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GASTRO > 4: Stomach > Flashcards

4: Stomach Flashcards

1
Q

What are the functions of the stomach? (3 things)

A
  1. Stores food
  2. Disinfects food
  3. Breaks food → chyme
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2
Q

How does the stomach break food down into chyme? (2 things)

A
  1. Chemical disruption: acid + enzymes
  2. Physical disruption: motility
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3
Q

What are the indents in the Stomach mucosa called?

A

Gastric pits

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4
Q

What do gastric pits open into?

A

Gastric glands

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5
Q

What are the cells of the Gastric Pits?

A

Neck cells

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6
Q

What are the cells of the Gastric Glands? (4 things)

A
  1. Parietal cells
  2. Chief cells
  3. Endocrine cells (G cells)
  4. SMC
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7
Q

What do Neck cells secrete? (2 things)

(Gastric Pit Cell)

A
  1. Mucus
    * Sticky so stays on stomach lining
  2. HCO3-
    * Secreted into mucus, provides buffer for H+ ions
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8
Q

What do Parietal cells secrete?

(Gastric Gland Cell)

A

HCl

  • Keeps stomach pH below 2
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9
Q

What do Chief cells secrete?

(Gastric Gland Cell)

A

Proteolytic enzymes (Pepsin)

  • Breaks down proteins →peptides
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10
Q

What do Endocrine cells secrete?

(Gastric Gland Cell)

A

Gastrin

Bind to receptor on Parietal cell → stimulates HCl secretion

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11
Q

What is the mechanism of HCl secretion? (4 steps)

A
  1. H2O in Parietal cell → H+ + OH-
  2. H+ pumped into Stomach through Canaliculi (invaginations in wall)
    * Canaliculi has proton pump: H+ pumped agains concentration gradient using ATP
  3. OH- combines with CO2 → HCO3-
  4. HCO3- secreted into blood / ECF

H+ and HCO3- secreted at 1:1 ratio

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12
Q

Why are the Canaliculi of the stomachs Parietal cells clinically important?

A

They can be inhibited by Proton Pump Inhibitor Drugs to reduce stomach acid

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13
Q

What are Parietal cells stimulated by? (3 things)

A
  1. Ach
  2. Gastrin
  3. Histamine
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14
Q

How does Ach stimulate Parietal cells? (3 steps)

A
  1. Food arrives → Gastric distension (stretching)
  2. Stretching causes Post-ganglionic PS neurones to release Ach
  3. Ach acts on Muscarinic (M3) receptors on Parietal cells
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15
Q

How does Gastrin stimulate Parietal cells? (2 steps)

A
  1. Presence of Ach stimulates → Endocrine Cells (G Cells) to secrete Gastrin
  2. Gastrin binds to surface receptors on Parietal cell
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16
Q

What is Gastrin inhibited by?

A

Low stomach pH (feedback control)

Because Gastrin makes Parietal cells make HCl so if pH already low then you don’t neeeeeeed it

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17
Q

How does Histamine stimulate Parietal cells? (3 steps)

A
  1. Gastrin + Ach stimulate Mast Cells → release Histamine
  2. Histamine binds to H2 receptors on Parietal cells
  3. Stimulates acid secretion via cAMP
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18
Q

What are the 3 phases of Gastric secretion?

A
  1. Cephalic Phase (High)
  2. Gastric Phase (High)
  3. Intestinal Phase (Low)
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19
Q

How is Gastric secretion stimulated in the Cephalic phase? (High acid) (3 steps)

A
  1. Sight, smell, swallowing → activates PNS
  2. PNS stimulates Ach release
  3. Ach stimulates Parietal cells
  • Directly
  • via Histamine

Called cephalic phase because sight smell and swallowing happens in the head innit

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20
Q

How is Gastric secretion stimulated in the Gastric phase? (High acid) (5 steps)

A
  1. When food reaches stomach → Gastric distensions (stretching)
  2. Stretching stimulates Ach release (via Post-ganglionic PS neurones)
  3. Food also buffers acid, increasing the pH, this disinhibits Gastrin → Gastrin secreted
  4. Acid + enzymes breakdown proteins → peptides
  5. Peptides stimulate Gastrin

Called gastric phase because everything happens in stomach innit

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21
Q

How is Gastric secretion inhibited in the Intestinal phase? (Low acid)

A
  1. When chyme leaves stomach → stimulates 2 hormones:
  2. Cholecystokinin (CCK)
  3. Gastric Inhibitory Polypeptide
  4. CCK & GIP antagonise Gastrin → Low acid secretion
  5. No food to buffer acid so pH decreases → low pH inhibits Gastrin → Low acid secretion

Called intestinal phase because food has gone to intestines now innit

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22
Q

What drugs can be used to reduce Gastric acid secretion? (2 things)

A
  1. Anti-histamine
  2. Proton Pump Inhibitor
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23
Q

How does Anti-histamine reduce gastric acid secretion? (2 steps)

A
  1. Inhibits histamine @ H2 receptors (on Parietal cells)
  2. Removes Gastrin / Ach signal amplification
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24
Q

How do Proton Pump Inhibitors reduce gastric acid secretion?

A

Prevent H+ from being pumped through Parietal cell Canaliculi

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25
Q

What are the properties of stomach mucus? (2 things)

A
  1. Sticky: stays on stomach lining
  2. Basic: buffers H+
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26
Q

What layer does mucus form in the stomach?

A

An “unstirred layer”

Where ions can’t move easily in

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27
Q

How does the “unstirred” layer of the stomach buffer H+? (3 steps)

A
  1. H+ ions diffuse into layer from stomach lumen
  2. HCO3- secreted into layer from Neck Cells (Gastric Pit Cells)
  3. Because layer is unstirred (ion can’t move easily in): HCO3- stays close to surface cells → surface pH stays above 6
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28
Q

What are HCO3- and Mucus secretions stimulated by?

A

Prostaglandins

  • (Which are promoted by most factors that stimulate acid secretion)
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29
Q

What things can breach the stomachs defences? (3 things)

A
  1. Alcohol
  2. Helicobacter Pylori
  3. NSAIDs
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30
Q

How does alcohol breach the stomachs defences?

A

Dissolves mucus → acid attacks stomach

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31
Q

How does Helicobacter Pylori breach the stomachs defences?

A

Infects surface cells → No mucus / HCO3- produced

32
Q

How do NSAIDS breach the stomachs defences?

A

Inhibit prostaglandins → no HCO3- / mucus produced

33
Q

What can form if the stomach defences are breached?

A

Peptic ulcers

34
Q

What is the treatment for breached stomach defences / peptic ulcers? (2 things)

A
  1. Reduce acid secretion (anti-histamine / proton pump inhibitors)
  2. Abx to eliminate Helicobacter Pylori (if needed)
35
Q

What reflex allows us to eat larger meals?

A

Receptive Relaxation

36
Q

What is Receptive Relaxation?

A

Stomach reflex: Gastric fundus dilates when food passes down pharynx + oesophagus

37
Q

How does Receptive Relaxation occur? (3 steps)

A
  1. Food goes down pharynx + oesophagus
  2. Neural reflex from Vagus nerve triggers stomach wall relaxtion → stomach pressure doesn’t increase
  3. Pressure not increasing limits reflux + allows us to eat larger meals
38
Q

What happens if the Vagus nerve is damaged? (Receptive relaxation)

A

Stomach pressure increase NOT inhibited by Receptive Relaxation → Reflux + Can’t eat large meals

39
Q

What are the rhythmic contractions of the stomach? (2 steps)

A
  1. Pacemaker in Cardiac region of Stomach → drives Longitudinal + Circular muscles contrctions
  2. Regular accelerating peristaltic contractions from Cardia → Pylorus
40
Q

How is the stomach emptied?

A
  1. Chyme reaches Pyloric region
  2. Small squirt ejected into intestine before peristaltic wave comes and shuts it
    * 3 persistaltic waves / min → 3 squirts / min
41
Q

What are the squirts of gastric emptying affected by? (3 things)

A
  1. Rate of peristaltic wave acceleration
  2. Intestinal hormones
  3. Fat + low pH slows down emptying
42
Q

What are some Gastric disordes? (4 things)

A
  1. Gastro-oesophageal Reflux Disease (GORD)
  2. Peptic Ulcer Disease (PUD)
  3. Helicobacter Pylori
  4. Gastrits
43
Q

What are the clinical features of Gastro-oesophogeal Reflux Disease (GORD)?

A

Dyspepsia (heart burn)

  • Worse @ lying down / bending / hot drinks
44
Q

How is Gastro-oesophogeal Reflux Disease (GORD) diagnosed and investigated? (2 things)

A
  1. Clinical diagnosis done on symptoms alone
  2. If Hiatus Hernia suspected: investigate by Endoscopy
45
Q

How is Gastro-oesophogeal Reflux Disease (GORD) managed? (6 things)

A
  1. Lifestyle
  • Lose weight
  • Reduce smoking / alcohol
  • Reduce chocolate + fatty foods
  1. Medication
  • Antacids
  • Proton Pump Inhibitor → reduces acid secretion from Parietal cells
  • Anti-histamines (H2 antagonists) → reduces acid secretion from Parietal cells
46
Q

What happens to the stomach cells in Peptic Ulcer Disease (PUD)?

A

Break in superficial epithelial cells → Penetrates down to Muscularis Mucosa

47
Q

What causes Peptic Ulcer Disease (PUD)?

A

NSAIDS

  • Inhibit prostaglandin production → reduces mucus production
48
Q

What are the clinical features of Peptic Ulcer Disease (PUD)? (2 things)

A
  1. Burning epigastric pain
  • Persistant + severe pain: suggests ulcer penetration into other organs
  • Back pain: suggests posterior penetration of ulcer
  1. Weight loss / anorexia
49
Q

How is Peptic Ulcer Disease (PUD) investigated? (2 things)

A
  1. Investigate H. Pylori infections
  2. Endoscopy for older patients → rule out cancer
50
Q

How is Peptic Ulcer Disease (PUD) managed? (2 things)

A
  1. If due to H. Pylori: Triple Therapy:
  • Proton Pump Inhibitors
  • Abx
  • Anti-histamine (H2 antagonists)
  1. If taking NSAIDs: Stop + review
51
Q

What are the complications of Peptic Ulcer Disease (PUD)? (2 things)

A
  1. Perforations of ulcer → into Peritoneal cavity
  2. Gastric outlet obstruction
52
Q

What is Chronic Gastritis caused by?

A

Helicobacter Pylori

53
Q

What are the features of Helicobacter Pylori? (3 things)

A
  1. Aerobic
  2. Produces urease enzyme
  3. Resides in stomach of infected person
54
Q

How does Helicobacter Pylori survive in the stomach?

A
  1. Produces urease enzyme → produces ammonia
  2. Ammonia neutralised acid → allows H. Pylori to survive
55
Q

How does Helicobacter Pylori damage the stomach? (2 things)

A

Damages epithelium by:

  1. Releasing enzymes
  2. Inducing apoptosis
56
Q

How is Helicobacter Pylori diagnosed? (3 things)

A
  1. igG in serum
  2. Urea breath test
  3. Culture gastric sample (taken by endoscopy)
57
Q

What is the treatment for Helicobacter Pylori?

A

Triple Therapy:

  • Proton Pump Inhibitors
  • Abx
  • Anti-histamine (H2 antagonists)
58
Q

What can chronic gastritis cause?

A

Ulceration

Endocrine cells (G cells) release gastrin (Hypergastrinaemia) → increases acid production → ulceration

59
Q

What are the 5 parts of the stomach?

A
  1. Cardia
  2. Fundus
  3. Body
  4. Antrum
  5. Pylorus
60
Q

What are the 2 stomach sphincters?

A
  1. Inferior Oesophageal Sphincter
  2. Pyloric Sphincter
61
Q

What is the Z line of the GI system?

A

Where Squamous mucosa of oesophagus meets Columnar mucosa of stomach

62
Q

What is superior to the Z line of the GI system?

A

Diaphragmatic musculature: forms LOWER OESOPHAGEAL SPHINCTER

63
Q

What is the Lower Oesophageal sphincter coupled with to prevent stomach reflex?

A

Cardiac notch of stomach

64
Q

What is the Pyloric sphincter made out of?

A

Thickened circular muscle coat

65
Q

What does the Pyloric sphincter of the muscle control?

A

The squirts of the stomach into the duodenum

66
Q

What is the gastric mucosa like when empty?

A
  1. Longitudinal folds (rugae)
  2. Gastric canal forms between folds along Lesser Curvature of stomah → allows saliva & small parts of food → Pylorus
67
Q

How are the different parts of the stomach histologically different?

A
  1. Cardia:
    * Neck cells → mucus
  2. Fundus & Body
  • Neck cells → mucus
  • Parietal cells → acid
  • Chief cells → pepsinogen
  1. Pylorus
  • Neck cells → mucus
  • Endocrine Cells (G cells) → Gastrin
68
Q

What are the peritoneal folds around the stomach? (2 things)

A
  1. Greater Omentum
  2. Lesser Omentum
69
Q

What is the Greater Omentum? (3 points)

A
  1. 4 layered peritoneal fold
  2. Hangs down from GREATER curvature of stomach
  3. Folds back up → attaches to anterior surface of transverse colon + its mesentry
70
Q

What is the Lesser Omentum? (3 points)

A
  1. 2 layered peritoneal fold
  2. Connects LESSER curvature of stomach + proximal part of duodenum → liver
  3. Connects stomach to portal triad
71
Q

What is the blood supply tree to the stomach?

A
72
Q

What is the blood supply to the Lesser Curvature of the stomach?

A

L & R Gastric Arteries

L esse R

73
Q

What is the blood supply to the Greater Curvature of the stomach?

A

L & R Gastro-omental Arteries

74
Q

What is the blood supply to the Fundus & Body of the stomach?

A

Posterior Gastric arteries

75
Q

What is the venous drainage of the stomach? (4 things)

A
  1. L & R Gastric → Hepatic portal vein (HPV)
  2. Short Gastric → Splenic vein → joins Superior Mesenteric Vein (SMV) → HPV
  3. L Gastro-omental → splenic vein → joins SMV → HPV
  4. R Gastro-omental → SMV → joins splenic vein → HPV

GASTRO (10 decks)

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