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P1: GI > Symptoms of GI Disease > Flashcards

Symptoms of GI Disease Flashcards

1
Q

What is emesis?

A

→Expels contents of upper GI tract via mouth
→Forceful (regurgitation, reflux)
→Complex, coordinated reflexive events
→Associated with relief

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2
Q

What is the difference between nausea and vomiting?

A

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

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3
Q

What causes nausea and vomiting?

A 
→GI infection
→Poisoning - contaminated food
→Emotional upset
→Obstruction
→GI disease
→Raised intracranial pressure
→Metabolic disturbance
→Other people being sick
→Travel sickness
→Excessive eating
→Excessive alcohol
→Pregnancy
→I.V drugs
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4
Q

What are the advantageous causes of vomiting?

A

→Poisoning
→excessive alcohol
→ excessive eating
→obstruction

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5
Q

What do chemoreceptive cells in the gut respond to?

A

→Irritants
→Inflammatory mediators
→Bacterial toxins

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6
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
→ non ingested toxins will have the same effect e.g chemotherapy, metabolic disturbance or systemic infections.

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7
Q

What is the chemoreceptor trigger zone?

A

→Area postrema in the brainstem

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8
Q

Why can the area postrema detect toxins in the blood?

A

→Blood-brain barrier is leaky

→Chemoreceptors can detect toxins in the blood

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9
Q

Describe the set up 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
→This is a protective mechanism so the brain is not in contact with most things that are transported

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10
Q

What is the vestibular system?

A

→The organ of balance but also a potent trigger for emesis

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11
Q

What does poisoning produce in the vestibular system?

A

→Poisoning is thought to produce aberrant activity in vestibular neural pathways

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12
Q

What are receptors in the vestibular system sensitive to?

A

→ chemicals

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13
Q

Why can traveling cause nausea?

A

→Travelling can cause nausea because it produces unnatural patterns of activity in the vestibular system.

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14
Q

What does aversion hardwire?

A

→Aversion may hardwire avoidance

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15
Q

What are the anti poison defenses coordinated by?

A

→The anti poison defenses are coordinated by the nucleus tractus solitarius

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16
Q

Where is the NTS found and what does it do?

A

→Found in the medulla of the brainstem

→Integrates cardiac, respiratory and GI functions

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17
Q

What are visceral afferent receptors associated with?

A

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

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18
Q

Where is the area postrema?

A

→sits below the cerebellum and the foramen magnum ( where the spinal cord is)

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19
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

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20
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

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21
Q

What do higher centres in the brain do?

A

→Things that make you sick in the past

→Other people being sick

22
Q

How does the NTS cause anti reflux barriers to relax?

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

23
Q

What are the 3 phases of nausea?

A

→Reduced mixing and peristalsis (reduction of parasympathetic)
→Proximal stomach relaxes (distensible)
→Giant retrograde contraction

24
Q

Why is there reduced mixing and peristalsis during vomiting?

A

→Prevents toxins from being carried further through the system

25
Q

Why does the proximal stomach relax during vomiting?

A

→Prepares stomach to receive additional contents

26
Q

Why are there giant retrograde contractions during vomiting?

A

→Returns upper intestinal contents to stomach

27
Q

What are the 2 phases of vomiting?

A

→ Retching

→Vomiting

28
Q

Describe what happens during retching?

A

→NTS triggers the phrenic nerve
→Coordinated contractions of abdominal muscles and diaphragm
→Waves of high pressure in abdomen
→Compresses stomach but anti-reflux barriers are intact so there is no expulsion

29
Q

Describe what happens during vomiting

A

→Esophageal sphincters and crural diaphragm relax

→Further waves of contraction expel stomach contents

30
Q

What do nociceptors respond to?

A

→Distension
→Inflammation
→Muscle spasm

31
Q

What happens when the gut is stretched and when does the brain produce pain?

A

→The more stretched the gut is the more action potentials are produced per second
→The brain produces pain when the frequency of action potentials increases

32
Q

What causes additional action potentials in nociceptors?

A

→ Inflammation

33
Q

What do nociceptors respond to?

A

→Nociceptors respond to inflammatory mediators

34
Q

What happens to nociceptors when they are depolarized?

A

→Release pro-inflammatory chemicals when depolarized

35
Q

What does continuous depolarization of nociceptors lead to?

A

→This causes a positive feedback loop that can contribute to inflammatory bowel disease
→Abnormal activity can potentiate synapses magnifying the nociceptor signals further
→Can become self-sustaining leading to chronic pain with no obvious cause

36
Q

What kind of pain is somatic pain?

A

→ precisely localized

37
Q

Where are the endings of nociceptors found?

A

→ under the skin

38
Q

What does activation of nociceptors trigger?

A

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

39
Q

What does the PSC have?

A

→The PSC has a map of the body

→The inputs to the somatic ‘map’ are discrete

40
Q

What is visceral pain?

A

→Visceral pain is referred to the surface of the body

41
Q

What pathway does visceral pain have?

A

→ shares the same pathway as somatic nociceptors

42
Q

What kind of pain is visceral pain?

A

→imprecise

43
Q

What are the oesophageal nociceptors?

A

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

44
Q

What can the stimulation of visceral nociceptors activate?

A

→The stimulation of receptors can activate a large part of the somato-cortex

45
Q

Where does pain appear to be coming from in visceral nociceptors?

A

→Pain appears to be coming from a wide surface

46
Q

What is a characteristic of viscerosomatic convergence?

A 
→Referred to regions of the body wall
→Due to viscerosomatic convergence
→Diffuse and poorly localized
→Relatively small number of afferents
→Imprecise wiring
47
Q

What does each organ have?

A

→characteristic pattern of referral

48
Q

What are dermatomes?

A

→Dermatomes are regions of the body sending somatic afferents to each spinal cord segment

49
Q

What do each of the visceral organs send?

A

→Each of the visceral organs send inputs to the spinal cord segment that correlates with the somite

50
Q

Describe the pattern of referral

A

→Diaphragm and peritoneum to C3-5, via phrenic nerve
→Gall bladder to T9 via greater splanchnic nerve
→Infections in the gall bladder often spread to the parietal peritoneum and diaphragm
→Afferents synapse in segments matching the embryonic origin of each organ

P1: GI (15 decks)

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