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SA gastro-intestine > S5) Function and Pathology of the Stomach > Flashcards

S5) Function and Pathology of the Stomach Flashcards

1
Q

What do epithelial cells do in the stomach?

A

Epithelial cells cover the surface and extend into pits/glands

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2
Q

Identify 4 epithelial cells in the stomach

A
  • Mucous cells
  • Parietal cells
  • Chief cells
  • G cells
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3
Q

Identify the muscle layers in the stomach

A
  • Circular
  • Longitudinal
  • Oblique

(the shape of the stomach also means that food has to travel downwards)

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4
Q

What is the effect of stomach muscle contractions?

A
  • Mix/grind contents
  • Move contents along
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5
Q

What is the function of the upper stomach?

A

The upper stomach has sustained contractions (tonic) to create basal tone

slow

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6
Q

The lower stomach is more muscular.

Describe its function

A

The lower stomach has strong peristalsis which mixes stomach contents

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7
Q

Describe how contractions occur in the stomach

A
  • Contractions are coordinated
  • Contractions occur every 20 seconds
  • Contraction are proximal to distal
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8
Q

What is receptive relaxation?

A

Receptive relaxation is the vagally mediated relaxation of orad stomach

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9
Q

What is the purpose of receptive relaxation?

A
  • Allows food to enter stomach without raising intra-gastric pressure too much
  • Prevents reflux of stomach contents when swallowing
  • Gastric mucosal folds (rugae) allow distension
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10
Q

Identify 3 functions of the acidic conditions of the stomach

A
  • Helps unravel proteins
  • Activates proteases: pepsinogen → pepsin
  • Disinfects stomach contents
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11
Q

Identify 4 substances which are secreted by the stomach

A
  • HCl
  • Intrinsic factor
  • Mucus/HCO3-
  • Pepsinogen (pepsin)
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12
Q

Identify the substances secreted from the following cells:

  • Parietal cell
  • G cell
  • Enterochromaffin like cell
A
  • Parietal cell: HCl & intrinsic factor
  • G cell: gastrin
  • Enterochromaffin like cell (ECL): histamine
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13
Q

Identify the substances secreted from the following cells:

  • Chief cell
  • D cells
  • Mucous cells
A
  • Chief cell: pepsinogen
  • D cells: somatostatin
  • Mucous cells: mucus
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14
Q

Identify the substances secreted from the following regions in the stomach:

  • Cardia
  • Fundus/body
  • Pylorus
A
  • Cardia: predominantly mucus secretion
  • Fundus/body: mucus, HCL, pepsinogen
  • Pylorus: gastrin, somatostatin
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15
Q

Identify the 3 substances which stimulate HCl production and state their origins

A
  • Gastrin from G cell
  • Histamine from ECL cells
  • Acetylcholine from vagus nerve
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16
Q

Where are G cells located?

A

G cells located in antrum

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17
Q

Identify the 2 factors which stimulate Gastrin secretion

A
  • Peptides/AA in stomach lumen
  • Vagal stimulation: (parasympathetic)

I. Acetylcholine

II. Gastrin-releasing peptide (GRP)

gastrin binds to CCK receptors

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18
Q

When food leaves the stomach, the pH drops.

How can HCl production be inhibted?

A
  • Low pH stimulates D cells which release somatostatin
  • Somatostatin inhibits G cells and ECL cells
  • Stomach distension reduces due to reduced vagal activity
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19
Q

Identify the 3 phases of digestion

A
  • Cephalic
  • Gastric
  • Intestinal
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20
Q

How much HCl is produced in the cephalic phase?

A

30% of total HCl

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21
Q

Outline the parasympathetic stimuli in the cephalic phase of digestion

A
  • Smelling, tasting, chewing, swallowing (sensory triggers)
  • Direct stimulation of parietal cells by vagus nerve
  • Vagus nerve releases GRP which stimulates of G cells
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22
Q

How much HCl is produced in the gastric phase of digestion?

A

60% of total HCl

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23
Q

State 4 events which occur in the gastric phase of digestion

A
  • Stomach distension and stretch stimulates vagus nerve
  • Vagus nerve stimulates parietal cells and G cells
  • Amino acids and small peptides stimulates G cells
  • Presence of food acts removes inhibition on Gastrin production (buffer) and the pH increases slightly
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24
Q

What is the role of the enteric nervous system in the gastric phase of digestion?

A

ENS and gastrin causes strong smooth muscle contractions

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25
Q

How much HCl is produced in the intestinal phase of digestion?

A

10% of total HCl production

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26
Q

State the 4 events occurring in the intestinal phase of digestion

A
  • Chyme stimulates gastrin secretion due to the detection of partially digested proteins by duodenum
  • G cells are then inhibited
  • Enterogastric reflex is activated by lipids which reduces vagal stimulation
  • Chyme then stimulates CCK and secretin
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27
Q

Which substances are released to protect the stomach lining?

A
  • Mucus
  • HCO3-
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28
Q

Where are mucus and hydrogen carbonate secreted from in the stomach?

A
  • Surface mucus cells
  • Neck cells in gastric glands
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29
Q

What are the effects of mucus and hydrogen carbonate secretion in the stomach?

A
  • Thick alkaline viscous layer is formed which adheres to epithelium
  • Epithelial surface kept at higher pH
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30
Q

Apart from mucus/HCO3-, identify and describe 2 other stomach defences

A
  • High turnover of epithelial cells to keep epithelia intact
  • Prostaglandins to maintain mucosal blood flow and supply epithelium with nutrients
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31
Q

Identify 3 substances that breach the stomach defences and state their effects

A
  • Alcohol – dissolves mucus layer
  • Helicobacter pylori – causes chronic active gastritis
  • NSAIDS – inhibits prostaglandins
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32
Q

Up to 40% of adults suffer from dyspepsia per year.

What is dyspepsia?

A

Dyspepsia is pain/discomfort in the upper abdomen

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33
Q

Identify 6 common gastric disorders

A
  • Gastro-oesophageal reflux disease (GORD)
  • Gastritis
  • Peptic ulcer disease
  • Zollinger-Ellison disease
  • Stress ulcers
  • Stomach cancer
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34
Q

What is GORD?

A

Gastro-oesophageal reflux disease (GORD) is a digestive disorder that affects the lower oesophageal sphincter and causes the reflux of stomach acid/contents into the oesophagus

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35
Q

Identify 4 symptoms of GORD

A
  • Heartburn
  • Cough
  • Sore throat
  • Dysphagia
36
Q

Identify 4 causes of GORD

A
  • LOS problems
  • Delayed gastric emptying (raised intra-gastric pressure)
  • Hiatus hernia
  • Obesity
37
Q

Identify 3 compound problems which can arise from GORD?

A
  • Oesophagitis → lots of bleeding
  • Strictures → hard to swallow
  • Barrett’s oesophagus (metaplasia)
38
Q

Identify 3 types of treatment for GORD

A
  • Lifestyle modifications: weight loss, smaller meals, don’t smoke
  • Pharmacological
  • Surgery (rare) fundoplication → wrap funds around spinster and lowers oesophagus below diaphragm
39
Q

Identify 3 types of pharmacological treatments for GORD

A
  • Antacids
  • H2 antagonists
  • Proton pump inhibitors ( reduces symptoms and heals inflammation)
40
Q

What is Barrett’s Oesophagus?

A
  • Barrett’s oesophagus is the metaplasia of squamous epithelium to columnar
  • It increases the risk of developing adenocarcinoma (30-40x) metaplasia can turn into dysplasia where there is no turning back
41
Q

What is gastritis?

A

Gastritis is a condition involving the inflammation of the stomach lining

42
Q

What are the 2 types of gastritis which can occur in the body?

A
  • Acute (can then lead to chronic)
  • Chronic
43
Q

Acute gastritis is an acute mucosal inflammatory process.

Identify 4 of its causes

A
  • Heavy use of NSAIDS
  • Lots of alcohol
  • Chemotherapy
  • Bile reflux
44
Q

Identify the possible symptoms which may arise from acute gastritis

A
  • Either: asymptomatic
  • Or: pain, nausea, vomiting and occasional bleeding
45
Q

What are the 2 types of chronic gastritis which can occur in the body?

A
  • Autoimmune
  • Bacterial
46
Q

Compare and contrast the causes of chronic autoimmune and bacterial gastritis

A
  • Bacterial Gastritis – caused by H. pylori infection (commonly)
  • Autoimmune Gastritis – caused by antibodies to gastric parietal cells
47
Q

Identify a complication of chronic autoimmune gastritis

A

Autoimmune gastritis can lead to pernicious anaemia

  1. antibodies attack parietal cells
  2. reduced acid production and intrinsic factor
  3. less intrinsic factor → reduced absorption of B 12
  4. less absorbed in the ilium
48
Q

Identify the possible symptoms which may arise from chronic bacterial gastritis

A
  • Either: asymptomatic
  • Or: pain, nausea, vomiting and occasional bleeding
49
Q

In chronic bacterial gastritis, symptoms may develop due to complications.

Identify 3 of its complications

A
  • Peptic ulcers
  • Adenocarcinoma
  • MALT lymphoma
50
Q

Identify the symptoms of chronic autoimmune gastritis

A
  • Symptoms of anaemia
  • Glossitis (swelling of tongue)
  • Anorexia (hard to eat)
  • Neurological symptoms
51
Q

What is peptic ulcer disease?

A

Peptic ulcer disease is a condition which occurs when ulcers form and extend into the muscularis mucosae of the stomach due to defects in the gastric/duodenal mucosa

52
Q

Identify 2 common locations of peptic ulcers

A
  • Most common in first part of duodenum
  • Commonly affects lesser curve of stomach
53
Q

Peptic ulcer disease is caused by mucosal injury.

Identify 3 factors which may cause/contribute to this injury

A
  • Stomach acid
  • H. pylori
  • NSAIDS
54
Q

A major symptom of peptic ulcer disease is epigastric pain.

Describe the features of this pain

A
  • Burning/gnawing
  • Follows meal times
  • Often at night (especially DU)
55
Q

Identify 3 serious symptoms of peptic ulcer disease

A
  • Bleeding/anaemia
  • Satiety (early)
  • Weight loss → early satiety as stomach can’t expand due to scar tissue
56
Q

What is Zollinger-Ellison syndrome?

A

Zollinger-Ellison syndrome is a condition when 1/more gastrin-secreting tumors (gastrinoma) form in your pancreas and duodenum

57
Q

What is stomach cancer?

A

Stomach cancer is a condition which involves tumour formation in the stomach lining

58
Q

Identify 4 different means of diagnosing gastric pathology

A
  • Upper GI endoscopy (biopsies/H-pylori)
  • Urease breath test
  • Erect chest X-ray (perforation)
  • Blood test (anaemia)
59
Q

Identify 3 ways of treating gastric pathologies

A
  • Eradicate H-pylori (PPI+ Clarithromycin + Amoxicillin)
  • Stop NSAIDS
  • PPIs
60
Q

Identify 2 pharmacological interventions for gastritis and provide examples for each

A
  • H2 blockers e.g. cimetidine, ranitidine
  • Proton pump inhibitors e.g. omeprazole
61
Q

Describe the structure, function and location of Helicobacter pylori

A
  • Structure: helix shaped, gram negative, flagellum
  • Function: produces urease, converts urea to ammonium, increases local pH
  • Location: mucus layer/adheres to gastric epithelia
62
Q

How does H.pylori spread?

A

Oral to oral/faecal to oral

63
Q

Identify 3 of H.pylori’s destructive functions

A
  • Releases enzymes (urease) causing direct epithelial injury
  • Degrades mucus layer
  • Promotes inflammatory response (self injury)
64
Q

State how the symptoms of H.pylori vary according to location

A
  • Antrum: duodenal ulceration
  • Antrum and body: asymptomatic
  • Body: leads to cancer
65
Q

Identify 5 causes of stress ulcerations

A
  • Severe burns
  • Raised intracranial pressure
  • Sepsis
  • Severe trauma
  • Multiple organ failure
66
Q

what are the different types of cells in the stomach

A
  • stratified squamous lines the oesophagus
  • simple columnar lines the cardia
67
Q

what is the role of the right crus of the diaphragm

A

it is around the lower oesophageal sphincter and it closes around it when pressure starts to increase in stomach

67
Q

what is the role of the right crus of the diaphragm

A

it is around the lower oesophageal sphincter and it closes around it when pressure starts to increase in stomach

68
Q

what cells do gastric glands contain

A
  • parietal cells (acid)
  • chief cell (inactive form of pepsin - pepsinogen)
  • enteroendocrine (G cells to release gastrin)
69
Q

how does acid secretion work

A
  • parietal cells use H/K proton pumps and exchange K for H
70
Q

parietal cells in their resting and active states

A
  • RESTING: apical membrane contains K and tubovesicles contain H, they are not in contact
  • STIMULATED: when stimulated the tubercles move up the K and H are now in contact
71
Q

how does histamine work to secrete acid

A
  • ECL cells (enters-chromaffin cells) secrete histamine
  • ECL can be stimulated by either vagus or Ach
  • then it secretes histamine
  • promotes acid secretion
72
Q

how is HCL actually produced in the parietal cell

A
  1. H20 + C02 → H2co3 (carbonic acid) in the cell
  2. H2co3 → Hco3- + H+ via carbonic anhydrase
  3. Hco3- exits cell into the Venous blood (alkaline) via Hco3/Cl transporter
  4. H passes into lumen of stomach through H/K atpase
  5. Cl enters the cell as Hco3- exits into blood
  6. cl moves out of the cell into lumen of stomach
  7. H + Cl → HCL
73
Q

what are some pathological changes in gastritis

A
  1. epithelial damage
  2. hyperplasia
  3. vasodilation
  4. neutrophil and lymphocyte response
  5. glandular atrophy
  6. fibrotic changes
74
Q

features of H pylori which make it easy to attack the stomach

A
  1. helix shape, gram negative, flagella and chemotaxis
  2. needs some 02 stomach has the perfect amount
  3. has adhesions that fix to the stomach epithelium and resist peristalsis
  4. produces ammonia to change stomach pH and adapt via urease (ammonia leads to cell damage)
75
Q

which 3 things does H pylori secrete to damage the stomach?

A
  1. CagA → causes inflammation and increases risk factor for stomach cancer
  2. VacA → toxic and increases paracellular permeability
  3. mucinase, protease and lipases that break down mucus and stomach wall epithelia
76
Q

how can H pylori spread to the duodenum?

A
  1. stimulate G cells in the antrum
  2. more parietal cells release more acid
  3. chyme more acidic
  4. damage cells of duodenum
  5. changes to gastric cells and so colonisation of H pylori
  6. can cause ulcers
77
Q

what happens if H pylori mainly colonises in the body of the stomach

A
  1. atrophy of parietal cells
  2. increase of cancer risk
78
Q

how to diagnose if someone is infected with H pylori

A
  • use a urease breath test and detect amount of c13 someone exhales.
  • if its higher than usual they are infected with H pylori
79
Q

treatment of H pylori

A

proton pump inhibitor and antibiotics for 7 days

80
Q

difference between acute and chronic ulcers

A

acute: develop as part of acute gastritis
chronic: occur at mucosal junctions

81
Q

what are some differences between gastric and duodenal chyme

A

Composition: Gastric chyme is acidic and contains large food particles that have been broken down by mechanical and chemical digestion in the stomach. Duodenal chyme, on the other hand, is neutralized by bicarbonate secreted by the pancreas and contains smaller food particles that have been further broken down by enzymes.

pH: Gastric chyme has a pH of around 2-3 due to the presence of hydrochloric acid secreted by the stomach, while duodenal chyme has a pH of around 7-8 due to the neutralizing effect of bicarbonate.

Digestive enzymes: Gastric chyme contains pepsin, an enzyme that breaks down proteins, while duodenal chyme contains pancreatic enzymes such as amylase, lipase, and proteases that break down carbohydrates, fats, and proteins, respectively.

Hormonal regulation: The release of gastric chyme into the duodenum stimulates the release of hormones such as secretin and cholecystokinin (CCK) that regulate the secretion of digestive enzymes from the pancreas and gallbladder, respectively.

82
Q

anatomy of peptic ulcer disease

A

scar tissue can be laid down and lead into peritonitis (inflammation of peritoneal cavity)

83
Q

erosion of ulcers into blood vessels

A
  1. ulcers can erode into the gastro-duodenal artery
  2. this lies behind the duodenum
  3. if so you get an upper GI bleed
  4. malaena is present due to digestion of blood
84
Q

how to treat peptic ulcer disease

A
  1. if H pylori is present, eradicate
  2. if its not, stop use of meds like NSAIDS

SA gastro-intestine (19 decks)

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