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Bioregulatory Systems: Upper GI Tract > Upper GI Tract Part 2 [Complete] > Flashcards

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?

A

Fundus

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
Q

Where are G cells mainly located?

A

Within the antrum of the stomach

26
Q

What paracrine substance is responsible for stimulating gastric secretion and where is it produced?

A

Histamine

Produced from ECL and mast cells within the gastric wall

27
Q

What hormone is produced to inhibit gastric secretion and where is it produced?

A

Secretin

Produced in the small intestines

28
Q

What paracrine substance is responsible for inhibiting gastric secretion?

A

Somatostatin

29
Q

List 5 paracrine/autocrine substances that can inhibit gastric secretion

A

PGs (E2 & I2), TGF-α & adenosine

(PG = prostaglandins)

(TGF= transforming growth hormone)

30
Q

What are the 4 types of mucosal protection?

A

Mucus film

HCO3- secretion

Epithelial barries

Mucosal blood perfusion (supplies mucosa with oxygen and HCO3-, and by removing H+ and toxic agents).

31
Q

Name 3 mechanisms that are in place to repair any epithelial defects.

A

Migration

Gap closed by cell growth

Acute wound healing

32
Q

Describe what happens in migration to repair epithelial defects

A

Adjacent epithelial cells flatten to close gap via sideward migration along basal membrane

33
Q

Cell growth used to repair epithelial defects is stimulated by which 5 substances?

A

EGF

TGF-α

IGF-1

GRP

gastrin

34
Q

Describe what happens during acute wound healing.

A

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
Q

What factors increases the risk of ulcer formation?

A

Helicobacter pylori

Increased gastric secretion

Decreased HC03- secretion

Reduced blood perfusion

Reduced cell formation

36
Q

What medications can increase risk of ulcer formation?

A

non-steroidal anti-inflammatory drugs (NSAIDs)

37
Q

What 3 substances does Helicobacter pylori release which can result in ulcer formation?

A

Urease

Exotoxins

Secretory enzymes

38
Q

How does urease contribute to ulcer formation?

A

Neutralise gastric acid by catalysing production of ammonia, leading to gastric mucosal injury

39
Q

Name 3 secretory enzymes produced by helicobacter pylori which could lead to ulcer formation?

A

Mucinase

Protease

Lipase

40
Q

What is the most common clinical outcome of helicobacter pylori if left untreated?

A

Asymptomatic or Chronic gastritis (>80%)

41
Q

What are 3 less common clinical outcome of helicobacter pylori infections?

A

Chronic atrophic gastritis

Intestinal metaplasia

Gastric or duodenal ulcer

(15-20%)

42
Q

What is a rare clinical outcome of a helicobacter pylori infection?

A

Gastric cancer

MALT lymphoma

43
Q

What are the most common treatment options for an ulcer?

A

PPI or H2 blocker

Triple Rx (amoxicillin, clarithromycin, pantoprazole) for 7-14 days)

44
Q

Most ulcers heal within 12 weeks after intial treatment. If this doesnt occur (which is rare), what is the next course of action?

A

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
Q

What is Zollinger-Ellison syndrome?

A

Zollinger–Ellison syndrome is a disease in which tumors cause the stomach to produce too much acid, resulting in peptic ulcers

46
Q

If treatment for an ulcer does not work, surgery is performed. What are the potential implications of this?

A

intractability (after medical therapy)

Haemorrhage

Obstruction

Perforation

Relative: continuous requirement of steroid therapy/NSAIDs

Bioregulatory Systems: Upper GI Tract (13 decks)

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