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Gastro nutrition > GI stomach > Flashcards

GI stomach Flashcards

1
Q

Explain the factors that prevent GORD?

A
  1. Upright posture
  2. Anatomical factors - angle of His, mucosal flap, posterolateral localtion of gastric fundus
  3. Sphincters 0 lower oesophageal and diaphragmatic crura with resting sphincter tone
  4. Resting sphincter tone regulation - neurogenic, myogenic, hormonal
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2
Q

What postural influences are their on GORD? (2)

A
  • Upright posture: gravity prevents the upward movement of stomach contents
  • Right lateral position decreases reflux, as it puts the pylorus in a dependent position, promoting gastric emptying (Loots et al, 2012)
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3
Q

What anatomical factors affect GORD?

A
  • The angle of His is an acute angle between the oesophagus and the gastric fundus, which contributes to the prevention of reflux mainly by creating a mucosal flap valve.
  • Mucosal flap valve: this is a “180-degree musculomucosal fold apposite to the lesser curvature of stomach” created by the intraluminal extension of the angle of His. It blocks the oesophageal opening.
  • Posterolateral location of the gastric fundus keeps gastric contents away from the oesophageal opening
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4
Q

What is the angle of His

A
  • The angle of His is an acute angle between the oesophagus and the gastric fundus, which contributes to the prevention of reflux mainly by creating a mucosal flap valve.
  • Mucosal flap valve: this is a “180-degree musculomucosal fold apposite to the lesser curvature of stomach” created by the intraluminal extension of the angle of His. It blocks the oesophageal opening.
  • Posterolateral location of the gastric fundus keeps gastric contents away from the oesophageal opening
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5
Q

Where is the opening of the oeosphaus relative to the stomach?

A
  • Posterolateral location of the gastric fundus keeps gastric contents away from the oesophageal opening
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6
Q

What sphincters function in the oesophagogastric region?

A

Lower GEJ sphincter
Diaphragmatic crura

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7
Q

Lower oesopheageal sphincter is characterised by? How is it different to surrounding smooth muscle?

A
  • Lower gastroesophageal sphincter is the smooth muscle that encircles the lower oesophagus.
    ◦ Structurally identical to the circular smooth muscle in the rest of the oesophagus
    ◦ Seems thicker because it is constantly tonically contracted.
    ◦ Myogenic influence on tone is mainly due to functional differences in the smooth muscle cells in the lower oesophagus, as compared to the rest of the oesophagus:
    ‣ Lower oesophageal smooth muscle has more α-actin and basic essential light chains
    ‣ That smooth muscle is constantly in a state of depolarization because of a higher resting membrane potential, though to be due to its greater chloride conductance
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8
Q

What part of the diaphragm interacts with the oesophagus?

A

right crus - band of skeletal muscle fibres forming the sides of the oesophageal hiatus

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9
Q

Resting sphincter tone of the lower oesophageal sphincter is?

A

15-25mmHg
Exerts a pressure generally greater than gastric pressure (2-3mmHg higher)

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10
Q

What factors influence resting lower oesophageal sphincter tone?

A

Neurogenic - vagal
Myogenic - functional difference in smooth muscle cells at this location with a higher resting membrane potential possibly due to chloride conductance promoting contraction
Hormonal

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11
Q

What hormones increased lower oesophageal sphincter tone?

A

‣ Gastrin
‣ Motilin
‣ Catecholamines (α-adrenergic effect)
‣ Substance P
‣ Bombesin
‣ Galanin
‣ Pancreatic polypeptide

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12
Q

What hormones decrease lower oesophageal sphincter tone?

A

‣ Secretin
‣ Glucagon
‣ VIP and GIP
‣ Cholecystokinin
‣ Somatostatin

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13
Q

What cell type produces gastric acid? What elso do they secrete?

A

Parietal cells
intrinsic factor

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14
Q

Where do you find acid producing cells

A

Parietal cells are in the neck of gastric glands

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15
Q

Describe the structure of a gastric parietal cell

A
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16
Q

How is acid secreted by parietal cells?

A

Negative potential in canaliculi created by chloride ion pumps, and sodium pumps causing K+ to flow outwards

H+/K+ exchange via ATPase

Water then passes via osmosis diluting the acid

pH of acid secretions is 0.8 but gets diluted

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17
Q

What transport protein moves acid out of a pareital cell?

A

H+/K+ ATPase

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18
Q

What factors stimulate acid production? 5

A

◦ PSNS - vagal innervation in cephalic phase of digestion via M3 receptors triggers increased secretion (Increased Ca intracellularly)
◦ Gastrin - cephalic and gastric phases of digestion due to central and mechanical signals. Gastrin receptors on parietal cells (HCl release) + CCK-B cells (histamine release)
‣ Both via cAMP secondary messenger
◦ Histamine - cephalic and gastric phases of digestion (central signals + gastrin cause release) binding to H2 receptors on parietal cells - via cAMP secondary messenger
◦ Mechanical stretch - local smooth muscle and Vagal-Vagal
◦ Peptides, caffeine, alcohol sensed by mucosal chemoreceptors –> gastrin

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19
Q

Pepsinogen is produced by? Activated by? What is also produced by this cell?

A

Chief cells from rough endoplasmic reticulum
Acid activates it by splitting into lower moelcular weight forms
Also produces gastric lipase

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20
Q

Pepsinogen does what? What stimulates its production?

A

protein digestion

Stimulated by
- Gastrin
- Vagal stimulation
- ACid

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21
Q

Is producing acid an energy consuming process?

A

1500calories per L of gastric juice

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22
Q

What is intrinsic factor? where is it produced?

A

Glycoprotein essential for absorption of vitamin B12 secreted by parietal cells

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23
Q

What is mucous in the stomach?

A

produced by GOBLET cells
- glycoproteins e.g. mucin
- Water
- viscous collloid - microscopic particles disperesed in water
- Antiseptic components - lysoszymes, IgA
- INorganic salts

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24
Q

What stimulates mucous production in the stomach?

A

Gastrin
Secretin increases HCO3 production from mucous glands
PGE2 and PGI2

Mucous production occurs in globlet cells

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25
Q

Gastrin secreted by?

A

G cells in pyloric antrum

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26
Q

What causes release of Gastrin?

A

protein/amino acids
Distension
Vagus

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27
Q

What does Gastrin do?

A

Binds to CCK B receptors to stimulate release of histamine in ECL cells

Induces insertion fo K+/H+ ATPase into apical membrane of parietal cells via CCK B cells and causes parietal cell maturation

Pepsinogen secretion weak stimulator as well as mucous secretion

Promotes stomach contraction, relaxation of pyloric sphincter and lower oesophageal sphincter and relaxes ileocaecal valve

Induces pancreatic secretion

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28
Q

What inhibits gastrin production

A

Acid
Somatostatin

Lesser extention - secretin, GIP, VIP, glucagon, calcitonin

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29
Q

What is a histamine secreting cell in the stomach called

A

ECL cell
Enterochromaffin cell

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30
Q

What is an ECL cell

A

Histamine releasing cell in the stomach mucosa stimulating acid production

Enterochromaffin cell

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31
Q

What stimulates ECL cells

A

Beta-adrenergic agents
cholinergic agents
gastrin-releasing peptides (Gastrin from G cells)
inhibited by enterogastric reflex and D cells release of Ghrelin

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32
Q

What is Ghrelin? What does it do?

A

Produced by P/D cells in the fundus of the stomach
Triggers satiety and rises before meals
Antagonised by Leptin

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33
Q

What does the vagus nerve act on in the stomach?

A
  1. ECL cells directly via muscurinic receptors stimulating action
  2. Mucous cells resulting in production of mucous and bicarbonate
  3. Direct action on parietal cells via muscurinic action
  4. Chief cells
  5. G cells
  6. Inhibition of D cells
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34
Q

What factors inhibit acid secretion?

A

Somatostatin
PGE2 and PGI2 - COX 1 action
GLP, secretin, CCK, GIP, VIP

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35
Q

How much gastric secretion is produced per day?

A

1-2L
100ml/hr

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36
Q

What is the content of gastric secretions?

A

95% water
HCl making pH 1.5-3
Cl 170mmol/L
K 12-20mmol/L
Na 10-60mmol/L
Ca 1mmolL
Mucous rich in bicarbonate
Pepsin, gastric lipase and intrinisc factor

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37
Q

Describe the mechanism of PSNS on acid secretion

A

◦ PSNS - vagal innervation in cephalic phase of digestion via M3 receptors triggers increased secretion (Increased Ca intracellularly)
◦ Gastrin - cephalic and gastric phases of digestion due to central and mechanical signals. Gastrin receptors on parietal cells (HCl release) + CCK-B cells (histamine release)
‣ Both via cAMP secondary messenger
◦ Histamine - cephalic and gastric phases of digestion (central signals + gastrin cause release) binding to H2 receptors on parietal cells - via cAMP secondary messenger
◦ Mechanical stretch - local smooth muscle and Vagal-Vagal
◦ Peptides, caffeine, alcohol sensed by mucosal chemoreceptors –> gastrin

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38
Q

Describe the mechanism of gastrin on acid secretion

A

◦ PSNS - vagal innervation in cephalic phase of digestion via M3 receptors triggers increased secretion (Increased Ca intracellularly)
◦ Gastrin - cephalic and gastric phases of digestion due to central and mechanical signals. Gastrin receptors on parietal cells (HCl release) + CCK-B cells (histamine release)
‣ Both via cAMP secondary messenger
◦ Histamine - cephalic and gastric phases of digestion (central signals + gastrin cause release) binding to H2 receptors on parietal cells - via cAMP secondary messenger
◦ Mechanical stretch - local smooth muscle and Vagal-Vagal
◦ Peptides, caffeine, alcohol sensed by mucosal chemoreceptors –> gastrin

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39
Q

Describe the mechanism of histamine affecting acid secretion

A

◦ PSNS - vagal innervation in cephalic phase of digestion via M3 receptors triggers increased secretion (Increased Ca intracellularly)
◦ Gastrin - cephalic and gastric phases of digestion due to central and mechanical signals. Gastrin receptors on parietal cells (HCl release) + CCK-B cells (histamine release)
‣ Both via cAMP secondary messenger
◦ Histamine - cephalic and gastric phases of digestion (central signals + gastrin cause release) binding to H2 receptors on parietal cells - via cAMP secondary messenger
◦ Mechanical stretch - local smooth muscle and Vagal-Vagal
◦ Peptides, caffeine, alcohol sensed by mucosal chemoreceptors –> gastrin

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40
Q

What factors other than histamine, gastrin, and PSNS influecne acid secretion

A

◦ PSNS - vagal innervation in cephalic phase of digestion via M3 receptors triggers increased secretion (Increased Ca intracellularly)
◦ Gastrin - cephalic and gastric phases of digestion due to central and mechanical signals. Gastrin receptors on parietal cells (HCl release) + CCK-B cells (histamine release)
‣ Both via cAMP secondary messenger
◦ Histamine - cephalic and gastric phases of digestion (central signals + gastrin cause release) binding to H2 receptors on parietal cells - via cAMP secondary messenger
◦ Mechanical stretch - local smooth muscle and Vagal-Vagal
◦ Peptides, caffeine, alcohol sensed by mucosal chemoreceptors –> gastrin

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41
Q

What are the function sof gastric secretions

A

Hormonal
* Gastrin, produced by G-cells, which stimulates gastric acid secretion
* Histamine, produced by enterochromaffin cells, which also stimulates acid secretion
* Somatostatin, produced by δ-cells, which inhibits gastric acid production

Immune function:
* pH acts to decontaminate bacteria in food.
* Proteolytic enzymes also act on microbial cell wall components and endotoxin

Barrier functions
* Gastric mucus acts as a barrier and neutralising agent against the gastric acid.

Macronutrient digestive function:
* Gastric acid
* Proteolytic enzymes begin the digestion of the protein in the food bolus (pepsin is the main one, and it accounts for about 15% of the total protein breakdown
* Gastric lipase hydrolyzes the ester bonds of triglycerides, contributing something like 30% of the total lipid catabolism in the gut

Micronutrient digestive function:
* Pepsin also helps ferric iron (Fe3+) conversion to the more soluble ferrous (Fe2+) ion
* Intrinsic factor binds to B12, creating a complex which can be absorbed in the terminal ileum

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42
Q

Define vomiting

A

vomiting is the involuntary, forceful, rapid expulsion of gastric contents through the mouth

43
Q

Where is the vomiting centre centrally?

A

The vomiting centre a scattered cluster of neurones within the lateral reticular formation of the medulla oblongata mediates both afferent and efferent impulses involved in vomiting.

44
Q

Afferents to the vomiting centre include

A

CTZ
NTS
Cranial nerve 8
Higher centres

45
Q

Where is the CTZ?

A

bilaterally on floor of the 4th ventricle of the medulla in the area postrema near vagal nuclei
◦ Receives blood directly from systemic circulation outside the BBB (fast vomiting response) - allows antiemetic drugs to act without crossing the BBB
◦ Stimuli triggering positive feedback to vomiting centre
‣ Dopamine - D2 - site of action of dopamine antagonists (Butyphenone) e.g. metoclopramide
‣ Serotonin - 5 HT3 - ondansetron site of action
‣ ACh
‣ Opioids
‣ Substance P - NK1

46
Q

What is special about the CTZ

A

bilaterally on floor of the 4th ventricle of the medulla in the area postrema near vagal nuclei
◦ Receives blood directly from systemic circulation outside the BBB (fast vomiting response) - allows antiemetic drugs to act without crossing the BBB
◦ Stimuli triggering positive feedback to vomiting centre
‣ Dopamine - D2 - site of action of dopamine antagonists (Butyphenone) e.g. metoclopramide
‣ Serotonin - 5 HT3 - ondansetron site of action
‣ ACh
‣ Opioids
‣ Substance P - NK1

47
Q

What triggers CTZ

A

bilaterally on floor of the 4th ventricle of the medulla in the area postrema near vagal nuclei
◦ Receives blood directly from systemic circulation outside the BBB (fast vomiting response) - allows antiemetic drugs to act without crossing the BBB
◦ Stimuli triggering positive feedback to vomiting centre
‣ Dopamine - D2 - site of action of dopamine antagonists (Butyphenone) e.g. metoclopramide
‣ Serotonin - 5 HT3 - ondansetron site of action
‣ ACh
‣ Opioids
‣ Substance P - NK1

48
Q

NTS has what role in vomiting? What receptor types are there?

A
  • Nucleus tractus solitarius - ascending inputs
    ◦ Pharyngeal inputs from CN IX (glossopharyngeal) involved in the gag reflex
    ◦ CNX - carrying afferent inputs from the enteric nervous system primarily mediated through mechanoreceptors sensing stretch, and chemoreceptors responding to infection, toxins, chemotherapy
    ‣ Primarily mediated by 5 HT3 - as seratonin released from enterochromaffin cells in the small intestine trigger ascending afferent inputs for vomiting
    ‣ Lesser mediators include: Acetylcholine and histamine receptors also involved
49
Q

How is CNVII involved in vomiting? What receptors?

A
  • Cranial nerve VIII - afferent information from vestibular system involving receptors (motion sickness)
    ◦ Histamine 1 receptors - histamine receptor antagonists e.g. cyclizine blocking afferent inputs promiting vomiting
    ◦ Muscurinic receptors - hyoscine antagonises these receptors working in motion sickness induced vomiting
50
Q

Vomiting centre effectors? 5

A

◦ Parasympathetic nervous system - salivary gland secretion
◦ SNS - sweating and tachycardia
◦ Respiratory centre - deep inspiration, closure of glottis with coordinated timing
◦ Smooth muscle via vagus, glossopharyngeal, hypoglossal and trigeminal
‣ Enteric smooth muscle - retrograde perstalisis of small intestine, pyloric contraction, relaxation of lower oesophageal sphincter
‣ Upper airway/aerodigestic tract smooth muscle - soft palate elevation
◦ Spinal nerves - Diaphragm, intercostal and abdominal muscle contraction

51
Q

What are the 3 phases to vomiting?

A

Pre-ejection
Retching
Ejection

52
Q

What characterises the pre-ejection phase of vomiting

A

◦ Nausea
◦ Decreased gastric motility
◦ Reverse peristalsis of small intestine pushing proximal small bowel contents back into stomach - increases pH of stomach contents (alkaline small bowel contents mixing)
◦ Secretion of HCO3 rich saliva mediated by PSNS
◦ Sweating and tachycardia - SNS

53
Q

What characterises the retching phase of vomiting?

A

◦ Deep inspiration
◦ Closure of glottis protecting trachea from aspiration
◦ Rhythmic contraction of intercostals, diaphragm and abdominal muscles against a closed glottis –> increased intrathroacic pressure compressing oesophagus preventing reflux of stomach contents

54
Q

What characterises the ejection phase of vomiting?

A

◦ Continuitation of glottic closure
◦ Contraction of pylorus- pushes gastric contents into body and fundus of stomach
◦ Relaxation of LOS and oeosphagus
◦ Sudden dramatic increase in intrabaomdinal pressure (abdominal muscle contraction, descent of diaphragm) pushing gastric contents out of stomach and into oesophagus
◦ Soft palate occludes nasopharyngx
◦ Reverse persistalsis of oesophagus rapidly expels its contents up

55
Q

Define gastric emptying

A

a coordinated emptying of chyme in the stomach into the duodenum determined by stomach contents and motility

56
Q

What happens to gastric emptying in a fasting state?

A
  • In fasting state - migrating motor complexes sweep stomach at regular intervals, slow peristaltic waves originating at the fundus to keep the stomach empty of secretions and debris
57
Q

How does the stomach handle a swallowed portion of food?

A

◦ Receptive relaxation shortly before swallowing leads to proximal stomach relaxation via vagal stimulus, and the middle area of the stomach contracts (transverse mid gastric band) to separate stored food from antrum and pyloric processes

58
Q

Gastric emptying physically involves what movement and process?

A

◦ Gastric emptying involves tonic contractions of the proximal regions of the stomach and phasic distal (antrum) contractions propelling food towards the pylorus which is tightly closed causing mixing with secretions –> pyrloric or antral pump
‣ Pyloric intermittent opening for <1-2mm particle passage maximises absorption by allowing digestion (pepsin). Preventing dumping - duodenal distension and osmotic diarrhoea

59
Q

What size particles are allowed through the pylorus usually

A

1-2mm

60
Q

Rate of gastric emptying in solid food characterised by?

A

◦ This is called the lag phase with solid food - minimal passage into duodenum for 30-90 minutes before linear emptying occurs where stable linear passage of small food particles. Nutrient poor solids exit faster than fatty solids - half time 30 - 120 minutes (empty in 3-4 hours)

61
Q

What rate is gastric emptying with solids? Over what time period

A

◦ This is called the lag phase with solid food - minimal passage into duodenum for 30-90 minutes before linear emptying occurs where stable linear passage of small food particles. Nutrient poor solids exit faster than fatty solids - half time 30 - 120 minutes (empty in 3-4 hours)

62
Q

What type fo solids exit faster in gastric emptying?

A

◦ This is called the lag phase with solid food - minimal passage into duodenum for 30-90 minutes before linear emptying occurs where stable linear passage of small food particles. Nutrient poor solids exit faster than fatty solids - half time 30 - 120 minutes (empty in 3-4 hours)

63
Q

How is liquid gastric emptying different to solids? Determinants (2)

A

◦ Liquids have no lag phase, and exit exponentially immediately and is determined by antral-duodenal pressure gradient and emptying rate proportional to volume of ingested fluid
‣ Pressure difference usually 5mmHg (as high as 40mmHg with peristalsis).
‣ 15min half time for non nutriousfoods

64
Q

What si the half time of liquid ingestion gastric emptying

A

◦ Liquids have no lag phase, and exit exponentially immediately and is determined by antral-duodenal pressure gradient and emptying rate proportional to volume of ingested fluid
‣ Pressure difference usually 5mmHg (as high as 40mmHg with peristalsis).
‣ 15min half time for non nutriousfoods

65
Q

What determinants are there of gastric emptying to liquids?

A

◦ Liquids have no lag phase, and exit exponentially immediately and is determined by antral-duodenal pressure gradient and emptying rate proportional to volume of ingested fluid
‣ Pressure difference usually 5mmHg (as high as 40mmHg with peristalsis).
‣ 15min half time for non nutriousfoods

66
Q

What is a MMC in the context of gastric emptying? When do you find this?

A

◦ Fasted - migratory motor complexes sweep secretions and residual food debris (stomach stretching abolishes MMC)

67
Q

What position changes gastric emptying?

A

Prone and left lateral decrease
Right lateral increases, seated increases

68
Q

Gastric emptying determinants

A
  1. Fed or fasted
  2. Position and anatomical obstructions e.g. pregnance
  3. Volume and consistency of chyme
  4. Gastric contents entering the duodenum

Regulators
1. Neural
2. Hormonal
3. Extrinsic

69
Q

What non regulatory functions determine gastric emptying?

A
  1. Fed or fasted
  2. Position and anatomical obstructions e.g. pregnance
  3. Volume and consistency of chyme
  4. Gastric contents entering the duodenum
70
Q

How does chyme characteristics influence gastric emtpying?

A

◦ Consistency of chyme - liquids pass faster than solids, pyloric sphincter constricts when solids approach until they are liquified
◦ Volume of chyme -
‣ increased gastric volume promotes gastric emptying via distension induced vasovagal excitatory reflexes increasing antral pump activity
‣ as well as antral distension induced gastrin secretion promoting antral pump
‣ Also increased pressure gradient

71
Q

Does a full or emptier stomach empty faster? Why?

A

◦ Consistency of chyme - liquids pass faster than solids, pyloric sphincter constricts when solids approach until they are liquified
◦ Volume of chyme -
‣ increased gastric volume promotes gastric emptying via distension induced vasovagal excitatory reflexes increasing antral pump activity
‣ as well as antral distension induced gastrin secretion promoting antral pump
‣ Also increased pressure gradient

72
Q

How does nutritional content influence gastric emptying?

A

Max emptying 200kcal/hr
More nutrients = slower emptying

73
Q

What major nutrient type empties the fastest fromt he stomach?

A

Carbohydrates
GIP inhibits gastric emptying in response to carbohydrates but is the least potent effector

74
Q

What major nutrient type empties the slowest from the stomach?

A

Fat - mediated by CCK release from duodenal mucosa in response to FFA in duodenum increasing pyloric tone and reducing gastric emptying

75
Q

What major nutrient empties neither slowest or fastest from the stomach?

A

Protein - stimulate sgastrin secretion with increases antral pump

76
Q

What effect does acidity have on gastric emptying? How?

A

Slows

mediated by enteric nervous system where H+ ions detected by dudodenal mucosa and relax information to interneurons in myenteric plexus and secretin is released from dudoenal mucosa inihibiting gastrin secretion –> inhibiting gastric smooth muscle

77
Q

What reflexes effect gastric emptying?

A

Duodenam enteric reflex - slows emptying

Gastric reflex promoting the antral pump and increasing emptying

78
Q

Does osmolality effect gastric emptying?

A

◦ Isoosmotic gastric contents empty fastest - osmoreceptors from duodenal receptors slow if hypo or hyperosmolar via enteric nervous system reflex

79
Q

Outline the innervation of the pylorus and how this influences gastric emptying?

A
  • Neural pyloric innervation - intrinsic myenteric and submucosal plexus integrating with extrinsic modulation from SNS (coeliac ganglion), and PSNS (vagal)
    ◦ PSNS - both excitatory and inhibitory functions
    ◦ SNS - minor inhibitory role
80
Q

What mediators increase gastric emptying?

A

‣ Nitric oxide - promotes pyloric relaxation released in response to vagal pathways
‣ 5-hydroxytryptamine (5HT) - 5HT3 receptors increase gastric emptying
‣ motilin increase frequency of action potentials and force of contraction
‣ Ghrelin - increased gastric acid secretion and emptying as highest pre meal

81
Q

What mediators slow gastric emptying?

A

‣ 5HT1
‣ CCK
‣ Secretin
‣ Gastric inhibitory peptide (GIP)
‣ GLP
‣ Leptin - from adipose tisssueand chief/parietal cells

82
Q

What extrinsic factors affect gastric emptying?

A

◦ Autonomic neuropathy, acute abdomen, ileus
◦ Pain slows emptying
◦ Opioids, alcohol, anticholinergic agents inhibit gastric motility
◦ Erythromycin, metoclopramide and cisaprie are prokinetic

83
Q

Define feed intolerance

A

An inability to reach or maintain the targeted rate of feed delivery during enteral nutrition, commonly due to large gastric residual volumes and delayed gastric emptying

84
Q

Describe characteristics of an ideal prokinetic

A

increase fundal tone and pressure wave frequency
stimulate antral wave amplitude and frequency
reduce pyloric wave frequency and abolish pyloric tone
the resulting gastroduodenal motor pattern would ensure antegrade movement of chyme and increase gastric emptying rate
does not affect intestinal transit nor impair nutrient absorption
optimises colonic function, facilitating normal bowel actions without causing diarrhoea
lacks adverse effects
remains effective despite continued use, as current therapies are limited by tachyphylaxis
has a wide therapeutic index and limited interaction with other drugs
metabolism unaffected by liver or kidney impairment

85
Q

How does metoclopramide act as a prokinetic

A

prokinetic action:
antagonism of D2 receptors in gut, and weak agonist at 5HT4 receptors
augmentation of peripheral cholinergic responses
increase smooth muscle tone
actions: increased tone of the lower oesophageal sphincter, accelerated gastric contractions, increased small bowel transit time (increased peristalsis in duodenum and jejunum)

86
Q

Problems with metoclopramide?

A

metabolised hepatically
adverse effects: sedation, dystonic reactions, dysrhythmias (methemoglobinemia in overdose)
not effective in patients with brain injury and may contribute to raised ICP
tachyphylaxis occurs

87
Q

Erythromycin mechanism as a prokinetic

A

prokinetic action due to agonism at motilin receptors
chronotropic effect on neuronal receptors
enhances motilin release from enterochromaffin cells in duodenum
enhanced contractile effects on gastric antrum and duodenum

88
Q

Describe problems with using erythromycin as a prokinetic

A

metabolised hepatically
drug interactions due to CYP450 3A4 inhibition
adverse effects: prolonged QT, hepatic dysfunction, overgrowth of non-susceptible organisms and clostridium difficile, possibly antibiotic resistance
most effective single agent, but is limited by tachyphylaxis (over 2-7 days)
dose dependent effects
combination with metoclopramide is more effective than either alone

89
Q

Define peristalsis

A
  • Successive waves of involuntary contraction passing along the walls of a hollow muscular structure (such as the esophagus or intestine) and forcing the contents onward”
90
Q

Describe the mechanism of peristalsis

A

◦ Coordinated movements of tunica musculari- fibres running in circular and longitudinal directions
◦ Behind the bolus circular muscles contract and longitudinal muscles relax, whereas opposite ahead

91
Q

Describe using a sensor effector model how peristalsis works

A

◦ The sensing of this is the myenteric reflex
‣ Stimulus - chemicals in lumen, mechanical deformation and radial stretch on muscles
‣ Sensor - blind chemoreceptor and stretch receptor nerve endings
‣ Afferent - enteric primary afferent neurons (cholinergic)
‣ Processing - Auerbach;s plexus via nicotinic and muscarinic receptors
‣ Efferent - inhibitor motor neurotransmission (nitric oxide, ATP, vasoactive inhibitory peptide), and excitatory (cholinergic via nicotinic receptors)

92
Q

What is the basal electrical rhythm of the gut

A

◦ The pacemaker current of the gut results in continuous peristaltic activity at lower amplitude (5-15mV) - 2-3 oscillations per 10 seconds on average, 20 beats at duodenum and slower distally.
‣ The duodenum is electrically quiescent and peristaltic waves do not continue the length of the gut - they only propogate a few centimetres before ceasing
‣ Pacemaker origin from interstitial cells of Cajal penetrating smooth msucel cels
‣ Long, slow action potentials - due to dihydropyridine resistance calcium channels

93
Q

At what speed does basal electrical activity of the gut occur

A

◦ The pacemaker current of the gut results in continuous peristaltic activity at lower amplitude (5-15mV) - 2-3 oscillations per 10 seconds on average, 20 beats at duodenum and slower distally.
‣ The duodenum is electrically quiescent and peristaltic waves do not continue the length of the gut - they only propogate a few centimetres before ceasing
‣ Pacemaker origin from interstitial cells of Cajal penetrating smooth msucel cels
‣ Long, slow action potentials - due to dihydropyridine resistance calcium channels

94
Q

How far do peristaltic waves propogate?

A

◦ The pacemaker current of the gut results in continuous peristaltic activity at lower amplitude (5-15mV) - 2-3 oscillations per 10 seconds on average, 20 beats at duodenum and slower distally.
‣ The duodenum is electrically quiescent and peristaltic waves do not continue the length of the gut - they only propogate a few centimetres before ceasing
‣ Pacemaker origin from interstitial cells of Cajal penetrating smooth msucel cels
‣ Long, slow action potentials - due to dihydropyridine resistance calcium channels

95
Q

What is the pacemaker origin of the peristaltic waves fo the gut?

A

◦ The pacemaker current of the gut results in continuous peristaltic activity at lower amplitude (5-15mV) - 2-3 oscillations per 10 seconds on average, 20 beats at duodenum and slower distally.
‣ The duodenum is electrically quiescent and peristaltic waves do not continue the length of the gut - they only propogate a few centimetres before ceasing
‣ Pacemaker origin from interstitial cells of Cajal penetrating smooth msucel cels
‣ Long, slow action potentials - due to dihydropyridine resistance calcium channels

96
Q

What is MMC?

A

◦ Migrating motor complex - during fasting, waves of electrical energy spreading throughout the intestine from stomach to terminal ileum in a regular cycle accompanied by peristalsis over 90-120 minutes (not a wave itself but moving region of high activity)
‣ Ghrelin, motilin, seratonin increase activity; somatostatin inhibits. Vagus increases stomach activity only ,

97
Q

When do MMC waves occur?

A

◦ Migrating motor complex - during fasting, waves of electrical energy spreading throughout the intestine from stomach to terminal ileum in a regular cycle accompanied by peristalsis over 90-120 minutes (not a wave itself but moving region of high activity)
‣ Ghrelin, motilin, seratonin increase activity; somatostatin inhibits. Vagus increases stomach activity only ,

98
Q

What increases MMC

A

◦ Migrating motor complex - during fasting, waves of electrical energy spreading throughout the intestine from stomach to terminal ileum in a regular cycle accompanied by peristalsis over 90-120 minutes (not a wave itself but moving region of high activity)
‣ Ghrelin, motilin, seratonin increase activity; somatostatin inhibits. Vagus increases stomach activity only ,

99
Q

How is the basal electrical rhythm of the gut modified?

A

Stretch/enteric contents
Chemical content
Electrlytes
Enteric hormones
Autonomic nervous system

100
Q

What electrolyte changes change gut motility?

A

Hypokalaemia, hypercalcaemia and hypermagnesaemia slow gut function

101
Q

What chemical characteristics of gut contents increase motility?

A

hyperosmolar
Acidic

Lipid inhibits

102
Q

What hormones increase perstalsis

A
  • Acetylcholine
    * Substance P
    * Motilin
    * Serotonin
103
Q
A

Gastro nutrition (7 decks)

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