Week 4- upper GI condition intro Flashcards

1
Q

what are the problems that people have to do with upper GI conditions due to acid?

A
• Wrong location (refluxing on oesphagus)
• Over-production 
• Faults with protective
mechanisms
• Dyspepsia
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2
Q

what is the treatment for upper GI conditions?

A

• Prevent acid from relocating
• Reduce acid production or
neutralise it
• Remove cause

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3
Q

what is the epidemiology for upper Gi conditions?

A
  • 20-40% of ppl

- a quarter will have some ulceration

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4
Q

what is gastric cancer? ppl its more likely to be in?

A
  • stomach cancer
  • 54% of cases are preventable
  • more common smoker and drinker
  • less likely in vegetarians
  • salt intake
  • infections related
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5
Q

what are some common upper GI conditions ?

A
  • Gastro-oesophageal reflux disease (GORD) 10-20%
  • Duodenal and stomach ulcer disease (PUD) 10-25%
  • Gastritis 30%
  • Functional dyspepsia 30%
  • Oesophageal & gastric cancer 2%
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6
Q

what type of cells secrete pepsinogen?

A

chief cells and mucus cells

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7
Q

how does pepsinogen have activity?

A
  • converts to pepsin and has to have acid conditions

- Hydrochloric acid from Parietal cells

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8
Q

what are the different phases of gastric activity associated with eating?

A
  • cephalic phase
  • gastric phase
  • intestinal phase
  • hormonal
  • these phases can overlap
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9
Q

acid secretion via Parietal Cells controlled by nervous control is done by how?

A

cephalic phase - parasympathetic

• Thought, smell, taste or sight of food

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10
Q

acid secretion via Parietal Cells controlled by local control is done by how?

A

gastric phase - parasympathetic

• Distension of stomach and chemical make up

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11
Q

acid secretion via horomal controlled by local control is done by how?

A

intestinal phase
• Food in duodenum (chyme) causes secretion of
somatostatin which inhibits acid production

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12
Q

what is the gastric physiology ?

A

• Secretion of H+ from the parietal cells into lumen through protn pump for HYDORGEN AND POTASSIUM,
-histamine, gastrin released from G cells when they detects amino acids and peptides & acetylcholine (ACh) secretion of acid stimulated by acetylcholine relased by vagal fibres
-Gastrin
• produced in response to vagal stimuli, rise in pH and ingested protein & calcium
• stimulates growth of gastric mucosa
• Within the parietal cell H+ is produced via the proton
pump, exchanges H+ with K+ in the gastric lumen

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13
Q

how do all the cells affect parietal cells?

A

• Parietal cell produces acid & directly stimulated by
• Vagus nerve – Acetylcholine (M3
receptor)
• Due to thought, sight, taste or smell
• Gastrin (G receptor)
• Due to contents of stomach
• Histamine (H2
receptor)
• Stimulation of enterochromaffin-like (ECL) cells by Gastrin & Vagus nerve
• Somatostatin is a prostaglandin and will suppress acid production
• Negative feedback due to contents of duodenum

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