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LS1 GI > Stomach > Flashcards

Stomach Flashcards

1
Q

What type of parietal cell receptor can be blocked pharmacologically to reduce stomach acid secretion?

A

H2 receptor (e.g. with H2 antagonists such as Ranitidine)

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2
Q

Name three receptors on parietal cells which when stimulated increase acid production

A
  1. H2 receptors (histamine receptor)
  2. Muscarinic receptor (ACh receptor)
  3. Gastrin receptor/ CCK receptor (gastrin and CCK have similar structures)
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3
Q

How do proton pump inhibitors (PPIs) work?

A

E.g. Omeprazole. They block the H+/K+ ATPase (proton pump), which actively transports H+ out of parietal cells onto the epithelial surface of the stomach

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4
Q

How does the stomach physically disrupt food?

A

Muscular contractions of the antrum - the antrum has thicker muscluar walls than the fundus or body

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5
Q

What the the function of receptive relaxation in the stomach?

A

It allows the stomach to distend when food enters to maintain a steady intraluminal pressure, preventing reflux

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6
Q

Stomach acid production is under neural, paracrine and endocrine control. Which substance is involved in paracrine control of stomach acid production?

A

Histamine released from ECL (enterochromaffin-like cells) (stimulates acid production by parietal cells)

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7
Q

Stomach acid production is under neural, paracrine and endocrine control. Which substance is involved in neural control of stomach acid production?

A

ACh neurotransmitter - stimulation from vagal nerve
GRP (gastrin-releasing peptide) - Released by nervous detection of stomach distension, which stimulates gastrin secretion and therefore stimulates H+ production in parietal cells

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8
Q

Stomach acid production is under neural, paracrine and endocrine control. Which substance is involved in endocrine control of stomach acid production?

A

Gastrin - released from G cells stimulates H+ production in parietal cells

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9
Q

Where are G-cells found?

A

Antrum

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10
Q

What is the effect of the hormone somatostatin?

A

It inhibits gastrin secretion in G cells which reduces the stimulation of gastrin on parietal cells, therefore less H+ is secreted into the stomach

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11
Q

Where is somatostatin secreted from and what stimulates this secretion?

A

Somatostatin is secreted from D cells in response to stimulation by stomach acid

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12
Q

Which two factors inhibit HCl secretion in the stomach?

A
  1. Low pH-> D-cell activation -> somatostatin release

2. Reduction in stomach distension -> decreased vagal activity…

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13
Q

What specialised cells in the stomach are responsible for the secretion of pepsinogen?

A

Chief cells

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14
Q

Which cells in the stomach produce mucous?

A

Mucous neck cells and surface mucous cells

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15
Q

What do parietal cells secrete?

A

Stomach acid and intrinsic factor

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16
Q

What do enteroendocrine cells secrete?

A

E.g. C-cells, D-cells and ECL cells. Hormones like gastrin and somatostatin

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17
Q

What type of chronic gastritis can lead to megaloblastic anaemia?

A

Chronic autoimmune gastritis - a process which attacks parietal cells which secrete intrinsic factor. Intrinsic factor is essential for absorption of vitamin B12. B12 deficiency leads to megaloblastic anaemia (pernicious anaemia)

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18
Q

What is megaloblastic anaemia?

A

A type of pernicious anaemia caused by inhibition of DNA synthesis during red blood cell production

19
Q

What type of anaemia can be caused by bacterial and reactive gastritis in severe cases?

A

Microcytic anaemia due to iron deficiency from blood loss

20
Q

What is the major function of the stomach?

A

Initial digestion - though salivary amylase in the oral cavity starts digestion

21
Q

What types of absorption occur in the stomach?

A

NO nutrient or water absorption

22
Q

What is the name of the first part of the duodenum which joins the stomach and what is it a common site for?

A

Duonenal bulb - a common site for peptic ulcers

23
Q

What is a peptic ulcer?

A

An umbrella term for any ulcer that happens in the stomach or duodenum

24
Q

What is receptive relaxation?

A

Relaxation and distension of the UPPER (thin-walled) portion of the stomach to maintain a steady pressure within the stomach, preventing reflux of contents into the oesophagus

25
Q

What triggers receptive relaxation?

A

Distension of distal oesophagus when food passes through it

26
Q

What gastric secretion can be considered part of the innate immune system?

A

Hydrochloric acid - kills many bacteria as they enter the stomach, therefore it acts as a chemical barrier to pathogens

27
Q

What is pepsinogen?

A

An inactive precursor to pepsin (protease), released by chief cells

28
Q

What do mucous cells secrete to protect the stomach epithelia from its own acid production?

A

mucus and bicarbonate ions

29
Q

What is the stomach’s “unstirred layer”?

A

A layer of mucus rich in bicarbonate ions that covers the stomach epithelium. This provides a physical barrier to H+ ions. H+ ions can only diffuse in slowly and they react with the basic groups in mucus and the bicarbonate ions -> neutralisation before they reach the epithelial cells

30
Q

What location of H. pylori colonisation in the stomach is most likely to result in gastric epithelial dysplasia?

A

It seems that body predominant colonisation of H.pylori in the stomach has an atrophic effect which can lead to stomach ulceration (and potentially dysplasia/cancer).

31
Q

What is the effect of H.pylori predominant colonisation of the antrum?

A

Results in the stimulation of G cells (and/or the suppression of D cells) and a resultant rise in acid secretion from parietal cells.
The increased acid secretion makes chyme more acidic as it leaves the stomach which can result in duodenal epithelial metaplasia. This metaplasia can allow H.pylori to colonise the duodenum which can lead to duodenal ulceration

32
Q

What is the effect of H.pylori colonisation of the body and antrum?

A

A diffuse colonisation in the body and antrum usually produces few symptoms

33
Q

What is the role of prostaglandin in the stomach?

A

Prostaglandins increase gastric mucosal blood flow. Good gastric mucosal blood flow is essential for maintaining a healthy cell turnover and cellular repair mechansims

34
Q

By what mechanism do NSAIDs promote epithelial damage and therefore increase the risk of peptic ulceration?

A

A number of mechanisms:

  1. Reduce prostaglandin synthesis -> reduced epithelial mucosa blood flow
  2. Reduces effectiveness of mucus barrier
  3. Topically irritant to the gastric epithelium
35
Q

What causes the ‘alkaline tide’ after a meal?

A

The movement of HCO3 across the basolateral membrane and into blood, causes the pH of the blood to rise transiently after a meal.

36
Q

How does H.pylori survive the acidic conditions of the stomach?

A

It produces urease an enzyme which converts naturally occuring urea in the stomach to ammonia and CO2. Ammonia forms a basic solution which raises the pH surrounding the H-pylori.

37
Q

Name two proposed mechanisms for how H-pylori cause chronic gastritis

A
  1. Release cytotoxins

2. Degrade the mucus layer of the stomach

38
Q

What type of pancreatic tumour causes Zollinger-Ellison syndrome?

A

Gastrin secreting tumour

39
Q

How is the severe ulceration of the stomach and small bowel, seen in Zollinger-Ellison syndrome, caused?

A

Gastrin-secreting tumour causes a proliferation of parietal cells and increased acid production.

40
Q

Which part of the stomach is particularly prone to ulceration?

A

Lesser curve of the stomach

41
Q

If a gastric ulcer were to erode through the posterior aspect of the body of the stomach, which major artery might be at risk of haemorrhage?

A

Splenic artery

42
Q

A gentlemen is admitted into hospital following severe abdominal pain and diarrhoea. Investigations reveal severe gastric ulceration that extends into the small intestine. A diagnosis of Zollinger-Elliosn syndrome (ZES) is made. What hormone is released in excess in ZES?

A

Gastrin - from a non-beta cell gastrin secreting tumour of the pancreas

43
Q

What is somatostatin stimulated by and what is its effect?

A

Its a hormone that is stimulated by low stomach pH and inhibits the production of gastrin (from G-cells) and therefore gastrin’s stimulation of HCl release from parietal cells

44
Q

What mechanisms prevent gastro-oesophageal reflux?

A
  1. Acute angle of the oesophagus into the stomach
  2. Positive intra-abdominal pressure -> walls of the intra-abdominal section of the oesophagus are compressed
  3. Folds of mucosa -> help occlude the lumen at the gastro-oesophageal junction
  4. The right crus of the diaphragm

LS1 GI (17 decks)

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