Practical Gastric Physiology Flashcards
What are the functions of the stomach?
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
What must fail for aspiration to happen?
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 can you minimize the risk of aspiration?
Minimize GOR by
- maintaining tone of LOS
- reducing gastro-oesophageal pressure gradient
- using gravity
Reduce gastric volume
Increase gastric emptying
Reduce gastric acidity
What is the LOS formed by?
The intrinsic circular smooth muscle of the lowest 2-4cm of the oesophagus, tonic contraction of which separates the gastric and oesophageal lumens
What is the normal pressure of the LOS?
Resting pressure 15-25 mmHg above the gastric pressure (this is called barrier pressure)
What is swallowing reflex mediated by?
Inhibitory neurotransmitters nitric oxide and vasoactive intestinal polypeptide - relaxes the LOS for 6-8 secs to allow passage of food
What would you expect the LOS pressure to be in oesophagitis?
<10 mmHg
What factors can increase LOS tone?
Physiological
- cholinergic stumulation
Pharmacological
- anticholinesterases (eg neostigmine)
- D2 antagonists (eg metoclopramide, domperidone)
- cyclizine
- succinylcholine
Pathological
- none
What factors can decrease LOS tone?
Physiological
- swallowing
- oestrogen, progesterone
Pharmacological
- antimuscarinics (eg glycopyrolate)
- dopamine
- opioids
- thiopental
Pathological
- alcohol
How does a hiatus hernia affect the angle of the gastro-oesophageal junction?
It straightens it out so there’s no diaphragmatic contribution to sphincter function and increased intra-abdominal pressure is transmitted to the stomach
How is chyme continuously output into the duodenum?
The fundus and body of the stomach act as a reservoir and they relax as the stomach expands
What happens to intragastric pressure as the stomach fills?
It remains consistent until the stomach contents exceed a litre due to vagal reflexes initiated by the stretch receptors in the oesphagus
What conditions increase intra-abdominal pressure?
Obesity
Pregnancy
Intestinal obstruction
Laparoscopic surgery
What can you do if your patient has a GI obstruction?
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
What is cricoid pressure?
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
What are the contraindications to cricoid pressure?
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 much acid per day does the stomach normally produce?
2L
What does stomach acid consist of ?
Hydrochloric acid Intrinsic factor Pepsinogens Mucous Water Electrolytes - K and Cl
What is the pH of the stomach?
1 - 1.5
What is the relationship between stomach volume and rate of emptying?
The rate of stomach emptying increases at an exponential rate proportional to the volume of the stomach
What is stomach emptying mediated by?
Vagal excitatory reflexes which are provoked by stomach distension and gastrin is also released in response to antral distension
= increased antral pump activity
Where is HCl released from in the stomach?
Parietal cells in the fundus and body
Where is pepsin released from in the stomach?
Cheif cells in the body
Where is intrinsic factor released from in the stomach?
Parietal cells, in the fundus
Where is mucus released from in the stomach?
Mucus cells
What causes HCl release in the stomach?
Gastrin ACh Vagal stimulation Distension of body of stomach (vagal reflex) Histamine (H2 receptors)
What causes pepsin release in the stomach?
Vagal stimulation
ACh
Acid pH
Secretin (from duodenum)
What causes intrinsic factor release in the stomach?
Gastrin ACh Vagal stimulation Distension of body of stomach (vagal reflex) Histamine (H2 receptors)
(same as things that stimulate gastric acid release)
What causes mucus release in the stomach?
Vagal stimulation
Prostaglandins E2 and I2
What inhibits HCl release in the stomach?
Acidity Anti-muscarinics Vagotomy Somatostatin Prostaglandin E2 H2 receptor antagonists PPIs
What is the function of HCl in the stomach?
Protein breakdown
Activates pepsinogens and provides optimal conditions for pepsin activity
Improves solubility and hence absorption of Ca and iron
Kills pathogenic microorganisms
What is the function of pepsin?
Proteolytic enzyme stores as inactive pepsinogens to facilitate protein digestion
What does intrinsic factor do in the stomach?
Glycoprotein than binds B12 (cobalamin) to protect it from enzyme destruction -complex then absorbed in terminal ileum
What is the purpose of mucus in the stomach?
It protects the mucosa from mechanical trauma and digestion by gastric acid and proteolyric enzymes
What factors increase gastric emptying?
Physiological
- stomach distension
- liquid content
- smaller particles
- parasympathetic stimulation
Pharmacological
- anti-cholinesterases (eg neostigmine)
- metoclopramide
- domperidone
- erythromycin
What factors decrease gastric emptying?
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
Where is gastrin released from?
G cells in stomach antrum and duodenum
What stimulates gastrin release?
Vagal stimulation Distension of gastric antrum Distension of duodenum Amino acids and pepties Alcohol Caffeine
What inhibits gastrin release?
Gastric acidity
Somatostatin
Secretin
Glucagon
What does gastrin do?
Stimulates gastric acid production Increases secretion of pepsinogens Increases mucus secretion Increases gastric motility Constricts pyloric sphincter Reduces gastric emptying
Where is secretin released from?
S cells in duodenum and jejunum
Where stimulates secretin release?
Increased acidity in duodenal chyme
What does secretin do?
Reduces gastric acid secretion
Reduces gastric emptying
Increases pancreatic secretions
What does CCK do?
Reduces gastric acid secretion
Reduces gastric emptying
Contracts gall bladder
Where is CCK released from?
I cells in the duodenum and jejunum
What stimulates release of CCK?
Increased fat in duodenal chyme
Where is somatostatin released from?
D cells in stomach
What does somatostatin do?
Inhibits gastrin secretion (and therefore gastric acid production)
Reduces gastric motility
Reduces gastric emptying
What stimulates somatostatin release?
Gastric acidity
What inhibits somatostatin release?
Vagal stimulation
What is motilin?
Released from entero-chromaffin-like cells in proximal small intestine
Increases gastric motility and emptying
What is metoclopramide?
Centrally and peripherally acting dopaminergic D2 antagonist
What are the SEs of metoclopramide?
Extra-pyramidal (acute dyskinesias and dystonic reactions, tardive dyskinesia, Parkinsonism, akinesia, akathisia, and neuroleptic malignant syndrome)
Tardive dyskinesia
Hyperprolactinaemia
What is erythromycin?
Macrolide antibiotic with prokinetic properties. It is an agonist at motilin receptors, stimulating strong antral contractions
What are the SEs of erythromycin?
Abdominal cramps
Nausea
Vomiting
Why is ranitidine preferred to cimetidine to reduce gastric acidity pre-op?
It has a longer duration of action and fewer drug interactions.
PPIs have no advantage over H2 receptor antagonists as a single preop dose
How do PPIs work?
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
What is sodium citrate?
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.
What would you do pre-op for someone with a potentially full stomach?
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)
What would you do at induction of anaesthesia for a patient with a full stomach?
Aspirate NG tube Give 30mls Sodium Citrate orally Position head up tilt Pre-oxygenate Apply cricoid pressure RSI Cuffed ETT
What would you do during theatre in a patient with a potentially full stomach?
Maintain head up
Avoid increased intraabdominal pressure
Ensure adequate depth of anaesthesia
How would you extubate a patient with a full stomach?
Left lateral position
When awake and gag and cough reflexes present
