gastric digestion Flashcards

(31 cards)

1
Q

Salvia production
-stimulated by
-inhibted by

A

Stimulated by sight, smell of food (autonomic control)

Inhibited during sleep, exercise, dehydration

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2
Q

Contents of saliva:

A

Electrolytes (hypotonic); high HCO3-
Mucin: lubricating of bolus and enhancing chewing action
Salivary amylase initiates digestion
Lactoferrin: lysozyme with anti-bacterial action

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3
Q

Loss of saliva effects?
Causes of lack of salvia

A

Dry mouth
Oral infections
Dental decay
Loss of taste

Causes: Sjogrens
Anti-cholingeric drugs

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4
Q

MAJOR ROLES OF THE STOMACH

A
  1. Mechanical
  2. Reservoir: Initial digestion, food passes thorugh in controlled amounts of semi-liquid paste (chyme)
  3. Adjusts osmolatity
    - prior to entry into the small intestine (duodenum)
    - Antrum: Grinding mill
    - Pylorus: regulates size of particles than can pass to duodenum
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5
Q

What does the stomach in general secrete?

A

intrinsic factor, pepsinogen, mucus, prostaglandins, gastric acid

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6
Q

What is DUMPING syndrome
-osmolarity effect

A

“Dumping” syndrome – nausea, vomiting, cramping, diarrhoea
- Food moves too quickly from stomach into duodenum and so are not completely digested

  • Undigested food particles result in a hyperosmolar chyme in small bowel
  • Rapid fluid shift into gut causing intestinal distension = pain
  • Diarrhoea due to osmotic effect
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7
Q

Causes of Delayed gastric emptying

A

Gastroparesis (delayed gastric empyting)

  1. Diabetes
  2. Autonomic neuropathy
  3. variable rate of glucose absorption
  4. Abdominal discomfort
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8
Q

Function of gastric acid

A
  1. Sterilise the stomach (minimal bacteria load)
  2. Limited role in digestion
  3. Helps abs B12 and iron
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9
Q

Condition with low or no gastric acid and the effects of this

A

Achlorhydria (absent or low gastric acid)
* bacterial overgrowth
- increased risk of gastric cancer
- absorption of iron slightly decreased

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10
Q

Cell types of stomach and what they secerete

A

Goblet: Mucusu (protect stomach lining)
Pareital (Gastric acid)
Cheif cells (Pepsinogen)
D cells (Somatostatin)
G cells (gastrin)

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11
Q

Parietal cell function: Diagram showing flow of bicarb and HCl relationship

A

Co2 and water enter cell forming H+ and Bicarbonate

Acid goes to lumen thorugh ATP’ase
Bicarb goes to blood through Cl channel

LEcture Slide

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12
Q

How is the gastric mucosa from acid protected from acid

A

Lecture Slide
Mucus layer with bicarbonate secretions protect the gastric epithelium

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13
Q

4 Controls of gastric acidity

A
  1. Neurotransmitter
    - Molecule that transmits a signal from a neuron
  2. Autocrine
    - Molecule released by a cell that targets itself
  3. Paracrine
    - Molecule released by a cell that targets adjacent cells
  4. Endocrine
    - Molecule (known as hormone) released by endocrine cells into circulation to target distant cell

LEcture Slide

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14
Q

Acetylcholine
- what nerve releaed by
-stimulate?

A

Released by vagus nerve and enteric neurons

Stimulates:
– Parietal cells to release
HCl
– ECL cells to release
histamine –> stimulates
parietal cells
– G cells to release gastrin –
> stimulates ECL and
parietal cells

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15
Q

Enterochromaffin-like (ECL) cells
-located?
-secretes?
-Stimulates?

A
  • Located in body of stomach
  • Secrete histamine
  • Histamine is a molecule with paracrine activity
  • Stimulates acid secretion directly by acting on adjacent
    parietal cells
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16
Q

G cells
-located?
-secretes?
-Stimulates? How?

A
  • Located in antrum of stomach
  • Secrete gastrin
  • Stimulates acid secretion indirectly via ECL and parietal cells
    – Enters blood circulation
    – Binds to ECL cells stimulating histamine release
    – Histamine stimulates parietal cells to secrete HCl
    – Binds to parietal cells
17
Q

D cells
-located?
-secretes?
-Stimulates? Inhibits?

A
  • Located in antrum of stomach
  • Secrete somatostatin
  • Somatostatin is a hormone with endocrine and paracrine
    activity
  • Inhibits acid secretion by acting on adjacent G cells and
    inhibiting gastrin release
18
Q

PHASES OF DIGESTION
and description

A
  1. Cephalic phase
    - Initiated by thought, sight, smell of food
    - Mediated via vagus nerve through acetylcholine
  2. Gastric phase
    - Distension of both body and antrum causes acid
    secretion mediated largely by the vagus nerve
    - Protein in the antrum (mainly breakdown products –
    amino acids and peptides) stimulates G cells – gastrin
    release
  3. Intestinal phase –
    inhibition of acid secretion
    - HCl in antrum causes release of somatostatin from D
    cells, which inhibits gastrin – main mechanism
    - HCl in duodenum stimulates secretin, which inhibits
    gastric acid and gastric emptying and stimulates
    pancreatic HCO3 secretion
    - Partially digested fats and proteins in duodenum
    stimulate cholecystokinin, which inhibits gastric acid and
    gastric emptying (hunger suppressant)
    - Cholecystokinin also stimulates release of pancreatic
    enzymes and gallbladder contraction to release bile
19
Q

What does gastric acid stimulate

What does gastric acid inhibit?

A

Stimulates release
* ECL cells – histamine
* G cells – gastrin
* Vagus and enteric nerves -
acetylcholine

Inhibits release
* D cells - somatostatin

20
Q

Examples of Abnormal gastric acid secretion:
Increased
Decreased

A

Increased
- H. pylori gastritis
- Tumours that produce gastrin (gastrinoma)

Decreased
- Loss of parietal cells e.g. pernicious anaemia (covered later)
- Vagotomy: loss of vagus nerve – reduced acetylcholine
- Drugs e.g. proton pump inhibitors and histamine 2 receptor antagonists
- Gastric surgery: removal of parts of stomach that contain cells involved in HCl
secretion

21
Q

Pepsinogen
- secreted by
- function
-Purpose

A

– Secreted from gastric chief cells

– Pepsin degrades/hydrolyses proteins
– Role in early digestion: hydrolysed proteins m ore active
stim ulus for gastrin
– If pH >4, pepsin not active

22
Q

DISEASES OF THE STOMACH AND DUODENUM
- Peptic ulcer disease
- what is it
-presentation findings

A

Break in the mucosa
- Erosion = Partial loss
- Ulcer = Full thickness loss
* Presentation
- Pain - “burning” epigastric pain
-Gastric ulcers - worse with food (during and after the meal)
- Duodenal ulcers - worse without food (empty stomach, night)
* Bleeding
* Perforation
* Obstruction (in pylorus or duodenum) from:
– Swelling
– Scarring causing stricture

23
Q

treatment for peptic ulcer disease

A

Medical:
- proton pump inhibitors
Omeprazole, Pantoprazole, Lansoprazole
- H2R antagonists

Surgery to reduce acid secretion (Historical)
- Gastrectomy: removes antrum, removes gastrin
- Vagotomy: divide vagus nerve, reduces acetylcholine

24
Q

Cause of peptic ulcer disease

A

Helicobacter pylori (most common)
* Other causes:
– Aspirin
– NSAIDs (non-steroidal anti-inflammatory drugs)

25
H. pylori - How has it adapted to become the only bacteria to survive in stomach acid
H. pylori is adapted to live in the mucus layer of the antrum and causes gastritis: - Produces enzymes (urease) - Degrades mucus -Elicits a cellular immune response
26
What are four conditions that H plyori can cause
– Gastritis – Peptic ulcer – Gastric cancer – Gastric MALToma * Mucosa-associated lymphoid tissue lymphoma
27
How can h plyori progress to gastric cancer
Long-term H. pylori gastritis (inflammation) can result in atrophic gastritis (loss of gastric cells such as parietal cells) Atrophic gastritis leads to impaired gastric secretion of various substances including gastric acid i.e. achlorhydria Achlorhydria (near absent acid secretion) allows for bacterial colonisation and formation of carcinogens This gastric environment plus dietary factors (high salt diet; low fruit and vegetables intake) gives higher risk for cancer
28
How does H.plyori cause Duodenal ulcer
H. pylori causes increased gastrin Raised gastrin causes increased gastric acid secretion High acid output causes gastric metaplasia in the duodenum H. pylori migrates from antrum to duodenal cap causing breakdown of mucosa
29
Treatment of H. pylori
First-line triple therapy – omeprazole, clarithromycin and amoxicillin for 14 days
30
Gastric cancer (adenocarcinoma) - 2 types and diffrences between them (differenitation, cell arrangment, location)
1. Intestinal 2. Diffuse Intestinal * Well-differentiated * Cells arranged in a tubular/glandular pattern * More likely to be in the antrum Diffuse: * Poorly differentiated * Lack glandular formation * Can infiltrate gastric wall – linitis plastica - May occur at a younger age
31
Gastric cancer Symptoms
- Upper abdominal discomfort (Dyspepsia) - Early satiety - Pain after meals - Anorexia - Weight loss