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TBL > Anti-emetics + GI disorders > Flashcards

Anti-emetics + GI disorders Flashcards

1
Q

What is NK?

A

Neurokinin

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2
Q

What is CB?

A

Cannabinoid

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3
Q

What is GR?

A

Glucocorticoid receptor

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4
Q

What are complications from N/V?

A

Dehydration

Electrolyte disturbances

Malnutrition

Aspiration pneumonia: gastric contents can get into respiratory system and cause inflammation

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5
Q

What are causes of N/V?

A

CNS: migraines, VESTIBULAR DYSFUNCTION (motion sickness)

GI: viral gastroenteritis, dysmotility, damage

Radiation = RINV

Surgery = PONV

Medications = CINV

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6
Q

What key receptors promote N/V?

A

H1, M1 = highly prevalent vestibular system

5HT3, NK1 = GI tract

D2

Opioid

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7
Q

Which receptors could be BLOCKED for potential anti-emetic effects?

A

H1
M1

5HT3
NK1

D2

Opioid

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8
Q

Which receptors inhibit N/V?

A

CB1

GR

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9
Q

Name 6 classes of antiemetics

A

5-HT3 antagonists

D2 Antagonists

M/H1 antagonists

NK1 antagonists

Corticosteroids

Cannabinoids

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10
Q

Name the 5-HT3 receptor antagonist drug

A

Ondansetron

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11
Q

What are the indications for ondansetron?

A

Acute CINV

RINV

PONV

Acute gastroenteritis

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12
Q

What drugs ENHANCE the effects of ondansetron?

A

NK1 blockers

Glucocorticoids

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13
Q

What AE’s are associated with ondansetron?

A

Headache

GI effects

Increase in LFTs

Increased QTc = inc. risk of TdP

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14
Q

Name the drug that is a D2 antagonist

A

Prochlorperazine

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15
Q

What is the MOA of prochlorperazine?

A

Blocks the following receptors:

D2
M
H1
Alpha1
Kr on heart
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16
Q

What is the indication for prochlorperazine?

A

“General purpose” antiemetics

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17
Q

What AEs are associated with prochlorperazine?

A

Drug-induced movement disorder from D2 blockade = tremor, slowness of movement, muscle rigidity

Involuntary movement of 👀, limbs => tardive dyskinesia

🍼Hyperprolactinemia from dopamine blockade

😡Anti-muscarinic side effects

💨 Orthostatic hypotension (dealing with alpha 1)

Increased QTc => increased TdP

😴 Sedation

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18
Q

What does hyperprolactinemia involve ?

A

Increased prolactin hormone

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19
Q

What are effects of having increased prolactin hormone?

A

Galactorrhea
Gynecomastia

Dec. sexual function
Dec. menses in women ⬇️🔴
ED in men ❌🍆

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20
Q

What is another D2 antagonist drug?

A

Metoclopramide

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21
Q

What is the MOA of metoclopramide?

A

Blocks:
D2
5HT3

Stimulates: 5HT4

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22
Q

What are the indications for metoclopramide?

A

PONV

GI motility induced problems = gastroparesis

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23
Q

What AEs are associated with Metoclopramide?

A

🍼🍼Hyperprolactnemia

🚷Movement disorders

◾️BLACK BOX WARNING: tardive dyskenesia

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24
Q

What are examples of D2 antagonists?

A

Prochlorperazine

Metoclopramide

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25
Q

What are examples of M/H1 antagonists?

A

Scopolamine

Meclizine

Dimenhydrinate

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26
Q

What is the MOA of scopolamine?

A

M receptor antagonist

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27
Q

What is the MOA of meclizine and dimenhydrinate?

A

Blocks H1 + M

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28
Q

What is the therapeutic use for M/H1 antagonists?

A

Motion sickness ONLY

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29
Q

What AEs are associated with M/H1 antagonists?

A

😡Anti-muscarinic effects

😴Sedation

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30
Q

What is Aprepitant?

A

NK1 antagonist

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31
Q

Name an NK1 antagonist

A

Aprepitant

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32
Q

What is the therapeutic use for aprepitant?

A

CINV

in combo with -setrons and glucocorticoids to increase treatment of delayed CINV

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33
Q

What AEs are associated with aprepitant?

A

📈Increased LFTs

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34
Q

What is dexamethasone?

A

Corticosteroid

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35
Q

What are the indications for dexamethosone?

A

CINV
(Need to combine with -setrons and NK1 antagonist)

PONV

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36
Q

What AEs are associated with dexamethasone?

A

👹Insomnia

🍭Increase in blood glucose

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37
Q

What is dronabinol?

A

Cannabinoid

38
Q

What is the MOA of dronabinol?

A

Stimulates CB1 receptors which can inhibit N/V

39
Q

What is the therapeutic use of Dronabinol?

A

refractory CINV

40
Q

What AEs are associated with dronabinol?

A

😝Increased laughing

😶Emotional changes

👾Hallucinations

41
Q

What drugs induce N/V?

A

Chemotherapy drugs

Opioids

Drugs that increase dopamine activity

SSRIs

Drugs that increase ACh in the brain

42
Q

Characterize GERD, PUD, and IBS as upper or lower GI disorders

A

GERD, PUD = upper GI

IBS = lower GI

43
Q

What are classical and atypical signs of GERD?

A

Classical =
Heartburn, regurgitation, dysphagia (difficulty swallowing)

Atypical =
Chest pain, cough/asthma, recurrent sore throat/hoarseness, dental enamel loss

44
Q

Describe the pathophysiology of GERD

A

Increased transient LES relaxations

Hypotensive LES

Hiatal hernia

45
Q

What complications can arise from GERD?

A

Esophagitis

Barrett’s esophagus = increased risk of esophageal cancer

Peptic strictures

46
Q

What lifestyle changes can help with GERD?

A

Weight loss

Elevation of head of bed approx. 6 inches

Avoid lying down right after a meal

Eliminate dietary triggers

Chew gum to increase salivation (bicarbonate)

47
Q

What are treatments for GERD?

A

Antacids

H2RAs

PPIs

Metoclopramide

48
Q

What is the MOA of antacids?

A

Neutralize acid to increase pH and eliminate pain

49
Q

What are side effects associated with Mg-containing antacids?

A

💩Osmotic diarrhea

Accumulation in decreased renal function

50
Q

What AEs are associated with Al-containing antacids?

A

Constipation

Accumulation in decreased renal function

51
Q

What AEs are associated with Ca-containing antacids?

A

Hypercalcemia

Belching + gastric distension

Metabolic alkalosis (increase in plasma pH)

52
Q

What AEs are associated with Na-containing antacids?

A

Increased sodium retention
(Which can inc. BP and edema in pts with HF)

Belching + gastric distension

53
Q

What DDIs are associated with antacids?

A

Decreased absorption of drugs that require acidic environment

Mg and Al can chelate some drugs => dec. absorption

54
Q

What are examples of H2RAs?

A

Cimetidine

Ranitidine

55
Q

What is the MOA of H2RAs?

A 
Block H2 receptors on parietal cells
⬇️
Decrease cAMP/PKA
⬇️
decreased activity from K/H ATPase
56
Q

What AEs are associated with H2RAs?

A

GI discomfort

🙇🏻‍♀️😴Headache, dizziness, drowsiness

Rash

Inc. in plasma creatinine

inc. risk of infections
dec. B12 absorption => over time can lead to deficiency => neurological damage + anemia

57
Q

Why is increase in plasma creatinine happen with H2RAs?

A

H2 blockers are competing with creatinine for renal secretion

**not necessarily a reflection of decreased kidney function

58
Q

What AE is associated with Cimetidine only?

A

Increase in prolactin in the blood = gynecomastia, galactorrhea, sexual dysfunction

Anti-androgen effects = gynecomastia, sexual dysfunction
(Double-whammy)

59
Q

What DDIs are associated with H2RAs?

A

Decreased drug absorption requiring acidic environment

Cimetidine only: inhibits multiple CYPs

60
Q

What is the MOA of omeprazole (PPI)?

A

Blocks K,H ATPase on parietal cell = decrease in basal, stimulated acid maximally

Needs to be absorbed into plasma

61
Q

When should PPIs be taken?

A

30 min to 1 hr BEFORE meal

62
Q

What AEs are associated with PPIs?

A

GI discomfort
🙇🏻‍♀️Headache, dizziness

Increased LFTs

Inc. risk of infections

Dec. B12 absorption => eventual deficiency
Dec. Ca absorption = inc. risk of osteoporosis
Dec. Mg absorption = hypomagnesemia = muscle spasms, seizures, arrhythmias

Increase in gastrin = ECL hyperplasia = rebound acid hypersecretion

63
Q

What DDIs are associated with PPIs?

A

Inhibit absorption of drugs that require acidic environment

Inhibition of CYPs

64
Q

What is the MOA of metoclopramide?

A

Blocks 5HT3, D2

Stimulates 5HT4 = motility effects (prokinetic) which will increase motility of upper GIT = inc. LES pressure

65
Q

What DDIs are associated with metoclopramide?

66
Q

What clinical findings are associated with peptic ulcer disease (PUD)?

A

Epigastric dyspeptic pain

Relieved by food, milk, and antacids

67
Q

What is the pathophysiology behind PUD?

A

Mucuosal defenses overwhelmed by HCl, pepsin

Major causes:
H. Pylori
NSAIDs

68
Q

What is a major complication that can result from PUD?

A

Perforations => bleeding => anemia

69
Q

What lifestyle changes should be adopted for PUD?

A

Stop NSAIDs

Dietary changes

Stop smoking

70
Q

What treatment options are available for PUD?

A

PPIs (or H2RAs) + antibiotics

Sucralfate

PG analogs

Bismuth salts

71
Q

What is the MOA of sucralfate?

A

Binds damaged area and increases protection

PG synthesis (more mucus)

72
Q

What AEs are associated with Sucralfate?

A

Not absorbed = no systemic effects

73
Q

What is misoprostol?

A

Prostaglandin analog

74
Q

What is the MOA of misoprostol?

A

Stimulates EP3 receptor on parietal and surface mucous cells

Parietal cell = dec. cAMP/PKA = dec. HCl secretion

Mucus cell = inc. mucus & HCO3 production

75
Q

What are the indications for misoprostol?

A

NSAID-induced ulcers

76
Q

What AEs are associated with Misoprostol?

A

Diarrhea

Abdominal cramping

Uterus contraction

** women of child-bearing age require negative pregnancy test before use

77
Q

What is the MOA of bismuth salicylate?

A

Binds to damaged area to increase mucus, bicarbonate production

Antimicrobial properties

78
Q

Does BSS have any effect on HCl secretion?

79
Q

What AEs are associated with BSS?

A

Black discoloration of tongue and stool

Absorption of salicylate can lead to salicylate toxicity (N/V, tinnitus, hearing loss, Reye’s syndrome)

80
Q

What clinical findings are associated with Irritable bowel syndrome (IBS)?

A

Recurrent abdominal pain

Changes in stool frequency

81
Q

How do you treat IBS?

A

Treatment varies for IBS where

Constipation predominates
Diarrhea predominates

82
Q

How do you treat IBS where constipation predominates?

A

Lactulose

Lupiprostone

83
Q

How do you treat IBS where diarrhea predominates?

A

Loperamide

84
Q

What is the MOA of Lactulose?

A

Osmotic agent that when metabolized will increase osmotic pressure

85
Q

What AEs are associated with lactulose?

A

Flatulence

Osmotic diarrhea

Abdominal pain

86
Q

What is the MOA of lupiprostone?

A

PGE1 analog binds to the EP4 receptor, causing increased chloride secretion

87
Q

What AEs are associated with Lupiprostone?

A

Nausea

Diarrhea

88
Q

What is the MOA of loperamide?

A

Stimulates GI opioid receptor, resulting in:

Increased non-propulsive contractions = segmentation

Decreased secretions = peristalsis

89
Q

What AEs are associated with loperamide

A

Abdominal pain

Constipation

90
Q

What drugs decrease pain for IBS?

A

Anti-spasmodic

91
Q

What is the MOA for hyoscyamine?

A

Blocks GI smooth muscle M3 receptor, resulting in decreased GI SM contractions

92
Q

What AEs are associated with hyoscyamine?

A

Anti-muscarinic

TBL (4 decks)

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