NEET-PG 2015 Practice Questions

Q: Amide group is present in which part of protein?

Peptide bond. ***Peptide bond*** - A **peptide bond** is formed between the **carboxyl group** of one amino acid and the **amino group** of another, releasing a water molecule. This bond has an **amide structure**. - The repeated formation of these amide (peptide) bonds links amino acids into long chains, forming a **polypeptide** or protein. *Amino-terminal* - The **amino-terminal (N-terminal)** end of a protein contains a free **amino group (-NH2)**, which is not part of an amide linkage within the polypeptide backbone. - It marks the beginning of the polypeptide chain and is typically involved in various cellular interactions and modifications. *Disulfide bond* - A **disulfide bond** is a covalent bond formed between two **sulfhydryl groups (-SH)** of **cysteine residues**, leading to the formation of a **cystine** residue. - This bond is crucial for stabilizing the **tertiary and quaternary structures** of proteins, but it does not contain an amide group. *Carboxy-terminal* - The **carboxy-terminal (C-terminal)** end of a protein contains a free **carboxyl group (-COOH)**, which is not part of an amide linkage within the polypeptide backbone. - It marks the end of the polypeptide chain and plays roles in protein processing, targeting, and regulation.

Q: What is the role of colipase in fat digestion?

Assists pancreatic lipase in fat digestion. ***Assists pancreatic lipase in fat digestion*** - Colipase **binds to pancreatic lipase** and the **lipid-water interface** of the fat droplet, providing a conformational change that enables lipase to access and hydrolyze triglycerides. - It also prevents bile salts from inactivating pancreatic lipase, ensuring efficient **fat emulsification and digestion**. *Is secreted in an inactive form* - Colipase is secreted as **procolipase** by the pancreas, which is then activated by **trypsin** in the duodenum. - While correct, this option describes its activation rather than its primary role in fat digestion. *Encoded by the gene CLPS* - The gene **CLPS** indeed encodes for colipase, but this is a genetic detail rather than its functional role in the digestive process. - Knowledge of the encoding gene is not directly relevant to understanding its biochemical function in fat digestion. *Is secreted by pancreatic cells* - Colipase is indeed synthesized and secreted by the **pancreas** into the small intestine. - This statement is true but describes the **origin** of colipase, not its specific functional role in fat digestion.

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

Positive Correlation with BMI. ***Positive Correlation with BMI (INCORRECT STATEMENT)*** - Adiponectin levels are **inversely correlated with BMI**, NOT positively correlated; as BMI increases, adiponectin levels generally decrease. - This inverse relationship is significant because lower adiponectin levels are associated with increased insulin resistance and **metabolic syndrome**. - This statement is **false**, making it the correct answer to this question. *Secreted by adipose tissue (Correct statement)* - Adiponectin is a **hormone primarily secreted by adipocytes** (fat cells). - It plays a crucial role in regulating glucose and lipid metabolism, and its secretion is altered in conditions like obesity. - This statement is **true**. *Lowers glucose (Correct statement)* - Adiponectin **enhances insulin sensitivity** in peripheral tissues like skeletal muscle and liver, leading to increased glucose uptake and utilization. - This action helps to **lower blood glucose levels** and improve glycemic control. - This statement is **true**. *Increases FFA oxidation (Correct statement)* - Adiponectin **promotes fatty acid oxidation** in muscle and liver, reducing intracellular lipid accumulation. - By increasing fatty acid burning, it helps to **decrease circulating free fatty acid (FFA) levels**, which can contribute to insulin resistance if elevated. - This statement is **true**.

Q: Vitamin D absorption is decreased by ?

Fat malabsorption. ***Fat malabsorption*** - **Vitamin D** is a **fat-soluble vitamin**, meaning it requires dietary fat for proper absorption in the small intestine. - Conditions causing **fat malabsorption**, such as **cystic fibrosis**, **celiac disease**, or **pancreatic insufficiency**, significantly reduce the uptake of vitamin D. *Proteins* - **Proteins** do not directly decrease vitamin D absorption; in fact, some dietary proteins can enhance vitamin D binding and transport in the bloodstream. - Their primary role is in structural and enzymatic functions, not impeding fat-soluble vitamin uptake. *Acid* - **Gastric acid** is important for the absorption of some nutrients, but it generally does not directly hinder the absorption of **fat-soluble vitamins** like vitamin D. - Conditions like **achlorhydria** primarily affect the absorption of minerals and vitamin B12, rather than vitamin D. *Lactose* - **Lactose** is a sugar found in milk, and its malabsorption (lactose intolerance) primarily causes gastrointestinal symptoms like bloating and diarrhea. - It does not directly interfere with the absorption of **fat-soluble vitamins**; rather, it affects carbohydrate digestion.

Q: Small intestinal peristalsis is controlled by :

Myenteric plexus. ***Myenteric plexus*** - The **myenteric (Auerbach's) plexus** is located between the longitudinal and circular muscle layers of the muscularis propria and is primarily responsible for **controlling gastrointestinal motility**, including peristalsis. - Its neurons coordinate the contractions and relaxations of these muscle layers to propel contents through the alimentary canal. *Meissners plexus* - The **Meissner's (submucosal) plexus** is located in the submucosa and mainly controls **glandular secretion**, local blood flow, and absorption, rather than muscle motility. - While it subtly influences motility through local reflexes, it is not the primary controller of peristalsis. *Vagus nerve* - The **vagus nerve (cranial nerve X)** provides parasympathetic innervation to the small intestine, modulating activity but not directly initiating or solely controlling peristalsis. - It influences the activity of the enteric nervous system (including the myenteric plexus) but does not itself generate the complex, coordinated patterns of muscle contraction. *Parasympathetic system* - The **parasympathetic nervous system**, through nerves like the vagus, generally **stimulates gastrointestinal motility**, but it acts by modulating the intrinsic enteric nervous system. - The local control and generation of specific peristaltic movements are primarily mediated by the enteric nervous system, especially the myenteric plexus.

Q: Cholecystokinin is produced from:

Duodenal mucosa. ***Duodenal mucosa*** - **Cholecystokinin (CCK)** is primarily secreted by **I cells**, which are specialized enteroendocrine cells located in the **mucosa of the duodenum** and jejunum. - The release of CCK is stimulated by the presence of **fatty acids** and **amino acids** in the small intestine. *Hepatocyte* - **Hepatocytes** are the main functional cells of the liver, responsible for bile production, metabolism, and detoxification. - They **do not produce regulatory hormones** like cholecystokinin. *Gastric mucosa* - The **gastric mucosa** primarily produces **gastrin**, hydrochloric acid, and pepsinogen, which are involved in gastric digestion. - It does **not secrete cholecystokinin**, which is involved in stimulating gallbladder contraction and pancreatic enzyme release. *Epithelial cells of distal common bile duct* - The **epithelial cells of the common bile duct** are involved in bile transport and modification, but **not in hormone production**. - Their primary role is to line the duct and contribute to the composition of bile.

Q: Somatomedin-C deficiency causes?

Growth retardation. ***Growth retardation*** - **Somatomedin-C** (also known as **Insulin-like Growth Factor 1 or IGF-1**) is a crucial mediator of **growth hormone's** effects on growth. - A deficiency in Somatomedin-C, therefore, directly leads to **impaired growth** and **stature**, manifesting as **growth retardation**. *Genetic dwarfism* - This term generally refers to dwarfism caused by various **genetic conditions** (e.g., achondroplasia), which may or may not involve the **growth hormone/IGF-1 axis**. - While Somatomedin-C deficiency can be genetic, "genetic dwarfism" is a broader term and not the most precise answer for the direct consequence. *Congenital hypothyroidism* - This condition results from **deficient thyroid hormone production** from birth. - It leads to neurological impairment and **growth failure**, but it is due to **thyroid hormone deficiency**, not Somatomedin-C deficiency. *Type 1 diabetes mellitus* - This is an **autoimmune disease** characterized by the **destruction of pancreatic beta cells**, leading to **insulin deficiency**. - It is entirely unrelated to **Somatomedin-C** or the growth hormone axis.

Q: Inotropic effect of thyroid hormone is by ?

Enhancement of Catecholamines. ***Enhancement of Catecholamines*** - Thyroid hormones **potentiate the effects of catecholamines** (like adrenaline and noradrenaline) on the heart, leading to increased heart rate and contractility, which is an **inotropic effect**. - This occurs by increasing the number and sensitivity of **beta-adrenergic receptors** on cardiac muscle cells. *Membrane receptors* - While thyroid hormones do have some rapid, non-genomic effects that may involve **membrane receptors**, their primary and well-established inotropic effect is mediated indirectly through catecholamine sensitivity. - The classic action of thyroid hormones is via intracellular receptors that modulate gene expression, not direct membrane receptor signaling for inotropic effects. *cAMP* - **cAMP** is a common second messenger for many hormones, particularly those acting via G protein-coupled receptors. - While catecholamines themselves act through cAMP to exert their cardiac effects, thyroid hormones *enhance the action* of catecholamines rather than directly using cAMP as their primary inotropic mechanism. *cGMP* - **cGMP** is a second messenger often associated with nitric oxide signaling and vasodilation, contributing to cGMP-dependent protein kinases. - It is not the primary mediator for the *positive inotropic effect* of thyroid hormones on the heart.

Q: What is the normal range of urinary pH?

6.0 - 6.5. ***6.0 - 6.5*** - This represents the **average normal urinary pH range** in healthy individuals. - While the kidney can produce urine with pH ranging from 4.5 to 8.0 (the full physiological range), the **typical urinary pH** in most healthy people is around 6.0, making this the most representative normal range. - This slightly acidic pH reflects normal renal handling of dietary acids and metabolic processes. *4.5 - 5.0* - This represents the **lower acidic end** of the physiological range. - While kidneys can produce urine this acidic in response to acid loads, this is **not the average normal range**. - Persistently low pH may indicate **metabolic acidosis**, high protein diet, or conditions like diabetic ketoacidosis. *5.0 - 5.5* - This range is **more acidic than average** but still within physiological limits. - This may be seen with high protein intake or mild acid loading, but it's not the most representative of typical normal urinary pH. *7.0 - 7.5* - This represents a **more alkaline urine**, which is at the upper end of the physiological range. - While healthy kidneys can produce alkaline urine (especially with alkaline diets), persistently elevated pH may indicate **urinary tract infections** with urea-splitting bacteria (Proteus species), renal tubular acidosis, or alkaline diet.

Q: Aortic valve closure occurs in which part of cardiac cycle?

Beginning of isovolumetric relaxation. ***Beginning of isovolumetric relaxation*** - Aortic valve closure marks the end of **ventricular systole** and the start of **isovolumetric relaxation**, as blood ceases to be ejected and the ventricle begins to relax while remaining closed. - This event corresponds to the **second heart sound (S2)** and signifies the beginning of a period where ventricular volume remains constant, but pressure drops. *Beginning of isovolumetric contraction* - This phase begins with the closure of the **mitral and tricuspid valves** (first heart sound, S1), as ventricular pressure rises but volume remains constant before ejection. - The aortic valve is still closed at this point, as ventricular pressure is not yet high enough to open it. *Beginning of ventricular ejection* - This phase begins when the **aortic valve opens** as ventricular pressure exceeds aortic pressure, allowing blood to be ejected from the left ventricle. - Aortic valve closure occurs *after* ejection, not at its beginning. *During rapid ventricular filling* - Rapid ventricular filling occurs when the **mitral valve opens** (following isovolumetric relaxation), allowing blood to flow from the atria into the ventricles. - During this phase, the aortic valve is closed, but its closure happened earlier, at the beginning of isovolumetric relaxation.

Question 1

Amide group is present in which part of protein?

Accepted Answer

Peptide bond

Answer

Amino-terminal

Answer

Disulfide bond

Answer

Carboxy-terminal

Question 2

What is the role of colipase in fat digestion?

Accepted Answer

Assists pancreatic lipase in fat digestion

Answer

Encoded by the gene CLPS

Answer

Is secreted in an inactive form

Answer

Is secreted by pancreatic cells

Question 3

Which of the following statements about adiponectin is incorrect?

Accepted Answer

Positive Correlation with BMI

Answer

Secreted by adipose tissue

Answer

Increases FFA oxidation

Answer

Lowers glucose

Question 4

Vitamin D absorption is decreased by ?

Accepted Answer

Fat malabsorption

Answer

Proteins

Answer

Acid

Answer

Lactose

Question 5

Small intestinal peristalsis is controlled by :

Accepted Answer

Myenteric plexus

Answer

Meissner's plexus

Answer

Vagus nerve

Answer

Parasympathetic system

Question 6

Cholecystokinin is produced from:

Accepted Answer

Duodenal mucosa

Answer

Hepatocyte

Answer

Gastric mucosa

Answer

Epithelial cells of distal common bile duct

Question 7

Somatomedin-C deficiency causes?

Accepted Answer

Growth retardation

Answer

Genetic dwarfism

Answer

Congenital hypothyroidism

Answer

Type 1 diabetes mellitus

Question 8

Inotropic effect of thyroid hormone is by ?

Accepted Answer

Enhancement of Catecholamines

Answer

Membrane receptors

Answer

cAMP

Answer

cGMP

Question 9

What is the normal range of urinary pH?

Accepted Answer

6.0 - 6.5

Answer

4.5 - 5.0

Answer

5.0 - 5.5

Answer

7.0 - 7.5

Question 10

Aortic valve closure occurs in which part of cardiac cycle?

Accepted Answer

Beginning of isovolumetric relaxation

Answer

Beginning of isovolumetric contraction

Answer

During rapid ventricular filling

Answer

Beginning of ventricular ejection

NEET-PG 2015

Biochemistry

Physiology