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Semester 4 > Case 2 > Flashcards

Case 2 Flashcards

1
Q

Definition of pH

A

pH = -log10[H+]

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2
Q

Normal range of INTRACELLULAR pH

A

6.8-7.2

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3
Q

Which macromolecules can do intracellular buffering?

A

Weak acids and base group on proteins

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4
Q

An open buffer system

A

CO2 and bicarbonate buffer system

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5
Q

Open buffer

A

Components of buffer reaction is in equilibrium?

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6
Q

What keeps Pco2 constant in the body?

A

Respiratory system

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7
Q

Acid extruding transporters involved in pHi regulation

A

Na+/H+ exchanger, H+ ATPases (pumps)

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8
Q

Base extruding transporters involved in pHi regulation

A

Na+/2HCO3- cotransporter, Cl-/HCO3- exchanger

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9
Q

What is the source of secreted H+ into the lumen?

A

CO2

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10
Q

Apical (lumen) acid secretion is driven by 3 transporters

A
  1. H+/K+ ATPase active transport of H+ into lumen, 2. K+ channels recycle K+ ions, 3. Cl- (CFTR) channels secrete Cl- into lumen.
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11
Q

Which subunit is necessary for the full function of H+/K+ ATPase proton pump?

A

Glycosylated Beta subunit

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12
Q

Similar to Na+/K+ ATPase, conformational change of H+/K+ ATPase is driven by

A

Phosphorylation and dephosphorylation

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13
Q

What causes the most common form of peptic ulcer disease?

A

Occurs within gastric Antrum or duodenum due to chronic, H.pylori-induced antral gastritis, associated with increased gastric acid secretion and decreased duodenal bicarbonate secretion.

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14
Q

Peptic ulcer disease within gastric fundus or body is accompanied by lesser acid secretion due to mucosal atrophy

A

….

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15
Q

How can perforated peptic ulcer be identified?

A

Detection of free air under the diaphragm on upright radiographs of abdomen

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16
Q

what are the 3 motor functions of stomach?

A

1) storage of food until it can be processed 2) mixing of food with gastric secretions until it forms chyme 3) gastric emptying of chyme into duodenum at the correct rate

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17
Q

what is the ORAD portion of stomach?

A

the first 2/3 of the ‘body’ of the stomach

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18
Q

what is the CAUDAD portion of stomach?

A

the last 1/3 of the ‘body’ of the stomach + antrum

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19
Q

When this food stretches the stomach wall, which reflex occurs that reduces the muscle tone of the muscular wall of the body of the stomach so that the wall can expand outwards progressively?

A

Vagovagal reflex

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20
Q

maximal stomach volume/ capacity is

A

0.8-1.5 litres

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21
Q

Digestive juices of the stomach are secreted by the gastric glands. Which part of body wall of stomach are they NOT present in?

A

Lesser curvature

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22
Q

what are ‘mixing waves’?

A

the weak peristaltic constrictor waves begin in the mid- to upper portions of the stomach wall and move toward the antrum about once every 15 to 20 seconds, as long as food is in the stomach.

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23
Q

what happens when these mixing waves become extremely intense?

A

provide powerful peristaltic action potential–driven constrictor rings that force the antral contents under higher and higher pressure toward the pylorus.

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24
Q

What is retropulsion?

A

An important mixing mechanism in the stomach - moving peristaltic constrictive ring, combined with upstream squeezing action of antral contents into body of stomach

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25
Q

what are hunger contractions?

A

rhythmical peristaltic contractions in the body of the stomach

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26
Q

does hypoglycemia trigger hunger contractions?

A

Yes

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27
Q

Name the pain in the stomach when hunger contractions occur

A

hunger pangs

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28
Q

Gastric emptying contractions

A

contractions become intense, beginning in mid-stomach and spreading through the caudad stomach no longer as weak mixing contractions but as strong peristaltic, very tight ring-like constrictions that can cause stomach emptying. When pyloric tone is normal, each strong peristaltic wave forces up to several milliliters of chyme into the duodenum. Thus, the peristaltic waves: 1. Cause mixing in the stomach. 2. Provide a pumping action called the “pyloric pump.”

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29
Q

is the pyloric sphincter open normally?

A

pylorus usually is open enough for water and other fluids to empty from the stomach into the duodenum with ease. Preventing passage of food until mixed in chyme.

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30
Q

how does the gastric food volume affect the rate of gastric emptying?

A

stretching of the stomach wall elicits local myenteric reflexes in the wall that greatly accentuate activity of the pyloric pump and at the same time inhibit the pylorus.

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31
Q

Gastrin secreted by

A

G-cells of antral mucosa

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32
Q

what stimulates the release of gastrin?

A
  • Stretching of the stomach wall.
  • Presence of protein food contents in the stomach.
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33
Q

what are the functions of gastrin?

A
  • Gastrin activates ECL cells, which release histamine, which is the primary initiator for parietal cell acid production.
  • enhances the activity of the pyloric pump, thus promoting stomach emptying.
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34
Q

Inhibitory Effect of Enterogastric Nervous Reflexes from the Duodenum. name the 3 routes by which this occurs

A
  1. Directly from the duodenum to the stomach through ENS in the gut wall.
  2. Through extrinsic nerves that go to the prevertebral sympathetic ganglia and then back through inhibitory sympathetic nerve fibres to the stomach.
  3. Through the vagus nerves to the brainstem, where they inhibit the normal excitatory signals transmitted to the stomach through the vagi. (minor role)
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35
Q

What effects do the ENS reflexes have on gastric emptying?

A
  1. Strongly inhibit the pyloric pump propulsive contractions.
  2. Increase the tone of the pyloric sphincter.
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36
Q

Which factors can initiate enterogastric inhibitory reflexes?

A
  1. Degree of distention of the duodenum
  2. Degree of irritation of the duodenal mucosa - especially sensitive to this
  3. Degree of acidity of the duodenal enzyme – especially sensitive to this (when chyme in duodenum has a pH below 3.5, the reflexes block further gastric emptying until the chyme is neutralised)
  4. Degree of osmolality of the chyme (Hypertonic and hypotonic (especially hypertonic) fluids elicit the inhibitory reflex.)
  5. Presence of breakdown products of protein and ~fats in the chyme. Slowing gastric emptying allows more time for proper digestion of these products.
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37
Q

Hormonal Feedback from the Duodenum Inhibits Gastric Emptying

A

Stimulus for hormone release - fats entering duodenum

fats bind to receptors on the duodenal and jejunal epithelium, thus extracting different hormones from the epithelium.

hormones are carried by blood into stomach, where they inhibit pyloric pump and increase the strength of contraction of pyloric sphincter.

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38
Q

Which hormone has the most potent effect in regards to hormonal feedback to inhibit gastric emptying?

A

cholecystokinin (CCK)

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39
Q

where and why is CCK released?

A

Where - duoenal and jejunal mucosa

why- in response to fatty substances in the chyme.

40
Q

How does CCK inhibit gastric emptying?

A

CCK acts as an inhibitor to block increased stomach motility caused by gastrin.

41
Q

which other hormones, apart form CCK, can inhibit gastric emptying?

A

Secretin

Gastric inhibitory peptide (GIP)

42
Q

Where and why are secretin released?

How does it work?

A

Where - duodenal mucosa (S cells in the crypts of Lieberkuhn)

Why - Released in response to gastric acid passed from the stomach through the pylorus

How - increase the strength of pyloric contraction and regulate gastric emptying

43
Q

Where and why are GIPreleased?

How does it work?

A

where - duodenal and jejunal mucosa

why - Released in response to fat in the chyme

how - although GIP weakly decreases the GI motility, its primary function is to stimulate secretion of insulin by the pancreas

44
Q

Which gastric factors increase gastric emptying?

A
  • increased stretching of stomach wall - increased pressure in stomach
  • Gastrin - enhanced pyloric pump + increased HCl production in parietal cells
45
Q

Stomach mucosa has 2 types of tubular glands. which and where are they?

A

oxyntic/gastric glands - on the inside surafces of body and fundus of stomach, proximal 80% of stomach

pyloric glands - antral portion, distal 20% of the stomach.

46
Q

Mucous neck cells in gastric glands secrete

A

Mucus

47
Q

Parietal cells in gastric glands secrete

A

HCl and intrinsic factor

48
Q

what is the function of intrinsic factor released from parietal cells?

A

Intrinsic factor is essential for the absorption of vitamin B12 in the ileum.

Patients lacking intrinsic factor gets pernicious anemia.

49
Q

Chief cells in gastric glands secrete

A

Pepsinogen

50
Q

what is the function of pepsinogen?

A

no digestive activity.

When it comes in contact with HCl , it is activated to form pepsin.

  • Pepsin is an active proteolytic enzyme for proein digestion, in an acid medium
  • optimum pH - 1.8-3.5
51
Q

what regulates pepesinogen secretion?

A

Pepsinogen is released in respose to:

  • Stimulation of chief cells by acetylcholine from vagus nerve or ENS
  • Stimulation of chief cell secretion in response to acid in the stomach, which elicits additional enteric nervous reflexes that support the original nervous signals to the peptic cells.

rate of pepsinogen secretion is influenced by the amount of acid in the stomach.

52
Q

What do pyloric glands secrete?

A

mainly mucus for protection of the pyloric mucosa from the stomach acid and hormone gastrin.

53
Q

Mechanism of HCl production

A

Check the notes

54
Q

what kind of celsdo pyloric glnads contain?

A

Few chief cells

NO parital cells

mainly mucous cells that secrete large amounts of thin mucus that helps lubricate food movement, as well as protect the stomach wall from digestion by the gastric enzymes

55
Q

surface mucous cells located between oxyntic and pyloric glands contian a continuous layer of surface mucous cells. what are their functions?

A

Surface mucous cells secrete large amounts of viscid mucus that cover stomach mucosa, providing lubrication and protection.

mucus is alkaline (contain HCO3-)

56
Q

How does enterochromaffin-like cell (ECL cell) exert an effect on stomach acid production?

A

ECL cells release histamine whihc act on histamine receptors on parietal cells to stimulate acid production and secretion.

Rate of formation and secretion of HCl is dependent on the amount of histamine secreted by ECL cells.

57
Q

How are ECL cells activated?

A
  1. Gastrin – when G-cells of the antral mucosa come into contact with amino acids, they pass gastrin to ECL cells through the digestive juices, which in turn secrete histamine.
  2. Acetylcholine – this is released from stomach vagal nerve endings.
  3. Hormonal substances secreted by the enteric nervous system
58
Q

what two froms of gastrin are secreted by G cells?

A

G-34 (34 amino acids)

G-17 (17 amino acids) - more abundant

59
Q

what main events happen during cephalic phase of gastric secretion?

A
  • cephalic phase results from the sight, smell, thought, or taste of food
  • Neuronal signals from appetite centres of the amygdala and hypothalamus are transmitted through the dorsal motor nuclei of the vagi through the vagus nerves to the stomach
  • This phase has stimulatory effects on HCl secretion:
    • stimulates vagus nerve, secrete more ACh –> activate more ECL and parietal cells
    • stimulates vagus to activate gastrin-releasing-peptide (GRP), which increases the secretion of gastrin.
  • 20% of gastric secretion
60
Q

what main events happen during gastric phase of gastric secretion?

A
  • once food enters stomach
  • has both stimulatory and inhibitory effects on HCl secretion
  • Stimulatory:
    • stimulates vagus nerve to release more Ach –> activate more ECLs and parietal cells
    • stimulates vagus nerve to activate GRP –> increase gastrin
    • increases pH of food, thus increasing gastrin secretion
    • stimulates secretagogues, increase H+ secretion
  • Inhibitory:
    • inhbits G-cells –> increases pH in stomach
  • 70% of gastric secretion
61
Q

what main events happen during intestinal phase of gastric secretion?

A
  • result of food in duodenum
  • both stimulatory and inhibitory effects on gastric secretions:
  • Stimulatory:
    • stimulates G-cells
  • Inhibitory:
    • 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
62
Q

How does chyme in duodenum inhibit gastric secretion?

A
  1. Presence of food in the small intestine initiates a reverse enterogastric reflex trabsmitted through myenteric nervous system and vagus nerves that inhibit gastric secretion.
  2. secretin is released in response to food in duodenum, opposes gastric secretion.
  3. other hormones - GIP, VIP and somatostatin inhibit gastric secretion
63
Q

how does somatostatin inhibit gastric secretion?

A

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

64
Q

what kind of stimuli increase indigestive gastric secretion?

A

Emotional stimuli

65
Q

the ptyalin in saliva breaks down starch into what in the mouth and stomach?

A

Maltose and 3 to 9 glucose polymers

66
Q

name the particular type of protein that can be very well broken down by pepsin.

A

Collagen

67
Q

which two things make up the gastric barrier?

A
  1. highly resistant mucous cells that secrete a viscid and adherent mucus
  2. tight junctions between adjacent epithelial cells
68
Q

what happens to the gastric barrier in gastritis?

A
  1. The permeability of the barrier is greatly increased
    • Hydrogen ions can now diffuse into the stomach epithelium, leading to stomach mucosal damage and atrophy
  2. The mucosa becomes susceptible to digestion by the peptic digestive enzymes
    • causes gastric ulcers
69
Q

Achlorhydria

A

diagnosed when the pH of the gastric secretions fails to decrease below 6.5 after maximal stimulation.

70
Q

Helicobacter Pylori

A
  • flagellated gram negative bacillus
  • contain high levels of the enzyme urease. These bacteria metabolise urea
71
Q

How are H.Pylori able to live in low pH environments?

A
  • it metabolises urea which releases NH3 (alkali).
  • This causes local alkaline conditions around the bacteria, allowing it to withstand the acidic conditions of the stomach.
72
Q

How are H.Pylori able to penetrate the mucosal barrier and increase acid secretion?

A
  • Its physical capability to burrow through the barrier.
  • Releasing bacterial digestive 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 (in 15% of patients).
  • H-pylori also inhibits somatostatin release in the antrum, thus causing an increase in acid secretion.
73
Q

Diagnosing H.Pylori infection

A

urea breath test (main one)

  • Patients swallow a meal consisting of non-radioactive carbon-13 urea and citric acid.
  • Breath sample taken by direct exhalation into test tubes 15 minutes later.
  • Urea is split by urease into NH3 and CO2.
  • The detection of the labelled CO2 in the exhaled breath indicates that the urea was split; this indicated that the urease is present in the stomach, and so H.pylori is present.

helicobacter stool antigen test

  • Based on amplification of H.pyloru RNA shed in stool
  • Sensitivity >90%; specificity 80-90%

serology

  • IgG indicates previous exposure, poor value
  • Sensitivity 90%; specificity 70-80%

CLO or Urease Test:

  • 2 gastric samples placed in a medium containing urea and a pH indicator.
  • Hydrolysis of urea by HP urease alters pH-pink colour develops in a few hours.

Gastric Biopsy for histopathology
Gastric Biopsy for culture of H.pylori

74
Q

How do NSAIDs cause peptic ulcers?

A
  • Normally, PGE2 works via the Gi intracellular protein pathway, inhibiting HCl secretion and stimulates mucus cell secretion (mucus and bicarbonate ions).
  • NSAIDs block the Arachadonic acid pathway by blocking COX and therefore increase HCl secretion and decreasing bicarbonate secretion.
  • NSAIDs inhibit PGE2 synthesis, thus increasing acid secretion and causing ulcers
75
Q

Zollinger-Ellison Syndrome

A

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

76
Q

Treatment of H.Pylori infection

A

Standard Triple Therapy

  • 2 antibiotics + 1 PPI.
  • “CAP” = Clarithromycin (500mg bd) + Amoxicillin (1g bd) + PPI (standard dose bd)
  • Metronidazole (400mg bd) can be used instead of Amoxicillin

Modern Bismiuth-Based Regimens

  • 2 antibiotics + 1 bismuth compound.
  • “CAR” = Clarithromycin (500 mg bd) + Amoxicillin (1 g bd) + Ranitidine bismuth citrate (400 mg bd)
  • Metronidazole (400 mg bd) can be used instead of Amoxicillin.
77
Q

H2 Histamine Receptor Antagonists

A
  • E.g. cimetidine, ranitidine
  • These 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.
78
Q

Proton pump inhibitors (PPIs)

A
  • thioamide compounds
  • Examples – Esomeprazole, Lansoprazole, Omeprazole, Pantoprazole, Rabeprazole sodium
  • block the action of the H+,K+ -ATPase pump permanently in the gastric parietal cell by binding to its sulphydryl group
79
Q

Bismuth Compounds

A

“coating compounds” which potentiate the action of antibiotics

80
Q

Antacids

A
  • Examples - Sodium Carbonate, Calcium Carbonate, Magnesium or Aluminium Hydroxide
  • weak bases which react with gastric HCl to form a salt and water, relieving dyspepsia and reflux pain, by neutralising the acid secreted in response to a meal
  • As the metal salts are absorbed by the kidneys, long term use of antacids is unsuitable for patients with serious renal disorders.
81
Q

Difference between 1st and 2nd generation PPIs

A

1st gen example - omeprazole

  • Forms irreversible S-S bond with H+,K+ ATPase, therefore blocks its action permanently
  • 1st generation PPIs are a mixture of optical (R and S) isomers.

2nd gen example - Esomeprazole / Nexium

  • The S-isomer is more active in humans.
  • Purified S-isomer is ‘esomeprazole/nexium’
82
Q

Visceral/ Parietal pain

A

Visceral pain - pain fibres that originate in the viscera are transmitted via C fibres, which only transmit colicky/ cramping, poorly localized types of pain.

Parietal peritoneum is innervated by extensions of the peripheral spinal nerves, which carry the same types of noxious pain sensations as those overlying the dermatomes. Results in sharp, localised pain.

83
Q

where does referred pain of peritonitis be sensed?

A

Peritonitis can cause irritation of diaphragm and so cause referred pain into the right shoulder via the C3, 4, 5 dermatome.

84
Q

What is dyspepsia?

A

the chronic or recurrent pain or discomfort centred in the upper abdomen

85
Q

What are the three phases of stress response?

A
  1. The alarm phase
  2. The resistane phase
  3. The exhaustion phase
    1.
86
Q

Which is the dominant hormone of the alarm phase?

A

Adrenaline

87
Q

In the alarm phase:

  1. Energy reserves are mobilized, mainly in the form of glucose
  2. The body prepares to deal with the stress-causing factor by “fight or flight” responses.

What are the other characteristics of the alarm phase?

A
  1. Increased mental alertness.
  2. Increased energy use by all cells, especially skeletal muscles.
  3. Mobilization of glycogen (Hepatocytes perform glycogenolysis) and lipid reserves (adipose tissue cells perform lipolysis).
  4. Icreased blood flow to skeletal muscles and decreased blood flow to the skin, kidneys, and digestive organs.
  5. A drastic reduction in digestion and urine production.
  6. Increased sweat gland secretion.
  7. Increases in blood pressure, heart rate, respiratory rate and metabolic rate.
88
Q

What is the resistance phase?

A

If a stress lasts longer than a few hours, the individual enters the resistance phase of the stress response.

89
Q

What are the dominant hormones of the resistance phase?

A

Glucocorticoids

Growth Hormone, ADH and glucagon are also involved.

90
Q

Key events happening during the resistance phase:

A
  1. Mobilization of remaining lipid and protein reserves:
    • hypothalmus produces growth hormone releasing hormone (GHRH) –> releasing growth hormone and glucocorticoids.
  2. conservation of glucose for neural tissues
  3. Elevation and stabilization of blood glucose concentrations:
    • when blood glucose declines, glucagon & glucocorticoids stimulate liver to do gluconeogenesis.
  4. Conservation of salts and water, and the loss of K+and H+:
    • Blood volume is conserved through the actions of ADH and aldosterone.
    • As Na+ is conserved, K+ and H+ are lost.
91
Q

Key events happening during exhaustion phase:

A
  • When the resistance phase ends, homeostatic regulation breaks down and the exhaustion phase begins.
  • Unless corrective actions are taken almost immediately, the failure of one or more organ systems will prove fatal.
  • Mineral imbalances:
    • production of aldosterone throughout the resistance phase results in a conservation of Na+ at the expense of K+.
    • As the body’s K+ content declines, a variety of cells—notably neurons and muscle fibers—begin to malfunction
92
Q

HPA axis: chronic stress result in excessive release of cortisol into blood. Where and why are they released?

A

Released form adrenal cortex in response to hign levels of adrenocorticotropic hormone (ACTH).

93
Q

HPA axis: Where are why is ACTH released?

A

ACTH released form anterior pituitary gland in response to corticotropin-releasing hormone (CRH)

94
Q

HPA axis: Where is CRH released from?

A

Released from parvocellular neurosecretory neurons in the paraventricular nucleus of the hypothalamus.

95
Q

Accodring to Lazarus’s Model of appraisal, in a primary appraisal, what are the four possible ways that a stressful event can be appraised as?

A
  1. Irrelevant
  2. Benign (gentle) and Positive
  3. Harmful and a Threat
  4. Harmful and a Challenge
96
Q

What happens during the secondary appraisal?

A

The individual evaluates the pros and cons of their different coping strategies.

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