Pharmacology 2 Exam 5 Quiz 6

Front 1

Which of the following is/are true about insulin
A. Produces the opposite effects in tissues of glucagon
B. Insulin is taken into cells by the GLUT2 transporter
C. C-peptide can be used as a marker of the amount of insulin release
D. Blocks ATP-dependent K channels
E. A and C
F. B and D

Back 1

E. A and C

Front 2

Insulin
A. Stimulates movement of glucose transporters to the cell membrane
B. Inhibits conversion of Triglycerides to fatty acids in adipose tissue
C. Is stored in the pancreas bound to zinc
D. Has a half-life of 3-9 minutes
E. All of the above
F. A and C

Back 2

E. All of the above

Front 3

Which of the following is/are true?
A. Lispro’s onset of action similar to regular insulin
B. Lente insulin is combined with protamine
C. Glargine is a ultra-long acting form of insulin
D. NPH insulin peak effect occurs around 2-4 hours
E. All of the above
F. None of the above

Back 3

C. Glargine is a ultra-long acting form of insulin

Front 4

Which of the following is/are true for the sulfonylureas
A. Block depolarization of the Beta cells of the pancreas
B. Metabolized in the liver
C. Directly inhibit gluconeogenesis
D. Major side effect is hypoglycemia
E. All of the above
F. B and D

Back 4

F. B and D

Front 5

Which of the following is/are true?
A. Glipizide increases insulin receptor number
B. Tolbutamide should be avoided in the elderly
C. Glimepride can be used in combination with insulin for better glucose control
D. Glyburide can be used safely in pregnancy
E. A and C
F. None of the above

Back 5

E. A and C

Front 6

Repaglinide
A. May be taken just prior to meals
B. Often used in combination with Glyburide
C. Has a peak at 1 hour and duration of 3-4 hours
D. May cause aplastic anemia
E. A and C
F. B and D

Back 6

E. A and C

Front 7

Metformin
A. Useful in insulin resistance
B. May cause lactic acidosis
C. Excreted unchanged by kidneys
D. Contraindicated in liver disease
E. A and C
F. All of the above

Back 7

F. All of the above

Front 8

Which of the following is/are true?
A. Pioglitazone increases tissue insulin sensitivity
B. Acarbose is rapidly absorbed and excreted unchanged in the kidneys
C. Rosiglitazone regulates transcription of insulin responsive genes
D. Miglitol decreases glucose production in the liver and peripheral tissues
E. A and C
F. All of the above.

Back 8

E. A and C

Front 9

Which of the following is/are true?
a) Cimetadine will block both basal and stimulated acid secretion
b) Omperazole reversibly inhibits the proton pump
c) H2 antagonsits increase the activity of Esomperazole
d) Pirenzipine inhibts acid secretion by an action on M3 receptors.
e) A and C
f) All of the above

Back 9

a) Cimetadine will block both basal and stimulated acid secretion

Front 10

Which of the following is/are true?
a) Cimetadine will block both basal and stimulated acid secretion
b) Omperazole reversibly inhibits the proton pump
c) H2 antagonists increase the activity of Esomperazole
d) Pirenzipine inhibits acid secretion by an action on M3 receptors.
e) A and C
f) All of the above

Back 10

a) Cimetadine will block both basal and stimulated acid secretion

Front 11

Antiemetic
a) Calcium carbonate
b) Famotidine
c) Magnesium hydroxide
d) Meclizine
e) Octreotide
f) Pirenzepine
g) Hydroxyzine

Back 11

g) Hydroxyzine

Front 12

Decreases acid production by action on parietal cells
a) Calcium carbonate
b) Famotidine
c) Magnesium hydroxide
d) Meclizine
e) Octreotide
f) Pirenzepine
g) Hydroxyzine

Back 12

b) Famotidine

Front 13

Contraindicated in intestinal obstruction
a) Calcium carbonate
b) Famotidine
c) Magnesium hydroxide
d) Meclizine
e) Octreotide
f) Pirenzepine
g) Hydroxyzine

Back 13

c) Magnesium hydroxide

Front 14

May cause kidney stones
a) Calcium carbonate
b) Famotidine
c) Magnesium hydroxide
d) Meclizine
e) Octreotide
f) Pirenzepine
g) Hydroxyzine

Back 14

a) Calcium carbonate

Front 15

Used in Zollinger-Ellison syndrome to decrease gastric release
a) Calcium carbonate
b) Famotidine
c) Magnesium hydroxide
d) Meclizine
e) Octreotide
f) Pirenzepine
g) Hydroxyzine

Back 15

e) Octreotide

Front 16

Decreases basal acid secretion more than stimulated acid release
a) Calcium carbonate
b) Famotidine
c) Magnesium hydroxide
d) Meclizine
e) Octreotide
f) Pirenzepine
g) Hydroxyzine

Back 16

f) Pirenzepine

Front 17

Strong antimuscarinic and antiemetic effects
a) Calcium carbonate
b) Diphenhydramine
c) Doxylamine
d) Hydroxyzine
e) magnesium hydroxide
f) Octrotide
g) Promethazine

Back 17

g) Promethazine

Front 18

Metabolite of dimenhydrinate used as antiemetic
a) Calcium carbonate
b) Diphenhydramine
c) Doxylamine
d) Hydroxyzine
e) magnesium hydroxide
f) Octrotide
g) Promethazine

Back 18

b) Diphenhydramine

Front 19

May produce kidney stones
a) Calcium carbonate
b) Diphenhydramine
c) Doxylamine
d) Hydroxyzine
e) magnesium hydroxide
f) Octrotide
g) Promethazine

Back 19

a) Calcium carbonate

Front 20

Contraindicated in renal failure and intestinal obstruction
a) Calcium carbonate
b) Diphenhydramine
c) Doxylamine
d) Hydroxyzine
e) magnesium hydroxide
f) Octrotide
g) Promethazine

Back 20

e) magnesium hydroxide

Front 21

Blocks gastrin release
a) Calcium carbonate
b) Diphenhydramine
c) Doxylamine
d) Hydroxyzine
e) magnesium hydroxide
f) Octrotide
g) Promethazine

Back 21

f) Octrotide

Front 22

List the 3 targets for treatment in peptic acid disease

Back 22

Neutralize acid
Reduce gastric secretions
Enahnce gastric mucosal defenses

Front 23

Aluminum hydroxide increases/decreases GI motility

Back 23

decreases

Front 24

Briefly explain the mechanism of action of Lansoprazole

Back 24

Irreversibly binds proton pump and inhibits its activity

Front 25

List indications for the use of insulin

Back 25

Type I diabetes
Diabetic ketoacidosis
Gestational diabetes
Hypercalcemia
Pregnant type II Hyperglycemic hyperosmolar non-ketotic coma
Type II not controlled with oral medications

Front 26

Briefly explain the difference between oral hypoglycemic and oral antihyperglycemics

Back 26

Hypoglycemic increase insulin release
Antihyperglycemics decrease glucose production and increase insulin sensitivity

Front 27

Briefly explain the mechanism of action of Glipizide

Back 27

Blocks ATP-dependent K channel in beta cells, increase in K depolarizes cells, opens Ca channels, increased Calcium releases insulin from storage sites

Front 28

List the physiological actions of Sitagliptin

Back 28

Inhibit DPP4 to increase GLP-1
Increase insulin
Decrease glucagon
No satiety/ appetite suppression
No weight loss
Oral administration

Front 29

List the 3 of the major symptoms of diabetes

Back 29

Polyuria
Weight loss
Polydipsia
Plasma glucose >200 mg/dl
Polyphagia

Front 30

Magnesium hydroxide increases/decreases GI motility

Back 30

increases

Front 31

Briefly explain the mechanism of action of Cimetidine

Back 31

Blocks H2 receptor on parietal cells, blocks histamine activation of the proton pump

Front 32

List indications for the use of insulin

Back 32

Type I diabetes Diabetic ketoacidosis
Gestational diabetes Hyperkalemia
Pregnant type II Hyperglycemic hyperosmolar non-ketotic coma
Type II not controlled with oral medications

Front 33

Briefly explain the difference between oral hypoglycemic and oral antihyperglycemics

Back 33

Hypoglycemic increase insulin release

Antihyperglycemics decrease glucose production and increase insulin sensitivity

Front 34

Briefly explain the mechanism of action of Repaglinide

Back 34

Blocks ATP-dependent K channel in beta cells, increase in K depolarizes cells, opens Ca channels, increased Calcium releases insulin from storage sites

Front 35

List the physiological actions of Exenatide

Back 35

Increase insulin release
Increase nausea and vomiting
Decrease glucagon release
Appetite suppressant
Decrease postprandial hyperglycemia
Weight loss
Slow gastric emptying
Injectable

Front 36

List the 4 major mechanisms of laxatives

Back 36

Bulk forming
Osmotic agents
Stimulant-irritant
Stool softeners

Front 37

Calcium carbonate increases/decreases GI motility

Back 37

decreases

Front 38

Briefly explain the mechanism of action of Octreotide

Back 38

Somatostatin analog that blocks gastrin release from stomach, prevents gastrin stimulation of histamine release

Front 39

Detemir has a longer/shorter duration of action than Lispro

Back 39

longer

Front 40

Briefly explain the mechanism of Acarbose

Back 40

Inhibits a-amylase and a-glucosidase in intestinal brush border, decreases glucose absorption

Front 41

Briefly explain the mechanism of action of Rosiglitazone

Back 41

Agonist of PPAR-gamma, regulates transcription of insulin responsive elements involved in glucose metabolism

Front 42

Compare the actions of Exenatide and Sitagliptin

Back 42

Exenatide
GLP-1 analog
Increase insulin release
Decrease glucagon release
Decrease postprandial hyperglycemia
Slow gastric emptying
Increase nausea and vomiting
Appetite suppressant
Weight loss
Injectable

Sitagliptin -
Inhibit DPP4 to increase GLP-1
Increase insulin
Decrease glucagon
No satiety/ appetite suppression
No weight loss
Oral administration

Front 43

Which of the following correctly describes the pharmacokinetic properties of the short acting insulins
(Humulin-R, Novolin-R) ‘?
A) Onset = 15 minutes, peak = 1-2 hours, duration = about 4 hours
B) Onset = 1-3 hours, peak = 6-14 hours, duration = 18-24 hours
C) Onset = 2-4 hours, peak = none, duration = 24 hours
D) Onset = 30-60 minutes, peak = 2-4 hours, duration = 5-7 hours.
E) Onset = 1-3 hours, peak = 1-2 hours, duration = 10-12 hours
F) None of the above

Back 43

D) Onset = 30-60 minutes, peak = 2-4 hours, duration = 5-7 hours.

Front 44

Which of the following insulin preparations does not exhibit a peak effect in its pharmacokinetic profile?
A) Insulin aspart (Novolog)
B) NPH (Humulin-N)
C) Velosulin BR
D) Glargine (Lantus)
E) All of the above exhibit a peak effect.

Back 44

D) Glargine (Lantus)

Front 45

Which of the following accurately states the goals of therapy as defined by the ADA's Standard of Medical Care for patients with diabetes mellitus.
A) Fasting plasma glucose = 60-120, postprandial PG = 100-160, HbA1c < 7
B) Fasting PG = 80-140, postprandial PG = 100-140, HbA1c < 7
C) Fasting PG = 80-120, postprandial PG = 100-135, HbA1c < 7
D) Fasting PG = 80-120, postprandial PG = 100-140, HbA1c < 8
E) Fasting PG = 80-120, postprandial PG = 100-140, HbA1c < 7
F) None of the above

Back 45

E) Fasting PG = 80-120, postprandial PG = 100-140, HbA1c < 7

Front 46

Which of the following undergo extensive metabolism in the liver.
A) Metformin (Glucophage)
B) Glipizide ( Glucotrol)
C) Acarbose (Precose)
D) Nateglinide (Starlix)
E) A and C
F) B and D

Back 46

F) B and D

Front 47

Which of the following drugs may require 10-12 weeks of therapy before maximal clinical effect on plasma glucose levels may be observed.
A) Metformin (Glucophage)
B) Glipizide ( Glucotrol)
C) Acarbose (Precose)
D) Nateglinide (Starlix)
E) Rosiglitazone (Avandia)
F) None of the above

Back 47

E) Rosiglitazone (Avandia)

Front 48

Which of the following medications is contraindicated in a patient with a transaminase level > 2.5 times the upper limit of normal at baseline?
A) Metformin (Glucophage)
B) Pioglitazone (Actos)
C) Glyburide ( Glynase)
D) Repaglinide (Prandin)
E) Glipizide (Glucotrol)
F) None of the above.

Back 48

B) Pioglitazone (Actos)

Front 49

Which of the following medications increase insulin release from the beta-cells?
A) Rosiglitazone ( Avandia)
B) Glipizide (Glucotrol)
C) Metformin (Glucophage)
D) Repaglinide (Prandin)
E) A and C
F) B and D

Back 49

F) B and D

Front 50

Which of the following is/are true with respect to the alpha-glucosidase inhibitors:
a. both drugs in this class have a positive effect on lipid metabolism
b. both drugs are rapidly absorbed and eliminated by the liver
c. the primary site of action is the muscle
d. the major complaint from users of these drugs is flatulence
e. all of the above are true statements

Back 50

d. the major complaint from users of these drugs is flatulence

Front 51

Which of the following is/are true for the hypoglycemic agents used to treat
Type 2 diabetes:
a. none of these agents have a positive effect on lipid metabolism
b. these agents are primarily metabolized by the liver
c. these agents are ineffective in patients that do not have a functioning pancreas.
d. major complication is hypoglycemia
e. all of the above are true statements

Back 51

e. all of the above are true statements

Front 52

Which of the following is/are true statements for the Biguanldes:
a. the major drug in this class has a positive effect on lipid metabolism
b. Metformin is mainly eliminated by the kidney
c. major site of action is at the liver
d. can be used in combination with sulfonlyureas or insulin
e. all are true statements

Back 52

e. all are true statements

Front 53

Which of the following is the most common effective dosing regiments for Type 1 diabetic patients:
a. two insulin injections per day (one long term and one short acting preparation)
b. four daily injection regiment (two short acting, two ultralente preparations)
c. five daily injection regiment (three short acting, one intermediate and one long term preparation)
d. five daily injection regiment (three short acting and two daily NPH preparations)
e. all are correct

Back 53

d. five daily injection regiment (three short acting and two daily NPH preparations)

Still correct?

Front 54

Which of the following is/are true statements for the Thiazolidinediones
(Glitazones):
a. agents in this class increase lipids
b. drugs in this class are primarily metabolized by the kidney
c. Primary site of action is the liver
d. Binds to nuclear transcription factors that stimulate the production of TNF-alpha
e. all of the above are true

Back 54

a. agents in this class increase lipids

Front 55

Which of the following statement(s) is/are false with regard to insulin therapy in diabetic patients:
a. the most rapid acting insulin preparation on the market is called lispro
b. Type 1 diabetic patients on insulin therapy will most likely reduce their insulin dosage when they are ill to avoid the development of hypoglycemia.
c. Insulin glargine (Lantus) is one of the newest insulin preparations. It is a clear solution that is peakless, effective within 2-4 hours, and lasts for up to 24 hours
d. complications include hypoglycemia and weight gain
e. all are false

Back 55

b. Type 1 diabetic patients on insulin therapy will most likely reduce their insulin dosage when they are ill to avoid the development of hypoglycemia.

Front 56

True/False
Since life-style changes alone are difficult in achieving the glycemic goal for diabetic patients, they are discarded and replaced with pharmacology therapy to more effectively treat Type 2 diabetes.

Back 56

False

Front 57

Concerning cetirizine, which of the following is NOT true:
a. It crosses the blood brain barrier very poorly
b. It is a member of the class called the piperazines
c. It is an active metabolite of hydroxyzine
d. It is administered intranasally
e. All of the above are true

Back 57

d. It is administered intranasally

Front 58

Which of the following does not stimulate gastric acid secretion:
a. Secretin
b. Gastrin
c. Histamine
d. Acetylcholine
e. All of the above stimulate

Back 58

a. Secretin

Front 59

Which of the following is true concerning the MOA of omeprazole:
a. Cornpetitively binds to muscarinic parietal cell receptors
b. Inhibits parietal cell carbonic anhydrase
c. Covalently binds to parietal cell proton pump protein
d. Competitively binds to histamine H2 receptors

Back 59

c. Covalently binds to parietal cell proton pump protein

Front 60

Concerning the H2 histamine antagonist, which of the following is true:
a. The bioavailability of cimetidine is around 90%
b. Nizatidine is metabolized more by the liver than the others
c. Ranitidine inhibits the cytochrome P450 system
d. All are secreted by the renal tubules
e. All of the above are true

Back 60

d. All are secreted by the renal tubules

Front 61

Concerning the MOA of bismuth subsalicylate, which of the following is NOT true:
a. It neutralizes gastric acid
b. It enhances secretion of cytoprotective factors
c. It inhibits pepsin activity
d. It preferentially accumulates in the craters of gastric ulcers
e. All of the above are true

Back 61

a. It neutralizes gastric acid

Front 62

Concerning misoprostol, which of the following is NOT true:
a. It is a PGE1 analog
b. It inhibits cytoplasmic release of calcium ions in parietal cells
c. It binds to receptors on columnar epithelial cells of the gastric mucosa
d. It inhibits histamine mediated acid release
e. All of the above are true

Back 62

b. It inhibits cytoplasmic release of calcium ions in parietal cells

Front 63

Concerning the dietary fiber and bulk-forming class of laxatives, which of the following is NOT true:
a. Psyllium, lignin, and pectin-containing forms bind bile acids and reduce their transport in the enterohepatic circulation
b. Fiber-containing forms support the growth of colonic bacteria
c. They aid in the prevention of diverticulitis
d. They can produce flatulence and borborygmi
e. All of the above are true

Back 63

e. All of the above are true

Front 64

Concerning difenoxin, which of the following is NOT true:
a. It penetrates the blood brain barrier poorly
b. lt is classified as an opioid
c. Its MOA is to enhance intestinal transit
d. It is a de-esterified derivative of diphenoxylate
e. All of the above are true

Back 64

c. Its MOA is to enhance intestinal transit

Front 65

Which of the following does NOT stimulate release of hydrogen ions from the gastric parietal cells:
a. direct effect of muscarinic stimulation on parietal cells
b. direct effect of decreased pH on parietal cells
c. indirect effect of muscarinic stimulation of ECL cells
d. direct effect of gastrin on parietal cells

Back 65

b. direct effect of decreased pH on parietal cells

Front 66

The H2 histamine antagonist having the highest bioavailability is:
a. Cimetidine
b. Ranitidine
c. Famotidine
d. Nizatidine

Back 66

d. Nizatidine

Front 67

The treatment of choice for Zollinger-Ellison Syndrome and for peptic ulcers that are unresponsive to other therapies is:
a. Ranitidine
b. Omeprazole
c. Bismuth subsalicylate
d. Misoprostol

Back 67

b. Omeprazole

Front 68

The drug used to promote healing of duodenal and gastric ulcers by forming a
protective coat of viscous gel and also binds bile salts is:
a. Bismuth subsalicylate
b. Misoprostol
c. Sucralfate
d. Danthron

Back 68

c. Sucralfate

Front 69

The antiemetic drug that also increases GI motility and is used to treat diabetic
gastroparesis is:
a. Metoclopramide
b. Octreotide
c. Diphenhydrarnine
d. Docusates

Back 69

a. Metoclopramide

Front 70

True/False
Milk of Magnesia (magnesium hydroxide) has the undesirable side effect of increasing GI motility.

Back 70

True

Front 71

True/False<BR>The compound found in antacids that has the potential of having the most serious side effects in patients with renal insufficiency is Mg(OH]2.

Back 71

False. CaCO3

Front 72

True/False
Prostaglandin E2 and prostaglandin I2 inhibit cyclic-AMP dependent acid secretion

Back 72

True

Front 73

True/False
The effectiveness of bismuth subsalicylate may be secondary to its antibacterial effect against Helicobacter pylori.

Back 73

True

Front 74

True/False
Senna and Cascara are naturally occurring compounds that inhibit colonic motility.

Back 74

False

Front 75

Briefly explain the mechanism of action of Cimetidine

Back 75

Blocks H2 receptor on parietal cells prevents activation of proton pump

Front 76

True / False
Omeprazole reversibly inhibits the proton pump

Back 76

False
irreversibly

Front 77

Briefly explain the antiemetic action of Metoclpromide

Back 77

D2 receptor antagonist blocks activation of Chemoreceptor trigger zone (CTZ) also acts on vomiting center D2 receptors

Front 78

List 3 indications for laxatives

Back 78

Prepare bowel for surgery, hasten excretion of toxins, minimize straining, temporary relief of constipation, post-operative stimulant

Front 79

Briefly explain the mechanism of release of insulin

Back 79

Glucose taken up by GLUT 2 transporter, glucose converted to ATP by Krebs cycle, ATP closes ATP dependent K channel, increases K causes depolarization which opens voltage sensitive calcium channels, Ca causes exocytoses of insulin

Front 80

GLUT 1 / GLUT 2 / GLUT 3 / GLUT 4 transporters are responsible for the insulin mediated uptake into muscle and adipose tissue

Back 80

GLUT 4

Front 81

Insulin Detemir differs from regular insulin by the addition of two ARG’s in position 31 and 32. True / False

Back 81

False

Front 82

Lispro insulin has an onset of action of 15 minutes and duration of 4 hrs.
True / False

Back 82

True

Front 83

Briefly explain the mechanism of action of Esomeprazole

Back 83

Irreversibly sulfates the proton pump and inactivates it

Front 84

The aluminum salt that is used to help heal stomach ulcerations is ________

Back 84

Sucralfate

Front 85

Briefly explain the antiemetic action of Dimenhydrinate

Back 85

Blocks H1 receptor in vomiting center, blocks signal from vestibular apparatus, also blocks in NTS

Front 86

List 3 mechanisms of action of laxatives

Back 86

Stimulants/irritants, stool softeners, bulk forming, osmotic agents (any three)

Front 87

Briefly explain how insulin stimulates glucose uptake into skeletal muscle

Back 87

Insulin binds tyrosine kinase receptor which phosphorylates itself and activates second messenger cascade to move preformed GLUT 4 transporters from intracellular site to membrane site where glucoise is taken up into cell

Front 88

GLUT 1 / GLUT 2 / GLUT 3 / GLUT 4 transporters are responsible for the basal glucose uptake into all cells

Back 88

GLUT 1

Front 89

Insulin Glulisine differs from regular insulin by the reversal of amino acids at position 29 and 30 of insulin True / False

Back 89

False

Front 90

Insulin Glargine has an onset of action of 2-4 hrs and a duration of 24 hrs.
True / False

Back 90

True

Front 91

Briefly explain the mechanism of action of Octreotide

Back 91

Somatostatin analog that blocks gastrin release and prevents gastrin stimulation of histamine release from paracrine cell and prevents gastrin from affecting parietal cell

Front 92

The agent used to increase mucous production in the stomach is _______

Back 92

Misoprstol

Front 93

Briefly explain the antiemetic action of Odansetron

Back 93

Blocks 5HT receptors in stomach, CTZ and NTS to prevent activation of vomiting center

Front 94

List 3 side effects of laxatives

Back 94

Abdominal cramps, GI muscle weakness, nausea, diarrhea, mucosal inflammation, atrophy of muscle, nerve damage, dehydration, malabsorbtion, (any three)

Front 95

Briefly explain why c-peptide can be used as a marker for insulin release

Back 95

C-peptide cleaved off of proinsulin in a 1-1 ratio with insulin

Front 96

GLUT 1 / GLUT 2 / GLUT 3 / GLUT 4 transporters are present of the Beta cells of the pancreas

Back 96

GLUT 2

Front 97

Insulin Lispro differs from regular insulin by a LYS for ASN substitution at position B3 and a GLU for LYS at position B29 True / False

Back 97

False

Front 98

NPH insulin has an onset of action of 1-3 hrs and duration of 18-24 hrs.
True / False

Back 98

True

Front 99

Sodium Bicarbonate
Calcium Carbonate
Aluminum Hydroxide
Magnesium Hydroxide
Magnesium Hydroxide + Aluminum Hydroxide (Maalox, Mylanta)

Back 99

Antacids

Front 100

Cimetidine
Nizatidine
Famotidine
Ranitidine

Back 100

H2 Antagonists

Front 101

Pantoprazole
Omeprazole
Lansoprazole
Esomeprazole
Robeprazole

Back 101

Proton Pump Inhibitors

Front 102

Pirenzepine
Telenzepine

Back 102

Anticholinergics - M1 Antagonists

Front 103

Octreotide

Back 103

Gastrin Inhibitor

Front 104

Sucralfate
Colloidal Bismuth
Misoprostol

Back 104

Mucousal Protecting Agent

Front 105

PPI or H2 Blocker + Clarithromycin + Amoxicillin or Metronidazole

Back 105

Triple Therapy

Front 106

PPI or H2 Blocker + Metronidazole + Tetracycline + Bismuth subsalicylate

Back 106

Quadruple Therapy

Front 107

Scopalamine

Back 107

Anti-Muscarinic

Front 108

Dimenhydrinate
Promethazine

Back 108

Anti-Histamine

Front 109

Dolasetron
Ondansetron
Granisetron

Back 109

Anti-Serotinergic - 5-HT3 Antagonists

Front 110

Chlorpromazine
Haloperidol
Metoclopramide
Prochlorperazine
Fluphenazine

Back 110

Anti-Dopaminergic - D2 Antagonists

Front 111

Dronabinol

Back 111

Cannabinoids

Front 112

Aprepitant

Back 112

Substance P Antagonists

Front 113

Metoclopramide
Erythromycin
Cisapride

Back 113

Prokinetic Drugs

Front 114

Bisacodyl
Senna
Phenothalin
Castor Oil

Back 114

Stimulant/Irritant Laxatives

Front 115

Psyllium
Methylcellulose

Back 115

Bulk-Forming Laxatives

Front 116

Glycerin
Mineral Oil
Docusate Sodium

Back 116

Stool Softener Laxatives

Front 117

Lactulose
Mannitol
Magnesium Sulfate
Magnesium Hydroxide

Back 117

Osmotic Laxatives

Front 118

Diphenoxylate
Loperamide
Difenoxin

Back 118

Anti-Diarrheal Opioids

Front 119

Kaolin-pectin
Bismuth Subsalicylate

Back 119

Other Anti-Diarrheals

Front 120

5HT3 Antagonist - Alosetron
5HT4 Partial Agonist - Tegaserod
PGE1 Analog - Lubiprostone

Back 120

Irritable Bowel Syndrome Treatments

Front 121

Olsalazine
Mesalamide
Glucocorticoids
Sulfasalazine
Cyclosporine
Azathiopurine
Methotrexate
Balsalazine
6-Mercaptopurine
Metronidazole
Infliximab
Ciprofloxacin
Clarithromycin

Back 121

Irritable Bowel Disease Treatments

Front 122

Glulisine
Aspart
Lispro

Back 122

Ultra-Short Insulin

Front 123

Regular

Back 123

Short-Acting Insulin

Front 124

NPH

Back 124

Intermediate Insulin

Front 125

Detemir
Glargine

Back 125

Long-Acting Insulin

Front 126

Tolazamide
Acetohexamide
Chlorpropamide
Tolbutamide
Glimepiride
Glipizide
Glyburide

Back 126

Sulfonylureas

Front 127

Repaglinide
Nateglinide

Back 127

Metglitinides

Front 128

Metformin

Back 128

Biguanides

Front 129

Troglitazone
Rosiglitazone
Pioglitazone

Back 129

Thiazolidinediones

Front 130

Acarbose
Miglitol

Back 130

Alpha-Glucosidase Inhibitors

Front 131

Exenatide
Liraglutide

Back 131

Incretins (GLP-1)

Front 132

Vildagliptin
Sitagliptin
Saxagliptin

Back 132

Dipeptidyl Peptidase-4 Inhibitors

Front 133

Dihydrotachysterol
Ergocalciferol
Calcifediol
Calcitriol

Back 133

Calciferols

Front 134

Cibacalcin
Miacalcin
Calcimar

Back 134

Calcitonins

Front 135

Risedronate
Zoledronate
Sodium etidronate
Pamidronate
Alendronate

Back 135

Biphosponates

Front 136

Raloxifene

Back 136

Hormone-Replacement Therapy

Front 137

Teriparatide

Back 137

Parathyroid Hormone

Front 138

Cinacalet

Back 138

Calcium Sensor Mimetics

Front 139

Fluoride
Vitamin K

Back 139

Other Calcium-Related Drugs

Front 140

Armour Thyroid
Bio-throid

Back 140

Natural Thyroid Drugs

Front 141

Propylthiouracil
Methimazole

Back 141

Anti-Thyroid Drugs

Front 142

131I
123I

Back 142

Radioactive Iodine

Front 143

Saturated potassium iodide solution
Lugol's solution

Back 143

Iodides

Front 144

Ipodate

Back 144

Iodinated Contrast Media