Practical Gastric Physiology Flashcards

1
Q

What are the functions of the stomach?

A

Temporary storage of food input
Mechanical breakdown of food into smaller particles
Chemical digestion, breakdown of proteins
Regulating chyme output into duodenum
Secretion of intrinsic factor, vital for Vit B12 absorption

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What must fail for aspiration to happen?

A

There must be gastroesophageal reflux, when gastric contents breach the LOS

The acid must then flow along 30cm of oesophagus and pass the upper oesophageal sphincter to contaminate the pharynx

If the patient’s gag/cough reflexes are obtunded then the gastric contents may then reach the tracheobronchial tree

Solid matter can obstruct the airways and acidic liquid can cause bronchospasm = severe hypoxia and resp failure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How can you minimize the risk of aspiration?

A

Minimize GOR by

  • maintaining tone of LOS
  • reducing gastro-oesophageal pressure gradient
  • using gravity

Reduce gastric volume
Increase gastric emptying
Reduce gastric acidity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the LOS formed by?

A

The intrinsic circular smooth muscle of the lowest 2-4cm of the oesophagus, tonic contraction of which separates the gastric and oesophageal lumens

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the normal pressure of the LOS?

A

Resting pressure 15-25 mmHg above the gastric pressure (this is called barrier pressure)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is swallowing reflex mediated by?

A

Inhibitory neurotransmitters nitric oxide and vasoactive intestinal polypeptide - relaxes the LOS for 6-8 secs to allow passage of food

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What would you expect the LOS pressure to be in oesophagitis?

A

<10 mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What factors can increase LOS tone?

A

Physiological
- cholinergic stumulation

Pharmacological

  • anticholinesterases (eg neostigmine)
  • D2 antagonists (eg metoclopramide, domperidone)
  • cyclizine
  • succinylcholine

Pathological
- none

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What factors can decrease LOS tone?

A

Physiological

  • swallowing
  • oestrogen, progesterone

Pharmacological

  • antimuscarinics (eg glycopyrolate)
  • dopamine
  • opioids
  • thiopental

Pathological
- alcohol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does a hiatus hernia affect the angle of the gastro-oesophageal junction?

A

It straightens it out so there’s no diaphragmatic contribution to sphincter function and increased intra-abdominal pressure is transmitted to the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How is chyme continuously output into the duodenum?

A

The fundus and body of the stomach act as a reservoir and they relax as the stomach expands

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What happens to intragastric pressure as the stomach fills?

A

It remains consistent until the stomach contents exceed a litre due to vagal reflexes initiated by the stretch receptors in the oesphagus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What conditions increase intra-abdominal pressure?

A

Obesity
Pregnancy
Intestinal obstruction
Laparoscopic surgery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What can you do if your patient has a GI obstruction?

A

Insert a large-bore NG tube and aspirate it to decompress the gut and relieve increased intra-abdominal pressure

Sit them up with hips and knees flexed to reduce tension in abdominal wall muscles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is cricoid pressure?

A

It’s external pressure on the cricothyroid (the only complete cartilage ring in the respiratory tract), compressing the oesophagus at C6 to discourage regurgitation.

10N whilst awake patient then 30N when they’re asleep

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the contraindications to cricoid pressure?

A

Suspected cricotracheal injury
Active vomiting - risk of oesophageal rupture
Unstable cervical spine injuries
Inadequate view of the cords on laryngoscopy
need for BVM ventilations (rescue ventilations in failed airway)
Decision made to site an LMA instead of performing intubation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

How much acid per day does the stomach normally produce?

A

2L

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does stomach acid consist of ?

A
Hydrochloric acid
Intrinsic factor
Pepsinogens
Mucous
Water
Electrolytes - K and Cl
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the pH of the stomach?

A

1 - 1.5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the relationship between stomach volume and rate of emptying?

A

The rate of stomach emptying increases at an exponential rate proportional to the volume of the stomach

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is stomach emptying mediated by?

A

Vagal excitatory reflexes which are provoked by stomach distension and gastrin is also released in response to antral distension
= increased antral pump activity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where is HCl released from in the stomach?

A

Parietal cells in the fundus and body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Where is pepsin released from in the stomach?

A

Cheif cells in the body

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Where is intrinsic factor released from in the stomach?

A

Parietal cells, in the fundus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Where is mucus released from in the stomach?

A

Mucus cells

26
Q

What causes HCl release in the stomach?

A
Gastrin
ACh
Vagal stimulation
Distension of body of stomach (vagal reflex)
Histamine (H2 receptors)
27
Q

What causes pepsin release in the stomach?

A

Vagal stimulation
ACh
Acid pH
Secretin (from duodenum)

28
Q

What causes intrinsic factor release in the stomach?

A
Gastrin
ACh
Vagal stimulation
Distension of body of stomach (vagal reflex)
Histamine (H2 receptors)

(same as things that stimulate gastric acid release)

29
Q

What causes mucus release in the stomach?

A

Vagal stimulation

Prostaglandins E2 and I2

30
Q

What inhibits HCl release in the stomach?

A
Acidity
Anti-muscarinics
Vagotomy
Somatostatin
Prostaglandin E2
H2 receptor antagonists
PPIs
31
Q

What is the function of HCl in the stomach?

A

Protein breakdown
Activates pepsinogens and provides optimal conditions for pepsin activity
Improves solubility and hence absorption of Ca and iron
Kills pathogenic microorganisms

32
Q

What is the function of pepsin?

A

Proteolytic enzyme stores as inactive pepsinogens to facilitate protein digestion

33
Q

What does intrinsic factor do in the stomach?

A

Glycoprotein than binds B12 (cobalamin) to protect it from enzyme destruction -complex then absorbed in terminal ileum

34
Q

What is the purpose of mucus in the stomach?

A

It protects the mucosa from mechanical trauma and digestion by gastric acid and proteolyric enzymes

35
Q

What factors increase gastric emptying?

A

Physiological

  • stomach distension
  • liquid content
  • smaller particles
  • parasympathetic stimulation

Pharmacological

  • anti-cholinesterases (eg neostigmine)
  • metoclopramide
  • domperidone
  • erythromycin
36
Q

What factors decrease gastric emptying?

A

Physiological

  • duodenal distension
  • chyme high in H+, fat or protein
  • secretin
  • pain/anxiety/stress
  • sympathetic stimulation

Pharmacological

  • antimuscarinics (eg glyopyrolate, atropine)
  • opioids

Pathological

  • alcohol
  • pyloric stenosis
  • intestinal obstruction
  • previous vagotomy
37
Q

Where is gastrin released from?

A

G cells in stomach antrum and duodenum

38
Q

What stimulates gastrin release?

A
Vagal stimulation
Distension of gastric antrum
Distension of duodenum
Amino acids and pepties
Alcohol
Caffeine
39
Q

What inhibits gastrin release?

A

Gastric acidity
Somatostatin
Secretin
Glucagon

40
Q

What does gastrin do?

A
Stimulates gastric acid production
Increases secretion of pepsinogens
Increases mucus secretion
Increases gastric motility
Constricts pyloric sphincter
Reduces gastric emptying
41
Q

Where is secretin released from?

A

S cells in duodenum and jejunum

42
Q

Where stimulates secretin release?

A

Increased acidity in duodenal chyme

43
Q

What does secretin do?

A

Reduces gastric acid secretion
Reduces gastric emptying
Increases pancreatic secretions

44
Q

What does CCK do?

A

Reduces gastric acid secretion
Reduces gastric emptying
Contracts gall bladder

45
Q

Where is CCK released from?

A

I cells in the duodenum and jejunum

46
Q

What stimulates release of CCK?

A

Increased fat in duodenal chyme

47
Q

Where is somatostatin released from?

A

D cells in stomach

48
Q

What does somatostatin do?

A

Inhibits gastrin secretion (and therefore gastric acid production)
Reduces gastric motility
Reduces gastric emptying

49
Q

What stimulates somatostatin release?

A

Gastric acidity

50
Q

What inhibits somatostatin release?

A

Vagal stimulation

51
Q

What is motilin?

A

Released from entero-chromaffin-like cells in proximal small intestine

Increases gastric motility and emptying

52
Q

What is metoclopramide?

A

Centrally and peripherally acting dopaminergic D2 antagonist

53
Q

What are the SEs of metoclopramide?

A

Extra-pyramidal (acute dyskinesias and dystonic reactions, tardive dyskinesia, Parkinsonism, akinesia, akathisia, and neuroleptic malignant syndrome)

Tardive dyskinesia
Hyperprolactinaemia

54
Q

What is erythromycin?

A

Macrolide antibiotic with prokinetic properties. It is an agonist at motilin receptors, stimulating strong antral contractions

55
Q

What are the SEs of erythromycin?

A

Abdominal cramps
Nausea
Vomiting

56
Q

Why is ranitidine preferred to cimetidine to reduce gastric acidity pre-op?

A

It has a longer duration of action and fewer drug interactions.

PPIs have no advantage over H2 receptor antagonists as a single preop dose

57
Q

How do PPIs work?

A

They irreversibly block the H+/K+ ATPase enzyme which catalyses the exchange of intracellular H+ for extracellular K+, the final step of acid production by the parietal cells

58
Q

What is sodium citrate?

A

It’s a non-particulate oral antacid which raises the pH of the stomach contents by neutralising gastric acid, but it increases gastric volume.

30mls is used, will work in 10 mins.

59
Q

What would you do pre-op for someone with a potentially full stomach?

A

Head up tilt
Insert large bore NG + aspirate + leave on free drainage
Keep NBM
Ranitidine 50mg IV
Metoclopramide 10mg IV (if no GI obstruction, perf or haemorrhage)

60
Q

What would you do at induction of anaesthesia for a patient with a full stomach?

A
Aspirate NG tube
Give 30mls Sodium Citrate orally
Position head up tilt
Pre-oxygenate
Apply cricoid pressure
RSI
Cuffed ETT
61
Q

What would you do during theatre in a patient with a potentially full stomach?

A

Maintain head up
Avoid increased intraabdominal pressure
Ensure adequate depth of anaesthesia

62
Q

How would you extubate a patient with a full stomach?

A

Left lateral position

When awake and gag and cough reflexes present