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ESA 3 > GI 5 > Flashcards

GI 5 Flashcards

1
Q

What mechanisms prevent gastric reflux?

A

Lower oesophageal sphincter (LES):

Usually closed, transiently relaxes to allow bolus through

Stomach:

Angle of His and mucosal flap valve, as well as the postero-lateral location of the fundus all prevent acid reaching the LES and refluxing

Diaphragm:

Right crus of diaphram acts as a sling around the oesophagus serving as an ‘extrinsic’ sphincter

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2
Q

The failure of anti-reflux mechanisms leads to what?

A

Prolonged contact of gastric juices with oesophageal mucosa

Gastro-oesophageal reflux disease and associated symptoms

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3
Q

What are the typical clinical features of Gastro-oesophageal reflux disease (GORD)?

A

Dyspepsia

Worsens on lying down, bending over or drinking hot drinks

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4
Q

What investigations are indicated by a history that leads you to suspect GORD?

A

No investigations done in typical clinical presentations

Only if worrying symptoms, such as dysphagia or hiatus hernia are suspected

Endoscopic investigation in this case

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5
Q

What are some of the risk factors for GORD?

A

Pregnancy or obesity

Fat, Chocolate, Coffee or Alcohol

Large meals

Smoking

Hiatus hernia

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6
Q

List lifestyle management techniques to prevent/treat GORD

A

Lose weight

Stop smoking

Reduce consumption of chocolate, coffee, alcohol, fatty foods

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7
Q

Outline the types of treatment available for GORD, including their mechanism and an examples of each type

A

Simple antacids:

Neutralises acid with a base

E.g. Calcium carbonate

Raft antacids (alginates):

Forms a protective raft that sits on top of stomach contents and prevents reflux

E.g. Gaviscon

PPIs:

Reduction of acid secretion by oxyntic cells

E.g. Omeprazole

H2 antagonists:

Blocks H2 receptor which reduces acid secretions

E.g. Ranitidine

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8
Q

What is a common complication of GORD?

A

Continual contact of gastric juices and oesophageal mucosa can lead to metaplastic change (Barrett’s Oesophagus)

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9
Q

What is Gastritis?

A

Chronic or acute inflammation of the gastric mucosa

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10
Q

Differentiate acute and chronic gastritis

A

Chronic:

Infection with H. pylori

Inflammatory changes to mucosa leadsing to atrophy and metaplasia (possible cancer)

Acute:

NSAIDs, Alcohol, Cocaine

Exfoliation of surface cells and decreased secretion of protective mucus

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11
Q

What are the common symptoms of gastritis?

A

Commonly asymptomatic

Symptoms when they appear include:

    • Dyspepia (Pain/Discomfort)*
    • Nausea*
    • Vomiting*
    • Haematemesis*
    • Melena*
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12
Q

Outline the complications of Gastritis

A

Increases risk of Peptic ulcer disease

Chronic gastritis can cause hypergastrinaemia due to increasing gastrin release from G cells, this in turn can lead to Duodenal ulceration (DU)

Chronic Antral H. Pylori gastritis can lead to Gastric cancer and mucosa associated lymphoid tissue lymphoma (MALT Lymphoma)

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13
Q

How is gastritis diagnosed?

A

Endoscopy/Biopsy

Testing for H. Pylori

Blood test (Anaemia due to GI bleed)

Stool test (Blood due to GI bleed)

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14
Q

What types of drugs are used to treat gastritis?

A

Antacids

PPIs

H2 antagonists

General theme is reduction in acid secretion for promotion of healing

Antibiotics

E.g. Clarithromycin/Amoxacillin

Treatment of H. Pylori infection

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15
Q

What is peptic ulcer disease?

A

A break in the superficial epithelial cells down to the muscularis mucosa of either stomach (GU) or duodenum (DU)

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16
Q

Where are peptic ulcers commonly found?

A

GU:

Lesser curvature and antrum

DU:

Duodenal cap

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17
Q

Outline the most common cause of peptic ulcer disease

Give statisitics

A

NSAIDs:

Inhibit prostaglandins and reduce production of unstirred layer of mucus

50% of patients with long term NSAIDs have mucosal damage

30% when endoscoped have petic ulcer(s)

5% are symptomatic

1-2% have complications such as GI bleed

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18
Q

What is the prevlance of the different forms of peptic ulcer disease and how do prevalence rates vary across ages and countries?

A

DU in 10% adult population

GU is 2-3x less common (3-5%)

Prevalence is lower among younger adults and higher in older

Developing countries have increasing prevalence of NSAID associated DU and decreasing prevalence of H. Pylori associated ulceration

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19
Q

What are the clinical features of Peptic ulcer disease?

A

Reccurent, burning epigastric pain:

Worse at night and when hungry in DU

Relieved by eating

Persistent severe pain:

Suggestive of penetrtion of ulcer into other organs

Back pain:

Suggests penetration of ulcer in posterior stomach

Nausea and vomitting:

Less common

Weight loss and anorexia:

GUs only

Sudden haematemesis:

Asymptomatic patients can suddenly present with haematemesis when a blood vessel is erroded

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20
Q

What are the common investigations for suspected Peptic ulcer disease?

A

Investigation of H. Pylori infection

In 55+ patients or those with alarming symptoms an endoscopy can be done to exclude cancer

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21
Q

How is peptic ulcer disease managed?

A

Triple therapy:

PPIs

H2 antagonists

Antibiotics for H. Pylori (Clarithromycin/Amoxicillin)

If taking NSAIDs, review use and perhaps use alternatives

Prevention:

NSAIDs and PPIs used together if NSAIDs are long term

22
Q

What are the complications of peptic ulcer disease?

A

Haemorrhage of blood vessels:

Haematemesis

Melena

Perforation:

More common in DUs, normally into peritoneal cavity

Gastric outlet obstruction:

Can be pre-pyloric, pyloric or duodenal

Occurs due to active ulcers w/oedema or due to healing of ulcer with associated fibrosis/scarring

Normally presents as vomiting without pain

23
Q

Describe H. pylori bacteria

A

Gram negatic, Aerobic

Helical

Urease producing

Found in the mucus layer of the stomach or adhered to gastric mucosa

24
Q

What is the significance of H. pylori producing urease?

A

Urease produces ammonia and CO2

Ammonia:

Used to neutralise surroundings and protect the bacterium

C13 Urea test:

C13 Urea can be ingested by the patient to test for H. Pylori infection

Urease breaks down C13 urea forming C13 CO2 which can be exhaled and detected

25
Q

How does H. Pylori colonisation of the gastric mucosa cause disease?

A

Secretion of enzymes and other substances that damage mucosa:

Ammonia is toxic to epithelia

Vacuolating cytotoxin A disrupts tight junctions and leads to apoptosis

Phospholipases

Inflammatory response to bacterium (Inflammatory cells and mediators)

26
Q

What are some of the diseases caused by H. pylori infection?

A

Chronic gastritis

Peptic ulcer disease

Gastric Cancers

MALT lymphoma

27
Q

How does H. pylori colonisation in different areas of the stomach affect clinical outcomes?

A

Antrum predominant colonisation:

DU risk

Antrum and body colonisation:

Largely asymptomatic

Body predominant:

GU and cancer risk

28
Q

How is a bacterium implicated only in the colonisation of the stomach cause DU?

A

Antral H. pylori infection leads to hypergastrinaemia and hence increased acid production from oxyntic cells

Duodenal cap is inflammed and damaged by excess acid and metaplasia can occur

H. pylori colonises inflammed duodenal cap

Duodenal immune response leads to duodenitis and development of ulceration which is common intermittent

29
Q

How can we test for H. pylori infection?

A

C13 Urea test

IgG serum levels

Endoscopy:

Gastric biopsy taken and H. pylori detected by histology and culture

30
Q

How is H. pylori infection treated?

A

Same as Gastritis, GU or DU with H. pylori being the cause

PPI, H2 antagonist, Antibiotics (Clarithromycin/Amoxicillin)

90% successful in treatment of H. pylori

31
Q

Outline the progression of H. pylori induced disease thus describing how it can lead to gastric carcinoma

A

Initial H pylori infection leads to chronic non-atrophic gastritis

Multifocal atrophy develops and leads to metaplasia of the underprotected mucosa

Dysplasia develops from metaplasia and progresses to carcinoma

Factors involved in progression:

H. pylori virulence factors

Virulence associated host gene polymorphisms (genetic predisposition)

Dietary and environmental factors alter progression

32
Q

Why is gastric cancer a particulalry deadly cancer?

A

Mildly symptomatic/Asymptomatic until late stage

5-6th biggest cause of cancer death

33
Q

Outline the mechanisms of drugs which reduce gastric acid production

A

PPIs:

Prevents H+ ions from being pumped into oxyntic cell canaliculi

H2 antagonists:

Removes amplification of the Gastrin/Ach signal for acid production

34
Q

Describe the gross anatomy of the stomach

A

Expanded part of the GI tract between the oesophagus and the duodenum

2-3 litres in capacity

Resembles letter J

Position depends on posture, body shape, distention

5 parts:

    • Body*
    • Cardia*
    • Fundus*
    • Pyloric canal*
    • Pyloric antrum*

2 Curvatures, greater and lesser

35
Q

Label the diagram

A

Horizontal boxes, top to bottom:

Cardiac notch of stomach

Fundus

Cardia

Body

Pylorus

Antrum

Diagonal boxes, left to right:

Lesser curvature

Greater curvaure

36
Q

What are the sphincters of the stomach and where are thy found?

A

Inferior oesophageal sphincter:

Found immediately superior to Z-line

In horizonatal plane with xiphoid process to the left of T11

Pyloric sphincter:

At the pyloric end of the stomach

37
Q

Describe the structure and function of the inferior oesophageal sphincter

A

Immediately superior to the Z-line the diaphragmatic musculature forms the oesophageal hiatus

This functions as a physiological sphincter

Contracts and relaxes to allow boluses to pass and prevent stomach contents from refluxing

38
Q

What is the Z-line?

A

The line where oesophageal mucosa abruptly changes to gastric mucosa

This marks the boundaries of each structure

39
Q

Describe the structure and function of the pyloric sphincter

A

Circular muscle coat at the end of the pyloric portion of the stomach is thickened to form an anatomical sphincter

Regulates the passage of chyme into the duodenum

40
Q

Label the boxes

A

From top left clockwise:

Diaphragm

Endothoracic fascia

Pleura

Upper phrenico-oesophageal ligament

Endoabdominal fascia

Cardiac notch

Lower phrenico-oesophageal ligament

Cardiac orifice of stomach

Z-line

Peritoneum

41
Q

Label the diagram

A

Top to bottom:

Pyloric canal

Pyloric orifice/sphincter

Duodenum

42
Q

What features of the stomach are most clearly seen when empty?

A

Rugae:

Longitudinal folds in the gastric mucosa

Gastric canal:

Found on the lesser curvature, a canal between gastric folds that allows saliva and small amounts of chewed food to reach the pylorus

43
Q

Label this diagram, answers given in columns

A

Column 1:

Gastric pit

Mucous epithelium

Lymph vessel

Lamina propria

Musc. Mucosa

Submucosa

Oblique muscle

Circular muscle

Longitudinal muscle

Serosa

Column 2:

Gastric pit

Artery + Veins

Gastric gland

Myenteric plexus

Column 3:

Mucous cells

Neck

Pariteal cells

Chief cells

Smooth muscle cell

G cell

44
Q

Outline how the stomach has regions that are histologically distinct from each other

A

Different zones carry different types of cells in their gastric pits

Cardia:

Only neck cells

Fundus and Body:

Neck cells

Parietal cells

Chief cells

Pylorus:

Neck cells

G-cells

45
Q

Describe the greater omentum

A

Prominent, four layered peritoneal fold hanging like an apron from the greater curvature

After descending it folds back up and attaches to the anterior transverse colon and its mesentery

46
Q

Describe the lesser omentum

A

Small, double layered peritoneal fold that connects the lesser curvature of the stomach and the proximal part of the duodenum to the liver

Also connects the stomach to the portal triad

47
Q

Describe the epiploic foramen

A

Opening siutated posterior to the free edge of the lesser omentum (hepatoduodenal ligament)

48
Q

Label the boxes

A

Top to botom, left to right:

Lesser omentum

Finger inserted into epiploic foramen

Greater omentum

49
Q

What is the coeliac trunk?

A

Branch of the abdominal aorta at the level of T12

Gives rise to the splenic, left gastric and common hepatic arteries

Supplies blood to the liver, stomach, abdominal, oesophagus, spleen and the superior half of both the duodenum and the pancreas.

50
Q

Label this diagram

A

Top left clockwise:

Left gastric artery

Oesophageal branch of left gastric

Aortic hiatus

Posterior gastric artery

Splenic artery

Short gastric arteries

Spleen

Left gastro-omental artery

Abd. Aorta

Right gastro-omental artery

Superior pancreaticoduodenal artery

Supraduodenal artery

Gastroduodenal artery

Common hepatic artery

Right gastric artery

Hepatic artery proper

Cystic artery

Coeliac trunk

51
Q

Describe the blood supply to the lesser and greater curvature and the fundus and body of the stomach

A

Lesser curvature:

Left gastric (branch of the coeliac trunk)

Right gastric (branch of the common hepatic)

Greater curvature:

Left gastro-omental (branch of the splenic)

Right gastro-omental (branch of the gastro-duodenal, in turn a branch of the common hepatic)

Fundus and body:

Posterior/small gastric arteries (branches of the splenic)

52
Q

Label this diagram

A

Top left anti-clockwise:

Left gastric vein

Right gastric vein

Portal vein

Pre-pyloric vein

Pancreaticoduodenal vein

Right gastro-omental vein

Splenic vein

Left gastro-omental vein

Middle gastric vein

Short gastric vein

ESA 3 (54 decks)

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