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GI- Week 6 > Fitzaekerly: Antiemetics and Treatments for IBD > Flashcards

Fitzaekerly: Antiemetics and Treatments for IBD Flashcards

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1
Q

What sensory inputs cause vomiting?

A
  1. Local irritation of GI tract → vagal & sympathetic afferents modulated by action on 5HT3 receptors → solitary tract nucleus (STN) and CTZ → vomiting center
  2. Inner ear (motion sickness, aminoglycoside abx) → cerebellum → vomiting center
  3. Glossopharyngeal & trigeminal afferents → STN → vomiting center (a.k.a. gag reflex)
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2
Q

What are blood borne emetics?

A

chemical agent irritates small intestine if oral or interacts w/ cells in the CNS outside the BBB>
stimulates vomiting center

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3
Q

What is anticipatory vomiting?

A

Learned response to chemo drugs that is controlled by higher centers that project into the vomiting center

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4
Q

What receptors are fundamental to the vomiting process? Where are they located?

A

5HT receptors

  • Enteric system
  • Chemoreceptive trigger zone
  • Solitary tract nucleus
  • Vomiting center
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5
Q

What are important anti-emetic drugs?

A

5HT antagonists

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6
Q

What receptors are OUTside the BBB in the GI tract?

A

5HT3 in the GI tract

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7
Q

What receptors act OUTside the BBB in the CTZ?

A

D2

Opiods

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8
Q

What receptors are located inside the BBB?

A

M1
H1
NK1
Cannabinonid

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9
Q

What receptors do emetics like L-dopa and apomorphine act on?

A

D2

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10
Q

What receptors do emetics like opiates act on?

A

opioid receptors

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11
Q

What drug acts on 5HT3 receptors and is used for chemotherapy?

A

“setrons”

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12
Q

What drugs are antiemetics that act on D2 receptors?

A

DROPERIDOL, METOCLOPRAMIDE
PROCHLORPERAZINE, PROMETHAZINE
THIETHYLPERAZINE

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13
Q

What drugs are antiemetics used for motion sickness that act on M1?

A

scopolamine

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14
Q

What drugs are antiemetics used for motion sickness that act on H1?

A

DIMENHYDRINATE, DIPHENHYDRAMINE, MECLIZINE

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15
Q

What antiemetics act on NK1 and are used for chemotherapy?

A

APREPITANT, FOSAPREPITANT

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16
Q

What drugs are antiemetics that act on corticosteroid receptors?

A

DEXAMETHASONE, METHYLPREDNISOLONE

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17
Q

What drugs are antiemetics that act on cannabinoid receptors?

A

DRONABINOL, NABILONE

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18
Q

What is used for GI contamination?

A
  1. Toxin binding (activated charcoal)
  2. cathartics (polyethylene glycol-electrolyte solution)
  3. emetic agents *(ipecac)
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19
Q

When would you use toxin binding activated charcoal and how does it work?

A

Used for upper GI Absorbs (binds to) many drugs and poisons d/t large surface area

Must be given in ratio of at least 10:1 (charcoal:toxin) by weight

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20
Q

What is toxin binding activated charcoal NOT good for?

A

Does not bind Fe, Li, or K

Binds alcohols and cyanide poorly

Not useful in cases of poisoning d/t corrosive mineral acids or bases

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21
Q

What are polyethelene glycol-electrolyte solutions used for? How does it work?

A

Lower GI problems or before endoscopic procedures

Removes toxins and reduces absorption, • May hasten removal of toxins and reduce absorption

*Whole bowel irrigation can enhance decontamination following ingestion of Fe tablets, enteric coated medicines, illicit drug-filled packets and FBs

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22
Q

How does ipecac work?

A

Local irritant effects and acts on CTZ (15-30 mins)> vomit if drug hasn’t effected the stomach (emesis may not occur if stomach is empty)

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23
Q

What is ipecac not good for?

A

dangerous is poison is corrosive, a petroleum distillate or a rapidly acting convulsant

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24
Q

What is the key mechanism for many antiemetics?

A

sedation

*more effective at PREVENTING vomiting than stopping it

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25
What are the 7 types of antiemetic drugs?
``` 5HT3 antagonists NK antagonists antimuscarinics Antihistamines D2 antagonists Cannabinoids Corticosteroids ```
26
Dolasteron, Granisteron, Ondansetron and palonsetron are...
5HT3 Antagonists (end in "etron")
27
What are the best antiemetics available that are commonly used to treat N/V from chemo?
Dolasteron, Granisteron, Ondansetron and palonsetron
28
What is the MOA of 5HT3 Antagonists?
BLOCK: peripheral 5HT3 receptors in GI tract on 1o afferents receptors in CTZ & VC
29
What is the TU for 5HT3 Antagonists?
Prevent and treat chemo induced vomiting *esp ACUTE phase if given 30 mins before chemo (not good for motion sickness or delayed phase)
30
What are SE of 5HT3 Antagonists?
well tolerated w/ good safety profile
31
Aprepitant and fosaprepitant are...
NK1 Receptor Antagonists
32
Is arepitatant or fosaprepitant oral or IV?
arepitant- oral | fosaprepitant- IV
33
What is MOA of aprepitant and fosaprepitant?
substance P receptor antag of HIGHER ORDER NK1 receptors
34
What is the TU of NK1 Antagonists? What is it often given with?
chemotherapy induced N/V given in combo w/ 5HT3 antagonist and Dexamethasone
35
What are the SE of NK1 Antagonists?
generally well tolerated, usually fatigue, dizziness, and diarrhea
36
What are NK1 Antagonists metabolized by? what SE can this worsen?
Met’d by CYP 3A4 (esp. some chemotherapeutic agents) → think about drug interactions and possibility of making other SEs worse (particularly BONE MARROW SUPPRESSION)
37
Dexamethasone and mehtylprednisone are both...
corticosteroids
38
What are corticosteroids used for?
reduce N/V * don't know MOA * used in combo w/ 5HT3 antag and aprepitant
39
What is an anticholinergic used to treat motion sickness?
scopalmine *distributes widely to CNS
40
What is the MOA of scopalmine?
Muscarinic & dopaminergic receptor antagonist, especially impt effects in cerebellum
41
What form of scopalmine has the fewest SE?
Given as transdermal patch to ↓ SEs compared to oral or parenterally
42
What are antihistamines that cause SUPER SEDATION?
Dimenhydrinate, Diphenhydramine, Meclizine
43
Which antihistamines cause the MOST sedation?
older H1
44
What are SE of antihistamines? When should they NOT be used?
anticholingergic SEs: confusion dry mouth urinary retention *Not to be used if PREGO
45
What are D2 receptor Antagonists?
``` Droperidol Metoclopramine Prochlorperazine Promethazine Thiethylperazine ```
46
Where do D2 receptor antagonists act?
at D2 receptors in the CTZ and possibly muscarinic receptors
47
What are D2 receptors antags "thought" to do?
reset GI motility | cause sedation
48
What are dronabiniol and nabilone?
Cannabinoids
49
Where do cannabinoids act?
central cannabinoid receptors> sedation
50
What are SE of cannabinoids?
hallucinations, euphoria, sedation, dry mouth, ↑ appetite (which can be good for cancer patients!)
51
What is IBD?
Chronic, progressive, disease d/t inflammation in the GI tract *give drugs that work in the LOWER part of the GI tract
52
What are tx options for IBD?
1. Anti-inflammatory agents (aminosalicylates) – based on 5-ASA (mesalamine- not absorbed in stomach and passes through to lg intestine) 2. Immunosuppressive agents (corticosteroids and antimetabolites) 3. Anti-TNFα therapy
53
What are Anti-Inflammatory Agents (Aminosalicylates):
Balsalazide mesalamine osalazine sulfasalazine
54
What is the MOA of anti-inflammatory agents?
gut bacteria break bond and release ASA → can work extremely LOCALLY in GI only *Also inhibits COX → ↓ PG synthesis
55
Where do anti-inflammatory agents act?
NO effects in the stomach, different drugs affect varying parts of GI tract (e.g. SI → rectum, or only distal colon→ rectum)
56
What are anti-inflammatory agents used for?
mild to mod. ulcerative colitis Not effective for Crohn’s disease b/c can’t get high enough dose at site of disease
57
What are SE of anti-inflammatory agents?
no systemic absorption → minimal SEs (only one exception)
58
What are hte SE of sulfasalazine?
hypersensitivity rxns and ↓ in folate absorption, GI upset, nausea, HA, arthralgia, and BM suppression
59
Budesonide, Prednisone, and Prednisolone are all....
Corticosteroids
60
What is the TU of Budesonide? Where does it act? How is it metabolized?
TU: mild to mod. Crohn’s disease involving the ileum and prox. colon Local in lung and GI trat Subject to extensive, rapid 1st pass met. → local rather than systemic effects
61
What are: Azathiorpine, 6-Mercaptopurine, Methotrexate
Antimetabolites
62
How are antimetabolites given?
Given in low doses for the induction and maintenance of remission of ulcerative colitis and Crohn’s disease Allow dose reduction or elimination of steroids (?)
63
What is the MOA of Anti-TNFa therapy (infliximab)?
Ab against TNFα
64
What is TNFa?
a cell signaling protein that has been increased d/t dysregulation of TH1 responses d/t IBD; TNFα usually activates complement
65
Why does infliximab not work for all pts?
1/3 of pts become refractory b/c develop Abs against the Abs
66
What is infliximab used for?
symptomatic improvement (60%) and remission in pts w/ severe Crohn’s disease
67
What are hte SE of infliximab?
infections (more common w/ Infliximab vs. other Abs) – especially think of reactivation of TB → so any pt receiving this drug must screen for TB 1st o Infusion rxns o Hepatic probs o Unique to these Abs → ↑ risk of lymphoma (although IBD pts more likely to get lymphoma or are drugs making it worse?)

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