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Gastrointestinal system > Stomach > Flashcards

Stomach Flashcards

1
Q

What are the basic functions of the stomach? (4)

A
  • short term food storage - disrupt food - Start of chemical digestion (mainly proteins) - Disinfect food
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2
Q

Describe the anatomical regions of the stomach

A
  • cardia at opening of oesphagus
  • Fundus at top
  • Body in middle
  • Antrum below this
  • Pylorus at end

(image doesnt show antrum)

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3
Q

What is the epithilial change from oesophagus to stomach?

A

stratified squamous to columnar

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4
Q

Are the rugae temporary or permenant?

A

temporary- allow distension of the stomach

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5
Q

How many layers of muscle cover the stomach? Name them from out to in

A

Londituitonal layer

circular muscle layer

oblique muscle layer

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6
Q

What is the name of the sphincter between the pylorus of stomach and the deodenum?

A

pyloric sphincter

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7
Q

From top to bottom, list the names of the cells found in the gastric pits (5)

A
  • Goblet cells
  • Parietal cells
  • Cheif cells
  • D cells
  • G cells
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8
Q

What is the function of parietal cells?

A

gastric acid production

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9
Q

What do cheif cells do?

A

pepsinogen secretion

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10
Q

What do D and G cells do?

A

D cells= somatostatin (GHRH) release (inhibits acid secretion)

G cells= Secrete gastrin (stimulates acid release)

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11
Q

Histamine is released at the base of many gastric pits, what secretes it?

A

Enteroendocrine cells/ enterochromaffin like cells (ECL cells)

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12
Q

Where are the most goblet cells found?

A

Many in cardia, but also in the body and fundus, few in the pylorus

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13
Q

What cells are found in aubundance in the fundus and body?

A

Goblet cells, cheif cells, parietal cells

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14
Q

What cells are most aubundant in the pylorus?

A

D and G cells

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15
Q

Describe the difference in stomach contractions between the upper and lower stomach?

A

upper- sustained contractions and thinner wall to move contents along

Lower- peristaltic contractions every 20s or so & thicker wall to gring contents

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16
Q

How does the stomach ensure only liquid chyme is passed into the duodenum?

A
  • Pyloric sphincter opens small amounts every 20s, so ejects liquid chyme
  • Stomach is cone shaped meaning lumps are left behind and only liquid chyme moves into the duodenum
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17
Q

What stimulates HCl release in the stomach?

A
  • Gastrin from G cells (multiple stimulators)
  • Histamine from enterochromaffin like cells (due to gastrin and vagal stimulation

Ach from the vagus nerve (due to sight/ smell/ taste of food)

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18
Q

Describe HCl release in the stomach?

A
  • In partietal cells
  • H+ extruded into lumen on H/K/ atpase (K+ in)
  • HCO3- extuded into blood
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19
Q

What receptors do gastrin, Histamine and Ach from the vagus nerve act on?

A

gastrin- CCK

Histamine- H2

Ach- Muscarinic Ach receptors

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20
Q

Describe the control of the release of gastrin

A

Stimulators: peptides and amino acids in lumen act on G cell receptors, Ach from vagus nerve (on seeing food), Gastrin releasing peptides (GRP) from stimulation of stretch receptors

Inhibitors: Somatostatin from D cells detecting low pH in lumen

Effector: G cells release/ dont release gastrin

21
Q

Describe the inhibition of HCl production in the stomach

A

When food leaves the stomach pH drops (as food normally acts as a buffer), low pH activates D cells, which release somatostatin. This inhibits gastrin release from G cells and histamine release from ECL cells.

Also less stomach distension and vagal activity reduces so less simtulation of parietal cells

22
Q

Describe how eating stimulates acid production in the stomach (overview)

A
  • Hedonistic inputs cause vagal stimulation which directly stimulates acid production in parietal cells, stimulates ECL cells to produce histamine and stimulate G cells to produce gastrin
  • Stretch receptors release GRP which stimulates G cells to produce gastrin
  • Peptides and amino acids reachin stomach stimulate G cells to produce gastrin
  • Gastrin also stimulates ECL cells to produce histamine
  • Gastrin, histmaine and vagus nerve all stimulate parietal cells to produce more stomach acid
23
Q

Describe control of pepsinogen release in the stomach

A

Vagus nerve and gastrin stimulate cheif cells to produce pepsinogens

24
Q

What are the 3 phases of digestion?

A

Cephalic phase- thought of food stimulating vagus nerve, GRP and Ach release- accounts for 30% total HCl production

Gastric phase- food in stomach= more GRP release, pH increase (food buffers)–> loss of D cell inhibition, stimulation of G cells ect, 60% of HCl production

Intestinal phase- chyme stimulates gastrin and as amino acids in intestine, but this is soon inhibited by lipids acitvating enterogastric reflex (reduced vagal activity) and secretin release

25
Q

What defenses does the stomach have against acid? (3)

A

Alkaline mucous produced from goblet cells

High turnover of epithelial cells keeps tract in tact

Prostaglandins vasodilate and maintain mucosal blood flow to supply the epithelium with nutrients

26
Q

Describe 3 causes of reduced HCl defence in the stomach

A

NSAIDS- inhibit prostaglandins, less vasodilation, less nutrient supply to epithelium

Alcohol thins mucous layer

H. Pylori damages ability to make mucus

27
Q

What are the symptoms of GORD? (4)

A

Heartburn, cough, sort throat, dysphagia

28
Q

Give 4 causes of GORD?

A
  • LOS problems
  • Delayed gastric emptying (raises intra- gastric pressure)
  • Hiatus hernia (stomach herniates into oesphagus)
  • Obesity (increases intra abonominal pressure)
29
Q

Give 3 consequences of reflux?

A

Oesphagitis

Stricutres (narrowing of oespahgus due to scar tissue formation from reflux)

Barretts oesophagus

30
Q

How is GORD treated?

A

Lifestyle modifications: loose weight, sleep upright, dont eat too much before bed

Pharmacological: antacids, H2 antagonists, proton pump inhibitors

Surgery (rare)

31
Q

What can cause acute gastritis?

A

heavy use of NSAIDs, Lots of alchol, Chemotherapy, Bile reflux

32
Q

Describe presentation of acute gastritis

A

Asymptomatic or pain, nausia, vomiting, malaena, haematemesis

33
Q

What can cause chronic gastritis (4)

A
  • H. Pylori infection
  • Autoimmune destruction of parietal cells (would also get anaemia, as they produce intrinsic factor needed for B12 absorbtion
  • Chronic alcohol abuse
  • Long term NSAID use
  • Reflux of bile (chronically)
34
Q

Other than chronic gastritis, what can H. Pylori cause?

A

peptic ulcers, adenocarcinoma, MALT lymphoma

35
Q

What is peptic ulcer disease?

A

Defects/ legions in the gastric or duodenal mucosa- the defect must extend through the muscular mucosa to be an ulcer

36
Q

Where is the most common location of a peptic ulcer?

A

Most commonly in the first part of the duodenum (duodenual ulcer), also quite common in the lesser curve of the stomach (gastric ulcer)

37
Q

Give risk factors/ causes for peptic ulcers

A

Excessive stomach acid

H. pylori

NSAIDs

Smoking (contribute to relapses)

Physiological stress (burns ect)

38
Q

How can you clinically differentiate between a gastric and duodenal ulcer?

A

gastric- pain 1/2 an hr after meal & weight loss

Duodenal- pain 2-3 hrs after meal & no weight loss

39
Q

How does peptic ulcer disease present?

A
  • epigastric pain, sometimes extending to the back, often following means and at night time
  • Pain described at burning or gnawing sensation
  • Bleeding/ anaemia if erodes into blood vessels
  • early fullness
  • weight loss at eating sore so dont eat
40
Q

What is a stress ulcer and how does it present

A

An ulcer following burns, raised ICP, sepsis, severe trauma, multiple organ failure

Presents w/ symptoms of gastritis/ ulceration

41
Q

What is functional dyspepsia? How is it diagnosed?

A

Symptoms of peptic ulcer disease without any physical evidence of ulcers

Diganosed by excluding other causes of the symptoms

42
Q

What investigations may be done to investigate stomach pathology?

A
  • Endoscopy
  • Urease breath test (detects H. Pylori)
  • Erect CXR (look for perforation)
  • Blood tests (anaemia)
  • Stool samples (malaena)
  • Abdo X ray- look for bowel obstruction
  • CRP (signs of inflammation)
43
Q

How is H. Pylori spread?

A

Oral- oral or faecal- oral

44
Q

What is H. Pylori’s gram stain characteristics?

A

Gram negative (red), rod

45
Q

How does H. Pylori protect itself from stomach acid?

A

produces urase, which converts urea to ammonia so increases local pH and protects itself from the acid

46
Q

How does H. pylori cause stomach injury?

A

Urase- increases pH and makes ammonium (toxic)

Cytotoxins which injury epithelium

Degrades mucus layer so promotes inflammatory response

47
Q

How is H. Pylori detected?

A

urase breath test

48
Q

Where do H. Pylori most commonly colonise and with what consequence?

A

Anturm (base)- which you find lots of peptic ulcers here

They may also reside in the body, but for some reason if they’re here they more commonly lead to cancer than ulcers

Gastrointestinal system (9 decks)

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