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Case 2 > Stomach > Flashcards

Stomach Flashcards

1
Q

What is the orad?

A

First 2/3 of the body of the stomach

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2
Q

What is the Caudad?

A

The last 1/3 of the body of the stomach and antrum

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3
Q

Storage Function of the Stomach

  • Which reflex allows distention of the stomach wall?
  • What is the maximal stomach volume?
A
  1. Vagovagal reflex: reduces muscle tone of the gastric wall so it can expand outwards
  2. Approx. 2 litres
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4
Q

The gastric glands are present everywhere in the wall of the stomach except for which region?

A

Lesser curvature of the stomach

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5
Q

What are mixing waves?

Where do they begin?

What initiates them?

A

Weak peristaltic constrictor waves

Begin in the mid to upper portions of the stomach wall and move toward the antrium every 15-20 seconds

Gut wall basic electrical rhythm

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6
Q

Mixing in the stomach by the constrictor ring is heavily reliant on what type of movement?

A

Retropulsion

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7
Q

Define hunger contractions

A

Rhythmical peristaltic contractions in the body of the stomach

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8
Q

Name two things that can initiate hunger contractions

A

High degrees of GI tonus

Hypoglycaemic state

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9
Q

What type of movement causes stomach emptying?

What is this known as?

A

Strong peristaltic very tight ring-like constrictions resulting in stomach emptying

“Pyloric pump”

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10
Q

How does an increased stomach volume effect the rate of emptying?

A

Stretching of the stomach wall elicits local myenteric reflexes in the stomach wall

These accentuate the activity of the pyloric pump and inhibit the pyloric sphinctor

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11
Q

Name two effects that gastrin has on stomach emptying

A
  1. Stimulates histamine release from ECL cells which then stimulates parietal cell to secrete acid
  2. Enhances the activity of the pyloric pump, promoting stomach emptying
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12
Q

Name three reflexes due to the passage of food into the duodenum which limit or prevent stomach emptying

A
  1. Enteric Nervous System in the gut wall, directly from the duodenum to the stomach
  2. Extrinsic nerves through the paravertebral sympathetic ganglia and then back through inhibitory sympathetic nerve fibres to the stomach
  3. Vagal nerve which inhibits excitatory signals transmitted to the stomach (minor role)
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13
Q

Name the two outcomes from the reflex pathways which act to inhibit stomach emptying

A
  1. Strongly inhibit the pyloric pump propulsive contractions

2. Increase the tone of the pyloric sphincter

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14
Q

Name five things which can initiate enterogastric inhibitory reflexes

A
  1. Duodenal distention
  2. Duodenal mucosal irritation
  3. Dudodenal pH <3.5
  4. Hyper/Hypotonic chyme osmolality
  5. Presence of protein breakdown products in chyme
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15
Q

What is CCK?

A

Cholecystokinin (CCK)

Released from duodenal and jejunal mucosa in response to fatty substances in the chyme

Blocks increased stomach motility caused by gastrin

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16
Q

Where is gastrin secreted from?

A

G cells in the antrum of the stomach

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17
Q

What are the three actions of gastrin?

A
  1. Increase gastric H+ secretion
  2. Increase growth of gastric mucosa
  3. Increase gastric motility
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18
Q

What stimulates gastrin secretion?

A

Stomach distention

Presence of amino acids and peptides

Vagal stimulation

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19
Q

What inhibits gastrin secretion?

A

Stomach pH <1.5

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20
Q

What cells secrete CCK?

A

I cells within the duodenum and jejunum

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21
Q

What are the three actions of CCK?

A

Increased pancreatic secretion

Increased gallbladder contraction

Decreased gastric emptying

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22
Q

What increases secretion of CCK?

A

Fatty acids and amino acids

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23
Q

Which cells secrete Secretin?

A

S cells within the duodenum

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24
Q

What are the three actions of Secretin?

A

Increased pancreatic HC03- secretion

Decreased gastric acid secretion

Increased bile secretion

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25
Q

What increases secretin secretion?

A

Acid and fatty acids within the lumen of the duodenum

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26
Q

Which cells secrete somatostatin?

A

D cells within the pancreatic islets and GI mucosa

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27
Q

What are the four actions of somatostatin?

A

Decreased:

  • gastric acid and pepsinogen secretion
  • pancreatic and small intestinal fluid secretion
  • gall bladder contraction
  • insulin and glucagon release
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28
Q

What increases somatostatin release?

What decreases somatostatin release?

A

Increase: acid

Decrease: vagal stimulation

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29
Q

What is GIP?

A

Gastric Inhibitory Peptide

Released from the duodenal and jejunal mucosa

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30
Q

What causes the release of GIP?

A

Fat within the chyme

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31
Q

What is the main function of GIP?

A

Stimulation of the secretion of insulin by the pancreas

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32
Q

Within the stomach there are two types of glands, name them

A

Oxyntic glands (Gastric glands)

Pyloric glands

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33
Q

Gastric glands contain what three types of cells?

A

Mucous neck cells - secrete mucous

Peptic (chief) cells - secrete large quantities of pepsinogen

Parietal (oxyntic) cells - HCL and intrinsic factor

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34
Q

Pyloric glands

What do they secrete?

Where are they located?

A

Secrete: mucous for the protection of pyloric mucosa from stomach acid and gastrin

Located: antral portion of the stomach i.e. distal 20%

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35
Q

Parietal cells secrete HCL name the first two stages to this process

A
  1. Cl- actively transported from parietal cell cytoplasm into the lumen of the canaliculus via chloride pumps. Na+ out via Na pump. -ve potential created within the canaliculus which causes K+ to enter the canaliculus from the cytoplasm
  2. Water dissociates into H+ and OH- in the cytoplasm. H+ actively enter canaliculus by H+/K+ ATPase (proton pump) and Na by Na pump. HCL formed in the canaliculus
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36
Q

Parietal cells secrete HCL name the last two stages of this process

A
  1. Water passes into the canaliculus via osmosis due to the increased ionic concentration within them
  2. OH- combines with CO2 via carbonic anhydrase to form HCO3-. This diffuses into the ECF in exchange for Cl- ions.
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37
Q

What is the function of pepsinogen?

A

On contact with HCL is forms pepsin which is a proteolytic enzyme

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38
Q

What is the optimal pH of pepsinogen?

A

1.8-3.5

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39
Q

Name two things which regulate the secretion of pepsinogen

A
  1. Stimulation of peptic cells by ACh released from the vagus nerve/gastric enteric nervous plexus
  2. Peptic cell secretion in response to acid in the stomach. The acid stimulates additional enteric nervous reflexes which summate with the original nervous signals to the peptic cells.
40
Q

Why is Intrinsic Factor important?

A

Absorption of Vit B12 in the ileum

41
Q

Which cell type secretes Intrinsic Factor?

A

Parietal (Oxyntic) cells

42
Q

What do the pyloric cells secrete?

A

Small amounts of pepsinogen

Large amounts of thin mucous

43
Q

What are ECL cells?

A

Enterochromaffin-like cells

44
Q

How do ECL cells cause secretion of HCL?

A

Secrete histamine
Histamine binds to H2 histamine receptors on parietal cells
Activates the parietal cells to form and secrete HCL

45
Q

Name three things which activate ECL cells

A
  1. Gastrin from G cells
  2. ACh from stomach branches of the vagal nerve
  3. Hormones secreted by the enteric nervous system of the stomach wall
46
Q

What causes the release of gastrin from G cells?

A

Amino acids reaching the antral end of the stomach

47
Q

Name the three stages of gastric secretion

A

Cephalic
Gastric
Intestinal

48
Q

Gastric Secretion: Cephalic phase

What causes this?

Where do the neuronal signals originate and what is their course?

A

Causes: sight, smell, thought or taste of food

Apeptite centres of the amygdala and hypothalamus transmitted through the dorsal motor nuclei of the vagi through the vagus nerve to the stomach

49
Q

During the cephalic phase of gastric secretion what are the two results of this stimulation?

A

Increases ACh release by the vagus nerve which activates more ECL and parietal cells

Stimulates the vagus nerve to activate gastrin-releasing-peptide (GRP) which increases the secretion of gastrin and activates parietal cells

50
Q

Gastric Secretion: Gastric phase

What are the four stimulatory effects of food entering the stomach?

A

Stimulatory effects:

  • Vagus nerve increased ACh and activates more ECL and parietal cells
  • Vagus nerve secretes gastrin-releasing-peptide (GRP) which increases the secretion of gastrin which activates parietal cells
  • Increased pH causes gastrin secretion
  • Stimulates secretagogues that increase gastrin secretion
51
Q

Gastric secretion: Gastric phase

What is the main inhibitory effect of HCL secretion?

A

Inhibition of G-cells within the antrum which decreases gastrin secretion which increases the pH in the stomach

52
Q

Gastric secretion: Intestinal Phase

What stimulates this process?

A

Presence of food within the upper portion of the small intestine (duodenum)

53
Q

Gastric secretion: Intestinal phase

What is the stimulatory effect?

A

Stimulates G-cells (duodenum) to secrete more gastrin resulting in an increased pH

54
Q

Gastric secretion: Intestinal phase

What is the inhibitory effect?

A

Inhibits chemoreceptors, causing a decrease in nerve reflexes which decreases H+ secretion

Secretin, CCK and GIP increase somatostatin which decreases H+ secretion

55
Q

Name two things which cause the inhibition of gastric secretion

A

Reverse enterogastric reflex

  • via myenteric reflex and vagus nerve
  • Inhibits stomach secretion
  • Initiated by: distention of the small bowel, acid in the upper intestine, presence of protein breakdown products and mucosal irritation

Secretin release

  • By the duodenum
  • Opposes stomach secretion
56
Q

Which enzyme is present within the saliva?

What does it do?

A

alpha-amylase

hydrolyses starch into maltose and small glucose polymers

57
Q

What is pepsin and what does it do?

A

Pepsin: Proteolytic enzyme

Hydrolyses protein into: proteoses, peptones and polypeptides by hydrolysis of the peptide bond in amino acids

58
Q

Name three things which cause gastritis

A

Chronic mucosal bacterial infection

Excess alcohol or aspirin ingestion

59
Q

What two things happen to the gastric barrier in gastritis?

A

Increased permeability of the barrier causing H+ diffusion into the stomach epithelium leading to mucosal damage and atrophy

Mucosa is susceptible to proteolytic peptic digestion resulting in a gastric ulcer

60
Q

What two conditions can result in gastric atrophy?

A

Achlorhydria

Percutaneous anaemia

61
Q

Name three things which usually protect from gastric juices

A

Mucous glands: viscid alkaline

Duodenal secretions/Pancreatic secretion: large [HCO3-] neutralise HCl in gastric juice and prevent pepsin activity

Brunner’s glands within the proximal duodenal wall which secretes alkaline mucous and bile from the liver

62
Q

What does presence of HCL within the duodenum cause?

A

Liberation of secretin from the duodenal mucosa which promotes rapid secretion of pancreatic juice which neutralises the acid

63
Q

What type of bacteria is H. Pylori?

A

Flagellated gram negative bacillus

64
Q

Why can H. Pylori survive in acidic environments?

A

Contains urease which metabolises urea
This releases NH3
Causes local alkaline conditions around the bacteria
Protects it from acidity

65
Q

Name two ways in which H. Pylori penetrates the mucosal barrier of the stomach

A

Innate burrowing action

Releases digestive enzymes, liquifies the mucosal barrier, preteolytic degradation of mucosal barrier by gastric juices and leads to peptic ulceration

66
Q

How does H. Pylori cause increased acid secretion?

A

Inhibition of somatostatin release within the antrum

67
Q

Name three non-invasive tests for H. Pylori diagnosis

A
  1. Urea breath test
  2. Heliobactor stool antigen test
  3. Serology
68
Q

Describe the urea breath test for H. Pylori

A
  • Pt swallows non-radioactive carbon-13 urea and citric acid
  • Breath sample taken by direct exhalation into test tube 15 minutes latter
  • Urea is split by urease into NH3 and C02
  • Detection of labelled C02 indicatives urease activity and presence of H. Pylori within the stomach

NB Sensitivity and specificity >95%

69
Q

Name three invasive tests for H. Pylori infection

A

CLO or Urease Test
Gastric biopsy for histopathology
Gastric biopsy for culture of H. Pylori

70
Q

How do NSAIDs predispose to ulcers?

A

Normally:

  • PEG2 inhibits HCl secretion and stimulates mucus cell secretion (mucus and bicarbonate ions)
  • NSAIDs block the arachadonic acid pway by blocking COX and increase HCl secretion and decreasing bicarbonate secretion

NSAIDs: inhibit PEG2 synthesis and thus increase acid secretion and causing ulcers

71
Q

Which G protein coupled pathway does histamine work to increase acid secreton?

A

Gs

72
Q

Which G protein coupled pathway does PGE2 work to decrease acid secretion?

A

Gi

73
Q

Treatment of H. Pylori

What is the standard triple therapy?

A

Triple Therapy “CAP”
Clarithromycin [500mg bd]
Amoxicillin [1g bd]
PPI [standard dose bd]

NB Metronidazole [400mg bd] can be used instead of amoxicillin

74
Q

Treatment of H. Pylori

What is the modern bismiuth-based regimen?

A

Modern Bismiuth-Based Regimen “CAR”

Clarithromycin [500mg bd]
Amoxixillin [1g bd]
Ranitidine Bismuthcitrate [400mg bd]

NB Metronidazole [400mg bd] can be used instead of amoxicillin

75
Q

Treatment of H. Pylori

What is quadruple therapy treatment?

A

Quadruple Therapy

  • PPI
  • Tetracycline [4x500mg]
  • Metronidazole [3x400mg/500mg]
  • Ranitidine Bimuthcitrate [4x100mg] or Bismuth Subsalicylate [4x 600mg]
76
Q

Proton pump inhibitors: 1st generation

  • Give an example of one
  • What are their characteristics?
  • How do they work?
A

Omeprazole

Lipid soluble and weak base which enters and accumulates in the the canaliculi of parietal cells

On contact with HCL, they are converted to their active sulphenamide form which is cationic so becomes trapped in the canaliculi. It forms an irreversible bond with H/K ATPase blocking its action permanenty

77
Q

Proton Pump Inhibitors: 2nd Generation

  • Give an example
  • What are their composition?
A

Esomeprazole (Nexium)

S-isomer only (1st generation are a mixture of both R and S)

78
Q

Define Rumination

A

Effortless regurgitation of undigested food after every meal

79
Q

Define dyspepsia

A

Chronic or recurrent pain or discomfort centered in the upper abdomen

80
Q

Name three clinical features of dyspepsia

A

Epigastric pain in central upper abdomen or lower retrosternal discomfort when eating

Postprandial fullness/unease

Accompanying symptoms such as: nausea, vomitting, bloating, belching and weight loss

81
Q

What is mass discharge?

A

During the initiation of the stress response and all sympathetic nerves fire simulataneously

82
Q

What is the alarm phase?

Which branch of the nervous system coordinates the response?

What is there an increased secretion of during this phase?

A

An immediate response to the stressor

Directed by the sympathetic nervous system

Causes increased secretion of adrenaline

83
Q

What is the resistance phase?

Which hormones are involved in this phase?

A

When stress lasts longer than a few hours

Glucocorticoids are the dominant hormones of the resistant phase (and GH, ADH, Glucagon)

84
Q

Name the four main endocrine outcomes of the resistance phase

A
  1. Mobilisation of remaining lipids and protein reserves
  2. Conservation of glucose for neural tissues
  3. Elevations and stabilisation of blood glucose concentrations
  4. Conservation of salts and water and the loss of K and H
85
Q

What is a main point regarding the resistance phase?

A

It can’t be maintained indefinitely

Side effects include:
1. Systemic anti-inflammatory activity results in immunocompromisation and slow wound healing

  1. ADH and aldosterone results in elevated blood volumes and higher BP
  2. Suprarenal cortex may become fatigued and unable to produce glucocorticoids thus causing abhorrent blood glucose concentrations
86
Q

What is the exhaustion phase?

What can result?

A

Homeostatic breakdown

Multiple organ failure and death due to hypokalaemia (due to ADH and aldosterone)

87
Q

How is CRH released?

A

Into the blood of the portal circulation by parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus

88
Q

How is ACTH released?

A

Anterior pituitary gland

In response to corticotropin-releasing hormone (CRH)

89
Q

How is cortisol released?

A

From the adrenal cortex in response to elevation in the blood level of adrenocorticotropic hormone (ACTH)

90
Q

Define stress reactivity

A

Changes in physiology to stress

91
Q

Regarding the model of appraisal, what is primary appraisal?

A

Initial appraisal of an event i.e. the outside world

  1. Irrelevant
  2. Benign (gentle) and positive
  3. Harmful and a threat
  4. Harmful and a challenge
92
Q

Regarding the model of appraisal, what is secondary appraisal?

A

Individual evaluating the pros and cons or their different coping strategies

i.e. appraisal of the individual themselves

93
Q

Define patient/agent-driven decision making

A

The physician presents all the options and the patients makes their choice

94
Q

Define physician recommendation decision making

A

The physician explains all the options and also makes a reccomendation

This recommendation is based on the patients values rather than on their own.

95
Q

Define shared decision making

A

The patient and physician work together to reach a mutual decision

96
Q

Define informed non-dissent decision making

A

The physician guided by the patients values determines the best course of action and fully informs the patient

Case 2 (1 decks)

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