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SGUL - Physiology 1 > Symptoms of GI Disease > Flashcards

Symptoms of GI Disease Flashcards

1
Q

Define nausea

A
  • personal, self-reported
  • associated with physiological changes (pale, sweaty)
  • Nausea is a SENSATION
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2
Q

Define vomiting (emesis)

A
  • Expels contents of the upper GI tract via the mouth
  • Forceful (regurgitation, reflux)
  • Emesis is a PHYSICAL ACT
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3
Q

List some things that could cause nausea and vomiting. PART 1

A
  • poisoning
  • GI infection
  • pregnancy
  • excessive alcohol
  • travel sickness
  • metabolic disturbance
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4
Q

List some things that could cause nausea and vomiting. PART 2

A
  • drugs
  • emotional upset
  • travel sickness
  • metabolic disturbance
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5
Q

Outline the importance of taste and smell against ingested toxins.

A
  • can potentially prevent indigestion
  • we have a built-in dislike for bitter flavours
  • children are naturally wary of novel flavours
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6
Q

Outline the importance of gastric and upper GI afferents against ingested toxins.

A
  • can potentially expel harmful agents before they have much chance to be absorbed
  • associated with chemoreceptors that respond to: irritants, inflammatory mediators and bacterial toxins
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7
Q

Outline the importance of the chemoreceptor trigger zone against ingested toxins

A
  • the postrema in the brainstem
  • Can detect toxins because the blood-brain barrier is leaky, chemoreceptors can detect toxins in the blood
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8
Q

Outline the importance of the vestibular system against ingested toxins

A
  • part of the ear that detects movements of the head and direction of gravity
  • trigger for emesis
  • poisoning is thought to produce aberrant activity in vestibular neural pathways
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9
Q

Outline the importance of learning against ingested toxins

A
  • if we survive a mistake we avoid repeating it
  • aversion may hardwire avoidance
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10
Q

List 4 things that will feed into and trigger nausea and vomiting.

A
  • visceral afferents (respond to toxins, irritants and distentions)
  • area postrema (responds to toxins in the blood)
  • vestibular system (responds to toxins in the blood, disrupting vestibular receptors)
  • higher centres of the brain (responds to aversive and emotional stimuli)
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11
Q

Where are signals sent by the factors that trigger nausea and vomiting?

A
  • To the brainstem i.e the NTS
  • Integrating centre for the heat, respiratory and GI systems
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12
Q

List the mechanisms of nausea. PART 1

A

Reduced mixing and peristalsis - prevents toxins from being carried further through the system
Proximal stomach relaxes - prepares stomach to receive additional contents

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13
Q

List the mechanisms of nausea. PART 2

A

Giant retrograde motion - sweeps up from the mid-intestine and returns upper intestinal contents to stomach

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14
Q

List the mechanisms of vomiting. PART 1

A

Retching
- coordinated contractions of abdominal muscles and the diaphragm
- waves of high pressure on the abdomen
- compresses stomach but anti-reflux barriers are intact so there’s no expulsion

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15
Q

List the mechanisms of vomiting. PART 2

A

Vomiting (emesis)
- oesophageal sphincters and the crural diaphragm relax
- further waves of contraction expel the stomach contents

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16
Q

What do pain receptors respond to?

A

Noxious stimuli

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17
Q

What are pain receptors commonly known as?

A

Nociceptors

18
Q

What do nociceptors respond to?

A
  • distention
  • inflammation
  • muscle spasms
19
Q

What do nociceptors do upon distension?

A
  • Nociceptors respond to the stretching of the wall, with the further stretching being potentially damaging.
  • The higher the distention, the higher the frequency firing.
20
Q

What factors can cause inflammation?

A

Injury, irritants, toxins, infection

21
Q

How does a nociceptor respond upon occurrence of inflammation?

A
  • Triggers additional nociceptor activity. RESULT - Pain
  • Positive feedback because the nociceptor releases inflammatory mediators when depolarised
22
Q

Describe nociceptor pathways.

A

Run along with sympathetic nerves and run into the spinal cord via splanchnic nerves

23
Q

Describe how chronic sensitisation of visceral pain pathways is thought to occur in GI disease.

A
  • Positive feedback between inflammation and the release of pro-inflammatory chemicals from nociceptors may contribute to inflammatory bowel disease.
24
Q

What can cause chronic pain?

A
  • Pain pathways can become potentiated, so normal signals from nociceptors are magnified, leading to chronic pain.
25
Q

How is visceral pain different from somatic pain?

A

Somatic pain is very precisely located. This is not the case for visceral pain.

26
Q

Why is somatic pain precisely located?

A

Ordered pathways, allowing for the pinpointing of the location of the pain

27
Q

What is the basis of viscero-somatic convergence?

A

REFERRED PAIN
- If there is pain in the internal organs, it will be felt in a precise location on the surface of the body.

28
Q

What are some characteristics of visceral pain? PART 1

A

Often diffuses and poorly localised.
- has a relatively small number of afferents
- imprecise wiring

Generally ‘referred’ to regions of the body wall due to viscero-somatic convergence

29
Q

What are some characteristics of visceral pain? PART 2

A

Each organ has a characteristic pattern of referral.
- a dermatome is an area of skin supplied by a single spinal nerve sending somatic afferents to each spinal cord segment
- initially, the pain is sent to dermatomes matching the embryonic origin of the organ
- however, this may evolve as other tissues are affected

30
Q

What is the difference between nausea and vomiting?

A

→Nausea is produced by the same stimuli as vomiting
→Nausea may clear up without triggering vomiting
→Vomiting can occur without prior nausea

31
Q

Why do receptors in the gut wall respond to non ingested toxins?

A

→Receptors in the gut wall that detect poison have a blood supply
→are in contact with the circulation so they respond to toxins in circulations

32
Q

Describe the setup of the blood-brain barrier.

A

→Within the brain the capillaries have endothelial walls that have tight junction
→ in other places there are big gaps between the endothelial cells so plasma can enter.
→Substances have to be carried across into and out of the brain tissue

33
Q

What are visceral afferent receptors associated with?

A

→ Afferents that run through the parasympathetic nerves through the vagus and into the brainstem.

34
Q

Where is the area postrema?

A

→sits below the cerebellum and the foramen magnum

35
Q

What happens if pressure goes up in the skull?

A

→If pressure goes up in the skull then it presses the brainstem down through the foramen magnum

36
Q

Why does vomiting occur if pressure goes up in the skull?

A

→The area postrema is sensitive to the change in pressure so vomiting occurs

37
Q

How does the NTS cause antireflux barriers to relax? PART 1

A

→The NTS integrates the information and produces the outputs
→NTS triggers the hypothalamus to increase ADH
→Fluid starts to be conserved
→Sympathetic activity increases

38
Q

How does the NTS cause antireflux barriers to relax? PART 1

A

→Reduced parasympathetic activity to upper GI tract
→Pallor and sweating (result of sympathetic activation)
→NTS coordinates muscular activity
→The antireflux barriers are relaxed

39
Q

Where are the endings of nociceptors found?

A

→ Under the skin

40
Q

What does activation of nociceptors trigger?

A

→The nociceptor triggers activity in a pathway that goes to the primary somatosensory cortex

41
Q

What are the oesophageal nociceptors?

A

→The oesophageal nociceptors have broad spreading axons that make connections.
- The stimulation of receptors can activate a large part of the somato cortex
- Pain appears to be coming from a wide surface

42
Q

What do each of the visceral organs send?

A

→Each of the visceral organs send inputs to the spinal cord segment

SGUL - Physiology 1 (68 decks)

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