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Digestive > 9 - Gastric Digestion and Disease > Flashcards

9 - Gastric Digestion and Disease Flashcards

1
Q

What part of the stomach is distal to the GO junction

A

Cardia

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2
Q

What part of the stomach is proximal to the pylorus

A

antrum

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3
Q

What are the major functions of the stomach

A
  • food reservoir (food moves from fundus to antrum)
  • digests food (mostly mechanical - antrum mixes and grinds food)
  • controls passage of food into SI (pylorus regulates size of particles and passage - slow and small digestive particles ensures effective digestion and absorption
  • gastric acid secretion (sterilisation, protective barrier and digestion)
  • other secretions
    > mucus
    > HCO3-
    > pepsinogen
    > prostaglandins (aid healing)
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4
Q

In gastric motility, the fundus acts as a …

A

food store

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5
Q

In gastric motility, the … and … mix/blend/churn food

A

The body and the antrum

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6
Q

The … contracts to … the exit of chyme

A

The pylorus contracts to limit the exit of chyme into the SI

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7
Q

What are the 4 steps of gastric motility?

A
  1. Relaxation of the fundus (vagovagal reflex) by the vagus nerve
  2. contraction of the body and antrum
  3. pylorus contracts
  4. contraction of body and antrum causes mixing by retropulsion
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8
Q

What does normal gastric function require?

A
  1. intact antrum, pylorus and duodenum
  2. normal vagal function to co-ordinate activity
  3. normal hormonal function - ensure they are released at the right time, feedback loop is okay, tumours can cause an increase release of hormones
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9
Q

2 types of abnormal gastric emptying

A

rapid gastric emptying

delayed gastric emptying

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10
Q

delayed gastric emptying

A

Causes food stasis
Can result in reflux as not emptying fast enough
Backlog
Bloated pain

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11
Q

Rapid gastric emptying

A
  • can occur post gastric surgery used to treat peptic ulcers
  • causes “Dumping Syndrome” where food moves too quickly into duodenum and isn’t completely digested. Causes vomiting, diarrhoea, cramping, nausea
  • undigested food particles results in a hyper-osmotic chyme resulting in osmotic diarrhoea
  • rapid fluid shift into SI causes distension and pain
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12
Q

What is the role of gastric acid?

A
  • limited digestion role
  • main roles is sterilisation; ensures an environment that is hostile to bacteria EXCEPT helicobacter pylori
  • helps with absorption of iron and B12
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13
Q

What bacteria is gastric acid not effective against?

A

Helicobacter pylori

Causes peptic ulcers and cancer

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14
Q

What is absent or low gastric acid called and what is a condition of an example of where it may occur?

A

Achlorhydria

Occurs in Pernicious anaemia (antibodies to parietal cells and IF)

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15
Q

How is HCl secreted

A

By parietal cells in the body of the stomach
Parietal cells have proton pumps that secrete HCl
Parietal cells secrete 2L of gastric acid a day

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16
Q

What controls acid secretion?

A

Positive and negative feed back loops

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17
Q

When will acid secretion be affected?

A
  • surgery of the body of the stomach

- parietal cells affected

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18
Q

Describe a parietal cell

A
  • have K+/H+ ATPases (proton pumps)
  • reflux medications inhibit these pumps
  • H+ pumped into stomach
  • HCO3- pumped into the blood
  • via carbonic anhydrase
  • K+ and Cl- in cell
  • HCO3- and H+ out of cell
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19
Q

How is the gastric mucosa protected from gastric acid?

A
  • mucus layer
  • HCO3- secretion by parietal cells gets trapped in the mucus secretion
  • ensures the mucosa pH stays neutral
20
Q

How does medicine affect the mucosa?

A

Alkaline mucus layer can be compromised by medication/NSAIDs
Exposes the epithelium to acid
Ulceration and problem with healing due to no mucus or HCO3- layer and inability to rebuild mucosa

21
Q

Neurotransmitter?

A

A molecule that transmits a signal from one NEURON to another

22
Q

Auto/para/endocrine

A
  • molecule released by a cell that targets itself/adjacent cells
  • molecule/hormone released by endocrine cells into blood circulation to target distant cells
23
Q

Where are the endocrine cells of the stomach found?

A

Parietal and ECL - body

G and D cells .- antrum

24
Q

ECL cells

A

Enterchromaffin-like cells
Body
Histamine
Paracrine and act on pariteal cells to secrete HCl

25
Q

G cells

A

antrum
gastrin
hormone/endocrine
stimulate acid secretion by stimulating ECL cells

26
Q

D Cells

A

antrum
somatostatin
endocrine and paracrine
INHIBITS acid secretion by inhibitng G cells

27
Q

Vagal control

A

Vagus nerve and enteric nerves release ACh neurotransmitter that stimulates parietal cells, G Cells and ECL Cells

28
Q

When do you get increased gastric acid secretion?

A

Tumours that produce gastrin called gastrinomas

Can cause ulceration

29
Q

4 ways you can get decreased acid secretion?

A
  1. Pernicious anaemia (antibodies against P cells)
  2. Gastric surgery either body or antrum
  3. Vagomtomy (loss of vagus nerve so reduced ACh stimulation)
  4. Drugs (receptors that block proton pumps or histamine receptors on parietal cells i.e. reflux or heart burn)
30
Q

What are 3 other things that are secreted by the stomach

A
  1. Pepsinogen by chief cells, cleaved to form pepsin that degrades protein
  2. Intrinsic Factor - released by parietal cells that binds B12 in the duodenum
  3. Prostaglandins - lipid molecules involved in the protection and repair of the gastric mucosa (NSAIDs can inhibit these resulting in disruption of the integrity of the mucosa and eventual ulceration
31
Q

What are the 3 phases of the stomach

A

Celiac, gastric and intestinal phase

32
Q

What happens in the celiac phase

A
  • the celiac phase is initiated by the thought, sight and smell of food
  • brain gets stimulated and stimulates vagus and enteric nerves
  • ACh is released
  • stimulates G cells, parietal cells and ECL cells

The celiac phase prepares the stomach for food by increasing gastric secretion

33
Q

What happens in the gastric phase?

A
  • food enters the stomach
    1. Released AAs stimulate G cells
    2. Gastric distension stimulates stretch receptors > enteric nerves > ACh

= exponential release of HCl

34
Q

What happens in the intestinal phase?

A
  • finish meal and food enters duo
    1. HCl increase in stomach stimulates D cells > somatostatin > inhibits G cells
    2. AA/FA in duo stimulate I cells > CCK > inhibits gastric secretion and emptying, Gb contraction, pancreatic enz secretion
    3. HCl in duo > S cells > secretin > inhibit gastric and stimulates HCO3- from ductal cells in pancreas and bile duct
35
Q

What 3 diseases of the stomach and duodenum should I know

A

peptic ulcer disease, H pylori infection and gastric cancer

36
Q

Helicobacter pylori?

A
  • causes inflammation of the stomach (gastritis)
  • destroys mucosa so vulnerable to ulceration
  • most common cause of peptic ulcer disease
  • increases risk of gastric cancer and MALTomas
  • only infects humans and usually the antrum
  • person to person transmission (probably oral route)
  • often a childhood infection and once treated doesn’t usually re-infect
37
Q

Describe how H pylori infection may develop into peptic ulcer disease

A
  • infection (antrum)
  • persistent inflammation of the mucosa that erodes the protective barrier
  • mucosa exposed to acid
  • acidic environ makes it difficult for the mucosa to heal
  • persistent chronic inflam (gastritis)
  • often asymptomatic
  • ulceration (cavity due to mucosa erosion)
  • pain, bleeding in stomach or duodenum if penetrates BV
38
Q

How is H pylori treated

A
  • single antibiotic treatment doesn’t work despite successful in lab
  • triple therapy
    > OMEPRAZOLE (proton pump inhibitor) and 2 antibiotics for 14 days
  • low recurrence (resistance) rate when successfully treated
  • main risk of infection 0-5
39
Q

What are the main causes of peptic ulcer disease?

A
  • most common is H pylori
  • others incl aspirin and NSAIDs like voltaren and ibuprofen that inhibit prostaglandins that protect the integrity of the mucosa
40
Q

How did peptic ulcer disease use to be treated?

A
  • surgeries to reduce gastric acid secretion to give the mucosa time to heal including
    > gastrectomy (remove antrum - G cells)
    > vagotomy (part of vagus nerve to reduce ACh)
    > pyloroplasty (cut and re-suture pylorus to relax the sphincter so stomach empties faster, food is in the stomach for a shorter amount of time so there is less stimulation of gastric acid release and more inhibition by secretin and CCK
41
Q

Why did treatment of peptic ulcer disease change in 1986?

A

This is when helicobacter pylori was isolated allowing a treatment to be developed

42
Q

What are some symptoms of

A

pain
bleeding
perforation
obstruction in duodenum or pylorus due to swelling or scarring causing stricture

43
Q

What are the 2 types of gastric adenocarcinoma?

A

Intestinal

Diffuse

44
Q

Intestinal gastric adencarcinoma

A

well differentiated - distinct cells with distinct shape and function
cells arranged in a tubular/glandular formation

45
Q

Diffuse

A

poorly differentiated and lacks glandular formation
homogenous with no qualities or structure
diffuse gastric cancer can infiltrate the gastric wall - this is called linitis plastica

46
Q

h pylori and gastric cancer?

A
  • there is an association between h pylori and gastric cancer that is stronger for the intestinal type
  • h pylori may produce widespread inflammation that destroys parietal cells resulting in reduced gastric secretion (achlorhydria)
  • low acid results in bacterial overgrowth that may produce carcinogens

Digestive (24 decks)

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