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nausea, vomiting and pain Flashcards

1
Q

What is Nausea

A

It is a sensation

It is personal and self reported
It is associated with physiological changes in the body
It makes the person feel unpleasant
It triggers the feeling of aversion in a person - This is a strong feeling of dislike towards something

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2
Q

What is Vomiting

A

It is a physical act

It is called emesis in medicinal terms
It expels contents of the upper GI tract via the mouth
It is forceful (unlike regurgitation and reflux)
There are complex coordinated reflex that lead to vomiting
It gives the person a sense of relief

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3
Q

What is the relationship between

Nausea and Vomiting?

A

Nausea is produced by the same stimuli as vomiting

Nausea is generally a prodrome (ie premonitory symptom) of vomiting hence warning

Nausea may clear up without triggering vomiting
AND vomiting can occur without prior nausea via powerful stimulus

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4
Q

Causes of nausea and vomiting:

A 
Poisoning (e.g. contaminated food, poisonous plants, chemical agents)
Gastroenteritis (e.g. norovirus)
Excessive alcohol
Pregnancy
Excessive eating
Travel sickness
Other people sick
Metabolic disturbance
Drugs (e.g. morphine, chemotherapy)
GI disease (e.g. gastritis, kidney stones, obstruction)
Emotional upset
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5
Q

Protection against ingested toxins

Taste and smell

A

Taste and smell
• these are receptors in the olfactory system
• they potentially prevent ingestion of harmful chemicals by detecting them
• they bind to chemicals and produce a dislike of the flavor (produce a bitter sensation)
- we have a built in dislike of bitter flavor

  • children are wary of novel flavors
  • we also learn from our elder what flavors and foods are safe

• people who have vomited to a specific flavor may have aversions towards that flavor

  • people undergoing chemotherapy may have aversions to perfectly good food
  • chemotherapy usually leads to vomiting
  • a person may have aversion
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6
Q

Protection against ingested toxins

Gastric & upper GI afferents

A

We can potentially expel harmful agents before they have much of a chance to be absorbed.

It is associated with chemoreceptive cells (that are in well perfused tissue, so can also respond to contaminants in blood circulation) that respond to:

Irritants, bacterial toxins, inflammatory mediators, some potentially harmful chemicals.

As stated in the brackets above, non-ingested toxins in the circulation can also act here e.g. chemotherapy, systemic infection, metabolic disturbance

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7
Q

Protection against ingested toxins

Chemoreceptor trigger zone

A

chemoreceptor trigger zone
which is the area postrema in the brain stem (medulla)

The blood brain barrier is leaky and chemoreceptors can detect toxins in the blood. But, they are also influenced by systemic infection, metabolic disturbances and therapeutic drugs.

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8
Q

Protection against ingested toxins

Vestibular system

A

it is the organ of balance but also a potential trigger of emesis.

It may be activated by toxins in the blood, or by disequilibrium resulting form poisoning.

But it also triggers nausea and vomiting in response to unnatural motion, as it assumes poison may have been ingested.

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9
Q

Mechanisms of Nausea and Vomiting

A

The nucleus tractus solitarius controls all the activity that needs to happen to expel food from the GI tract

This structure is located in the medulla of the brain stem
It integrates cardiac, respiratory, and GI functions

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10
Q

Mechanisms of Nausea and Vomiting

Visceral afferents

A

that could trigger N+V include toxins, irritants and distension.

The receptors can be found in the fundus and duodenum.

The afferents take this info to the medulla. (NTS)

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11
Q

Mechanisms of Nausea and Vomiting

area postrema

A

Signals from the area postrema also come into the NTS

This is located on the base of the 4th ventricle of the brain
Toxins detected here will send signals to the NTS causing vomiting

If you have raised intracranial pressure, it causes serious nausea + vomiting -> increased intracranial pressure will mean that the brain swells, pressure squeezed out of forama magnum and the brain pressed down into apenture. The area postrema and NTS gets pressed down

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12
Q

Mechanisms of Nausea and Vomiting

Vestibular system

A

Signals from the vestibular system also go to the NTS

Toxins disrupt vestibular receptors and therefore cause imbalance in the body
Unnatural movements will also stimulate the receptors here
This sends signals to the NTS causing vomiting

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13
Q

Mechanisms of Nausea and Vomiting

Higher centres

A

Higher centers in the brain also detect signals and send to the NTS

• higher centers process what is going on around the world and may detect observable emesis stimuli
• stimuli may be visual, emotional or aversive
• stimuli in these centers also lead to anticipatory nausea and vomiting (eg anticipating
chemotherapy)

• they send signals to the NTS causing vomiting

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14
Q

Mechanisms of Nausea and Vomiting

A

Fibres from the area postrema (detecting toxins in the blood), abdominal afferents travelling by the vagus nerve (detecting toxins, irritants, distension in the gut), higher centres of the brain (bringing aversive and emotional stimuli) as well as the fibres from the vestibular system (detecting toxins or disequilibrium) travel to the NTS where the information is processed.

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15
Q

5HT3 receptors

A

The receptors involved in the area postrema and the abdomen are 5HT3 receptors
• nausea and vomiting due to stimulation of the receptors in the area postrema and the
abdomen can be reduced by using 5HT3 antagonists

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16
Q

How Does Nausea Happen

A

• The NTS sends signals to the frontal cortex and
some limbic area causing the sensation of
nausea

• The NTS also sends signals to the
hypothalamus which increases secretion of
ADH/vasopressin

• ADH will retain water as fluid will be lost while
vomiting

• The NTS will also send signals via autonomic
afferents to various organs leading to:
• changes in gut motility
- reducing movement in the gut so less of the
substance passes through

• vasoconstriction of gut will reduce the ability
of the gut to absorb toxins
• sweating and salivation (salviation will give fluid lining for mucosa to protect it from acid)

  • The motility of the gut reduces
  • prevents toxins from being carried further through the system
  • The proximal stomach relaxes
  • this prepares stomach to receive additional contents in the next step (from upper part of SI)
  • Giant retrograde contraction
  • sweeps up from mid-small intestine
  • returns upper intestinal contents to stomach

• All the above processes are under parasympathetic control via the vagus nerve

17
Q

How Does Vomiting Happen

A

• All the processes mentioned above for nausea happen

• There is retching (dry heaves)
There is coordinated contraction of the abdominal muscles and diaphragm by the somatic
and phrenic nerves

There are now waves of high pressure in the abdomen

The stomach gets compressed but there are anti reflux barriers (esophageal sphincters and
crural diaphragm) which do not allow the food to leave the stomach

• Vomiting takes place
The esophageal sphincters and crural diaphragm relax

There are further waves of contraction which lead to expulsion of food content of the
stomach

18
Q

Why Vomit in Certain Situations

A

• Poisoning (contaminated food, poisonous plants, chemical agents)
to remove harmful substances detected by chemoreceptors

• Gastroenteritis (noravirus)
to remove toxins produced by virus detected by chemoreceptors

• Excessive alcohol
is poisonous and will be detected by chemoreceptors

• Pregnancy
certain chemicals and hormones are produced during pregnancy which stimulate the chemoreceptors

• Emotional upset
this is done through the higher centers of the brain

• Excessive eating
evolutionary so that early man could re-eat undigested matter

• GI diseases (gastritis, kidney stones, obstruction)
this is so that food doesn’t go through to obstructed area

• Raised intracranial pressure
pressure presses down on the NTS

• Drugs
poisonous detected by chemoreceptors

• Metabolic disturbance

• Other people being sick
people usually eat in groups so it can be a precautionary measure to prevent poisoning from food being eaten by the group

Travel sickness
• stimulates the vestibular system in the same way as poisons do

19
Q

Visceral Pain

A

Visceral pain is caused by stimulation of nociceptors
• most GI nociceptor afferent axons run in the greater and lesser splanchnic (sympathetic)
nerves

  • these nerves go to the thoracic segments
  • pain is a result of activation of these nociceptors
20
Q

Receptors for visceral pain

A

The sensory receptors for pain are known as “nociceptors” (these are both arc stretch receptors and chemoreceptors).

Nociceptors respond to “noxious” stimuli, such as—

Distension
Inflammation
Ischaemia 
Traumatic injury
Muscle spasm

Most GI nociceptor afferent axons run in the sympathetic nerves (the greater and lesser splanchnic nerves)

21
Q

Receptors for visceral pain

Distention

A

distention - there are two types of afferents that cause pain:

  • wide dynamic range cell
    they respond to all levels of distention non pathological gut distention leads to low frequency afferents
    these low level signals are use for local control
    the low frequency afferents are not noticeable and are ignored by the brain so do not result in pain
    as the frequency gets really high (during pathological levels of distention) the brain realizes there is something wrong and sends signals for pain
  • nociceptor specific cell
    these only respond to pathological levels of distention
    as soon as these start firing the brain interprets that something is wrong resulting in pain
22
Q

Receptors for visceral pain

Inflammation

A

inflammation
- nociceptors respond to inflammatory mediators such as: injury, irritants, toxins, infections and autoimmunity

  • on response to these mediators, the receptors depolarize and send APs to the CNS
  • nociceptors also begin to produce their own inflammatory mediators as a response to stimulation by
    inflammatory mediators (positive feedback) thus producing more inflammation
  • inflammation makes the nociceptors hypersensitive
  • signals from nociceptors are now fired at even normal levels of distention
  • the brain interprets the lower level of distention as damaging
  • therefore now the normal function of gut causes pain
  • this may also result in chronic pain
  • due to the hypersensitivity of the nociceptors normal distention while digestionn becomes painful
  • prolonged inflammation will lead to this normal level of distention becoming permanently painful
  • this is because new synapses and connections will be made which will result in normal levels of distention being detected by the brain as abnormal
23
Q

somatic pain is precisely localised

A

E.g pinprick will activate somatic nocioceptors which will be projected to the spinal chord and from that location enter the spinal chord at lets say T3.

Synapse pathways to carry info to somatosensory cortex and this sends info to precise region of somatosensory homunculus map so there is a highly localised sensation of pain

24
Q

Viscero-somatic convergence aka referred pain

A

Visceral nocioceptors don’t have own pathways to somatosensory cortex so they piggyback onto the somatic pathways hence they will send an axon down and synapse at same pathway activated by somatic nocioceptor. This will produce sensation in the position of the somatic location hence is called referred pain

BUT there are also very less number of afferents
and the wiring of the afferents is imprecise SO the visceral nocioceptor can terminate between few different terminals which will mean there is pain over an extended part of the mao and a wide region so the pain is poorly localised.

25
Q

Each organ has a specific pattern of referral

A

initially the site of the pain is on the dermatome it was linked to in the embryo

• this may change as other tissues are affected
- eg gall bladder inflammation pain leads to pain in the T9 dermatome
- inflammation in the gall bladder + inflammation in the diaphragm will lead to pain in the
shoulder

26
Q

Characteristics of visceral pain

A

Generally “referred” to regions of the body wall
due to viscero-somatic convergence

Often diffuse and poorly localised
relatively small number of afferents
imprecise wiring

Each organ has a characteristic pattern of referral
initially to dermatomes matching the embryonic origin of the organ
but may evolve as other tissues are affected

GI (19 decks)

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