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Life Maintenance > Visceral afferents in GI > Flashcards

Visceral afferents in GI Flashcards

1
Q

What is sensation?

A

Activation of sensory/afferent neurones

Bidirectional cross-talk between these neurones and the surrounding cells and the CNS

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2
Q

What kinds of cells are involved in the cross-talk that mediates sensation?

A

enteroendocrine cells
immune cells
fibroblasts, glia, enterocytes
interstitial cells of Cajal

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3
Q

Do all sensory inputs from the gut mediate sensation?

A

No, sensory inputs are tightly modulated by the brain and spinal cord before sensation precipitates

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4
Q

What kind of sensations can be felt from the gut?

A 
oesophageal distension
gastric distension i.e. fullness 
nutrient density in stomach, duodenum 
toxins or excess nutrients causing nausea
gas
pain
urgency 
awareness of rectal content
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5
Q

What are the 5 types of sensory neurones?

A 
serosal
mesenteric 
mucosal 
muscular 
musculo-mucosal
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6
Q

What are the 6 types of visceral afferents in the gut?

A 
intraganglionic (vagal and pelvic)
enteric viscerofugal 
intramuscular (vagal and pelvic) 
vascular 
muscular-mucosal 
mucosal (vagal and pelvic)
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7
Q

What are the 3 main pathways involved in visceral pain sensation from the gut?

A

PRIMARY SENSITISATION: of primary sensory afferents innervating the viscera
CENTRAL SENSITISATION: hyper-excitability of spinal afferents reacting to sensory input from gut viscera
DYSREGULATION: of descending pathways that modulate spinal nociceptive transmission

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8
Q

Describe the nature of the 6 visceral afferents in the gut?

A

intraganglionic: low threshold mechanoreceptor (pelvic and vagal)

enteric viscerofugal: interneurons with mechanosensitivity

intramuscular: mechanosensitive (pelvic and vagal)
vascular: extramural and intramural blood vessels, mechano-nociceptive (splanchnic and pelvic)

muscular-mucosal: mucosal stroking and distension/contraction (pelvic and vagal)

mucosal: mucosal distortion and entero-endocrine cell mediators (pelvic and vagal)

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9
Q

What are 5 entero-endocrine mediators of mucosal afferents?

A 
CCK
PYY
5-HT (serotonin)
ghrelin
secretin
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10
Q

What are the different types of pain?

A

somatic
visceral
neuropathic
phantom

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11
Q

What is visceral pain?

A

Activation of nociceptors in the thoracic, pelvic and abdominal organs
Usually most sensitive to distension (stretch), ischaemia and inflammation
usually referred pain

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12
Q

What is somatic pain?

A

activation of pain receptors in tissues (e.g. skin, muscle, connective tissue)
Usually activated by pressure, temperature, vibration or swelling
often describes as cramping sort of pain
usually well localised

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13
Q

What is dysesthesia?

A

abnormal sensation

often as a result of neuropathic pain

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14
Q

What is allodynia?

A

Pain presenting from normally non-painful stimuli

often as a result of neuropathic pain

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15
Q

What is neuropathic pain?

A

Damage or disease to the somatosensory nervous system

Can result in either dysesthesia or allodynia

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16
Q

What is phantom pain?

A

Pain from a body part that is no longer there

Some evidence to suggest this is not entirely psychological, pain sensations do original from the spinal cord and brain

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17
Q

Why are not all internal organs sensitive to pain?

A

Many organs e.g. liver, lungs, kidneys do not contain nociceptors (pain receptors) and so cannot ‘feel’ direct pain in the same way as somatic pain is felt
Also, several visceral converge onto the same spinal cord neurones and so localised pain is not felt
Severe visceral discomfort may be referred onto cutaneous structures e.g. within a dermatome

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18
Q

What stimuli can result in visceral pain?

A 
inflammation 
ischaemia
traction
hollow organ distension
acids/irritant chemical 
electrical stimulation
'pinching' only causes pain when hyperalgesia is present
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19
Q

What is hyperalgesia?

A

Increased sensitivity to pain receptors etc
Can be caused by neuropathic damage
Also caused by consumption of opiods

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20
Q

How can visceral pain be caused by ‘structural’ conditions?

A

Inflammatory: gastric-acid/peptic disease
Neoplastic: tumours

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21
Q

How can visceral pain be caused by ‘functional’ conditions?

A 
IBS (inc. bloating)
functional dyspepsia (nausea)
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22
Q

What is dyspepsia?

A

Simply indigestion

Can be caused by pathology in oesophagus, stomach, duodenum or intestine

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23
Q

What is ‘somatic’ abdominal pain?

A

Pain from abdominal wall or inguinal ligaments
Often well localised, reproduces pain
Can present asymmetrically
Affected by position, movement, straining
Unaffected by defecation, or food
e.g. painful rib syndrome, spinal pain

24
Q

How can appendicitis migrate from visceral to somatic pain?

A

Early phase: visceral pain presenting as peri-umbilical, centralised and colicky
Later phase: parietal peritoneal inflammation pushes pain towards right iliac fossa (RIF)
worse with movement or straining
Tenderness at McBurney’s point

25
Q

What can be used to treat visceral pain?

A

Treat underlying cause/disease
Use anti-spasmodics e.g. mebeverine for IBS
Use tricyclics e.g. amitryptiline for visceral hypersensitivity (hyperalgesia)
[latter is effective when used at sub anti-depressant doses, with main side effect being sedation]

26
Q

How does hyper-vigilance relate to visceral pain?

A

Mild pain is often exacerbated by awareness of pain, which causes anxiety or panic. This anxiety can also result in hyper vigilance which causes a vicious cycle of pain etc
e.g. painful rib syndrome - patients exhibit pain reduction when they are told it is not serious

27
Q

What is achalasia?

A

Oesophageal motility disorder
Results in aperistalsis and incomplete lower sphincter relaxation
Causes dysphagia
Can be treated by botulinum toxin, myotomy, pneumatic dilatation

28
Q

What is myotomy?

A

Heller’s myotomy for achalasia
surgical procedure in which muscles of the cardia (gastric) aka the lower oesophageal sphincter are cut to allow for food to pass more easily

29
Q

What is pneumatic dilation?

A

Endoscopic therapy for achalasia

Placement of a balloon over the lower oesophageal sphincter to loosen the muscles and therefore allow food to pass

30
Q

How can botulinum toxin be used to treat achalasia?

A

Injection of the lower oesophageal sphincter with botulinum toxin causes temporary paralysis of the muscles
This causes them to relax and therefore allows food to pass through into the stomach cardia

31
Q

What are the main features of gastric oesophageal reflux disease (GORD)?

A

incompetent lower oesophageal sphincter, but normal resting pressure
Normal gastric acid secretion
Oseophagitis observed by endoscopy but usually non-erosive lesion seen

32
Q

What are the 3 types of hypersensitivity evoked by gastric acid exposure?

A

Hyperalgesia: primary, local focal point of hypersensitivity
Allodynia: to non-painful stimuli
Secondary hyperalgesia: generalised hypersensitivity

33
Q

What are the clinical subdivisions of GORD?

A

Erosive reflux disease (20-30%)
Non-erosive reflux disease, NERD (60-70%)
Barrett’s Oesophagus (5-10%)

34
Q

What are the 2 main ion channels in the oesophagus?

A

TRPV1: transient receptor potential vanilloid 1
ASIC: acid sensing ion channel

35
Q

What happens when (gastric) acid is exposed to the TRPV1 channels?

A

neurogenic inflammation

release of pro-inflammatory mediators

36
Q

What stimuli are the ion channels in the oesophagus sensitive to?

A

Mechanical
Electrical
Thermal

37
Q

What are the clinical subtypes of NERD?

A

pH positive vs pH negative
pH neg: if symptoms are associated with pH changes then its hypersensitive oesophagus (40%)
pH neg: if symptoms are not associated with pH changes then its functional heartburn - reflux negative (60%)

38
Q

How do the vagus, gastrin and Ach affect gastric motility?

A

They promote acid secretion

39
Q

Delayed gastric emptying can be present in dysmotility conditions. What are examples where this may be exacerbated?

A

gastroparesis (weakened muscular contractions in stomach)

post-infective diabetes

40
Q

How is delayed gastric emptying monitored or identified?

A

Isotope gastric emptying study

41
Q

How can delayed gastric emptying be treated?

A

pro-kinetic drugs
e.g. domperidone, metocloperaminde
These also function as anti-emetics

42
Q

What are the demographics for GORD?

A 
10-15% prevalence
greater anxiety, lower QoL
F > M
No excess mortality 
Assessed using Rome and Manning Criteria
43
Q

What are the Rome and Manning criteria?

A

2x algorithm used to assess IBS Dx

Consists of a series of questions asked by the doctor to the patient

44
Q

How does the Rome IV criterial describe IBS?

A 
disorders of the gut-brain interaction 
Motility disturbance
visceral hypersensitivity 
altered mucosal and immune function 
altered gut microbiota
Altered CNS processing
45
Q

What are the 3 types of IBS relating to stool consistency?

A

IBS with constipation
>25% hard stools, <25% loose stools

IBS-mixed
both hard and loose stools

IBS with diarrhoea
>25% loose stools, <25% hard stools

46
Q

What are common causes of constipation?

A

low fibre diet
medications e.g. opiates
hypercalcaemia
hypothyroidism

47
Q

What are the functional types of constipation?

A 
colonic inertia (slow transit, assessed by marker studies)
Pelvic floor dysyngergia (pelvic floor muscles do not relax with defecation) 
management is similar between both types
48
Q

Which dietary fibre types have been shown to more effective to combat constipation in RCTS?

A

Sorbitol (prunes)
Kiwifruit
Vegetable and wholegrain powder
Fruit and fibre to porridge

49
Q

Why are osmotic laxatives such as macrogol considered to be more effective and better tolerated than lactulose?

A 
Proven efficacy in long term treatment 
improved stool frequency 
improved pain
less need for other top-up laxatives
side effects: diarrhoea and bloating
50
Q

What are the first line laxative used to treat IBS with constipation?

A

Osmotic (e.g. macrogol)
Stimulant (Sodium picosulphate, Bisacodyl, Senna)
Stool softeners (sodium docusate)

Side effects:
Osmotic: bloating
Stimulant: cramps

51
Q

What is the mechanism of action for secretagogues used to treat IBS?

A

Increases water-Cl- secretion into intestinal lumen

Therefore softens stools correcting constipation

52
Q

Name two examples of secretagogues used to treat IBS with constipation?

A

Lubiprostone (Cl channel activator)
SE nausea, diarrhoea, cramps

Linaclotide (guanylate cyclase C agonist)
IBS-C (improves abdo pain)
SE diarrhoea

53
Q

What diet advice could be given to patients with IBS?

A 
should be individualised to patient
Regular, small meals
Fat reduction
Caffeine
Reduce lactose and fructose
Reduce gas-producing foods
Modify soluble/insoluble fibre
Reduce wheat
Low FODMAP diet (reduces bifidobacteria)
54
Q

How would you treat a patient with opiod-induced constipation?

A

Use a Peripherally Acting Mu Opioid Antagonist (PAMORA)

e.g. Naloxegol (pegylated naloxone)

55
Q

What embryological structuer is Meckel’s diverticulum derived from?

A

the vitello-intestinal duct

it is a congenital diverticulum of the small intestine, containing exotic ileal, gastric or pancreatic mucosa

56
Q

What is the “rule of 2’s” for Meckel’s diverticulum?

A 
affects 2% of population
2 inches (5cm) long
2 feet (60cm) from the ileocaecal valve
2x more common in men
2 types of tissue involved

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