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Primary FRCA > Physiology 17 > Flashcards

Physiology 17 Flashcards

1
Q

What is intrinsic factor?

A
  • Glycoprotein
  • Secreted by parietal cells into gastric lumen
  • Essential for absorption of vit B12, binding it in the stomach and protecting it from destruction in the GI tract
  • IF-B12 complex absorbed in the terminal ileum
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2
Q

What is the most likely cause of anaemia post-gastrectomy?

A

IDA due to impaired absorption from loss of acidic environment

B12 deficiency due to lack of IF also relevant, but above is main driver

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3
Q

What is pepsin?

A
  • Collection of proteolytic enzymes facilitating protein digestion
  • Stored as inactive precursor, pepsinogen in membrane-bound zymogen granules in chief cells
  • Activated in acidic environ of stomach (maximal activity at pH <3
  • Act by hydrolysing peptide bonds producing polypeptides and amino acids
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4
Q

What factors stimulate release of pepsin?

A
  • Vagal stimulation
  • low gastric pH
  • Gastrin
  • β stimulation
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5
Q

Where is gastric mucus produced?

A
  • Gastric mucus neck cells

- Surface epithelial cells

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6
Q

How thick is the gastric mucus layer?

A

200 um

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7
Q

What factors stimulate gastric mucus production?

A
  • Vagal stimulation
  • Gastrin
  • PGE2/PGI2 (synthesised within mucosa)
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8
Q

What are the components of the gastric ‘mucosal barrier?’

A
  • Alkaline mucus

- Tight junctions between epithelial cells

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9
Q

Through what mechanism does H. pylori cause gastric ulcers?

A

H. pylori infection is associated with sustained gastrin release, which increases acid production and reduces the pH gradient between the gastric lumen and mucosa, causing ulceration.

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10
Q

What are the physiological effects of gastrin?

A
  • Increased gastric acid secretion
  • Release of gastric enzymes and mucus
  • Increases gut motility
  • Regulates mucosal growth
  • Unclear effect on gastric emptying and pyloric sphincter
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11
Q

How does the secretion and composition of gastric juice vary in the fed state?

A

3 phases:

  1. Cephalic (30%)
    - Anticipation of food
    - Mediated by efferent vagal stimulation
    - Causes increased gastric motility, juice secretion and release of gastrin and histamine
  2. Gastric (60%)
    - Arrival of food into stomach
    - Initiated by gastric distension -> vagal reflex and stimulation of gastrin release due to antral peptide and amino acid detection
    - Self-limiting (~30 mins) due to inhibition of gastrin production when pH <2 and by release of somatostatin by D cells.
  3. Intestinal (10%)
    - Arrival of chyme into duodemun
    - Initial increase in gastrin production due to duodenal stretch
    - Subsequent reduction in gastric secretion due to duodenal production of secretin (by S cells)
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12
Q

What are the main functions of secretin with regard to digestion?

A
  1. Reduction of duodenal pH through:
    - Stimulation of pancreatic secretion
    - Increasing somatostatin release
    - Inhibiting gastrin release
    - Directly downregulating parietal cell acid secretion
  2. Triggering increased insulin release in response to increasing glycaemia
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13
Q

Summarise the absorptive capacity of the stomach

A

Little absorption

Notable exceptions:

  • Alcohol (due to lipid solubility)
  • Aspirin (due to pKa 3.5 -> mostly unionised in stomach lumen)
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14
Q

What are the main drivers of physiological gastric emptying?

A
  • In general, rate of emptying is proportional to stomach volume
  • This is due to vagal reflexes increasing antral pump activity in response to gastric distension
  • Rate also affected by food particle size
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15
Q

What is the difference in gastric transit time between clear fluid and solid food?

A

Clear fluid: 95% in 1 hour

Solid meal: 50% in 2 hours

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16
Q

What methods can be used to measure gastric emptying?

A
  • Paracetamol absorption (none absorbed in stomach)
  • Ultrasound studies
  • Applied potential tomography
  • Scintigraphy
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17
Q

What factors increase gastric emptying?

A
  • Stomach distension
  • Cholinergics / anticholinesterases
  • Small particle size of gastric contents
  • Prokinetic drugs
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18
Q

What factors delay gastric emptying?

A
  • Duodenal distension
  • Antimuscarinics
  • Duodenal chyme high in [H+], fat, protein or osmolality
  • Sympathetic stimulation
  • Opioids
  • Alcohol
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19
Q

Explain how the contents of duodenal chyme influence gastric emptying

A

Low pH - secretin release
High fat - CCK release
High protein - Gastrin release (though effect on emptying contested)
Hypertonia - osmoreceptor reflex

20
Q

Outline the phases of swallowing

A
  1. Voluntary movement of food bolus to back of mouth by tongue
  2. Sensory receptor reflex from tonsillar pillars initiate involuntary phase. This begins with lifting of the soft palate to occlude access to the nasal cavity and formation of a ‘sagittal slit’ through which food passes to the posterior pharynx
  3. Vocal cords are adducted and larynx is drawn anteriorly and cephalad, widening the upper oesophagus. Epiglottis swings over closed glottis. Upper oesophageal sphincter relaxes.
  4. Enlargement of upper oesophagus initiates peristaltic wave which is propagated down the oesophagus
21
Q

How is swallowing coordinated?

A

By swallowing centre in reticular substance of the medulla and lower pons. The swallowing centre inhibits the respiratory centre, preventing respiration during swallowing.

22
Q

How long does a co-ordinated swallowing sequence last?

A

1-2 seconds

23
Q

How is oesophageal barrier pressure defined?

A

OBP = LOSP - GP

LOSP - Lower oesophageal sphincter pressure
GP - Gastric pressure

24
Q

Describe the reflex arc involved in regulating LOS tone

A

-Spinal and vagal sensory afferents -> NTS -> vagal motor nucleus

25
Q

What are the substances involved in LOS relaxation?

A

NO
ATP?
VIP?
CO?

26
Q

What anaesthetic factors affect oesophageal barrier pressure?

A

Reduce OBP:

  • LMA
  • Cricoid pressure in awake patient
  • Volatile anaesthesia
  • N2O
  • Thiopental

No effect:

  • Propofol
  • Remi
  • NMBs (except vecuronium and pancuronium)

Increase OBP:
-Vec- / Pancuronium

27
Q

What is the overall incidence of PONV following elective surgery without prophylaxis?

A

33%

28
Q

Contrast vomiting and regurgitation

A

Vomiting: Active, forceful, coordinated expulsion of GI contents from the mouth

Regurgitation: Passive, effortless flow of undigested stomach contents back into oesophagus

29
Q

Summarise the vomiting reflex

A

Two phases:

Pre-ejection phase:

  • Gastric relaxation
  • Retrograde peristalsis
  • Airway protective reflexes immediately preceding ejection (deep inspiratory breath, elevation of larynx + hyoid, opening of upper oesophageal sphincter, closure of glottis, elevation of soft palate)

Ejection phase:

  • Contraction of abdominal and diaphragmatic muscles
  • Retrograde oesophageal contraction
  • Crural relaxation
  • Dilatation of upper oesophageal sphincter
30
Q

What evidence is there to suggest that nausea and vomiting have at least partially separate mechanisms?

A
  • Nausea is harder to treat than vomiting
  • Some situations (eg. raised ICP, radiotherapy, pregnancy) can cause vomiting without nausea
  • Vomiting is attenuated post-vagotomy but nausea can still occur
  • Sensation of nausea requires involvement of higher (conscious) centres in CNS
31
Q

List the main pathways for stimulation of nausea and vomiting

A
  1. Toxins in GI lumen
  2. Toxins in bloodstream
  3. GI/visceral pathology
  4. CNS stimuli
  5. Vestibulocochlear disturbance
32
Q

What is the mechanism of N&V stimulation by toxins in the gut lumen?

A

Enterochromaffin (EC) cells in the gut mucosa release paracrine intermediates

  • 5-HT
  • Substance P
  • CCK

5-HT3 receptors in the gut are coupled to Na+ channels, causing vagal afferent activity

5-HT3 receptors also found in NTS and CTZ

33
Q

What is the mechanism of N&V stimulation by toxinaemia?

A

Mediated by CTZ (area postrema)

CTZ expresses many receptors including 5-HT3, dopamine receptors and neurokinin-1 (substance P receptor)

34
Q

Where is the CTZ found?

A
  • Circumventricular organ

- Midline brainstem structure found in the dorsal medulla, at the caudal border of the 4th ventricle

35
Q

What is the mechanism of N&V stimulation by GI or visceral pathology?

A

Not well understood, varied

May include obstruction, cardiac vagal afferents stimulation and renal failure (azotaemia?)

36
Q

What is the mechanism of N&V stimulation by CNS stimuli?

A
  • Not usually associated with nausea
  • Poorly understood
  • Include emotional stimuli eg. fear, anticipation and physical stimuli eg. brain trauma and raised ICP
37
Q

What is the mechanism of N&V stimulation by vestibulocochlear disturbance?

A
  • Thought to modulate sensitivity of brainstem to emetogenic stimuli
  • Afferents to vomiting centre involve ACh and H1 receptors
38
Q

Classify the dopamine receptor subtypes and their actions

A

D1-5

D1-like (D1, D5) - Adenylate cyclase stimulation
D2-like (D2, D3, D4) - Adenylate cyclase inhibition

39
Q

How are dopamine receptors implicated in N&V?

A

D2 receptors clearly linked with N&V

D3 receptors may evoke vomiting or facilitate vomiting induced by D2Rs

40
Q

Where is the vomiting centre found?

A
  • No clearly defined area

- Consists of neural network in NTS

41
Q

List the risk factors for PONV

A

Patient-specific / anaesthetic / surgical

Patient-specific:

  • Female sex
  • Non-smokers
  • History of PONV/motion sickness

Anaesthetic:

  • Use of volatiles
  • N20
  • Perioperative opioid use

Surgical:

  • Prolonged surgery
  • Specific procedures (laparoscopy/laparotomy, ENT, neurosurgery, breast, strabismus, plastics)
42
Q

How are children affected by PONV?

A

<2 years - rare
>3 years - incidence 40%
No difference between sexes prior to puberty

43
Q

What are some important complications of PONV?

A

Surgical site:

  • Wound dehiscence
  • Anastomotic breakdown

Poor analgesia, patient distress

Aspiration

Electrolyte disturbances

44
Q

Which induction agents are implicated in PONV?

A

All but propofol

45
Q

What receptor subtypes are involved in N&V

A 
D2/3
H1
M3/5
5-HT3
NK1

Primary FRCA (34 decks)

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