Upper GI Tract Part 2 [Complete] Flashcards

1
Q

What investigations are usually performed to determine if someone has GORD and to rule out other potential causes for symptoms?

A

OGD: To exclude cancer, oesophagitis, peptic stricture & Barretts oesophagus

Oesophageal manometry

24-hr Oesophageal pH recording

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2
Q

What are the treatment options for someone with GORD?

A

Lifestyle changes: Weight loss, smoking, alocohol

PPIs (Proton pump inhibitors)

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3
Q

What are some of the surgical treatments for a person with GORD?

A

Dilatation peptic strictures

Laparoscopic Nissen’s fundoplication

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4
Q

What are the 3 main functions of the stomach?

A

Breaks food into smaller particles (acid & pepsin)

Holds food, releasing it in controlled steady rate into duodenum

Kills parasites & certain bacteria

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5
Q

State what different regions of the stomach secrete.

A

Cardia & Pyloric Region: Mucus only

Body & Fundus: Mucus, HCl, pepsinogen

Antrum: Gastrin

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6
Q

What does the cardia and pyloric regions of the stomach produce?

A

Mucus

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7
Q

What does the body and fundus of the stomach produce?

A

Mucus

HCL

Pepsinogen

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8
Q

What does the antrum of the stomach produce?

A

Gastrin

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9
Q

How much stomach acid is produced each day and how does the concentration compare to that of blood?

A

2L/day

150mM H+ (3 mill x that in blood)

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10
Q

What are mucins?

A

A glycoprotein gel coating which protects the gastrointestinal tract from acids, trauma, microorganisms and digestive enzymes.

HCO3- trapped in mucus gel to neutralise H+

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11
Q

How does the pH on the epithelial surface compare to the pH of the lumen of the stomach?

A

Epithelial surface = 6-7 (most likely due to mucins)

Lumen = 1-2

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12
Q

Inflammation in the lining of the stomach is known as?

A

Gastritis

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13
Q

Name the 4 main types of gastritis

A

Erosive & haemorrhagic gastritis

Nonerosive, chronic active gastritis

Atrophic gastritis (Fundal gland gastritis)

Reactive gastritis

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14
Q

Define gastritis

A

Inflammation of the stomach lining

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15
Q

Erossive, haemorhhagic gastritis has numerous causes. What is the most common cause?

A

Acute ulcer (Characterised by gastric bleeding and perforation)

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16
Q

What is the main cause of non-erossive, chronic active gastritis?

A

Helicobacter pylori

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17
Q

Non-erossive, chronic active gastritis occurs mostly in which region of the stomach?

A

Antrum

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18
Q

What is the treatment for non-erosive chronic gastritis caused by helicobacter pylori?

A

Give them tripple antibiotics for 7-14 days

amoxicillin

clarithromycin

pantoprazole

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19
Q

What is the main cause of atrophic gastritis?

A

Antibody targeting of parietal cells and their products

(Leads to parietal cell atrophy and decreased secretion of acid and intrinsic factors)

20
Q

Which region of the stomach is most affected by atrophic gastritis?

21
Q

An alternative name for atrophic gastritis is?

A

Fundal gland gastritis

22
Q

What systems are responsible for regulating gastric secretion?

A

Nervous system

Endocrine

Paracrine

23
Q

What neurotransmitter and cranial nerve is responsible for stimulating gastric secretion?

A

ACh

Vagus nerve (Cranial nerve X)

(ACh is the postganglionic transmitter of vagal parasympathetic fibres which innervate the stomach)

24
Q

What peptide hormone is responsible for stimulating gastric secretion and where is it produced?

A

Gastrin

Produced by G cells in the antrum

25
Where are G cells mainly located?
Within the antrum of the stomach
26
What paracrine substance is responsible for stimulating gastric secretion and where is it produced?
Histamine Produced from ECL and mast cells within the gastric wall
27
What hormone is produced to inhibit gastric secretion and where is it produced?
Secretin Produced in the small intestines
28
What paracrine substance is responsible for inhibiting gastric secretion?
Somatostatin
29
List 5 paracrine/autocrine substances that can inhibit gastric secretion
PGs (E2 & I2), TGF-α & adenosine (PG = prostaglandins) (TGF= transforming growth hormone)
30
What are the 4 types of mucosal protection?
Mucus film HCO3- secretion Epithelial barries Mucosal blood perfusion (supplies mucosa with oxygen and HCO3-, and by removing H+ and toxic agents).
31
Name 3 mechanisms that are in place to repair any epithelial defects.
Migration Gap closed by cell growth Acute wound healing
32
Describe what happens in migration to repair epithelial defects
Adjacent epithelial cells flatten to close gap via sideward migration along basal membrane
33
Cell growth used to repair epithelial defects is stimulated by which 5 substances?
EGF TGF-α IGF-1 GRP gastrin
34
Describe what happens during acute wound healing.
Destruction of basal membrane attracts leukocytes & macrophages. phagocytosis of necrotic cells soon occurs followed by angiogenesis. There is eventual regeneration of epithelial cell membrane after repair of basal membrane Finally epithelial closure by cell division.
35
What factors increases the risk of ulcer formation?
Helicobacter pylori Increased gastric secretion Decreased HC03- secretion Reduced blood perfusion Reduced cell formation
36
What medications can increase risk of ulcer formation?
non-steroidal anti-inflammatory drugs (NSAIDs)
37
What 3 substances does Helicobacter pylori release which can result in ulcer formation?
Urease Exotoxins Secretory enzymes
38
How does urease contribute to ulcer formation?
Neutralise gastric acid by catalysing production of ammonia, leading to gastric mucosal injury
39
Name 3 secretory enzymes produced by helicobacter pylori which could lead to ulcer formation?
Mucinase Protease Lipase
40
What is the most common clinical outcome of helicobacter pylori if left untreated?
Asymptomatic or Chronic gastritis (\>80%)
41
What are 3 less common clinical outcome of helicobacter pylori infections?
Chronic atrophic gastritis Intestinal metaplasia Gastric or duodenal ulcer (15-20%)
42
What is a rare clinical outcome of a helicobacter pylori infection?
Gastric cancer MALT lymphoma
43
What are the most common treatment options for an ulcer?
PPI or H2 blocker Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)
44
Most ulcers heal within 12 weeks after intial treatment. If this doesnt occur (which is rare), what is the next course of action?
Change medication and observe for another 12 weeks Also check serum gastrin to rule out antral G-cell hyperplasia or gastrinoma [Zollinger- Ellison syndrome] Perform an OGD and biopsy all 4 quadrants of ulcer to rule out malignancy
45
What is Zollinger-Ellison syndrome?
Zollinger–Ellison syndrome is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers
46
If treatment for an ulcer does not work, surgery is performed. What are the potential implications of this?
intractability (after medical therapy) Haemorrhage Obstruction Perforation Relative: continuous requirement of steroid therapy/NSAIDs