Pharm Test 2 Gi Drugs

Front 1

Antacids

1) What are they

2) When do you use them?

3)What increasing the pH does?

Back 1

1) Weak bases that react with HCL in stomach to raise intra gastric pH

2) Use when unable to tolerate primary therapy for symptom relief in GERD, gastritis, peptic ulcers

3)get inc weak base antibiotics (quinidine), dec weak acid antibiotics (warfarin), decreased tetracycline antibiotics (chelation)

Front 2

Aluminum Hydroxide

1)MOA

2)AE

Back 2

1) Antacid, reacts with HCL to form a complex of aluminum chloride

2) Constipation, Can reduce bioavailability of Digoxin, antimuscarinic drugs, and TC

Front 3

Magnesium Hydroxide

1)MOA

2)AE

Back 3

1) Antacid; reacts wtih HCL to form magnesium chloride

2) Mg poorly absorbed in GIT and has osmotic effect -> diarrhea
-dec digoxin and TC absorption (bioavailability)

Front 4

Calcium Carbonate

1)MOA

2)AE

3)Other Use?

Back 4

1)Antacid; reacts with HCL to form complex of calcium chloride

2) Nephrolithiasis and Dense Fecal Matter Formation

3) Adjuvant in Osteoporosis

Front 5

H2 Receptor Blockers

1)What do they do?

2) Effect on Ulcers?

3)Effect on Acid Secretion by Ach or Bethanechol

4) Why give to major trauma patients in ICU

Back 5

1) reduce gastric acid secretion by 80 to 90 percent

2) heal gastric and duodenal ulcers and prevent their recurrence (but recurrence common when treatment is stopped)

3) Only partially inhibits gastric acid secretion induced by these

4)It treats acute stress ulcers in these patients

Front 6

H2 Receptor Blockers

5) Why give them preop?

6) Effect on GERD

7)AE

8)Effect on Ketoconazole

Back 6

5) To prevent aspiration pneumonia

6)Only 50 percent of patients find benefit, so PPIs are drug of choice for this

7) headache, dizziness, diarrhea, muscle pain
- in elderly, confusion or hallucinations

8)Ketoconazole absorption depends on gastric acid, so wont be absorbed as efficiently if give H2 blocker

Front 7

Cimetidine

1)MOA

2)Pharmacokinetics

3)AE

4) Slows metabolism of what drugs?

Back 7

1)H2 Receptor Blocker

2) Short half life, increased in renal failure; most excreted unchanged in urine

3)Inhibits CYP 450
- Acts as Non steroidal anti androgen -> cause gynecomastia, galactorrhea, dec sperm count

4) warfarin, diazepam, phenytoin, carbamazepine, theophylline, imipramine

Front 8

Ranitidine (Zantac)

1)MOA

2)Pharmacokinetics

3)AE

Back 8

1) H2 Receptor Blocker

2) Longer acting and 5 to 10 times more potent then cimetidine

3) NO antiandrogenic, NO prolactin stimulating, and NO inhibition of CYP 450

Front 9

Famotidine (Pepcid)

1)MOA

2)Pharmacokinetics

3)AE

Back 9

1)H2 Receptor Blocker

2)20 to 50 times more potent then cimetidine; 3 to 20 times more potent then ranitidine

3)NO antiandrogenic, NO prolactin stimulating, and NO inhibition of CYP 450

Front 10

Nizatidine

1)MOA

2) Pharmacokinetics

3)AE

Back 10

1)H2 Receptor Blocker

2)NO first pass metabolism, thus 100 percent bioavailability; Eliminated by kidney (no IV Form available)

3) NO antiandrogenic, NO prolactin stimulating, and NO inhibition of CYP 450

Front 11

Proton Pump Inhibitors (PPIs)

1)MOA

2)Are they active?

Back 11

1) Inhibits H+/K+ ATPase proton pump on parietal cell, suppressing secretion of H+ into gastric lumen

2)No, they are Prodrugs (weak base)

3) Are enteric coated so resistant to degradation by gastric acid. Coating removed by alkaline duodenum, and absorbed and transported to parietal cell. In the cell, gets converted to active form which reacts with cysteine of H+/K+ ATPase, forming covalent irreversible bond

Front 12

Proton Pump Inhibitors

4) How long for acid suppression to begin? How long does it last?

5)Reduces basal and stimulated gastric acid secretion by how much?

6)CU

7)Why use with Aspirin/NSAIDS?

8)Effect on H. pylori

Back 12

4) 1 to 2 hours; 18 hours because thats how long it takes for enzyme to be resynthesized

5) >90 percent

6)Peptic ulcers, erosive esophagitis, duodenal ulcer, LONG TERM treatment of Zollinger Ellison syndrome, GERD

7) They dec risk of bleeding from the ulcers these drugs cause. Do it by supporting platelet aggregation and maintaining clot integrity

8)Use with combo therapy to eliminate H. pylori

Front 13

Proton Pump Inhibitors

9)AE

Back 13

9)inhibits metabolism of warfarin, phenytoin, diazepam, cyclosporine

Front 14

Effect of H2 Antagonists and PPIs on Vit B12

Back 14

Will get low vit B12 because gastric acid required for its absorption

Front 15

Omeprazole

Back 15

Proton Pump Inhibitor

Front 16

Esomeprazole

Back 16

Proton Pump Inhibitor

Front 17

Sucralfate

1)What is it?

2)MOA

3)CU

4) Contra

Back 17

1) Mucosal Protective Agent; complex of aluminum hydroxide and sulfalated sucrose

2)- binds to proteins and forms a complex gel with epithelial cells -> creating a physical barrier against a HCL and prevents degradation of mucus by pepsin and acid

- stimulates prostaglandin release and mucus and bicarbonate output

3) Long Term Maintenance therapy of Mucosa

4) Requires acidic pH for activation, thus should NOT be given with H2 antagonists of antacids

Front 18

Bismuth Subsalicylate

1)What is it?

2)MOA

Back 18

1) Mucosal Protective Agent

2) inhibits pepsin, inc mucous secretion, interacts with glycoproteins in necrotic mucosal tissue to protect ulcer crater; has Antimicrobial actions

Front 19

Misoprostol (PGE1)

1)What is it?

2)Prostaglandins normally do what in Stomach?

3)Contra

Back 19

1) Mucosal Protective Agent

2) Normally, prostaglandins inhibit HCL secretion, and stim secretion of mucous and bicarbonate; Deficiency of PG thought to cause peptic ulcers

3) Prevention of Gastric Ulcers induced by NSAIDS
-Prophylaxis for elderly or patients prone to NSAID induced uclers

3)Pregnancy (because causes uterine contractions)

Front 20

Pirenzepine

1)MOA

2)CU

3)AE

Back 20

1)anticholinergic (muscarinic antagonists)
-inhibits M1 on ECL cells (dec histamine) and inhibits M3 on parietal cells (dec H+)

2)Peptic Ulcer

3)Sympathomimetic

Front 21

Dicyclomine

1)MOA

2)CU

3)AE

Back 21

1)Muscarinic Antagonist
-inhibits M1 on ECL cells (dec histamine) and inhibits M3 on parietal cells (dec H+)

2) Irritable Bowel Syndrome

3)Sympathomimetic

Front 22

Clarithromycin

Back 22

Antimicrobial for H. pylori eradication

Front 23

Amoxicillin

Back 23

Antimicrobial for H. pylori eradication

Front 24

Metronidazole

Back 24

Antimicrobial for H. pylori eradication

Front 25

Tetracycline

Back 25

Antimicrobial for H. pylori eradication

Front 26

1)Effect of dec H. pylori on peptic ulcers

2)What is bismuth

Back 26

1) Dec H. pylori allows peptic ulcers to heal

2)Bismuth helps dec pepsin, and inc mucus secretion -> forms barrier (they do not neutralize stomach acid)

Front 27

Metoclopramide

1)MOA

2)CU

3)AE

4)Contra

Back 27

1)A Prokinetic Agent
D2 Antagonist, and mixed 5HT3 antagonist/5HT4 agonist

2)Anti emetic (antagonizes activity at D2 in CTZ zone in brain); GERD

3)Parkinsons Symptoms d/t dopamine antagonist effect

4)Hyperprolactinemia, because Dopamine is a prolactin inhibiting hormone (so inhibit dopamine -> inc prolactin)

Front 28

Cisapride

1)MOA

2)CU

3)AE

Back 28

1) A prokinetic
-Releases Ach in myenteric plexus ->inc muscle tone in esophageal sphincter

2)GERD
Diabetic Gastroparesis (because inc gastric emptying)
Bowel Constipation

3)Long QT Syndrome ->Arrhythmias

Front 29

Senna

1)MOA

2)CU

3)Combine with what to make stools softer

Back 29

1)Laxative (stimulant)
-causes H20 and electrolyte secretion into bowel

2)Evacuates bowel in 8 to 10 hours

3)Docusate

Front 30

Bisacodyl

1)MOA

2)How is it taken

3)AE

4)Contra

Back 30

1)Laxative (stimulant)
-Acts on nerve fibers on colon mucosa

2)Suppository, enteric coated tablets

3)Abdominal cramps, Atonic Colon (if prolonged use)

4)Antacids (PPI, H2) (dissolves enteric coating of drug leading to drug dissolving to fast in stomach and getting stomach irritation and pain)

Front 31

Castor Oil

1)MOA

2)Contra

Back 31

1)Laxative (stimulant)
-Converted to Ricinoleic Acid ->irritates gut ->Increases peristalsis

2)Pregnancy because can cause uterine contractions

Front 32

Methylcellulose, Psyllium seeds, Bran

1)MOA

2)What are they made of?

3)Use cautiously in who?

Back 32

1)Laxative (Bulk Forming)
-hydrophillics form gel in LI ->water retention and intestinal distension ->inc peristalsis

2)indigestible parts of fruits and veggies

3)Bed bound

Front 33

Magnesium citrate, Mg sulfate, Mg phosphate, Mg hydroxide

1)MOA

Back 33

1)Laxative (saline and osmotic laxative)
-Hold water in intestine via osmosis, distend bowel causing stimulation of defecation

Front 34

Lactulose

1)MOA

Back 34

Saline and Osmotic Laxatives
-large doses degraded by colonic bacteria to form lactic, formic, and acetic acid, which increases osmotic effects

Front 35

Polyethylene Glycol (PEG)

1)MOA

2)CU

Back 35

1)Laxative (saline and osmotic laxative)

2)colonic lavage for endoscopic and radiological procedures

Front 36

Docusate Sodium/Calcium/Potassium

1)MOA

Back 36

1)Stool Softner

Emulsifies with stool to make stool softer and easier to pass

Front 37

Lubricant Laxatives

1)Examples

Back 37

1)Mineral oil and glycerin suppositories

Front 38

Apomorphine

1)MOA

2)CU

Back 38

1)causes emesis by stimulating the CTZ and by gastric mucosa irritation

2)treats accidentals poisoning

Front 39

Apomorphine

1)MOA

2)CU

Back 39

1)causes emesis by stimulating the CTZ and by gastric mucosa irritation

2)treats accidentals poisoning

Front 40

Diphenoxylate (imodium)

1)MOA

2)Any analgesic Effects?

3)Any abuse potential

4)AE

Back 40

1)Antidiarrheal
opioid like action in gut by activating presynaptic opioid receptors in enteric nervous system to inhibit Ach release and decrease peristalsis

2)NONE

3)Yes, thus need to give with atropine to discourage abuse

4)drowsiness, cramps, toxic megacolon in young kids or severe colitis

Front 41

Loperamide (imodium)

1)MOA

2)Any analgesis effects

3)Any abuse potential

4)AE

Back 41

1)Antidiarrheal
opioid like action in gut by activating presynaptic opioid receptors in enteric nervous system to inhibit Ach release and decrease peristalsis

2)NONE

3)NONE

4)drowsiness, cramps, toxic megacolon in young kids or severe colitis

Front 42

Bismuth Subsalicylate (pepto bismol)

1)MOA

Back 42

1)Antidiarrheal
coats intestinal epithelium and decreases GI irritation

Front 43

1)What is the chemoreceptor trigger zone (CTZ)

2)Where is a second vomiting center located?

3)Receptors that play role in vomiting:

4)Vagal contribution in vomiting

Back 43

1) located in area postrema outside the BBB, so can respond directly to stimuli in blood or csf, and TRIGGER VOMITTING

2) Medulla; coordinates motor mechanism of vomiting, and also responds to afferent input from vestibular system (motion sickness) or pharynx and GI tract

3)D2, 5HT3

4) Ach, Neurokinin-1, Substance P in CNS

Front 44

Scopolamine

1)MOA

Back 44

1)Antiemetic drug

Also used in motion sickness

Front 45

Dimenhydrinate

Back 45

Anti Emetic
H1 receptor antagonist that treats motion sickness

Front 46

Meclizine

Back 46

Anti Emetic
H1 receptor antagonist that treats motion sickness

Front 47

Cyclizine

Back 47

Anti Emetic
H1 receptor antagonist that treats motion sickness

Front 48

Prochlorperazine

1)MOA

2)CU

3)AE

Back 48

1)Anti emetic
D2 Receptor antagonist

2)treatment in low or moderately emetogenic chemotherapy

3)hypotension and restlessness, extrapyramidal symptoms

Front 49

Ondansetron

1)MOA

2)CU

Back 49

1)Anti emetic
5HT3 antagonist in periphery and in brain (CTZ)

2)Admin prior to chemo

Front 50

Granisetron

1)MOA

2)CU

Back 50

1)Anti emetic
5HT3 antagonist in periphery and in brain (CTZ)

2)Admin prior to chemo

Front 51

Dolasetron

1)MOA

2)CU

3)AE

Back 51

1)Anti emetic
5HT3 antagonist in periphery and in brain (CTZ)

2)Admin prior to chemo

3)Prolongs QT interval

Front 52

Metoclopramide

1)MOA

2)CU

3)AE

Back 52

1)Anti Emetic
D2 antagonist, mixed 5-HT3 antagonist/5HT4 agonist

2)treatment of vomit in highly emetegenic chemo drug cisplatin

3)anti dopa side effects of sedation, diarrhea

Front 53

Droperidol

1)MOA

2)AE

Back 53

1)Anti Emetic
D2 anatagonist

2)Prolong QT (so only use for Refractory cases)

Front 54

Haloperidol

1)MOA

2)AE

Back 54

1)Anti Emetic
D2 anatagonist

2)Prolong QT (so only use for Refractory cases)

Front 55

Lorazepam

1)MOA

2)CU

Back 55

1)Antiemetic
Benzodiazepine
Beneficial effect due to sedative, anxiolytic, and amnesic properties

2)Anticipatory vomiting assoc with chemo

Front 56

Alprazolam

1)MOA

2)CU

Back 56

1)Antiemetic
Benzodiazepine
Beneficial effect due to sedative, anxiolytic, and amnesic properties

2)Anticipatory vomiting assoc with chemo

Front 57

Dexamethasone

1)MOA

2)CU

3)AE

Back 57

1)Anti Emetic
Corticosteroid
Anti vomit property might be due to blockade of prostaglandins

2)Mild to Mod Emetogenic chemo, in combo with other drugs

3)Insomnia, hyperglycemia, DM

Front 58

Methylprednisolone

1)MOA

2)CU

3)AE

Back 58

1)Anti Emetic
Corticosteroid
Anti vomit property might be due to blockade of prostaglandins

2)Mild to Mod Emetogenic chemo, in combo with other drugs

3)Insomnia, hyperglycemia, DM

Front 59

Dronabinol

1)MOA

2)CU

3)AE

Back 59

1)Antiemetic
Marijuana Derivative

2)mild to mod emesis assoc with cemo
Not first line

3)Dysphoria, hallucinations, sedation

Front 60

Nabilone

1)MOA

2)CU

3)AE

Back 60

1)Antiemetic
Marijuana Derivative

2)mild to mod emesis assoc with cemo
Not first line

3)Dysphoria, hallucinations, sedation

Front 61

Aprepitant

1)MOA

2)How do you use it?

3)AE

Back 61

1)Antiemetic
Blocks neurokinin-1/substance P in the brain

2)Oral with dexamethasone and palonosetron

3)Metabolized extensively by CYP3A4, and also INDUCES CPY3A4, so decreases warfarin levels

Front 62

Sulfasalazine

1)MOA

2)CU

Back 62

1)broken down into sulfapyridine and 5-ASA; 5ASA has the anti inflam effects (inhibits prostaglandins and leukotrienes

2)Inflam Bowel Disease Maintenance therapy (Crohns and UC)

Front 63

Infliximab

1)MOA

2)CU

Back 63

1)monoclonal antibody to TNF

2)IBD (crohns and UC)
Rheumatoid Arthritis

Front 64

Methotrexate

1)MOA

2)CU

Back 64

1)inhibits dihydrofolate reductase

2)UC and Crohns

Front 65

6-Mercaptopurine

1)MOA

2)CU

Back 65

1)inhibits purine nucleotide synthesis

2)Immunosuppressant in UC and Crohns

Front 66

Prednisone/Prednisolone

1)CU

Back 66

2)acute inflamm assoc with Crohns and UC

Front 67

Irritable Bowel Syndrome (IBS) Classification

1)IBS-D

2)IBS-C

3)IBS-A

4)IBS-PI

Back 67

1)diarrhea predominates

2)constipation predominates

3)alternating between diarrhea and constipation

4)post infectious

Front 68

1)how to treat IBS-D

2)how to treat IBS-C

Back 68

1)anti diarrheals like loperamide, diphenoxylate, codeine

2)use dietary fiber, osmotic agents like PEG, sorbitol, lactulose

Front 69

Hyoscyamine

1)CU

Back 69

1)Antispasmodic to treat cramps/diarrhea

Front 70

Dicyclomine

Back 70

1)Antispasmodic to treat cramps/diarrhea

Front 71

1)When do you use pancreatic enzymes?

Back 71

1)used in pancreatic insufficiency due to chronic pancreatitis, malabsorption, steattorhea, cystic fibrosis

Front 72

What are these used for?

1)Alpha Amylase
2)Lipase/Phospholipase A/Colipase

3)Proteases (trypsin, chymotrypsin, elastase, carboxypeptidase)

4)Trypsinogen

Back 72

1)starch digestion

2)fat digestion

3)protein digestion

4)converted to active enzyme trypsin by enterokinase.enteropeptidase (secreted from duodenal mucosa)

Front 73

Octreotide

1)MOA

2)CU

Back 73

1)Antidiarrheal

2)A somatostatin derivative used to control diarrhea assoc with metastatic carcinoid tumors and vasoactive intestinal peptide tumors

Front 74

Ipecac Syrup

1)MOA

2)CU

Back 74

Emetic Drug

1)causes emesis by stim CTZ and by gastric mucosa irritation

2)Accidental Poisoning