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sem 2 Liver and GI > Regulation and disorders of gastric secretion > Flashcards

Regulation and disorders of gastric secretion Flashcards

1
Q

name the contents of gastric juice (fasting state)

A
  • Cations: Na+, K+, Mg2+, H+
  • Anions: Cl-, HPO42+, SO42-
  • Pepsinogen
  • Lipase
  • Mucus
  • Intrinsic factor
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2
Q

what is the pH of this gastric juice

A

approx pH 3.0

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3
Q

what is intrinsic factor important for?

A
  • important for absorption of vitamin b12

- prevents pernicious anaemia

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4
Q

why is mucus important?

A

for protection

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5
Q

what are lipase involved in?

A

digestion of TG’s to glycerol and 3 FA’s

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6
Q

what does the fundus secrete a lot of?

A

mucus, pepsinogen and HCL

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7
Q

what does the antrum secrete a lot of?

A

mucus, pepsinogen and gastrin

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8
Q

what is 2 things is gastrin involved in and how does it act?

A
  1. contraction
  2. secretion of acid

-gastrin can act on its own or act on ECL cells, which produce histamine

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9
Q

approximately how many litres does gastric juice add to intestinal contents?

A

2.5 litres

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10
Q

what type of cell do gastric glands contain?

A

parietal cells-responsible for HCL production

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11
Q

what do these gastric glands secrete?

A

HCL and intrinsic factor

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12
Q

what is a gastric gland?

A

any of the branched tubules in the inner lining of the stomach that secrete gastric juice and protective mucus

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13
Q

how many types of gastric glands are there and how are they distinguished from one another?

A

there are 3 types of gastric gland, distinguished from one another by location and type of secretion

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14
Q

name the 3 types of gastric glands and where they are located:

A
  1. cardiac gastric glands - beginning of the stomach
  2. intermediate/true gastric glands - narrow tubules in central stomach areas
  3. pyloric glands - terminal stomach portion
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15
Q

what do the cardiac and pyloric glands secrete?

A

mucus:

  • coats the stomach
  • protects stomach from self-digestion by helping to dilute acids and enzymes.
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16
Q

what do intermediate gastric glands produce?

A

most of the digestive substances secreted by the stomach

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17
Q

what are intermediate gastric glands composed of?

A

three major cell types

  1. zymogenic
  2. parietal
  3. mucous neck cells.
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18
Q

Where are the 3 cell types located in the gland?

A

zymogenic/chief cells are located at the base of the gland
-thought to produce the enzymes pepsin and rennin. (pepsin digests proteins, rennin curdles milk)

parietal cells which occur throughout the length of the gland

mucous neck cells secrete mucus

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19
Q

what is the fundus?

A

thin-walled upper portion of the stomach

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20
Q

what is the antrum?

A

thick-walled lower portion

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21
Q

which out of the fundus and antrum secrets less HCL?

A

the antrum secretes less HCL

there is conflicting data about this-look at notes

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22
Q

what does the body of the stomach have?

A

numerous epithelial cells with numerous tubular glands

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23
Q

what type of cell are the walls of the glands lined with?

A

parietal cells, which secrete HCl and intrinsic factor

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24
Q

exocrine secretion of the stomach

A

mucus, acid, pepsinogen

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25
Q

what is the pylorus and what does it provide?

A

lower portion of the stomach

provides the sphincter and the passageway through which the chyme (partially digested food) will enter the duodenum

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26
Q

what are ECL cells, where are they located and what do they secrete?

A

secrete paracrine agents, e.g. histamine. Paracrine means local action for local effects- don’t want histamines going everywhere

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27
Q

what does the stomach wall contain

A

gastric mucosa that contains gastric pits

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28
Q

what are at the base of these gastric pits?

A
  • gastric glands whose chief cells create gastric juice
  • a mucous fluid that contains digestive enzymes
  • parietal cells
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29
Q

what is HCO3- exchanged for in the blood

A

Cl-

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30
Q

HCO3- and Cl- are exchanged via what?

A

a secondary active transporter

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31
Q

The HCO3- and Cl- exchange causes what change in blood?

A

↓ of acidity of venous blood from stomach compared to blood that is arriving at it, so there is essentially a neutralising agent that will decrease the acidity

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32
Q

carbonic acid dissociates into what?

A

HCO3- and H+

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33
Q

what happens to the H+?

A

can either form water or H+ gets pumped into stomach lumen

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34
Q

where does excess CL- go?

A

Excess Cl- diffuses into the stomach through chloride channels as the H+ is pumped into the stomach lumen

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35
Q

How does H+ get transported to lumen side?

A

K+/H+-ATPase pumps H+ out into stomach lumen. The proton has the capacity to flux into the luminal side of the stomach and get exchanged for potassium using the ATPase transporter.

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36
Q

how is HCL made?

A

both H+ and Cl- in the stomach lumen, they come together to make HCL

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37
Q

so what is the net effect?

A

net flow of H+ Cl - out of the parietal cell and into stomach lumen

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38
Q

approx how many litres of HCL does the stomach secrete every day?

A

approx 2 litres

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39
Q

what is some gastric juice described as?

A

resting juice

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40
Q

what is the pH of resting juice, and why is this?

A

pH 7.4-7.7

-pH that is close to plasma pH and but more alkaline because there is a lot of bicarbonate being secreted

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41
Q

name 4 gastric secretions:

A
  1. mucus
  2. rennin
  3. lipase
  4. intrinsic factor
  5. HCL
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42
Q

mucus

A
  • alkaline
  • thick and sticky
  • ↑HCO3-
  • forms water-insoluble gel on epithelial surface
  • protects against H+ secretion
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43
Q

what does rennin do?

as we get older what is rennin replaced by?

A
  • curdles milk into casein clot (particularly in children)

- as we get older, renin is replaced by pepsin

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44
Q

what will happen if you do not release lipase?

A

given lipase breakdown TG’s to fatty acid and glycerol, to releasing lipase means you cannot benefit from lipids or fatty meals

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45
Q

HCL roles

A
  • kills bacteria
  • acid denaturation of digested food
  • activates pepsinogen (protein digestion)
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46
Q

which cells contain resting juice

A

non-parietal cells

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47
Q

when is there an increase in HCL secretion?

A

at meal times

48
Q

what 2 ways is HCl secretion is regulated by?

A
  • neuronal pathways

- duodenal hormones

49
Q

how does the HCL regulation occur?

A
  1. Directly, act on parietal cells → ↑ acid secretion
  2. Indirectly, influence the secretion of gastrin and histamine → ↑ acid secretion

essentially, some of the factors when secreted act directly on the relevant cell, initiating acid secretion. some factors cause release of histamines which will then bind to parietal cells, causing secretion of acid.

50
Q

what are the 3 phases involved in acid secretion?

A
  1. Cephalic
  2. Gastric
  3. Intestinal phases
51
Q

name 3 types of acid secretion

A
  • gastrin mediated (hormonal)
  • ACH mediated acid secretion
  • histamine mediated acid secretion
52
Q

which of the 3 phases is the most regulatory?

A

Intestinal phase is more regulatory because we don’t want too much acid in the duodenum because this will inhibit some of the enzymes from working cell

53
Q

when does the cephalic (1st) phase occur?

A

before the food has even entered the stomach (smell, sight, taste, chewing)

54
Q

what does the cephalic phase involve?

A

parasympathetic innervation!!!
• ACh and Gastrin stimulate histamine release from ECL cells.
• ACh acts directly on parietal cells → HCl secretion. Gastrin can also act directly on parietal cells

55
Q

Hyper secretion of acid would essentially cause a hole in our stomach, what prevents this?

A

D-cells/somatostatin releasing cells

  • stop acid secretion
  • too much acid stimulates them to secrete somatostatin which has inhibitory effects on parietal cells, ECL cells etc - reducing acid secretion.
56
Q

explain what happens in the gastric (second) phase?

A
  • Acidity of lumen of stomach is ↑ before a meal (no buffers)
  • After a meal there are more proteins therefore more peptides in the stomach
57
Q

What do proteins do to luminal acidity?

A

-Proteins act as buffers in the gastric lumen, meaning they decrease the acidity in the lumen

58
Q

relationship between acid secretion and acidity of the lumen?

A

Acid secretion increases as the acidity of the lumen decreases

59
Q

so, how do proteins affect acid secretion?

A

HCL secretion increases

  • proteins remove the inhibitory powers of somatostatin on gastrin secretion and hence acid secretion
  • illicits feedback inhibition
60
Q

what can increased parasympathetic effects stimulate?

A

acid secretion via the parietal cells

61
Q

how do things from the stomach enter the duodenum? what rate does the stomach secrete at?

A

Via the pyloric canal

Stomach secretes at a pace that the duodenum can handle

62
Q

what important balance needs to be made in the intestinal phase?

A

balance between the secretory activity of the stomach and the digestive and absorptive capacities of small intestine

63
Q

in the third phase, what inhibits acid secretion?

A

high acidity of duodenal contents reflexly inhibits acid secretion

64
Q

why is high acidity bad in the duodenum?

A

Increased acidity will inhibit the activity of digestive enzymes, bicarbonate and bile salts

65
Q

what else inhibits acid secretion, and how do they work?

A
  • Distension of duodenum (food goes in and are swells)
  • hypertonic solution
  • amino acids
  • fatty acids
  • monosaccharides
  • ->
66
Q

what else inhibits acid secretion, and how do they work?

A
  • Distension of duodenum (food goes in and are swells)
  • hypertonic solution
  • amino acids
  • fatty acids
  • monosaccharides
  • -> cause release of factors by enterogastrones (CCK involved in lipids, secretin involved in HCO3-, etc…)
67
Q

inhibition of acid secretion in the small intestine depends on what 2 factors overall:

A
  • Composition and volume of chyme

* Distention of duodenum

68
Q

do hormonal or neuronal pathways inhibit acid secretion, and how do they work?

A

both

inhibit acid secretion by the parietal cells or gastrin secretion by the G cells, which is inhibited by somatostatin

69
Q

which 2 neuronal reflexes inhibit acid secretion?

A

short and long (nerves that move from brain to gut)

Long neural reflexes:
o increase sympathetic (inhibitory) discharge
o decrease parasympathetic (stimulatory) discharge
o decrease contractions (NO and VIP are involved)

Short neural reflexes
o (via enteric neurons)

70
Q

what type of hormones inhibit acid secretion

A

enterogastrones

e.g. secretin, CCK and GIP

71
Q

Histamine, Ach and gastrin bind to what to increase acid secretion?

A

Histamine, ACh, and gastrin binding to their receptors on parietal cells
causes an ↑ in HCl secretion

72
Q

does somatostatin have a direct or indirect effect on inhibition of HCL secretion?

A

both

73
Q

what is the effect of PGE2?

A
  • negatively regulates HCl secretion caused by those various mediators/hyperacidity of parietal cells
  • promotes bicarbonate and mucus secretion
74
Q

describe the indirect and direction actions of Act, gastrin and histamine:

A

DIRECT
-the 3 stimulate the parietal cell which the releases H+ into the lumen

INDIRECT

  • Ach and gastrin only stimulate the ECL cell
  • ECL cell secretes histamine
  • histamine acts on the parietal cell
75
Q

list some factors/stimulants that increase HCL secretion:

A
  • Histamine
  • Acetylcholine
  • Gastrin
  • Caffeine*
  • Alcohol*
  • NSAIDs*
  • Nicotine*
  • Helicobacter pylori
  • Zollinger-Ellison syndrome
  • Hyperparathyroidism
  • Stress
  • Bile salts
  • Genetic

*avoid these drugs if you have a peptic ulcer

76
Q

what is HCL essential for in life?

A
  • Defence
  • Protein digestion: activates pepsinogen to pepsin
  • Stimulates flow of bile and pancreatic juice
77
Q

a lack of HCL causes what?

A

-failure of protein digestion, leading to achlorhydria

achlorhydria/hypochlorhydria is when production of gastric acid in the stomach is absent or low

78
Q

what stimulates secretion of pepsinogen?

A
  • inputs to chief cells from nerve plexus

- causes pepsinogen to be secreted by chief cells

79
Q

what acts on pepsinogen to convert it to pepsin?

A

HCL, in the stomach lumen

80
Q

when is pepsin inactivated?

A

Inactivated upon entry of food in the small intestine

81
Q

What is the point of pepsin secretion?

A

Initiates digestion of proteins - degrades food proteins into peptides

BUT pepsin is not required for food digestion

82
Q

Which other enzymes could digest proteins?

A

o Trypsin
o Chymotrypsin
o Elastases

83
Q

what is a required substance secreted by the parietal cells?

A

intrinsic factor

84
Q

what does NSAIDs stand for?

A

Nonsteroidal anti-inflammatory drugs

85
Q

what are NSAIDs?

A
  • acidic
  • causes topical irritation of the gut particularly if taken without food
  • Impair the barrier properties of mucosa
  • blocks PGE2
  • Suppress gastric prostaglandin synthesis
  • ↓ gastric mucosal blood flow
  • Interfere with the repair of superficial injury
  • Inhibit platelet aggregation
  • Presence of acid in the stomach promotes NSAID-mediated gastric disorder
86
Q

how do NSAIDs work?

A
  • Impairs restitution process
  • Inactivates FGF (fibroblast growth factor) which interferes with the haemostasis process (you can get bloody faeces)
  • Way forward = discover and develop stomach–sparing NSAIDs
87
Q

name some disorders of gastric secretion:

A
  • GIT function: digestion, absorption of nutrients, salts, water, metabolism and elimination of (undigested) wastes
  • Malformation of GIT: ↓ nutrient status
88
Q

what is a peptic ulcer?

A

a lesion in the lining (mucosa) of the digestive tract, typically in the stomach or duodenum, caused by the digestive action of pepsin and stomach acid.

89
Q

describe the mechanism of a peptic ulcer formation:

A
  • Breakage of mucosal barrier-imbalance between protective and damaging factors
  • Exposure of tissues to the erosive effects of HCl and pepsin
90
Q

what 3 sites are affected by peptic ulcers?

A

Oesophagus, stomach and duodenum

91
Q

name some factors responsible for gastric acid secretion:

A
  • Histamine
  • ACH
  • gastrin
  • food/protein, alcohol, smoking, caffeine, NSAIDs
  • zollinger-ellison syndrome
  • hyperparathyroidism
  • stress-can it aggravate once ulcer is present
  • genetic?
  • helicobacter pylori
92
Q

list the symptoms of peptic ulcers:

A
  • nausea
  • vomiting (blood)
  • anaemia
  • black stools
  • epigastric pain
  • chest discomfort
  • weight loss
  • anorexia
  • dispepsia (complex combination of symptoms, look at tutorial sheet)
93
Q

where are peptic ulcers common?

A
  • Duodenal cap: first part of the duodenal cap
  • The stomach – junction of antrum and body
  • Distal oesophagus, especially in Barrett’s oesophagus
  • Meckel’s diverticulum
  • After gastroenterostomy (weight loss, recurrent pains, ulcers)
  • this is the surgical creation of a connection between the stomach and the jejunum
94
Q

what is the outcome of peptic ulcers?

A

Complete healing and replacement of tissue and some scarring

95
Q

what type of peptic ulcer is common? describe it

A

chronic peptic ulcer is common

  • Occurs in upper GIT (pepsin and HCl)
  • Asymptomatic in >80% of people
  • Low incidence in young; common in over 50s
  • 90% incidence in developing countries
  • Inflammation plays a key role in the disease process
96
Q

what type of peptic ulcer is less frequent? describe it

A

acute peptic ulcer is less frequent

  • Develops from areas of corrosive gastritis (oesophagus, stomach, proximal duodenum), severe stress or shock (burns, trauma)
  • Acute hypoxia of surface epithelium (i.e., ischaemia of gastric mucosa)
97
Q

what is the outcome of an acute peptic ulcer?

A
  • Severe bleeding
  • Heal with no scarring
  • Chronic peptic ulcer
98
Q

name a major risk factor for peptic ulceration:

A

Gastric and duodenal infection with H. pylori is a major risk factor

(if you have duodenal ulcer, there is 80% chance that you have H. pylori infection)

99
Q

when can H. pylori be acquired?

A

childhood

100
Q

what determines the distribution and colonisation of H. pylori in the stomach?

A

Environmental and host factors

101
Q

what does a H. pylori infection do?

A
  • causes hyperacidity in the stomach

- decreases the number of D and G cells

102
Q

what are some factors that prevent infection of the gastric mucosa?

A
  • HCL and pepsin
  • Mucus production
  • Peristalsis and fluid movement
  • Seamless epithelium with tight junctions
  • Fast cell turnover
  • IgA secretion at mucosal surfaces
  • Peyer’s patches
103
Q

what are peyers patches?

A

Small masses of lymphatic tissue found throughout the ileum region of the small intestine (also known as aggregated lymphoid nodules).

Form an important part of the immune system by monitoring intestinal bacteria populations and preventing the growth of pathogenic bacteria in the intestines

104
Q

HCL has damaging effects, so what protects the GIT? List some protective factors that prevent autodigestion of the stomach:

A
  • Secretion of alkaline mucus and HCO3-
  • Protein content of food
  • Presence of tight junction between the epithelial cells lining the stomach and fibrin coat
  • Replacement of damaged cells within the gastric pits
  • Prostaglandins (E and I): inhibit acid secretion and enhance blood flow
  • Mucus layer protects the gastric mucosa from the low pH by forming a water-insoluble gel that coats the mucosa
105
Q

what is H. Pylori (Helicobacter Pylori)?

A
  • Gram negative; spiral shaped (can be coccoid too) aerobic bacterium
  • Penetrates gastric mucosa (able to survive under the harsh condition of the stomach)
  • Highly pathogenic, with many virulence factors
  • The flagella enables its “corkscrew” motility towards the gut epithelium
106
Q

name some virulence factors of H. pylori:

A
  • Motility: flagella; moves close to the epithelium (pH 7)
  • Produces urease (converts urea to ammonia, which buffers gastric acid and produces CO2)
  • Cytotoxin-associated antigen (CagA) – inserts pathogenicity islands and confers ulcer-forming potential
  • Vacuolating toxin A (VacA) – alters the trafficking of intracellular protein in gastric cells
107
Q

what are virulence factors?

A
  • molecules produced by H. pylori (malaria, viruses, and fungi) that add to their effectiveness and enable them to achieve the colonisation of a niche in the host (e.g. attachment to cells)
  • The virulence factors enable H. Pylori to attach and colonise the gastric epithelium
108
Q

what is the commonest cause of peptic ulcer? give stats:

A

H. Pylori is the commonest cause of peptic ulcer – ↑ peptic ulcer risk by 10 to 20%

works by disregulating and increasing gastrin secretion

109
Q

describe urease and its role In the H. Pylori infection:

A
  • one of the most important features of H. pylori infection-without it, the bug could not survive in the stomach
  • enzyme that breaks urea into carbon dioxide and ammonia-the carbon dioxide gets blown off, but the ammonia stays and surrounds the bug, raising the pH and allowing the bug to sit comfortably in this otherwise deadly environment – note that it is deadly as highly acidic.
110
Q

describe mucinase and its role In the H. Pylori infection:

A

-busts apart the thick mucin layer that normally overlies the gastric epithelium, allowingH. pylorito walk on through this layer of protection and get right onto the surface of the epithelial cells.

111
Q

what is the role of H pylorus corkscrew motility?

A

H. pylori is curved, and it has a few nice flagellae at one end

  • it corkscrews itself down through the mucin to reach the epithelial layer
  • much more effective than a regular old straight rod trying to push its way through
112
Q

what is CagA and describe its negative effects in the body

A
  • a virulence factor that disrupts cell junctions, affects cell proliferation and differentiation, and induces inflammation
  • patients who have CagA positive strains generally have more severe gastritis, and a significantly increased risk of developing ulcers and carcinoma compared to those with Cag negative strains
113
Q

what is VacA and describe its negative effects in the body

A
  • does many things: making vacuoles, inhibiting apoptosis, disrupting cellular pathways, inducing inflammation, and modulating the immune system (it allows H. pylori to live in macrophages, and also inhibits T-cell production by decreasing IL-2 production)
  • patients with VacA positive strains also have an increased risk of severe gastritis, ulcers and carcinoma.
114
Q

name some aggravators of peptic ulcer:

A
  • Regurgitated bile acids
  • NSAIDS
  • Genetics
  • Smoking, alcohol, spicy foods
  • Chronic gastritis
  • H. pylori infection
  • Ureases and proteases, which work by interfering with epithelial protection
115
Q

what are some complications of peptic ulcer?

A
  • Haemorrhage (GI bleeding)
  • Perforation (peritonitis) and penetration (liver and pancreas may be affected); leakage of luminal contents
  • Narrowing of pyloric canal (stricture causing acquired pyloric stenosis in the stomach) or oesophageal stricture
  • Malignant change becomes 3-6 times likely with H. pylori infection
116
Q

suspected tests for peptic ulcers:

A
  • Endoscopy (oesophagogastroduodenoscopy, EGD)
  • Histological examination and staining of an EGD biopsy
  • Stool antigen test
  • also test for virulence factors (eg. CagA and VacA)
  • Evaluate urease activity
  • Urea breath test

sem 2 Liver and GI (11 decks)

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