Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

BMS150 - Post Test 2 > Stomach Physiology and Pathology (Week 11) > Flashcards

Stomach Physiology and Pathology (Week 11) Flashcards

1
Q

True or False: The stomach is a J-shaped enlargement directly inferior to the diaphragm and is the most distensible part of the GI tract

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the functions of the stomach?

A

1) serves as a reservoir for food before release into small intestine

2) mixes saliva, food, and gastric juice to form chyme

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two sphincters of the stomach?

A

1) lower esophageal

2) pyloric

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

True or False: The lower esophageal sphincter separates the esophagus and the stomach

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the main arterial supply of the stomach?

A

celiac trunk of the aorta

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the 4 arteries that supply the stomach?

A

1) hepatic artery –> right gastric artery
2) hepatic artery –> right gastro-omental artery
3) celiac trunk –> left gastric artery
4) splenic artery –> left gastro-omental artery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What veins does the stomach drain into?

A

1) hepatic portal vein

2). superior mesenteric vein

Note: the veins run parallel with the arteries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

The left gastric vein and right gastric vein drain into the ______________

A

hepatic portal vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The left gastro-omental vein and right gastro-omental vein drain into the __________________

A

superior mesenteric vein

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the parasympathetic innervation of the stomach?

A

anterior and posterior vagal trunks from vagus nerve

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the sympathetic innervation of the stomach?

A
  • from T5-T9 segments of sympathetic trunk
  • passes to celiac plexus via greater splanchnic nerve
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the three layers of stomach mucosa?

A

1) epithelium (on the surface)
2) lamina propria
3) muscularis mucosae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

In which mucosal layer of the stomach would you find loose connective tissue, smooth muscle, and lymphoid cells?

A

lamina propria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Which mucosal layer of the stomach is organized into three layers: inner circular, outer longitudinal, outermost circular?

A

muscularis mucosae

Note: this is NOT talking about the muscularis externa which has an oblique layer, circular layer, and longitudinal layer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

The epithelium and lamina propria are arranged into glands. What are the three regions of these glands?

A

1) gastric pit
2) neck (isthmus)
3) base

Note: there are different cell types that are found in different regions of the glands

Note: different regions of the stomach have different glands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What type of cells are found in the surface epithelium and gastric pits?

A

simple columnar cells

Note:
- lines the surface of the stomach and gastric pits
- lots of mucin granules in apical surface (apical = means side of the lumen; mucin = large glycoprotein that lubricates)
- short microvilli also at the apical surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What type of cells are found in the neck/isthmus?

A

simple columnar cells

Note:
- usually interspersed between parietal cells (parietal cells make HCl)
- shorter and contain LESS mucin granules in apical surface

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What type of cells are in both the neck & base?

A

parietal cells (oxyntic)

Note:
- mainly in upper half of gastric gland
- rounded/pyrimidal shape
- tubulovesicular structures in apical region; rearrange to form lumen canaliculi when active
- function = to produce HCl and IF (IF = intrinsic factor; helps us absorb B12)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of cells are found in the base?

A

chief cells (zymogenic)

Note:
- found in lower regions of gastric glands
- have abundant RER for synthesizing proteins
- contain granules that contain pepsinogen (in the presence of acid breaks down to give pepsin; pepsin is used to break down protein)
- function = pepsinogen secretion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What type of glands/enteroendocrine cells are found deep within the gastric pits?

A
  • enterochromaffin-like cells (secrete histamine)
  • G-cells (secrete gastrin)
  • D cells (secrete somatostatin)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

The ____________ of the stomach contains dense, irregular connective tissue and a rich vascular and lymphatic network draining the lamina propria

A

submucosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the three layers of the muscularis externa?

A

1) inner oblique
2) middle circular
3) outermost longitudinal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Underneath the muscularis externa is the ___________

A

serosa

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are four stages of stomach motility?

A

1) food entry into stomach
2) storage in fundus
3) mixing (aka churning)
4) emptying into small intestine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

The _________________ controls movement of food into the stomach and prevents reflux of gastric contents into the esophagus

A

lower esophageal sphincter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

How is the resting tone of the lower esophageal sphincter maintained?

A

via intrinsic myogenic properties of sphincter muscles & cholinergic regulation

Note: relaxation is required to allow entry of food into the stomach

Recall: cholinergic = parasympathetic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Food entry into the stomach is initiated by a vasovagal reflex called _________________

A

receptive relaxation

Note: this reflex is triggered by swallowing and esophageal distension

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Following receptive relaxation, then a wave of _______________ from the esophagus approaches the stomach and pushes food into the stomach

A

peristalsis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

The presence of food in the stomach stretches the stomach wall, reducing the tone of the wall. This is known as what?

A

gastric accomodation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

How much volume can a completely relaxed stomach hold?

A

0.8-1.5L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When waves that start in the middle to upper portion of the stomach move the bolus toward the pyloric antrum

A

propulsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

contractions in the pyloric antrum that grinds the food bolus

A

grinding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

When antral stomach contents are pushed back upstream toward the body of the stomach due to contents being forced into the very small opening of the pylorus

A

retropulsion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

True or False: Only liquid can leave the stomach via the pyloric sphincter. If particles are greater than 2mm in size, mixing continues

A

True

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

the movement of liquid chyme from the stomach into the small intestine

A

gastric emptying

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

The rate of gastric emptying is governed by signals from the ____________________

A

stomach and duodenum

Note: this ensures pH inside the duodenum does not become too acidic (too acidic = can cause damage/ulcers) + ensures travel time is slow enough for nutrient absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Gastric acid is released from __________ cells

A

parietal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What is the pH of gastric acid?

A

pH 1-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

What is gastric acid composed of?

A
  • hydrochloric acid (HCl) *
  • large amounts of KCl
  • small amounts of NaCl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What is the function of gastric acid?

A
  • digestion of protein (denatures them)
  • bacteriostatic (prevents growth but doesn’t kill them)
  • conversion of pepsinogen to pepsin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What enzyme facilitates the conversion of CO2 and OH- to bicarbonate ions?

A

carbonic anhydrase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

How does H+ get into the lumen of the canaliculus?

A

H+/K+ ATPase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

How does Cl- get into the lumen of the canaliculus?

A

passive transport from cytoplasm of parietal cell into lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

H+/K+ ATPase is blocked by what type of drug?

A

proton pump inhibitors (PPI)

Note: this would lower acidity in the stomach, since we block the transport of H+ ions into the lumen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What can stimulate parietal cells?

A
  • acetylcholine
  • gastrin
  • histamine

Note: all of these promote acid production (more H+ ions being pumped into the lumen)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Acetylcholine acts on what type of receptor in the stomach?

A

muscarinic receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Gastrin acts on what type of receptor in the stomach?

A

CCK2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Histamine acts on what type of receptor in the stomach?

A

H2 receptors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

function of histamine in stomach

A
  • stimulates release of gastric acid
  • stimulates vasodilation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

What drug works by blocking the H2 receptor?

A

H2 receptor antagonists

Note: usually used for GERD; result = decreased acid production in stomach

51
Q

Gastrin is secreted in response to what?

A
  • stomach distension
  • vagal stimulation
  • presence of partially digested proteins (peptides and amino acids)
52
Q

function of gastrin in the stomach

A
  • acts on ECL cells (ECL cells release histamine) to stimulate the release of histamine –> leads to increased gastric acid
  • directly stimulates parietal cells
53
Q

What can inhibit parietal cells, thereby reducing acid production?

A
  • somatostatin
  • prostaglandins
54
Q

function of somatostatin

A
  • act on parietal cells to reduce secretion of gastric acid
  • reduce release of gastrin, secretin, and histamine
  • suppresses release of pancreatic hormones
55
Q

What is somatostatin secreted in response to?

A

luminal H+

Note: this is negative feedback

56
Q

True or False: Gastric acid is substantially lower after meals and high between meals

A

False.

Gastric acid is substantially HIGHER after meals and LOW between meals

57
Q

What are the phases of gastric acid secretion after meals?

A

1) cephalic
2) gastric
3) intestinal

58
Q

What is the cephalic stage of gastric acid secretion triggered by?

A

smell, sight, taste, thought, and swallowing food

59
Q

The cephalic stage is mediated by what nerve?

A

vagus nerve

60
Q

The vagus nerve releases ____________

A

acetylcholine (Ach)

61
Q

REVIEW: Ach acts directly on ___________ cells to release H+ ions

A

parietal

62
Q

REVIEW: Ach acts on _____________ cells to release histamine

A

ECL

63
Q

REVIEW: Ach acts on _____________ cells, inhibiting the release of somatostatin

A

D cells

64
Q

The vagus nerve releases gastrin-releasing peptide (GRP) to induce the release of _________ from G cells

A

gastrin

65
Q

The cephalic stage accounts for _____ % of gastric acid secretion

A

30%

66
Q

During the gastric phase of gastric acid secretion, food enters the stomach, distending the gastric mucosa and activates the _______________

A

vasovagal reflex & local ENS reflex

67
Q

During the gastric phase of gastric acid secretion, partially digested proteins stimulate G cells to produce ___________

A

gastrin

Note: carbs nor lipids participate in gastric acid secretion, BUT components of wine, beer, and coffee CAN promote gastric secretion by stimulating G cells (these same three things can trigger GERD)

68
Q

Low luminal pH stimulates D cells to secrete _________, which INHIBITS gastrin production

Note: this is negative feedback

A

somatostatin

69
Q

The gastric phase accounts for _____ % of gastric acid secretion

A

50-60%

70
Q

In the intestinal phase of gastric acid secretion, we have the presence of amino acids and partially digested peptides in the proximal intestine, that stimulates G cells in the duodenum to secrete __________

A

gastrin

71
Q

The intestinal phase accounts for _____ % of gastric acid secretion

A

5-10%

72
Q

Intrinsic factor is a ___________ secreted by parietal cells

A

glycoprotein

73
Q

What is the function of intrinsic factor?

A

required for the absorption of vitamin B12 in the ileum (last part of the small intestine)

74
Q

Pepsinogen is secreted by chief cells via ___________

A

exocytosis

75
Q

Pepsinogen is spontaneously cleaved into __________ in the presence of HCl

A

active pepsin

76
Q

What is the function of pepsin?

A

digestion of protein (via hydrolysis of the peptide bond)

Note: function of pepsin is dependent on low pH (optimal = 1.8-3.5)

77
Q

Secretion of pepsinogen is stimulated by what?

A

1) Ach release from vagus nerve or enteric nervous system (ENS), whereby Ach binds to M receptors on chief cells

2) presence of acid in the duodenum triggers secretin from S cells; secretin also stimulates chief cells to release more pepsinogen

78
Q

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

A

Gastric diffusion barrier

  • mucus gel layer on surface epithelium
  • bicarbonate microclimate adjacent to surface epithelial
  • tight junctions in gastric glands
79
Q

What does mucus combine with to form the mucus gel layer on the epithelium?

A
  • phospholipids
  • water
  • electrolytes
80
Q

What does the mucus gel layer on the surface epithelium protect against?

A
  • acid
  • pepsin
  • bile acid
  • ethanol
  • also minimizes abrasions from food
81
Q

Mucin secretion is induced by what?

A

1) vagal stimulation
2) chemical irritation

82
Q

True or False: Surface epithelial cells secrete HCO3, which remains trapped in the mucus gel layer.

A

True

83
Q

________ can neutralize most acid that diffuses through the mucosal layer and inactivate any pepsin that penetrates the mucus

A

HCO3-

84
Q

What is HCO3- secretion induced by?

A

1) vagal stimulation
2) PGE2 (prostaglandin E2)
3) intraluminal pH

85
Q

inflammation of stomach mucosa

A

gastritis

Note: may be acute or chronic

86
Q

damage is limited to the gastric mucosa (e.g., does not penetrate beyond the lamina propria)

A

gastric erosiion

87
Q

damage extends beyond lamina propria

A

peptic ulcer

88
Q

loss of gastric glandular cells

A

gastric atrophy

89
Q

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

A

acute gastritis

Note: ranges in severity (can be asymptomatic and discovered incidentally or can cause catastrophic blood loss, anemia, or peritonitis

90
Q

What is the etiology of acute gastritis?

A
  • NSAID toxicity
  • alcohol
  • bile
  • shock/sepsis
  • intracranial lesions
  • H. pylori

Note: H. pylori more closely linked to chronic gastritis

91
Q

How can NSAIDs contribute to the development of acute gastritis?

A

Inhibits prostaglandins

Recall: What is the role of prostaglandins on gastric acid secretion? –> Prostaglandins REDUCE acid secretion (therefore inhibiting = indirectly increasing acid secretion in the stomach)

Additionally, prostaglandins (i.e., PGE2) promote bicarbonate secretion, so inhibiting prostaglandins = your protective layer is diminished

Note: this effect is more significant for nonselective inhibitors (aspirin, ibuprofen, and naproxen); but can also occur with selective COX-1 inhibitors (celecoxib)

92
Q

How can alcohol consumption contribute to the development of acute gastritis?

A

causes direct cellular damage

93
Q

How can intracranial lesions contribute to the development of acute gastritis?

A

thought to stimulate the parasympathetic nervous system

94
Q

True or False: Acute gastritis usually starts with mild inflammation and progresses to active inflammation

A

True

95
Q

What is the difference between mild inflammation and active inflammation in acute gastritis?

A

Mild inflammation:
- lamina propria shows moderate edema and slight vascular congestion
- surface epithelium intact with scattered neutrophils

Active inflammation:
- lots of neutrophils found above the basement membrane in direct contact with epithelial cells

96
Q

True or False: In severe cases of acute gastritis, mucosal damage may progress to erosions and bleeding

A

True

97
Q

acute erosive hemorrhagic gastritis = erosion + __________

A

bleeding

98
Q

erosion = loss of superficial epithelium (damage does not penetrate ___________)

A

the lamina propria

99
Q

What are the clinical features of acute gastritis?

A

May be asymptomatic, but often includes:

  • dyspepsia (upset stomach/discomfort; very common)
  • nausea
  • vomiting
  • loss of appetite
  • belching
  • bloating
  • acute abdominal pain
100
Q

What are some complications to be aware of regarding acute gastritis?

A
  • perforation (leading to peritonitis = medical emergency**)
  • bleeding
  • chronic gastritis
101
Q

True or False: Chronic gastritis is one of the most common GI disorders

A

True-ish

Note: However, recent research shows that it’s not AS common as we thought; Canadian guidelines have yet to be updated… so many people who “have chronic gastritis” actually don’t

102
Q

What is the most common cause of chronic gastritis?

A

H. pylori

Note: prevalence in Canada = 20-30%

Other causes:
- pernicuous anemia, Crohn’s disease, radiation toxicity, amyloidosis

103
Q

gram negative motile curved rod bacteria that lives in the mucous layer

A

H. pylori

104
Q

What is the most commonly infected site in chronic gastritis?

A

stomach antrum

Note: can progress to gastric body or fundus

105
Q

What are the two main types of chronic gastritis?

A

1) non-atrophic
2) atrophic

106
Q

Which type of chronic gastritis is characterized by inflammation WITHOUT loss of gastric glandular cells and is caused by H. pylori?

A

non-atrophic

107
Q

Which type of chronic gastritis is characterized by a loss of gastric glandular cells (replaced by intestinal epithelium, pyloric-type glands, and fibrous tissue), is associated with the development of gastric carcinoma, and is caused by H. pylori and autoimmunity?

A

atrophic

108
Q

Summarize the pathogenesis of chronic H. pylori gastritis

A

Overall mechanisms are poorly understood…

  • virulence factors allow for survival of bacteria in the stomach (e.g., have a flagella allowing them to be motile, they produce ammonia that’s toxic to our epithelial cells + increasing alkalinity for themselves, they produce adhesins allowing for better adhesion to epithelial cells, and release toxins linked to the development of malignancy)
  • elicit a robust inflammatory response (neutrophils, plasma cells, lymphocytes)
  • bacteria seem to reduce mucous and bicarbonate secretion, and increase gastric acid secretion
109
Q

What are the clinical features of chronic H. pylori gastritis?

A

May be asymptomatic but can cause:

  • epigastric pain
  • nausea
  • vomiting
  • anorexia (from eating tiny amounts)
  • early satiety
  • weight loss
110
Q

How do you diagnose chronic H. pylori gastritis?

A
  • presence of antibodies to H. pylori in serum (note: least reliable because these antibodies can last for a very very long time)
  • fecal bacteria detection
  • urea breath test (GOLD STANDARD)
111
Q

What are some complications to be aware of for chronic H. pylori gastritis?

A
  • PUD (peptic ulcer disease)
  • gastric adenocarcinoma
  • MALT lymphoma
112
Q

What is the treatment for chronic H. pylori gastritis?

A

-triple therapy (two antibiotics + PPI)

Note: eradication of bacteria tends to cure the disease

Note: when it gets to the point of gastritis, often natural treatments are not enough; however, natural remedies + the triple therapy = improves outcomes/one round of triple therapy seems to be enough

113
Q

REVIEW: Change of one differentiated cell type to another is called what?

A

metaplasia

114
Q

Atrophic gastritis is associated with increased risk of __________

A

gastric adenocarcinoma

115
Q

Overgrowth of MALT associated with H. pylori may be associated with ___________

Recall: MALT = mucosal associated lymphoid tissue (e.g., Peyer’s patches, tonsils, etc.)

A

gastric lymphoma

116
Q

What are the two main types of peptic ulcer disease (PUD)?

A

1) duodenal (4x more common)
2) gastric

117
Q

True or False: Duodenal PUD has a higher likelihood of perforation and malignancy compared to gastric PUD

A

False

Duodenal PUD = lower likelihood of perforation and malignancy

Gastric PUD = 4% are malignant + higher likelihood of perforation

118
Q

What are some of the causes of peptic ulcer disease (PUD)?

A
  • H. pylori infection (most common)
  • NSAIDs
  • cigarette smoking
119
Q

True or False: PUD is a complication of chronic gastritis

A

True

120
Q

Summarize the pathogenesis of peptic ulcer disease (PUD)

A
  • occurs due to an imbalance between defense mechanisms and damaging factors causing chronic gastritis (aka develops as a result of chronic gastritis)
  • duodenal ulcers and antral gastric ulcers not well understood but linked to H. pylori colonization leading to decreased bicarbonate secretion in duodenum and increased gastric acid secretion in the stomach
  • gastric ulcers in the fundus or body = caused by mucosal atrophy, slightly higher acid secretion, and greatly decreased mucin production + other protective factors
121
Q

What do peptic ulcers look like?

A
  • round to oval shaped, sharply punched-out defect
  • granulation tissue below fibrous scar
  • larger vessels within scarred area that are thickened and thrombosed
122
Q

What are the clinical features of peptic ulcer disease?

A
  • vague, sometimes intense pain sometimes with meals
  • duodenal ulcers = BETTER with food, but worsened 2-3 hours after eating
  • duodenal ulcers commonly awaken patients at night
  • gastric ulcers = pain shortly after meal
  • gastric ulcers = weight loss is common

may also present with:
- iron-deficient anemia, bleeding, nausea/vomiting, bloating, belching

123
Q

How do you treat peptic ulcer disease?

A
  • withdraw offending agent
  • eradicate H. pylori infection
124
Q

What are some complications that can occur with peptic ulcer disease?

A
  • performation that can lead to peritonitis (medical emergency)
  • bleeding
  • gastric adenocardinoma
  • MALT lymphoma

BMS150 - Post Test 2 (9 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions