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Pharmacology > Gastrointestinal Medicines > Flashcards

Gastrointestinal Medicines Flashcards

learn the GI meds, MOA, SE, contraindications, and considerations.

1
Q

Name one medication to tx gallstones

A

Ursodiol (Actigall)

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2
Q

How does urosiol protect cholangiocytes against cytotoxicity of hydrophobic bile acids?

A
  1. modulation of the composition of mixed phospholipid-rich micelles
  2. reduction of bile acid cytotoxicity
  3. decrease concentration of bile acids in cholangiocytes
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3
Q

How does ursodiol stimulate hepatobiliary secretion?

A

through Calcium and protein kinase C alpha dependent mechanisms or activation of p38 MAPK and extracellular signal related kinases, which results in insertion of transporter molecules (bile salt export pump (BSEP) or conjugate export pump (MRP3)

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4
Q

How does ursodiol protect hepatocytes against bile acid-induced apoptosis?

A

it inhibits mitochondrial permeability transition (MMPT) and stimulates a survival pathway
aka stabilizes hepatocyte canalicular membranes

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5
Q

What is ursodiol used for?

A

dissolution of gallstones and decreases hepatic cholesterol secretion

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6
Q

What are the side effects of ursodiol?

A

diarrhea, abd pain, HA, dyspepsia, nausea, viral infections

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7
Q

Name 2 drug interactions with ursodiol?

A
  1. aluminum based antacids decrease the effect of ursodiol

2. estrogen and clofibrate negate ursodiol’s effects

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8
Q

What are the functions of gastric acids in the body? (3 main)

A
  1. protein digestion
  2. absorption of B12, iron, and calcium
  3. prevents some enteric infections
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9
Q

What is the composition of TUMS?

A

calcium carbonate

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10
Q

What is the chemical composition of Alka-seltzer?

A

sodium bicarbonate

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11
Q

What is the chemical composition of maalox?

A

aluminum hydroxide

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12
Q

The condition in which antacids should be used cautiously

A

renal insufficiency

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13
Q

What does the aluminum in maalox cause?

A

constipation

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14
Q

What does the magnesium in mylanta cause?

A

diarrhea (due to unabsorbed salts)

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15
Q

What is the general MOA of antacids?

A

they are weak bases therefore they neutralize acids and raise the pH to greater than 3.5

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16
Q

What is the end product of antacids? (2)

A
  1. sodium and water
    or
  2. salt and CO2 (sodium bicarbonate)
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17
Q

What are major SE of antacids?

A

metabolic alkalosis, cardiac disease, fluid/electrolyte imbalances

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18
Q

Drug interactions of antacids?

A

any - binds with other drugs so take 1-2 hours after taking other meds, also the decrease in gastric acids could cause inefficient absorption

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19
Q

What is the result of blocking Histamine 2 receptors?

A

decreased stomach acid production

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20
Q

What can the decrease of stomach acid cause?

A

increased bacterial growth in the stomach, leading to increased bacterial colonization in the lungs, and pneumonia in COPD pt

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21
Q

SE of IV formulations of H2 receptor antagonists

A

confusion, mental changes

esp. if pre-existing renal or hepatic impairment

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22
Q

Famotidine brand name

A

pepcid

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23
Q

ranitidine brand name

A

zantac

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24
Q

cimetidine brand name

A

tagamet

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25
Q

what is the chemical composition of mylanta?

A

magnesium hydroxide

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26
Q

common SE of antacids NOT containing AlOH or MgOH?

A

eructation

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27
Q

what is eructation

A

bleching

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28
Q

Considerations for chronic antacid use in renal compromised pt

A

monitor ALP, ALT, AST, serum creatinine, BUN

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29
Q

What do parietal cells do?

A

produce gastric acid

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30
Q

What stimulates parietal cells?

A

histamine, acetylcholine, and gastrin receptors

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31
Q

What releases histamine, ach and gastrin?

A

antral G cells and enterochromaffin-like cells (ECL)

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32
Q

Examples of H2 antagonists?

A

famotidine, ranitidine, nizatidine, cimetidine

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33
Q

nizatidine brand name

A

axid

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34
Q

endocrine effects associated with cimetidine?

A

increased prolactin, decreased metabolism of estradiol, and blockage of androgen receptors

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35
Q

how does cimetidine block androgen receptors?

A

inhibits binding of DHT (dihydroxytestosterone)

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36
Q

Adverse endocrine effects of cimetidine (2)

A

glactorrhea in women, gynecomastia in men

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37
Q

cautions for H2 antagonists

A

pregnancy category B, monitor renal or hepatic dysfunction for mental status changes

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38
Q

IV administration of H2 antagonists may cause ___ in renally or hepatic impaired pt

A

mental status changes, confusion, depression

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39
Q

What enzymes could cimetidine affect?

A

cytochrome p450 enzymes

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40
Q

drug interactions with cimetidine?

A

other drugs using the same p450 pathway - warfarin, phenytoin, theophylline, lidocaine

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41
Q

examples of proton pump inhibitors

A

esomeprazole, omeprazole, lansoprazole, pantoprazole, rabeprazole

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42
Q

brand name esomeprazole

A

nexium

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43
Q

brand name lansoprazole

A

prevacid

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44
Q

brand name omeprazole

A

prilosec

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45
Q

brand name pantoprazole

A

protonix

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46
Q

brand name rabeprazole

A

aciphex

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47
Q

MOA proton pump inhibitors

A

directly inhibiting proton pumps, which plays a role in gastric acid production in the stomach

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48
Q

adverse effects of OTC PPI? (3)

A

increase of stomach bacteria, abdominal discomfort, diarrhea

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49
Q

adverse effect of high dose, chronic PPI? (3)

A

atrophic gastritis, osteoporosis related bone fx, magnesium deficiency

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50
Q

cautions for PPI

A

pregnancy category B, liver impaired patients due to the increased half life and impaired metabolism of the drug

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51
Q

Drug interactions with PPI’s

A

ketoconazole and atazanavir (decreases the bioavailability of these drugs, since they need a certain pH to work); cyp 2c19 and cyp3A4 metabolized drugs; taking PPI and warfarin inc risk of bleeding

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52
Q

How are PPI’s metabolized?

A

cytochrome P450 pathways, CYP 2C19 and CYP2A4

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53
Q

2 treatments for H. pylori

A
  1. PPI plus clarithromycin and amoxicillin OR PPI plus metronidazole for 14 days
  2. a PPI or H2 antagonist plus bismuth, metronidazole, and tetracycline (bismuth quadruple therapy) for 10-14 days
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54
Q

what is an alternative treatment for H. pylori NOT including bismuth-based quadruple therapy?

A

a PPI plus amoxicillin for 5 days, followed by a PPI plus clarithromycin and tinidazole for another 5 days

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55
Q

what is bismuth subsalicylate?

A

pepto bismol

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56
Q

absolute contraindictions for pepto bismol?

A

never give to children, especially after flu and varicella shots. salicylate is a causative agent of Reye’s syndrome

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57
Q

How are mucosal protectants different than antacids, H2 antagonists, or PPI’s?`

A

they do not affect gastric acid secretion, rather, shield gastric mucosa

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58
Q

MOA of sucralfate

A

due to limited solubility, becomes thick and sticky in acid solutions. <3% of intact drug absorbed.
utilizes negative charges to adhere to gastric erosions (with positively charged proteins) to protect from further damage and promote healing

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59
Q

MOA bismuth subsalicylate

A

coats stomach lesions and can bind to microbes to provide protection from gastric acids, for diarrhea can bind to and absorb toxins and inhibit intestinal prostaglandin and chloride secretion

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60
Q

MOA misoprostol (cytotec)

A

activates prostaglandin E1 receptors on gastric parietal cells and inhibits gastric acid production via G protein coupled receptor-mediated inhibition of adenylate cyclase. this decreases intracellular cyclic adenosine monophosphate and proton pump activity.

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61
Q

what combination of drugs is given to prevent GI erosions ?

A

NSAID and misoprostol, due to NSAID decreasing prostaglandin synthesis

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62
Q

Adverse effects bismith subsalicylate? (3)

A

dark brown-black stools, constipation or salicylate toxicity with chronic use

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63
Q

adverse effects misoprostol? (5)

A

abdominal discomfort with or without diarrhea, N/V, flatulence, dyspepsia

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64
Q

Pregnancy risk categories for sucralfate, bismuth subsalicylate, and misoprostol?

A

B, C, X

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65
Q

Drug interactions with sucralfate?

A

should not be given with any other drugs bc will bind to them and inhibit their absorption

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66
Q

drug interactions with misoprostol?

A

none

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67
Q

drug interactions with bismuth subsalicylate?

A

chemical reactions with tetracyclines and quinolone antibiotics, decreases antibiotic absorption; may increase hypoglycemic effects of insulins/DM meds, increase risk of bleeding in concurrent warfarin d/t synergistic effects of antiplatelets; decrease effectiveness of probenecid and sulfinpyrazone (for gout); avoid using with other salicylates like aspirin

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68
Q

Drugs to stimulate GI motility are called?

A

Gastroprokinetic drugs

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69
Q

How do gastroprokinetic drugs work?

A

increased frequency of small intestine contractions WITHOUT disrupting rhythm

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70
Q

What conditions can be relieved by gastroprokinetic drugs? (11)

A

IBS, acid reflux disease, gastroparesis, gastritis, functional dyspepsia, abdominal discomfort, bloating, constipation, heartburn, nausea, vomiting

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71
Q

2 types of gastroprokinetic drugs?

A

cholinergic mimetic agents, dopamine receptor antagonists

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72
Q

specific MOA of cholinergic mimetic agents? (2)

A
  1. antagonize M1 receptor (which usually inhibits ach release), therefore increasing ach production
  2. inhibit acetylcholineesterase (less ach broken down)
  3. MAY stimulate muscarinic M3 receptors on muscle cells and myenteric plexus synapses
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73
Q

General MOA of gastroprokinetic drugs?

A

increasing availability of acetylcholine which increases GI peristalsis which increases pressure on lower esophageal sphincter (increases GI motility)

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74
Q

Considerations for cholinergic mimetic agents?

A

never administer IV (fast absorption may lead to heart block or severe hypotension, d/t drug being in the wrong location) , never use if there is a mechanical obstruction of gastric or urinary tracts

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75
Q

Example of a cholinergic mimetic agent?

A

bethanechol (urecholine)

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76
Q

SE of cholinergic mimetic agents? (8)

A

abd discomfort, diarrhea, hypotension, reflex tachycardia, lacrimation, miosis, salivation, urinary urgency

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77
Q

General MOA of dopamine receptor blockers

A

stimulates the GI tract without increasing gastric secretions

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78
Q

example of D2 receptor blocker?

A

metoclopramide (reglan)

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79
Q

Adverse effects of D2 receptor blockers? (10)

A

parkinsonian like symptoms, tardive dyskinesia, acute dystonia, drowsiness, confusion, elevated prolactin levels, galactorrhea, gynecomastia, impotence, menstrual disorders

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80
Q

Drug interactions with D2 receptor blockers?

A

alcohol, tranquilizers, sleep meds, narcotics, use caution with hypertensive pt

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81
Q

Types of drugs to control diarrhea? (3)

A

opioid agonists, bismuth compounds, octredotide

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82
Q

opioid agonist monotherapy drug

A

loperamide (imodium)

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83
Q

combination opioid agonists?

A

diphenoxylate plus atropine (lomotil) and difenoxin plus atropine (motofen)

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84
Q

characteristics of loperamide (3 major)

A

does not cross blood brain barrier, no analgesic properties or potential for addiction, nonprescription

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85
Q

characteristics of diphenoxylate (2 major)

A

prescription only, analgesic properties at higher/nonstandard doses

86
Q

general MOA of opioid agonists?

A

act directly on intestine to slow peristalsis, allow more fluid and electrolyte absorption in colon, anticholinergic properties of atropine contribute as well

87
Q

Considerations for opioid agonists?

A

acute tx of diarrhea d/t CNS depression, take with adequate fluids to prevent constipation and electrolyte imbalance, FIRST rule out c. diff

88
Q

SE Lomotil? (4)

A

dry mouth, abd pain, tachycardia, blurred vision (d/t atropine)

89
Q

Considerations for the patient for opioid agonist users?

A

if diarrhea continues, fever, abdominal pain or bloody stools occur, contact prescriber asap

90
Q

Drug interactions with opioid agonists?

A

additive sedation with CNS depressants or alcohol, hypertensive crisis when taken with MAOIs (because they both increase synaptic 5-HT which can be toxic)

91
Q

3 MOA of octreotide (sandostatin)

A
  1. prevents secretion of hormones and transmitters like gastrin, serotonin, and other active peptides causing diarrhea
  2. directly inhibits intestinal and pancreatic secretion and enhances absorption
  3. slows GI motility
92
Q

Octreotide is usually used to tx diarrhea related to these 5 conditions

A

cancer, vagotomy, dumping syndrome, short bowel syndrome, AIDS

93
Q

Adverse effects of octreotide (4)

A

nausea, abdominal pain, flatulence, diarrhea

94
Q

adverse effects of chronic octreotide use (4)

A

acute cholecystitis, hyperglycemia, hypothyroidism, bradycardia

95
Q

Considerations for octreotide for impaired pancreatic secretion?

A

may cause steatorrhea, leading to fat soluble vitamin deficiency

96
Q

Types of stool according to Bristol Stool Chart (7)

A
  1. separate hard lumps like nuts (hard to pass)
  2. sausage shaped but lumpy
  3. sausage but with surface cracks
  4. sausage or snake, smooth and soft
  5. soft blobs with clear cut edges (passed easily)
  6. fluffy pieces with ragged edges (mushy stool)
  7. watery, no solid pieces, entirely liquid
97
Q

Normal frequency of bowel movements?

A

once per week to 2-3 times per day

98
Q

Subcategories of laxatives (5)

A

bulk forming laxatives, stimulant laxatives, stool softeners/surfactants, osmotic laxatives, miscellaneous

99
Q

Considerations for prescribing laxatives

A

sufficient fluids must be consumed, take a thorough hx of laxative use d/t potential to cause fecal impaction, adequate fiber and fluid intake

100
Q

Examples of bulk forming laxatives?

A

calcium polycarbophil (fibercon), psyllium mucilloid (metamucil)

101
Q

MOA of bulk forming laxatives?

A

absorb water to form a bulky emollient gel that distends the colon to promote peristalsis

102
Q

Characteristics of bulk forming laxatives

A

indigestible, hydrophillic colloids, safest class, produce less abdominal cramping, but more flatulence or bloating

103
Q

Drug interactions of bulk forming laxatives?

A

may decrease absorption of warfarin, digoxin, nitrofurantoin, antibiotics, salicylates

104
Q

examples of stimulant laxatives

A

bisacodyl (dulcolax), castor oil (emulsoil)

105
Q

Pregnancy categories dulcolax and emulsoil?

106
Q

General MOA of stimulant laxatives?

A

activate bowel movement by irritating mucosa and enteric nervous system in the colon and altering intestinal electrolyte and fluid absorption

107
Q

Concern for stimulant laxatives?

A

more abdominal cramping and depletion of fluid and electrolytes, potential dependence and destruction of myenteric plexus MAY be safe for long term use

108
Q

drug interactions for stimulant laxatives?

A

do not give with milk or dairy, as this will dissolve enteric coating and cause dyspepsia, take on empty stomach for faster action and to avoid decreased absorption

109
Q

example of stool softener/surfactant?

A

docusate sodium (colase)

110
Q

general MOA of colase?

A

soften stool by absorbing water and lipids, take with 6-8 oz water

111
Q

Colase is commonly used in these (3) situations to prevent constipation?

A

recent surgery, traumatic injury, MI

112
Q

adverse effects of colase? (2)

A

abdominal cramping, diarrhea, caution with elderly d/t risk of nutritional deficits

113
Q

pregnancy category of colase?

114
Q

Drug interactions with Colase?

A

do not use in sodium restricted patients, do not give concurrent with mineral oil (increases systemic absorption of docusate), long term use may impair absorption of fat soluble vitamins ADEK (decreased contact time in GI tract)

115
Q

Examples of osmotic laxatives?

A

magnesium hydroxide (milk of magnesia), polyethylene glycol (miralax), sodium biphosphate (fleet phospho-soda)

116
Q

general MOA of osmotic laxatives?

A

attract water and create more fluid stools, cause a concentration gradient

117
Q

considerations for milk of magnesia?

A

very potent, so only use in fecal impaction where bowel obstruction has been ruled out

118
Q

Adverse effects of osmotic laxatives?

A

abdominal cramping, diarrhea

119
Q

Use osmotic laxatives with caution in these patients

A

elderly d/t dehydration and electrolyte imbalance, renal impairment d/t risk of hypermagnesemia (decreased ability of mg elimination)

120
Q

Drug interactions with osmotic laxatives?

A

Milk of magnesia may decrease absorption of histamine2 receptor antagonists, iron salts, phenytoin, digoxin and tetracyclines

121
Q

Collection of medications to control IBS? (5)

A

antidiarrheal, laxatives, anticholinergics, serotonin 5HT receptor antagonists/agonists, chloride channel activators

122
Q

What are anticholinergics used to treat in IBS?

A

reduce bowel motility, prevent painful cramping spasms

123
Q

Commonly used anticholinergic/antimuscarinics for IBS?

A

dicyclomine (bentyl) and hycosamine

124
Q

general MOA of anticholinergics in IBS?

A

bind to muscarinic receptors in GI mucosa, relaxing intestinal spasms, may inhibit intestinal gland secretion (reduce diarrhea)

125
Q

Anticholinergic effects (4 examples)

A

dry mouth, visual disturbance, urinary retention, constipation

126
Q

Examples of 5HT3 antagonists (5)

A

alosetron, ondansetron, graisetron, dolasetron, palonosetron

127
Q

Which 5HT antagonist was removed from market due to cardiovascular deaths?

A

tegaserod, is now used in emergency situations for short term treatment in women with IBS with predominant constipation

128
Q

What is the difference between alosetron and tegaserod?

A

alosetron is a highly potent and selective 5HT3 antagonist with a longer duration of effect (higher affinity and slower dissocation from receptors), tegaserod is a 5HT4 receptor partial agonist

129
Q

Considerations for alosetron

A

restricted to women with diarrhea-predominant IBS who have not responded to conventional therapies (due to ischemic colitis and constipation risks), be very aware of sx of lightheadedness and chest pain due to cardiovascular risks associated with this and tegaserod

130
Q

Adverse effects of tegaserod

A

angina, heart attack, stroke (pt must register with the manufacturer when they receive this medication)

131
Q

Strict duration of treatment for alosetron and tegaserod

A

4-6 weeks ONLY

132
Q

Example of a chloride-channel activator for IBS

A

lubiprostone

133
Q

Lubiprostone target

A

type 2 volume regulated chloride channel located in gastric parietal cells, small intestinal and colonic epithelia

134
Q

Restrictions for lubiprostone

A

used in women with constipation-predominant IBS

135
Q

Lubiprostone MOA

A

prostanoic acid derivative from a metabolite of prostaglandin E1, activates selective type 2 volume regulated Cl channel to accelerate small bowel and colon transit times to increase secretion of fluid and electrolytes

136
Q

Adverse effects of lubiprostone

A

diarrhea, nausea, DO NOT use for known or suspected bowel obstruction

137
Q

Drug interactions with lubiprostone

138
Q

What stimulates nausea and vomiting?

A

center of medulla stimulated when receives input from digestive tract, inner ear, or chemoreceptor trigger zone (in postrema)

139
Q

6 classes of antiemetics

A
  1. 5HT3 receptor antagonists
  2. corticosteroids
  3. neurotonin 1 receptor antagonists
  4. dopamine receptor antagonists
  5. antihistamines/anticholinergics
  6. cannabinoids
140
Q

Examples of 5HT3 receptor antagonists (4)

A

ondansetron (zofran), granisetron (kytril), dolasetron (anzemet), palonosetron (aloxi)

141
Q

What effect do cytotoxic drugs or radiation have on GI cells?

A

causes release of serotonin from enterochromaffin cells in the GI mucosa, which stimulates 5HT3 receptors on sensory nerve terminals peripherally, initiating emesis or cause sensory nervous system to initiate emesis

142
Q

5HT3 antagonists work on the receptors to create an antiemetic response through selective antagonism at ____?

A

peripheral 5HT3 receptors

143
Q

Mild SE of 5HT3 antagonists? (5)

A

mild HA, dizziness, constipation, diarrhea, transient elevation of hepatic aminotransferase levels (AST, ALT)

144
Q

drug interactions with 5HT3 antagonists?

145
Q

Examples of corticosteroids used to treat N/V (2)

A

dexamethasone (decadron), methyprednisolone (solu-medrol)

146
Q

Long term effects of corticosteroids? (5)

A

risk for DM2, hypertension, osteoporosis, hyperadrenalism, hypoadrenalism

147
Q

Cautions for corticosteroids

A

avoided or monitored in hyperglycemic or diabetic pt

148
Q

adverse events in dexamethasone specifically (7)

A

insomnia, indigestion, epigastric discomfort, agitation, increased appetite, weight gain, acne

149
Q

example of neurokinin-1 (NK1) receptor antagonist

A

aprepitant (emend)

150
Q

MOA of NK1 RA?

A

inhibits substance P, which is involved in the emesis reflex centrally and peripherally

151
Q

What is substance P?

A

a neuropeptide that acts as a NT by preferentially binding to NK1 receptor that is involved in the emesis reflex

152
Q

common SE of aprepitant (6)

A

fatigue, HA, anorexia, diarrhea, hiccups, mild transaminase elevation

153
Q

Drug interactions with NK1 RA

A

induces CYP3A4 and CYP 2C9, and dexamethasone is a substrate of CYP2C9, so decrease dexamethasone 50%; warfarin, phenytoin, itraconazole, terfenadine, oral contraceptives (synergistic effects on same CYP 450 subtype system)

154
Q

Categories of dopamin-receptor antagonists (3)

A
  1. phenothiazine, butyrophenones, substituted benzamides
155
Q

examples of phenothiazines (3)

A

promethazine (phengergan), prochlorperazine (compazine), thiethylperazine

156
Q

examples of butyrophenones (1)

A

droperidol (inapsine)

157
Q

examples of substituted benzamides (2)

A

metoclopramide (reglan), trimethyobenzamide (tigan)

158
Q

General MOA of central dopamine antagonists

A

inhibits dopamine and muscarinic receptors, selective for D2 receptors

159
Q

Adverse effects of central dopamine antagonist long term use? (5)

A

sedation, extrapyramidal symptoms (restlessness, dystonias, parkinsonian symptoms)

160
Q

Additional adverse effects of droperidol (inapsine) (2)

A

hypotension, prolonged QT interval

161
Q

Pregancy class of the phenothiazines?

162
Q

Pregnancy class of metoclopramide

163
Q

Drug interactions with phenothiazines

A

synergistic with streptomycin, erythromycin, oleandomycin, spectinomycin, levofloxacin, azithromycin, amoxicillin-clavulanic acid

164
Q

Contraindications of metoclopramide

A

pt who take antipsychotics, HIGH LIKELIHOOD of tardive dyskinesia with long term use

165
Q

Drug given for motion sickness, and type of drug

A

scopolamine (hyoscine), anticholinergic

166
Q

Examples of H1 antihistamines

A

diphenhydramine (benadryl), dimenhydrinate (dramaine), meclizine (antivert)

167
Q

MOA for H1 antihistamines and anticholinergics for antiemesis?

A

inhibits H1 and muscarinic cholinergic M1 receptors

168
Q

Adverse effects of antihistamines and anticholinergics?

A

dizziness, sedation, dry mouth, confusion, cycloplegia, urinary retention

169
Q

Cannabinoids used as antiemetics

A

dronabinol (marinal), nabilone (cesamet)

170
Q

What is dronabinol (marinal) used to tx? (2)

A

appetite stimulant, antiemetic

171
Q

Hypothesized MOA of cannabinoids?

A

modulates 5HT3 receptor activation in nodose ganglion and substance P release in the spinal cord

172
Q

Effects of cannabinoids? (9)

A

euphoria, dysphoria, sedation, hallucinations, dry mouth, increased appetite, tachycardia, conjunctival injection, orthostatic hypotension

173
Q

What is IBD?

A

inflammatory bowel disease, combines ulcerative colitis and Crohn’s Disease

174
Q

IBD drugs that affect the immune system (6)

A

immunosupressants, purine analogs, methotextrate, monoclonal antibodies, antitumor necrosis factor agents, anti-integrin agents

175
Q

Categories of IBD drugs (3)

A

aminosalicylates, corticosteroids, immune system drugs

176
Q

Two subtypes of aminosalicylates

A

5-ASA/mesalamine and azo compounds

177
Q

Drugs with azo compounds (3)

A

sulfasalazine, balsalazide, olsalazine

178
Q

Drugs with 5-ASA formulations (6)

A

pentasa, asacol, apriso, lialda, rowasa, canasa

179
Q

Primary MOA of salicylates and NSAIDS

A

blockage of prostaglandin synthesis by inhibiting COX

180
Q

Potential MOA of salicylates in the GI tract (4)

A
  1. modulation of inflammatory mediators derived by COX and lipoxygenase pathways
  2. interference with the production of inflammatory cytokines
  3. inhibitory effects on nuclear factor kB
  4. other inhibitory effects on NK cells, mucosal lymphocytes, and macrophages
181
Q

SE of olsalazine (4)

A

secretory diarrhea, subtle renal tubular changes, rare interstitial nephritis, rare hypersensitivity reactions

182
Q

SE of sulfasalazine (15)

A

nausea, GI upset, HA, malaise, arthralgias, myalgias, bone marrow supression, hypersensitivity reactions causing fever, exfoliative dermatitis, pancreatitis, pneumonitis, hemolytic anemia, pericarditis, hepatitis

183
Q

Drug interactions with sulfasalazine

A

may interfere with folic acid absorption and processing, take 1mg/day folic acid

184
Q

examples of glucocorticoids used to treat IBD (4)

A

prednisone, prednisolone, topical hydrocortisone, budesonide

185
Q

MOA of glucocorticoids

A

inhibits production of inflammatory cytokines and chemokines like TNFalpha, interleukin 1 (IL-1) and interleukin 8 (IL-8)
reduction of expression of adhesion molecules, inhibition of gene transcription of nitric oxide synthesis, phospholipase A2, COX2, and NF-kB

186
Q

Examples of purine analogs

A

azathioprine, 6-mercaptopurine (6-MP)

187
Q

When are purine analogs used

A

when IBD patients are unresponsive to aminosalicylates or glucocorticoids, or who relapse when glucocorticoids are withdrawn

188
Q

Proposed MOA of purine analogs

A

metabolized to nucleotide 6-thioinosinic acid, thioguanylic acid, and 6-methylmercaptopurine ribotide. these are thought to inhibit purine ribonucleotide synthesis, which then impedes DNA synthesis and proliferation of fast growing cells (T and B lymphocytes)

189
Q

Dose dependent adverse effects of purine analogs

A

nausea, vomiting, bone marrow suppression, hepatic toxicity, hypersensitivity reactions with fever, rash, pancreatitis, diarrhea, hepatitis

190
Q

considerations for purine analogs

A

monitor CBC and hepatic function tests

191
Q

Drug interactions with purine analogs

A

allopurinal reduces xanthine oxide catabolism of purine analogs, increasing active 6-thioguanine nucleotides, increasing risk for leukopenia
allopurinol inhibits xanthine oxidase (which breaks down 6-MP)

192
Q

MOA of methotrexate

A

inhibits dihydrofolate reductase, which participates in tetrahydrofolate synthesis, and therefore inhibits production of purines and thymidines; may interfere with inflammatory actions of IL-1, simulate release of adenosine, and induce apoptosis of activated T-lymphocytes

193
Q

Adverse effects methotrexate

A

with lower dose, don’t see bone marrow suppression, megaloblastic anemia, alopecia, and mucositis, and low risk of hepatic damage.

194
Q

Interactions with methotrexate

A

caffeine (coffee, tea, soda, chocolate) (effectiveness is reduced), alcohol (liver dysfunction), NSAIDS can increase blood levels of methotrexate

195
Q

Anti-tumor necrosis factor drugs approved for IBD tx (3)

A

infliximab, adalimumab, certolizumab

196
Q

When are anti-TNF drugs used?

A

pt with IBD who have shown inadequate response to conventional treatment

197
Q

What is TNF?

A

important pro-inflammatory cytokine in the pathogenesis of IBD

198
Q

MOA of anti-TNF agents

A

bind to soluble and membrane bound TNF and prevents the binding of TNF to TNFr that are present on helper T cell type 1 and other innate immune/non-immune cells
-binding of anti-TNF to membrane bound TNF induces reverse signaling, suppressing cytokine release

199
Q

Adverse effects of anti-TNF agents

A

due to suppression of helper T cell type 1 (TH1), this immunosuppression may allow infections to flourish, like bacterial sepsis, TB, invasive fungal organisms, reactivation of Hep B, listeriosis, and opportunistic infections

200
Q

considerations for anti-TNF agents

A

test for TB before starting, administer prophylactic tx for positive TB, may increase the risk of lymphoma

201
Q

Why does anti-TNF cause drug resistance?

A

production of antibodies to TNF antibodies (ATA) or non-ATA mechanisms

202
Q

Reactions to drug resistance/TNF antibody development

A

acute or delayed infusion reactions = fever, HA, dizziness, urticaria, mild cardiopulmonary sx

203
Q

Delayed infusion reactions to anti-TNF agents

A

myalgia, jaw tightness, rash, edema

may occur 1-2 weeks after therapy is initiated

204
Q

Example of anti-integrin therapy

A

natalizumab

205
Q

What are integrins

A

integrins are adhesion molecules located on the surface of leukocytes, which interact with selectins on the surface of vascular endothelial cells. this allows circulating leukocytes to adhere to the vascular endothelium and move though blood vessel wall into the tissue

206
Q

MOA of natalizumab

A

humanized IgG4 monoclonal antibody targets the alpha-4 subunit of integrins and blocks the interaction of integrins with selectin, therefore preventing leukocyte migration into the surrounding tissue
= prevents IBD progression in chronic disease process

207
Q

Risk of natalizumab

A

induces progressive multifocal leukoencephalopathy due to the reactivation of a human polyomavirius in pt receiving concurrent immunomodulators
aka do not take with immunomodulators/immune suppressants

208
Q

pregnancy class of milk of magnesia?

209
Q

pregnancy class of miralax?

210
Q

pregnancy class of colase?

211
Q

pregnancy class of dulcolax

Pharmacology (5 decks)

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