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ESA 3 > GI 5 > Flashcards

GI 5 Flashcards

(52 cards)

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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?

Study These Flashcards
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?

Study These Flashcards
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

Study These Flashcards
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?

Study These Flashcards
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
How does H. Pylori colonisation of the gastric mucosa cause disease?
**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
What are some of the diseases caused by H. pylori infection?
Chronic gastritis Peptic ulcer disease Gastric Cancers MALT lymphoma
27
How does H. pylori colonisation in different areas of the stomach affect clinical outcomes?
**Antrum predominant colonisation:** DU risk **Antrum and body colonisation:** Largely asymptomatic **Body predominant:** GU and cancer risk
28
How is a bacterium implicated only in the colonisation of the stomach cause DU?
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
How can we test for H. pylori infection?
**C13 Urea test** **IgG serum levels** **Endoscopy:** Gastric biopsy taken and H. pylori detected by histology and culture
30
How is H. pylori infection treated?
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
Outline the progression of H. pylori induced disease thus describing how it can lead to gastric carcinoma
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
Why is gastric cancer a particulalry deadly cancer?
Mildly symptomatic/Asymptomatic until late stage 5-6th biggest cause of cancer death
33
Outline the mechanisms of drugs which reduce gastric acid production
**PPIs:** Prevents H+ ions from being pumped into oxyntic cell canaliculi **H2 antagonists:** Removes amplification of the Gastrin/Ach signal for acid production
34
Describe the gross anatomy of the stomach
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
Label the diagram
**Horizontal boxes, top to bottom:** Cardiac notch of stomach Fundus Cardia Body Pylorus Antrum **Diagonal boxes, left to right:** Lesser curvature Greater curvaure
36
What are the sphincters of the stomach and where are thy found?
**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
Describe the structure and function of the inferior oesophageal sphincter
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
What is the Z-line?
The line where oesophageal mucosa abruptly changes to gastric mucosa This marks the boundaries of each structure
39
Describe the structure and function of the pyloric sphincter
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
Label the boxes
**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
Label the diagram
**Top to bottom:** Pyloric canal Pyloric orifice/sphincter Duodenum
42
What features of the stomach are most clearly seen when empty?
**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
Label this diagram, answers given in columns
**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
Outline how the stomach has regions that are histologically distinct from each other
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
Describe the greater omentum
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
Describe the lesser omentum
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
Describe the epiploic foramen
Opening siutated posterior to the free edge of the lesser omentum (hepatoduodenal ligament)
48
Label the boxes
**Top to botom, left to right:** Lesser omentum Finger inserted into epiploic foramen Greater omentum
49
What is the coeliac trunk?
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
Label this diagram
**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
Describe the blood supply to the lesser and greater curvature and the fundus and body of the stomach
**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
Label this diagram
**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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