Internal Medicine
3 questionsWhich of the following statements about Alport's syndrome is incorrect?
Which of the following statements about Gilbert syndrome is false?
What is the most appropriate initial management for paralysis resulting from organophosphorus poisoning?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 311: Which of the following statements about Alport's syndrome is incorrect?
- A. Nerve deafness
- B. Glomerulonephritis
- C. Autosomal dominant (Correct Answer)
- D. X-linked
Explanation: ***Autosomal dominant*** - While there are rare autosomal dominant forms, the most common and classic presentation of **Alport's syndrome is X-linked recessive**, affecting males more severely. - This statement is incorrect because it implies that autosomal dominant inheritance is the primary or typical mode, which is not true for the majority of cases. *Nerve deafness* - **Sensorineural hearing loss**, particularly for high frequencies, is a common and characteristic extra-renal manifestation of Alport's syndrome. - This symptom typically progresses with age and is a key diagnostic feature. *Glomerulonephritis* - **Progressive glomerulonephritis** is the hallmark renal feature of Alport's syndrome, leading to hematuria, proteinuria, and eventually end-stage renal disease. - It is caused by mutations in collagen type IV genes, which disrupt the integrity of the glomerular basement membrane. *X-linked* - The majority of Alport's syndrome cases (about 85%) are **X-linked recessive**, caused by mutations in the *COL4A5* gene located on the X chromosome. - This explains why males are more severely affected and typically present with earlier onset and more rapid progression of renal disease.
Question 312: Which of the following statements about Gilbert syndrome is false?
- A. Normal liver histology
- B. Autosomal dominant
- C. Elevated bilirubin levels are present
- D. Causes cirrhosis (Correct Answer)
Explanation: ***Causes cirrhosis*** - **Gilbert syndrome** is a benign condition characterized by intermittent unconjugated hyperbilirubinemia and does **not lead to cirrhosis** [1]. - Cirrhosis is a severe form of **liver scarring** resulting from chronic damage, which is not a feature of Gilbert syndrome. *Normal liver histology* - The liver structure and function in individuals with Gilbert syndrome are typically **normal**, distinguishing it from other liver disorders [2]. - Histological examination of liver biopsies usually reveals no abnormalities, reflecting the **benign nature** of the condition. *Autosomal dominant* - Gilbert syndrome is inherited in an **autosomal recessive** pattern, not autosomal dominant [2]. - It results from a reduction in the activity of the **UGT1A1 enzyme**, which is responsible for bilirubin conjugation [1], [2]. *Elevated bilirubin levels are present* - Individuals with Gilbert syndrome experience **intermittent unconjugated hyperbilirubinemia**, meaning their indirect bilirubin levels are elevated [3]. - This elevation is usually mild and can be exacerbated by stress, fasting, or illness, but it is typically **harmless** [1], [2].
Question 313: What is the most appropriate initial management for paralysis resulting from organophosphorus poisoning?
- A. Supportive care, including respiratory support (Correct Answer)
- B. Atropine to counteract muscarinic symptoms
- C. Oximes to reactivate acetylcholinesterase
- D. No specific antidote
Explanation: **Supportive care, including respiratory support** * **Paralysis** in organophosphorus poisoning (OPP) is often due to **nicotinic effects** at the neuromuscular junction, leading to respiratory muscle weakness and failure [2]. * **Respiratory support** through mechanical ventilation is crucial to maintain oxygenation and prevent complications while awaiting the effects of antidotal therapy [1], [2]. * *Atropine to counteract muscarinic symptoms* * **Atropine** primarily blocks **muscarinic receptors**, effectively treating symptoms like bradycardia, bronchorrhea, and miosis [2]. * It does **not reverse the nicotinic effects** responsible for muscle paralysis and respiratory failure. * *Oximes to reactivate acetylcholinesterase* * **Oximes (e.g., pralidoxime)** reactivate **acetylcholinesterase**, thereby addressing the underlying cause of acetylcholine accumulation [2]. * They are most effective if given **early** before irreversible aging of the enzyme occurs, but their effect on established paralysis can be limited without concurrent respiratory support [2]. * *No specific antidote* * This statement is incorrect; **atropine** and **oximes** are specific antidotes for organophosphorus poisoning [2]. * While these antidotes are vital, initial management prioritizing **airway and breathing support** is paramount due to the life-threatening respiratory paralysis [1].
Pharmacology
6 questionsWhich drug has the highest plasma protein binding?
What is the mechanism of metabolism for alcohol, aspirin, and phenytoin at high doses?
In the context of pharmacology, which plasma protein do acidic drugs primarily bind to?
Muscarinic cholinergic receptors are seen at all sites, except?
Which urinary bladder spasmolytic has local anesthetic properties?
Which dopamine receptor is known for its inhibitory action in the central nervous system?
NEET-PG 2013 - Pharmacology NEET-PG Practice Questions and MCQs
Question 311: Which drug has the highest plasma protein binding?
- A. Warfarin (Correct Answer)
- B. Verapamil
- C. Aspirin
- D. GTN
Explanation: ***Warfarin*** - **Warfarin** exhibits very **high plasma protein binding**, typically greater than 99%, primarily to albumin. - This high binding capacity means that only a small fraction of the drug is free and pharmacologically active. - Due to high protein binding, warfarin is susceptible to drug interactions when displaced from albumin. *Verapamil* - **Verapamil** has a relatively high plasma protein binding, around 90%, but it is not as high as warfarin. - Its binding is predominantly to **albumin** and alpha-1-acid glycoprotein. *Aspirin* - **Aspirin** (acetylsalicylic acid) has moderate plasma protein binding, usually between 50-90%, depending on the dosage. - It binds to **albumin** and can displace other protein-bound drugs. *GTN* - **Glyceryl trinitrate (GTN)** has moderate plasma protein binding, approximately 60%. - Its rapid onset and short duration of action are primarily due to its extensive first-pass metabolism and quick redistribution, rather than protein binding characteristics.
Question 312: What is the mechanism of metabolism for alcohol, aspirin, and phenytoin at high doses?
- A. First pass kinetics
- B. First order kinetics
- C. Zero order kinetics (Correct Answer)
- D. Second order kinetics
Explanation: ***Zero order kinetics*** - This mechanism occurs when the **metabolic enzymes become saturated at high drug concentrations**, leading to a constant amount (not a constant percentage) of drug being eliminated per unit time. - Alcohol, aspirin, and phenytoin are examples of drugs that exhibit **saturable metabolism**, transitioning from first-order to zero-order kinetics at higher doses. *First pass kinetics* - This describes the **metabolism of a drug by the liver or gut wall enzymes before it reaches systemic circulation** after oral administration. - While relevant to the oral bioavailability of these drugs, it does not describe the specific mechanism of elimination at high doses. *First order kinetics* - In this mechanism, a **constant fraction or percentage of the drug is eliminated per unit of time**, meaning the rate of elimination is directly proportional to the drug concentration. - Most drugs follow first-order kinetics at therapeutic doses because metabolizing enzymes are not saturated. *Second order kinetics* - This is a **less common pharmacokinetic model** where the rate of elimination is proportional to the square of the drug concentration or involves two reactants. - It does not typically describe the common elimination patterns of most drugs, including alcohol, aspirin, and phenytoin.
Question 313: In the context of pharmacology, which plasma protein do acidic drugs primarily bind to?
- A. Globulin
- B. Albumin (Correct Answer)
- C. α1-acid glycoprotein
- D. None of the options
Explanation: ***Albumin*** - **Albumin** is the most abundant plasma protein and has multiple binding sites for a wide range of drugs, particularly **acidic drugs**. - Its high concentration and diverse binding capabilities make it the primary transporter for many **lipophilic** and **anionic drugs**. *Globulin* - **Globulins** are a diverse group of proteins, some of which bind to drugs, but they primarily transport **hormones**, **metals**, and **vitamins**, not acidic drugs. - They are less significant for binding acidic drugs compared to albumin. *α1-acid glycoprotein* - **α1-acid glycoprotein** primarily binds to **basic drugs** due to its numerous acidic residues. - While it plays a crucial role in binding basic compounds, it has limited affinity for acidic drugs. *None of the options* - This option is incorrect because **albumin** is a well-established and significant plasma protein for binding acidic drugs. - Specific plasma proteins are known to bind different types of drugs, and for acidic drugs, albumin is the primary binder.
Question 314: Muscarinic cholinergic receptors are seen at all sites, except?
- A. Stomach
- B. CNS
- C. Glands
- D. Neuromuscular junction (Correct Answer)
Explanation: ***Neuromuscular junction*** - The **neuromuscular junction** primarily contains **nicotinic cholinergic receptors**, not muscarinic receptors. - Activation of these nicotinic receptors by acetylcholine causes muscle contraction. *Stomach* - The stomach contains **muscarinic M3 receptors** which mediate gastric acid secretion and smooth muscle contraction. - Activation by acetylcholine via the vagus nerve promotes digestion. *CNS* - The **central nervous system** has various subtypes of **muscarinic receptors (M1-M5)** distributed throughout, playing roles in learning, memory, and motor control. - These receptors modulate neuronal excitability and neurotransmitter release. *Glands* - Most exocrine glands (e.g., salivary, lacrimal, sweat glands) are richly supplied with **muscarinic receptors**, primarily **M3**. - Activation leads to increased glandular secretion.
Question 315: 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.
Question 316: 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.
Psychiatry
1 questionsWhich of the following develop first during dependence of a substance ?
NEET-PG 2013 - Psychiatry NEET-PG Practice Questions and MCQs
Question 311: Which of the following develop first during dependence of a substance ?
- A. Tolerance
- B. Physical dependence
- C. Psychological dependence (Correct Answer)
- D. Withdrawal symptoms
Explanation: ***Psychological dependence*** - **Psychological dependence** often develops first, characterized by an emotional need for the substance to experience pleasure or avoid discomfort. - This involves a strong **craving** and compulsive drug-seeking behavior despite negative consequences, driven by the substance's effect on brain reward pathways. *Tolerance* - **Tolerance** means that increasing doses of the substance are required to achieve the same effect previously achieved with lower doses. - While it often develops early in substance use, the initial "need" to use the substance is often psychological before physiological adaptations occur. *Physical dependence* - **Physical dependence** describes the body's physiological adaptation to the substance, leading to withdrawal symptoms if use is stopped or reduced. - It typically develops after consistent, prolonged use and is usually preceded by psychological dependence and often tolerance. *Withdrawal symptoms* - **Withdrawal symptoms** are the physiological and psychological signs that occur when a dependent person stops or drastically reduces their substance intake. - These are a direct manifestation of physical dependence and thus develop once physical dependence has been established.