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GI Pharmacology > GI Pharmacology > Flashcards

GI Pharmacology Flashcards

1
Q

Cimetidine

A
  • H2 Receptor Antagonist
  • do not effect H1 or H3 receptors
  • least potent (1)
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2
Q

Ranitidine

A
  • H2 Receptor Antagonist
  • do not effect H1 or H3 receptors
  • more potent (4-10)
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3
Q

Nizatidine

A
  • H2 Receptor Antagonist
  • do not effect H1 or H3 receptors
  • more potent (4-10)
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4
Q

Famotidine

A
  • H2 Receptor Antagonist
  • do not effect H1 or H3 receptors
  • most potent (20-50)
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5
Q

Clinical Utility of H2-Antagonists

A
  • suppress basal and meal-stimulated acid section in a linear dose-dependent manner
  • their effect is most pronounced on nocturnal acid secretion, which depends largely on histamine
  • although still prescribed, H2-receptor antagonists are being steadily replaced by the more potent acid inhibiting PPIs for most clinical indications
  • however, over-the-counter (OTC) preparations are heavily used by the public for nonulcer dyspepsia
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6
Q

H2-Antagonists for GERD

A
  • intermittent administration is useful for infrequent (<3 times/week) heartburn or dyspepsia
  • may be taken prophylactically before meals to reduce likelihood of heartburn
  • frequent heartburn is best treated with twice-daily H2 antagonists or w/ PPIs
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7
Q

H2- Antagonists for Peptic Ulcer Disease

A
  • PPIs have largely replaced H2 antagonists for the treatment of acute peptic ulcer disease
  • that said, nocturnal acid suppression by H2 antagonists affords effective ulcer healing in most patients with uncomplicated gastric and duodenal ulcers
  • once-daily administration at bedtime results in ulcer healing rates of >80-90% after 6-8 wks of therapy
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8
Q

H2-Antagonists Adverse Effects

A
  • H2-receptor antagonists are safe drugs
  • adverse effects occur in <3% of patients and include diarrhea, headache, fatigue, myalgias, and constipation
  • H2 antagonists cross the placenta and, therefore, should not be administered to pregnant women unless absolutely necessary
  • H2 antagonists are secreted into breast milk and may thus affect nursing infants
  • cimetidine (inhibits CYP3A4) slows the hepatic metabolism of many drugs, with ranitidine having a lesser effect. Famotidine and nizatidine do not alter hepatic drug metabolism
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9
Q

Omeprazole

A

-proton pump inhibitor (PPI)

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10
Q

Esomeprazole

A

-proton pump inhibitor (PPI)

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11
Q

Lansoprazole

A

-proton pump inhibitor (PPI)

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12
Q

Dexlansoprazole

A

-proton pump inhibitor (PPI)

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13
Q

Pantoprazole

A

-proton pump inhibitor (PPI)

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14
Q

Rabeprazole

A

-proton pump inhibitor (PPI)

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15
Q

PPI Facts

A
  • prodrugs (require activation via protonation in the acid environment of the secretory canaliculus of the gastric parietal cell
  • activated rug forms a covalent disulfide bond with the H+, K+ ATPase and irreversibly inactivates the enzyme
  • markedly suppress both fasting and meal-stimulated acid secretion (latter being significantly more pronounced than H2-antagonist)
  • PPIs inhibit 90-98% of 24-hour acid secretion
  • different PPI agents show little difference in clinical efficacy
  • bioavailability decreased ~50% when taken with food
  • should be administered 1 hour before a meal (usually breakfast) so that peak serum conc. coincide with max proton pump activity
  • short half life (0.5-2.0 hrs), but acid inhibition lasts up to 24 hrs. due to the irreversible inactivation of the pump
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16
Q

PPIs and GERD

A
  • most effective agents for txt of nonerosive and erosive GERD
  • once-daily dosing provides effective sx relief and tissue healing in 85-90% of pts, with up to 15% of pts requiring twice-daily dosing
  • increasing first-line therapy for pts with symptomatic GERD
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17
Q

PPIs and Peptic Ulcer Disease

A
  • compared to H2-antagonists, PPIs afford more rapid sx relief and faster ulcer healing for duodenal ulcers and, to a lesser extent, gastric ulcers
  • all PPIs heal >90% of duodenal ulcers w/i 4 wks and a similar percentage of gastric ulcers within 6-8 wks
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18
Q

Triple Therapy for H. pylori Associated Ulcers

A
  1. PPI 2x/day
  2. amoxicillin (1g) 2x/day
  3. either clarithromycin 500 mg or metronidazole 500 mg 2x/day
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19
Q

Prevpac

A

-lansoprazole/amoxicillin/clarithromycin

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20
Q

Quadruple Therapy for H. pylori Associated Ulcers

A
  • both antibiotics is proving more effective for eradication of H. pylori, and is now recommended for initial treatment
  • effectiveness of triple therapy regimens is diminishing due to increasing rates of resistance to clarithromycin or to metronidazole, but simultaneous resistance to both drugs remains relatively rare
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21
Q

PPIs and NSAID Associated Ulcers

A
  • for pts with ulcers caused by aspirin or other NSAIDs, H2 antagonists or PPIs provide rapid ulcer healing so long as the NSAID is discontinued
  • in pts with NSAID-induced ulcers who require continued NSAID therapy, once- or twice-daily PPI treatment more reliably promotes ulcer healing
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22
Q

PPI Adverse Rxns

A
  • quite safe
  • diarrhea, headache, and abd pain in 1-5% of pts
  • increases in gastric bacterial conc. have been reported in pts taking PPIs, due to suppression of the gastric acid barrier to ingested bacteria
  • an increased risk of enteric infection may therefore exist in pts taking PPIs, particularly those traveling to underdeveloped countries
  • hospitalized pts may have an increased risk for C. difficile infection
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23
Q

Antacids

A
  • weak bases that react with gastric HCl to form a salt and water
  • usefulness lies in their ability to reduce gastric acidity as well as peptic activity (pepsin is inactive in sol’ns above pH 4.0)
  • principal constituents are Mg(OH)2 or Al(OH)3, alone or in combination
  • vary widely in potency, with differing doses of different antacids being required to achieve a desired degree of neutralizing capacity
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24
Q

Antacids Clinical Utility

A
  • primarily used for txt of intermittent heartburn
  • effective in promoting healing of duodenal ulcers, but benefit in treating gastric ulcers has not been demonstrated
  • tablets are weak in their neutralizing capability - not recommended for high dose regiments, since a large number of tablets would be required
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25
Q

Gaviscon

A

-antacids in combination with the mucosal protective agent alginic acid (Gaviscon) can reduce the sxs of GERD, but do not affect the natural hx of the disease

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26
Q

Sucralfate

A
  • drug that promotes mucosal defense
  • viscous substance that si insoluble in water and has a weak buffering action
  • thought to selectively bind necrotic ulcer tissue, where it acts as a barrier to acid, pepsin, and bile
  • may stimulate the synthesis of prostaglandins, which, in turn, stimulate the secretion of mucus and HCO3-
  • effective in preventing and healing duodenal ulcers
  • requires acidic conditions to be activated and thus should NOT be taken together with antacids, H2-receptor antagonists, or PPIs
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27
Q

Bismuth Subsalicylate (Pepto-Bismol)

A
  • colloidal bismuth compound
  • appears to work by selective binding to an ulcer, coating it, and protecting it from acid and pepsin
  • bismuth compounds have direct antimicrobial activity against H. pylori and bind enterotoxins
  • when combines with antibiotics such as tetracycline and metronidazole, H. pylori-associated ulcer healing rates of up to 98% have been seen
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28
Q

Bismuth Subcitrate Potassium

A
  • colloidal bismuth compound
  • appears to work by selective binding to an ulcer, coating it, and protecting it from acid and pepsin
  • bismuth compounds have direct antimicrobial activity against H. pylori and bind enterotoxins
  • when combines with antibiotics such as tetracycline and metronidazole, H. pylori-associated ulcer healing rates of up to 98% have been seen
  • **bismuth subcitrate is only available as a combination prescription product with tetracycline and metronidazole
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29
Q

Misoprostol

A
  • prostaglandin analog
  • a methyl analog of prostaglandin E1 (PGE1), and is approved for the prevention of NSAID-induced ulcers
  • has both mucosal protective and acid inhibitory properties
  • its mucosal protective effects stem from stimulation of mucus and HCO3- secretion as well as enhancement of mucosal blood flow
  • also reduces histamine-stimulated cAMP production, resulting in modest acid inhibition
  • TOXICITY: causes dose-dependent diarrhea and is contraindicated in women with childbearing potential, due to its stimulant effect on the uterus
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30
Q

Prokinetic Agents

A
  • agents that increase lower esophageal sphincter pressure may be useful for GERD
  • agents that increase gastric emptying may be helpful for gastroparesis and delay of post-surgical gastric emptying
  • many prokinetic agents have serious cardiac, cholinergic, and/or CNS side effects that limit usage
  • because of such untoward effects, cisapride, tegaserod, and domperidone are not available in the U.S. and bethanecol is seldom used
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31
Q

Metoclopramide

A
  • hastens esophageal clearance, raises lower esophageal sphincter pressure, and accelerates gastric emptying
  • antagonism of dopamine D2-receptors is thought to underlie its prokinetic properties
  • can produce symptomatic relief in pts with gastric motor failure due to diabetes and post-surgical disorders
  • sometimes used in combination with antisecretory agents, for the txt of refractory heartburn
  • also effective as an antiemetic agent (prevention of vomiting.. usually given for this)
  • TOXICITY: multiple CNS untoward effects, including extrapyramidal sxs (e.g. Parkinsonism and tardive dyskinesia), anxiety, depression, and drowsiness
  • much lower dose needed for antiemetic effects, so usually given for this due to less toxicity
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32
Q

Lubiprostone

A
  • a fatty acid derived from prostaglandin E1 that activates type 2 chloride channels in GI epithelial cells, producing a chloride-rich fluid secretion
  • secretion softens stool, increases motility, and promotes spontaneous bowel movements
  • useful for the management of chronic idiopathic constipation and irritable bowel syndrome with constipation
  • not approved for use in children
  • COMMON SIDE EFFECTS include nausea, diarrhea, headache, and abd pain
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33
Q

Linaclotide

A
  • peptide agonist of guanylate cyclase 2C that activates CFTR chloride ion channels in GI epithelial cells, producing a chloride-rich fluid secretion that increases motility and promotes spontaneous bowel movements
  • also reduces pain by reducing activation of colonic sensory neurons (helps with abd cramps)
  • useful in the txt of chronic idiopathic constipation and IBS with constipation
  • MOST COMMON SIDE EFFECT is diarrhea, which can occasionally be severe enough to warrant cessation of txt
  • not recommended for children 17 and younger
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34
Q

Psyllium

A
  • bulk-forming laxative
  • indigestible, hydrophilic colloid that absorbs water, forming a bulky, emollient gel that distends the colon and promotes peristalsis
  • SIDE EFFECT: bacterial digestion of plant fibers in the colon can lead to bloating and flatus
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35
Q

Methylcellulose

A
  • bulk-forming laxative
  • indigestible, hydrophilic colloid that absorbs water, forming a bulky, emollient gel that distends the colon and promotes peristalsis
  • SIDE EFFECT: bacterial digestion of plant fibers in the colon can lead to bloating and flatus
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36
Q

Polycarbophil

A
  • bulk-forming laxative
  • synthetic fiber
  • indigestible, hydrophilic colloid that absorbs water, forming a bulky, emollient gel that distends the colon and promotes peristalsis
  • SIDE EFFECT: bacterial digestion of plant fibers in the colon can lead to bloating and flatus
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37
Q

Docusate

A
  • stool softener
  • soften stool material, permitting water and lipids to penetrate
  • may be administered orally or rectally
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38
Q

Glycerin suppository

A
  • stool softener
  • soften stool material, permitting water and lipids to penetrate
  • may be administered orally or rectally
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39
Q

Mineral Oil

A

-lubricates fecal material, retarding water absorption from the stool (acts via emulsification)

40
Q

Mg(OH)2 (Milk of Magnesia)

A
  • osmotic laxative
  • soluble but non-absorbable compound that results in increased stool liquidity due to an obligate increase in fecal fluid
  • PEG solutions are used for colonic cleansing prior to GI endoscopic procedures
  • can help in patients with IBS who have constipation
41
Q

Sorbitol

A
  • osmotic laxative
  • soluble but non-absorbable compound that results in increased stool liquidity due to an obligate increase in fecal fluid
  • PEG solutions are used for colonic cleansing prior to GI endoscopic procedures
  • can help in patients with IBS who have constipation
42
Q

Lactulose

A
  • osmotic laxative
  • soluble but non-absorbable compound that results in increased stool liquidity due to an obligate increase in fecal fluid
  • PEG solutions are used for colonic cleansing prior to GI endoscopic procedures
43
Q

Polyethylene glycol

A
  • osmotic laxative
  • soluble but non-absorbable compound that results in increased stool liquidity due to an obligate increase in fecal fluid
  • PEG solutions are used for colonic cleansing prior to GI endoscopic procedures
44
Q

Magnesium citrate and Sodium phosphate

A
  • osmotic laxative

- for rapid (1-3 hrs) bowel evacuation (purgation)

45
Q

Bisacodyl

A
  • stimulant laxative
  • induces bowel movements through mechanisms that include stimulation of the enteric nervous system and secretion of colonic electrolytes and fluid
  • typically produce a bowel movement in 6-12 hrs when given orally and within 2 hrs when given rectally
  • bisacodyl is used in conjunction with PEG solutions (Dulcolax + MiraLAX) for colonic cleansing prior to colonoscopy
46
Q

Aloe Vera

A
  • stimulant laxative
  • induces bowel movements through mechanisms that include stimulation of the enteric nervous system and secretion of colonic electrolytes and fluid
  • typically produce a bowel movement in 6-12 hrs when given orally and within 2 hrs when given rectally
47
Q

Senna

A
  • stimulant laxative
  • induces bowel movements through mechanisms that include stimulation of the enteric nervous system and secretion of colonic electrolytes and fluid
  • typically produce a bowel movement in 6-12 hrs when given orally and within 2 hrs when given rectally
48
Q

Cascara Sagrada

A
  • stimulant laxative
  • induces bowel movements through mechanisms that include stimulation of the enteric nervous system and secretion of colonic electrolytes and fluid
  • typically produce a bowel movement in 6-12 hrs when given orally and within 2 hrs when given rectally
49
Q

Diphenoxylate

A
  • antidiarrheal agent
  • may be used safely in pts with mild to moderate acute diarrhea, but should not be used in pts with bloody diarrhea and high fever
  • act by inhibiting acetylcholine release through presynaptic opioid receptors in the enteric nervous system
  • TOXICITY: has the potential for CNS effects, and prolonged use can lead to dependence
50
Q

Loperamide

A
  • antidiarrheal agent
  • may be used safely in pts with mild to moderate acute diarrhea, but should not be used in pts with bloody diarrhea and high fever
  • act by inhibiting acetylcholine release through presynaptic opioid receptors in the enteric nervous system
  • helpful in treating IBS
  • available OTC
  • ** does not cross the blood-brain barrier and has no potential for addiction **
51
Q

Amitriptyline

A
  • antidepressant
  • for pain and severe IBS
  • for chronic abd pain, low doses appear to be helpful w/o altering mood
52
Q

Desipramine

A
  • antidepressant
  • for pain and severe IBS
  • for chronic abd pain, low doses appear to be helpful w/o altering mood
53
Q

Alosetron

A
  • for pain and severe IBS
  • inhibition of 5-HT3-receptors in the GI tract inhibits unpleasant visceral afferent pain and nausea
  • approved for the treatment of pts with severe IBS with diarrhea
54
Q

5-aminosalicylic acid (5-ASA, mesalamine)

A
  • have been used successfully for decades for txt of IBDs (ulcerative colitis and Crohn’s disease)
  • believed to work topically (not systemically) in areas of diseased GI mucosa
  • considered first-line agents for the txt of mild to moderate ulcerative colitis
  • although their efficacy in Crohn’s disease is unproven, they are also used as first-line therapy for mild to moderate disease involving the colon or distal ileum
55
Q

Sulfasalazine

A

commonly used formulation of 5-aminosalicylate

56
Q

Olsalazine

A

commonly used formulation of 5-aminosalicylate

57
Q

Balsalazide

A

commonly used formulation of 5-aminosalicylate

58
Q

Prednisone

A

glucocorticoid often used in the txt of pts with moderate to severe active IBD

59
Q

Prednisolone

A

glucocorticoid often used in the txt of pts with moderate to severe active IBD

60
Q

Hydrocortisone

A
  • glucocorticoid often used in the txt of pts with moderate to severe active IBD
  • used in the form of enemas, foams, and suppositories to maximize colonic and rectal tissue effects, while minimizing systemic absorption (though 15-30% of administered dosage is still absorbed)
61
Q

Budesonide

A
  • glucocorticoid often used in the txt of pts with moderate to severe active IBD
  • controlled-release oral formulation that releases the drug in the distal ileum and colon, where it is absorbed
  • oral controlled-release is commonly used in the txt of mild to moderate Crohn’s disease involving the ileum and proximal colon
  • subject to rapid fast-pass hepatic metabolism and capsules have a bioavailability of ~10%
  • usually used as an inhaled steroid for asthma due to crappy bioavailability, but even with crappy bioavailability it still works b/c very potent
62
Q

Azathioprine

A
  • purine antimetabolite that has immunosuppressive properties
  • important agents in the induction and maintenance of remission of ulcerative colitis and Crohn’s disease
  • after 3-6 months of txt, 50-60% of pts with active disease achieve remission
  • help maintain remission in up to 80% of pts
63
Q

6-mercaptopurine (6-MP)

A
  • purine antimetabolite that has immunosuppressive properties
  • important agents in the induction and maintenance of remission of ulcerative colitis and Crohn’s disease
  • after 3-6 months of txt, 50-60% of pts with active disease achieve remission
  • help maintain remission in up to 80% of pts
64
Q

Methotrexate

A

-another antimetabolite used to induce and maintain remission in pt’s with Crohn’s disease, but its efficacy in ulcerative colitis is uncertain

65
Q

Inflaximab

A
  • anti-tumor necrosis factor (anti-TNF) therapy
  • TNF is one of the key proinflammatory cytokines in IBD
  • approved for acute and chronic txt of pts with moderate to severe Crohn’s, where response to conventional therapies is inadequate
  • with induction therapy, all three agents lead to symptomatic improvement in 60% and disease remission in 30% of pts with moderate to severe Crohn’s
  • ** also approved for the acute and chronic txt of ulcerative colitis in cases of inadequate response to mesalamine or corticosteroids **
  • MOST SIGNIFICANT EFFECT (in up to 6% of patients with anti-TNF therapy) is opportunistic infection (e.g. bacterial sepsis, TB, fungal, and listeriosis) from suppression of the helper T-cell type 1 inflammatory response
66
Q

Adalimumab

A
  • anti-tumor necrosis factor (anti-TNF) therapy
  • TNF is one of the key proinflammatory cytokines in IBD
  • approved for acute and chronic txt of pts with moderate to severe Crohn’s, where response to conventional therapies is inadequate
  • with induction therapy, all three agents lead to symptomatic improvement in 60% and disease remission in 30% of pts with moderate to severe Crohn’s
  • MOST SIGNIFICANT EFFECT (in up to 6% of patients with anti-TNF therapy) is opportunistic infection (e.g. bacterial sepsis, TB, fungal, and listeriosis) from suppression of the helper T-cell type 1 inflammatory response
67
Q

Certolizumab

A
  • anti-tumor necrosis factor (anti-TNF) therapy
  • TNF is one of the key proinflammatory cytokines in IBD
  • approved for acute and chronic txt of pts with moderate to severe Crohn’s, where response to conventional therapies is inadequate
  • with induction therapy, all three agents lead to symptomatic improvement in 60% and disease remission in 30% of pts with moderate to severe Crohn’s
  • MOST SIGNIFICANT EFFECT (in up to 6% of patients with anti-TNF therapy) is opportunistic infection (e.g. bacterial sepsis, TB, fungal, and listeriosis) from suppression of the helper T-cell type 1 inflammatory response
68
Q

Natalizumab

A
  • anti-integrin therapy
  • humanized monoclonal antibody that targets the integrin alpha-4 subunit, thereby blocking several integrins on circulating inflammatory cells
  • integrins are adhesion proteins on the surface of circulating leukocytes that allow them to adhere to the vascular endothelium, and subsequently move through the vessel wall into the tissue
  • in initial clinical trials, 3/3100 pts developed progressive multifocal leukoencephalopathy due to reactivation of latent human polyoma virus
  • withdrawn in 2005, it was approved in 2008 for pts with moderate to severe Crohn’s who have failed other therapies, through a carefully restricted program
  • approx 50% of pts respond to initial therapy, with a long-term response being maintained in 60% and remission in over 40% of those pts
69
Q

Ondansetron

A
  • antiemetic
  • selective 5-HT3 receptor antagonist
  • primary agents for the prevention of ACUTE chemotherapy-induced nausea and emesis
  • also effective at preventing and treating postoperative and postradiation nausea and vomiting
  • efficacy is enhanced by combination therapy with a corticosteroid (e.g. dexamethasone) and NK1-receptor antagonist (e.g. aprepitant)
70
Q

Granisetron

A
  • antiemetic
  • selective 5-HT3 receptor antagonist
  • primary agents for the prevention of ACUTE chemotherapy-induced nausea and emesis
  • also effective at preventing and treating postoperative and postradiation nausea and vomiting
  • efficacy is enhanced by combination therapy with a corticosteroid (e.g. dexamethasone) and NK1-receptor antagonist (e.g. aprepitant)
71
Q

Dolasetron

A
  • antiemetic
  • selective 5-HT3 receptor antagonist
  • primary agents for the prevention of ACUTE chemotherapy-induced nausea and emesis
  • also effective at preventing and treating postoperative and postradiation nausea and vomiting
  • efficacy is enhanced by combination therapy with a corticosteroid (e.g. dexamethasone) and NK1-receptor antagonist (e.g. aprepitant)
72
Q

Palonosetron

A
  • antiemetic
  • selective 5-HT3 receptor antagonist
  • primary agents for the prevention of ACUTE chemotherapy-induced nausea and emesis
  • also effective at preventing and treating postoperative and postradiation nausea and vomiting
  • efficacy is enhanced by combination therapy with a corticosteroid (e.g. dexamethasone) and NK1-receptor antagonist (e.g. aprepitant)
73
Q

Aprepitant

A
  • neurokinin (NK)-receptor antagonist
  • NK1-receptor antagonists have antiemetic properties
  • used in combination with 5-HT3-receptor antagonists and corticosteroids for the prevention of ACUTE AND DELAYED nausea and vomiting from highly emetogenic chemotherapeutic regimens
74
Q

Fosaprepitant

A
  • neurokinin (NK)-receptor antagonist
  • NK1-receptor antagonists have antiemetic properties
  • used in combination with 5-HT3-receptor antagonists and corticosteroids for the prevention of ACUTE AND DELAYED nausea and vomiting from highly emetogenic chemotherapeutic regimens
75
Q

Diphenhydramine

A
  • H1 antihistamine

- although weakly antiemetic, they are particularly useful for the prevention and txt of motion sickness

76
Q

Dimenhydrinate

A
  • H1 antihistamine

- although weakly antiemetic, they are particularly useful for the prevention and txt of motion sickness

77
Q

Meclizine

A
  • H1 antihistamine
  • although weakly antiemetic, they are particularly useful for the prevention and txt of motion sickness
  • meclizine has less anticholinergic properties and is less sedating than the other two agents
78
Q

Goals of HBV Therapy

A
  • goals are to sustain suppression of HBV, so as to:
    1. slow the progression of the disease (with retardation of hepatic fibrosis and even reversal of cirrhosis)
    2. prevent complications (i.e. cirrhosis, hepatic failure, and hepatocellular carcinoma)
    3. reduce the need for liver transplantation
  • achieving these goals leads to 3 endpoints:
    1. suppress HBV DNA to undetectable levels
    2. seroconversion of hepatitis B e antigen (HBeAg) from + to -
    3. reduction in elevated hepatic transaminase levels
79
Q

Tenofovir Disoproxil Fumerate

A
  • nucleoside analog
  • treatment of chronic HBV infection
  • inhibit HBV DNA synthesis by inhibiting HBV DNA polymerase (virus hijacks host mechanisms except it brings along its own DNA polymerase)
  • first line therapy
80
Q

Entecavir

A
  • nucleoside analog
  • treatment of chronic HBV infection
  • inhibit HBV DNA synthesis by inhibiting HBV DNA polymerase (virus hijacks host mechanisms except it brings along its own DNA polymerase)
  • first line therapy
81
Q

Adefovir

A
  • nucleoside analog
  • treatment of chronic HBV infection
  • inhibit HBV DNA synthesis by inhibiting HBV DNA polymerase (virus hijacks host mechanisms except it brings along its own DNA polymerase)
82
Q

Lamivudine

A
  • nucleoside analog
  • treatment of chronic HBV infection
  • inhibit HBV DNA synthesis by inhibiting HBV DNA polymerase (virus hijacks host mechanisms except it brings along its own DNA polymerase)
83
Q

Telbivudine

A
  • nucleoside analog
  • treatment of chronic HBV infection
  • inhibit HBV DNA synthesis by inhibiting HBV DNA polymerase (virus hijacks host mechanisms except it brings along its own DNA polymerase)
84
Q

Pegylated Interferon alpha-2a and 2b

A
  • nucleoside analog
  • treatment of chronic HBV infection
  • cytokines that induce signals which inhibit viral penetration, translation, transcription, protein processing, maturation, and release
  • first line therapy
85
Q

Anti-HBV Efficacy

A
  • nucleoside analog therapies are typically better tolerated and produce higher (though less rapid) response rates than the interferon therapies
  • however, the responses to nucleoside analogs may be less sustained after discontinuation of therapy than responses to interferons
  • in addition, oral nuceloside analog therapy is chronic, whereas interferon therapy is finite (you will get too sick if you keep taking interferon therapy)
86
Q

Primary Goal of HCV Therapy

A
  • viral eradication
  • achieving this goal translates into the following endpoint:
  • a sustained viral response (SVR), as indicated by the absence of detectable viremia for a period of 6 months after completion of therapy
  • oral regimens are generally well tolerated
  • nausea is a common side effect that can be minimized by taking the oral regimens with food
87
Q

Sofosbuvir and Ribavirin

A
  • treatment of HCV genotypes 2 and 3
  • taken oral daily in combination with weight-based ribavirin
  • sofosbuvir is a nucleotide analog that inhibits the HCV RNA polymerase (nonstructural protein 5B, NS5B)
  • ribavirin is a nucleoside analog that inhibits GTP synthesis and capping of viral mRNA
  • this dual drug combination markedly reduces the duration of treatment compared to previous combination regimens
  • *** Recommended Treatment Duration:
  • 12 wks for genotype 2
  • 24 wks for genotype 3
88
Q

Treatment of HCV Genotype 1a (worst genotype)

A
  • three oral options with similar efficacy are recommended:
    1. fixed-dose combination of Ledipasvir/Sofosbuvir (Harvoni) for 12 wks
    2. fixed-dose combination of Paritaprevir/Ritonavir/Ombitasvir plus twice daily Dasabuvir (packaged together as Viekira Pak) for 12 wks (no cirrhosis) or for 24 wks (with cirrhosis)
    3. daily Sofosbuvir in combination with Simeprivir with or without weight-based ribavirin for 12 wks (no cirrhosis) or for 24 wks (with cirrhosis)
89
Q

Ledipasvir

A

inhibits the HCV nonstructural 5A (NS5A) phophoprotein, thereby inhibiting viral replication, assembly, and secretion

90
Q

Ombitasvir

A

inhibits the HCV nonstructural 5A (NS5A) phophoprotein, thereby inhibiting viral replication, assembly, and secretion

91
Q

Paritaprevir

A

inhibits the HCV nonstructural 3/4A (NS3/4A) serine protease, thereby inhibiting the processing of viral proteins

92
Q

Simeprivir

A

inhibits the HCV nonstructural 3/4A (NS3/4A) serine protease, thereby inhibiting the processing of viral proteins

93
Q

Dasabuvir

A

a non-nucleotide analog that inhibits the HCV NS5B polymerase

94
Q

Ritonavir

A
  • given to boost paritaprevir potency by inhibiting CYP3A4

- it has no intrinsic anti-HCV activity

95
Q

Treatment of HCV Genotype 1b

A
  1. fixed-dose combination of Ledipasvir/Sofosbuvir (Harvoni) for 12 wks
  2. fixed-dose combination of Paritaprevir/Ritonavir/Ombitasvir plus twice daily Dasabuvir (packaged together as Viekira Pak) for 12 wks in pts with no cirrhosis. Add weight-based Ribavirin in pts with cirrhosis
  3. Daily Sofosbuvir in combination with Simeprivir for 12 wks (no cirrhosis) or for 24 wks (with cirrhosis)
96
Q

Treatment of HCV Genotype 4

A
  1. fixed-dose combination of Ledipasvir/Sofosbuvir for 12 wks
  2. fixed-sode combination of Paritaprevir/Ritonavir/Ombitasvir and weight-based Ribavirin for 12 wks
  3. daily sofosbuvir in combination with and weight-based Ribavirin for 24 wks

GI Pharmacology (1 decks)

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