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CV > NV > Flashcards

NV Flashcards

1
Q

Specific event involving forceful expulsion of gastric contents in retrograde fashion up the esophagus and out of the mouth

A

Vomiting

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2
Q

Vomiting is not to be confused with _ , which is a passive event, associated with reflux and not typically associated with nausea

A

regurgitation

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3
Q

Feeling of upper abdominal discomfort, typically after eating; May include several symptoms (Bloating, Early satiety, Epigastric pain)Not a specific diagnosis, rather is a cluster of symptoms that can be associated with a variety of causes

A

Dyspepsia

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4
Q

Triggers for n and v converge in which nucleus? What does this nucleus then connect to?

A

nucleus tractus solitarius (NTS); connects to the emetic center (all in medulla)

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5
Q

Triggers for n/v converge on the NTS in the medulla. Where do these triggers arise (4)?

A
  • GI tract (and other visc. organs via vagus)
  • Vestibular system via cerebellum
  • CTZ (area postrema; floor of 4th ventricle)
  • Cerebral Cortex (and limbic system)
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6
Q

What is the function of the chemoreceptor trigger zone (in area postrema)?

A

Samples chemical inputs from the bloodstream outside the blood-brain barrier

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7
Q

List 7 NTs involved in the neural pathway of n/v

A
  • Dopamine
  • Serotonin
  • Histamine
  • Acetylcholine
  • NK-1
  • SP
  • Endocannabinoids
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8
Q

Which NT involved in neural pathways…

Activates emesis center; the final endpoint in activation of vomiting

A

DA

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9
Q

Which NT involved in neural pathways…

Causes dopamine release at the emesis center?

A

SERT

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10
Q

Which NT involved in neural pathways…

inhibit activation of the emesis center>

A

Endocannabinoids

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11
Q

What is the mechanism for development of nausea in a patient with viral gastroenteritis?

A

Viral infection and inflammation of gastric mucosa stimulate afferent nerve fibers in the stomach (via the vagus nerve) to the NTS; Serotonin released by NTS neurons triggers dopamine release in the emetic center (via D2 receptors)

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12
Q

What is the mechanism for development of nausea in a patient with gastric outlet obstruction form a peptic ulcer?

A

Distension of the gastric antrum activates mechanoreceptors which trigger afferent nerve fibers (via the vagus nerve) to the NTS; Serotonin released by NTS neurons triggers dopamine release in the emetic center (via D2 receptors)

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13
Q

Nausea and vomiting can be triggered by many processes affecting the GI tract. Signals communicating these processes are transmitted (for the most part) by the _

A

vagus nerve

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14
Q

Which class of drugs may be used to treat nausea in a patient with viral gastroenteritis?

A

Dopamine Receptor Antagonists (DRAs)

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15
Q

List two types of DRAs

A

phenothiazines; benzamides

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16
Q

In addition to D2 blockade, DRAs also have what type of effects?

A

anticholinergic

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17
Q

List three phenothiazine DRAs

A

Promethazine (Phenergan)
Prochlorperazine (Compazine)
Chlorpromazine (Thorazine)

18
Q

List the prototype Benzamide DRA

A

Metoclopramide (Reglan)

19
Q

Which class of DRAs also stimulate gut motility so should not be used with cases of obstruction (e.g. peptic ulcer) for the risk of perforation?

A

benzamides (Metoclopramide (Reglan))

20
Q

List the major side effects of DRAs

A

those related to DA blockade: dystonia (acutely) and TD (chronic use)
may also cause drowsiness
Benzamides stimulate motility

21
Q

What is the mechanism for development of nausea in a patient with an acute MI?

A

the NTS receives afferent inputs from some other visceral organs, including the pharynx, heart, ureters, and testicles, as well as the parietal peritoneum. These travel via the vagus nerve as well as sympathetic neurons.
Processes affecting these structures such as infection, inflammation, or ischemia, can produce nausea and vomiting

22
Q

What is the mechanism for development of nausea and vomiting in a patient with motion sickeness?

A

Neurons transmit signals from the vestibular system to the NTS; these inputs depend much more on histaminergic (H1-receptors) and muscarinic (M1-receptors) transmission of signals than neurons from other areas

23
Q

What causes motion sickness?

A

Motion sickness: caused by a mismatch between visually observed motion and motion sensed by the vestibular system

24
Q

Which class of drugs may be used to treat nausea in a patient with obstruction (e.g. due to PUD)?

A

DRAs (must use phenothiazidines; benzamides CI as they cause gut motility)

25
Q

Which classes of drugs may be used to treat nausea in a patient with motion sickenss? (2)

A
  • Anticholinergics
  • Antihistaminergics

(DA blockers do not work well for vestibular induced nausea)

26
Q

What is the prototype anticholinergic?

A

Scopolamine

27
Q

List some examples of antihistaminergics (4)

A

Diphenhydramine (Benadryl)
Meclizine
Dimenhydrinate (Dramamine)
Hydroxyzine

28
Q

Antihistaminergics act via blockade of H1-receptors, but also have some _ activity

A

anticholinergic activity.

29
Q

List some side effects of anticholinergics

A

dry mouth/eyes, urinary retention

30
Q

What is the mechanism for development of nausea and vomiting in a patient with chemotherapy-induced nausea and vomiting?

A

Some chemotherapeutic agents can stimulate the chemoreceptor trigger zone (CTZ) in the area postrema in the floor of the 4th ventricle.
They can also cause activation of peripheral afferent sensory nerves by serotonin release, resulting in signals transmitted via the vagus nerve

(These same mechanisms are responsible for most other medication-induced nausea and vomiting)

31
Q

In addition to chemo, list three other toxins that may stimulate the CTZ

A
  • urea
  • excessive acid (DKA)
  • bacterial toxins
32
Q

What neurotransmitters are involved in these symptoms of nausea and vomiting?

Acute onset: e.g. within first 24 hours after beginning chemotherapy

A

Mostly mediated by serotonin (peripherally-released)

33
Q

What neurotransmitters are involved in these symptoms of nausea and vomiting seen with chemotherapy induced n/v?

Delayed onset: begins more than 24 hours after starting chemotherapy

A

Primarily mediated by substance P (in the CTZ)

34
Q

Which classes of drugs may be used to treat nausea in a patient with chemotherapy induced n/v?

A

5HT-3 Receptor (Serotonin) Blockers
Substance P Blockers (blockagde of NK-1 receptors)

Now, these are usually given as premedication prior to initiating chemotherapy

35
Q

List the two serotonin blockers

A
  • Odansentron

- Graniesetron

36
Q

List the proto substance P blocker

A

Aprepitanat (blocks NK-1)

37
Q

What is the mechanism for development of nausea and vomiting in a patient with anticapatory n/v?

A

Results from stimulation of the vomiting center from inputs from the cerebral cortex and limbic system

38
Q

How can posteoperative n/v (related to effects of medications given periopratively) be prevented?

A

Prophylactic Targeting of Serotonin and Substance P (similar to chemo induced n/v)

39
Q

Pregnancy-induced n/v is typically seen in which period of pregnancy?

A

first trimester

40
Q

Mechanisms for Pregnancy-induced n/v are not well-understood but the severity of nausea seems to correlate with _

A

with serum HCG levels

41
Q

Which form of n/v can result from trauma, malignancy/neoplasm, vascular injury, or idiopathic process (e.g. pseudotumor cerebri)

A

Increased ICP n/v

42
Q

What is the difference between the medications used for chemotherapy-induced nausea and those used for motion sickness?

A

target different NTs

CV (2 decks)

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