

1
Q

What are the three components (layers) of the mucosa?

A
  1. A lining epithelium with mucosal and submucosal glands and ducts
  2. Lamina propria
  3. Muscularis mucosa
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2
Q

What kind of epithelium is on the oral cavity, oropharynx, esophagus, and anal canal?

A

Stratified squamous.

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3
Q

What kind of epithelium is on the stomach, small and large intestine and the rectum?

A

Simple columnar.

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4
Q

In what specific layer are lymphatic nodules and immune cells located in the GI?

A

Lamina propria.

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5
Q

What is muscularis mucosal layer made up of?

A

Thin double layer of smooth muscle.

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6
Q

What are intestinal villi?

A

finger-like extension of the mucosal layer into the lumen which serves to increase surface area.

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7
Q

What makes up the muscularis externa ?

A

Two layers of smooth muscle.

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8
Q

How does the orientation of the muscularis layer help conduct GI function?

A

The two layers of smooth muscle, one is circular and the other is longitudinal. The Contraction of the circular layer decreases the lumen and thus helps with mixing of content. The contraction of the longitudinal layer shortens the tube and thus helps with paristalsis.

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9
Q

What’s the difference between Adventitia and serosa?

A

They’re both the outermost layer of the GI tube. Adventitia is outside of the peritoneal cavity and thus is found in most of esophagus, and duodenum. Serosa is within the peritoneal cavity and is the outer layer of those organs that are within the peritoneum.

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10
Q

Which of the esophageal sphicter is involuntary?

A

LES

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11
Q

Where is the UES located?

A

near the cricopharyngesu msucle.

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12
Q

What kind of epithelium does the esophagus have?

A

non-keratinized stratified squamous.

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13
Q

What is the muscularis mucosa made up of in the upper esophagus?

A

Thin elastic fibers instead of smooth muscle cells.

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14
Q

How does the muscularis layer change as you go down the esophagus?

A

It goes from skeletal muscle in the upper third for voluntary swallowing to smooth muscle in the lower 2/3s that controls peristalsis.

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15
Q

At the gastroesophageal junction, how does the mucosa change?

A

Mucosa changes from stratified squamous epithelium of the esophagus to simple columnar epithelium and glandular secretory mucosa.

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16
Q

Are there glands in the mucosal and submucosal layers of the esophagus?

A

Yes, they continuously produce a thin layer of mucous to lubricate the epithelial surface.

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17
Q

Where do you start to see cardiac glands?

A

at the esophagus/stomach junction

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18
Q

In GERD, how does the epithelium change, and what are consequences?

A

Changes to columnar (like stomach). Presents with chronic esophagitis/ulceration, dysphagis, fibrosis, esophageal strictures.

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19
Q

What is Barrett’s esophagus?

A

A condition in whcih an abnormal columnar epithelium replaces the stratified squamous epithelium that normally lines the distal esophagus.

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20
Q

Barrett’s esophagus predisposes patients to development of _?

A

adenocarcinomoa of the esophagus.

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21
Q

What causes sliding hiatal hernia?

A

Widening of the muscular hiatal tunnel and circumferential laxity of the phrenoesophagea membrane allowing a portion of the gastric cardia to hernia upward into the posterior mediastium. Associated with GERD.

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22
Q

What causes paraesophageal hiatal hernia?

A

Localized defect in the phrenoesophgeal membrane while the gastroesophgeal junction remains fiexed to th pre aortic fascia and the median arcuate ligament. Part of the fundus herniates up into the thorax. This doesn’t really have a reflux complication but more mechanical complication.

23
Q

In order for you to be able to swallow, what parts of the GI must relax?

A

The orad area and the LES.

24
Q

What are rugae?

A

Longitudinal fold of the gastric mucosa and submucosa that protrudes into the lumen.

25
Q

How are the cardiac glands different in appearance from glands from other parts of the stomach?

A

Cardiac glands have a coiled lower end.

26
Q

What are cell types that can be found in gastric glands?

A
  1. Mucous neck cells
  2. chief cells
  3. Parietal cells
  4. Stem cells
  5. gastroenteroendocrine cells.
27
Q

What part of gastric glands are mucous neck cells found?

A

At the isthmus of gastric gland ( by the narrow neck area near the pit)

28
Q

Where are Chief cells found in the gastric glands?

A

Body of the gland. They predominate at the lower third of the gastric gland.

29
Q

where are parietal cells found in the gastric glands?

A

Lower part of the body of the glands

30
Q

Where are gastroentero-endocrince cells found in the gastric gland?

A

In the lower part of the body.

31
Q

What are types of mucous cells found in the stomach?

A
  1. surface mucous cells lining the pit

2. mucous neck cells located at the opening of the gastric gland into the pit.

32
Q

What are the function of the mucous cells in the stomach?

A

Produce an insoluble gel that attaches to the surface of the gastric mucosa thus forming a thick protective gastric mucosal barrier. This mucus blanket traps bicarbonate ions and neutralies the microenvironment adjacent to the apical region of the surface mucous cells to an alkline pH.

33
Q

What parts of the stomach are chief cells mainly found?

A

Fundus and body.

34
Q

What is the function of chief cells?

A

They release zymogenic pepsinogen and chymosin. Pepsinogen is activated into pepsin after it comes in contact with acid produced by gastric parietal cells. Pepsin act to degrade food proteins into peptides.

35
Q

Where are parietal cells located in the gastric gland?

A

In the neck of the gastric gland of the fundus and body of the stomach.

36
Q

What is the function of parietal cells?

A

Parietal cells are also called oxyntic cells, which secrete HCl and intrinsic factor in humans. The cytoplasm of parietal cells displays numerous tubulovescucles and an intracellular canaliculus continuous with the lumen of the gastric gland.

37
Q

What causes autoimmune gastritis?

A

Autoantibodies to H+,K+ dependent ATPase, a parietal cell antigen, and intrinsic factor. Destruction causes a reduction in HCl and gastric juice and intrinsic factor. Lack of intrinsic factor will cause pernicious anemia.

38
Q

What stimulates parietal cells to release HCl?

A

parasympathetic nt Ach release, and gastrin released by enteroendocrine cells of the pyloric antrum.

39
Q

How does H. Pylori cause ulcer?

A

H. Pylori likes to live in the pylorus of the stomach, they evade the acidic environment by diving deep inside the epithelium and also produces urease to enutralize the acidic evironemnt around it. That part of the stomach now loses the protective enviroment and so now, gastric juice and acids can now touch the epithelium and slowly erode it leading to ulcer and predisposing people to adenocarcinoma.

40
Q

What cell types regulate the function of the alimentary tube?

A

Gastroenteroendocinces and neuroendocrine mediators. Gastroenteroendocine cells produces peptide hormones that regulate GI functions.

41
Q

What are the specific functions of peptide hormoens produced by gastrointestinal endocrine cells?

A
  1. regulation of water, electorlyte metabolism, and enzyme secretion
  2. regulation of gastrointestinal motility and mucosal growth
  3. stimulation of the release of other peptide hormones.
42
Q

What are some examples of peptide hormones produced by the gastroendoteroendocrince cells?

A
  1. secretin
  2. gastrin
  3. CCK
  4. GIP (glucose-dependent insulinotripic peptide)
  5. Motilin
  6. Ghrelin
43
Q

What part of the GI is secretin released from?

A

Released by S cells in the duodenal glands of lieberkuhn when gastric contents enter the duodenum.

44
Q

What function do secretin serve?

A
  1. Stimulate release of bicarb from the pancreatic centroacinar and bile duct.
  2. increase water and bicar secretion from duodenal Brunner’s glands to buffer the incoming protons of acidic chyme.
  3. enhances effect of CCK to induce secretion of digestive enyzymes and bile from pancreas and gallbladder.
  4. counteracts blood glucose by triggering increased insulin release from pancreas.
  5. inhibits gastrin release from normal stomach, and thus reduce acid secretion by pariteal cells of the stomach
  6. stimulates pepsinogen secretion from chief cells which helps break down protein in food.
  7. stimulates glucagon, pancreatic polypeptide and somatostatin.
45
Q

Where are gastrin released from?

A

G cells in the pyloric antrum.

46
Q

What is the main function of gastrin?

A
  1. Stimulate HCl productio by pariteal cells.

2. activate CCK to stimulate gallbladder contraction

47
Q

Where is CCK produced?

A

Duodenum

48
Q

What is the function of CCK

A

stimulates gallbladder contraction and relaxation of the sphincter of Oddi when protein-and fat-rich chyme enters the duodenum.

49
Q

Where is GIP produced?

A

duodenum.

50
Q

What is the function of GIP?

A

Stimulates insulin release (insulinotropic effect) when glucose is detected in the small intestine.

51
Q

What is the function of motilin?

A

Relased cyclically every 90 mins during fasting from the upper smal intestine and stimulates GI motility. A neural control mechanism regulates the release of motilin. This ensures that all of the contents of the stomach is been sqeezed out during fasting.

52
Q

Where is Ghrelin produced?

A

Fundus of the stomach.

53
Q

What is the function of grelin?

A

Binds to its receptor present in gorwht hormone-secreting cells of the anterior pittuitary and stimulates the secretion of growth hormone. Ghrelin plasma levels increase during fasting triggering hunger by acting on hypothalamic feeding centers.

54
Q

What forms the annular pyloric sphicter?

A

The circular muscle layer of the muscularis externa layer.

GI Midterm (11 decks)

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