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PBL SEM 4 > CASE 2 > Flashcards

CASE 2 Flashcards

1
Q

HCl is produced by what cells of the stomach?

A

parietal cells

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2
Q

describe how acid is produced in the stomach?

A

• to begin with, H2O and CO2 combine within the parietal cell cytoplasm to produce carbonic acid (H2CO3), which is catalysed by carbonic anhydrase
• carbonic acid then spontaneously dissociates into a H+ and a bicarbonate ion (HCO3-)
• the H+ formed is transported into the stomach lumen via the H+/K+ ATPase ion pump
• this pump uses ATP as an energy source to exchange K+ ions into the parietal cells of the stomach with the H+ ions
• the HCO3- is transported out of the cell into the blood via a transporter protein called anion exchanger which transports the bicarbonate ion out of the cell in exchange for a Cl-
• this chloride ion is then transported into the stomach lumen via a chloride channel
• this results in both H+ and Cl- being present in the stomach lumen
• their opposing charges leads to them associating with each other to form HCl

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3
Q

control of gastric acid production

• at rest, the number of H+/K+ ATPases present within the parietal cell membrane is ____
• the rest are sequestered within ________ in the parietal cell
• upon stimulation the _____ fuse with the cell membrane which leads to the _______ insertion of H+/K+ ATPase into the membrnae, hence allowing for the increased movement of ___ into the stomach thus increasing acid production

A

control of gastric acid production

• at rest, the number of H+/K+ ATPases present within the parietal cell membrane is minimal
• the rest are sequestered within tubulovesicles in the parietal cell
• upon stimulation the vesicles fuse with the cell membrane which leads to the increased insertion of H+/K+ ATPase into the membrnae, hence allowing for the increased movement of H+ into the stomach thus increasing acid production

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4
Q

how does ACh release affect gastric acid production and what is it realised by?

A

ACh released from vagus nerve increases gastric acid production

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5
Q

when is ACh released in the stomach?

A
  • released firstly during the cephalic phase of digestion, which is activated upon seeing or chewing food, leading to direct stimulation of parietal cells via the vagus nerve
  • also produced in the gastric phase of digestion when intrinsic nerves detect distention of the stomach, stimulating the production of ACh by the vagus nerve
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6
Q

the main regulation pathway of gastric acid production involves what?

A

gastrin — secreted from G cells in the stomach

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7
Q

what are G cells activated by?

A

vagus nerve, gastrin related peptide and by peptides in the stomach lumen produced via protein digestion

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8
Q

what does the activation of G cells lead to?

A

the production of gastrin which is released into the blood and travels through the blood until it reaches the parietal cells. gastrin binds to CCK receptors on parietal cells which also elevates calcium levels causing increased vesicular fusion

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9
Q

what do enterochromaffin like cells (ECL cells) do in the stomach?

A

secrete histamine which binds to H2 receptors on the parietal cells — activates parietal cells to form and secrete HCl

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10
Q

what do ECL cells secrete histamine in response to?

A

the presence of gastrin (from G cells in antral mucosa) and ACh (from stomach vagal endings)

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11
Q

what does histamine release from ECL cells lead to?

A

increased fusion, however it is via the secondary messengers cAMP as opposed to calcium in the other methods to increase gastric production

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12
Q

what does accumulation of acid in the empty stomach between meals cause?

A

decreased gastric acid production

  • increase in acid leads to a lower pH — inhibits gastrin secretion via the production of somatostatin from D cells
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13
Q

once food has been broken down into chyme, it passes into the duodenum, triggering the what?

A

enterogastric reflex

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14
Q

what can stimulate the enterogastric reflex?

A
  • distention of small bowel
  • excess acid in upper intestine
  • presence of protein breakdown products
  • irritation to mucosa
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15
Q

what is the enterogastric reflex?

A
  • A nervous reflex whereby stretching of the wall of the duodenum results in inhibition of gastric motility and reduced rate of emptying of the stomach.
  • It is a feedback mechanism to regulate the rate at which partially digested food (chyme) leaves the stomach and enters the small intestine.
  • Receptors in the duodenal wall detect distension of the duodenum caused by the presence of chyme and also raised acidity (i.e. low pH) of the duodenal contents due to excess gastric acid. They send signals via the parasympathetic nervous system, causing reflex inhibition of stomach-wall muscles responsible for the stomach emptying.
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16
Q

enterogastric reflex:

____ signals are sent to the stomach via the ____, as well as signals to the medulla — reducing ___ stimulation of stomach. the enterogastric reflex is important in slowing down gastric _____ when the intestines are already filled.

A

inhibitory signals are sent to the stomach via the ENS, as well as signals to the medulla — reducing vagal stimulation of stomach. the enterogastric reflex is important in slowing down gastric emptying when the intestines are already filled.

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17
Q

the presence of chyme within the duodenum stimulates entero-endocrine cells to release what?

A

cholecystokinin and secretin — both inhibit gastric acid secretion

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18
Q

what is secretin released by and when?

A

secretin is released by the S cells of the duodenum when there is excessive acid production in the stomach

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19
Q

what other hormones work to decrease acid production in the stomach?

A

glucose dependent insulin tropic peptide (GIP) and vasoactive intestinal polypeptide

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20
Q

gastrin binds to ___ receptors on parietal cells which acts to increase ____ levels within the cell, which in turn promotes ______ and thus acid production

A

gastrin binds to CCK receptors on parietal cells which acts to increase Ca++ levels within the cell, which in turn promotes vesicular fusion and thus acid production

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21
Q

G cells are activated by the ____ nerve, gastrin related peptide and by peptides in the stomach. activation of G cells leads to production of ____, in turn _____ acid production and release

A

G cells are activated by the vagus nerve, gastrin related peptide and by peptides in the stomach. activation of G cells leads to production of gastrin, in turn increasing acid production and release

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22
Q

increased acid ___ the pH of the stomach which stimulates _____ production by __ cells. _____ subsequently inhibits gastrin secretion, thus reduces acid release

A

increased acid reduces the pH of the stomach which stimulates somatostatin production by D cells. somatostatin subsequently inhibits gastrin secretion, thus reduces acid release

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23
Q

ACh released by ____ stimulation excites secretion of _____ by peptic cells, ___ by parietal cells, and ___ by mucous cells

A

ACh released by parasympathetic stimulation excites secretion of pepsinogen by peptic cells, HCl by parietal cells, and mucus by mucous cells

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24
Q

what is achlorhydria?

A
  • a state where there is a decrease in the volume of stomach acid produced
  • can result in an increased risk of salmonella and cholera and H. pylori infection
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25
Q

what secrete gastric acid and intrinsic factor?

A

parietal cells

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26
Q

what secrete pepsin and gastric lipase?

A

chief cells

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27
Q

intrinsic factor is important in the absorption of what?

A

vitamin B12

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28
Q

what inhibits gastrin release?

A

somatostatin - hence decreases acid production

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29
Q

regulation of pepsinogen secretion by the peptic cells in the oxyntic glands occurs in response to 2 types of signals?

A
  1. stimulation of peptic cells by ACh released from the vagus nerves or from the gastric enteric nervous plexus
  2. stimulation of peptic cell secretion in response to acid in stomach
    - acid doesn’t stimulate the peptic cells directly, instead it elicits additional enteric nervous reflexes that support the original nervous signals to the peptic cells
    - the rate of pepsinogen secretion is influenced by the amount of acid in the stomach
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30
Q

intrinsic factor is secreted by the parietal (oxyntic) cells along with what?

A

the secretion of HCl

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31
Q

what happens when the parietal cells are destroyed eg. in chronic gastritis?

A

the person develops achlorhydria (lack of stomach acid secretion) and also pernicious anaemia (because of failure of maturation of RBCs in the absence prof vitamin B12 stimulation of the bone marrow)

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32
Q

what are the phases of gastric secretion?

A
  1. cephalic
  2. gastric
  3. intestinal
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33
Q

when does the cephalic phase occur and result from?

A

• occurs before food enters the stomach, especially whilst in the mouth
• results from the sight, smell, thought, or taste of food
• the greater the appetite, the more intense the stimulation

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34
Q

cephalic phase : neuronal signals from appetite centres of the _________ + __________ are transmitted through the _____________ through the vagus nerves to the stomach

A

neuronal signals from appetite centres of the amygdala + hypothalamus are transmitted through the dorsal motor nuclei of the vagi through the vagus nerves to the stomach

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35
Q

what effects does the cephalic phase have on HCl secretion?

A

stimulatory

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36
Q

the cephalic phase stimulates the vagus nerve to release more what? effect?

A

more ACh — thus activating more ECL cells and parietal cells

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37
Q

the cephalic phase stimulates the vagus nerve to activate what? effect?

A

activate gastrin-releasing-peptide — increases the secretion of gastrin, thus activating parietal cells

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38
Q

the cephalic phase accounts for what % of gastric secretion associated with eating a meal?

A

20%

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39
Q

what effects does the gastric phase have on HCl secretion?

A

both stimulatory and inhibitory

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40
Q

what stimulatory effects does the gastric phase have on HCl secretion?

A

—> stimulates the vagus nerve to release more ACh, thus activating more ECL and parietal cells
—> stimulates the vagus nerve to activate gastrin-releasing-peptide (GRP) which increases the secretion of gastrin, thus activating parietal cells
—> increases the pH of the food, thus causing an increase in gastrin secretion
—> stimulates secretagogues, which increase H+ secretion

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41
Q

what inhibitory effects does the gastric phase have on HCl secretion?

A

—> low pHs stimulate D cells to release somatostatin, which inhibits the G-cells (antrum) which decreases the secretion of gastrin and so increases the pH in the stomach

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42
Q

the gastric phase accounts for what % of gastric secretion associated with eating a meal?

A

70%

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43
Q

the intestinal phase of gastric secretion occurs as a result of what?

A

the presence of food in the upper portion of the SI, particularly the duodenum

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44
Q

what effects does the intestinal phase have on HCl secretion?

A

stimulatory and inhibitory

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45
Q

what stimulatory effects does the intestinal phase have on HCl secretion?

A

stimulates G cells (duodenum) which secrete more gastrin, resulting in an increase in the secretion of H+

46
Q

what inhibitory effects does the intestinal phase have on HCl secretion?

A

—> inhibits chemoreceptors which cause a decrease in nerve reflexes, thus decreasing H+ secretion
—> secretin, CCK and GIP increase the secretion of somatostatin, thus decreasing H+ secretion

47
Q

why would the presence of food continue to cause stomach secretion of small amounts of gastric juice?

A

because small amounts of gastrin is released by the duodenal mucosa

48
Q

what initially increases gastric secretion, but later inhibits it?

A

chyme

49
Q

how does chyme inhibit gastric secretion?

A
  1. presence of food in the SI initiates a reverse enterogastric reflex, transmitted through the myenteric nervous system + vagus nerves, that inhibits stomach secretion
  2. the hormone secretin is secreted as a result of the presence of acid in the upper intestine, by the presence of protein breakdown products or by irritation of the mucosa. secretin OPPOSES stomach secretion
50
Q

what can the reverse enterogastric reflex be initiated by?

A
  • distending the small bowel
  • by the presence of acid in the upper intestine
  • by the presence of protein breakdown products
  • by irritation of the mucosa

secretin is released in response to some of these

51
Q

what other hormones than secretin have a slight effect on inhibiting gastric secretion?

A

GIP, vasoactive intestinal polypeptide and somatostatin

52
Q

what is the purpose of inhibition of gastric secretion by intestinal factors?

A

to slow passage of chyme from the stomach when the SI is already filled or already overactive

53
Q

what does somatostatin do?

A

inhibits G cells, ECL cells and if there is an excess of acid in the duodenum, it inhibits the parietal cells

54
Q

increased stomach emptying — gastric factors

A
  1. increased stretching of stomach wall — increased pressure in the stomach
  2. gastrin — enhanced pyloric pump and increased HCl production in parietal cells
55
Q

decreased stomach emptying — duodenal factors

A
  1. nervous reflexes (via ENS, extrinsic nerves and CN X) — inhibit pyloric pump and increase pyloric sphincter tone
  2. hormonal feedback — inhibit pyloric pump and increase pyloric sphincter tone
56
Q

what factors affect the duodenal mucosa and initiate the nervous reflexes, leading to decreased stomach emptying?

A
  • distention
  • irritation of the mucosa
  • acidity of digestive enzymes
  • osmolarity of chyme (hyper/hypotonic)
  • protein breakdown products
57
Q

what hormones are released due to the presence of fat in the duodenum, leading to decreased stomach emptying?

A
  • secretin (released from duodenal mucosa in response to gastric acid) — inhibit gastrin, thus lowering acid secretion
  • cholecystokinin (CCK) — released from jejunal mucosa in response to fat in chyme — inhibit gastrin, thus lowering acid secretion
  • gastric inhibitory peptide (GIP) — released from jejunal mucosa in response to fat in chyme — weakly decrease GI motility
58
Q

enterogastric inhibitory nerbvous feedback reflexes and hormonal feedback by CCK work together to slow the rate of emptying when what?

A
  1. too much chyme is already in the small intenstine
  2. the chyme is excessively acidic, contains too much unprocessed protein or fat, is hypotonic or hypertonic, or is irritating

• in this way, the rate of stomach emptying is limited to that amount of chyme that the small intestine can process

59
Q

Stimulation of the vagus excites _______ _________ neurons in the stomach, which then release _______ onto ________ cells to stimulate acid secretion.

A

Stimulation of the vagus excites postganglionic parasympathetic neurons in the stomach, which then release acetylcholine onto parietal cells to stimulate acid secretion.

60
Q

what does a peptic ulcer refer to?

A

both gastric and duodenal ulcers

61
Q

what is associated with about 95% of duodenal ulcers and 80% gastric ulcers?

A

Helicobacter pylori infection

62
Q

what are some causes of ulcers?

A

• H.pylori
• NSAIDs
• pepsin
• smoking
• alcohol
• bile acids
• steroids
• stress
• changes in gastric mucin consistency (may be genetically
determined)
• Zollinger-Ellison syndrome

63
Q

why is smoking thought to be linked to ulcers?

A

presumably because of the increased nervous stimulation of the stomach secretory glands

64
Q

what is Zollinger-Ellison syndrome?

A

a condition where there is a gastrin-secreting tumour thus leading to excess acid secretion

65
Q

what are some of the ulcer defence mechanisms?

A

mucus, bicarbonate, mucosal blood flow and prostaglandins

66
Q

symptoms of peptic ulcers

A
  • epigastric pain, usually 1-3 hours after a meal (postprandial) — may sometimes wake a patient in the night, and be relieved by food
  • nausea
  • oral flatulence, distension and intolerance of fatty food (last is also associated with gallstones)
  • heartburn (although more typically associated with GORD)
  • a posterior ulcer may cause pain radiating to the back
  • symptoms relived by antacids
67
Q

peptic ulcer risk factors

A
  • old age
  • male sex
  • smoking
  • H.pylori infection
68
Q

signs of peptic ulcers

A
  • epigastric tenderness
  • if gastric emptying is slow, there may be a succussion splash
69
Q

what are the 3 mechanisms that control protection against excess acid?

A
  1. vagal and local reflexes — increase secretion of mucus
  2. secretin — increase secretion of bicarbonate ions
  3. prostaglandin E2 (PGE2)
70
Q

what effect does PGE2 normally have on HCl and mucus?

A

normally it inhibits HCl secretion and stimulates mucus cell secretion (mucus and bicarbonate ions)

71
Q

how do NSAIDs affect H+?

A

NSAIDs block the arachidonic pathway by blocking COX and therefore increase HCl secretion and decrease bicarbonate secretion

eg. misoprostol : stimulates mucus secretion (surface mucous cells and intestinal goblet cells) and inhibits H+ secretion from parietal cells

72
Q

NSAIDs inhibit _____ synthesis, thus increasing acid secretion and causing ulcers

A

PGE2

73
Q

what effect does alcohol tend to have on mucosal barrier?

A

breaks it down

74
Q

how does histamine affect acid secretion?

A

works via the Gs intracellular protein pathway, causing an increase in acid secretion

75
Q

PGE2 works via what pathway to cause a decrease in acid secretion?

A

Gi intracellular protein pathway

76
Q

what type of bacterium are H.pylori? where are they found?

A

flagellated gram negative bacillus found on the luminal surface of the gastric epithelium

77
Q

H. pylori contain high levels of what?

A

the enzyme urease — these bacteria metabolise urea (this urease production is the basis for diagnostic tests)

78
Q

how can H. pylori live in low pH environments?

A

these bacteria metabolise urea which releases NH3 (alkali), causing local alkaline conditions around the bacteria — this enables it to withstand the acidic conditions of the stomach

79
Q

how is H. pylori capable of penetrating the mucosal barrier?

A
  • its physical capability to burrow through the barrier
  • releasing bacterial enzymes that liquefy the barrier, allowing the strong acidic digestive juices to penetrate the underlying epithelium and digesting the gastroduodenal wall, thus leading to peptic ulceration
  • also inhibits somatostatin release in the antrum thus causing an increase in acid secretion
80
Q

peptic ulcer investigations

A
  • FBC may show iron-deficiency anaemia
  • testing for H. Pylori — stool antigen test (PPI will interfere with result), 13urea breath test (PPI will interfere with result), serology (cannot distinguish between active and previous infection), CLO test (gold standard, biopsy during endoscopy)
81
Q

irrespective of age, endoscopy is required if what red flags are present?

A
  • iron-deficiency anaemia
  • chronic blood loss
  • progressive dysphagia
  • persistent vomiting
  • an epigastric mass
82
Q

in patients over 55. referral should also be considered if there is what?

A
  • previous gastric ulcer
  • previous gastric surgery
  • pernicious anaemia
  • NSAID use
  • family history of carcinoma
83
Q

peptic ulcer management : modification of behaviour

A
  • stop any drugs that could be causing ulcer eg. steroids, NSAIDs, anticoagulants, low-dose aspirin, SSRIs
  • smoking cessation — smoking increases the risk of peptic ulcer and delays healing, as well as opposing the action of H2-receptor antagonists. it has many effects on other parts of the gut, including facilitating GORD
84
Q

peptic ulcer management : H.pylori positive

A

treatment mainly directed at eradication of infection - antibiotics (amoxicillin + metronidazole/clarithromycin)

85
Q

peptic ulcer management : H.pylori negative, NSAID-induced

A
  • stop NSAIDs
  • while H2-receptor antagonists will heal NSAID-induced ulcers, PPIs are more effective
86
Q

peptic ulcer management : H. pylori negative, not NSAID-induced

A
  • rare
  • careful history of NSAID and aspirin use is important
  • exclude rare conditions such as Zollinger-Ellison syndrome — take samples from ulcer and surrounding mucosa
87
Q

when does pain typically arise? gastric vs duodenal ulcers

A

gastric - pain shortly after meals

duodenal - pain 2-3 hours after meals

88
Q

name 2 H2 histamine receptor antagonists

A

cimetidine and ranitidine

89
Q

how do H2 histamine receptor antagonists work?

A
  • they block the H2 histamine receptors on the parietal cells
  • as a result, histamine secreted by ECL cells can no longer activate parietal cells, thus preventing the secretion of HCl into the stomach lumen
90
Q

how do proton pump inhibitors work?

A
  • comprise of thioamide compounds
  • block the action of H+ K+ ATPase pump permanently in the gastric parietal cell by binding to its sulphydryl group
  • given in encapsulated formulation to avoid breakdown by stomach acid
  • absorbed in the SI and travels to parietal cells in the blood
91
Q

peptic ulcers are defects in the gastric or duodenal mucosa that extend through what layer?

A

muscularis mucosa

92
Q

most patients with duodenal ulcers have impaired what?

A

duodenal bicarbonate secretion, which has been proven to be caused by H pylori because it’s eradication reverses the defect

93
Q

aggressive factors such as NSAIDs, H pylori infection, alcohol, bile salts, acid, and pepsin, can alter the mucosal defence by allowing what?

A

the back diffusion of H+ and subsequent epithelial injury

94
Q

what 2 things can lead to peptic ulcers?

A
  1. excess secretion of acid and pepsin by the gastric mucosa
  2. diminished ability of the gastroduodenal mucosal barrier to protect against the digestive properties of the stomach acid-pepsin secretion
95
Q

what is the duodenum protected by?

A

intestinal secretions

—> an important secretion is pancreatic secretion : contains large amounts of sodium bicarbonate that neutralises the HCl of the gastric juice, thus also inactivating pepsin and preventing digestion of the mucosa

96
Q

feedback mechanism for neutralisation of gastric juices:

  1. when ___ acid enters the duodenum, it reflexly _____ gastric secretion and peristalsis in the stomach, both by ________ and ___________ from the duodenum, thereby decreasing the rate of gastric emptying
  2. the presence of acid in the small intestine liberates ______ from the intestinal mucosa, which then passes by way of the blood to the pancreas to promote rapid secretion of pancreatic juice — this juice causes __________ of the acid
A

feedback mechanism for neutralisation of gastric juices:

  1. when excess acid enters the duodenum, it reflexly inhibits gastric secretion and peristalsis in the stomach, both by nervous reflexes and hormonal feedback from the duodenum, thereby decreasing the rate of gastric emptying
  2. the presence of acid in the small intestine liberates secretin from the intestinal mucosa, which then passes by way of the blood to the pancreas to promote rapid secretion of pancreatic juice — this juice causes neutralisation of the acid
97
Q

what is gaviscon?

A

a combination of 2 antacids (calcium carbonate and sodium bicarbonate) and an alginate

98
Q

what do antacids do?

A

neutralise stomach acid and inhibit pepsin

99
Q

what does sodium alginate do?

A

forms a sticky layer that works as a mechanical barrier on top of stomach contents, preventing reflux into the gullet

100
Q

describe the clarithromycin and statin interaction

A
  • clarithromycin is a potent inhibitor of the cytochrome P450 (CYP450)
  • CYP450 metabolises statins
  • therefore get increased statin levels
  • increased risk of rhabdomyolysis
101
Q

peritontitis can cause irritation of the diaphragm. where is referred pain of the inferior part of the diaphragm?

A

goes to right shoulder — C3/4/5

102
Q

parietal vs visceral peritoneal pain

A

parietal pain = well localised, sharp pain
visceral pain = not well localised, dull ache/cramp

103
Q

what is the only place that the parietal peritoneum cant localise pain?

A

inferior part of diaphragm

104
Q

what cause epigastric pain?

A

foregut organs

105
Q

right upper quadrant pain normally involves what?

A

the liver or biliary tree, such as acute hepatitis, gallstones, or acute cholecystitis, but it may radiate to the back or epigastrum

106
Q

left upper quadrant pain normally involves what?

A

can overlap with causes of epigastric pain, such as pancreatitis which causes pain that radiates to the back, but amy also be due to the spleen

107
Q

what causes periumbilcial pain?

A

midgut organs (rest of SI, caecum, appendix)

108
Q

what does small bowel obstruction cause?

A
  • periumbilcial pain
  • vomiting, abdominal distention, severe constipation
109
Q

what causes suprapubic/hypogastric pain?

A

hindgut organs (rest of large intestines, as well as the intraperitoneal portions of the genitourinary tract)

110
Q

in older patients, pain associated with a change in bowel habits and iron deficiency anaemia can be the first signs of what?

A

colorectal cancer

111
Q

what is a secretagogue? example?

A

secretagogue = a substance that causes another substance to be secreted

eg. gastrin : stimulates the H/K ATPase in the parietal cells (increased gastric acid)

112
Q

read anaemia notes

A

ew

PBL SEM 4 (50 decks)

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