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GI Physiology > 47 Gastrointestinal Disorder II > Flashcards

47 Gastrointestinal Disorder II Flashcards

1
Q

H.pylori can be detected 100% in GU and 95% in DU.
Which of the below describes H.Pylori?
A. Gram-negative
B. Non-invasive spiral bacterium
C. spread infection via oral transmission

A

All of the above

C. Infected via oral transmission (e.g. contaminated endoscopy/ chopticks)

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2
Q

How H.pylori survive in low pH?

A
  • Urease is highly expressed on cell wall of H.pylori, which causes H+ + urea to become HCO3- and NH4+
  • With HCO3- leak out of the cell, cause neutralisation
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3
Q

How pylori cause epithelial mucosal cell damage, leading to PUD? (3 points)

A
  1. NH4+ is a cytotoxic agent that increases gastric mucosal damage.
  2. NH4+ produces endotoxin and exotoxin that increases mucosal ulceration
  3. Chemotactic factors recruit and activate inflammatory cells to increase mucosal inflammation.
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4
Q

What is the difference in location of H.pylori in GU and DU?

A

GU: gastric body, acid-secreting area by parietal cells (therefore it is due to diminishing gastric mucosal barrier rather than increased acid secretion)

DU: gastric antrum, hormone-secreting area (damage to D-cells, somatostatin decreased, no inhibitory effect on acid secretion)

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5
Q

Invasive tests for diagnosis of H.Pylori infected PUD:
Antral biopsy, requires tissue sample via endoscopy.
Name the 2 tests.

A
  1. Gram’s stain

2. Urease test

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6
Q

Name the 2 non-invasive tests for diagnosis of H.Pylori infected PUD. Briefly describe the 2nd one.

A
  1. Serological testing for antibody to H.Pylori (but positive test doesn’t imply active infection)
  2. Urea breath test
    - high sensitivity and specificity for H.pylori
  • 13C or 14C labelled urea (capsule/liquid). 13C is radioactive: health problem; 14C is expensive
  • Swallowed together with ascorbic acid (citric acid), thus delay gastric emptying (acid is a potent gastric emptying inhibitor) for increasing contact time of urea and the H.pylori if present
  • Collect samples and check isotope activity

***The bacteria contains urease to turn urea to HCO3- (and NH4+)

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7
Q

Briefly state the target of treating
A. GU
B. DU

A

A. Mucosal defence enhancement

B. Acid suppression

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8
Q

Name all the 5 treatments to suppress acid secretion.

Give examples.

A
  1. Antacids
    - Al(OH)3, Mg(OH)2
    - Nonspecific, side effects like Mg-induced diarrhea and Al induced constipation
  2. H2 receptor antagonists
    - cimetidine, ranitidine, famotidine
    - inhibition of histamine-dependent acid secretion
  3. PPI/ H+/K+-ATPase inhibitors
    - omeprazole, iansoprazole
    - inhibition of proton pump thus acid secretion
    - more potent and long lasting (acts on the ATPase, need to wait for 24 hours after new ATPase are synthesized )
  4. Muscarinic receptor antagonists
    - Pirenzepine, atropine
    - Inhibition of Acetylcholine-stimulated acid secretion
  5. Vagotomy/Antrectomy
    - remove vagal nerve/ antrum
    - Removal of Ach- or gastrin mediated acid secretion
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9
Q

Name the treatment to enhance mucosal defense.

A

Prostaglandin agonists

  • misoprostol
  • Inhibition of acid secretion; direct cytoprotection (mucous and HCO3- secretion)
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10
Q

Name the 2 treatments to eradicate H.Pylori directly.

A
  1. Triple therapy:
    use of PPI (omeprazole) or H2 receptor antagonist (Ranitidine)
    + 2-3 antibiotics (Amoxycillin, metronidazole, clarithromycin)
    - enhance healing rate and decrease recurrence
  2. Bismuth salts
    - toxic to H.Pylori
    - Coat ulcer base
    - adsorb pepsin
    - enhance PG synthesis
    - Stimulate HCO3- secretion
    Side effects: Black tongue and stool
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11
Q

Balance between intestinal absorption and secretion (A>S = normal)
State 3 features of diarrhea.

A
  1. Absorption decreased
  2. Secretion increased
  3. GI motility increased
    (Hypersecretion and Hypermotility)
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12
Q

What cells are responsible for absorption in GI?

In what scenario will these cells cause diarrhea?

A

Absorptive villus cells;
Villus cell damaged by inflammation and infection > also glucose/AA/Peptide carrier system

A

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13
Q

What cells are responsible for secretion in GI?

In what scenario will these cells cause diarrhea?

A

Crypt cells
- Overstimulation by bacteria (endotoxins), increased liquidity of luminal contents

S>A, causing diarrhrea

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14
Q

What are the neural and hormonal agents that stimulate intestinal secretion?
Briefly describe when each agent causes an “oma”.

A 
Neural:
VIP 
○ Stimulate intestinal secretion
○ VIPoma results in pancreatic cholera (watery diarrhea)
Mediator: cAMP (2nd messenger)

Hormonal:
Gastrin
Gastrinoma (excessive gastrin, act on parietal cells to produce HCl and IF) results in persistent watery diarrhea

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15
Q

What are the 3 broad categories of diarrhea? State the definition of each diarrhea.
Can they occur simultaneously?

A
  1. Malabsorptive diarrhea
    - diarrhea due to impaired absorption by intestine
    (e. g. infection, inflammation)
  2. Osmotic diarrhea
    - diarrhea due to accumulation of non-absorbable solutes in intestines
  3. Secretory diarrhea
    - diarrhea due to over stimulation of secretory crypt cells in villi by enteric pathogens/toxins.

Yes.

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16
Q

What is Celiac disease?

Which diarrhea is it related to ?

A

Celiac disease is a gluten (gliadin) -sensitive enteropathy (degeneration of villus cells)

Gluten, a wheat protein activates immunological reaction in GALT, causing inflammation and then loss of villous architecture (blunted/flattened villi)

Malabsorptive diarrhea.

17
Q

Give examples of causes of osmotic diarrhea.

A

Glucose malabsorption (genetic defect of SGLT 1 in neonates)

Lactase deficiency (lactose intolerance in adults)

18
Q

Explain the mechanism of osmotic diarrhea resulting from lactase deficiency.

A

Lactase deficiency > accumulation of lactose in bowel lumen, increased luminal osmolality in lumen > fluid accumulation in lumen (hypersecretion) > luminal distension > enhanced peristalsis (hypermotility) > watery diarrhea (lactose free diet helps)

19
Q

Secretory diarrhea can be further subdivided into inflammatory and non-inflammatory diarrhea. What are the differences in nature of the two?

A

Inflammatory:

  • Pathogens invade intestinal mucosa, elaborate toxins resulting in loss of mucosal integrity & inflammation
  • E.g. invasive & cytotoxin-producing Salmonella

Non-inflammatory diarrhea:

  • Pathogens colonize intestinal lumen/ produce toxins with intact mucosal integrity & no inflammation
  • e.g. Enterotoxins from Vibrio cholerae or enterotoxigenic E. coli
20
Q

Briefly state the effects of Vibrio cholerae on stimulating cholera toxin receptor (GM1-ganglioside) located on the crypt cell.

A
  1. When cholera toxin receptor is activated, cAMP increases, which activates protein phosphorylation and therefore cAMP-dependent CFTR channels (Cl- channels).
  2. Anion secretion (Na+ and Cl-)

Excessive loss of water and ions
e.g. K+ and HCO3-

21
Q

Briefly state the effects of heat stable enterotoxigenic E.Coli on stimulating STa receptor and guanylate cyclase located on the crypt cell.

A
  1. Activation of heat stable enterotoxin receptor, cGMP increase > G kinase increases > protein phosphorylation increases Therefore cGMP-dependent CTFR channels
  2. Anion secretion (Na+ and Cl-)
22
Q

State the differences of inflammatory and non-inflammatory diarrhea in terms of stool.

A

Inflammatory: bloody, mucoid

Non-inflammatory: watery

23
Q

State the differences of inflammatory and non-inflammatory diarrhea in terms of volume.

A

Inflammatory: small volume, frequent bowel movements, dehydration is unusual

Non-inflammatory: Large, dehydration possible

24
Q

State the differences of inflammatory and non-inflammatory diarrhea in terms of fecal leukocytes.

A

Inflammatory: many, frequently occult blood

Non-inflammatory: absent

25
Q

State the differences of inflammatory and non-inflammatory diarrhea in terms of clinical symptoms.

A

Inflammatory: tenesmus, fever, severe abdominal pain

Non-inflammatory: no blood, no pus, no tenesmus, no fever, abdominal pain usually not prominent

26
Q

State the differences of inflammatory and non-inflammatory diarrhea in terms of causes.

A

Inflammatory: Invasive and cytotoxin-producing microorganisms

e.g. Salmonella, Shigella, Invasive E.Coli

Non-inflammatory: Enterotoxin-producing bacteria, minimally destructive viruses

e.g. Vibro cholarae (cAMP dependent),
Enterotoxingenic E. coli (cGMP depedent),
Rotavirus (Gastroenteristis_

27
Q

Why is oral rehydration therapy is not suitable for inflammatory type of diarrhea, but only non-inflammatory?

A

Villous cells are damaged and thus the glucose/AA/Peptide carrier system (e.g. SGLT 1) too, no effect when oral rehydration therapy is given,

GI Physiology (11 decks)

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