NEET-PG 2013 Practice Questions

Q: Arch of Aorta develops from which aortic arch artery?

Left 4th. ***Left 4th*** - The **arch of the aorta** develops from the **fourth left aortic arch artery**. [1] - This artery connects the **aortic sac** to the **dorsal aorta** on the left side during embryonic development. *Right Truncus arteriosus* - The **truncus arteriosus** gives rise to the **ascending aorta** and the **pulmonary artery**, not the arch of the aorta. - The term "right truncus arteriosus" is not standard in describing normal aortic arch development. *Right 3rd* - The **third aortic arch arteries** primarily contribute to the development of the **common carotid arteries** and the proximal part of the **internal carotid arteries**. - The right third aortic arch forms the proximal part of the right common carotid artery. *Left 3rd* - The **left third aortic arch artery** forms the proximal part of the **left common carotid artery** and the proximal part of the left internal carotid artery. - It does not directly form the arch of the aorta itself.

Q: Which muscle is derived from the third pharyngeal arch?

Stylopharyngeus. ***Stylopharyngeus*** - The **stylopharyngeus muscle** is uniquely derived from the **third pharyngeal arch**. - It is innervated by the **glossopharyngeal nerve (CN IX)** and plays a role in elevating the pharynx and larynx during swallowing. - This is the **only muscle** derived from the third pharyngeal arch, making it a key anatomical landmark. *Tensor tympani* - The **tensor tympani muscle** is derived from the **first pharyngeal arch**. - It is innervated by the **mandibular nerve (V3)** and dampens sound by tensing the tympanic membrane. *Cricothyroid* - The **cricothyroid muscle** is derived from the **fourth and sixth pharyngeal arches**. - It is innervated by the **external branch of the superior laryngeal nerve (CN X)** and tenses the vocal cords. *Stapedius* - The **stapedius muscle** is derived from the **second pharyngeal arch**. - It is innervated by the **facial nerve (CN VII)** and dampens sound by stabilizing the stapes bone.

Q: What is the first permanent tooth to erupt?

First molar. ***First molar*** - The **first molars** are typically the first permanent teeth to erupt, usually around **6 years of age**. - They erupt distal to the primary second molars and are not preceded by primary teeth, making them crucial for establishing the **occlusion**. *First premolar* - **First premolars** typically erupt later, between **10 and 11 years of age**, replacing the primary first molars. - Their eruption is part of the **exchange of primary teeth** for permanent successors. *Second premolar* - The **second premolars** erupt even later, usually between **11 and 12 years of age**, replacing the primary second molars. - They are also involved in the **replacement of primary teeth**, not the initial permanent eruption. *Second molar* - **Second molars** erupt much later than the first molars, typically between **11 and 13 years of age**, distal to the first molars. - They are part of the **later stages of permanent dentition development**.

Q: Migraine is due to

Cortical spreading depression. ***Cortical spreading depression*** - The current understanding is that **cortical spreading depression (CSD)** is the initiating event in migraine with aura, characterized by a wave of neuronal and glial depolarization that spreads across the cerebral cortex, leading to a temporary shutdown of neuronal activity [1]. - CSD is thought to activate the **trigeminal nerve**, subsequently causing the release of inflammatory neuropeptides and contributing to the pain phase [1]. *Dilatation of cranial blood vessels* - While **vasodilation of intracranial and extracranial blood vessels** does occur during the headache phase of migraine, it is now considered a *consequence* of the initial neurological events rather than the primary cause [1]. - This vasodilation contributes to the throbbing sensation of migraine pain but does not explain the aura or the initiation of the attack. *Constriction of cranial blood vessels* - **Vasoconstriction** was previously thought to be the cause of the migraine aura, but this theory has largely been disproven. - While some temporary constriction may precede CSD, it is not the primary mechanism behind the migraine attack. *Inflammation of the meninges* - While **neurogenic inflammation** of the meninges, involving the release of inflammatory mediators like **calcitonin gene-related peptide (CGRP)**, does play a role in sensitizing the trigeminal system and contributing to migraine pain, it is a downstream effect. - It is not the initial trigger for a migraine attack but rather part of the pain pathway activated by events like CSD.

Q: Which antiglaucomatous drug is known to cause spasm of accommodation?

Pilocarpine. ***Pilocarpine*** - **Pilocarpine** is a **direct-acting muscarinic agonist** that contracts the **ciliary muscle**. - Contraction of the ciliary muscle leads to **accommodation spasm** and a forward movement of the **iris-lens diaphragm**, which also helps to open the **trabecular meshwork**, facilitating aqueous outflow. *Timolol* - **Timolol** is a **beta-blocker** that reduces aqueous humor production by blocking beta-adrenergic receptors on the ciliary epithelium. - It does not directly affect the **ciliary muscle** or cause accommodation spasm. *Dorazolamide* - **Dorzolamide** is a **carbonic anhydrase inhibitor** that reduces aqueous humor production. - Its mechanism of action does not involve the ciliary body's mechanical action and therefore does not cause **accommodation spasm**. *Latanoprost* - **Latanoprost** is a **prostaglandin analog** that increases uveoscleral outflow of aqueous humor. - It does not directly affect the ciliary muscle's contraction or cause **accommodation spasm**.

Q: Which of the following is classified as an antispasmodic agent?

Dicyclomine. ***Dicyclomine*** - **Dicyclomine** is an **anticholinergic** medication that works by blocking muscarinic receptors, thereby reducing smooth muscle spasm in the gastrointestinal tract. - It is commonly used to treat symptoms of **irritable bowel syndrome (IBS)**, such as abdominal pain and cramping. *Physostigmine* - **Physostigmine** is a **cholinesterase inhibitor** that increases the concentration of acetylcholine at the synaptic cleft. - It is used to treat **anticholinergic poisoning** by reversing the effects of anticholinergic drugs, rather than acting as an antispasmodic itself. *Tropicamide* - **Tropicamide** is an **anticholinergic** agent primarily used as a **mydriatic** (pupil dilator) and **cycloplegic** (paralyzes the ciliary muscle) for ophthalmic examinations. - Its action is localized to the eye and it does not have significant systemic antispasmodic effects. *None of the options* - This option is incorrect because one of the listed medications is indeed classified as an antispasmodic agent. - When "None of the options" appears as a choice, it should only be selected if all other options are clearly incorrect.

Q: Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it

Produces no miosis. ***Produces no miosis*** - Timolol, a **non-selective beta-blocker**, decreases intraocular pressure without affecting pupillary size. - This is a **key advantage** in glaucoma treatment as miosis (pupil constriction) can worsen vision, especially in patients with cataracts. - Unlike **miotics** (e.g., pilocarpine), timolol does not cause pupillary constriction, making it better tolerated. *Possesses membrane stabilizing activity* - While some beta-blockers possess **membrane-stabilizing activity** (local anesthetic effect), this property is not a primary reason for timolol's preference in glaucoma. - This action is more relevant in antiarrhythmic uses of beta-blockers due to its effect on cardiac action potentials. *Increases outflow of aqueous humor* - Timolol primarily reduces intraocular pressure by **decreasing the production of aqueous humor**, not by increasing its outflow. - Drugs like **pilocarpine** (a cholinergic agonist) or **prostaglandin analogs** increase outflow. *Is a selective beta-adrenoceptor blocker* - Timolol is a **non-selective beta-blocker**, meaning it blocks both beta-1 and beta-2 adrenergic receptors. - Its non-selectivity is associated with systemic side effects (e.g., bronchospasm, bradycardia), and selective beta-blockers like **betaxolol** exist but are not the primary reason for timolol's preference in glaucoma.

Q: Which dopamine receptor is known for its inhibitory action in the central nervous system?

Dopamine Receptor D2. ***Dopamine Receptor D2*** - The **D2 receptor** is a member of the D2-like family (D2, D3, D4), which are **G-protein coupled receptors** that inhibit adenylyl cyclase activity. - Its activation typically leads to a **decrease in neuronal excitability** and neurotransmitter release, providing an inhibitory effect in the CNS. *Dopamine Receptor D5* - The **D5 receptor** belongs to the D1-like family (D1, D5), which are **G-protein coupled receptors** that stimulate adenylyl cyclase activity. - Activation of D5 receptors typically leads to **excitatory effects** rather than inhibitory ones in the CNS. *No inhibitory dopamine receptor present* - This statement is incorrect as specific dopamine receptor subtypes, particularly the **D2-like family**, are well-established to exert inhibitory actions in the CNS. - These inhibitory effects are crucial for various physiological processes, including motor control and reward pathways. *Dopamine Receptor D1* - The **D1 receptor** is part of the D1-like family (D1, D5) and is known for its **excitatory effects** in the CNS. - Activation of D1 receptors leads to an **increase in intracellular cAMP** and generally enhances neuronal activity.

Q: Which of the following statements about clonidine is incorrect?

First line for AMI. ***First line for AMI*** - Clonidine is **not first-line** for **Acute Myocardial Infarction (AMI)** as it can cause **bradycardia** and **hypotension**, potentially worsening cardiac output. - First-line AMI treatments include **thrombolytics**, **antiplatelet agents** (aspirin), **beta-blockers**, and **ACE inhibitors** for optimal cardiac protection. *Alpha 2 receptor agonist* - Clonidine is indeed an **alpha-2 adrenergic receptor agonist** that acts centrally in the **medulla oblongata**. - It reduces **sympathetic outflow** from the CNS, leading to decreased **heart rate**, **blood pressure**, and **peripheral vascular resistance**. *Sudden withdrawal causes rebound hypertension* - Abrupt clonidine discontinuation causes dangerous **rebound hypertension** due to sudden loss of **sympathetic inhibition**. - **Gradual tapering** over 1-2 weeks is essential to prevent this potentially life-threatening complication. *Controls loose motions due to diabetic neuropathy* - Clonidine effectively treats **diabetic diarrhea** by stimulating **alpha-2 receptors** in the enteric nervous system. - It **slows intestinal transit** and **enhances fluid absorption**, making it useful for **autonomic neuropathy-related** gastrointestinal symptoms.

Q: Which urinary bladder spasmolytic has local anesthetic properties?

Oxybutynin. ***Oxybutynin*** - Possesses both **anticholinergic properties** (bladder smooth muscle relaxation) and **direct local anesthetic properties**, which contribute to its spasmolytic effect on the detrusor muscle. - The **local anesthetic action** directly reduces bladder detrusor muscle contractions, explaining its efficacy in treating urge incontinence and overactive bladder. - This dual mechanism makes it unique among bladder spasmolytics. *Tamsulosin* - Is an **alpha-1 adrenergic receptor blocker** used for benign prostatic hyperplasia (BPH) by relaxing smooth muscle in the prostate and bladder neck. - Does **not have local anesthetic properties** and is not a bladder detrusor spasmolytic. *Terazosin* - Also an **alpha-1 adrenergic receptor blocker**, similar to tamsulosin, used for BPH and hypertension. - Acts via **vascular and prostatic smooth muscle relaxation**, without local anesthetic or bladder spasmolytic effects. *Yohimbine* - Is an **alpha-2 adrenergic receptor antagonist** known for increasing sympathetic outflow. - Does **not have bladder spasmolytic effects** or local anesthetic properties.

Question 1

Arch of Aorta develops from which aortic arch artery?

Accepted Answer

Left 4th

Answer

Right 3rd

Answer

Left 3rd

Answer

Right Truncus arteriosus

Question 2

Which muscle is derived from the third pharyngeal arch?

Accepted Answer

Stylopharyngeus

Answer

Tensor tympani

Answer

Cricothyroid

Answer

Stapedius

Question 3

What is the first permanent tooth to erupt?

Accepted Answer

First molar

Answer

First premolar

Answer

Second premolar

Answer

Second molar

Question 4

Migraine is due to

Accepted Answer

Cortical spreading depression

Answer

Dilatation of cranial blood vessels

Answer

Constriction of cranial blood vessels

Answer

Inflammation of the meninges

Question 5

Which antiglaucomatous drug is known to cause spasm of accommodation?

Accepted Answer

Pilocarpine

Answer

Timolol

Answer

Dorzolamide

Answer

Latanoprost

Question 6

Which of the following is classified as an antispasmodic agent?

Accepted Answer

Dicyclomine

Answer

Physostigmine

Answer

Tropicamide

Answer

None of the options

Question 7

Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it

Accepted Answer

Produces no miosis

Answer

Is a selective beta-adrenoceptor blocker

Answer

Increases outflow of aqueous humor

Answer

Possesses membrane stabilizing activity

Question 8

Which dopamine receptor is known for its inhibitory action in the central nervous system?

Accepted Answer

Dopamine Receptor D2

Answer

Dopamine Receptor D5

Answer

No inhibitory dopamine receptor present

Answer

Dopamine Receptor D1

Question 9

Which of the following statements about clonidine is incorrect?

Accepted Answer

First line for AMI

Answer

Alpha 2 receptor agonist

Answer

Sudden withdrawal causes rebound hypertension

Answer

Controls loose motions due to diabetic neuropathy

Question 10

Which urinary bladder spasmolytic has local anesthetic properties?

Accepted Answer

Oxybutynin

Answer

Tamsulosin

Answer

Terazosin

Answer

Yohimbine

NEET-PG 2013

Anatomy

Dental

Internal Medicine

Pharmacology