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Semester 4 > PBL 2 > Flashcards

PBL 2 Flashcards

1
Q

What are mixing waves in the stomach?

A

Weak peristaltic constrictor waves that begin in the mid-upper portions of the stomach and move toward the pyloric antrum

The waves are initiated by the gut wall and neural activity

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2
Q

How does the pylorus control stomach emptying?

A

At the pylorus, there is a thick muscular wall which is slightly contracted almost all the time - the pyloric sphincter
The pyloric sphincter is open enough for water and other fluids to empty upon contraction of stomach wall
Constriction of the sphincter prevents passage of food until it has mixed with chyme

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3
Q

How does CCK help to control stomach emptying?

A

When fat enters the duodenum, it binds to epithelial cells which cause the release of CCK
CCK is carried to the pyloric pump to inhibit it
CCK increases the contraction of the pyloric sphincter

Less food can exit the stomach

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4
Q

What are the two types of tubular gland present in the stomach?

Where are they located in the stomach?

A

Gastric glands - located in the body and fundus of the stomach
Pyloric glands - located in the antrum of the stomach (distal 20%)

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5
Q

What types of cell are present in Gastric Glands?

What do they secrete?

A

Mucous neck cells - secrete mucus
Chief cells - secrete pepsinogen
Parietal cells - secrete HCL + intrinsic factor
Enterochromaffin (ECL) cells - secrete histamine

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6
Q

How much gastric juice is secreted each day?

A

1500mL

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7
Q

What type of cell secretes intrinsic factor? What is the role of intrinsic factor?

A

Secreted by parietal cells

Intrinsic factor binds to vitamin B12 to help it be absorbed across the intestinal lining

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8
Q

What is the pH of HCL?

A

0.8

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9
Q

What are the villus like projections inside of a parietal cell called?

A

Canaliculi

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10
Q

What is the mechanism of HCL secretion from parietal cells at the apical membrane?

A

H+ is actively secreted in exchange for K+
K + is recycled via K+ ion channels
Cl- is secreted via Cl- ion channels

H+ and Cl- then combine in the lumen of the gastric gland to make HCL

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11
Q

What occurs at the basolateral membrane of the parietal cells?

A

HCO3- is exchanged passively for Cl- ions

Na+K+ ATPase pumps K+ into parietal cells

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12
Q

How is HCL secretion from parietal cells controlled?

A

Ach - from vagus nerve
Gastrin - from G cells
Histamine - from ECL cells

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13
Q

What controls histamine release from ECL cells?

A

Ach - from vagus

Gastrin - from G cells

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14
Q

How does histamine lead to HCL secretion by parietal cells?

A

Histamine binds to receptors on parietal cells which leads to an increase in intracellular cAMP
Intracellular cAMP causes tubulovesicles to inset themselves into the membrane to form ‘canaliculus’ structure
This increases the surface area of the lumen, increasing the proton pump number, increasing acid secretion

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15
Q

What do chief cells secrete?

A

Pepsinogen - inactive pepsin

Gastric lipase - accounts for some fat digestion in the stomach

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16
Q

How is pepsinogen activated?

A

By HCL

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17
Q

At what pH does pepsin work best?

A

Strong acidic pH: 1.5-2.0

It is inactive at pH >5

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18
Q

What is pepsinogen secreted in response to?

A

Ach - from vagus

Acid in stomach

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19
Q

What cells are present in the pyloric glands?

What do they secrete?

A

Mucous neck cells - secrete mucus
G cells - secrete gastrin
D cells - secrete somatostatin

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20
Q

What stimulates gastrin release from G cells?

A

The presence of digested proteins

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21
Q

What are the three phases of gastric secretion?

How much gastric secretion does each account for?

A

Cephalic phase - 40%
Gastric phase - 50%
Intestinal phase - 10%

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22
Q

What happens during the cephalic stage of gastric secretion?

A

Occurs when you see, smell, taste or think of food
Vagus nerve releases Ach which stimulates gastric acid secretion
Vagus nerve releases gastric releasing peptide - stimulates gastrin release from G cells, which in turn stimulate HCL secretion

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23
Q

What happens during the gastric phase of gastric secretion?

A

Food in stomach stimulates:

  • local enteric reflexes, activates mixing waves
  • long vagovagal reflexes, release of Ach to stimulate gastric secretion
  • gastrin and histamine stimulation and secretion of HCL
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24
Q

What happens during the intestinal stage of gastric secretion?

A

Chyme present in the duodenum causes:

  • G cells in the deodenum to secret gastrin
  • enterogastric reflex causes inhibition of gastric production and secretion in the stomach
  • CCK and PIP release which increase the secretion of somatostatin from D cells which in turn inhibits gastrin secretion
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25
Q

What is a secretagogue

A

A substance which promotes another substance to be secreted

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26
Q

What is the enterogastric reflex?

A

The presence of food in the small intestine triggers a reflex
This reflex is transmitted through extrinsic sympathetic and vagus nerves, which inhibit stomach gastric acid secretion

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27
Q

How does protein buffering in the stomach inhibit gastric secretion?

A

The presence of protein in the stomach acts as a buffer to keep luminal pH > 3
As the stomach empties, the luminal pH falls below pH 3
This causes D cells to release somatostatin, which inhibits gastric acid secretion

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28
Q

What is the role of somatostatin

A

Inhibits:

  • Histamine release from ECL cells
  • HCL release from parietal cells
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29
Q

What are the intestinal hormones that inhibit gastric acid secretion?

A

Secretin
Gastric Inhibitory peptide (GIP)
Vasoactive intestinal polypeptide (PIP)
CCK

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30
Q

What are the two layers of mucus found in the GI tract?

A

Loose layer - upper layer where bacteria live

Adherent layer - thick dense lower layer attached to epithelial cells

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31
Q

What does it mean by mucus is a viscoelastic material?

A

Vicious properties - it can flow like a liquid

Elastic properties - it is elastic like a solid (if deformed it can return to original material)

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32
Q

What is the composition of mucus?

A

Water and ions - 90%
Proteins (glycoproteins) - 5-10%
Mucus glycoproteins (mucins) - 1-5%

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33
Q

What is the consistency of mucus dependant on?

A

The amount of mucins present:
Liquid mucus (Saliva) - small amount of mucins
Thick stick mucus (Gut)- large amount of mucins

34
Q

What are mucins?

A

Long glycoprotein polymers which are connected by disulphide bones
Protein glycoprotein core allows lots of monosaccharide sugars to bind

35
Q

How do mucins form mucus?

A

Entanglement to form a gel
Bind to water and expand
Mucins link together to form cross links

36
Q

What are the different types of mucins and where are they found in the GI Tract?

A

Saliva - MUC5B
Stomach - MUC5AC & MUC6
Intestines - MUC2

37
Q

How does the thickness of mucus layer vary through the GI Tract?

A

Firmly adherent layer - thin in the small intestine

Loosely adherent layer - thick in the large intestine

38
Q

How are mucins protease resistant?

A

They have a large protein core covered in sugars, so there are very few places where protease is able to cut

39
Q

In which mucus layer do the gut bacteria live?

A

The loose adherent (upper) layer

40
Q

How come only 10-20% of protein digestion takes place in the stomach?

A

Because pepsin can only attack certain peptide bonds and not all of them

41
Q

Why does nutrient absorption not occur in epithelial cells in the stomach?

A

Epithelial cells are covered by alkaline mucus so are not directly exposed to chyme
Epithelial cells lack specialised transport mechanisms
Digestion has not been completed by the time that chyme leaves the stomach, and nutrients have only been partially broken down

42
Q

What drugs are absorbed in the stomach?

A

NSAIDs

Alcohol

43
Q

What is dyspepsia?

A

Indigestion

44
Q

What is gastritis?

A

Inflammation of the gastric mucosa

45
Q

What is the gastric barrier

A

A physical barrier in the stomach which prevents absorption:

  • thick mucus layer
  • tight junction epithelial cells
46
Q

What is the pathophysiology of gastritis?

A

The permeability of the gastric barrier is increased for some reason
H+ ions are able to diffuse into the stomach epithelium leading to mucosal damage and atrophy
This makes the epithelium susceptible to digestion by peptic enzymes

47
Q

What is achlorhyria?

A

Where the stomach fails to secrete HCL

48
Q

In what organs are G cells found?

What do they secrete?

A

Stomach
Duodenum
Pancreas

Gastrin - leads to stimulation of HCL secretion

49
Q

Where are Brunners Glands Found?

What is their purpose?

A

In the submucosa of the duodenum

Secrete mucus and bicarbonate ions to help neutralise the HCL coming from the stomach

50
Q

What is the role of prostaglandins in gastric acid production?

A

They inhibit gastric acid secretion

They stimulate mucus and bicarbonate secretion to neutralise acidic stomach environment

51
Q

How do NSAIDs lead to gastric ulcers?

A

Inhibit the COX enzyme - which is involved in the synthesis of prostaglandins

Prostaglandins have a protective role in the gastric mucosa as they reduce acid secretion and stimulate bicarbonate release

52
Q

Where are the two locations of peptic ulcers?

Which type is more common

A

Stomach - gastric ulcer
Duodenum (1st part) - duodenal ulcer

Duodenal ulcers are more common

53
Q

What is the pathophysiology of a peptic ulcer?

A

Excess acid secretion by gastric mucosa
Decreased mucous protection by the mucosal barrier

Allows for small punched out holes in the mucosa epithelial lining

54
Q

Where are gastric ulcers most likely to occur in the stomach?

A

On the lesser curvature

55
Q

Where are duodenal ulcers most likely to occur?

A

Right after the pyloric sphincter

56
Q

What is Zollinger-Ellison syndrome and what does it increase your risk of?

A

It is a neuroendocrine tumour typically located in the duodenal wall or pancreas
It secretes abnormal amounts of gastrin
This can stimulate parietal cells to secrete excess HCL

57
Q

What are the clinical features of a peptic ulcer?

A

Epigastric pain
Nausea
Weight loss (gastric ulcer) or weight gain (duodenal ulcer)

58
Q

What are the 3 main complications of a peptic ulcer? Explain them

A

Haemorrhage in GI tract - due to deep ulcers which can damage nearby arteries
Perforation - when an ulcer erodes all the way through the wall allowing gastrointestinal contents to get into peritoneal space
Obstruction - long standing ulcers near the pyloric sphincter can cause so much scaring that it obstructs normal passage of food contents

59
Q

How are peptic ulcers treated?

A

Antibiotics - if the cause is H.pylori infection
Proton pump inhibitors (PPI)
H2 receptor antagonists
Antacids and Alginates

60
Q

What are the common antibiotics used to treat H.Pylori infection?

A

Amoxicillin
Clarithromycin
Metronidazole
Tetracycline

61
Q

How do proton pump inhibitors work?

A

Reduce the amount of acid secreted in the stomach

Block the apical H+K+ ATPase to prevent acid secretion

62
Q

How does Omeprazole work?

A

It accumulates in acidic spaces e.g, canaliculi and tubulovesicles of the parietal cell
It is activated by H+ to its active form sulphonamide
Sulphonamide forms irreversible disulphide bonds with the H+K+ ATPase to block H+ secretion into the stomach

63
Q

Why is omeprazole given in encapsulated form?

A

So it is not broken down by the staunch acid

It can be absorbed in the small intestine, so it can travel to the parietal cells via the blood

64
Q

What is the onset time of omeprazole?

A

1-2 hours

65
Q

What is the difference between 1st and 2nd generation proton pump inhibitors

A

1st generation PPI is a mixture of R & S isomers

2nd generation PPI contains only the active S isomer

66
Q

How are H2 receptor antagonists used to treat peptic ulcers?

A

They bind to the histamine receptor on parietal cells

This blocks the action of histamine to incude HCL production - therefore inhibiting HCL production

67
Q

What is Cimetidine?

A

A H2-receptor antagonist

68
Q

What is Ranitidine?

A

A H2 receptor antagonist

69
Q

How do antacids work?

A

They are a combination of magnesium and aluminium salts

Help to neutralise the HCL in the stomach by raising the pH

70
Q

What is alginate?

A

Creates a protective coating on the lining of your stomach

71
Q

What kind of bacterium is H.Pylori?

A

Gram negative bacterium

72
Q

Where in the stomach does H.Pylori colonise?

A

The antrum, under the mucous layer in the gastric pits

73
Q

What features does H.Pylori have which make it able to colonise the stomach more easily?

A

Flagellum - can ‘swim’ to epithelium

Urease - converts urea to ammonia + CO2, ammonia neutralises the acidity of the stomach

74
Q

What are the different consequences of H.Pylori infection?

A

Gastritis
Peptic ulcers
Gastric carcinoma

75
Q

What are the two toxic genes that H.Pylori expresses and what do they do?

A

CagA - disrupts tight junctions at epithelial cells and promotes inflammation

VacA - causes epithelial cell apoptosis

76
Q

How does H.Pylori adhere to the mucosal layer?

A

Has BabA gene on bacterial surface which binds to Lewis antigen expressed on the glycans of MUC5AC mucins

77
Q

How does H.Pylori infection in the antrum of the stomach lead to ulcers in the duodenum?

A

The antrum is the location of D cells
Inflammation of the antrum inhibits somatostatin release from D cells
This leads to an increase in gastrin production by G cells
This leads to an increase in acid production by parietal cells
High acid stomach content leads to high duodenal acid content

78
Q

How is H.Pylori induced ulcers treated?

A

Triple therapy: 2 x antibiotic + PPI/H2 antagonist

Quadruple therapy: 2 x antibiotic + PPI/H2 antagonists + bismuth

79
Q

Why is a bismuth compound often added to the treatment of H.Pylori infection?

A

Bismuth compounds block H+ influx into H.Pylori
This reduces the acidity inside of the bacteria
This enables the bacteria to survive and divide more
Dividing bacteria are easier to target with antibiotics

80
Q

How does a Urea C13 breath test work for diagnosis of H.Pylori?

A

Labelled carbon in urea is ingested
H. Pylori breaks down urea into CO2 + NH3
CO2 is now labelled
Labelled CO2 is breathed out

81
Q

What is the maximum stomach capacity?

A

1.5L

82
Q

How does ingestion of predominantly liquid meals effect gastric emptying?

A

Reduces the gastric emptying time

Semester 4 (10 decks)

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