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

Fitzaekerly: Antiemetics and Treatments for IBD Flashcards

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
Q

What are the 7 types of antiemetic drugs?

A 
5HT3 antagonists
NK antagonists
antimuscarinics
Antihistamines
D2 antagonists
Cannabinoids
Corticosteroids
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26
Q

Dolasteron, Granisteron, Ondansetron and palonsetron are…

A

5HT3 Antagonists (end in “etron”)

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27
Q

What are the best antiemetics available that are commonly used to treat N/V from chemo?

A

Dolasteron, Granisteron, Ondansetron and palonsetron

28
Q

What is the MOA of 5HT3 Antagonists?

A

BLOCK:
peripheral 5HT3 receptors in GI tract on 1o afferents

receptors in CTZ & VC

29
Q

What is the TU for 5HT3 Antagonists?

A

Prevent and treat chemo induced vomiting

*esp ACUTE phase if given 30 mins before chemo (not good for motion sickness or delayed phase)

30
Q

What are SE of 5HT3 Antagonists?

A

well tolerated w/ good safety profile

31
Q

Aprepitant and fosaprepitant are…

A

NK1 Receptor Antagonists

32
Q

Is arepitatant or fosaprepitant oral or IV?

A

arepitant- oral

fosaprepitant- IV

33
Q

What is MOA of aprepitant and fosaprepitant?

A

substance P receptor antag of HIGHER ORDER NK1 receptors

34
Q

What is the TU of NK1 Antagonists? What is it often given with?

A

chemotherapy induced N/V

given in combo w/ 5HT3 antagonist and Dexamethasone

35
Q

What are the SE of NK1 Antagonists?

A

generally well tolerated, usually fatigue, dizziness, and diarrhea

36
Q

What are NK1 Antagonists metabolized by? what SE can this worsen?

A

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
Q

Dexamethasone and mehtylprednisone are both…

A

corticosteroids

38
Q

What are corticosteroids used for?

A

reduce N/V

  • don’t know MOA
  • used in combo w/ 5HT3 antag and aprepitant
39
Q

What is an anticholinergic used to treat motion sickness?

A

scopalmine

*distributes widely to CNS

40
Q

What is the MOA of scopalmine?

A

Muscarinic & dopaminergic receptor antagonist, especially impt effects in cerebellum

41
Q

What form of scopalmine has the fewest SE?

A

Given as transdermal patch to ↓ SEs compared to oral or parenterally

42
Q

What are antihistamines that cause SUPER SEDATION?

A

Dimenhydrinate, Diphenhydramine, Meclizine

43
Q

Which antihistamines cause the MOST sedation?

A

older H1

44
Q

What are SE of antihistamines? When should they NOT be used?

A

anticholingergic SEs:
confusion
dry mouth
urinary retention

*Not to be used if PREGO

45
Q

What are D2 receptor Antagonists?

A 
Droperidol
Metoclopramine
Prochlorperazine
Promethazine
Thiethylperazine
46
Q

Where do D2 receptor antagonists act?

A

at D2 receptors in the CTZ and possibly muscarinic receptors

47
Q

What are D2 receptors antags “thought” to do?

A

reset GI motility

cause sedation

48
Q

What are dronabiniol and nabilone?

A

Cannabinoids

49
Q

Where do cannabinoids act?

A

central cannabinoid receptors> sedation

50
Q

What are SE of cannabinoids?

A

hallucinations, euphoria, sedation, dry mouth, ↑ appetite (which can be good for cancer patients!)

51
Q

What is IBD?

A

Chronic, progressive, disease d/t inflammation in the GI tract

*give drugs that work in the LOWER part of the GI tract

52
Q

What are tx options for IBD?

A
  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
Q

What are Anti-Inflammatory Agents (Aminosalicylates):

A

Balsalazide
mesalamine
osalazine
sulfasalazine

54
Q

What is the MOA of anti-inflammatory agents?

A

gut bacteria break bond and release ASA → can work extremely LOCALLY in GI only

*Also inhibits COX → ↓ PG synthesis

55
Q

Where do anti-inflammatory agents act?

A

NO effects in the stomach, different drugs affect varying parts of GI tract (e.g. SI → rectum, or only distal colon→ rectum)

56
Q

What are anti-inflammatory agents used for?

A

mild to mod. ulcerative colitis

Not effective for Crohn’s disease b/c can’t get high enough dose at site of disease

57
Q

What are SE of anti-inflammatory agents?

A

no systemic absorption → minimal SEs (only one exception)

58
Q

What are hte SE of sulfasalazine?

A

hypersensitivity rxns and ↓ in folate absorption, GI upset, nausea, HA, arthralgia, and BM suppression

59
Q

Budesonide, Prednisone, and Prednisolone

are all….

A

Corticosteroids

60
Q

What is the TU of Budesonide? Where does it act? How is it metabolized?

A

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
Q

What are: Azathiorpine, 6-Mercaptopurine, Methotrexate

A

Antimetabolites

62
Q

How are antimetabolites given?

A

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
Q

What is the MOA of Anti-TNFa therapy (infliximab)?

A

Ab against TNFα

64
Q

What is TNFa?

A

a cell signaling protein that has been increased d/t dysregulation of TH1 responses d/t IBD; TNFα usually activates complement

65
Q

Why does infliximab not work for all pts?

A

1/3 of pts become refractory b/c develop Abs against the Abs

66
Q

What is infliximab used for?

A

symptomatic improvement (60%) and remission in pts w/ severe Crohn’s disease

67
Q

What are hte SE of infliximab?

A

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?)

GI- Week 6 (14 decks)

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