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Which of the following statements correctly describes the mechanism of action of Invokana (Canagliflozin)?

a. Increase insulin sensitivity towards blood glucose.
b. Stimulates insulin release from functioning beta cells of pancreas.
c. Delayed the absorption of glucose from gut to blood.
d. Increase gluconeogenesis in the liver.
e. Increase excretion of glucose through kidney.



Which of the following statements correctly describes the mechanism of action of Invokana (Canagliflozin)?

a. Increase insulin sensitivity towards blood glucose.
b. Stimulates insulin release from functioning beta cells of pancreas.
c. Delayed the absorption of glucose from gut to blood.
d. Increase gluconeogenesis in the liver.
e. Increase excretion of glucose through kidney.

Answer: (e). Sodium-glucose co-transporter 2 (SGLT2), expressed in the proximal renal tubules, is responsible for the majority of the reabsorption of filtered glucose from the tubular lumen. Canagliflozin is an inhibitor of SGLT2. By inhibiting SGLT2, Canagliflozin reduces reabsorption of filtered glucose and lowers the renal threshold for glucose (RTG), and thereby increases urinary glucose excretion (UGE).

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Which of the following drugs interacts with Invokana (Canagliflozin)? [SELECT All THAT APPLY]

a. Digoxin
b. Rifampin
c. Ketoconazole
d. Trazodone
e. Tramadol


Which of the following drugs interacts with Invokana (Canagliflozin)? [SELECT All THAT APPLY]

a. Digoxin
b. Rifampin
c. Ketoconazole
d. Trazodone
e. Tramadol

Answer: (a and b). Co-administration of Canagliflozin with rifampin, a nonselective inducer of several UGT enzymes, including UGT1A9, UGT2B4, decreased Canagliflozin area under the curve (AUC) by 51%. This decrease in exposure to Canagliflozin may decrease efficacy.

If an inducer of these UGTs (e.g., rifampin, phenytoin, phenobarbital, ritonavir) must be co-administered with Invokana (Canagliflozin) (Canagliflozin), consider increasing the dose to 300 mg once daily if patients are currently tolerating Invokana (Canagliflozin) 100 mg once daily, have an eGFR greater than 60 mL/min/1.73 m2, and require additional glycemic control.

Consider other antihyperglycemic therapy in patients with an eGFR of 45 to less than 60 mL/min/1.73 m2 receiving concurrent therapy with a UGT inducer and require additional glycemic control.

There was an increase in the AUC and mean peak drug concentration (Cmax) of digoxin (20% and 36%, respectively) when co-administered with Invokana (Canagliflozin) 300 mg. Patients taking Invokana (Canagliflozin) with concomitant digoxin should be monitored appropriately.

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Which of the following information is TRUE about Invokana (Canagliflozin)? [SELECT ALL THAT APPLY]

a. The 300-mg dose of Invokana is proven to show greater A1C reductions than Januvia.
b. It is a once-daily pill that works around the clock.
c. It is not for weight loss, but may help a patient to lose weight-on average 3%.
d. In most clinical trials, the majority of people taking Invokana reached an A1C goal of less than 7%.
e. The most common side effect associated with the use of Invokana is hypoglycemia.


Which of the following information is TRUE about Invokana (Canagliflozin)? [SELECT ALL THAT APPLY]

a. The 300-mg dose of Invokana is proven to show greater A1C reductions than Januvia.
b. It is a once-daily pill that works around the clock.
c. It is not for weight loss, but may help a patient to lose weight-on average 3%.
d. In most clinical trials, the majority of people taking Invokana reached an A1C goal of less than 7%.
e. The most common side effect associated with the use of Invokana is hypoglycemia.

Answer: (a,b,c, and d). Invokana (Canagliflozin) is a sodium-glucose co-transporter 2 (SGLT2) inhibitor indicated as an adjunct to diet and exercise to improve glycemic control in adults with type 2 diabetes mellitus.

The recommended starting dose is 100 mg once daily, taken before the first meal of the day. Dose can be increased to 300 mg once daily in patients tolerating Invokana (Canagliflozin) 100 mg once daily who have an eGFR of 60 mL/min/1.73 m2 or greater and require additional glycemic control.

Invokana (Canagliflozin) is limited to 100 mg once daily in patients who have an eGFR of 45 to less than 60 mL/min/1.73 m2. Assess renal function before initiating Invokana (Canagliflozin). Do not initiate Invokana (Canagliflozin) if eGFR is below 45 mL/min/1.73 m2. Discontinue Invokana (Canagliflozin) if eGFR falls persistently below 45 mL/min/1.73 m2.

It can increase the risk of hypoglycemia when combined with insulin or an insulin secretagogue. A lower dose of insulin or insulin secretagogue may be required to minimize the risk of hypoglycemia when used in combination with Invokana (Canagliflozin).

It causes intravascular volume contraction. Symptomatic hypotension can occur after initiating Invokana (Canagliflozin), particularly in patients with impaired renal function (eGFR <60 mL/min/1.73 m2), elderly patients, patients on either diuretics or medications that interfere with the renin‐angiotensin‐aldosterone system, or patients with low systolic blood pressure.

The most common side effects of Invokana (Canagliflozin) include genital yeast infections, urinary tract infection, and changes in urination.

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After completing the therapy, H. pylori follow-up status testing shall be done within what time frame to ensure H. Pylori has been completely eradicated?

a. 7 days
b. 72 hours
c. 4 weeks
d. 6 months
e. a month


After completing the therapy, H. pylori follow-up status testing shall be done within what time frame to ensure H. Pylori has been completely eradicated?

a. 7 days
b. 72 hours
c. 4 weeks
d. 6 months
e. a month

Answer: (c) Before the seriousness of H. pylori infections was fully appreciated and when it was still believed that H. pylori eradication therapy could routinely cure more than 90% of patients, confirmation of cure testing was not routinely recommended.

Although confirmation for cure testing is currently considered the standard of care, preferably with noninvasive tests such as the stool antigen or a urea breath test, it is often not done.

Post eradication testing is not only useful to confirm H. pylori eradication but also serves to alert the clinician when resistance begins to undermine their locally effective current regimens. In this issue of Clinical Gastroenterology and Hepatology, Gatta et al report a pilot study suggesting that it may be possible to accurately assess cure using changes in serum pepsinogen II levels.

A positive urea breath test (UBT), histology, culture, or rapid urease test (RUT) any time after therapy is considered as evidence of treatment failure. However, it has been recommended that posttreatment testing be delayed for at least 4 weeks after the end of therapy.

This recommendation is based on the fact that it takes time for any remaining bacteria to recover and repopulate the stomach in sufficient numbers to be detected reliably. By 4 weeks, the accuracy of a negative test is in the range of 98% to 100%.

There is little or no gain by repeating negative tests to ensure success (e.g, 2 negative urea breath tests) as a second urea breath test has not shown an increase in accuracy and adds an incremental cost with little clinical benefit.

One caveat among available noninvasive tests is that when using the stool antigen to assess outcome, it may be best to increase the interval from 4 to 6 or 8 weeks to ensure that a positive result is not false positive.

The available data show that the stool antigen tests that use monoclonal anti-H. pylori antibodies are more reliable than polyclonal stool antigen tests and monoclonal antibody-based stool antigen tests are recommended.

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Which of the following is/are false positive tuberculin skin test reactions? [Select All that apply]

a. Infection with non-tuberculosis mycobacteria
b. Cutaneous anergy
c. Previous BCG vaccination
d. Very old TB infection
e. Recent live-virus vaccination


Which of the following is/are false positive tuberculin skin test reactions? [Select All that apply]

a. Infection with non-tuberculosis mycobacteria
b. Cutaneous anergy
c. Previous BCG vaccination
d. Very old TB infection
e. Recent live-virus vaccination

Answer: (a,c). The Mantoux tuberculin skin test (TST) is the standard method of determining whether a person is infected with Mycobacterium tuberculosis. Reliable administration and reading of the TST requires standardization of procedures, training, supervision, and practice.

The TST is performed by injecting 0.1 ml of tuberculin purified protein derivative (PPD) into the inner surface of the forearm. The injection should be made with a tuberculin syringe, with the needle bevel facing upward. The TST is an intradermal injection. When placed correctly, the injection should produce a pale elevation of the skin (a wheal) 6 to 10 mm in diameter.

The skin test reaction should be read between 48 and 72 hours after administration. A patient who does not return within 72 hours will need to be rescheduled for another skin test.

The reaction should be measured in millimeters of the induration (palpable, raised, hardened area or swelling). The reader should not measure erythema (redness). The diameter of the indurated area should be measured across the forearm (perpendicular to the long axis).

Skin test interpretation depends on two factors:

1. Measurement in millimeters of the induration
2. Person's risk of being infected with TB and of progression to disease if infected

What Are False-Positive Reactions?

Some persons may react to the TST even though they are not infected with M. tuberculosis. The causes of these false-positive reactions may include, but are not limited to, the following:

1. Infection with non-tuberculosis mycobacteria
2. Previous BCG vaccination
3. Incorrect method of TST administration
4. Incorrect interpretation of reaction
5. Incorrect bottle of antigen used

What Are False-Negative Reactions?

Some persons may not react to the TST even though they are infected with M. tuberculosis. The reasons for these false-negative reactions may include, but are not limited to, the following:

1. Cutaneous anergy (anergy is the inability to react to skin tests because of a weakened immune system)
2. Recent TB infection (within 8-10 weeks of exposure)
3. Very old TB infection (many years)
4. Very young age (less than 6 months old)
5. Recent live-virus vaccination (e.g., measles and smallpox)
6. Overwhelming TB disease
7. Some viral illnesses (e.g., measles and chicken pox)
8. Incorrect method of TST administration
9. Incorrect interpretation of reaction

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Thiazide diuretics should NOT be used as a first line treatment for hypertension in patient suffering from:

a. Hyperlipidemia
b. Heart failure
c. COPD
d. Gout
e. Peripheral artery disease


Thiazide diuretics should NOT be used as a first line treatment for hypertension in patient suffering from:

a. Hyperlipidemia
b. Heart failure
c. COPD
d. Gout
e. Peripheral artery disease

Answer :(d). Thiazide diuretics may increase the reabsorption of uric acid from renal tubules and may cause hyperuricemia. It should NOT be used as a first line treatment for hypertension in patient suffering from gout.

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Which of the following inhibits CYP 3A4?

a. Omeprazole
b. Lansoprazole
c. Pantoprazole
d. Rabeprazole
e. Esomeprazole


Which of the following inhibits CYP 3A4?

a. Omeprazole
b. Lansoprazole
c. Pantoprazole
d. Rabeprazole
e. Esomeprazole

Answer: (a) Below is the list of drugs that inhibit specifically CYP 3A4:

1. Amiodarone
2. Anastrozole
3. Azithromycin
4. Cannabinoids
5. Cimetidine
6. Clarithromycin
7. Clotrimazole
8. Cyclosporine
9. Danazol
10. Delavirdine
11. Dexamethasone
12. Diethyldithiocarbamate
13. Diltiazem
14. Dirithromycin
15. Disulfiram
16. Entacapone (high dose)
17. Erythromycin
18. Ethinyl estradiol
19. Fluconazole
20. Fluoxetine
21. Fluvoxamine
22. Gestodene
23. Grapefruit juice
24. Indinavir
25. Isoniazid
26. Ketoconazole
27. Metronidazole
28. Mibefradil
29. Miconazole
30. Nefazodone
31. Nelfinavir
32. Nevirapine
33. Norfloxacin
34. Norfluoxetine
35. Omeprazole
36. Oxiconazole
37. Paroxetine (weak)
38. Propoxyphene
39. Quinidine
40. Quinine
41. Quinupristin and Dalfopristin
42. Ranitidine
43. Ritonavir
44. Saquinavir
45. Sertindole
46. Sertraline
47. Troglitazone
48. Troleandomycin
49. Valproic acid

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Home ovulation tests usually detect a preovulatory surge in which of the following in the urine?

a. Prolactin
b. Oestrogen
c. Oxytocin
d. Progesterone
e. Luteinizing hormone


Home ovulation tests usually detect a preovulatory surge in which of the following in the urine?

a. Prolactin
b. Oestrogen
c. Oxytocin
d. Progesterone
e. Luteinizing hormone

Answer: (e). An ovulation home test is used by women to help determine the time in the menstrual cycle when getting pregnant is most likely. The test detects a rise in luteinizing hormone (LH) in the urine. A rise in this hormone signals the ovary to release the egg.

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Which of the following rating scales is commonly used to evaluate the severity of extrapyramidal symptoms (EPS)? [Select ALL that apply]

a. SAS
b. BARS
c. AIMS
d. ESRS
e. PDS


Which of the following rating scales is commonly used to evaluate the severity of extrapyramidal symptoms (EPS)? [Select ALL that apply]

a. SAS
b. BARS
c. AIMS
d. ESRS
e. PDS

Answer: (a,b,c,d). Extrapyramidal symptoms (EPS) are drug-induced movement disorders that include acute and tardive symptoms.

These symptoms include dystonia (continuous spasms and muscle contractions), akathisia (motor restlessness), Parkinsonism (characteristic symptoms such as rigidity, bradykinesia, and tremor), and tardive dyskinesia (irregular, jerky movements).

Since it is difficult to measure extrapyramidal symptoms, rating scales are commonly used to assess the severity of movement disorders.

The Simpson-Angus Scale (SAS), Barnes Akathisia Rating Scale (BARS), Abnormal Involuntary Movement Scale (AIMS), and Extrapyramidal Symptom Rating Scale (ESRS) are rating scales frequently used for such assessment and are not weighted for diagnostic purposes.

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Poison Ivy rash is an example of:

a. Type I Hypersensitivity
b. Type II Hypersensitivity
c. Type III Hypersensitivity
d. Type IV Hypersensitivity
e. Type V Hypersensitivity


Poison Ivy rash is an example of:

a. Type I Hypersensitivity
b. Type II Hypersensitivity
c. Type III Hypersensitivity
d. Type IV Hypersensitivity
e. Type V Hypersensitivity

Answer: (d), Type 4 hypersensitivity is often called delayed type. Delayed hypersensitivity does not start to be noticeable until several hours to a full day after exposure to the antigen. It may last for over a week.

Poison ivy rash is caused by an allergic reaction to an oily resin called urushiol (u-ROO-she-ol). This oil is in the leaves, stems and roots of poison ivy, poison oak and poison sumac. Urushiol, which is a hapten, when absorbed through the skin from a poison ivy plant, it (urushiol) undergoes oxidation in the skin cells to generate the actual hapten, a reactive molecule called a quinone, which then reacts with skin proteins to form hapten adducts.

T lymphocytes recognize the foreign substances, usually after the antigen is eaten, degraded, and presented (in pieces) by so-called antigen-presenting cells such as Langerhans cells in the skin, or macrophages. Urushiol metabolites (metabolite of Poison Ivy) are presented by this and other mechanisms. The T lymphocytes pour out inflammatory signal substances called cytokines. These call in armies of white blood cells called monocytes, which become macrophages. The macrophages become activated by the cytokines and attack everything in the vicinity, and can cause severe tissue damage.

Usually, the first exposure causes only sensitization, in which there is a proliferation of effector T-cells. After a subsequent, second exposure, the proliferated T-cells can become activated, generating an immune reaction that produces typical blisters of a poison ivy exposure.


In addition to poison ivy, a good example is the skin reaction to injected tuberculosis antigen. In fact, when tuberculosis bacteria infect the lung, it is the delayed hypersensitivity against them which destroys the lung. Unlike the other types, it is not antibody mediated but rather is a type of cell-mediated response.

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