Anatomy
2 questionsArch of Aorta develops from which aortic arch artery?
Which muscle is derived from the third pharyngeal arch?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 71: Arch of Aorta develops from which aortic arch artery?
- A. Right 3rd
- B. Left 4th (Correct Answer)
- C. Left 3rd
- D. Right Truncus arteriosus
Explanation: ***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.
Question 72: Which muscle is derived from the third pharyngeal arch?
- A. Tensor tympani
- B. Stylopharyngeus (Correct Answer)
- C. Cricothyroid
- D. Stapedius
Explanation: ***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.
Dental
1 questionsWhat is the first permanent tooth to erupt?
NEET-PG 2013 - Dental NEET-PG Practice Questions and MCQs
Question 71: What is the first permanent tooth to erupt?
- A. First premolar
- B. Second premolar
- C. First molar (Correct Answer)
- D. Second molar
Explanation: ***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**.
Internal Medicine
1 questionsMigraine is due to
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 71: Migraine is due to
- A. Cortical spreading depression (Correct Answer)
- B. Dilatation of cranial blood vessels
- C. Constriction of cranial blood vessels
- D. Inflammation of the meninges
Explanation: ***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.
Pharmacology
6 questionsWhich antiglaucomatous drug is known to cause spasm of accommodation?
Which of the following is classified as an antispasmodic agent?
Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it
Which dopamine receptor is known for its inhibitory action in the central nervous system?
Which of the following statements about clonidine is incorrect?
Which urinary bladder spasmolytic has local anesthetic properties?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 71: Which antiglaucomatous drug is known to cause spasm of accommodation?
- A. Timolol
- B. Pilocarpine (Correct Answer)
- C. Dorzolamide
- D. Latanoprost
Explanation: ***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**.
Question 72: Which of the following is classified as an antispasmodic agent?
- A. Dicyclomine (Correct Answer)
- B. Physostigmine
- C. Tropicamide
- D. None of the options
Explanation: ***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.
Question 73: Besides its properties of decreasing intraocular pressure, timolol is preferred in the treatment of glaucoma because it
- A. Is a selective beta-adrenoceptor blocker
- B. Increases outflow of aqueous humor
- C. Produces no miosis (Correct Answer)
- D. Possesses membrane stabilizing activity
Explanation: ***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.
Question 74: Which dopamine receptor is known for its inhibitory action in the central nervous system?
- A. Dopamine Receptor D5
- B. No inhibitory dopamine receptor present
- C. Dopamine Receptor D2 (Correct Answer)
- D. Dopamine Receptor D1
Explanation: ***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.
Question 75: Which of the following statements about clonidine is incorrect?
- A. Alpha 2 receptor agonist
- B. Sudden withdrawal causes rebound hypertension
- C. Controls loose motions due to diabetic neuropathy
- D. First line for AMI (Correct Answer)
Explanation: ***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.
Question 76: Which urinary bladder spasmolytic has local anesthetic properties?
- A. Tamsulosin
- B. Terazosin
- C. Oxybutynin (Correct Answer)
- D. Yohimbine
Explanation: ***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.