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1. GI > Physiology of Nausea and Vomiting > Flashcards

Physiology of Nausea and Vomiting Flashcards

1
Q

What is Nausea?

A

sinking feeling, doesn’t necessarily lead to vomiting, pallor, excessive sweating
relaxation of the stomach and lower oesophagus, upper intestinal contractions, forcing reverse peristalsis into the stomach

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2
Q

What is Vomiting/Emesis?

A

forceful expulsion of stomach contents through the mouth/nose by contraction of the abdominal muscles and diaphragm

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3
Q

What is Retching?

A

repetitive reverse peristalsis of the stomach and oesophagus without vomiting
Forceful, involuntary contraction of the abdominal muscles and diaphragm
Increased saliva can neutralise the acid chyme coming into the oesophagus

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4
Q

What is Regurgitation?

A

the effortless movement of swallowed food contents/ stomach acid back into the mouth

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5
Q

What are the two stimulis for vomiting?

A 
Systemic toxins (e.g. cytotoxic drugs)  
Toxic materials in gut lumen (e.g. bacterial toxins, salts of heavy metals, ethanol)
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6
Q

What do the two stimulus stimulate?

A

Enterochromaffin cells in mucosa releasing 5-HT mediators

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7
Q

What does the release of 5-HT mediators cause?

A

Depolarization of sensory afferent terminals in mucosa (e.g. via 5-HT3 receptors)
Action potential discharge in vagal afferents to brainstem (CTZ and NTS)
Co-ordination of vomiting by the ‘vomiting centre’

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8
Q

What are the CTZ and NTS?

A

CTZ - chemoreceptor trigger zone within the area postrema (AP)
NTS – nucleus tractus solitarius

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9
Q

What do absorbed toxic material and drugs in the blood stimulate to cause vomiting?

A

CTZ within the AP of the brainstem

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10
Q

What do mechanical stimuli, pathology within the GI tract or other viseral organs stimulate to cause vomiting?

A

Vagal afferents to the brainstem CTZ and NTS

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11
Q

What does the vestibular system (e.g. motion sickness) stimulate to cause vomiting?

A

CTZ

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12
Q

What does stimuli in the CNS like pain, odours, repulsive sites stimulate to cause vomiting?

A

Cerebral cortex, lumbic system - i.e. straight to the vomiting centre

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13
Q

What are the steps of vomiting?

A
  1. Suspension of intestinal slow wave activity
  2. Retrograde contractions from ileum to stomach
  3. Suspension of breathing (closed glottis - prevents aspiration)
  4. Relaxation of LOS- contraction of diaphragm and abdominal muscles compresses stomach
  5. Ejection of gastric contents through open UOS
  6. Repeats of the cycle

Vomiting does not involve stomach contractions, it is due to an increased intraabdominal pressure

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14
Q

What is the Vomiting centre?

A

a group of interconnected neurones within the medulla that receives input from the NTS

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15
Q

What is an efferent?

A

leaves the CNS and goes to peripheries

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16
Q

What are the autonomic/somatic efferents that preceed vomiting?

A

increased heart rate and force
increased salivation
pallor, cold sweating
constriction of bladder and anus

17
Q

What are the vagal efferents that occur during vomiting?

A

Shortening of the oesophagus
Proximal relaxation of the stomach
Giant retrograde contraction of the small intestine

18
Q

What are the somatic neuron effects that happen during vomiting?

A

diaphragm contraction

contraction of the anterior abdominal muscle

19
Q

What are the consequences of severe vomiting?

A

Dehydration
Loss of gastric protons and chloride – causes hypochloraemic metabolic alkalosis
Metabolic acidosis may occur due to duodenal bicarbonate loss
Hypokalaemia - potassium excretion by kidneys
Aspiration of the vomitus into the air passage and lungs
Mallory-Weiss tear due to profuse vomiting that tears the inner mucosal walls of the oesophagus

20
Q

What drugs and radiation can induce vomiting?

A

cancer chemotherapy (cisplatin, doxorubicin) and radiotherapy. Chemotherapy drugs release 5-HT and substance P from enterochromaffin cells in the gut

Operations involving the administration of general anaesthetic (post operative nausea and vomiting)

Levodopa used in Parkinson disease (dopamine agonist properties have a high density of D2 receptors which are prevalent in the CTZ)

Morphine and other opiate analgesics

Cardiac glycosides (digoxin)

Drugs enhancing 5-HT function – SSRIs, 5HT, receptors prevalent in the CTZ)

21
Q

What are the major classes of anti-emetic drugs?

A 
Dopamine antagonists
5HT3-Receptor Antagonists
Muscarinic receptor antagonist
H1 Antihistamines
Anticholinergics
Adjuvant Antiemetics
Prokinetic Drugs

22
Q

Describe the names and action of dopamine antagonists?

A

Prochlorperazine, droperidol,trifluoperazine chlorpromazine, haloperidol, levomepromazine
Choose domperidone because it cannot cross the BBB so the brain is protected and it is specific targeting

act centrally by blocking the chemoreceptor trigger zone
available as rectal suppositories, buccal tablets

Prophylaxis/treatment of nausea and vomiting associated with neoplastic disease, radiation sickness, and drug-induced emesis

23
Q

Describe the names and action of 5HT3-Receptor Antagonists?

A

Granisetron, ondansetron, palonosetron, Setron

block 5HT3 receptors in the GIT and CNS.

Frequent side effect is constipation and headache, not effective in motion sickness

24
Q

Describe the names and action of muscarinic receptor antagonists?

A

To treat motion sickness
Hyosine and scoplamine
Prolonged duration of action

25
Q

Describe the names and action of H1 Antihistamines?

A

Promethazine, cyclizine, cinnarizine
Blockade of H1 receptors in vestibular nuclei and NTS Cause CNS depression and sedation

Many agents exert an additional Antimuscarinic effect that probably contributes to their activity

Useful in Motion sickness (prophylaxis and treatment) morning sickness, PONV

26
Q

Describe the names and action of Anticholinergics?

A

Hyosine (scopolamine), Dicyclomine
Block muscarinic receptors in vestibular nuclei, NTS, vomiting centre
Motion sickness
Frequent side effects include: blurred vision, urinary retention, dry mouth, sedation

27
Q

Describe the names and action of Prokinetic drugs?

A 
GI Tract 
-Increase Gastric peristalsis
-Increase Lower Esophageal sphincter tone
CNS 
- blocks D2 receptors in CTZ

Metoclopramide (antiemetic, GORD, Migraine)
Domperidone (does not cross the blood-brain barrier)

28
Q

Name some Ajuvant Antiemetics?

A 
Role in CINV
NK1 receptor antagonists
- antagonism of substance P
Corticosteroids
- Dexamethasone, methylprednisolone 
- Augmentate the effect of ondansetron & metoclopramide
Benzodiazepines 
- Lorazepam, diazepam
- No intrinsic antiemetic action 
- Sedative, antianxiety, amnesia inducing effect
Cannabinoids
- Nabilone, Dronabinol
- Sedation, Hallucinogenic, dry mouth

1. GI (61 decks)

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