Upper GIT Physiology and disorders Flashcards

1
Q

Exocrine cells

A

Mucous cells – secrete mucus

  • Important because it sits at the top of internal muscuso and acts as a cell layer to prevent burning of ACID
  • seen as the protective cells

• Chief cells – secrete pepsinogen & gastric lipase
- is in active form

• Parietal cells – secrete HCl & intrinsic factor (glycoprotein for B12 absorption)
- B12 is absorbed at the end of small intenstine

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2
Q

Endocrine/ Paracrine cells

A
  • Enterochromaffin-like (ECL) cells
  • G cells
  • D cells

other cells
Stem cells filled in Stomach and small intestine

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3
Q

Roles of HCl

A

• Activates pepsinogen (zymogen) -
converts it in active pepsin
• Contributes to nonspecific disease resistance by destroying most ingested pathogens

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4
Q

Mucus is a protective barrier

A
  1. Impermeable mucosal cells: luminal membranes are impermeable to H+
  2. Tight junctions: prevent HCl from penetrating
  3. Mucous coat: physical barrier to HCl
  4. Chemical barrier: HCO3- neutralizes HCl
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5
Q

Regulation of gastric secretion

- neural control

A

Acetylcholine (ACh) – released by intrinsic nerve plexuses within the stomach, under the control of short local reflexes and vagal stimulation

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6
Q

Regulation of gastric secretion

- hormonal control

A

• Enterochromaffin-like (ECL) cells – secrete histamine among the parietal and chief cells (oxyntic mucosa)
• G cells – secrete gastrin into the bloodstream
- Food reaches mouth > g cells release gastin > stimulates
ECL and D cells > Histamine

• D cells – secrete somatostatin in response to acid

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7
Q

Shut down system

A

d cells sense change in pH and produce somatostatin

And has opposite affect and shuts down system

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8
Q

Control of gastric secretion involves three phases:

A
  1. cephalic phase -factors arising before food reaches the stomach (thinking of food - long reflex)
  2. gastric phase -factors resulting from food in the stomach (food is present)
  3. intestinal phase -factors in the duodenum after food has left the stomach
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9
Q
  1. Cephalic phase
A

– sight and thought of food increase gastric juices.

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10
Q
  1. Gastric phase
A

– begins when food is in the stomach (especially proteins).

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11
Q
  1. Intestinal phase
A

factor that originates in the small intestine (duodenum). Inhibitory phase, which helps with stomach emptying.

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12
Q

Gastritis

A

Breakdown of the mucus barrier can result in inflammation. >
Chemical breakdown of mucosal barrier: alcohol, aspirin and non steroidal
anti-inflammatory drugs (NSAIDs such as ibuprofen) > GASTRITIS
Redness (erythema) is caused by excessive production of HCl and gastric juices when no need it

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13
Q

Gastritis treatment

A

• antacids tablets: neutralize HCl
• lifestyle changes: avoid aggravating food (spicy food, coffee, chocolate, mint and
tomato).

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14
Q

Peptic ulcers

A

Extreme gastritis or bacterial infection increase the chance of developing peptic ulcers.

Discovery of the acid-resistant bacteria Helicobacter pylori
• Flagella
• Prefer to settle in the
antrum (no parietal
cells)
• Production of urease
to buffer HCl
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15
Q

Peptic ulcers trmt and diagnosis

A

Diagnosis: urea breath test (UBT), if positive endoscopy to check for ulcers
Treatment:
• antibiotics (2 weeks)
• proton pump inhibitors (action on H+-K+ ATPase pump)
• blocker for histamine receptor 2 (H2) (cimetidine): inhibits production of HCl, no effect on H1 receptors (involved in allergic respiration disorders)
• lifestyle changes

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16
Q

Pernicious anemia

A

Autoimmune disease that affects the parietal cells. > Absence of intrinsic factors (glycoprotein) release by
parietal cells.
> Impossibility of the body to absorb enough vitamin
B12 in ileum
> Defective erythrocyte production
Treatment:
• Regular injections of vitamin B12