PBL 1 Flashcards
(77 cards)
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
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
3
Q
what is the main part of the stomach called?
A
Body
4
Q
What shape is the pylorus and what does it do?
A
funnel shaped, connects the stomach to the duodenum
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
6
Q
What is the pyloric sphincter? what does it do?
A
smooth muscle which controls emptying/flow of chyme from stomach to SI
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
8
Q
What are the main histological layers of the stomach including plexuses
A
Mucosa Submucosa - - - SUBMUCOSAL PLEXUS - - - Muscularis externa - - - MYENTERIC PLEXUS - - - Serosa
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
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
11
Q
function of surface mucus cells
A
secrete protective, thick alkaline mucus which provides lubrication and protects from acidic HCl
12
Q
function of parietal cells and where they’re found?
A
Fundus/body
Secretes HCl and intrinsic factor
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
14
Q
What is the function of intrinsic factor ?
A
needed for vitamin B12 absorption
15
Q
What is the function of chief cells?
A
Secrete pepsinogen
16
Q
What is pepsinogen and its function?
A
precursor of pepsin
Breaks down protein into peptides and amino acids
17
Q
Where are G cells found and what is their function
A
Antrum
Secrete the hormone Gastrin
18
Q
Function of gastrin?
A
stimulates secretion of gastric acid
19
Q
What is the function of mucus neck cells? where are they found?
A
secrete thin, acidic mucus
fundus/body
20
Q
how do mucus neck cells differ from surface mucus cells
A
Mucus neck: acidic
Surface mucous: alkaline
21
Q
What do ECL cells secrete?
A
Histamine
22
Q
What do D cells secrete?
A
Somatostatin
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
24
Q
between what muscle layers is the myenteric plexus found?
A
Between circular and longitudinal
25
The portion of the serosa covering the stomach is known as ?
visceral peritoneum
26
At the lesser curvature of the stomach, the visceral peritoneum extends upwards to the liver as the _______?
lesser omentum
27
At the greater curvature of the stomach, the visceral peritoneum that hangs down from the stomach like an apron is known as_______?
greater omentum
28
Where are Brunner's glands found and what is their role?
Duodenum
| They secrete alkaline mucus which neutralises the gastric acid in chyme
29
What are the 4 parts of the duodenum?
superior, descending, horizontal and ascending
30
in which part of the duodenum is the duodenal bulb found? what is the duodenal bulb the common site for?
superior
| Duodenal ulcerations
31
In which part of the duodenum is the major duodenal papilla found?
Descending
32
What are the contents of gastric juice?
Hydrochloric acid
Pepsin
Mucin
Intrinsic factor
33
What are the phases of gastric secretion and what proportion of gastric acid is made in each?
* Cephalic phase (35% of total)
* Gastric phase (60% of total)
* Intestinal phase (5% of total)
34
For the cephalic phase: explain what stimulates it and its process of increasing gastric secretion
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
How long does the gastric phase last and what triggers it?
3-4 hours
| triggered by entry of food into the stomach
36
Describe how there is increased gastric secretion in the Gastric phase
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
Describe the intestinal phase of gastric secretion
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
gastriN secretion is inhibited at lumen pH
pH < 2
39
Describe the action of AcetylCholine
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
Describe the action of Gastrin and where is it released from?
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
Describe the action of Histamine
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
What is the role of carbonic anhydrase in Parietal cells?
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
What produces Somatostatin and describe its action
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
What is the action of prostaglandins once released into the stomach and duodenum?
They stimulate mucous and bicarbonate secretion and also have an inhibitory effect on ECL cells
45
Define peptic ulcer disease
The erosion of the mucosal lining down to the muscularis mucosa, which is more than 5mm in diameter.
46
Gastric ulcers typically form in the ?
lesser curvature of the antrum
47
List 5 clinical features of peptic ulcer disease
```
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
List causes of Peptic Ulcer Disease
```
o H. Pylori bacteria
o NSAIDs
o Zollinger Ellison Syndrome
o Smoking
Alcohol
Stress
```
49
List features of H pylori (description of the bacteria)
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
H. Pylori is usually found in ___% of people
50%
51
What region of the stomach do H.pylori colonise and how are they able to do this?
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
How is H. pylori able to survive the acidic conditions of the stomach?
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
How do H.Pylori adhere to gastric epithelial cells?
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
What are the 2 endotoxins secreted by H. pylori ?
Cag A
| Vac A
55
What is the role of Cag A? Describe its action
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
What is the role of Vac A? Describe its action
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
Describe how NSAIDs cause peptic ulcers
NSAIDs inhibit the enzyme cyclooxygenase which inhibits the synthesis of prostaglandins. This leaves the gastric mucosa susceptible to damage
58
Describe Zollinger-Ellison Syndrome
Presence of a gastrinoma (neuroendocrine tumour). It secretes abnormal amounts of gastrin which increases stomach acid and causes ulcers.
59
List the non-invasive methods of diagnosis peptic ulcer disease
Serological tests
13C-Urea breath test
Stool antigen test
60
What does the serological test check for?
blood test to detect IgG antibodies
61
Describe the 13C-Urea breath test
13C urea sample is ingested. Using a spectrometer, the amount of CO2 in the patient’s breath is measured after ingestion
62
Describe the stool antigen test
monoclonal antibodies are used to detect H. pylori antigens in stool
63
what are the two types of peptic ulcer disease?
gastric ulcer
| Duodenal ulcer
64
list complications of peptic ulcer disease
Perforation
| haemorrhage
65
List the invasive methods of diagnosis peptic ulcer disease
```
Endoscopy (biopsy may also be taken)
Histology (section of biopsy is stained)
Biopsy urease test
Culture medium
Barium Swallow (X-ray)
```
66
Describe the Biopsy urease test
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
explain the use of culture mediums in the diagnosis of PUD
Biopsies can be cultured in a medium and sensitivities to antibiotics can be checked to identify an appropriate antibiotic regimen
68
Describe the treatment regimen for PUD
Triple therapy comprising a PPI and 2 antibiotics
69
List the treatments for Peptic Ulcer Disease with examples
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
In what situation would surgery be considered as a treatment option for PUD?
Surgery – only used if complications occur (perforation or haemorrhage).
71
list ways of managing PUD
* Healthy diet – including probiotics
* Eliminate milk
* Control stress
* Don’t smoke
* Limit or avoid alcohol
* Stop ingestion of NSAIDs
72
Discuss how H2 receptor antagonists work
Completely inhibit histamine actions at all H2 receptors
Therefore inhibit gastric secretions too.
Also promote healing of gastric and duodenal ulcers.
73
Discuss how PPIs work
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
List some side effects of PPIs
Reduced gastric acid production:
Reduces nutrient absorption
Reduced gastric antimicrobial function
Increase in serum Gastrin levels
Neoplasia
Osteoporosis
75
In what percentage of people is H pylori found in?
50%
76
Discuss the epidemiology of peptic ulcer disease
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
Where are glands that produce pepsinogen and hydrochloric acid found?
Body and Fundus of the stomach
