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Physiology for Anaesthetists > GIT - Stomach And Vomiting > Flashcards

GIT - Stomach And Vomiting Flashcards

1
Q

List the functions of the stomach

A
  1. Storage of large meals - releasing ingested food slowly into the small intestine
  2. Secretion: Digestive enzymes (gastrin)
  3. Mixing: mix with enzymes and liquify into chyme
  4. Secretion gastric acid: (defence micro-organsims + absorption Vit C / Iron)
  5. Secretion Intrinsic Factor: for B12 absorption
  6. Endocrine: Hormones to control gastric emptying
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2
Q

What quantity of fluid is produced + secreted by the following organs over 24 hours:

  1. Salivary glands
  2. Stomach
  3. Bile
  4. Pancreas
  5. Intestines
  6. Total
A
  1. Salivary glands - 1.5 L
  2. Stomach - 2.5 L
  3. Bile - 0.25 L
  4. Pancreas - 0.75 L
  5. Intestines - 3 L
  6. Total: 8 - 9 L/day
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3
Q

List the substances secreted by the stomach

A
  1. HCl
  2. Pepsinogen
  3. Gastrin
  4. Intrinsic Factor
  5. Mucus
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4
Q

Describe the structures, mechanism and function of HCl secretion into the stomach

A

Structures - Parietal cells

Mechanism (Parietal cell function –> Draw cell)
Page 280 Chambers

BASOLATERAL

  1. . CO2 inward diffusion
  2. Na-K ATPase pump
  3. CL-/HCO3 antiport
  4. M receptor
  5. G receptor
  6. H2 receptor

ECL cell (enterochromaffin like cell)

  1. Release Histamine to stimulate H2
  2. Have somatostatin inhibitory receptors

CELL LUMEN
Bicarbonate equilibrium reaction with CA

LUMINAL
Proton pump = H+/K+ ATPase exchanger
Cl- channel (into GIT)
K+ channel (into GIT)

HCl reduces pH which:

  1. Converts pepsinogen to pepsin
  2. Destroys ingested bacteria
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5
Q

What is the concentration and equivalent pH of the Hcl secreted into the stomach

A

150mml/L

pH = 0.8

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6
Q

How is HCL secretion regulated

A

DIRECT STIMULATION on parietal cell

  1. Histamine (H2 receptors)
  2. Ach (M3 receptors)
  3. Gastrin (G receptors)

INDIRECT STIMULATION
1. Gastrin stimulates ECL cells to release histamine

INHIBITION
1. Somatostatin receptors on ECL cells are inibitory

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7
Q

How is protein catabolism initiated and where does this occur

A

In the stomach

Gastrin and Ach (PSNS) stimulate CHIEF cells to secrete pepsinogen which is converted to pepsin by the acidic environment

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8
Q

Which cells secrete Gastrin, when is it released and what is its function. How is gastrin secretion regulated.

A

G cells

Function of gastrin

  1. PARIETAL CELLS –> Secrete HCl
  2. CHIEF CELLS –> Secrete Pepsin
  3. GASTRIC MOTILITY

Regulation

Release:

  1. PSNS –> Ach
  2. Distension of stomach
  3. Presence of partially digested proteins in stomach

Inhibition
1. High levels of gastrin –> release of somatostatin from DELTA cells in the stomach. –> inhibits further gastrin release

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9
Q

Which cells secrete intrinsic factor and explain the nature and site of its release and function

A

Parietal cells

Intrinsic Factor is an important co-factor for the absorption of vitamin B12.

IF does not bind to B12 in the acid environment of the stomach

B12 is released from digested animal proteins in the stomach

Haptocorrin binds a protects B12 from the acid environment in the stomach

Trypsin digests haptocorrin in the small intestine re-releasing vitamin B12

IF now binds to B12

Receptors for IF-B12 complexes in the terminal ileum allow for the absorption of B12 here.

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10
Q

What is pernicious anaemia

A

Autoimmune destruction of parietal cells in the stomach with deficiency of IF –> low B12 –> megaloblastic anaemia

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11
Q

What cells secrete mucus in the stomach and what is the function

A

Mucus cells –> HCO3- rich mucus

Function

  1. protection of stomach mucosa from acid
  2. Lubrication stomach wall
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12
Q

Differentiate between particulate and non-particulate antacids and their mechanism of action

A

Both particulate and non-particulate antacids react directly with HCl to neutralise the gastric pH.

PARTICULATE ANTACIDS

  1. Aluminium Hydroxide
  2. Magnesium Hydroxide
  3. Calcium Carbonate

Particulate = Aluminium / Magnesium and Calcium Salts formed are non-absorbable and form particulate matter –> if this formed particulate matter is aspirated into the lungs, pulmonary damage will still occur

NON-PARTICULATE ANTACIDS
1. Sodium Citrate

Non-particulate
Rapid onset of action

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13
Q

Why do gastric acid inhibitors take longer than antacids to work

A

Antacids work immediately via an immediate reaction with HCl in the stomach.

Gastric acid inhibitors prevent gastric acid from being secreted from parietal cells –> takes longer to work but there is a prolonged duration of action

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14
Q

What are the risks associated with chronic PPI use

A 
Clostridium difficile infection
Calcium deficiency and osteoporosis
Magnesium deficiency
B12 deficiency
Iron deficiency anaemia
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15
Q

Name and describe the phases of gastric secretion

A
  1. Cephalic (30%)
    - thought, smell, taste –> Vagus –> Ach –> Gastrin/HCl/Pepsinogen
  2. Gastric (60%)
    - Distension –> gastrin release
  3. Intestinal
    - chyme entry –> secretin from brush border –> HCO3- from pancreatic ductal cells and inhibits gastrin from G cells
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16
Q

What is secretin, where and when is it secreted and what is its function

A

As chyme enters the duodenum, secretin is secreted by the intestinal mucosa. Secretin then has the following effects:

  1. Stimulates pancreatic ductal cell secretion of HCO3- to neutralize acidic chyme
  2. Inhibits release of gastrin from G cells –> reduces HCL output from parietal cells
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17
Q

What is gastric dumping syndrome

A

Normally, chyme enters duodenum very slowly.

After gastric surgery –> rapid gastric emptying –> largely undigested chyme passes into the small intestine

  1. Duodenal distension (EARLY DUMPING SYNDROME)
    - -> Large amounts of hyperosmolar chyme draws in water from ECF –> cramping pains/nausea and bloating. EARLY DUMPING (soon after meal ingestion)
  2. Hypoglycaemia (LATE DUMPING SYNDROME)
    –> Rapid absorption of large amounts of CHO –> triggers B cells of islets of Langerhans in pancreas to secrete large amounts of insulin.
    –> Rapid blood glucose uptake
    –> Slower insulin metabolism
    Leading to hypoglycaemia
    Occurs 1 - 3 hours after a meal (LATE)
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18
Q

What is the rate of gastric emptying depend on?

A

DEPENDS ON CHARACTERISTICS OF THE DUODENAL AND GASTRIC CONTENTS

DUODENAL CONTENTS

  1. Duodenal distension –>reflex inhibition of enteric nervous system –> closing pylorus.
  2. Acid –> low pH –> secretin release –> HCO3 secretion and inhibition of gastrin –> reduced gastrin –> slowed emptying
  3. Fat –> CCK released when fat enters duodenum –> increased pyloric sphinter tone –> allows intestine more time to digest fat
  4. Hyperosmolarity –> inhibits gastric emptying

GASTRIC CONTENTS

  1. Consistency of chyme - solids –> Constriction of pyloric sphincter. liquids pass through.
  2. Gastric Volume –> increased volume promotes emptying
  3. Content: Protein faster than CHO faster than fat (slow)
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19
Q

Summarise the intrinsic and extrinsic factors that reduce gastric emptying

A 
INTRINSIC
Gastric contents
1. Solids
2. Low Volume
3. Fat > CHO > Protein

Duodenal contents

  1. High volume chyme with duodenal distension
  2. Acidic (secretin release –> inhibit gastrin)
  3. Fat (CCK increases pyloric sphincter tone)
  4. Hyperosmolar chyme (complex mechanism)

EXTRINSIC

  1. SNS acitivity
  2. PAIN
  3. DRUGS (opioids)
  4. DISEASES: diabetic autonomic neuropathy, acut abdomen, ileus
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20
Q

Draw the graph the demonstrates the rate of gastric emptying which differs between ingestion of solids and liquids.

A

Solids –> 30 minute lag where remains 100%
then linear decline until about three hours. 30 minute lag is for mixing in stomach and action of pepsin

Liquids –> exponential decline
–> unless liquids contain fats or acidic –> may mimmic solids linear emptying line

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21
Q

What are the disadvantages of pre-operative fasting

A
  1. Patient discomfort
  2. Dehydration
  3. Electrolytes
  4. PONV increased
  5. Glycaemic disturbance in diabetics
  6. Increased body muscle catabolism following major surgery
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22
Q

Define vomiting

A

Involuntary, rapid, forceful expulsion of gastric contents through the mouth. Nausea often precedes vomiting and is an unpleasant upper abdominal sensation

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23
Q

Where is the vomiting center

A

The vomiting centre is an anatomically ill defined area in the medulla oblongata in close contact with three important structures

  1. Respiratory centre
  2. Nucleus tractus solitaris (receives afferents from various cranial nerves)
  3. Chemoreceptor trigger zone (CTZ) (floor of fourth ventricle of the medulla = area postrema)
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24
Q

What is significant about the chemoreceptor trigger zone

A

It is located outside of the blood brain barrier and receives systemic blood directly. This:

  1. Provides a faster vomiting response to emetic stimuli
  2. Antiemetic drugs do not have to cross BBB to reach their target receptors.
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25
Q

Summarise the inputs into the vomiting centre that can trigger vomiting

A

CTZ

  • Dopamine (D2)
  • Serotonin (5-HT3)
  • ACh
  • Opioid
  • Substance P (NK-1)
CN 8 (Vestibulocochlear)
- Vestibular: Muscarinic and H1 receptors
CN 9 (Glossopharyngeal)
- Afferent for the gag reflex
CN 10 (Vagus)
- Distension, Infection, chemotherapy, radiotherapy --> stimulation serotonin 5-HT3 receptors in GIT --> vomiting

Higher centres
- Limbic system –> anxiety / extreme emotional states

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26
Q

Describe the three phases and what happens in each of the phases during vomiting

A

Pre-ejection

  • nausea
  • decreased gastric motility
  • Reverse peristalsis duodenum
  • HCO3 rich saliva (PSNS)
  • Sweating + tachycardia (SNS)

Retching phase

  • Deep inspiration –> closure of glottis
  • Rhythmic contraction of intercostal muscles, diaphragm, abdominal muscles against a closed glottis.
  • Alkaline contents of SI are vigorously mixed with gastric contents increasing pH.
  • Increased intrathoracic pressure compresses the oesophagus, preventing reflux of stomach contents

Ejection phase

  • Continuation of glottic closure
  • Contraction pylorus forcing gastric contents into body and fundus of stomach
  • Relaxation LOS and oesophagus
  • Sudden dramatic increased intra-abdominal pressure (contraction of abdominal muscles and descent of the diaphragm)
  • Soft palate occludes nasopharynx
  • Reverse peristalsis in the oesophagus rapidly expels contents upwards and out of the mouth
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27
Q

Describe the anaesthetic factors contributing toward PONV

A

Volatiles
N2O
Opioids
Anticholinesterases (Neostigmine)

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28
Q

Describe the surgical factors that contribute towards PONV

A

Longer duration of surgery
Middle-ear surgery
Laparoscopic surgery
Neurosurgery

29
Q

Describe the patient factors that contribute toward PONV

A 
Female
Child
PONV history
Motion sickness history
Non-smoker
30
Q

What anaesthetic techniques can be implemented to avoid PONV

A
  1. Avoid opioids / N2O / Volatiles
    - -> use regional / TIVA
  2. IV fluid therapy
  3. Antiemetic drugs
31
Q

How long can PONV persist after surgery

A

up to 5 days

32
Q

Define nausea

A

A feeling of sickness with an inclination or an impending desire to vomit

33
Q

Define retching

A

Laboured, spasmodic, rhythmic contractions of the respiratory muscles without expulsion of gastric contents

34
Q

Define regurgitation

A

The effortless expulsion of food from the stomach or return of food to the mouth

35
Q

Define vomiting

A

Forceful, involuntary and rapid ejection of gastric contents from the mouth

36
Q

Draw a simplified diagram of the various afferents into the vomiting centre. List these afferents

A
  1. CTZ (Area postrema of the 4th ventricle)

2. GIT (Mechanoreceptors and serotonin release –> CTZ)

37
Q

What receptors does the CTZ contain and what is the function of the CTZ in health

A

Receptors

  1. 5 HT3
  2. D2
  3. H1
  4. u (MOP)
  5. Substance P (NK-1)

Function
Blood Pressure regulation
Sleep
Food intake

38
Q

Describe the afferents to the vomiting centre in the Medulla Oblongata

A
  1. Chemoreceptor Trigger Zone in the area postrema of the 4th ventricle: H1/D2/5HT3/MOP/NK-1
  2. GIT Receptors (CN 10)
    - Mechanoreceptors
    - Chemoreceptors (5HT3, NK-1 ——-> Vagal —-> VC)
  3. Peripheral pain receptors (trauma)
  4. Nucleus solitaris (CN 9 –> gag reflex)
  5. Vestibular system (CN 8 –> CTZ–>motion sickness)
  6. Ocular (CN 5 –> opthalmic branch)
  7. Cerebral Cortex (Smell/physiological stress)
  8. Limbic system (emotional stress/anxiety)

Memory aid below:

BRAIN
CTZ (D2/5HT3/H1/MOP/NK-1)
Cerebral cortex (Physiological stress)
Limbic (Anxiety and emotional stress)

CRANIAL NERVES
10 - Vagus (GIT mechanoreceptors and chemoreceptors)
9 - Glossopharyngeal (gag reflex - nucleus solitarius)
8 - Vestibulocochlear (Motion sickness)
5 - Trigeminal (ophthalmic) - ocular pressur/pain
1 - Olfactory (smells)
2 - Optic (Visual stimuli)
7,9,10 - taste stimuli
PERIPHERAL NERVES
Peripheral pain receptors (vomiting after trauma)

39
Q

Summarise the process of vomiting

A 
PROTECTION of lungs and nasopharynx
Deep inspiration
Hyoid bone rises
Glottis closes
Soft palate lifted
PROTECTION FROM pH
Reversed peristalsis into stomach from SI
Increased salivation (HCO3)

RELAXATION
LOS + Oesophagus

CONTRACTION 
Abdominal wall
Thoracic muscles
Diaphragm
--> RIAP
---> ejection
40
Q

How can the risk factors for PONV be classified

A

Patient
Medical
Surgical
Anaesthetic

41
Q

What is the APFEL score

A

1 point - Female
1 point - Non-smoker
1 point - History PONV or motion sickness
1 point - Postop opioids

Score  (Risk PONV)
0 (10)
1 (20)
2 (40)
3 (60)
4 (80)
42
Q

What are the medical risk factors for PONV

A 
GIT disease (hiatus hernia / GORD)
Metabolic disease (DM, Uraemia, Electrolyte)
Pregnancy 
Pre-operative Anxiety
The underlying surgical problem 
Intracranial stimulation (tumour)
Acute abdomen, intestinal obstruction
Chemotherapy or radiation
43
Q

Which types of surgery are associated with a higher risk of PONV

A 
ENT
Dental
Breast
Orthopedic shoulder surgery
Laparoscopy
Ophthalmology (strabismus)
Varicose vein stripping)
44
Q

How does duration of surgery affect risk of PONV

A

Longer –> increase risk PONV

Adults > 60 minutes –> increased risk
Kids > 35 minutes –> increased risk

For every 30 minutes after these times the risk increases by 60%

45
Q

Describe anaesthetic factors that increase and decrease risk of PONV

A

DECREASE

  1. Benzodiazepines (Premed anxiolysis)
  2. Regional anaesthesia/TIVA (vs. GA) - avoid all of below
  3. PROPOFOL TIVA/TCI - avoid all of below
  4. Higher FiO2 (reduces bowel distension/ischaemia)
  5. Atropine (crosses BBB unlike glycopyrrolate)
  6. IV Fluids

INCREASE

  1. N2O
  2. Volatiles
  3. Opioids
  4. Neostigmine
  5. Dehydration
  6. Hypotension (>35% decrease SBP)
46
Q

Classify and list the dopamine receptor antagonists

A

Phenothiazines

  1. Chlorpromazine
  2. Promethazine

Butyrophenones
1. Droperidol

Benzamides
1. Metoclopramide

47
Q

Compare phenergan to chlorpromazine including classification, MOA and side effects

A 
Phenergan = Promethazine = phenothiazine 
Dose 12.5 - 25 mg 4 - 6 hrly
MOA
1. D2 receptor antagonist CTZ
2. H1 receptor antagonist 
3. M receptor antagonist
4. Alpha adrenergic antagonist - reduces hormone release from hypothalamus/Pituitary
5. Reduces stimuli to brainstem/RAS

Chlorpromazine = phenothiazine
Dose: 10 - 25 mg IM 4 - 6 hourly

MOA

  1. D2 receptor antagonist CTZ
  2. M receptor antagonist
  3. Alpha adrenergic antagonist - reduces hormone release from hypothalamus/Pituitary
  4. Reduces stimuli to brainstem/RAS

Adverse effects (both)

  1. Drowsiness
  2. Extra-pyramidal side effects
  3. PROLONG QT (more significant in chlorpromzine)
48
Q

What are two examples of a butyrophenones. What is the Dose, MOA and adverse effects. Which agent is preferred and why

A

Droperidol
Dose:
PONV Rx: Max initial: 2.5 mg IM/IV
PONV Prevent: 1.25 IM/IV ±30 min before end of surgery (then 6hrly)

MOA

  1. D2 receptor antagonist
  2. Alpha adrenergic antagonist (low)
  3. H1 receptor antagonist (low)
  4. 5HT 1 + 2 antagonist (low)

Haloperidol
Dose: 2mg 30 minutes before end of surgert

Same MOA

Haloperidol has been associated with higher frequency of adverse effects:

  1. Drowsiness
  2. Dysphoria
  3. Extra-pyramidal side effects
  4. Prolonged QT
49
Q

What are the benzamides? MOA,

A

Metoclopramide

MOA
CTZ
1. D2 antagaonist CTZ
2. 5HT3 antagonist (at high doses)
Also GIT
1. Increase LOS tone
2. Facilitation gastric emptying into small intestine

Side effects

  1. Drowsiness
  2. Extra-pyramidal SE
  3. Prolonged QT
50
Q

What is benadryl: MOA, dose and clinical use

A

Diphenhydramine
Dose: 20mg ± 30 minutes before end of surgery
MOA:
1. H1 receptor antagonist
2. M receptor antagonsit
3. alpha adrenergic antagonist
Inhibition of integrative functioning of the vestibular nuclei in the inner ear by decreasing vestibular and visual input

Clinical use

  1. Motion sickness
  2. Inner ear disease
51
Q

Give an example of a muscarinic receptor antagonist used for nausea and vomiting

In which perioperative setting is this usually used

What is the MOA and Side effects

A

Scopolamine transdermal patch

Used Middle Ear Surgery –> disruption of vestibular apparatus

MOA: Blocks transmission to the medulla (vomiting center) of impulses arising from overstimulation of the vestibular apparatus

Apply patch before induction of anaesthesia

Takes 2 - 4 hours to work

Adverse effects

  1. Dry mouth
  2. Dizziness
  3. Problems with accommodation
  4. Delirium
52
Q

Are the serotonin antagonists more effective at treating nausea or vomiting

A

Vomiting

53
Q

Name 4 serotonin receptor antagonists

Which of these agents is said to be effective when other ‘setron’s’ fail to be effective and why is this the case

A

Ondansetron
Granisetron
Tropisetron
Dolasetron

Granisetron is often effective despite failed efficacy of another setron. This is because, unlike the other drugs in this group, Granisetron is not dependent on CYP2D6 for metabolism, it depends on CYP3A4. Genetic polymorphism for CYP2D^ is very common. Therefore, Granisetron may be effective when the other three drugs fail for rescue PONV.

54
Q

Apart from 5HT3 receptors what other receptors do Ondansetron and Tropisetron bind to

A

alpha adrenergic
MOP

Unknown clinical relevance

55
Q

Why and how do the setrons prolong QT

A

Granisetron blocks sodium channels in the heart

Ondansetron blocks potassium channels in the heart

56
Q

What is apomorphine, what is it used for and what happens when it is combined with one of the setrons

A

D1 and D2 agonist used in Parkinsons

Combined with setron: significant hypotension and loss of consciousness

57
Q

Differentiate Ondansetron and Granisetron

A

Both effective in treating established PONV rather than preventing it.

Ondansetron
Less selective
T1/2 = 4 hours
Dose: Adults 4 - 8 mg. Paeds: 0.1 mg/kg 
Side effects
1. HA, dizziness, transient transaminitis, 
2. GIT: Warm epigastric sensation and constipation
3. Prolong QT

Granisetron
More selective
T1/2 = 9 hours
Dose: 3mg Paeds: 0.02 mg/kg

58
Q

What is Aprepitant

A

Neurokinin-1 (NK-1) receptor antagonist

Substance P (Visceral afferent stimuli e.g. gastric distension) is a natural ligand for the NK-1 receptor

Aprepitant is said to be superior to ondansetron in preventing PONV in first 24 - 48 hours

59
Q

What is the mechanism of action whereby steroids reduce PONV

A

Unknown

Maybe: inhibition of PG synthesis / stimulation of endorphin release / decreased central uptake serotonin

60
Q

How long does dexamethasone take to elicit its antiemetic effect?

A

2 hours

Repeated doses not recommended

61
Q

What is the minimum effective dose of dexamethasone to prevent PONV in adults and children

A

5 mg

Kids: 0.15 mg/kg

62
Q

How does midazolam elicit its anti-emetic effect

A

Potentiation of GABA
–> decreases dopaminergic neuronal activity and 5HT release in the CTZ

Also reduces catecholamine levels

63
Q

Does propofol elicit an anti-emetic effect subsequent to bolus administration at induction of anaesthesia

A

NO –> continuous sub-hypnotic propofol infusion required.

64
Q

Describe the effective plasma concentration of propofol for the following indications:

  1. Antiemesis
  2. Sedation
  3. Anaesthesia
A

TCI Schnider: Cpl

  1. Antiemesis: 0.35 ug/mL
  2. Sedation: 0.9 - 3 ug/mL
  3. Anaesthesia: 3 - 10 ug/mL
65
Q

How do alpha 2 adrenergic agonists possibly exhibit antiemetic effects

A
  1. Reduced SNS outflow
  2. Analgaesic properties (reduced opioids needed)
  3. Sedation (reduced volatile needed)

BUT sometimes dexmedetomidine causes hypotension which causes nausea and vomiting

66
Q

How do cannabinoids reduce vomiting

A

CB - 1 receptor within the vagal nucleus complex –> mediation of serotonin and substance P

67
Q

How does inhaled isopropyl alcohol reduce nausea and vomiting

A

Unclear mechanism

Possibly: Depressant effect on CNS

68
Q

Ideal anaesthesia for patient with previous severe PONV

A
  1. Dexamethasone
  2. Droperidol
  3. Ondansetron
  4. TIVA/TCA (Propofol/Remifentanyl)
  5. Aggressive IVF 25 ml/kg
  6. No N2O
  7. No neuromuscular blockade
  8. Analgaesia: Paracetamol / ketorolac

Physiology for Anaesthetists (61 decks)

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