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Pharm Exam 5 -- Smooth Muscle, GI and OTC > GI (pt 4/5) PONV > Flashcards

GI (pt 4/5) PONV Flashcards

1
Q

What are some conditions that can cause N/V?

A

Adverse effects from medications
Systemic disorders
Infections
Pregnancy
Vestibular dysfunction
↑ICP or CNS infection
Peritonitis
Hepatobiliary disorders
Chemo/radiation (XRT)
GI obstruction
Pain/Anxiety/Stress
Noxious stimuli (Sights, smells, tastes)

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2
Q

What receptors are found in the vomiting center (Nucleus of Tractus Solitarius)?

A

H1 receptors
M1 receptors
NK1 receptors
5-HT3 receptors

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3
Q

What are the 4 sources of input to the Vomiting Center?

A

-Chemoreceptor trigger zone
-Vestibular System
-GI Tract
-CNS

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4
Q

What receptors are found in the Chemoreceptor trigger zone (Area Postrema)?

A

Chemoreceptors
D2 receptors
NK1 receptors
5-HT3 receptors
H1 ?
M1 ?

CTZ is located outside the BBB. Prevents poisons and stuff from getting into the brain.

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5
Q

What receptors are found in the Vestibular System?

A

Motion sickness via cranial nerve VIII:
-H1
-M1

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6
Q

What makes up CNS input to the Vomiting Center?

A

Cortex
Thalamus
Hypothalamus
Meninges

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7
Q

What receptors around found in the GI tract that contribute to the Vomiting Center?

A

Mechanoreceptors
Chemoreceptors
5-HT3 receptors

CN IX (GP - gag reflex) and CN X (Vagus).

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8
Q

What does the Vomiting (emetic) center consist of?

A

The emetic center consists of various scattered groups of neurons that control the components of vomiting through interactions with cranial nerves VIII, IX, and X, and neural networks in the nucleus tractus solitarius.

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9
Q

Sensory input from which areas of the body can activate the emetic center?

A

1) Afferent impulses from the pharynx, GI tract, and mediastinum and direct stimulation from the cerebral cortex (anticipation, fear, memories)
2) Signals from the sensory organs (disturbing sites, smells, pain)
3) Input from the chemoreceptor trigger zone in the fourth ventricle
4) Signals from the vestibular apparatus of the inner ear can all stimulate the emetic center to initiate vomiting.

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10
Q

What is the Chemoreceptor Triggering Zone (CTZ)?

A

Located outside of the BBB, so sensitive to chemicals in the blood.
-Located in the area postrema in the floor of the 4th Ventricle.

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11
Q

What types of substances can stimulate the Chemoreceptors?

A

Opioids, analgesics, chemotherapy agents, poisons, Substance P

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12
Q

What are examples of antagonist drugs to the receptors in the Chemoreceptor triggering zone?

A

-5HT3 –Zofran
-H2-Promethazine, compazine
-Muscarinic—Atropine , Phenergan, compazine
-Dopamine- Droperidol, Haldol, Compazine, Reglan
-NK-1 aprepitant

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13
Q

Which cranial nerves report to the vomiting center?

A

VIII, IX, and X

Vestibulocochlear (8)
Glossopharyngeal (9)
Vagus (10)

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14
Q

What Neural Networks contribute to the Vomiting Center?

A

Neural networks from:
Nucleur tractus solitaris- (afferent sensory cell bodies in brainstem) it has high concentrations of M1,H1, NK1, 5HT3 receptors.

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15
Q

Where does sensory/afferent input to the Vomiting Center come from?

A

CNS-Smells, sight, pain, fear, anxiety, memories

GI tract-mechanoreceptors, chemoreceptors, 5HT3-R

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16
Q

If you block all 4 pathways (CNs, Neural Networks, CNS/GI tract afferent signals, and input from the CTZ), you will not get vomiting, except for when given _____.

A

Block all these pathways you should not get vomiting. However, it will not prevent vomiting when given IPECAP syrup which will cause severe irritation and vomiting.

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17
Q

What is Ipecap Syrup?

A

Ipecap syrup was the front line tx for treating acute poisoning by having fast acting forceful vomiting. However, newer studies show charcoal binding to be more effective at keeping blood levels from getting too high from poison. Risks for ipecap was esophagitis and aspiration pneumonia.

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18
Q

What is the MOA of Serotonin (5HT3) Antagonists?

A

Selectively block serotonin 5-HT3 receptors in the:
-vomiting center
-CTZ centrally
-peripherally on extrinsic intestinal vagal and spinal afferent nerves.

19
Q

Serotonin (5HT3) Antagonists have a greater ____ effect than a ____ effect.

A

Antiemetic is greater than anti-nausea. May still be nauseated, but they won’t vomit

20
Q

When should you administer Serotonin Antagonists?

A

Best given at the end of surgery. Some are long acting. Good for post-discharge N/V.

21
Q

What are the clinical uses for Serotonin (5HT3) Antagonists?

A

-Chemotherapy induced N/V
-PONV and Post-radiation N/V
-Post Discharge N/V (PDNV)

22
Q

Which Serotonin (5HT3) Antagonist has a half-life of 40 hrs (second gen)?

A

Palonosetron

23
Q

Which Serotonin (5HT3) Antagonist is no longer used due to QT issues?

A

Dolasetron

24
Q

Which Serotonin (5HT3) Antagonist is the GOLD STANDARD for PONV and Post-radiation N/V?

A

Ondansetron (Zofran)

25
Q

T/F: Combination therapy enhances the efficacy of Serotonin (5HT3) Antagonists.

A

True: usually combined with Corticosteroids & NK1-receptor antagonist.
-Ex: give steroid at the beginning, and Zofran at the end.

26
Q

What are the most commonly reported adverse effects associated with Serotonin 5-HT3 Antagonists?

A

Headache
Dizziness
Constipation

27
Q

What is important to know about Serotonin 5-HT3 Antagonists and patients with cardiac issues?

A

-Small, statistically significant prolongation of the QT interval in doses of Zofran 16mg (ondansetron) for chemo.
-Should not be administered to patients with prolonged QT or with other medications that may prolong the QT interval-(block some cardiac sodium channels)
-Risk of cardiac arrhythmias and Torsades de Pointes

28
Q

95% of Serotonin is secreted in the ____. It modulates the _______ nervous system.

A

95% of Serotonin is secreted in the gut. It modulates the Enteric Nervous System.

29
Q

What should you do with Serotonin 5-HT3 Antagonist administration in a patient with liver failure?

A

Reduce the dose.

30
Q

What drug interactions occur with Serotonin 5-HT3 Antagonists?

A

No significant interactions reported.

31
Q

How are Serotonin 5-HT3 Antagonists metabolized?

A

All undergo some metabolism by the hepatic Cytochrome P450 system.
-Potentially reduced hepatic clearance & altered 1/2 life.

32
Q

What is the MOA of corticosteroids in the use of PONV prevention?

A

Unknown MOA. Appear to enhance the efficacy of 5-HT3 Receptor antagonists in prevention of N&V

33
Q

Why should you give corticosteroids after induction?

A

Female patients will complain of heat and burning pain sensation in perineal region, pts may be embarrassed and not report it.

34
Q

What patient condition is contraindicated with the administration of corticosteroids for N/V?

A

C/I in brittle diabetics - increases BG for up to 6-12 hrs

35
Q

T/F: One dose of Corticosteroids significantly decreases wound healing.

A

False; one dose has no effect on wound healing.

36
Q

How do Neurokinin Receptor Antagonists have N/V prevention effects?

A

Antiemetic properties mediated through central blockade in the area postrema

37
Q

What are the two drug examples for the Neurokinin Receptor Antagonists?

A

-Aprepitant (-emend)
-Fosaprepitant

38
Q

What is Aprepitant?

A

A Neurokinin Receptor Antagonist.
-Oral formulation – 65% oral bioavailability
-Highly selective NK1-receptor antagonist
-Crosses blood-brain barrier to occupy brain NK1 receptors
-Serum t ½ = 12h, however DOA=24 hours!
-Hepatic metabolism – CYP3A4

39
Q

What is Fosaprepitant?

A

A Neurokinin Receptor Antagonist.
-IV formulation
-Converted within 30 minutes after infusion to Aprepitant

40
Q

What are the clinical uses for the Neurokinin Receptor Antagonists?

A

Prevention of acute & delayed N&V from highly emetogenic chemotherapeutic regimens

41
Q

What combo therapy is used with the Neurokinin Receptor Antagonists?

A

Used in combination with 5-HT3 receptor antagonists and corticosteroids. Effective in 80-90% of patients.

42
Q

What are the adverse effects of the Neurokinin Receptor Antagonists (Aprepitant)?

A

-Fatigue, dizziness, and diarrhea
-Decreases INR in patients taking warfarin (!! blue box!)
-Metabolized by CYP3A4.

43
Q

What is important to know regarding Aprepitant (Neurokinin Receptor Antagonist) and other drugs metabolized by the CYP3A4?

A

Aprepitant may inhibit the metabolism of other drugs metabolized by this pathway (Chemotherapeutic agents- multiple use this pathway).
-Drugs that inhibit CYP3A4 metabolism may increase aprepitant plasma levels
-Examples: Ketoconazol, Ciprofloxacin, Clarithromycin, Ritonavir, Nelfinavir, Verapamil, and Quinidine

Pharm Exam 5 -- Smooth Muscle, GI and OTC (10 decks)

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