Gastrointestinal Pharmacology I

Front 1

2. Which has a higher pH, the area close to the mucosa or the lumen?

Back 1

a. Area close to the mucosa
b. Higher HCO3 concentration

Front 2

3. How can you decrease gastric acidity?

Back 2

a. Block histamine receptor on parietal cells
b. Block muscarinic receptors
c. Inhibit H/K ATPase to block gastric acid secretion from all stimuli
d. Use a drug directly against the acid

Front 3

5. What are the most potent drugs against high gastric acidity?

Back 3

a. H/K ATPase

Front 4

a. How can you identify a PPI?

Back 4

i. -prazole

Front 5

b. What is the MOA of PPIs?

Back 5

i. React with H/K ATPase to IRREVERSIBLY inactivate the enzyme

Front 6

c. What type of secretion do PPIs inhibit?

Back 6

i. Fasting
ii. Meal-stimulated

Front 7

d. In what form are PPIs administered?

Back 7

i. Oral progdrug

Front 8

e. Where are PPIs activated?

Back 8

i. Small intestine parietal cells

Front 9

f. How fast is the onset of action for PPIs?

Back 9

i. Slow onset of action

Front 10

g. What decreases the bioavailability of PPIs?

Back 10

i. Presence of food

Front 11

h. How does first-pass hepatic metabolism affect PPIs?

Back 11

i. Rapid first-pass metabolism

Front 12

i. What is the first line drug for peptic ulcer disease?

Back 12

i. PPI

Front 13

j. What is the first line drug for GERD?

Back 13

i. PPI

Front 14

k. What can be used to treat nonulcer dyspepsia?

Back 14

i. PPI

Front 15

l. What is used for prevention of stress-related mucosal bleeding?

Back 15

i. PPI

Front 16

m. What is used for gastric acid hypersecretion due to gastrinoma?

Back 16

i. Surgical resection of tumor if possible
ii. PPI to increase pH

Front 17

n. What is used to prevent NSAIDS-induced GI side effects?

Back 17

i. PPI

Front 18

o. What are the adverse effects of PPIs?

Back 18

i. Well-tolerated and safe
ii. Nausea, diarrhea, abdominal pain

Front 19

p. What will long-term use of PPIs lead to?

Back 19

i. Reduced plasma vitamin B12 levels
ii. Increase respiratory and enteric bacterial infection

Front 20

a. How can you identify an H2 histamine receptor antagonist?

Back 20

i. -tidine
ii. Cimetidine, ranitidine

Front 21

b. What is the MOA of H2 histamine receptor antagonists?

Back 21

i. Competitively and selectively bind to H2 receptors
ii. Reduce histamine-induced acid secretion

Front 22

c. What is the clinical use for H2 histamine receptor antagonists?

Back 22

i. Same as PPIs

Front 23

d. What are the adverse effects of histamine receptor antagonists?

Back 23

i. Extremely safe

Front 24

a. What is the MOA of antacids?

Back 24

i. Neutralize gastric acids

Front 25

b. What salts are most common in antacids?

Back 25

i. Mg, Al, Na, Ca salts most common

Front 26

c. What is the clinical use for antacids?

Back 26

i. Short-term relief of symptoms
ii. PNR

Front 27

d. What are the adverse effects of antacids?

Back 27

i. Constipation→ aluminum
ii. Diarrhea→ Mg
iii. Altered electrolyte balance

Front 28

a. What is triple therapy for H. pylori peptic ulcer?

Back 28

i. PPI and two antibiotics for 14 days

Front 29

b. What is quadruple therapy for H. pylori peptic ulcer?

Back 29

i. PPI or H2 receptor antagonist
ii. Bismuth subsalicylate
iii. 2 antibiotics for 14 days

Front 30

c. What is sequential therapy for H. pylori peptic ulcer?

Back 30

i. 1 antibiotic +PPI for 5 days
ii. Followed by 2 antibiotics+PPI for 5 days

Front 31

a. What are the therapeutic strategies for IBD?

Back 31

i. Inhibit the inflammatory responses
ii. Suppress immune responses

Front 32

i. What are inflammatory suppressors used to treat?

Back 32

1. IBD

Front 33

ii. What are inflammatory suppressors?

Back 33

1. 5-aminosalicylaters (5-ASA)→
2. Mesalamine and sulfasalazine

Front 34

iii. What is the MOA of inflammatory supressors?

Back 34

1. NOT CLEAR

Front 35

iv. What is used for mildly to moderately active ulcerative colitis?

Back 35

1. Inflammatory suppressors

Front 36

v. What is used to induce and maintain remission of UC?

Back 36

1. Inflammatory suppressors

Front 37

vi. What is modestly effective in Chron’s Disease in inducing remission?

Back 37

1. Inflammatory suppressors

Front 38

vii. What can be used to treat rheumatoid arthritis?

Back 38

1. Inflammatory suppressors

Front 39

viii. What are the adverse effects of inflammatory suppressors?

Back 39

1. Nausea
2. Vomiting
3. Headache
4. Abdominal pain

Front 40

i. What are the two corticosteroids?

Back 40

1. Prednisone
2. Prednisolone

Front 41

ii. What is the MOA of corticosteroids?

Back 41

1. Inhibit expression of inflammatory mediators
2. Increase expression of anti-inflammatory mediators

Front 42

iii. What can be used to control acute moderate to severe active IBD?

Back 42

1. Corticosteroids

Front 43

iv. Which is more potent, corticosteroids or 5-ASAs?

Back 43

1. Corticosteroids

Front 44

v. What is the term of use for corticosteroids?

Back 44

1. Short-term only

Front 45

vi. What is the purpose of corticosteroid use for IBD?

Back 45

1. Induce remission
2. Taper symptoms

Front 46

i. What are the two immunomodulators?

Back 46

1. 6-mercaptopurine
2. Azathioprine

Front 47

ii. What is the MOA of immunomodulators?

Back 47

1. Inhibit purine synthesis→ produce anti-proliferative effects and induce apoptosis in T-cells

Front 48

iii. What would you use to maintain remission of UC and CD?

Back 48

1. Immunomodulators

Front 49

iv. What is used to assist steroid tapering in UC and CD?

Back 49

1. Immunomodulators

Front 50

v. What is used to treat steroid-unresponsive IBD?

Back 50

1. Immunomodulators

Front 51

vi. What will decrease formation of antibodies for TNF inhibitors?

Back 51

1. Immunomodulators

Front 52

vii. What will prevent CD recurrence after surgical resection?

Back 52

1. Immunomodulators

Front 53

i. What is the MOA of methotrexate?

Back 53

1. Unclear

Front 54

ii. What would you use to for moderate to severe steroid-dependent and steroids-resistant CD to induce and maintain remission?

Back 54

1. Methotrexate

Front 55

i. What is the MOA of cyclosporine?

Back 55

1. Inhibit first phase of T-cell activation

Front 56

ii. What would you use for sever steroid-resistant UC to induce and maintain remission?

Back 56

1. Cyclosporine

Front 57

iii. What is tacrolimus?

Back 57

1. An alternative to cyclosporine

Front 58

i. What are some anti-TNFα drugs?

Back 58

1. INFLIXIMAB
2. Adalimumab
3. Glimumab
4. Certolizumab

Front 59

ii. What is the MOA of anti-TNFα drugs?

Back 59

1. Monoclonal antibodies bind TNFα

Front 60

iii. What would you use for moderate to severe CD and UC?

Back 60

1. Anti-TNFα drugs

Front 61

iv. What is the contraindication for anti-TNFα drugs?

Back 61

1. Uncontrolled infection

Front 62

1. What is the MOA for natalizumab?

Back 62

a. Monoclonal antibody directed against α4 integrin

Front 63

vi. What would be effective for moderate to severe CD for patients who do not respond to or could not tolerate anti-TNFα drugs?

Back 63

1. Natalizumab

Front 64

vii. What are the adverse effects of natalizumab?

Back 64

1. PML
2. Severe hepatic toxicity

Front 65

i. For what is metronidazole used?

Back 65

1. Anaerobic bacteria
2. Bacteroides fragilis

Front 66

ii. What is ciprofloxacin used to treat?

Back 66

1. Gram positive and negative bacteria

Front 67

iii. What is rifaximin used to treat?

Back 67

1. Enteric gram+ and gram - organisms

Front 68

iv. What are antibiotics used for in CD?

Back 68

1. Induce and maintain remission of CD

Front 69

i. What is a probiotic?

Back 69

1. Nonpathogenic microorganisms→bacteria or yeasts

Front 70

ii. What is the MOA of probiotics?

Back 70

1. Lower intestinal pH and inhibit growth of pathogenic bacteria
2. Prevent adhesion and colonization of pathogenic bacteria
3. Induce or enhance an immune response
4. Inhibit the pathogenicity of bacterial toxins

Front 71

iii. What would you use to maintain remission of UC, especially with pouchitis?

Back 71

1. Probiotics

Front 72

iv. What are the adverse effects of probiotics?

Back 72

1. Bloating
2. Flatulence
3. Diarrhea
4. Hiccups

Front 73

a. What is the treatment strategy to promote mucosal defense?

Back 73

i. Create a physical barrier on GI lining
ii. Increase the secretion of mucus and bicarbonate
iii. Improve blood supply

Front 74

i. What is the prototype colloidal bismuth compound?

Back 74

1. Bismuth subsalicylate

Front 75

ii. What is the MOA of colloidal bismuth compounds?

Back 75

1. Coat ulcer and erosions
2. Stimulate the secretion of prostaglandin, mucus, and bicarbone
3. Reduces stool frequency and liquidity
4. Bind to bacteria and enterotoxins

Front 76

iii. What drug can be used for traveller’s diarrhea?

Back 76

1. Colloidal bismuth compounds

Front 77

iv. What is the non-RX clinical use for colloidal bismuth compounds?

Back 77

1. Treat dyspepsia and prevent traveler’s diarrhea
2. H. pylori infection-caused peptic ulcer

Front 78

v. What are the adverse effects of colloidal bismuth compounds?

Back 78

1. Excellent safety profile
2. Black stool

Front 79

i. What is sucralfate?

Back 79

1. Complex of aluminum hydroxide and sulfated sucrose

Front 80

ii. What is the MOA of sucralfate?

Back 80

1. Physical barrier
2. Inhibit pepsin-mediated hydrolysis of mucosal protein
3. Stimulates mucosal prostaglandin and bicarbonate secretion

Front 81

iii. What are the clinical uses for sucralfate?

Back 81

1. Peptic ulcer
2. Oral mucositis
3. Bile reflux gastropathy

Front 82

iv. What are the adverse effects of sucralfate?

Back 82

1. Possible constipation due to aluminum salt