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BMS150 Post-MT2 > Physiology and Pathology: The Stomach > Flashcards

Physiology and Pathology: The Stomach Flashcards

1
Q

What is the most distensible part of the GI tract?

A

Stomach

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2
Q

Two general functions of the stomach?

A
  1. Reservoir for food before release into SI
  2. Mixes saliva, food, and gastric juices to form chyme
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3
Q

4 main regions of the stomach?

A
  • Cardia
  • Fundus
  • Body
  • Pyloric
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4
Q

Two sphincters of the stomach?

A
  • Lower esophageal
  • Pyloric
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5
Q

Main arterial supply of the stomach?

A

Celiac trunk

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6
Q

Main arteries that supply the stomach?

A
  • Hepatic artery
  • Celiac trunk
  • Splenic artery
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7
Q

Branches of hepatic artery supplying stomach?

A
  • Right gastric
  • Right gastro-omental
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8
Q

Branch of celiac trunk supplying stomach?

A
  • Left gastric
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9
Q

Branch of splenic artery supplying stomach?

A
  • Left-gastro-omental
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10
Q

Veins that drain the stomach?

A
  • Hepatic portal vein
  • Superior mesenteric vein
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11
Q

Veins that drain into hepatic portal vein?

A

Left gastric and right gastric veins

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12
Q

Veins that drain into superior mesenteric vein?

A

Left and right gastro-omental veins

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13
Q

Parasympathetic supply of the stomach?

A

Vagus nerve

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14
Q

Sympathetic supply of the stomach?

A
  • From T5-T9
  • Passes to celiac plexus via greater splanchnic nerve
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15
Q

Epithelium and lamina propria are arranged into ______

A

Glands

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16
Q

Glands have 3 regions:

A
  1. Pit
  2. Neck
  3. Base
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17
Q

Cell types in surface epithelium and gastric pit? (3)

A
  • Simple columnar epithelium
  • Mucin granules
  • Short microvilli
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18
Q

Cell types in neck/ismuth?

A
  • Simple columnar epithelium
  • Shorter and contain less mucin granules
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19
Q

Cell type in neck and base?

A
  • Parietal cells (Oxyntic)
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20
Q

What are parietal cells? Function?

A

Cells found mainly in upper half of gastric gland that produce HCl and IF

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21
Q

Cell type in base?

A

Chief cells (zymogenic)

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22
Q

What are chief cells? What is their function?

A

Cells found in lower regions of gastric glands with lots of RER and granules. Function of granules is to secrete pepsinogen

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23
Q

Cell types in glands (deep in gastric pits)? Subdivisions and functions?

A

Entero-endocrine cells
- Enterochromaffin-like (histamine)
- G-cells (Gastrin)
- D-cells (Somatostatin)

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24
Q

3 layers of muscularis externa?

A
  • Inner oblique
  • Middle circular
  • Outer longitudinal
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25
Q

4 stages of motility?

A
  1. Food entry into stomach
  2. Storage in fundus
  3. Mixing
  4. Emptying into small intestine
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26
Q

Functions of LES? (2)

A
  • Controls movement of food into stomach
  • Prevents reflux
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27
Q

Resting tone of LES is maintained via ________ properties of sphincter muscles & cholinergic regulation

A

Intrinsic myogenic

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28
Q

To allow food to enter the stomach, a wave of ______ moves along the esophagus, LES, and into stomach and SI initiated by ________

A

Relaxation; vasovagal reflex (receptive relaxation)

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29
Q

What is gastric accomodation?

A

Presence of food in stomach stretches wall of body of stomach (reduces muscular tone)

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30
Q

Presence of food in the stomach triggers mixing waves, initiated by what?

A

Gastric pacemakers

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31
Q

Waves start where and move toward what? What is this called?

A

Mid- to upper portion ad move toward pyloric antrum - Propulsion

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32
Q

What is retropulsion?

A

Pylorus opening is very small so antral contents are pushed back upstream toward body of stomach

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33
Q

Only what can leave the stomach through the pyloric sphincter?

A

Liquid

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34
Q

What is the rate of gastric emptying governed by?

A

Signals from stomach and duodenum

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35
Q

What do gastric emptying signals ensure? (2)

A
  • pH inside duodenum doesn’t become too acidic
  • Travel time slow enough for nutrient absorption
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36
Q

Gastric acid:
- Released from _____
- pH ____
- Composed of _____ (3)
- Functions _______ (3)

A
  • G-cells
  • pH 1-2
  • HCl (main), KCl (lots), NaCl (little)
  • Functions: digestion of proteins, bacteriostatic, conversion of pepsinogen to pepsin
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37
Q

Gastric acid secretion mechanism: CO2 combines with OH to form what? Using what enzyme?

A

Bicarbonate via carbonic anhydrase

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38
Q

What is pumped into the lumen of the canaliculus and what is passively transported there?

A
  • Pump: H+
  • Passive: Cl-
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39
Q

What ATPase is blocked by PPIs?

A

H+/K+ ATPase

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40
Q

What can stimulate parietal cells? (3)

A
  • Ach on muscarinic receptors
  • Gastrin on CCK2 receptors
  • Histamine on H2 receptors
41
Q

Functions of Histamine? (3)

A
  • Acts on muscarinic receptors of parietal cells
  • Stimulates release of gastric acid
  • Stimulates vasodilation
42
Q

What is gastrin secreted in response to? (3)

A
  • Stomach distension
  • Vagal stimulation
  • Presence of partially digested proteins
43
Q

Functions of gastrin? (2)

A
  • Acts on ECL to stimulate Histamine release
  • Directly stimulates parietal cells by binding to CCK2 receptors
44
Q

What can inhibit parietal cells? (2)

A
  • Somatostatin
  • PGs
45
Q

Somatostatin as also known as what?

A

Growth hormone inhibiting hormone

46
Q

Functions of somatostatin? (3)

A
  • Reduce secretion of gastric acid by parietal cells
  • Reduces secretin and histamine
  • Suppresses release of pancreatic hormones
47
Q

What is somatostatin released in response to?

A

Luminal H+

48
Q

When is gastric acid secretion higher? Lower?

A
  • Higher after meal
  • Lower between meals
49
Q

Phases of gastric acid secretion? (3)

A
  • Cephalic
  • Gastric
  • Intestinal
50
Q

What is cephalic phase triggered by?

A

Smell, sight, taste, thought and swallowing food

51
Q

Cephalic phase is primarily mediated by what?

A

Vagus nerve

52
Q

Vagus nerve releases?

A

Ach and GRP

53
Q
  • Ach acts directly on ______ cells to release H+
  • Ach acts on ______ cells to release histamine
  • Ach acts on D cells, inhibiting release of ______
A
  • Parietal cels
  • ECL cells
  • somatostatin
54
Q

Vagus nerve releases GRP to induce what?

A

Gastrin release from G cells

55
Q

What is the gastric phase triggered by?

A

Food entering stomach, distending gastric mucosa

56
Q

Gastric phase is mediated by what?

A

Vagal reflex and ENS reflex

57
Q

Partially digested proteins stimulate what?

A

G cell release of gastrin

58
Q

Low luminal pH stimulates what?

A

D cells to secrete somatostatin = inhibit gastrin production

59
Q

What is the intestinal phase triggered by?

A

Presence of amino acids and partially digested peptides in proximal intestine

60
Q

What is intrinsic factor? What is its function?

A
  • Glycoprotein secreted by parietal cells
  • Required for absorption of B12 in ileum
61
Q

Where is pepsinogen secreted from?

A

Chief cells via exocytosis

62
Q

What is required for pepsinogen => pepsin?

A

Spontaneous cleavage in presence of HCl

63
Q

Pepsin function?

A

Digestion of protein

64
Q

What is pepsinogen secretion stimulated by? (2)

A
  • Ach release from vagus nerve
  • Presence of acid in the duodenum triggers secretin from S cells => pepsinogen from chief cells
65
Q

What receptor does Ach bind to on chief cells?

A

M receptors

66
Q

How is the stomach able to withstand the low pH and high pepsin levels?

A

Gastric diffusion barrier

67
Q

How is the gastric diffusion barrier maintained? (3)

A
  • Mucus gel layer on surface epi
  • Bicarb microclimate
  • Tight junctions in gastric glands
68
Q

What cells secrete gastric mucin?

A

Simple columnar epithelium

69
Q

How does the gel layer form?

A

Mucous + phospholipids + electrolytes + water

70
Q

Functions of mucus layer? (2)

A
  • Protect against acid, pepsin, bile acid, ethanol
  • Lubricates gastric mucosa to minimize abrasions
71
Q

Mucin secretion is induced by? (2)

A
  • Vagal stimulation
  • Chemical irritation
72
Q

What does the bicarbonate microclimate do?

A

Neutralize most acid that
diffuses through the mucosal layer
and inactivate any pepsin that penetrates the mucus

73
Q

HCO3- secretion induced by? (3)

A
  • Vagal stimulation
  • PGE2
  • Intraluminal pH
74
Q

Inflammation of stomach mucosa?

A

Gastritis

75
Q

Damage is limited to the gastric mucosa (ie. does not penetrate beyond the lamina propria)?

A

Gastric erosion

76
Q

What is acute gastritis?

A

Gastric mucosal inflammation caused by an imbalance between protective factors and secretion of acid and pepsin

77
Q

Etiology of acute gastritis? (6)

A
  • NSAID toxicity
  • Alcohol
  • Bile
  • Shock/sepsis
  • Intracranial lesions
  • H. pylori (more often chronic)
78
Q

What happens in acute gastritis when mild inflammation progresses to active inflammation?

A

Lots of neutrophils above basement membrane contacting epithelial cells

79
Q

In severe cases where erosion and bleeding occur, what is acute gastritis called?

A

Acute erosive hemorrhagic gastritis

80
Q

Clinical features of acute gastritis?

A
  • Dyspepsia
  • Nausea, vomiting, loss of appetite, belching, bloating
  • Acute abdominal pain
81
Q

Complications of acute gastritis?

A
  • Perforation leading to peritonitis
  • Bleeding
  • Chronic gastritis
82
Q

Most common cause of chronic gastritis?

A

H. pylori

83
Q

Most common site in the stomach for H. pylori infection?

A

Stomach antrum

84
Q

Types of chronic gastritis? (2)

A
  • Non-atrophic = inflammation without loss of gastric glandular cells
  • Atrophic = loss of gastric glandular cells
85
Q

What are gastric glandular cells replaced by in chronic atrophic gastritis?

A

Intestinal epithelium, pyloric-type glands, fibrous tissue (metaplasia)

86
Q

Common cause of non-atrophic and atrophic chronic gastritis?

A
  • Non-atrophic = H. pylori
  • Atrophic = H. pylori and autoimmunity
87
Q

What do H. pylori bacteria seem to cause the reduction of?

A

Mucous and bicarb secretion

88
Q

What may overgrowth of MALT associated with H. pylori be associated with?

A

Gastric lymphoma

89
Q

Clinical features of chronic gastritis?

A
  • Epigastric pain
  • Nausea, vomiting, anorexia, early satiety
  • Weight loss
90
Q

Complications of chronic gastritis?

A
  • PUD
  • Gastric adenocarcinoma
  • MALT lymphoma
91
Q

Two main types of peptic ulcer disease?

A
  • Duodenal - lower likelihood of perforation/malignancy
  • Gastric
92
Q

Etiology of PUD?

A
  • H. pylori infection
  • NSAIDs
  • Cigarette smoking
93
Q

Pathogenesis of PUD?

A

Occurs due to imbalance between defense mechanisms and damaging factors causing chronic gastritis

94
Q

Duodenal ulcer and gastric ulcer pathogenesis?

A

H. pylori colonization due to:
- decreased bicarb in duodenum
- increased gastric acid in antrum

95
Q

Gastric ulcer in fundus or body pathogenesis?

A

Caused by mucosal atrophy

96
Q

Peptic ulcers are round to oval shaped, sharply _______ defect

A

punched-out

97
Q

What can happen to larger vessels within scarred area of ulcer?

A

They can become thickened and thrombosed

98
Q

Clinical features of PUD?

A
  • Intense pain associated with perforation, bleeding, peritonitis
  • Duodenal ulcers relieved by eating and awake patient at night
  • Gastric ulcers weight loss is common
  • Can also present with iron-deficiency anemia, bleeding, nausea/vomiting, bloating, and belching
99
Q

Complications of PUD?

A
  • Perforation leading to peritonitis
  • Bleeding
  • Gastric adenocarcinoma & MALT lymphoma

BMS150 Post-MT2 (17 decks)

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