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Pathophysiology > Disorders of the GI Tract Pt.2 > Flashcards

Disorders of the GI Tract Pt.2 Flashcards

1
Q

Diverticular Disease: What are some factors that contribute to the development of this disease?

A

lack of fiber, decrease in physical activity, and poor bowel habits (aging)

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2
Q

In this disease, what are pseudodiverticula? How are these different from diverticula?

A

mucosa and submucosa being herniated through the other layers. Found mainly in the sigmoid colon and doesn’t have a muscularis layer.

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3
Q

Diverticular Disease Complications

A

peritonitis, hemorrhage, and bowel obstruction

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4
Q

Why is it important to increase fiber in the diet for patients with diverticular disease?

A

Causes bulk and more regular defecation. This leads to a decrease in intraluminal pressure.

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5
Q

Intussusception

A

folding of the intestinal wall in such a way that the intestine “telescopes” (a
section of bowel folds into the section immediately ahead) More common in children.

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6
Q

Vovulus

A

part of the intestine twists over on itself, like a kink in a garden hose, and is more common in older men

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7
Q

Inguinal Hernia

A

part of the intestine protrudes through a weak spot in the abdominal wall muscles

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8
Q

Non-celiac gluten sensitivity

A

Not an IgE mediated disease. Symptoms include GI discomfort, headaches, fatigue, joint and muscle pain, skin rashes, asthma and rhinitis and some nutritional deficiencies.

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9
Q

Wheat Allergy

A

IgE involved allergy to any wheat components. Symptoms can include rash, nausea, abdominal pain, itching, swelling of the lips and tongue and even anaphylaxis

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10
Q

Celiac Disease

A

Flattens enterocyte villi and has malabsorption problems. Involved a product of wheat call Gliadin.

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11
Q

What other names is celiac disease known by?

A

celiac sprue, non-topical sprue or gluten sensitive enteropathy

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12
Q

Which 2 portions of the digestive tract are most affected by celiac disease?

A

duodenum and proximal jejunum

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13
Q

Know the 3 main gluten-containing grains.

A

Barley, wheat, and rye

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14
Q

What is gluten and what are its two main subcomponents?

A

glutenin: allows for elasticity
gliadin: increases viscosity (triggers gluten intolerant folks)

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15
Q

What does zonulin do?

A

Gliadin increases the release of zonulin. It’s a protein produced by the enterocytes in the intestine and by the liver.

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16
Q

What does IL-15 do?

A

triggers intraepithelial lymphocyte (IEL) cell proliferation and also causes these cells to express NKG2D which is a receptor for MIC-A.

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17
Q

What is MIC-A and what does it do?

A

expressed by enterocytes under conditions of stress such as with bacterial infections, cancer, gliadin or other antigen exposure. Will make IEL kill enterocyte.

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18
Q

What does the enzyme tissue transglutaminase (TTG) do to gliadin in the lamina propria?

A

deaminates gliadin in the lamina propria.

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19
Q

Having which of the HLA subtypes will increase the risk for having celiac disease?

A

D8Q

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20
Q

Name 3 antibodies that can be measure in the blood as part of the diagnosis for celiac disease

A

Anti-TTG, anti-gliadin and anti-endomysium antibodies

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21
Q

Describe 3 morphological changes that occur with celiac disease

A 
villous blunting (no villi), IEL
proliferation and crypt elongation (because of IEL proliferation)
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22
Q

What are 4 important clinical features that may be experienced by those with celiac disease?

A

diarrhea, bloating, chronic fatigue and anemia

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23
Q

Why do children with untreated celiac disease often have short stature?

A

because of malabsorption of nutrients during crucial times of growth

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24
Q

Why is there an increased

risk for malignancy with celiac disease and which 2 cells may become cancerous?

A

because of increased IEL proliferation (leading to lymphoma) and increased enterocyte division (leading to small intestine adenocarcinoma)

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25
Q

What is the most important treatment for celiac disease?

A

Gluten free diet!

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26
Q

Recognize the listed causes of dysphagia

A

esophageal narrowing such as strictures and scleroderma (fibrous replacement of tissues in the
muscularis layer of the GI tract). Lack of saliva my also be a cause (Sjogren’s). Syndromes that lead to muscle weakness. Also neural network disorders that causes an inability to relax the LES.

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27
Q

What is a diverticulum of the esophagus?

A

an outpunching of the esophageal wall caused by weakness of the
muscularis layer or motility issues

28
Q

What are some manifestations of an esophageal diverticulum and what complications can arise if this is left untreated?

A

food getting stuck in the diverticula which can lead to halitosis. Complications such as esophagitis and ulceration may occur.

29
Q

What is Mallory-Weiss syndrome and what can cause it?

A

non-penetrating mucosal tears at the gastroesophageal junctions. Caused by severe retching or vomiting in conditions like chronic alcoholism, bulimia, sickness, or pregnancy.

30
Q

What is the difference between a sliding and para esophageal hiatal hernia?

A

Sliding: depicted as a bell-like protrusion of stomach above the diaphragm
Para: separate portion of the stomach, usually the fundus, enters the thorax through a widened opening

31
Q

Hiatus Hernia

A

small portion of the stomach comes into the thoracic cavity through the
esophageal hiatus

32
Q

“Angle of His”

A

angle created between the esophagus and the stomach at the esophagogastric junction. This angle forms a valve that prevents reflux of gastric contents from entering the esophagus.

33
Q

Secretory products of the gastric area

A

Parietal Cells: release HCl and intrinsic factor
Chief cells: make pepsinogen
Mucous cells: make mucous
ECL: make histamine

34
Q

What are the 3 main ingredients necessary for hydrochloric acid production by the parietal cells of the stomach?

A

Cl-, CO2 and H20

35
Q

What is the name of the enzyme inside the parietal cells that makes carbonic acid?

A

Carbonic anhydrase

36
Q

What is the name of the transporter that uses ATP to pump hydrogen ions into the lumen of the stomach and potassium ions into the cytosol of the parietal cell?

A

hydrogen/potassium ATPase

37
Q

What happens to the bicarbonate that is made in the parietal cells?

A

the bicarbonate goes into the blood and uses a transporter that exchanges bicarbonate for Cl-

38
Q

Name 3 receptors located on the parietal cells that when activated will increase the activity of the
hydrogen/potassium ATPase

A

acetylcholine, histamine and gastrin

39
Q

Two drug classes that decrease acid production

A
  • H-2 blockers: block histamine from activating H-2 receptors (DRUGS: pepcid and zantac)
  • Proton pump inhibitor (PPI): inhibit hydrogen/potassium pump (DRUGS: omeprazole, lansoprazole, and esomeprazole)
40
Q

Most common cause of GERD

A

inappropriate relaxation of the lower esophageal sphincter (LES), overproduction of gastric acid, and large meals

41
Q

Why does lying on the right side make GERD symptoms worse than lying on the left side?

A

This is due to heartburn, because the heart is on the right side.

42
Q

What is laryngopharyngeal reflux (LPR). What are the symptoms associated with LPR?

A

Affect air passages and cause chronic cough and hoarseness.

43
Q

What are esophageal strictures and what are they caused by?

A

Occurs when the esophagus tightens or narrows leading to swallowing difficulties. It is a complication of GERD.

43
Q

What are esophageal strictures and what are they caused by?

A

Occurs when the esophagus tightens or narrows leading to swallowing difficulties. It is a complication of GERD.

44
Q

What is Barret esophagus and how is it caused? Barrett esophagus increases the risk for what cancer?

A
  • Epithelial cells in esophagus are replaced by columnar epithelium cells.
  • Increases risk for adenocarcinoma.
45
Q

What are some lifestyle modifications that are important in the treatment and prevention of GERD?

A

Eating smaller meals, eliminating offending foods, weight loss, head of the bed elevation for sleeping, and not eating 3 hours before bed.

46
Q

Antacids

A
  • Neutralize stomach acid and provide rapid relief

- Not long lasting because the stomach increases acid to react

47
Q

Elements in the antacids

A

Aluminum: increase constipation
Calcium: increase constipation and risk for calcium containing kidney stones.
Magnesium: cause diarrhea

48
Q

What is Systemic Mastocytosis?

A

Mast cells accumulate in the body which produces a lot histamine. Histamine stimulates H-2 receptors and produces stomach acid.

49
Q

What is Zollinger-Ellison Syndrome?

A

produce excess amounts of gastrin in the pancreas (might be from tumor).
At higher risk for peptic ulcers

50
Q

Describe the mechanisms that make up the gastric mucosal barrier that protect the gastric cells from the low pH environment of the stomach lumen.

A
  • an impermeable layer of epithelial cells

- tight junctions and a protective mucus layer above the cells

51
Q

Acute gastritis

A

acute inflammatory process in the mucosa of the stomach. may involve bleeding into the mucosa and sloughing off of the superficial mucosal cells.

52
Q

Know how NSAID use increases risk of gastritis

A

NSAIDS are protonated at the low pH of the stomach acid, and this helps them cross the mucosal cell membrane. Once crossed they lose the proton and become ionized which traps them in the mucosal cell to inhibit COX. COX helps produce prostaglandins and prostaglandins help keep up a thick and healthy layer of mucus on the membrane to protect from acid. NSAIDS inhibit COX therefore making a thinner layer of mucus.

53
Q

What is Chronic Autoimmune Gastritis?

A

autoantibodies to gastric and parietal cells that produce intrinsic factor.
Lack of b-12 absorption can lead to megaloblastic anemia and atrophic glossitis (beefy red and smooth tongue)

54
Q

Which portions of the stomach are mostly affected by H. pylori gastritis?

A

antrum and body of the stomach

55
Q

What is the mode of transmission for H. pylori?

A

oral-oral and fecal-oral route

56
Q

What is the name of the enzyme produced by H. pylori that affects urea and what reaction does this enzyme catalyze?

A

urease: catalyzes urea into CO2 and ammonia or NH3. NH3 becomes NH4+ and helps neutralize acid around H. pylori

57
Q

What are some cruciferous vegetables and why are they believed to inhibit the growth of H. pylori?

A

Brussel sprouts, cauliflower and broccoli. Contain a chemical called sulforaphane that has been shown to have bactericidal effects on H. pylori

58
Q

Describe how the carbon urea breath test can be used in the diagnosis of H. pylori.

A

by having the patient drink C13 labeled urea. The H. pylori will make CO2 from the urea that will be breathed out. C13 will be detected

59
Q

What can be tested in the blood and urine or stool to aid in the diagnosis of an H. pylori infection?

A

blood: H. pylori antibodies

urine and stool: H. pylori antigens

60
Q

What is the most accurate diagnostic method for an H. pylori infection?

A

take a biopsy from two different locations and culture the biopsy specimens or do a urease test on the specimens.

61
Q

Tx of H. pylori

A
  • Prevpac: contains 2 antibiotics and a proton pump inhibitor (increases the pH) to create an environment more conducive to healing
  • Bismuth can prevent binding of H. pylori and even cause lysis of H. pylori
62
Q

Name the places that peptic ulcers tend to form

A

stomach or proximal duodenum

63
Q

What are the two most significant risk factors for peptic ulcer development?

A

H. pylori and the chronic use of aspirin and NSAIDS

64
Q

Complications of peptic ulcers

A

hemorrhage, perforation, and gastric outlet obstruction

65
Q

What would you expect to happen to the blood pressure of an individual with an actively bleeding ulcer?

A

Blood pressure is dangerously low because a lot of blood can be lost from actively bleeding ulcers.

Pathophysiology (10 decks)

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