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Semester 4 > Case 12 > Flashcards

Case 12 Flashcards

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1
Q

What are the phases of gastric secretion

A
  • Cephalic
  • Gastric
  • Intestinal
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2
Q

What are the 4 important stimuli for the cephalic phase

A
  • Sight of food
  • Thougt of food
  • Smell of food
  • Taste of food
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3
Q

What are the inhibitory events for the cephalic phase

A

Anything that triggers the sympathic nervous system so anxiety, or any emotional upset

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4
Q

What do parietal cells secret

A

HCl and intrinsic factor

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5
Q

What do chief cells secrete

A

Pepsinogen that gets activated into pepsin

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6
Q

How does the stimulation of the cephalic phase cause activation of the parietal and chief cells

A

The senses of food activates the cortex of the brain which sends a signal to the hypothalamus, the hypothalamus then has descending neurons that stimulate the Dorsal Nucleus of Vagus (DNV) which activates the vagus nerve and leads to the stimulation of the parietal and chief cells

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7
Q

How does the sympathic nervous system inhibit parietal and chief cell activation

A

Sympathetic fibers from T1 to L2 (Greater splanchnic nerve) goes to the stomach and inhibits the action of the vagus nerve (parasympathetic) on the parietal and chief cells

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8
Q

What are the stimulations for the gastric phase

A
  • Stomach distention
  • Partially digested proteins
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9
Q

Describe the Vagovagal reflex and what type of reflex arc it is

A

The Vagovagal reflex is a long reflex arc that begins with the distention of the stomach, stretch receptors in the muscularis externa of the stomach send signals to the Dorsal nucleus of Vagus through the afferent vagus nerve. The stimulation of the DNV then sends signals down the efferent vagus nerve to the parietal and chief cells to increase gastric secretions

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10
Q

Describe the short arc reflex to do with the stomach

A

Stomach distention activates the afferent vagus nerve (sensory) which then also sends signals to the submucosal plexus which can stimulate the parietal and chief cells to produce gastric secretion (can also activate the myenteric plexus for stomach motility)

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11
Q

Explain the effect of partially digested proteins on the stomach

A

Partially digested proteins can activate antral enteroendocrine G-cells which release the hormone gastrin in the blood stream. Gastrin then travels to parietal and chief cells and binds to CCK-2 receptors which will lead to increased intercellular calcium and activate them to release HCl and Pepsinogen

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12
Q

Explain how parietal cells make H+ and explain the Alkaline Tide phenomenon

A

Parietal cells have a lot of mitochondria and so because of respiration there is alot of CO2 and H2O, with the presence of Carbonic Anhydrase carbonic acid (H2CO3) is produced, H2CO3 dissociates into H+ and HCO3- (bicarbonate) ions. The H+ goes through the H+/K+ pump into the stomach and the bicarbonate ions leave into the blood in the gastric veins leading the blood to be more alkaline then when it came (Alkaline Tide)

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13
Q

Explain how parietal cells gain Cl- and how it leads to the creation of HCl

A

Because the parietal cell is getting of negative ions (HCO3- bicarbonate ions) it must gain negative ions back which is how Cl- ions enter the cell. Cl- then exits the parietal cell into the stomach via special ion channels and HCl is created

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14
Q

Explain the inhibitory events of the gastric phase

A
  • Sympathic activation (emotional upset)
  • Too much H+ ions present in stomach (or too low pH) which activates the D-cells (via chemoreceptors) in the antrum to release somatostatin, somatostatin then acts on parietal and chief cells to decrease their gastric secretions
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15
Q

Describe the receptors on the parietal cell, what they respond to, and their effects

A

Parietal cells have 5 receptors that all influence the H+/K+ proton pump:
- CCK-2 receptors that respond to gastrin leading to increased HCl production

  • SST receptors that respond to somatostatin that decrease HCl production

-M3 receptors that respond to Ach released by the vagus nerve that increases HCl production

-H2 receptors that respond to histamine released by enterochromaffin-like cells that increase HCl production

  • EP3 receptors that respond to prostaglandins that decrease HCl production
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16
Q

Describe the receptors found on chief cells and what they respond to and do

A

There are 4 receptors that are all stimulatory
- CCK2 receptors that’s respond to gastrin and increase Pepsinogen release

  • M3 receptors that respond to Ach that increases Pepsinogen release
  • H2 receptors that respond to histamine and increases Pepsinogen release
  • Receptors that respond to secretin which increases Pepsinogen release
  • Somatostatin receptors too
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17
Q

What do enterochromaffin-like cells do and respond to

Study These Flashcards
A
  • They are located in the stomach and release histamine
  • They respond to Ach via M3 receptors to increase histamine release
  • response to Gastrin via CCK-2 receptors to increase histamine release
  • respond to somatostatin via SST receptors to decrease histamine release
18
Q

Two types of D-cells and where they’re found and do

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A
  • Antral D-cells respond to decreases pH or increased H+ ions and release somatostatin in the blood
  • D-cells found in the body of the stomach have M3-receptors and respond to Ach released by vagus nerve which inhibits the D-cell causing decreased somatostatin released to the ECL cells so the ECL cells get activated more, release more Histamine and so increase gastric secretions
19
Q

What is the actions the stomach undergoes that pushes chyme back towards the body

20
Q

What does the mucosal barrier consist of in the stomach

Study These Flashcards
A
  • 90% water and ions
  • 5-10% glycoproteins
  • 1-5% mucus glycoproteins known as mucins
21
Q

Two stains for mucins

Study These Flashcards
A
  • Periodate Schniff’s (PAS)
  • Alcian blue (AB)
22
Q

Describe the structure of mucins

Study These Flashcards
A

Mucins are very large glycoproteins that are the cause for the gel/hydrogel like property of the mucosal barrier

23
Q

What is the functions of mucins

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A
  • The help in pathogen binding/ evasion (can shed when pathogens attach to it)
  • lubricate chyme
  • forms a gel like protective layer
24
Q

Describe the Helicobacter Pylori bacteria

Study These Flashcards
A
  • Gram negative rod bacteria, the have flagellum, circular DNA and lipopolysaccharides
  • H. Pylori have the enzyme Urease on their surface which converts urea and and water into ammonia (basic) and CO2.
  • H. Pylori releases two toxins, CagA and VacA
25
What are the two toxins released by H. Pylori and what do they do
- CagA is one and it disrupts the tight junctions between stomach cells and increases inflammation via IL-8 - VacA is the other which is a cytotoxin that causes stomach cell apoptosis
26
What do the mucin variations do against H. Pylori
- MUC5AC is the first mucin to come in contact with H. Pylori, it is a binding mucin and so binds and restricts the H. Pylori bacteria - MUC6 is the second mucin to come in contact with H. Pylori and it has growth inhibition properties that inhibit cell wall synthesis of H. Pylori and so acts like a natural antibiotic - MUC1 is the final and deepest mucin layer that H. Pylori comes in contact with and it has a shedding property which means that when H. Pylori attached to it to try to get through the mucous layer MUC1 will shed and go back into the lumen of the stomach
27
How does H. Pylori cause gastric and duodenal ulcers
- H. Pylori has urease on its surface which means that it can break down urea to produce ammonia, ammonia can neutralize the HCl and allow H. Pylori to dig into the acidic lining of the stomach - H. Pylori also has a flagellum which allows it to go deep into mucosal layer and adhere to the gastric epithelial cells via its lipopolysaccharides - H. Pylori then secretes VacA and CagA which cause cell death and disrupt the tight junctions respectively, this leads to HCl eroding the affected area and an ulcer to form - CagA also causes inflammation which leads to histamine release and so increased HCl production meaning the chyme that entered the duodenum is more acidic than usual leading to ulcer formation there too
28
How to diagnose H. Pylori infection
- Urea breath test - Urea with a marked carbon atom is ingested by the patient, if H. Pylori is present it will break down this urea and turn it into CO2, this CO2 will be breathed out and so tested - Stool test - H. Pylori antigens can be present in the stool and so you can test for H. Pylori infection by looking at the stool
29
H. Pylori treatment
Triple therapy which includes: - Proton pump inhibitor such as: Omeprazole, Esomeprazole and pastorale - Clarithromycin, which is a macro life antibiotic that inhibits bacterial protein synthesis - Amoxicillin or Metronidazole, Amoxicillin is effective against H. Pylori and metronidazole is used in cases of penicillin allergy
30
What stimulates the intestinal phase
Intestinal gastrin (G34)
31
How is intestinal gastrin released
When chyne enters the duodenum, duodenal G-cells encounter partially digested proteins (peptones) which activates then to release intestinal gastrin which acts in the parietal cell and chief to further increase gastric secretions
32
What are common symptoms of gastric and duodenal diseases?
Indigestion, heartburn, reflux, hematemesis, malaena, weight loss, anorexia, early satiety, dysphagia, dyspepsia, upper abdominal pain, nausea, vomiting ## Footnote Symptoms can vary in severity and can indicate different underlying conditions.
33
What is hematemesis?
Internal bleeding in the upper GI tract, leading to vomiting of blood ## Footnote It is a serious symptom that requires immediate medical evaluation.
34
What does malaena refer to?
Passing of jet black, tarry, smelly stools ## Footnote This indicates potential upper GI bleeding.
35
What is early satiety?
Feeling of fullness soon after beginning to eat ## Footnote This can be a sign of various gastrointestinal issues.
36
What are the red flag symptoms that indicate a need for urgent medical attention?
For people of any age : Dysphagia For people >55 yrs: weight loss, any symptoms of the following symptoms: Dyspepsia, Upper abdominal pain and acid reflux ## Footnote These symptoms can suggest serious conditions such as cancer.
37
What is dysphagia?
Difficulty swallowing ## Footnote Can be associated with various esophageal or neurological disorders.
38
What is dyspepsia?
Complex collection of GI symptoms that include: - Upper abdominal pain or discomfort - Heartburn - Acid reflux - Nausea - Vomiting - Typically > 4 weeks ## Footnote Often associated with eating, it can have multiple causes.o
39
What does the term 'reflux' refer to?
The backward flow of stomach contents into the esophagus ## Footnote This can lead to heartburn and other symptoms.
40
What is the gold standard investigation for upper GI problems
OGD (Oesophago-Gastro-Duodenscopy)
41
Peptic ulcers risk factors
- H. Pylori infection (90% of cases) - Smoking - NSAIDS - Caffeine - Stress ulcers - Steriods, Crohn’s, drugs etc

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