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Physiology III > Lecture 32: Gastroduodenal Mucosal Protection, Ulcers > Flashcards

Lecture 32: Gastroduodenal Mucosal Protection, Ulcers Flashcards

1
Q

What is the function of the gastrointestinal barrier

A
  1. Allow efficiency transport of nutrients across epithelium
  2. Protect epithelial cells from destructive acidity, hostile microorganisms, toxins, and digestive activity of pepsin
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2
Q

__cells support the continual repair of GI epithelium

A

Stem cells

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3
Q

What maintains the H+ gradient in the gastrointestinal barrier

A

Bicarbonate microenvironment on epithelial cells

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4
Q

What is the function of the mucus gel layer

A

Provide protection to cells

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5
Q

What are 2 examples of immune cells in the GI tract

A
  1. Paneth cells
  2. Peyers patches
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6
Q

What are the 3 components of the mucosal barrier

A
  1. Tight junctions that connect enterocytes
  2. Mucus layer, unstirred H20 layer
  3. Immune cells
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7
Q

What layers create the microenvironment separating the lumen and apical membrane

A

Glycocalyx, mucus, unstirred water layer

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8
Q

What cells secrete mucus in the mucus layer

A

Goblet

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9
Q

Is the SI mucus layer thick or thin compared to LI

A

Thin- has buffers to combat acidity

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10
Q

Why is the LI mucus layer thick

A

To protect from microbial activity

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11
Q

What cells produce mucins

A

Surface mucous, surface neck and glandular cells

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12
Q

What triggers mucus secretion

A
  1. Vagal stimulation
  2. Stroking causes release of PG—> VIP—> CFTR Cl- channel to release H20 and goblet cells activated
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13
Q

How can acid and pepsinogen pass the mucus layer

A

Via small channels

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14
Q

What creates the neutral character of the mucus gel layer

A
  1. Water layer
  2. Bicarbonate secretion via surface epithelial cells
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15
Q

What is responsible for stimulating release of bicarbonate at the mucus layer

A

PGE2

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16
Q

How does PGE2 inhibit gastric acid secretion

A
  1. Inhibits AC of parietal cells
  2. Inhibits histamine
  3. Inhibits gastrin cells
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17
Q

How does PGE2 impact blood flow

A

Simulates mucosal blood flow and oxygen delivery by vasodilation

18
Q

Microbial/pathogen recognition leads to what 3 things

A
  1. Activation of immune response
  2. Production of effector molecules
  3. Commensal bacteria create hostile environment for pathogenic bacteria
19
Q

What are paneth cells

A

Immune cells located in the SI crypts

20
Q

What are Peyers patches

A

Mass of lymphatic tissue in the SI, especially the ileum

21
Q

What is the function of pattern recognition receptors

A

Recognize and discriminate pathogenic bacteria vs commensal bacteria

22
Q

What are the two types of PPR’s

A
  1. Toll like receptors (transmembrane)
  2. NOD like receptors (intracellular)
23
Q

What do PRR’s recognize on pathogenic bacteria

A
  1. Lipolysaccharides
  2. Flagella
  3. DNA/RNA
24
Q

PPR recognition leads to production of what effector molecules

A

IL-18, IL-1B, TNFalpha

25
Q

What are alpha-Densins (aka cryptidins)

A

Antimicrobial peptides secreted by paneth cells that have activity against bacteria, some yeast, and giardia trophozoites

26
Q

How do commensal bacteria provide protection (3)

A
  1. Production of inhibitory compounds (stop growth)
  2. Competing for adhesion sites
  3. Modulating the immune response
27
Q

What factors contribute to the development of IBD

A
  1. Impaired immunity (cytokines)
  2. Genetic predisposition (NOD-like receptors)
  3. Microbial flora dysfunction (metabolites, dysbiosis)
28
Q

Inflammatory stimuli (HCl injury) induce ___release from mast cells and ____synthesis by epithelial cells

A

Histamine, prostaglandins

29
Q

The constant repair of GI epithelium helps prevent defects but bears risk of ___

A

Malignancy

30
Q

What causes an ulcer

A

Excessive exposure to HCl or SCFA

31
Q

NSAID’s inhibit COX activity which thereby inhibit the production of ___

A

Prostaglandins

32
Q

What are the 2 ways in which NSAIDs cause toxic effects

A
  1. Inhibit COX and affect in PG synthesis
  2. Become trapped in epithelial cells causing damage/death
33
Q

How do NSAIDS effect mucus, bicarbonate, blood flow, cell restitution and inflammation

A

Decrease all except inflammation which increases

34
Q

How do NSAIDs become trapped in the epithelial cells

A
  1. Carboxylic acids such as NSAIDS are non-ionized in acidic gastric lumen
  2. Migrate to inside cell lumen which is neutral and become ionized and trapped
  3. Elevated intracellular NSAID levels cause cell death and injury
35
Q

How does H. Pylori result in gastritis, peptic ulcers and potentially a higher rate of gastric neoplasia

A
  1. Burrow into mucus gel layer
  2. Adhesins facilitate attachment to mucus layer
  3. Disturb HCO3- release and digest mucus layer therefore decrease pH causing ulcers and damage to epithelial lining
36
Q

How do parasites cause damage to GI mucosa/epithelium

A
  1. Mechanical damage to mucus gel layer and mucosa
  2. Chronic exposure of mucosal cells to acidic environment
  3. Inability of mucosal repair/epithelial proliferation (b/c injury is continuous)
37
Q

What are the two types of disorders that can cause gastrointestinal ischemia

A
  1. Non-occlusive ischemia
  2. Occlusive ischemia
38
Q

What is occlusive ischemia and what are some causes

A

Conditions that directly disrupt gastrointestinal flow

Causes: strangulation, volvulus, thromboembolism, bloat/tympany, FB, herniation

39
Q

What is non-occlusive ischemia

A

Ischemia due to reduce capillary flow or shunting blood away from GI tract so that blood bypasses gastric mucosa

40
Q

Why can stress and Cushings result in non-occlusive ischemia

A

Both cause an increase in glucocorticoids which results in vasoconstriction

Physiology III (34 decks)

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