UPSC-CMS 2010 - Pharmacology PYQs Practice Questions

Q: Treatment with Herceptin in breast cancer is indicated for

Tumours with over-expressed HER2/C-erbB-2 protein. **tumours with over-expressed C-erb B-2 protein** - **Herceptin** (trastuzumab) is a monoclonal antibody that specifically targets the **HER2/neu receptor**, which is encoded by the *ERBB2* gene. - Its efficacy depends on the **overexpression of C-erbB-2 protein** (also known as HER2/neu) on the surface of breast cancer cells, which indicates **HER2-positive breast cancer**. *K : 67 stain +ve tumours* - **Ki-67** is a proliferation marker that indicates the **growth fraction of a tumor**, and a positive stain suggests a rapidly dividing tumor. - While Ki-67 positivity is associated with more aggressive tumors, it does **not directly indicate suitability for Herceptin** treatment. *PR receptor +ve tumours* - Tumors positive for the **progesterone receptor (PR)** are typically treated with **hormonal therapies**, such as tamoxifen or aromatase inhibitors. - **PR positivity** does not indicate responsiveness to Herceptin, which targets the HER2 receptor. *ER receptor +ve tumours* - Tumors positive for the **estrogen receptor (ER)** are also treated with **hormonal therapies** due to their dependence on estrogen for growth. - Similarly to PR-positive tumors, **ER positivity** does not determine eligibility for Herceptin therapy. [Practice more Pharmacology PYQs on OnCourse]

Q: The mechanism of action by which clomiphene citrate induces ovulation is

through its anti-estrogenic effect. ***Correct: Through its anti-estrogenic effect*** - **Clomiphene citrate** is a selective estrogen receptor modulator (SERM) that acts as an **estrogen antagonist** at the hypothalamus and pituitary gland - By blocking estrogen receptors, it prevents the hypothalamus from sensing circulating estrogen, thereby removing the **negative feedback** normally exerted by estrogen - This perceived low estrogen state triggers increased **GnRH secretion**, leading to elevated **FSH and LH release**, which stimulates follicular development and ovulation *Incorrect: Through the hypothalamic estrogenic effect* - Clomiphene citrate is an **anti-estrogen**, not an estrogen agonist at the hypothalamic level - An estrogenic effect would **enhance negative feedback**, inhibiting GnRH and gonadotropin release, thereby **suppressing** rather than inducing ovulation *Incorrect: Through negative feedback on gonadotrophins* - This is the opposite of clomiphene's mechanism - Clomiphene works by **blocking negative feedback**, not establishing it - By antagonizing estrogen receptors, it tricks the hypothalamus into perceiving low estrogen levels, leading to **increased** (not decreased) gonadotropin release *Incorrect: Through positive feedback on gonadotrophins* - While clomiphene ultimately results in increased gonadotropin release, it does so by **disrupting negative feedback**, not by directly creating positive feedback - True positive feedback occurs naturally during the late follicular phase when sustained high estrogen levels trigger the LH surge - Clomiphene's mechanism is distinct—it removes the brake (negative feedback) rather than adding an accelerator (positive feedback) [Practice more Pharmacology PYQs on OnCourse]

Q: Which parenteral iron preparation does not cause anaphylaxis on intravenous administration?

Iron sucrose. ***Iron sucrose*** - **Iron sucrose** is a newer generation parenteral iron preparation with the **lowest risk of anaphylaxis** among IV iron formulations - This safety profile is primarily due to its **lack of dextran content**, which is responsible for the anaphylactic reactions seen with iron dextran - **Does not require a test dose** before administration, unlike iron dextran - Preferred for **intravenous administration** in patients requiring parenteral iron therapy [1] *Iron fumarate* - **Iron fumarate (ferrous fumarate)** is an **oral iron preparation only**, not a parenteral formulation - Since it is not administered intravenously, this option is **not applicable** to the question about parenteral IV iron preparations - As an oral preparation, it does not carry the risk of anaphylaxis associated with intravenous iron administration *Iron dextran* - **Iron dextran** is an older parenteral iron preparation with the **highest risk of anaphylactic reactions** due to the presence of dextran [2] - **Test dose is mandatory** before full administration due to significant hypersensitivity risk [2] - Can cause both **anaphylactoid reactions** (non-IgE mediated) and **true anaphylaxis** (IgE-mediated) [2] *Iron sorbitol* - **Iron sorbitol** is a parenteral iron preparation primarily used for **intramuscular administration**, not typically given intravenously - Can cause **allergic reactions** and has potential for **cardiovascular side effects** - Less commonly used today due to availability of safer alternatives like iron sucrose and ferric carboxymaltose [3] [Practice more Pharmacology PYQs on OnCourse]

Q: The following drugs can cause osteoporosis, except

mifepristone. ***Mifepristone***- **Mifepristone** is the **least commonly associated** with osteoporosis among these options in typical clinical practice, making it the best answer to this "EXCEPT" question.- While mifepristone is an anti-progestin and anti-glucocorticoid used for conditions like Cushing's syndrome, its osteoporosis risk is **less direct and less well-established** compared to the other drugs listed.- In chronic use, mifepristone can paradoxically increase cortisol levels through negative feedback disruption, which theoretically could affect bone, but this is **not a primary clinical concern** in its typical therapeutic applications.*Corticosteroid*- **Corticosteroids** are the **most common cause** of drug-induced osteoporosis (glucocorticoid-induced osteoporosis - GIOP) [1, 2].- They increase bone resorption by stimulating osteoclast activity and decrease bone formation by inhibiting osteoblast function [2].- Even short-term use can lead to rapid bone loss, with fracture risk increasing within 3-6 months of therapy.*Danazol*- **Danazol** is a synthetic androgen that causes a **hypoestrogenic state** by suppressing ovarian function.- This reduction in estrogen levels leads to **accelerated bone loss and osteoporosis**, particularly in women [1, 2].- Prolonged use requires bone density monitoring.*GnRH analogue*- **GnRH analogues** suppress sex hormone production (estrogen and testosterone) by pituitary desensitization.- The resulting **hypogonadism** directly causes **rapid bone loss** and significantly increased osteoporosis risk [1, 2].- Bone loss can occur within 6 months of therapy, often requiring prophylactic bone-protective agents. [Practice more Pharmacology PYQs on OnCourse]

Q: Consider the following drugs : 1. Rifampicin 2. Dapsone 3. Clofazimine 4. Minocycline Which of the above drugs are used in the standard treatment of pauci-bacillary leprosy in adults?

1 and 2 only. ***1 and 2 only*** - The **WHO standard treatment regimen** for **pauci-bacillary leprosy** in adults consists of only two drugs: **Rifampicin** and **Dapsone** [1]. - **Rifampicin 600 mg** is administered once monthly under supervision for 6 months, while **Dapsone 100 mg** is given daily for 6 months [3]. - This regimen is sufficient for PB leprosy, which has fewer bacilli and 1-5 skin lesions with no nerve involvement or only one nerve trunk involved [1], [2]. *1, 2 and 3* - This combination includes **Clofazimine**, which is part of the **multi-bacillary (MB) leprosy** regimen, not pauci-bacillary [2], [3]. - MB leprosy requires triple therapy (Rifampicin + Dapsone + Clofazimine) for 12 months due to higher bacterial load and more extensive disease. - Pauci-bacillary leprosy has a lower bacterial load and requires only a 6-month two-drug regimen [1]. *1 and 4* - **Minocycline** is used in **alternative regimens** for leprosy, particularly for patients with drug intolerance or in single-lesion PB leprosy (ROM regimen). - It is **not part of the standard first-line WHO treatment** for pauci-bacillary leprosy in adults. - The standard PB regimen requires **Rifampicin plus Dapsone**, not Rifampicin plus Minocycline. *2, 3 and 4* - This option misses **Rifampicin**, which is the **most crucial bactericidal drug** for all forms of leprosy (both PB and MB) [3]. - **Clofazimine** and **Minocycline** are not part of the standard PB leprosy regimen—Clofazimine is reserved for MB leprosy, and Minocycline is used only in alternative regimens. - Without Rifampicin, the treatment would be inadequate and risk development of drug resistance [3]. [Practice more Pharmacology PYQs on OnCourse]

Question 1

Treatment with Herceptin in breast cancer is indicated for

Accepted Answer

Tumours with over-expressed HER2/C-erbB-2 protein

Answer

PR receptor +ve tumours

Answer

ER receptor +ve tumours

Answer

Ki-67 stain +ve tumours

Question 2

The mechanism of action by which clomiphene citrate induces ovulation is

Accepted Answer

through its anti-estrogenic effect

Answer

through the hypothalamic estrogenic effect

Answer

through negative feedback on gonadotrophins

Answer

through positive feedback on gonadotrophins

Question 3

Which parenteral iron preparation does not cause anaphylaxis on intravenous administration?

Accepted Answer

Iron sucrose

Answer

Iron fumarate

Answer

Iron dextran

Answer

Iron sorbitol

Question 4

The following drugs can cause osteoporosis, except

Accepted Answer

mifepristone

Answer

corticosteroid

Answer

danazol

Answer

GnRH analogue

Question 5

Consider the following drugs :
1. Rifampicin
2. Dapsone
3. Clofazimine
4. Minocycline
Which of the above drugs are used in the standard treatment of pauci-bacillary leprosy in adults?

Accepted Answer

1 and 2 only

Answer

1, 2 and 3

Answer

1 and 4

Answer

2, 3 and 4

UPSC-CMS 2010 — Pharmacology