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Y2 GI block > PBL 1 > Flashcards

PBL 1 Flashcards

1
Q

What region of the stomach is the cardia?

A

point where the oesophagus connects to the stomach and through which food passes into the stomach

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2
Q

What shape is the fundus and whereabouts in the stomach is it ?

A

dome shaped, upper region of stomach, above and to the left of the cardia

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3
Q

what is the main part of the stomach called?

A

Body

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4
Q

What shape is the pylorus and what does it do?

A

funnel shaped, connects the stomach to the duodenum

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5
Q

Pyloric antrum: BLANK end of pylorus which connects to BLANK

Pyloric canal – BLANK end of pylorus which connects to BLANK

A

Pyloric antrum – wider end of pylorus which connects to body of the stomach
Pyloric canal – narrower end of pylorus which connects to duodenum

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6
Q

What is the pyloric sphincter? what does it do?

A

smooth muscle which controls emptying/flow of chyme from stomach to SI

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7
Q

What are rugae and what do they allow the stomach to do?

A

They are folds in the stomach

They allow the stomach to stretch to accommodate large meals

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8
Q

What are the main histological layers of the stomach including plexuses

A 
Mucosa
Submucosa 
- - - SUBMUCOSAL PLEXUS - - - 
Muscularis externa
- - - MYENTERIC PLEXUS - - -
Serosa
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9
Q

what are the divisions of the mucosal layer of the stomach and what type of epithelium is found ?

A

Epithelium - simple columnar epithelium
Lamina Propria
Muscularis Mucosae

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10
Q

What is the role of the muscularis mucosae in the stomach?

A

thin layer of smooth muscle that contracts and helps break down food

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11
Q

function of surface mucus cells

A

secrete protective, thick alkaline mucus which provides lubrication and protects from acidic HCl

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12
Q

function of parietal cells and where they’re found?

A

Fundus/body

Secretes HCl and intrinsic factor

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13
Q

List the functions of Hcl

A
  • converts pepsinogen into pepsin
  • connective tissue and muscle fibre breakdown
  • Denatures protein
  • Barrier immunity from harmful bacteria/microbes
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14
Q

What is the function of intrinsic factor ?

A

needed for vitamin B12 absorption

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15
Q

What is the function of chief cells?

A

Secrete pepsinogen

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16
Q

What is pepsinogen and its function?

A

precursor of pepsin

Breaks down protein into peptides and amino acids

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17
Q

Where are G cells found and what is their function

A

Antrum

Secrete the hormone Gastrin

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18
Q

Function of gastrin?

A

stimulates secretion of gastric acid

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19
Q

What is the function of mucus neck cells? where are they found?

A

secrete thin, acidic mucus

fundus/body

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20
Q

how do mucus neck cells differ from surface mucus cells

A

Mucus neck: acidic

Surface mucous: alkaline

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21
Q

What do ECL cells secrete?

A

Histamine

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22
Q

What do D cells secrete?

A

Somatostatin

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23
Q

How many layers of muscle does the musculAris externa of the stomach have? What are they in order From inner to outer?

A

3
Inner to outer:
Oblique, circular, longitudinal

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24
Q

between what muscle layers is the myenteric plexus found?

A

Between circular and longitudinal

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25
Q

The portion of the serosa covering the stomach is known as ?

A

visceral peritoneum

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26
Q

At the lesser curvature of the stomach, the visceral peritoneum extends upwards to the liver as the _______?

A

lesser omentum

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27
Q

At the greater curvature of the stomach, the visceral peritoneum that hangs down from the stomach like an apron is known as_______?

A

greater omentum

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28
Q

Where are Brunner’s glands found and what is their role?

A

Duodenum

They secrete alkaline mucus which neutralises the gastric acid in chyme

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29
Q

What are the 4 parts of the duodenum?

A

superior, descending, horizontal and ascending

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30
Q

in which part of the duodenum is the duodenal bulb found? what is the duodenal bulb the common site for?

A

superior

Duodenal ulcerations

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31
Q

In which part of the duodenum is the major duodenal papilla found?

A

Descending

32
Q

What are the contents of gastric juice?

A

 Hydrochloric acid
 Pepsin
 Mucin
 Intrinsic factor

33
Q

What are the phases of gastric secretion and what proportion of gastric acid is made in each?

A
  • Cephalic phase (35% of total)
  • Gastric phase (60% of total)
  • Intestinal phase (5% of total)
34
Q

For the cephalic phase: explain what stimulates it and its process of increasing gastric secretion

A

Stimulated by the sight, thought, taste or smell of food.
This increases parasympathetic activity and stimulates the vagus nerve to release ACh.
ACh stimulates parietal cells to increase gastric acid secretion

35
Q

How long does the gastric phase last and what triggers it?

A

3-4 hours

triggered by entry of food into the stomach

36
Q

Describe how there is increased gastric secretion in the Gastric phase

A

Distention of the stomach due to food entry –> activates stretch receptors –> stimulates parasympathetic nerves to release Acetyl Choline –> acts on gastrin-releasing cells, Histamine releasing cells and parietal cells –> increased gastric secretion

Partially digested proteins (chyme), caffreine, RISING pH –> stimulate G cells to release Gastrin –> induces parietal cells to increase HCL production

37
Q

Describe the intestinal phase of gastric secretion

A

Entry of partially digested foods in the duodenum: results in a brief stage of gastrin secretion from Duodenal G cells

As chyme distends the duodenum, it triggers an enterogastric reflex, which suppresses gastric secretory activity. This is due to:

Presence of low pH = S cells release Secretin which inhibits gastrin releases and reduces the affinity of parietal cells to gastrin.

Presence of lips and carbohydrates = release of CCK and Gastric Inhibitory Peptide (GIP) which both inhibit gastrin release

38
Q

gastriN secretion is inhibited at lumen pH

A

pH < 2

39
Q

Describe the action of AcetylCholine

A

Acts on G cells to stimulate Gastrin release
Acts on Parietal cells to stimulate HCl release
Acts on Chief cells to stimulate pepsinogen release
Acts on ECL cells to stimulate Histamine release

40
Q

Describe the action of Gastrin and where is it released from?

A

Gastrin is released from antral G cells.

Gastrin binds to Cholecystokinin receptors (CCK-2R) on the surface of enterochromaffin-like (ECL) cells, which in turn release Histamine.
Alternatively, Gastrin can bind directly to CCK-2R receptors on Parietal cells

41
Q

Describe the action of Histamine

A

The Histamine binds to H2 receptors on parietal cells. promotes HCL acid secretion

This leads to the secretion of Hydrogen (H+) ions into the stomach in exchange for Potassium (K+) ions by a K+/H+ ATPase (protein pump) at the apical membrane.

42
Q

What is the role of carbonic anhydrase in Parietal cells?

A

Carbonic anhydrase catalyses the combination of CO2 and water to form carbonic acid.
Carbonic acid dissociates into Bicarbonate and H+ ions. Bicarbonate ions exchange across the basal membrane for Cl-. (Cl released into stomach)

43
Q

What produces Somatostatin and describe its action

A

Somatostatin is produced by D cells and binds to the SST2R receptors. It has an inhibitory effect on ECL cells, parietal cells and G cells.

44
Q

What is the action of prostaglandins once released into the stomach and duodenum?

A

They stimulate mucous and bicarbonate secretion and also have an inhibitory effect on ECL cells

45
Q

Define peptic ulcer disease

A

The erosion of the mucosal lining down to the muscularis mucosa, which is more than 5mm in diameter.

46
Q

Gastric ulcers typically form in the ?

A

lesser curvature of the antrum

47
Q

List 5 clinical features of peptic ulcer disease

A 
	Recurrent, burning abdominal pain 
	Patient points with single finger to the epigastrium as the site of pain
	DU pain typically occurs at night
	Epigastric tenderness
	Nausea or vomiting
	Weight loss/anorexia
	Fatty food intolerance 
	Feeling of fullness, bloating, belching
48
Q

List causes of Peptic Ulcer Disease

A 
o	H. Pylori bacteria 
o	NSAIDs
o	Zollinger Ellison Syndrome
o	Smoking
        Alcohol
        Stress
49
Q

List features of H pylori (description of the bacteria)

A

o Gram-negative, spiral shaped bacteria
o Multiple flagella
o Has lipopolysaccharides (adhesions) –help them adhere to cells
o Urease enzyme on surface
o Secretes cytotoxins which damage cells (e.g. VacA – causes cell apoptosis, CagA – disrupts cell structure/integrity and causes inflammation

50
Q

H. Pylori is usually found in ___% of people

A

50%

51
Q

What region of the stomach do H.pylori colonise and how are they able to do this?

A

H. pylori colonise the mucous layer in the gastric antrum.

Their multiple flagella make them motile and allows them to burrow and live under the mucous layer.

52
Q

How is H. pylori able to survive the acidic conditions of the stomach?

A

H. pylori are able to surpass the gastric acid due to the urease on their surface.

This is an enzyme that converts urea (naturally present in stomach) into carbon dioxide and ammonia.

The ammonia neutralises the acidity and the flagella help it burrow down to the epithelial cells.

53
Q

How do H.Pylori adhere to gastric epithelial cells?

A

The lipopolysaccharides help H. Pylori adhere to the gastric epithelial cells. (adheres via these adhesion molecules e.g. BabA. BabA binds to Lewis antigen which is expressed on the surface of gastric mucosal cells)

54
Q

What are the 2 endotoxins secreted by H. pylori ?

A

Cag A

Vac A

55
Q

What is the role of Cag A? Describe its action

A

Cag A breaks down the junctions between epithelial cells. It also stimulates the production of cytokines (IL-8) to induce an inflammatory response.

The inflammatory response results in even more HCl being secreted by parietal cells due to histamine. This can enter the duodenum, which is usually basic, so H. pylori infection can result in duodenal ulcer

56
Q

What is the role of Vac A? Describe its action

A

Vac A causes apoptosis of the epithelial cells. The acid and mucus layer come in/down and damage the surrounding tissue, creating an ulcer.

57
Q

Describe how NSAIDs cause peptic ulcers

A

NSAIDs inhibit the enzyme cyclooxygenase which inhibits the synthesis of prostaglandins. This leaves the gastric mucosa susceptible to damage

58
Q

Describe Zollinger-Ellison Syndrome

A

Presence of a gastrinoma (neuroendocrine tumour). It secretes abnormal amounts of gastrin which increases stomach acid and causes ulcers.

59
Q

List the non-invasive methods of diagnosis peptic ulcer disease

A

Serological tests
13C-Urea breath test
Stool antigen test

60
Q

What does the serological test check for?

A

blood test to detect IgG antibodies

61
Q

Describe the 13C-Urea breath test

A

13C urea sample is ingested. Using a spectrometer, the amount of CO2 in the patient’s breath is measured after ingestion

62
Q

Describe the stool antigen test

A

monoclonal antibodies are used to detect H. pylori antigens in stool

63
Q

what are the two types of peptic ulcer disease?

A

gastric ulcer

Duodenal ulcer

64
Q

list complications of peptic ulcer disease

A

Perforation

haemorrhage

65
Q

List the invasive methods of diagnosis peptic ulcer disease

A 
Endoscopy (biopsy may also be taken)
Histology (section of biopsy is stained)
Biopsy urease test
Culture medium
Barium Swallow (X-ray)
66
Q

Describe the Biopsy urease test

A

Biopsy is added to a substrate containing urea and phenol red. If peptic ulcer is present, the urease from H. pylori will break down the urea into ammonia and CO2. This raises the pH of the solution and causes a colour change.

67
Q

explain the use of culture mediums in the diagnosis of PUD

A

Biopsies can be cultured in a medium and sensitivities to antibiotics can be checked to identify an appropriate antibiotic regimen

68
Q

Describe the treatment regimen for PUD

A

Triple therapy comprising a PPI and 2 antibiotics

69
Q

List the treatments for Peptic Ulcer Disease with examples

A

o Antibiotics e.g. Amoxycillin, Clarithromycin, Metronidazole
o Proton Pump Inhibitors E.g. Omeprazole, Lansoprazole
o Histamine (H-2) receptor antagonists e.g. cimetidine, ranitidine
o Antacids e.g. Pepto-Bismol, milk of magnesia
o Cytoprotective medication (that protect the lining of the stomach and small intestine) e.g. sucralfate
o Surgery – e a gastrectomy or vagotomy

70
Q

In what situation would surgery be considered as a treatment option for PUD?

A

Surgery – only used if complications occur (perforation or haemorrhage).

71
Q

list ways of managing PUD

A
  • Healthy diet – including probiotics
  • Eliminate milk
  • Control stress
  • Don’t smoke
  • Limit or avoid alcohol
  • Stop ingestion of NSAIDs
72
Q

Discuss how H2 receptor antagonists work

A

Completely inhibit histamine actions at all H2 receptors
Therefore inhibit gastric secretions too.
Also promote healing of gastric and duodenal ulcers.

73
Q

Discuss how PPIs work

A

irreversibly inhibit H+ K+ ATPase (protein pump)
PPIs are weak bases and they accumulate in the acidic environment of the secretory canaliculus of the stimulated parietal cell, where the pH is 1.0. It is converted into an achiral form and is able to react with and inactivate the ATPase.

74
Q

List some side effects of PPIs

A

Reduced gastric acid production:
 Reduces nutrient absorption
 Reduced gastric antimicrobial function

Increase in serum Gastrin levels
 Neoplasia
 Osteoporosis

75
Q

In what percentage of people is H pylori found in?

A

50%

76
Q

Discuss the epidemiology of peptic ulcer disease

A

Prevalence of H. pylori is high in developing countries (80-90%) and much lower in developed countries (20-50%).

In the developed world, incidence of NSAID-induced peptic ulcers is higher, as the H. pylori prevalence is lower.

77
Q

Where are glands that produce pepsinogen and hydrochloric acid found?

A

Body and Fundus of the stomach

Y2 GI block (25 decks)

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