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Pharm II New Stuff Final > Gastrointestinal Agents > Flashcards

Gastrointestinal Agents Flashcards

1
Q

Proton Pump Inhibitors (PPI)

  1. ADR’s?
  2. How to discontinue drug?
  3. DDI’s?
A
  1. Vit b12 deficiency, osteoporosis, community acquired pneumonia
  2. Taper to avoid rebound hypersecretion of acid
  3. ketoconazole, itraconazole, atazanavir, rilpivirine, calcium carbonate, iron salts
    • Omeprazole + clopidogrel = therapeutic failure of clopidogrel
      • increase risk for MI
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2
Q

Name miscellaneous anti-emetics that can be used? ( 4 things)

A
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3
Q

What drug category would you used for what areas of inflammation?

A
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4
Q

Linaclotide

  1. MOA?
  2. What else can this drug do?
  3. ADR’s?
  4. Indication?
A
  1. Activates guanylate cyclase in response to a meal → increase cGMP→stimulates stimulates chloride sodium bicarbonate and water secretion into intestinal lumen
  2. Also activates colonic sensory and motor neurons
    • reduces abdominal pain and increases smooth muscle contraction ( increases peristalsis)
  3. Serious dehydration -BBW
    • Do not use with pts < 18 years of age
  4. Constipation
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5
Q

Saline Laxative

  1. MOA?
  2. OTC agents available?
  3. Caution with?
A
  1. MOA: draws water into the intestine(sm &lg), increasing intraluminal pressure, which acts as a stimulus to increase intestinal motility
    • Magnesium citrate
    • Magnesium hydroxide
    • Sodium phosphate/diphosphate
  3. Caution in elders with uncontrolled cardiac and renal disease
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6
Q

Aminosalicylate ADEs/DDI’s

  • Mesalamine ADR’s?
  • Osalazine ADR’s?
  • Sulfasalazine ADR?

How can you “treat” ADR’s of Sulfasalazine?

DDI’s of all agents?

A
  • M: well tolerated
  • O: secretory diarrhea
  • Sulfa: “lupus like syndrome”
    • Folate deficiency
    • rash
    • photosensitivity
  • Supplement with 1 mg daily of folic acid
  • DDI’s: Medicaitons that can alter stomach pH
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7
Q

Lubiprostone

  1. Indication?
  2. What is the MOA?
  3. ADR’s?
A
  1. Take for chronic constipation -agent derived from PE1
  2. MOA: activates cholride channel in GI epithelial cells → efflux of Cl, Na, H2O into lumen of GI tract → increased fluid secretion and intestinal transport
  3. ADR’s: Nausea (31%)
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8
Q

Aminosalicylates

  1. MOA?
  2. efficacy is dependent on?
  3. C/I?
A
  1. Unknown
  2. works topically needs to be high concentration at SITE of DISEASE
  3. salicylate allergy (LIKE ASPIRIN)
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9
Q
  1. Parietal cells secrete acid into the lumen of the stomach in response to ?
  2. Importances of the lower esophageal sphincter?
A
  1. ACh, histamine, gastrin
  2. prevents stomach contents from refluxing into the esophagus
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10
Q

Misoprostol

  1. MOA?
  2. Indication?
  3. ADR’s?
A
  1. PGE1 analog
    • Increases mucosal blood flow and bicarbonate secretion
      • stomach protectant
  2. Used for prevention of NSAID-related ulcers or to induce labor
  3. Uterine contractions
    • dont use if pregnant
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11
Q

Proton Pump Inhibitors (PPI)

  1. Agents available?
  2. Bioavailability?
  3. Indicaiton?
  4. Benefits pts with?
A
  1. anything that ends in prazole like omeprazole
    • Omeprazole (Prilosec®), esomeprazole (Nexium®), lansoprazole (Prevacid®), dexlansoprazole (Dexilant®), pantoprazole (Protonix®), rabeprazole (Aciphex®)
  2. bioavailbility decreases with food. take on empty stomach 30-60 mins prior to meal (exceptions are bolded drugs aboved)
  3. Indicated to use for 3-4 days to get maximum supression of acid ( not for symptomatic relief)
  4. Benefits pts with- renal insufficiency
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12
Q
  1. Loperamide abuse leads to ?
  2. When shoud you suspect overdose?
  3. When do fatal doses occur?
A
  1. cardiac arrthythmias, fainting or MI
  2. fainting, tachycardia, unresponsiveness
  3. 4-100 times reccommended dose is ingested
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13
Q

What is the MOA for 5-HT3 receptor antagoinists?

A
  • Central blocakde of CTZ and Vomiting center
  • Peripheral blockade on intestinal vagal and spinal afferent nerves →drives antiemetic benefit
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14
Q
A
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15
Q

Bulking forming OTC laxative

  1. MOA?
  2. OTC agents available?
  3. DOC for?
A
  1. Dissolves or swells in the intestinal fluid, forming emollient gels that facilitate the passage of intestinal contents and stimulate peristalsis
    • Methycellulose
    • Polycarbophil
    • Psyllium
  3. Pt’s with constipation on low fiber diets
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16
Q

Budesonide

  1. ) Drug class?
  2. ) Indication
  3. ) MOA?
A
  1. Corticosteroids
  2. For acute flare up of inflammartory bowel disease
  3. pH controlled, delayed release
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17
Q

Methylnaltrexone

  1. MOA?
  2. ADR’s?
  3. C/I’s?
A
  1. Peripheral acting mu opioid receptor ANTAGONIST (PAMORA)
    • ​ Minimal absorption in the GIT
    • Does not cross BBB
  2. Abdominal pain or distention, diarrhea
    • ​​Don’t use Methylnaltrexone if the patient has a history of GI Obstruction
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18
Q

Aminosalicyclates are broken down into what two groups?

Describe the agents in each group and considerations about each?

A
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19
Q

Diphenoxylate/atropine

  1. Drug class?
  2. Why is it beneficial to be combined with atropine?
  3. ADR’s?
A
  1. Peripheral mu opioid agonist
  2. discourages overdoses
  3. dry mouth constipatation
    1. Euphoria (CNS effects) @ high doses
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20
Q

Bismuth subsalicylate

  1. MOA?
  2. Indication?
  3. C/I?
  4. ADR’s?
A
  1. MOA- reacts with HCL to form bismuth and salicylic acid
    • Bismuth → have direct antimicrobial effect
    • Salicylic acid → inhibits chloride secretion in intestine to reduce liquid content of stools
  2. For diarrhea- pepto bismol (brand name)
    • Avoid if documted allergy or sensitivity to aspirin
    • don’t use in children less than 12 years of age
  4. Blackening of tongue and stools (benign)
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21
Q

Hyperosmotic Laxatives

  1. MOA?
  2. OTC agents available?
A
  1. MOA: draws water into rectum to stimulate a bowl movement
    • Glycerin
    • Polyethylene glycol 3350 (miralax)
      • Must take with 4-8 ounces of water
22
Q
  1. What Dopamine receptor antagoinist do we have available?
  2. ADR’s?
  3. What drug is also used for gastroparesis?
A
    • ​​Prochlorperazine
      • hits more D2
      • hypotension
    • Promethazine
      • hits more muscarinic
      • hypotension
    • Olanzapine
    • Trimethobenzamide
    • Metoclopramide
      • also used for gastroparesis (slows gastric emptying)
  2. Dystonia, akathesia, parkinsonian, sedation, hyperprolactinemia, hypotension, dry mouth
23
Q
  1. Symtpoms of laxative abuse?
  2. Abuse may lead to ?
  3. When to suspect laxative abuse?
A
  1. due to loss of Na, K, Mg, and PO4
    • Tremors
    • weaknesss
    • blurry vision
    • kidney injury
    • arrhythmias
  2. Lazy colon, infecton, colon cancer
    • more common in women
    • concomitant eating disorder
    • inconsistencies in medical history
    • complaints of alternating diarrhea and constipation
24
Q

Thiopurines

  1. MOA?
  2. Agents available?
  3. ADR’s ?
  4. DDI’s?
  5. Indication?
A
  1. ​Purine antagonists → inhibition of DNA/RNA synthesis → decreased T-cell function → immunosupression
    • 3-6 month to clinical benefits
  2. Azathioprine (pro-drug) metabolized to 6-mercaptopurine (active metabolite)
  3. bone marrow supression (leukopenia), hepatotoxicity
  4. Allipurinol and febuxostate LEADS to INCREASE in azathiprine
  5. UC+ Crohns
25
Q

Sucralfate

  1. MOA?
  2. C/I?
  3. ADRs?
A
  1. MOA - Sucrose + aluminum hydroxide
    • forms paste that binds to interal ulcers and erosions to help decrease gastric pain and protect stomach lining
  2. aluminum toxicity can occur in renal disease (C/I)
  3. constipation due to aluminum
26
Q
  1. Corticoidsteriods are used for?
A

* For acute flares of inflammatory bowel disease

For acute use only not for long term because of systemic side effects

27
Q
  1. DDI’s of antacids?
  2. Agents available?
A
  1. Decrease absorption of drugs that require acid to be absorbed
    • tetracycline, FQ, iron, itraconazole
      • separate doses by 2-4 hours
    • Calcium carbonate
    • Sodium bicarbonate
    • Magnesium & aluminum hydroxide
28
Q

Histamine-2 receptor antagonists

  1. MOA:
  2. Indication?
  3. Onset of action, durtion of relief?
A
  1. Reversible decreases fasting and food stimulated acid secretion by inhibiting histamine on the H2 receptor of the parietal cell
  2. Indicated for the reatment of mile-moderate infrequent, episodic heart burn (60-70% acid supression)
  3. Onset of action (30-45 mins) and duration of relief (6-10 hrs)
29
Q

DDI’s of NK-1 receptor antagonists? Example?

A
  • CYP 3A4 substrate and inhibitor
  • Aprepitant and warfarin = decreased INR
    • Increased risk for stroke or DVT
30
Q

Methotrexate

  1. MOA?
  2. ADR’s?
  3. What disease state is this used for?
  4. How is it administered?
A
  1. MOA: immunosupressents (inhibits DNA synethesis, repair, replication)→ may suppress inflammation associated with Crohns disease
  2. Hepatotoxicity
  3. Crohn’s disease
  4. Given IM/SC only
31
Q

Lubricants

  1. MOA?
  2. OTC agents available?
  3. DOC for?
A
  1. MOA: Soften fecal contents by coating them so fecal water can’t be reabsorbed
  2. Mineral oil
  3. Not a DOC - there is safety concern of lipid pneumonia
32
Q

1.) What Neurokinin-1 (NK-1) antagonist agents do we have available?

2.) How are NK-1 antagonist used ? What is their indication for use?

A
  • Aprepitant
  • Netupitant
    • really long half life 90-180 hrs
  • Rolapitant
    • really long half life 90-180 hrs
  • Fosaprepitant
    • Converted to aprepitant 30 ins after infusion

2.) Used for prevention of CINV along with 5HT-3 antagonist and corticosteroids

33
Q

Alvimopan

  1. MOA?
  2. ADR’s?
  3. C/I’s?
A
  1. Peripheral acting mu opioid receptor ANTAGONIST (PAMORA)
    • ​ Minimal absorption in the GIT
    • Does not cross BBB
  2. Abdominal pain or distention, diarrhea
  3. Long term use of alvimopan increases risk of MI
    • Short term use only
34
Q

Histamine2-receptor antagonists

  1. Agents available
  2. What drug has the most minimal first pass effect compared to the other agents?
A
  • Cimetidine
  • Ranitidine
  • Famotidine
  • Nizatidine (minimal first pass effect)
35
Q

What is the MOA of Neurokinin-1 (NK1) antagonists?

A
  • MOA: central blockade of NK1 receptors in CTZ
    • blocks the binding substance P
36
Q
  1. What 5HT-3 receptor antagonist agents are available?
  2. These agents are the corner stone for?
  3. What agent is the most effective?
  4. What agent has the longest half life and binding affinity in what type of formulation?
A

1.)

  • Ondansetron
  • Granisetron
  • Dolasetron
  • Palonsetron
  1. ) chemotherapy induced N/V
  2. ) All equally effective at equipotent doses

4.) Palonsetron has longer half life (40 hrs) and has greater binding affinity (IV)

37
Q

What acid supression therapy is better for nighttime what is better for the day?

A

H2 blocker -night time

PPI-day

38
Q
  1. What agent has receptor affinities to the most varied type of receptors?
  2. ADR’s of 5HT-3 receptor antagonists?
  3. What ADR is rare but you should still check to make sure they are on what medications?
A
  1. Ondansetron
  2. OTc interaval prolongation
    • Due to K+ channel blockade
    • Palonsetron has the least amount of ADR’s
  3. Serotonin syndrome
    • Check to make sure they aren’t on triptans or tramadol
39
Q
  1. Why do opiods cause constipation?
  2. Can pts develop a tolerance to opiod induced constipation
A
  • delay gastric emptying
  • interrupts bowel peristalsis
  • reduce intestinal secretion of fluid

2.) NO

40
Q

Emollients (“stool softners”)

  1. MOA?
  2. OTC agents available?
  3. DOC for?
A
  1. MOA: Inrease the wetting efficacy of intestinal fluid and facilitate a mixture of aqueous and fatty substances to soften the fecal mass
  2. Docusate sodium
  3. DOC: pts with dry stools, straining when defecating
41
Q

Antacids

  1. MOA?
  2. Purpose?
  3. Onset of action/ duration of relief ?
  4. ADR’s?
A
  1. Neuralize gasric pH
  2. provides symptom relief to GERD and sour stomach
  3. Liquids have faster onset of action then pills (<5 mins) (duration of relief 20-30 mins)
  4. If product contains this salt the result will be….
    • Magnesium salit → diarrhea
    • Calcium, aluminum→constipation
    • Sodium → farts/ burps, edema
      • Watch out for renal insufficiency
42
Q

Inflammatory bowel disease

  • Ulcerative colitis vs. crohns
A

UC:

  • Involves colon/rectum
    • proctitis =inflammation of rectum
    • continuous inflammation of colon
    • affects the inner most lining of the colon

CD:

  • Involves entire GIT
    • mix of healthy and inflammed areas
    • can effect all layers of the bowl walls
43
Q

Importance of HCL? (4 things)

A
  1. 1st line defense against pathogenic bacteria from food
  2. Activates pepsin needed for the initial breakdown of protein
  3. Signals pancreas to produce digestive enzymes
  4. Essential for the absorption of vitamin b12
44
Q

Cyclosporine

  1. MOA?
  2. ADR’s?
  3. What disease state is this used for ?
A
  1. Calcineurin inhibitor (decreases proinflammatory factors)
  2. Nephrototxicity
  3. Ulcerative colitis (UC)
45
Q

Stimulant Laxative

  1. MOA?
  2. OTC agents available?
  3. These agents can lead to ?
A
  1. MOA: Increases peristalisis by local irritation of the mucosa. Stimulates the secretion of water and electrolytes in the large instentine
    • ​​Senna
    • Bisacodyl
  3. Electrolyte and fluid deficiencies due to malabsorption
46
Q

Why would someone abuse Loperamide?

A
  • OTC and Cheap
  • euphoria
  • self treat withdrawal symptoms
  • often used with other drugs its exposure
47
Q

Loperamide

  1. MOA?
  2. What does it also do?
  3. ADR’s?
A
  1. peripheral mu opioid agonist that stimulates receptors located in the intestinal muscles
    • Slows intestinal contractions
    • Inhibits secretion of electrolytes and water
      • NO tolerance has been reported
  3. Dizziness, mild constipation
    • At high doses CNS effects
48
Q

Define constipation?

What mediation should you not give them?

A
  • A decrease in the frequency of fecal elimination characterized by the difficult passage of hard, dry, stools
    • don’t give them meds that will increase the number of stools they have because you don’t want these patients to strain
49
Q

Proton Pump Inhibitors (PPI)

  1. MOA?
  2. How does it get to the site of action?
  3. Onset of action/duration of relief? what is imporant about DOR?
A
  1. Irreversibly inactivates the hydrogen potassium ATPase “proton pump” resulting in impairment of acid secretion
  2. Pro-drug is protected by enteric coating (EC)
    1. In the intestinal lumen, EC dissovles and the drug is released and aborbed back into the stomach to interact with the parietal cell for activation → forms strong covalent bond with proton pump
  3. OOA=2-3 hrs. DOR= 24 hrs
    • Most potent inhibitor of acid suppressoin (90-98% of acid is suppressed)
50
Q

What are the different areas of the brain and what are their receptors that when activated will lead to N/V?

A

Pharm II New Stuff Final (2 decks)

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