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Pathophysiology > Gastrointestinal Disorders > Flashcards

Gastrointestinal Disorders Flashcards

1
Q

What is the esophageal hiatus?

A

Hole in diaphragm where esophagus passes through thoracic cavity into the abdominal cavity

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2
Q

Where does majority of digestion occur?

A

In small intestine

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3
Q

What are the three components of the small intestine?

A

Duodenum, jejunum, ileum

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4
Q

What is the main job of the large intestine?

A

Absorption of water and electrolytes, forms a denser package to prepare to expel

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5
Q

What is the innermost region of the GI wall?

A

The mucosa, lined with epithelial cells

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6
Q

What lies beneath mucosa?

A

Sub-mucosa= home to vessels, immune cells, some glands

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7
Q

What is the outermost region of the GI wall?

A

Serosa/ adventitia= layer of connective tissue, supports and attaches to the mesentary (attaches to abdominal wall)

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8
Q

What is the enteric nervous system?

A

Located solely in the GI tract, controlled by local and autonomic nervous system stimuli–neurons regulate motility reflexes, blood flow, absorption, secretions, immune response

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9
Q

What is the role of IgA antibodies?

A

B cells–> plasma cells–> produce IgA antibodies that are secreted into lumen and keep the commensal bacteria in check

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10
Q

What are some key immune cells involved in the GI tract?

A

Dendritic cells extend into the lumen, take up molecules and present them to T cells (regulatory T cells)

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11
Q

What are some of the important roles of the liver?

A

Detoxification, storage of nutrients, production of bile salts, and production of plasma proteins

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12
Q

What is the main role of the gallbladder?

A

Stores bile salts, secretes them into the duodenum

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13
Q

What is the role of bile salts?

A

Emulsify fats–able to get between fat molecules, take them from globs to smaller molecules through emulsification

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14
Q

What is the role of acinar cells?

A

Produce enzymes

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15
Q

What is the role of duct cells?

A

Secrete bicarb, neutralize stomach acid, protect small intestine

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16
Q

How do exocrine secretions enter duodenum?

A

Via ampulla, shared region between gallbladder and pancreas

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17
Q

How are digestive enzymes synthesized?

A

Inactive form, have to be activated by enteropeptidase

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18
Q

What is the role of trypsin?

A

Enzyme that aids in digestion of proteins, serves to activate other proenzymes from pancreas

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19
Q

What are some risk factors for GERD?

A

Sliding hiatal hernia, obesity, smoking, alcohol, certain foods and conditions/activities that increase abdominal pressure

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20
Q

What is the key issue in GERD?

A

Lower esophageal sphincter becomes more relaxed, reduced resting pressure

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21
Q

Where does the LES sit in relation to the esophagus hiatus?

A

Just above!

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22
Q

What is Barrett’s esophagus?

A

Some individuals with GERD experience abnormal repair processes following exposure to acidic chyme, epithelium changes and squamous epithelium is replaced by metaplastic columnar epithelium and goblet cells *increases risk for esophageal adenocarcinoma

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23
Q

Who is chronic gastritis more likely to occur in?

A

Those with H.Pylori infections, autoimmune reactions, chronic use of alcohol/tobacco/NSAIDs

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24
Q

What is autoimmune metaplastic atrophic gastritis?

A

Autoimmune reaction against gastric parietal cells, autoantibodies target intrinsic factor and proton pumps (facilitate the production of HCl)

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25
Q

What is the role of parietal cells?

A

Produce hydrochloric acid and intrinsic factor

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26
Q

What is the role of intrinsic factor?

A

Protein that binds to Vit B12, helps it be absorbed within the ileum

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27
Q

What can autoimmune metaplastic atrophic gastritis result in?

A

Destruction of parietal cells= less intrinsic factor= less HCl= Vit B12 deficiency= pernicious anemia

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28
Q

What is pernicious anemia?

A

Deficiency of Vit B12–RBC’s need Vit B12 to synthesize their DNA

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29
Q

What is peptic ulcer disease?

A

Ulceration of the esophagus, stomach, or duodenum, can be acute or chronic

30
Q

What are the risk factors for peptic ulcer disease?

A

NSAIDs, H. Pylori (most common)

31
Q

What is the mechanism of action of NSAIDs?

A

Inhibit cyclo-oxygenase enzymes which synthesize prostaglandins from arachidonic acid

32
Q

What is the role of prostaglandins?

A

Signaling molecules, can be produced by immune cells or epithelial cells–production of them stimulate inflammation, cause pain. Also produced and present in the stomach and have HELPFUL roles (produce bicarb and mucin, protective against HCl in stomach, inhibit HCl secretion, facilitate platelet aggregation)

33
Q

What is H.Pylori?

A

Gram negative helical/spiral bacteria with flagella, infects approx 50% of the world’s population, only bacteria that can survive harsh conditions of the stomach

34
Q

How does H.Pylori survive the harsh environment of the stomach?

A

Neutralizes stomach acid, secretes mucinase which breaks down the mucus lining the stomach so it can burrow within and adhere to the epithelium

35
Q

What harm does H.Pylori do?

A

Can damage the mucosa epithelial cells, attaches to them and produces toxins (ex: VacA= toxin that makes epithelial cell membrane permeable to ions, promotes apoptosis) and mucinase (can get rid of mucus in other areas, allows HCl to damage), initiates inflammation and ROS production

36
Q

What is the most common place for peptic ulcer to occur?

A

The duodenum

37
Q

What are some of the symptoms of duodenal ulcers?

A

Some asymptomatic, most common symptom is chronic, intermittent pain in epigastric area often happening 2-3 hours after eating (time when food starting to be released into duodenum), pain can be relived with eating (sphincters tightening) and antacids

38
Q

What are some causes of gastric ulcers?

A

NSAIDs, H.Pylori, duodenal reflux of bile salts (can be damaging to epithelial cells, not normally in stomach)

39
Q

What are some symptoms of gastric ulcers?

A

Similar to duodenal ulcers, but nature of pain is different and eating does not relieve it/onset of pain is much more rapid

40
Q

What are the two subtypes of IBD?

A

Crohn’s and ulcerative colitis

41
Q

What is Crohn’s disease?

A

Inflammation that can affect any portion of the GI tract (typically in the terminal ileum and proximal colon), discontinuous inflammation with skip lesions, affects ENTIRE thickness of the GI wall (resulting in ulceration, severe inflammation, can cause perforations and holes)

42
Q

What occurs as response to the severe inflammation in Crohn’s?

A

Fibrous scar tissue develops, narrows the lumen and can cause strictures, increases risk of developing colon cancer

43
Q

What are some of the symptoms of Crohn’s?

A

Abdo pain, diarrhea with blood and mucus, pernicious anemia, weight loss, anal fissures, intestinal obstruction

44
Q

What areas does ulcerative colitis affect?

A

Begins in the rectum, extends more proximally through portion of large intestine

45
Q

What is the pattern of inflammation in ulcerative colitis?

A

Continuous, no skip lesions and not as deep or penetrating (limited to the mucosal cells)

46
Q

What occurs as result of ulcerative colitis?

A

Inflammation, distortion of the mucosa, loss of goblet cells, edema/redness, can cause polyps in the colon and increase risk for colon cancer

47
Q

What are the symptoms of Crohn’s?

A

Frequent diarrhea (blood/mucus), cramping, urge to defecate, bowel obstructions, if severe can have fever/tachycardia

48
Q

What causes the increased exposure of immune cells to intestinal contents?

A

Occurs b/c mucus barrier along the wall is thinner in those with IBD and epithelial cells are more permeable and leaky

49
Q

What other immune changes occur in IBD?

A

Reduction of regulatory T cells, increased IL-17, impaired T cell apoptosis

50
Q

What immune arm characterizes Crohns?

A

Th1, T cell

51
Q

What immune arm characterizes UC?

A

TH2, B cells, plasma cells, etc.

52
Q

What are the most common forms of hepatitis?

A

Hep A, B, and C

53
Q

What is the transmission method of Hep A?

A

Fecal-oral route, usually contamination of water

54
Q

How does hepatitis affect the liver?

A

Nutrients from GI tract enter liver through portal vein, hepatocytes become infected, virus replicates in hepatocytes and gets shed into bile, virally infected hepatocytes attacked by immune system

55
Q

What is the severity of Hep A?

A

Usually self-limiting, individuals develop immunity. If severe, can cause liver failure (usually less severe than Hep B or C)

56
Q

How is Hep B transmitted?

A

Through infected blood, contaminated needles, bodily fluid/sexual contact, from mom to babe in 3rd trimester

57
Q

What can be the result of Hep B?

A

In 70%, self-limiting, can progress to chronic inflammation and scarring/cirrhosis and liver failure

58
Q

What is typical of Hep C?

A

Acute inflammatory response often unable to clear virus, often results in chronic inflammation/hepatitis and liver failure

59
Q

What is cholelithiasis?

A

Development of gall stones in the gall bladder that can result in obstruction of bile, supersaturation of cholesterol

60
Q

What are some potential causes of cholethiasis?

A

Genetic predisposition, decreased secretion of bile salts (results in bile stasis), decreased reabsorption of bile salts from ileum, enzyme defects that increase cholesterol synthesis

61
Q

What causes jaundice?

A

Build up of bile salts

62
Q

What is cholecytitis?

A

Inflammation of the gall bladder, commonly occurs by obstructions in common bile duct from gallstones, see distension and inflammation of gall bladder

63
Q

What are some symptoms of cholecystitis?

A

Acute abdominal pain, fever, rebound tenderness

64
Q

What is the cause of acute pancreatitis?

A

Intrapancreatic activation of proteases and lipases, usually caused by obstruction to the outflow tract

65
Q

What are the symptoms of acute pancreatitis?

A

Pain, fever, nausea, vomiting

66
Q

What is the main cause of chronic pancreatitis?

A

Chronic alcohol abuse

67
Q

What is the duct from the gall bladder to the small intestine?

A

Common bile duct

68
Q

How does chronic alcohol abuse contribute to pancreatitis?

A

Alcohol metabolized by acinar cells, converted into toxic metabolites that damage these cells–results in them releasing enzymes and becoming prematurely activated

69
Q

What is the role of pepsin?

A

Digestion of proteins

70
Q

What does bilirubin come from?

A

Breakdown of hemoglobin from aged red blood cells by Kuppfer cells in the liver

71
Q
A

Pathophysiology (12 decks)

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