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GI/Pulm > GI Pharm > Flashcards

GI Pharm Flashcards

1
Q

5-Aminosalicylates (5-ASA)

A

Original indication: rheumatoid arthritis

Administration: Oral, topical (rectal)

Multiple immune system effects

Therapeutic uses:

  • UC: induction, maintenance of mild to moderate disease (YES!)
  • CD: induction (weak), ? Maintenance (EH)
  • Chemoprophylaxis (colon cancer)

Toxicity:

  • Dose-related malaise, nausea, abdominal pain
  • Impaired folic acid absorpion (supplement)
  • Oligospermia
  • Severe skin reactions (rare)
  • Nephrotoxicity
  • Bone marrow suppression
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2
Q

Antibiotics in IBD

A

Crohn disease:
ciprofloxacin, metronidazole
- treat colonic and perianal disease

AE: Cipro: c. diff, arthropathy, tendon rupture
Metronidaxole: metallic taste, peripheral neuropathy, antabuse-like effect

Ulcerative colitis: rifaximin
- Elevated CRP

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3
Q

Systemic glucocorticoids in IBD

A

Treatment in severe IBD: abdominal pain, fever, leukocytosis, rectal bleeding

  • remission in 90% cases
  • Orally, 40 mg/day (IV for severe cases)

Binds GC receptors–> inhibits inflamm. mediators, WBC migration/function

+ induction, NOT maintenance

  • No benefit >40-60 mg prednisone
  • Divided ~ once-daily dosing
  • Intravenous, oral, rectal
  • Time Course: 5-10 days
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4
Q

Budesonide

A

Non-systemic steroid for IBD:

  • High first pass metabolism, fewer systemic side-effects
  • Time-dependent release in small bowel

Efficacy:

  • CD: ileal/R colon
  • UC: ulcerative proctitis (enema)
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5
Q

Methotrexate

A

Induction and maintenance therapy for Crohn Disease

MOA: Folate analog; reversible competitive inhibition of dihydrofolate reductase–> interferes with DNA synthesis, multiple anti-inflammatory effects

AE: pulmonitis, hepatotoxicity, BM suppression, teratogen/abortifacient

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6
Q

Cyclosporine

A

Use: Severe, refractory ulcerative colitis NOT responding to steroids

MOA: lipophilic peptide, downregulates IL-2–> inhibits T(H) cells
- Calineurin inhibitor suppresses proinflammatory factors

AE: nephrotoxicity, neurotoxicity, HTN

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7
Q

Natalizumab

A

Use: Induction, maintenance in Crohn Disease

MOA: decreases WBC trafficking to sites of inflammation

AE: progressive multifocal leukoencephalopathy (JC virus exposure)

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8
Q

Anti-TNF monoclonal antibodies

A

MOA: neutralize membrane-bound & soluble TNF (TNF= pro-inflammatory factor)
- TNF-alpha increased in mucosa of Crohn patients

Used in treatment of IBD:

  • Chimeric monoclonal antibody (infliximab): single infusion induces single remission (reduces fistulizing disease)
  • Human monoclonal antibody (adalimumab)
  • Pegylated humanized antibody (Certolizumab pegol)

Toxicity: infrequent: nausea, low risk for infections and malignancy (lymphomas- hepatocellular t-lymphoma)

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9
Q

Azathioprine (AZA)/ 6-mercaptopurine (6-MP)

A

Cytotoxic agents for IBD after gaining control of severe symptoms (second line therapy) - Maintenance

MOA: AZA–> 6-MP–> 6-TGN–> proliferation activated lymphocytes; apoptosis (suppresses lymphocyte proliferation)

Use: Steroid withdrawal, maintenance
Maximal clinical benefit: 3-4 months

Early reactions: fever, pancreatitis
Adverse reactions: leukopenia, hepatotoxicity, infection (viral), lymphoma, non-melanoma skin cancer

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10
Q

Cimetidine

A

H2-receptor antagonist

Clinical use:

  • Promotes gastric and duodenal ulcer healing
  • Prevents ulcer recurrence
  • Suppression of nocturnal acid secretion maximizes efficacy

PK: rapidly absorbed, little hepatic metabolism, excreted by kidneys

Leads to 90% reduction in acid secretion
NO value in combining with antacids; can reduce efficacy of PPIs

    • Cimetidine inhibits P450: slows metab. of other drugs (eg. warfarin, phenytoin)
  • Can also cause confusion in elderly, gynecomastia
  • Can lead to tachyphylaxis over days (upregulates H2 receptors)
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11
Q

Ranitidine

A

H2-receptor antagonist

Clinical use:

  • Promotes gastric and duodenal ulcer healing
  • Prevents ulcer recurrence
  • Suppression of nocturnal acid secretion maximizes efficacy

PK: rapidly absorbed, little hepatic metabolism, excreted by kidneys

Leads to 90% reduction in acid secretion
NO value in combining with antacids; can reduce efficacy of PPIs

  • Can lead to tachyphylaxis over days (upregulates H2 receptors)
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12
Q

Famotidine

A

H2-receptor antagonist

Clinical use:

  • Promotes gastric and duodenal ulcer healing
  • Prevents ulcer recurrence
  • Suppression of nocturnal acid secretion maximizes efficacy

PK: rapidly absorbed, little hepatic metabolism, excreted by kidneys

Leads to 90% reduction in acid secretion
NO value in combining with antacids; can reduce efficacy of PPIs

Fewest side effects, most effective (headache)

  • Can lead to tachyphylaxis over days (upregulates H2 receptors)
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13
Q

Nizatidine

A

H2-receptor antagonist

Clinical use:

  • Promotes gastric and duodenal ulcer healing
  • Prevents ulcer recurrence
  • Suppression of nocturnal acid secretion maximizes efficacy

PK: rapidly absorbed, little hepatic metabolism, excreted by kidneys

Leads to 90% reduction in acid secretion
NO value in combining with antacids; can reduce efficacy of PPIs

  • Can lead to tachyphylaxis over days (upregulates H2 receptors)
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14
Q

Omeprazole (prilosec)

A

Irreversible inhibition of gastric-parietal proton pump (single dose can inhibit 97% of acid secretion)

Clinical use:

  • Short term treatment of GU and DU
  • Superior to H2/misoprostol in healing of NSAID-induced ulcers
  • Tx of choice for Zollinger Ellison, MEN, systemic mastocytosis
  • Used in combination with antibiotics for H.Pylori
  • Treatment of GERD

PK: Rapidly absorbed

  • Highly protein bound
  • Excreted by kidneys
  • Metabolized by and inhibits some P450 (decreased benzo, warfarin, phenytoin clearance)
  • Prodrugs that require activation in an acid milieu (thus best administered with meals)

Toxicities:

  • Inhibition of P450–> decreased clearance of benzos, warfarin, phenytoin
  • Nausea, abdominal pain, change in bowel habits
  • Elevated gastrin: lack of acid feedback inhibition. Carcinoid tumors only observed in animals
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15
Q

Lansoprazole (Prevacid)

A

rreversible inhibition of gastric-parietal proton pump (single dose can inhibit 97% of acid secretion)

Clinical use:

  • Short term treatment of GU and DU
  • Superior to H2/misoprostol in healing of NSAID-induced ulcers
  • Tx of choice for Zollinger Ellison, MEN, systemic mastocytosis
  • Used in combination with antibiotics for H.Pylori
  • Treatment of GERD

PK: Rapidly absorbed

  • Highly protein bound
  • Excreted by kidneys
  • Metabolized by and inhibits some P450 (decreased benzo, warfarin, phenytoin clearance)
  • Prodrugs that require activation in an acid milieu (thus best administered with meals)

Toxicities:

  • Inhibition of P450–> decreased clearance of benzos, warfarin, phenytoin
  • Nausea, abdominal pain, change in bowel habits
  • Elevated gastrin: lack of acid feedback inhibition. Carcinoid tumors only observed in animals
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16
Q

Rabeprazole (aciphex)

A

rreversible inhibition of gastric-parietal proton pump (single dose can inhibit 97% of acid secretion)

Clinical use:

  • Short term treatment of GU and DU
  • Superior to H2/misoprostol in healing of NSAID-induced ulcers
  • Tx of choice for Zollinger Ellison, MEN, systemic mastocytosis
  • Used in combination with antibiotics for H.Pylori
  • Treatment of GERD

PK: Rapidly absorbed

  • Highly protein bound
  • Excreted by kidneys
  • Metabolized by and inhibits some P450 (decreased benzo, warfarin, phenytoin clearance)
  • Prodrugs that require activation in an acid milieu (thus best administered with meals)

Toxicities:

  • Inhibition of P450–> decreased clearance of benzos, warfarin, phenytoin
  • Nausea, abdominal pain, change in bowel habits
  • Elevated gastrin: lack of acid feedback inhibition. Carcinoid tumors only observed in animals
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17
Q

Pantoprazole (protonix)

A

rreversible inhibition of gastric-parietal proton pump (single dose can inhibit 97% of acid secretion)

Clinical use:

  • Short term treatment of GU and DU
  • Superior to H2/misoprostol in healing of NSAID-induced ulcers
  • Tx of choice for Zollinger Ellison, MEN, systemic mastocytosis
  • Used in combination with antibiotics for H.Pylori
  • Treatment of GERD

PK: Rapidly absorbed

  • Highly protein bound
  • Excreted by kidneys
  • Metabolized by and inhibits some P450 (decreased benzo, warfarin, phenytoin clearance)
  • Prodrugs that require activation in an acid milieu (thus best administered with meals)

Toxicities:

  • Inhibition of P450–> decreased clearance of benzos, warfarin, phenytoin
  • Nausea, abdominal pain, change in bowel habits
  • Elevated gastrin: lack of acid feedback inhibition. Carcinoid tumors only observed in animals
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18
Q

Esomeprazole (nexium)

A

rreversible inhibition of gastric-parietal proton pump (single dose can inhibit 97% of acid secretion)

Clinical use:

  • Short term treatment of GU and DU
  • Superior to H2/misoprostol in healing of NSAID-induced ulcers
  • Tx of choice for Zollinger Ellison, MEN, systemic mastocytosis
  • Used in combination with antibiotics for H.Pylori
  • Treatment of GERD

PK: Rapidly absorbed

  • Highly protein bound
  • Excreted by kidneys
  • Metabolized by and inhibits some P450 (decreased benzo, warfarin, phenytoin clearance)
  • Prodrugs that require activation in an acid milieu (thus best administered with meals)

Toxicities:

  • Inhibition of P450–> decreased clearance of benzos, warfarin, phenytoin
  • Nausea, abdominal pain, change in bowel habits
  • Elevated gastrin: lack of acid feedback inhibition. Carcinoid tumors only observed in animals
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19
Q

Treatment of GERD

A
  • PPIs are more effective than H2s

- An empirical trial of PPIs is appropriate in the absence of alarm symptoms (wt loss, dysphagia)

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20
Q

Treatment of NERD

A

Non-erosive reflux disease (heartburn sensation without damage)
Acid suppression effective in ~ 50%

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21
Q

Treatment of peptic ulcer disease

A
  • PPIs promote more rapid healing than H2s

- IV PPIs have a role in acute bleeding

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22
Q

Treatment of stress ulceration

A
  • Burn and head trauma victims

- Acid suppressive therapy is beneficial

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23
Q

Carbechol

A
  • Activation of muscarinic receptors on the smooth muscle cells
  • Increases intracellular Ca++–> enhanced motility (cholinergic drug)
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24
Q

Bethanecol

A
  • Activation of muscarinic receptors on the smooth muscle cells (cholinergic drug)
  • Increases intracellular Ca++–> enhanced motility
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25
Q

Metaclopramide

A

Clinical uses:

  • Gastroparesis (diabetic)
  • Anti-emesis
  • Heartburn in GERD

Targets:

  • Dopamine antagonist: ENS- blocks dopamine (which blocks Ach), thus increases motility (enhances Ach effects)
  • 5-HT3 antagonist: ECL cells and ENS promotes motility
  • 5-HT4 agonist: enhances motility

Toxicity:

  • Somnolence
  • Nervousness
  • Tardive dyskinesia in elderly
  • Prolactin secretion
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26
Q

Tegeserod maleate (Zelnorm)

A

Serotonin receptor modulator used in constipation-predominant IBS

MOA: 5-HT4 agonist= modules excitatory response (enhanced motility)

27
Q

Erythromycin

A

Motilin agonist used in diabetic gastroparesis and intestinal pseudo-obstruction

  • Stimulation enhances MMC (migrating motor complex= fasting state sweep of bowel in 80-110 minutes)
28
Q

Botox

A

Inhibits Ach release

  • Intrapyloric injection to inhibit pylorospasm, seen in diabetic gastroparesis
  • Enhances solid, not liquid emptying
  • Improves post-prandial fullness, bloating
29
Q

Pancreatin

A

Extract of hog pancreas

Uses: aids with digestion

  • Helps shuts down pancreas to lower pain caused by inability to secrete pancreatic enzymes (food stimulates pancreas)
  • Prevents steatorrhea (pancreatic output < 10% of normal)

Dosed with meals, titrated to therapeutic effect
- Higher gastric pH enhances activity

30
Q

Pancrelipase

A

Enriched with lipase

Uses: aids with digestion

  • Helps shuts down pancreas to lower pain caused by inability to secrete pancreatic enzymes (food stimulates pancreas)
  • Prevents steatorrhea (pancreatic output < 10% of normal)

Dosed with meals, titrated to therapeutic effect
- Higher gastric pH enhances activity

31
Q

Antibiotics in IBD

A

Metronidazole, ciprofloxacin

  • Useful in mild to moderate Crohn disease
  • Induces remission
32
Q

Mesalamine

A

Coated 5-ASA

  • Lacks sulfa component (causes toxicities)
  • Asacol= coating dissolves in alkaline ileum, colon
  • Pentasa= semi-permeable coating, releases drug through jejunem and colon
  • Rowasa Enema= local delivery for distal colitis, rectal disease
33
Q

Olsalazine

A
  • 2 5-ASA molecules linked by diazo bond
  • Bond cleaved by bacterial flora
    Used for IBD treatment
34
Q

Treatment for severe Ulcerative Colitis

A

First: Glucocoticoids

Improvement with Glucocorticoids:

  • 5-ASA
  • Cytotoxic agents (Azathioprine, 6-mercaptopurine)

No improvement with glucocorticoids:

  • Cyclosporine
  • Surgery
35
Q

Treatment for mild/moderate Ulcerative colitis

A
  • Sulfasalazine
  • Mesalamine
  • Olsalazine

Improvment: maintenance on above tx
No improvement: Glucocorticoids

36
Q

Treatment for severe Crohn Disease

A

First: Glucocorticoids

Improvement:

  • 5-ASA
  • Cytotoxic agents (Azathioprine, 6-mercaptopurine)

No improvement with glucocorticoids:

  • TNF-alpha inhibitors
  • Surgery
37
Q

Treatment for mild/moderate Crohn Disease

A
  • Antibiotics
  • Sulfasalzine (colon only)
  • Mesalamine (small bowel)
  • Budesonide (ileal)

Improvement: maintenance therapy on above
No improvement: Glucocorticoids

38
Q

Octreotide

A

Synthetic somatostatin analogue to inhibit gastric secretions (peptic ulcers), treats severe refractory secretory diarrhea (endocrine tumor), vasoconstriction in GI bleeding

MOA: targets somatostatin receptors on ECL cells–> decreased acid secretion; hyperpolarizes gut neurons–> decreases Ach, slowing peristalsis

Use: Zollinger-Ellison syndrome, anti-diarrheal

Contraindications: hypersensitivity; can cause gallbladder stasis

39
Q

Chenodiol

A

Bile salt used to solubilize cholesterol in gallstones (oral)
- Use limited by diarrhea

40
Q

Ursodiol

A

Bile salt used to solubilize cholesterol in gallstone therapy and primary biliary cirrhosis

  • Epimer of chenodiol
  • Less toxicity (diarrhea)
41
Q

Bulk-forming agents

A

Psyllium, carboxymethycellulose

MOA: absorb water and form gels in large intestine–> intestinal distention, peristalsis

Uses: chronic constipation or diarrhea (BULK forming)

Contraindications: GI obstruction, perforation, gastric retention, abdominal pain, vomiting (appendicitis), toxic colitis, ileus, megacolon
- Avoid in pts with swallowing difficulties, slow colon, diverticulitis

Adverse effects: bloating, flatulence, abdominal cramps; can effect drug absorption (separate by 1 hour)

42
Q

Osmotic/saline/hyperosmotic agents

A

Magnesium citrate, magnesium hydroxide, sodium phophates, polyethylene glycol + electrolytes, lactulose, sorbitol, glycerin suppositories

MOA: non-absorbable/non-digestable salts/sugars hold water in intestine (osmotic force)–> distends colon–> peristalsis

Uses: constipation, colon prep for GI procedures, removal of toxins

Contraindications: GI obstruction, perforation, gastric retention, undiagnosed abdominal pain, vomiting/ appendicitis, toxic colitis/ileus/megacolon; ulcerative colitis, diverticulitis, colonoscopy/ileostomy, renal insufficiency, heart block (Na/K changes), rectal bleeding

Adverse effects: electrolyte abnormalities

Interactions: Antibiotics (Mg-containing laxatives)

43
Q

Surfactant laxatives

A

Docusate dioctyl sodium sulfocussinate

MOA: anionic detergent–> emulsify stool, softens

Indications: stool softener, hemorrhoids

Contraindications: GI obstruction, perforation, gastric retention, undiagnosed abodominal pain, vomiting/appendicitis, toxic colitis/ileus/megacolon, fecal impaction/obstruction, acute surgical abdomen. AVOID mineral oil use

Adverse effects: cramping

  • NOT useful once constipation has occurred
44
Q

Lubricant laxatives

A

Mineral oil

MOA: penetrates/lubricates feces for easier passage, prevents water reabsorption

Indications: fecal impaction; post-MI, surgery, partum (avoid straining)

Contraindications: aspiration risk, appendicitis, diverticulitis, ulcerative colitis, colostomy/ileostomy

Adverse effects: aspiration, incontinence/anal leakage; chronic use–> malabsorption of fat-soluble minerals, chronic intestinal hypomotility

45
Q

Irritant/stimulant/contact laxatives

A

Anthraquinones, cassia, aloe, castor oil, diphenylmethane, bisacodyl

MOA: contact irritant on enterocytes, enteric neurons, muscle–> accumulation of water/electrolytes in lumen + stimulation of intestinal motility

*Prodrugs- need to be digested to be effective

Indications: constipation, prep for delivery, surgery, GI exam

Contraindications: acute abdomen, bowel obstruction, appendicitis, gastroenteritis. NOT for chronic use

Adverse effects: melanosis coli, cathartic colon, cramps, severe diarrhea, dependency, mucosal damage (castor oil, diphenylmethanes)

Interactions: antacids, milk

46
Q

Methylnaltrexone

A

MOA: Muscarinic opioid receptor antagonist. Cannot cross BBB (no effects on opioid receptors)

Use: opioid-induced constipation; post-operative ileus

Contraindications: known/suspected mechanical GI obstruction

Adverse effects: diarrhea, abdominal pain, nausea, dizziness

47
Q

Sucraflate

A
  • Sucrose based compound that becomes a viscous paste in the stomach and duodenum
  • Mechanical barrier to caustic acid, pepsin, bile salts
  • Promotes the mucous/bicarbonate layer and the mucoid cap promoting epithelial regeneration

Adverse effects: minor

48
Q

Bismuth subsalicylate

A

Uses:

  • Non-specific anti-diarrheal: binds bacterial toxins, anti-secretory effects
  • Ulcer treatment: Mechanism felt to be related to formation of a glycoprotein-bismuth complex over ulcer crater preventing further ulceration and promoting healing

Contraindications: hypersensitivity to ASA, not for children < 16 with viral infections, avoid chronic use in renal failure patients

49
Q

Misoprostol for Gastric Ulcers

A

Prostaglandin analog (PGE1)

  • Improves mucosal blood flow–> enhances the mucous/bicarbonate layer
  • Decreases acid production

Side effects limit use: Diarrhea, Uterine muscle contraction (NO pregnant women)

*Most commonly used for patients who must be maintained on NSAIDs

50
Q

H. pylori therapy

A
  1. PPI + 2 antibiotics= PPI + amoxicillin + clarithromycin (PPI-AC)
  2. Acid suppressing agent + 3 antibiotics= PPI/H2RA + bismuth + metronidazole + tetracyclines
    * metronidazole + clarithromycin resistance more common–> use amoxicillin
51
Q

Medical management of Gastric ulcers

A

1) Proton pump inhibitors: decreases gastric acidity by 97%
2) H2 receptor antagonists: only first line when given in IV high dose infusion
3) Sucralfate: becomes past in stomach–> mechanical barrier to allow healing
4) Bismuth: forms glycoprotein-bismuth complex over ulcer crater
5) Prostaglandin anaglogs (misoprostol- PGE1): mucosal blood flow enhanced

52
Q

Pharmacotherapy for Upper GI bleed

A
  • PPI (IV)
  • IV erythromycin (enhance motility for endoscopy)
  • IV Octreotide: lower portal pressure, decreases splanchnic blood flow
  • Vasopressin (decrease portal venous inflow- splanchnic vasoconstriction) + nitrates (to prevent end-organ ischemia)
53
Q

Alvimopan

A

MOA: muscarinic receptor antagonist

Uses: short-term, in-hospital use for post-operative ileus

Contraindication: therapeutic dose of opioids used for more than 7 days

54
Q

Lubiprostone

A

MOA: Agonist of GI CLC-2 chloride channels; activates channel–> increased chloride-rich intestinal fluids without affecting serum Na+ or K+
- Structural prostaglandin with osmotic laxative properties

Use: Chronic idiopathic constipation, IBS with constipation (females > 18)

Adverse effects: nausea, diarrhea, abdominal pain

*No evidence of tolerance, dependence, or rebound effects

55
Q

Drugs causing diarrhea

A 
Antibiotics
Adrenergic neuron blockers
Cholinergic agonists, cholinesterase inhibitors
Laxatives (osmotic, stimulant)
Prokinetic agents (metoclopramide)
Prostaglandins
Quinidine
56
Q

Narcotic analogs for diarrhea

A

Phenylpiperidine analgesic analog, loperamide, diphenoxylate + atropine, diphenoxin + atropine

MOA: Stimulates opioid receptors in myenteric plexus–> slows intestinal transit/ decreases secretions

Uses: Acute, non-specific diarrhea

Contraindications: NOT for infectious diarrhea, toxigenic E. coli, salmonella, shigella

Adverse effects: constipation, toxic megacolon

57
Q

Bile acid binders for diarrhea

A

Cholestyramine, colestipol

MOA: anion exchange resin, binds bile acids

Uses: secretory diarrhea, post-op

Contraindications: patients prone to constipation

58
Q

Components of antacids

A

Al and Mg hydroxide: Al slower than Mg
Na and Ca bicarbonate: fast rate of reaction
Non-acid neutralizing components: simethicone, alginic acid

  • Do not use in renal failure patients
59
Q

IBS treatments

A

Constipation-predominant disease

  • Bulking agents
  • Prokinetics (metoclopramide)
  • Tegaserod maleate
  • Lubiprostone

Diarrhea-predominant:

  • Antispasmodics/anticholinergics
  • Antidepressants
60
Q

Gastroparesis treatments

A
  • Metoclopramide (prokinetic)
  • Erythromycin (MMC effects)
  • Cisapride (prokinetic like metoclopramide)
  • Botox: intrapyloric injection
61
Q

Asacol

A

Coated 5-ASA for IBD: released in terminal ileum and colon

62
Q

Pentasa

A

Semipermeable coated 5-ASA for IBD: semi-permeable allows release from jejunem through colon

63
Q

Rowasa

A

Mesalamine (5-ASA) in wax matrix to treat rectal form of IBD

GI/Pulm (7 decks)

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