Diseases Of The GIT Flashcards
what is the anatomy of the stomach( parts of the stomach, its position in relation to the oesophagus,state one function of the , state the
two sphincters in th stomach and the layers of the smooth muscle of the stomach, what is the function of the pyloric sphincter, where does the duodenum terminate at?
state the types of cells in the stomach and where they can be found as well as their functions, what is stomatostatin, what is the mucosal barrier made up of? what is the function of prostaglandins in the stomach?
Structure
The stomach occupies a small area immediately distal to the
oesophagus (the cardia), the upper region (the fundus, under
the left diaphragm), the mid-region or body and the antrum,
which extends to the pylorus
It serves as a reservoir
where food can be retained and broken up before being actively expelled in to the proximal small intestine.
The smooth muscle of the wall of the stomach has three
layers: outer longitudinal, inner circular and innermost oblique
layers. There are two sphincters, the gastro-oesophageal
sphincter and the pyloric sphincter. The latter is largely made
up of a thickening of the circular muscle layer and controls the exit of gastric contents into the duodenum.
The duodenum has outer longitudinal and inner smooth
muscle layers. It is C-shaped and the pancreas sits in the concavity. It terminates at the duodenojejunal flexure where
it joins the jejunum.
The mucosal lining of the stomach can stretch in size with feeding. The greater curvature of the undistended
stomach has thick folds or rugae. The mucosa of the upper two-thirds of the stomach contains parietal cells that secrete hydrochloric acid, and chief cells that secrete pepsinogen (which initiates proteolysis).
The antral mucosa secretes bicarbonate and contains
mucus-secreting cells and G cells, which secrete
gastrin, stimulating acid production. There are two major forms of gastrin, G17 and G34, depending on the number of amino-acid residues. G17 is the major form found in the antrum. Somatostatin, a suppressant of acid secretion, is also produced by specialized antral cells (D cells).
Mucus-secreting cells are present throughout the
stomach and secrete mucus and bicarbonate. The
mucus is made of glycoproteins called mucins.
The ‘mucosal barrier’, made up of the plasma
membranes of mucosal cells and the mucus layer,
protects the gastric epithelium from damage by acid
and, for example, alcohol, aspirin, NSAIDs and bile
salts. Prostaglandins stimulate secretion of mucus,
and their synthesis is inhibited by aspirin and
NSAIDs, which inhibit cyclo-oxygenase (see
Fig. 15.30).
The duodenal mucosa has villi like the rest of the
small bowel, and also contains Brunner’s glands that
secrete alkaline mucus. This, along with the pancreatic
and biliary secretions, helps to neutralize the acid
secretion from the stomach when it reaches the
duodenum
how is acid produced in the stomach, state the phases of acid secretion
Acid secretion is central to the functionality of the stomach;
factors controlling acid secretion.
Acid is not essential for digestion but does prevent some
food-borne infections. It is under neural and hormonal control
and both stimulate acid secretion through the direct action of histamine on the parietal cell. Acetylcholine and gastrin also release histamine via the enterochromaffin cells.
Phases of acid secretion
1. Cephalic
Thought, sight or smell of food stimulate
the vagus, producing acetylcholine
2. Gastric
Distension by food directly stimulates
secretory cells( chief cells( pepsinogen), parietal cells(intrinsic factor and acid) and G cells(gastrin) and gastrin release
3. Intestinal
Passage of food into duodenum
stimulates GI hormone(Digestive hormones - Gastrin, Secretin, cholecystokinin, Gastric Inhibitory Peptide and Motilin; VASOACTIVE INTESTINAL PEPTIDE(VIP), Somatostatin https://gastrodigestivesystem.com/digestion/digestive-hormones) release
Somatostatin inhibits both histamine and gastrin release and
therefore acid secretion.
Other major gastric functions are:
Reservoir for food
Emulsification of fat and mixing of gastric contents
Secretion of intrinsic factor
Absorption (of only minimal importance
what is the shape of H pylori, is it Gram neg or pos,where is it found in greater numbers in the stomach and which cells do they specifically adhere to, what features of H pylori help it to cause damage
H. pylori is a slow-growing spiral Gram-negative flagellate urease-producing bacterium which plays a major role in gastritis and peptic ulcer disease. It colonizes the mucous layer in the gastric antrum, but is also found in the duodenum in areas of gastric metaplasia. H. pylori is found
in greatest numbers under the mucous layer in gastric pits, where it adheres specifically to gastric epithelial cells. It is protected from gastric acid by the juxtamucosal mucous layer which traps bicarbonate secreted by antral cells, and ammonia produced by bacterial urease.Furthermore, the bacterium is
capable of penetrating the mucosal barrier both by
virtue of its physical capability to burrow through the
barrier and by releasing bacterial digestive enzymes
that liquefy the barrier. As a result, the strong acidic
digestive juices of the stomach secretions can then penetrate into the underlying epithelium and literally digest
the gastrointestinal wall, thus leading to peptic
ulceration.
. Four features are linked to H. pylori
virulence:
* Flagella, which allow the bacteria to be motile in viscous mucus
* Urease, which generates ammonia from endogenous
urea, thereby elevating local gastric pH around the organisms and protecting the bacteria from the acidic pH of the stomach
* Adhesins, which enhance bacterial adherence to surface
foveolar cells
* Toxins, such as that encoded by cytotoxin-associated
gene A (CagA), that may be involved in ulcer or cancer
development by poorly defined mechanisms
These factors allow H. pylori to create an imbalance between
gastroduodenal mucosal defenses and damaging forces that
overcome those defenses. Over time, chronic antral H. pylori
gastritis may progress to pangastritis, resulting in multifocal atrophic gastritis, reduced acid secretion, intestinal
metaplasia, and increased risk of gastric adenocarcinoma in
a subset of patients. The underlying mechanisms contributing
to this progression are not clear, but interactions between
the host immune system and the bacterium seem to be
critical.
signs and symptoms of PUD
A peptic ulcer consists of a break in the superficial epithelial
cells penetrating down to the muscularis mucosa of either
the stomach or the duodenum; there is a fibrous base and
an increase in inflammatory cells. Erosions, by contrast,
are superficial breaks in the mucosa alone. Episodic abdominal pain (often aggravated by dietary indiscretions
and lifestyle)
y May be a minor discomfort, gnawing, burning, dull ache or very
severe pain
y Typically pain is in the epigastrium or right hypochondrium
y Occasionally high up behind the sternum or low down around
the umbilicus
y In duodenal ulcer, pain typically comes on when the patient is
hungry and may wake the patient up in the middle of the night.
y In gastric ulcer, it is typically worsened by food, and may be relieved by vomiting
y Is relieved by alkalis and food in duodenal ulcer
y Vomiting may occur in both duodenal and gastric ulcers. It is usually
a complication in duodenal ulcer (gastric outlet obstruction) but may
be self-induced in gastric ulcer to relieve pain
Signs
y There may be no abdominal signs
y Weight loss (sometimes in gastric ulcer)
y Weight gain (sometimes in duodenal ulcer)
y Tenderness - epigastrium, right hypochondrium or umbilical region
investigations for PUD
Investigations
y Haemoglobin
y H. pylori stool antigen
y Oesophago-gastro-duodenoscopy (endoscopy)
y Barium meal (in the absence of endoscopy)
y Stool examination (to exclude intestinal parasites)
do urease test as youre treating for PUD to make sure the treatment is working properly but you do upper GI ENDOCOPY to diagnose
Invasive (endoscopy)
Biopsy urease test. Gastric biopsies, usually antral
unless additional material is needed to exclude
proximal migration, are added to a substrate containing
urea and phenol red. If H. pylori are present, the urease
enzyme that they produce splits the urea to release
ammonia which raises the pH of the solution and causes
a rapid colour change (yellow to red). This enables a
patient’s H. pylori status to be determined before they
leave the endoscopy suite. The test may be falsely
negative if patients are taking PPIs or antibiotics at the
time.
Histology. H. pylori can be detected histologically on
routine (Giemsa) stained sections of gastric mucosa
obtained at endoscopy. The sensitivity is reduced if a
patient is on PPIs, but less so than with the urease
test. This can be improved with immunohistochemical
staining using an anti H. pylori antibody.
Culture. Biopsies obtained can be cultured on a special
medium, and in vitro sensitivities to antibiotics can be
tested. This technique is typically used for patients with
refractory H. pylori infection to identify the appropriate
antibiotic regimen and routine culture is rare
how is PUD treated
Non-pharmacological treatment
y Avoid alcohol and tobacco intake
y Avoid foods that aggravate the pain
y Allay anxiety and stress
y Surgical treatment: for chronic cases with severe periodic attacks,
failed medical treatment and complications e.g. perforation, gastric
outlet obstruction and haemorrhage)
Helicobacter pylori Eradication
Majority of patients presenting with duodenal ulcer are infected with
Helicobacter pylori. Eradication of H. pylori should therefore be done using
a 10-14 day course of treatment consisting of a PPI plus a combination of
two of the antibiotics indicated in the table below.
Table 1-5: Helicobacter pylori Eradication Therapy
Helicobacter pylori Eradication therapy
PPI Antibiotic
Amoxicillin,
oral ξ
Clarithromycin, oral Metronidazole,
1.Esomeprazole, oral
20 mg 12 hourly and either Amoxicillin
oral-1 g 12 hourly and
Clarithromycin-500 mg 12 hourly or
clarithromycin 500 mg 12 hourly and
oral Metronidazole-400 mg 12 hourly
Or
2.Omeprazole, oral
20 mg 12 hourly and either amoxicillin
1 g 12 hourly and clarithromycin 500 mg 12 hourly or amoxicillin 500 mg 8 hourly and metronidazole 400 mg 8 hourly or
clarithromycin- 500 mg 12 hourly and metronidazole 400 mg 12 hourly
Or
3.Pantoprazole, oral
40 mg 12 hourly and amoxicillin
1 g 12 hourly and clarithromycin 500 mg 12 hourly ——or clarithromycin 500 mg 12 hourly and metronidazole 400 mg 12 hourly
ξ Avoid treatment regimens including Amoxicillin in patients with penicillin allerg
NSAID-associated duodenal or gastric ulcer and gastro-duodenal
erosions
Evidence Rating: [A]
y Esomeprazole, oral,
— Peptic Ulcer Disease —
Standard Treatment Guidelines, 7th Edition, 2017
24
Adults
20 mg daily for 4 weeks. Repeat course if ulcer is not fully healed.
Or
y Omeprazole, oral,
Adults
20 mg daily for 4 weeks. Repeat course if ulcer is not fully healed.
Or
y Pantoprazole, oral,
Adults
20-40 mg daily for 4 weeks. Repeat course if ulcer is not fully healed
Dyspepsia
1st Line treatment
Evidence Rating: [A]
y Magnesium trisilicate, oral, 15 ml 8 hourly (in-between meals and at
bedtime to control dyspepsia)
Or
y Aluminium hydroxide, oral, 500 mg 6 hourly (in-between meals and
at bedtime)
Note 1-6
Avoid taking antacids within 2 hours of proton pump inhibitors (PPIs) e.g. omeprazole, esomeprazole, pantoprazole
state and explain five complications of PUD, state the signs and symptoms of gastric outlet obstruction
Haemorrhage
See page 256.
Perforation (Box 6.4; see also p. 299)
. DUs perforate
more commonly than GUs, usually into the peritoneal cavity;
perforation into the lesser sac also occurs. Detailed management of perforation is described on page 301. Laparoscopic surgery is usually performed to close the perforation and drain the abdomen. Conservative management using nasogastric suction, intravenous fluids and antibiotics is occasionally used in elderly and very sick patients.
Gastric outlet obstruction
The obstruction may be prepyloric, pyloric or duodenal. The obstruction occurs either because of an active ulcer with surrounding oedema or because the healing of an ulcer has been followed by scarring. However, obstruction due to peptic ulcer disease and gastric malignancy are now
uncommon; Crohn’s disease or external compression from a pancreatic carcinoma are more common causes. Adult
hypertrophic pyloric stenosis is a very rare cause.
After gastric outlet obstruction the stomach becomes full of gastric juice and ingested fluid and food, giving rise to the
main symptom of vomiting, usually without pain as the characteristic ulcer pain has abated owing to healing.
Vomiting is infrequent, projectile, large in volume, and the
vomitus contains particles of previous meals. On examination
of the abdomen there may be a succussion splash. The
diagnosis is made by endoscopy but can be suspected by
the nature of the vomiting; by contrast, psychogenic vomiting
is frequent, small volume and usually noisSevere or persistent vomiting causes loss of acid from the
stomach and a metabolic alkalosis (see p. 666). Vomiting will
often settle with intravenous fluid and electrolyte replacement, gastric drainage via a nasogastric tube and potent acid
suppression therapy. Endoscopic dilatation of the pyloric
region is useful, as is luminal stenting, and overall, 70% of
patients can be managed without surge
anatomy of the oesophagus
What are haemorrhoids
Hemorrhoids are swollen blood vessels in the lower rectum.
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