Antiplatelet Drugs — MCQs
Mechanism of action of exenatide in diabetes mellitus is
What is the mechanism of action of ticagrelor?
Which of the following is an antiplatelet drug?
Which enzyme is irreversibly inhibited by aspirin?
What is the mechanism of action of ticagrelor?
A 34-year-old woman has Raynaud's phenomenon associated with systemic sclerosis (scleroderma). Which of the following is the most appropriate management for this condition?
The following drugs are effective in the management of menorrhagia except :
An 85-year-old patient was brought to the ER, BP: 180/100, right hemiparesis was seen. What is the next best step in management?
A 30-year-old male chronic smoker presents with this condition. Which of the following drugs is the preferred drug for improving circulation?
Treatment with Herceptin in breast cancer is indicated for
Antiplatelet Drugs Indian Medical PG Practice Questions and MCQs
Question 1: Mechanism of action of exenatide in diabetes mellitus is
- A. It is DPP-4 inhibitor and results in decreased breakdown of GLP
- B. It is amylin analogue and decreases glucagon
- C. It is analogue of GLP released from gut and increases glucose dependent insulin secretion (Correct Answer)
- D. It inhibits SGLT-2 and causes glucosuria
Explanation: ***It is analogue of GLP released from gut and increase glucose dependant insulin secretion*** - **Exenatide** is a **glucagon-like peptide-1 (GLP-1) receptor agonist**, mimicking the action of naturally occurring GLP-1 [1]. - It stimulates **glucose-dependent insulin secretion**, suppresses glucagon release, slows gastric emptying, and promotes satiety, all contributing to improved glycemic control [2]. *It inhibits SGLT-2 and cause glucosuria* - This describes the mechanism of **sodium-glucose co-transporter 2 (SGLT-2) inhibitors**, such as empagliflozin or canagliflozin, which promote glucose excretion in urine. - **Exenatide** does not directly affect renal glucose reabsorption. *It is DPP-4 inhibitor and result in decreased breakdown of GLP* - This mechanism belongs to **dipeptidyl peptidase-4 (DPP-4) inhibitors** (e.g., sitagliptin, saxagliptin), which prevent the rapid degradation of endogenous GLP-1, thus prolonging its action [1]. - **Exenatide** directly activates GLP-1 receptors rather than modulating the enzyme that breaks down endogenous GLP-1 [1]. *It is amylin analogue and decrease glucagon* - This describes **pramlintide**, an amylin analogue used in diabetes management, which primarily suppresses postprandial glucagon secretion, slows gastric emptying, and promotes satiety. - While **exenatide** also decreases glucagon, its primary mechanism is via GLP-1 receptor agonism [2].
Question 2: What is the mechanism of action of ticagrelor?
- A. PAR1 activator
- B. P2Y12 inhibitor (Correct Answer)
- C. P2Y12 activator
- D. PAR1 inhibitor
Explanation: ***P2Y12 inhibitor*** - Ticagrelor is an **oral antiplatelet agent** that works by reversibly binding to the **P2Y12 receptor** on platelets. - This binding prevents adenosine diphosphate (ADP) from activating the P2Y12 receptor, which is crucial for **platelet aggregation** and **thrombus formation**. *PAR1 inhibitor* - **PAR1 inhibitors** (e.g., vorapaxar) block the thrombin receptor on platelets, leading to antiplatelet effects. - This mechanism is distinct from ticagrelor's action on the P2Y12 receptor. *PAR1 activator* - Activating **PAR1** would promote platelet aggregation and activation, which is the opposite effect of an antiplatelet medication like ticagrelor. - This mechanism would increase the risk of thrombosis. *P2Y12 activator* - Activating the **P2Y12 receptor** would lead to increased platelet aggregation and is not the mechanism of action for an antiplatelet drug. - Drugs that activate P2Y12 would promote the formation of blood clots.
Question 3: Which of the following is an antiplatelet drug?
- A. Clopidogrel (Correct Answer)
- B. Streptokinase
- C. Hirudin
- D. Tranexamic acid
Explanation: ***Clopidogrel*** - Clopidogrel is an **antiplatelet agent** that works by irreversibly inhibiting the **P2Y12 ADP receptor** on platelets, preventing platelet activation and aggregation. - It is commonly used for the prevention of **thrombotic events** in patients with acute coronary syndrome, stroke, or peripheral artery disease. *Tranexamic acid* - Tranexamic acid is an **antifibrinolytic drug** that inhibits the activation of plasminogen to plasmin, thereby preventing the breakdown of fibrin clots. - It is primarily used to **reduce bleeding** in various conditions such as heavy menstrual bleeding, surgical procedures, and trauma. *Streptokinase* - Streptokinase is a **thrombolytic agent** that acts by forming a complex with plasminogen, leading to its conversion to plasmin, which then breaks down fibrin clots. - It is used to dissolve existing blood clots in conditions such as acute myocardial infarction, pulmonary embolism, and deep vein thrombosis. *Hirudin* - Hirudin is a direct **thrombin inhibitor** originally isolated from the salivary glands of medicinal leeches. - It directly binds to and inactivates thrombin, thereby preventing the conversion of fibrinogen to fibrin and inhibiting clot formation.
Question 4: Which enzyme is irreversibly inhibited by aspirin?
- A. Lipooxygenase
- B. Cyclooxygenase (Correct Answer)
- C. Thromboxane synthase
- D. Phospholipase
Explanation: ***Cyclooxygenase*** - **Aspirin** irreversibly inhibits **cyclooxygenase (COX-1 and COX-2)** by acetylating a serine residue in the enzyme's active site. - This irreversible inhibition prevents the production of **prostaglandins, thromboxane**, and **prostacyclin**, thereby reducing inflammation, pain, fever, and platelet aggregation. *Lipooxygenase* - **Lipooxygenase** is involved in the synthesis of **leukotrienes**, which are mediators of inflammation and allergic responses. - Aspirin does not directly inhibit lipooxygenase; rather, it primarily targets the COX pathway. *Thromboxane synthase* - **Thromboxane synthase** is an enzyme downstream of COX, responsible for converting prostaglandin H2 into **thromboxane A2**. - While aspirin's effect on platelet aggregation is due to reduced thromboxane A2 synthesis via COX inhibition, it does not directly inhibit thromboxane synthase itself. *Phospholipase* - **Phospholipase A2** is responsible for releasing **arachidonic acid** from cell membrane phospholipids, which is the initial step in both the cyclooxygenase and lipooxygenase pathways. - Aspirin does not directly inhibit phospholipase A2; its action occurs later in the cascade.
Question 5: What is the mechanism of action of ticagrelor?
- A. P2Y12 receptor antagonist (Correct Answer)
- B. Cox inhibition
- C. Inhibition of thromboxane synthase
- D. GPIIb/IIIa inhibition
Explanation: ***P2Y12 receptor antagonist*** - **Ticagrelor** is an **oral antiplatelet drug** that reversibly binds to the **P2Y12 ADP receptor** on platelet surfaces. - By blocking this receptor, it prevents **ADP-mediated platelet activation** and subsequent aggregation, reducing the risk of thrombotic events. *Cox inhibition* - **COX inhibitors** like **aspirin** prevent the synthesis of **thromboxane A2**, a powerful platelet aggregator. - This mechanism is characteristic of **NSAIDs** and **aspirin**, not ticagrelor. *GPIIB/IIIA inhibition* - **GPIIb/IIIa inhibitors** (e.g., abciximab, eptifibatide, tirofiban) directly block the final common pathway for platelet aggregation by preventing **fibrinogen binding** to the GPIIb/IIIa receptor. - While also an antiplatelet mechanism, this is distinct from ticagrelor's action on the P2Y12 receptor. *Inhibition of thromboxane synthase* - Inhibition of **thromboxane synthase** would reduce the production of **thromboxane A2**, similar to the effect of COX inhibition. - This is not the primary mechanism of action for ticagrelor; drugs like **dazoxiben** or **picotamide** act through this pathway.
Question 6: A 34-year-old woman has Raynaud's phenomenon associated with systemic sclerosis (scleroderma). Which of the following is the most appropriate management for this condition?
- A. ergotamine
- B. calcium channel blockers (nifedipine)
- C. beta-blocking drugs
- D. warm clothing (Correct Answer)
Explanation: ***Warm clothing*** - Maintaining **core body temperature** and direct protection of extremities from **cold exposure** is the primary non-pharmacological management for Raynaud's phenomenon. - This helps prevent the **vasospasm** triggered by cold, reducing the frequency and severity of attacks. *ergotamine* - **Ergotamine** is a powerful **vasoconstrictor** and would worsen Raynaud's phenomenon by further narrowing blood vessels. - It is primarily used for **migraine treatment** and is contraindicated in conditions involving vasoconstriction. *calcium channel blockers (nifedipine)* - While **calcium channel blockers** like nifedipine are often used as **second-line pharmacological treatment** for Raynaud's, warm clothing represents a more fundamental and universally applicable management strategy. [1] - Nifedipine works by causing **vasodilation**, which can reduce the severity and frequency of attacks when non-pharmacological methods are insufficient. [1] *beta-blocking drugs* - **Beta-blockers** can worsen Raynaud's phenomenon by causing **vasoconstriction** due to unopposed alpha-adrenergic activity. [1] - These drugs are generally **contraindicated** in patients with Raynaud's syndrome. [1]
Question 7: The following drugs are effective in the management of menorrhagia except :
- A. Progestational agents
- B. Prostaglandins (Correct Answer)
- C. Non-steroidal anti-inflammatory drugs
- D. Anti-fibrinolytic drugs
Explanation: ***Prostaglandins*** - Prostaglandins, particularly **PGE2** and **PGF2α**, are generally associated with **increased uterine contractions** and **vasodilation**, which can worsen menstrual bleeding rather than reduce it. - While cyclooxygenase inhibitors (NSAIDs) work by inhibiting prostaglandin synthesis, exogenous prostaglandins themselves are not used to treat menorrhagia and can exacerbate it. *Progestational agents* - Progestins help to **stabilize the endometrium**, reducing excessive bleeding by inducing decidualization and limiting endometrial growth. - They can be administered orally, via injection, or through an **intrauterine device (IUD)** like the levonorgestrel-releasing IUD (Mirena), which is highly effective. *Non-steroidal anti-inflammatory drugs* - NSAIDs reduce menorrhagia by **inhibiting prostaglandin synthesis** in the endometrium, which leads to reduced vasodilation and uterine contractions. - They also help alleviate associated **dysmenorrhea** (menstrual pain). *Anti-fibrinolytic drugs* - These drugs, such as **tranexamic acid**, work by **inhibiting plasminogen activation**, thereby preventing the breakdown of fibrin clots within the uterus. - This promotes clot stability and reduces menstrual blood loss significantly.
Question 8: An 85-year-old patient was brought to the ER, BP: 180/100, right hemiparesis was seen. What is the next best step in management?
- A. Reduce BP
- B. NCCT (Correct Answer)
- C. MRI
- D. Aspirin 300mg and anticoagulants
Explanation: ***NCCT*** - A **non-contrast CT (NCCT) scan of the brain** is the most crucial initial step to differentiate between **ischemic stroke** and **hemorrhagic stroke** [1]. - This distinction is vital because management, especially the use of thrombolytics or anticoagulants, differs significantly based on stroke type [1]. *Reduce BP* - While blood pressure management is important in stroke, immediate and aggressive lowering of BP in acute ischemic stroke can **worsen cerebral perfusion** and **increase infarct size**. - In hemorrhagic stroke, BP control is often necessary, but the decision to lower BP and by how much depends on the cause and extent of the bleed, and this can only be determined after imaging [1]. *MRI* - **MRI** is more sensitive for detecting acute ischemic changes than CT, especially in the posterior fossa [1]. - However, **MRI is not typically the first-line imaging** in an emergency setting for an acute stroke due to its longer acquisition time and potential contraindications (e.g., pacemakers, metallic implants) [1]. *Aspirin 300mg and anticoagulants* - These medications are indicated for **ischemic stroke** (aspirin is an antiplatelet, anticoagulants may be used in specific cases like cardioembolic stroke). - Administering these agents in the event of a **hemorrhagic stroke** would be contraindicated and could significantly worsen the bleeding, leading to severe neurological damage or death [1].
Question 9: A 30-year-old male chronic smoker presents with this condition. Which of the following drugs is the preferred drug for improving circulation?
- A. Prasugrel
- B. Naftidrofuryl
- C. Cilostazol (Correct Answer)
- D. Xanthine nicotinate
Explanation: ***Cilostazol*** - The image shows **gangrenous toes** in a **chronic smoker**, suggesting peripheral arterial disease (PAD) or Buerger's disease (thromboangiitis obliterans), which is typically seen in young to middle-aged males who are heavy smokers and presents with limb ischemia. - **Cilostazol** is a phosphodiesterase-3 inhibitor that inhibits platelet aggregation and is a direct arterial vasodilator, making it the preferred drug for improving **claudication** and circulation in PAD. *Prasugrel* - **Prasugrel** is an antiplatelet drug used primarily in acute coronary syndromes undergoing percutaneous coronary intervention (PCI) to reduce thrombotic events. - While it reduces platelet aggregation, it does not directly improve peripheral circulation or symptoms of claudication as effectively as cilostazol in PAD. *Naftidrofuryl* - **Naftidrofuryl** is a peripheral vasodilator and serotonin 5-HT2 receptor antagonist used primarily for treating intermittent claudication and has some evidence for improving pain-free walking distance. - However, it is generally considered a second-line agent, and its efficacy is often less pronounced than cilostazol, particularly in severe cases of peripheral ischemia. *Xanthine nicotinate* - **Xanthine nicotinate** is a derivative of nicotinic acid with vasodilator properties, sometimes used to improve circulation in peripheral vascular disease. - Its efficacy in severe peripheral ischemia or symptomatic claudication is generally considered limited compared to other agents like cilostazol, and it is not typically a preferred first-line treatment.
Question 10: Treatment with Herceptin in breast cancer is indicated for
- A. Tumours with over-expressed HER2/C-erbB-2 protein (Correct Answer)
- B. PR receptor +ve tumours
- C. ER receptor +ve tumours
- D. Ki-67 stain +ve tumours
Explanation: **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.
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