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MOD 3 > Upper GI Inflammatory Disorders > Flashcards

Upper GI Inflammatory Disorders Flashcards

1
Q

Food is the main stimulant for acid production. What are the 3 pahses of food-stimulated acid production? Which phase results in the most acid secretion?

A
  • Cephalic, Gastric, Intestinal
  • Gastric phase results in the most acid secretion
  • G cells –> gastrin –> ECL cells (histamine –> H2 receptor on parietal cell) + parietal cells
  • D cells –> somatostatin –> inhibits gastrin release
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2
Q

What are the 3 stimulatory receptors on the basolateral surface of parietal cell? Which is the most important? What does stimulation of these receptors lead to?

A
  1. M3 Muscarinic Receptor
  2. CCK-B gastrin receptor
  3. H2 receptor ** most important

Stimulation leads to activation of the proton pump (secretes H, neighboring Cl pump = HCl secretion)

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3
Q

Channels involved for successful secretion of HCl in the parietal cell

A
  1. H+K+ ATPase (antiporter)
  2. Cl channel
  3. K channel
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4
Q

What are the four major components of Gastric Mucosal Defense?

What are they all regulated by?

A
  1. Mucus secretion
  2. Bicarbonate secretion (buffer)
  3. Mucosal blood flow
  4. Cell restitution/turn over

Mucosal prostaglandins regulate

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5
Q

General key cause for inflammatory disorders of upper GI tract

A

imbalance between aggressive and **defensive mucosal forces **

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6
Q

Primary regions of gastric acid-related diseases, and primary findings (3)

A

Lower esophagus: Acid Reflux

  • esophagitis
  • strictures
  • Barret’s esophaguse
  • esophageal adenocarcinoma

Stomach:

  • gastritis
  • gastric ulcer

Duodenum

  • duodenitis
  • duodenal ulcer (more common than gastric)
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7
Q

Balance of aggressive factors (3) and protective factors (5): View from mucosa

A

Aggressive factors: Acid + pepsin, H. Pylori

Protective Factors (top/lumen to bottom):

  • prostaglandins
  • mucus layer
  • bicarbonate
  • surface epithelial cells
  • mucosal blood supply
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8
Q

In terms of a balance beam between healthy mucosa and peptic ulcer formation, list the hostile factors (4) and protective factors (4)

A

Hostile factors:

  • H. Pylori
  • Gastric Acid
  • Pepsin
  • NSAIDs

Aggressive factors

  • Bicarbonate
  • Prostaglandins
  • mucus production
  • blood flow to mucosa
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9
Q

What are the 3 main causes of Peptic Ulcer Disease?

A
  1. Helicobacter pylori infection
  2. NSAID and ASA
  3. Zollinger-Ellison Syndrome
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10
Q

What does H. pylori produce thats potent and why ?

What layer does H. Pylori reside in?

A

Urease: converts urea to ammonia and carbon dioxide

Resides in the mucus layer overlying the gastric epithelium (mucus layer is adjacent to the lumen). Has flagella to swim through it

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11
Q

What factors may contribute to colonization of gastric mucosa by H. pylori? 3 mains ones with subsets.

A
  1. Urease activity
    * may neutralize acid in local environment
  2. Motility
  • spiral, corscrew shape (gram negative bacteria)
  • flagellae
  • proteases (local mucus layer digestion)
  1. Adherence
  • attachment pedestals
  • bacterial adhesins specific for gastric-type epithelium
  • epithelial cell receptors
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12
Q

H. Pylori is present only in the following types of mucosa

A
  1. Human gastric mucosa
  2. Ectopic or metaplastic gastric-type mucosa elsewhere in GI tract
  • Esophagus
  • Duodenum
  • Meckel’s diverticlum
    • (true diverticulum, persistence of the vitelline duct: may contain ectopic acid-secreting gastric mucosa and/or pancreatic tissue)
  • Rectum
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13
Q

Mechanisms responsible for H. pylori-induced GI injury are not clearly defined. What are 3 proposed mechanisms?

A
  1. production of toxic products –> local tissue injury
  2. induces local mucosal immune responses
  3. causes increased gastrin and may increase acid secretion
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14
Q

Explain the proposed mechanism by which H. Pylori possible increases acid secretion

A

H. pylori infection —> decreased number of D-cells —> decreased somatostain release —> decreased G cell inhibition –> increased Gastrin secretion –> incresed number of parietal cells –> increased gastric acid secretion

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15
Q

Study done about H. Pylori and D-cell density

A

eradiation of H. pylori:

  • increases antral D-cell density and somatostain
  • decreases antral gastrin
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16
Q

What are peptic ulcers strongly associated with? (and which etiologic factor for the peptic ulcers in specific)

A

Peptic ulcers are strongly associated with antral gastritis, and there was a much stronger correlation between non-NSAID associated ulcers (H. pylori) than NSAID associated ones.

**histological antral gastritis is usually due to H. pylori)

17
Q

What is likelihood of developing an ulcer with H. pylori infection?

A

10-15% (and 10% ulcer gastritis)

18
Q

True or false: eradiation of H. pylori dramatically reduces ulcer recurrence

A

True. Slightly more effective at getting rid of duodenal ulcers than gastric.

19
Q

Antral gastritis associated with:

Pan (entire stomach) gastritis associated with: (2)

A

Antral gastritis: PUD

Pan gastritis: gastric cancer and MALT lymphoma

20
Q

H. pylori therapy

What type of mechansim is used

Success rate

A

Dual mechanism therapy

  • Acid suppression (Bismuth or PPI)
  • Antibiotics: Macrolides, Penicillins, Tetracyclincs, Metronidazole, Floxins all used

Success rate is about 75-90%, not ideal

21
Q

Definition of dyspepsia

Which type of ulcers have increased dyspepsia while eating and which type has decreased dyspepsia while eating?

Which type of ulcers have no pain or dyspepsia?

A

Dyspepsia: Epigastric burning

**Note: Dyspepsia does NOT equal PUD

  • Gastric ulcer: increased dyspepsia with eating (more acid production in stomach to digest the incoming food)
  • Duodenal ulcer: decreased dyspepsia with eating (duodenum secretes protective factors to prepare for acidic gastric contents)
  • NSAID ulcers often have no pain or dyspepsia
22
Q

Complications of PUD and their associated symptom (3)

A
  • obstruction —> vomiting
  • melena (black tarry feces) or hematemesis —> bleeding
  • perforation —> pain, distention, sepsis
23
Q

Which type of ulcer is more frequent

A

Duodenal ulcers occur 4x more than gastric ulcers.

24
Q

H. pylori prevalance

A

Colombia, Narino

25
Q

Pathophysiology of NSAID ulcer formation

A

Aspirin causes the loss of gastric surface mucous cells (the weak organic acid can cause cell membrane damage directly, despite if its coated)

26
Q

What do NSAIDs/ASA block, and what effects does this have?

A

They block COX-1 and COX-2 that converts arachidonic acid to prostaglandins

COX-1: prostaglandins –> protection of gastric mucosa, hemostasis

COX-2: prostaglandins –> mediation of pain, inflammation, and Fever

27
Q

Best site specific therapies for parietal cell secretion

A

H2 blocker (histamine receptor blocker)

PPI (most successful, because blocks the actual H+ pump)

28
Q

MOA of H2 receptor antagonists

what happens to intragastric pH and pH control

Long term efficacy?

A

MOA: competitively and reversibly blocks H2 receptors on the surface of the parietal cell

Modest increase in intragastric pH, but large variability in pH control

Long term efficacy LIMITED due to tachyphylaxis (tolerance)

29
Q

Side effects of H2 receptor antagonists (3)

A

Renal disease, rash, thrombocytopenia

30
Q

Describe the “cumulative effect” of proton pump inhibtors (PPIs) and their mechanism of action

A
  • steady state inhibition isn’t reached until 48-72 hour: as the drug irreversibly binds the acid pump, the pump is no longer utilized. But some pumps are still active, so you need multiple doses to block the max amount of pumps possible
  • restoration of secretion requires new pump synthesis since PPI’s irreversibly bind to pumps
  • 30% capacity restored by 24 hours
  • biologic half-life > plasma half-life
31
Q

Omeprazole (Prilosec- PPI) : selective localization and covalent binding

A

Selective localization:

  • pKa 4 (weak base)
  • concentrates exclusively in secretory canaliculus where it becomes ionized

Covalent binding:

  • omeprazole is activated at LOW pH (Acidic) to form an active sulfur group
  • this sulfur group forms a covalent disulfide bond at a critical luminal site on the H+/K+ ATPase
32
Q

Side effects of PPIs: (3)

Long term use associations (4)

A

Side effect: diarrhea, headache, rash

Associations with long-term use: Fundal Gland Polyps, C. Dif Colitis, Osteoporosis, Hypomagnesaemia

33
Q

What is Zollinger Ellison Syndrome?

A

Non-beta islet cell gastrin-secreting tumor

  • maximally stimulates the parietal cells
  • Acid hypersecretion leads to significant gastrointestinal mucosal ulceration
34
Q

When does ZE syndrome normally manifest?

What disorder is ZES sometimes a manifestation of?

A
  • normallly manifests in 40s, ZES is infrequent cause of PUD and occurs in only 1% of all patients with duodenal ulcers
  • ZES can be a manifestation of multiple endocrine neoplasia type 1 (MEN 1) Autosomal Dominant
35
Q

Symptoms of ZES (4)

A
  • Abdominal pain
  • Diarrhea
  • PUD with multiple uclers in unusual places in small intestine
  • severe reflux with strictures (narrowings)
36
Q

Treatment of ZES

Is the tumor malignant?

A

To control the acid: PPI

To control the diarrhea: Octreotide

Removal of lesions (but challening to find at times)

Tumor is malignant and can cause metastasis

MOD 3 (19 decks)

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