NEET-PG 2015 Practice Questions

Q: Which of the following is a positive acute phase protein that enhances the acute phase response?

Fibrinogen. ***Fibrinogen*** - **Fibrinogen** is a key **positive acute phase protein** whose concentration increases significantly during inflammation - Its elevation contributes to the acute phase response by promoting **blood clotting** and influencing **erythrocyte sedimentation rate (ESR)** - Along with C-reactive protein (CRP), haptoglobin, and serum amyloid A, fibrinogen is among the major positive acute phase reactants *Transferrin* - **Transferrin** is a **negative acute phase protein**, meaning its concentration decreases during inflammation - This reduction is part of the body's iron-sequestration strategy to limit iron availability for invading pathogens - The decrease in transferrin helps restrict bacterial growth by reducing available iron *Albumin* - **Albumin** is a prominent **negative acute phase protein**, with its concentration decreasing during acute inflammation due to redistribution and reduced synthesis - It plays a vital role in maintaining **oncotic pressure** and transporting various substances - Its decline reflects the severity of inflammation and is used as a marker of the acute phase response *Prealbumin* - **Prealbumin** (also known as transthyretin) is a **negative acute phase protein** and a sensitive marker of nutritional status - Its rapid decline during inflammation makes it a useful indicator, as its synthesis is quickly reduced - It has a short half-life (2-3 days), making it more sensitive to acute changes than albumin

Q: Chicken fat clot is seen in -

Postmortem clot. ***Postmortem clot*** - **"Chicken fat" clot** is a classical postmortem finding observed during autopsy in the **heart chambers and large blood vessels**. - It appears as a **yellowish, gelatinous layer** (plasma with lipids) overlying a **darker red layer** (settled red blood cells) due to gravitational separation of blood components after cessation of circulation. - This appearance indicates **postmortem blood coagulation** and helps distinguish postmortem clots from antemortem thrombi. - **Key differentiating features**: Postmortem clots are smooth, shiny, unattached to vessel walls, and rubbery in consistency. *Antemortem thrombus* - **Antemortem thrombi** form during life and show attachment to the vessel wall (**lines of Zahn**), dull surface, and friable consistency. - They are **firmly adherent** to the endothelium and show evidence of organization with inflammatory response. - The texture is **uniform** without the characteristic yellow-red separation seen in chicken fat clots. *Currant jelly clot* - **Currant jelly clot** is another type of postmortem clot that appears **dark red and gelatinous** throughout. - It forms when red blood cells remain relatively mixed with plasma, unlike the separated appearance of chicken fat clots. - Both are postmortem findings, but have different gross appearances. *Antemortem wound* - **Antemortem wounds** show vital reactions including hemorrhage, inflammation, and tissue response. - Blood at antemortem injury sites shows **active coagulation** during life, not the passive gravitational separation characteristic of chicken fat clots. - The chicken fat appearance is specific to **intravascular postmortem clots**, not wound sites.

Q: What is the primary effect of beta blockers in the management of thyroid storm?

Provides rapid relief of symptoms. Detailed management of thyrotoxic crisis (thyroid storm) is a medical emergency where patients should be given propranolol, either oral or intravenous, to manage life-threatening symptoms [1]. ***Provides rapid relief of symptoms*** - Beta blockers primarily address the **adrenergic manifestations** of thyroid storm, such as **tachycardia**, **tremors**, anxiety, and palpitations [1]. - By blocking **beta-adrenergic receptors**, they provide rapid symptomatic relief and reduce cardiovascular stress, without affecting hormone levels [2]. Thyroid hormones normally increase the expression of genes for beta-adrenergic receptors and G-proteins, leading to increased heart rate and force of contraction [2]. *Increases metabolism of thyroxine* - Beta blockers do not increase the **metabolism** or breakdown of thyroxine; their action is primarily on the **peripheral effects** of thyroid hormones. - While some beta blockers like **propranolol** can inhibit the peripheral conversion of T4 to T3, this is a secondary effect and not their primary role in providing rapid symptomatic relief [1]. *Blocks thyroxine receptors* - Beta blockers do not block **thyroxine receptors**; thyroid hormones exert their effects by binding to intracellular receptors, not adrenergic receptors [2]. - Their action is on the **adrenergic system**, which is overstimulated by the high levels of thyroid hormones. *Decreases synthesis of thyroxine* - Beta blockers do not directly decrease the **synthesis of thyroxine** by the thyroid gland. - That action is performed by **antithyroid drugs** like methimazole and propylthiouracil, which inhibit hormone production [1].

Q: What is the mode of inheritance for the most common form of hypophosphatemic rickets?

X-Linked Dominant (XD). ***X-Linked Dominant (XD)*** - The most common form of hypophosphatemic rickets is **X-linked hypophosphatemic rickets (XLH)**, which is inherited in an X-linked dominant pattern. - This condition is caused by mutations in the **PHEX gene** on the X chromosome, leading to impaired phosphate reabsorption in the kidneys. *Autosomal Recessive (AR)* - While some rare forms of hypophosphatemic rickets exist with **autosomal recessive** inheritance, they are not the most common. - These forms typically involve mutations in genes affecting phosphate transport or vitamin D metabolism, distinct from the primary defect in XLH. *Autosomal Dominant (AD)* - There are also rare **autosomal dominant** forms of hypophosphatemic rickets, such as hereditary hypophosphatemic rickets with hypercalciuria (HHRH) or autosomal dominant hypophosphatemic rickets (ADHR). - However, these are less common than the X-linked dominant form (XLH). *X-Linked Recessive (XR)* - **X-linked recessive** inheritance typically affects males more severely and exclusively, with carrier females usually unaffected or mildly affected. - In X-linked dominant conditions like XLH, both males and females are affected, though females may exhibit variable expressivity.

Q: Where is the benzodiazepine binding site located on GABA receptors?

γ-subunit. ***γ-subunit*** - The **benzodiazepine binding site** is located at the interface between the **α and γ subunits** of the GABA-A receptor, with the **γ-subunit (especially γ2) being essential** for benzodiazepine sensitivity. - The presence of the **γ2 subunit** is **mandatory** for benzodiazepine binding - receptors lacking this subunit are **insensitive to benzodiazepines**. - Benzodiazepines bind to this site and act as **positive allosteric modulators**, increasing the frequency of **chloride channel opening** in response to GABA. - This is the **standard answer** for NEET-PG and medical PG examinations in India. *α-subunit* - The **α-subunit** contributes to forming the benzodiazepine binding pocket at the α-γ interface. - Different **α-subunit isoforms** (α1, α2, α3, α5) determine the pharmacological profile and tissue distribution of benzodiazepine effects. - However, the **α-subunit alone** cannot bind benzodiazepines without the γ-subunit. *β-subunit* - The **β-subunit** contains the primary binding site for **GABA** itself. - It does not participate in benzodiazepine binding but is crucial for the receptor's overall function and GABAergic signaling. *δ-subunit* - The **δ-subunit** replaces the γ-subunit in certain GABA-A receptor subtypes that mediate **tonic inhibition**. - Receptors containing **δ-subunits** are **insensitive to benzodiazepines** but sensitive to neurosteroids and certain general anesthetics. - This is a key distinguishing feature between phasic (γ-containing) and tonic (δ-containing) GABA-A receptors.

Q: Which sympathomimetic drug is primarily known to increase heart rate?

Isoprenaline. ***Isoprenaline*** - **Isoprenaline** (isoproterenol) is a non-selective beta-adrenergic agonist, with a strong affinity for **β1 and β2 receptors** [1]. - Its activation of **β1 receptors** in the heart leads to a significant increase in **heart rate (positive chronotropy)** and contractility (positive inotropy) [1]. - It is the **most potent chronotropic agent** among sympathomimetics and is primarily known for increasing heart rate [2]. *Phenylephrine* - **Phenylephrine** is a selective **α1 adrenergic agonist** that causes vasoconstriction [4]. - It increases blood pressure but typically causes **reflex bradycardia** (decreased heart rate) due to baroreceptor activation. - Does NOT directly increase heart rate. *Noradrenaline* - **Noradrenaline** (norepinephrine) primarily acts on **α1 receptors** causing vasoconstriction, and to a lesser extent on **β1 receptors** [3]. - While it can stimulate β1 receptors, its predominant effect is to increase **mean arterial pressure** through vasoconstriction, often causing **reflex bradycardia** [3]. *Adrenaline* - **Adrenaline** (epinephrine) acts on **α1, β1, and β2 receptors** [4]. While it does increase heart rate via **β1 receptor** stimulation, it also causes significant **vasoconstriction** (via α1) and **vasodilation** (via β2). - Its cardiovascular effects are more complex and dose-dependent compared to isoprenaline's specific chronotropic action.

Q: At which receptor is the primary action of antipsychotic medications required?

D2 dopaminergic. ***D2 dopaminergic*** - The **antipsychotic effects** of typical (first-generation) antipsychotics are primarily mediated through **D2 receptor blockade** [1]. - Blocking D2 receptors in the **mesolimbic pathway** helps reduce positive symptoms of psychosis like hallucinations and delusions [2]. *M, muscarinic* - **Muscarinic receptor blockade** is a common adverse effect of some antipsychotics, leading to anticholinergic side effects such as **dry mouth** and **blurred vision**, rather than their primary therapeutic action. - This action does not directly contribute to the antipsychotic effect. *D1 dopaminergic* - While D1 receptors are involved in dopamine signaling, they are **not the primary target** for the antipsychotic action of most drugs [1]. - Some atypical antipsychotics may affect D1 receptors, but it's secondary to their D2 antagonism and serotonin modulation. *5HT4 serotonergic* - **Serotonin receptors (5HT)**, particularly 5HT2A, are important targets for atypical (second-generation) antipsychotics. - However, 5HT4 receptors are **not a primary target** for the antipsychotic effects, and 5HT2A blockade modulates dopamine release, which is still connected to the D2 hypothesis.

Q: What effect does morphine have on muscle tone?

Increased muscle tone. ***Increased muscle tone*** - Morphine **increases skeletal muscle tone** and can cause muscle rigidity, particularly with rapid IV administration (truncal rigidity). - It significantly increases **smooth muscle tone** in various organs including the sphincter of Oddi (causing biliary colic), bladder sphincter (causing urinary retention), and GI tract (causing constipation). - This increased tone in sphincters and smooth muscle is a well-documented effect mediated through **opioid receptor activation**. *Bradycardia (not increased heart rate)* - Morphine typically causes **bradycardia** (decreased heart rate) due to vagal stimulation and central effects, not tachycardia. - Increased heart rate would be atypical and not a primary pharmacological effect of morphine. *Miosis (not mydriasis)* - Morphine characteristically causes **miosis** (pinpoint pupils) due to stimulation of the Edinger-Westphal nucleus of the oculomotor nerve. - Mydriasis (dilated pupils) is seen with anticholinergics or sympathomimetics, not opioids. *Respiratory depression (not stimulation)* - Morphine causes **respiratory depression**, not stimulation, by reducing the responsiveness of brainstem respiratory centers to CO2. - This is one of the most dangerous adverse effects and the primary cause of death in opioid overdose.

Q: Which hormone is primarily responsible for maintaining the luteal phase of the menstrual cycle?

Progesterone. ***Progesterone*** - **Progesterone**, secreted by the **corpus luteum** after ovulation, is crucial for maintaining the luteal phase by preparing the **endometrium** for implantation. - It causes the endometrial lining to thicken and become more vascularized, creating a suitable environment for a fertilized egg. *Estrogen* - While **estrogen** is important throughout the menstrual cycle for endometrial proliferation, its primary role is in the **follicular phase**, not the maintenance of the luteal phase. - Estrogen levels are higher during the follicular phase, promoting the growth of the dominant follicle. *Follicle-stimulating hormone (FSH)* - **FSH** is primarily responsible for stimulating the growth and development of **ovarian follicles** during the follicular phase. - Its levels decrease significantly after ovulation, and it does not play a direct role in maintaining the luteal phase. *Luteinizing hormone (LH)* - **LH** triggers **ovulation** and the formation of the **corpus luteum** from the ruptured follicle. - While essential for initiating the luteal phase, its levels decline afterward, and it's not the primary hormone for *maintaining* the corpus luteum's function.

Q: All of the following are true about Down syndrome except for one.

Incidence of Robertsonian translocation is 1:1000. **Incidence of Robertsonian translocation is 1:1000** - This statement is **not accurate** for Down syndrome. Robertsonian translocation accounts for only about **3-4% of Down syndrome cases**, not a general population incidence of 1:1000. - The vast majority of Down syndrome cases (~95%) are due to trisomy 21 from nondisjunction, not translocation. - This is the **correct answer** as it is the FALSE statement. *Extra chromosome is of maternal origin* - In approximately **90-95% of Down syndrome cases**, the extra copy of chromosome 21 originates from the mother due to **nondisjunction** during meiosis. - This maternal origin is strongly correlated with **advanced maternal age**. *Most common cause is trisomy 21* - **Trisomy 21** (due to meiotic nondisjunction) accounts for about **95% of all Down syndrome cases**, making it the most common genetic mechanism. - This results in three separate copies of chromosome 21 in all body cells. *Mosaicism 21 has no association with maternal age* - **Mosaic Down syndrome** occurs when nondisjunction happens *after fertilization* in early embryonic development, leading to a mixture of cells with normal and trisomic cells. - Because it is a **post-zygotic event**, its incidence is independent of **maternal age**, unlike full trisomy 21. *Incidence increases with advanced maternal age* - **TRUE statement** - The risk of Down syndrome (particularly trisomy 21) increases significantly with **maternal age**. - Risk is approximately 1:1500 at age 20, 1:1000 at age 30, 1:400 at age 35, and 1:100 at age 40. - This is due to increased risk of meiotic nondisjunction in older oocytes.

Question 1

Which of the following is a positive acute phase protein that enhances the acute phase response?

Accepted Answer

Fibrinogen

Answer

Transferrin

Answer

Albumin

Answer

Prealbumin

Question 2

Chicken fat clot is seen in -

Accepted Answer

Postmortem clot

Answer

Antemortem thrombus

Answer

Currant jelly clot

Answer

Antemortem wound

Question 3

What is the primary effect of beta blockers in the management of thyroid storm?

Accepted Answer

Provides rapid relief of symptoms

Answer

Increases metabolism of thyroxine

Answer

Blocks thyroxine receptors

Answer

Decreases synthesis of thyroxine

Question 4

What is the mode of inheritance for the most common form of hypophosphatemic rickets?

Accepted Answer

X-Linked Dominant (XD)

Answer

Autosomal Recessive (AR)

Answer

Autosomal Dominant (AD)

Answer

X-Linked Recessive (XR)

Question 5

Where is the benzodiazepine binding site located on GABA receptors?

Accepted Answer

γ-subunit

Answer

β-subunit

Answer

δ-subunit

Answer

α-subunit

Question 6

Which sympathomimetic drug is primarily known to increase heart rate?

Accepted Answer

Isoprenaline

Answer

Phenylephrine

Answer

Noradrenaline

Answer

Adrenaline

Question 7

At which receptor is the primary action of antipsychotic medications required?

Accepted Answer

D2 dopaminergic

Answer

M, muscarinic

Answer

5HT4 serotonergic

Answer

D1 dopaminergic

Question 8

What effect does morphine have on muscle tone?

Accepted Answer

Increased muscle tone

Answer

Respiratory stimulation

Answer

Decreased muscle tone

Answer

Mydriasis

Question 9

Which hormone is primarily responsible for maintaining the luteal phase of the menstrual cycle?

Accepted Answer

Progesterone

Answer

Estrogen

Answer

Follicle-stimulating hormone (FSH)

Answer

Luteinizing hormone (LH)

Question 10

All of the following are true about Down syndrome except for one.

Accepted Answer

Incidence of Robertsonian translocation is 1:1000

Answer

Most common cause is trisomy 21

Answer

Mosaicism 21 has no association with maternal age

Answer

Extra chromosome is of maternal origin

Answer

Incidence increases with advanced maternal age

NEET-PG 2015

Biochemistry

Forensic Medicine

Internal Medicine

Pharmacology

Psychiatry