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Introduction to medicine (Year 1) > Nausea, Vomiting & Pain: Symptoms of GI disease > Flashcards

Nausea, Vomiting & Pain: Symptoms of GI disease Flashcards

1
Q

What is nausea?

A
  • A sensation
  • Personal, self reported
  • Associated with physiological changes
  • Unpleasant
  • Triggers aversion
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2
Q

What is retching?

A

Co-ordinated contractions of abdominal muscles and diaphragm

Waves of high pressure in abdomen

Compresses stomach but anti-reflex barriers intact so no expulsion of GI contents

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3
Q

Define aversion

A

A strong dislike or disinclination

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4
Q

What is vomiting?

A
  • Physical act
  • Expels contents of upper GI tract via mouth
  • Forceful (regurgitation, reflux)
  • Complex, coordinated reflexive events
  • Associated with sensation of relief
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5
Q

What is the relationship between nausea and vomiting?

A
  • Nausea is produced by the same stimuli as vomiting
  • Nausea is generally a produce (permonitory system) of vomiting
  • Nausea may clear up without triggering vomiting
  • Vomiting can occur without prior nausea if the stimulus is powerful enough
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6
Q

What causes nausea and vomiting?

A
  • Poisoning (contaminated food, plants, chemical agents)
  • GI infection (norovirus)
  • Excessive alcohol
  • Pregnancy
  • Excessive eating
  • Travel sickness
  • Other people being sick
  • Metabolic disturbance
  • IV drugs (morphine, chemotherapy)
  • Raised intracranial pressure
  • GI disease (e.g. gastritis)
  • Obstruction
  • Emotional upset
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7
Q

How does aversion protect the body?

A

Taste and smell:

  • Can potentially prevent ingestion or poisons/toxins
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8
Q

How does nausea and vomiting protect the body against ingested toxins?

A
  • Can potentially expel harmful agents before they have (much) chance to be absorbed
  • Association with chemoreceptive cells that respond to:

Naturally occurring toxins
Damaging chemicals
Inflammatory mediators

Nausea is a potent trigger for memory and can in future induce:

Avoidance
Aversion

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9
Q

Describe the chemoreceptor trigger zone

A

The area postrema in the brainstem

Blood-brain barrier is ‘leaky’

Chemoreceptors that can detect toxins in the blood

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10
Q

Describe the vestibular system

A
  • The organ of balance, but also a potent trigger for emesis (vomiting)
  • Poisoning is thought to produce aberrant activity in vestibular neural pathways
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11
Q

What are our anti-poison defences co-ordinated by?

A
  • Nucleus Tractus Solitarius (NTS)
  • Found in the medulla of the brainstem
  • Also integrates cardiac, respiratory and gastrointestinal functions
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12
Q

Describe the 4 main inputs received by the NTS

A

1 - Visceral (abdominal) afferents for nausea and vomiting - afferent signals (toxins, irritants, inflammation, distension), lead to excitatory signals of vagus nerve to area postrema.

2 - Area postrema - Chemoreceptive trigger zone, receives signal from vagus nerve, inputs to NTS. There’s no blood-brain barrier, therefore receptors here can detect toxins in the blood

3 - Vestibular system - Organ of balance, sits in inner ear - toxins in the blood disrupt vestibular signals. Nausea and vomiting thought to arise from mismatch between vestibular and other sensory (especially visual) input. It sends its axons out through the 8th cranial nerve, and straight into the brainstem, into the NTS

4 - Higher brain centres - e.g. others around you being sick, things that have made you sick before, things you find disgusting

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13
Q

How does the NTS coordinate the response to detecting and eliminating ingested harmful agents?

A

NTS in medulla coordinates cardiac, respiratory and GI functions = NTS is regulatory/coordinator and is used to coordinate processes needed to expel contents of GI tract

  1. NTS receives input from abdominal visceral afferents (toxins, irritants and distension) receptors found in fundus and duodenum
  2. Fibres from area prostrema (detecting toxins in blood) travel to NTS
  3. Higher centres of brain (aversive and emotional stimuli) travel to the NTS
  4. Fibres from vestibular system (detecting toxins and disequilibrium) also travel to the NTS for info processing
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14
Q

What are the outputs from the nucleus tractus solitarius?

A
  • Hypothalamus - releases ADH, vasopressin
  • Higher centres (cerebral cortex, limbic) - higher centres
  • Autonomic efferents - Changes in gut motility, increased salivation, vasoconstriction in GIT (GI tract)
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15
Q

How does the NTS trigger nausea and vomiting?

A
  1. Reduced mixing and peristalsis
    1. Prevents toxins from being carried further through the system
  2. Proximal stomach relaxes
    1. Prepares stomach to receive additional contents
  3. Giant retrograde contraction
    1. Sweeps up from mid-small intestine
    2. Returns upper intestinal contents to stomach
  4. Retching (dry heaves)
    1. Co-ordinated contractions of abdominal muscles and diaphragm
    2. Waves of high pressure in abdomen
    3. Compresses stomach but anti-reflux barriers intact so no-expulsion
  5. Vomiting (emesis)
    1. Oesophageal sphincters and crural diaphragm relax
    2. Further waves of contraction expel stomach contents
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16
Q

What are the symptoms of nausea?

A
  • Lack of appetite
  • Profuse sweating
  • Repeated rhythmic contractions of respiratory and abdominal muscles that happen without your contract (retching)
  • Stomach ache
  • Uneasy feeling in your chest, upper abdomen, or back of your throat
17
Q

Describe the neural mechanism when a person feels nauseous

A
  • NTS will signal to hypothalamus to increase release of ADH - conserves fluid in prep for fluid loss due to vomiting
  • NTS signals frontal cortex and limbic areas to induce nausea
  • NTS will activate autonomic efferents - Stimulates salivation, sweating, vasoconstriction of GIT (prevents absorption of toxins)
  • NTS stimulates parasympathetic efferents (vagus nerve) to change GI motility:

Reduce gut motility to prevent further carrying of toxins

Proximal stomach relaxes - prep stomach to receive additional contents

Giant retrograde contraction - peristalsis halts, returns upper intestinal contents to stomach, sweeping up from middle small intestine

18
Q

What are the mechanical events of retching and vomiting?

A
  1. Retching (dry heaves)
    1. Co-ordinated contractions of abdominal muscles and diaphragm
    2. Waves of high pressure in abdomen
    3. Compresses stomach but anti-reflux barriers intact so no-expulsion
  2. Vomiting (emesis)
    1. Oesophageal sphincters and crural diaphragm relax
    2. Further waves of contraction expel stomach contents
19
Q

What are the receptors called in the pain pathways that respond to ‘noxious’ stimuli?

A

Nociceptors

20
Q

What are noxious stimuli in the GI tract? Why do they trigger nausea and vomiting?

A
  • Distension - As the gut distension increases, nociceptors detect this and afferent nerve action potentials also increase. This would increase the signalling of the vagus nerve to the area postrema, which would then trigger the NTS to induce vomiting
  • Inflammation - Nociceptors are sensitised by inflammatory mediators, which can then leads to vomiting due to this sensitisation
    • Nociceptors also release chemicals that increase inflammatory responses
    • This creates a positive feedback loop, that may become self-sustaining
    • Chronic sensitisation of visceral pain pathways is through to occur in GI disease
  • Muscle spasm
21
Q

List some emetic stimuli that can trigger nausea and vomiting and describe why they may cause vomiting

A

Emetic - (substance) causes vomiting

Gastroenteritis– and gastric diseases produce irritation and inflammatory mediators that activate toxin defences. Virses trigger receptors to detect poisons

Excessive eating– triggers defence against obstruction

Travel sickness– fast speed triggers vestibular system (disequilibrium)

Pregnancy, metabolic disturbances, drugs– produce toxins in blood detected by area prostrema

Emotional upset– could be by-product of info from emotional centres being relayed to NTS

Other people being sick– hunter gatherer seeing other people sick you probably had the same food = GI on high alert

Intracranial pressure– pressure presses on tissue near foramen magnum = pushes it through which is near area prostrema = stimulated

22
Q

Identify classes of anti-emetics that can be used to treat nausea and vomiting caused by toxins in the gut and/or blood stream

A

Area prostrema and abdominal afferents signalling can be reduced by 5-HT antagonist = decreased nausea and vomiting if caused by toxins in blood or abdominal afferents

23
Q

Describe the origin and characteristics of ‘visceral pain’

A

Nociceptors = sensory receptors for pain which responds to noxious stimuli

  • Distension, inflammation, ischaemia, traumatic injury, muscle spasm

Most GI nociceptor afferents run in sympathetic nerves (greater and lesser splanchnic) into thoracic segments of spinal cord:

  • Greater T1-T9
  • Lesser T10-T12
24
Q

What are characteristics of visceral pain?

A

Diffuse and poorly localised - relatively small number of afferents and imprecise wiring = referred pain

Accompanied by motor actions - guarding (protective spinal level reflex)

Trigger autonomic responses - Increased HR, BP, sweating, pale skin

25
Q

What is the neural pathway for referred pain originating from the GI tract? Give an example

A

Afferents synapse in segments matching the embryonic origin of each organ

Imprecise wiring = gastric pain referred to body wall due to viscera-somatic convergence (visceral afferents travel with somatic nerves innervating certain/similar part of body wall)

Initially pain referred to dermatomes matching the embryonic origin of organ but site and nature can change- can cause pain nowhere near organ

Example:

Gallbladder normally at T9 if small, but if spread - pain can be felt in neighbouring structures and peritoneum for example the diaphragm or C3,4,5 = shoulder pain

26
Q

What is the neural pathway of direct pain for the GI?

A

Nociceptors act on same vertebral level as pain receptors of skin so brain localises this to that region

27
Q

Describe the physiological changes that may be involved in the aetiology of functional bowel disease

A
  • As nociceptors release inflammatory mediators in response to inflammation = nociceptors activated more strongly and persistently = may potentiate synapses magnifying signals further
  • Intrinsic pain control becomes less active so hypersensitivity outlasts pathology = chronic GI pain as entire GI is hypersensitised

Introduction to medicine (Year 1) (59 decks)

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