NEET-PG 2013 Practice Questions

Q: Which muscle receives a muscular branch from the ulnar nerve?

Both FCU and FDP. ***Both FCU and FDP*** - The **flexor carpi ulnaris (FCU)** is solely innervated by the **ulnar nerve** in the forearm. - The **flexor digitorum profundus (FDP)** has dual innervation: the **ulnar nerve** supplies the medial half (tendons to ring and little fingers), while the anterior interosseous nerve (branch of median nerve) supplies the lateral half (tendons to index and middle fingers). - Both muscles receive muscular branches from the ulnar nerve, making this the most complete and accurate answer. *FCU* - While the FCU does receive innervation from the ulnar nerve (and only the ulnar nerve), this option is incorrect because the FDP also receives branches from the ulnar nerve. - Selecting only FCU ignores the dual innervation of FDP and is therefore an incomplete answer when "Both FCU and FDP" is available. *FDP* - While the medial half of FDP does receive innervation from the ulnar nerve, this option is incorrect because FCU also receives innervation from the ulnar nerve. - Selecting only FDP ignores the complete innervation of FCU and is therefore an incomplete answer when "Both FCU and FDP" is available. *None of the options* - This option is incorrect because both the **flexor carpi ulnaris** and the medial portion of the **flexor digitorum profundus** definitively receive muscular branches from the ulnar nerve. - The ulnar nerve provides motor innervation to these specific forearm muscles before continuing into the hand.

Q: Glucagon stimulates

Gluconeogenesis. ***Gluconeogenesis*** - **Glucagon** is a hormone that primarily acts to raise **blood glucose levels** by stimulating the production of glucose from non-carbohydrate sources. - This process, **gluconeogenesis**, occurs mainly in the liver and is initiated by glucagon to counteract hypoglycemia. *Glycogenesis* - **Glycogenesis** is the process of synthesizing **glycogen** from glucose and is primarily stimulated by insulin when blood glucose levels are high. - Glucagon's role is to *inhibit* glycogen synthesis and instead promote glycogen breakdown. *Fatty acid synthesis* - **Fatty acid synthesis** is an anabolic process that primarily occurs when there is an excess of energy and glucose, often stimulated by **insulin**. - Glucagon generally has an **inhibitory effect** on fatty acid synthesis, as its main goal is to mobilize energy stores, not create them. *Glycolysis* - **Glycolysis** is the breakdown of glucose to produce energy, and it is stimulated when glucose is abundant and energy is needed. - Glucagon primarily acts to *inhibit* glycolysis in the liver, thereby conserving glucose for use by other tissues and promoting its release into the bloodstream.

Q: Chronic atrophy of adrenal gland will result in which hormone deficiency ?

Cortisol. ***Cortisol*** - **Chronic atrophy of the adrenal gland**, often seen in conditions like **Addison's disease** [1], primarily leads to a deficiency of **glucocorticoids**, the main one being cortisol [2]. - **Cortisol** is produced in the **zona fasciculata** of the adrenal cortex, which is highly susceptible to damage in atrophic conditions [2]. *Aldosterone* - While aldosterone is produced in the adrenal cortex (**zona glomerulosa**), its deficiency is more characteristic of primary adrenal insufficiency affecting the entire cortex, not necessarily solely from 'chronic atrophy' which can have varied pathophysiology [2]. - In some autoimmune forms of adrenal atrophy (Addison's disease), **aldosterone deficiency** can occur, but **cortisol deficiency** is a more universal and defining feature [1][3]. *Dehydroepiandrosterone (DHEA)* - **DHEA** is an adrenal androgen produced in the **zona reticularis** of the adrenal cortex [2]. Its deficiency is also common in adrenal atrophy. - However, **cortisol deficiency** generally has more immediate and life-threatening clinical consequences compared to DHEA deficiency. *Epinephrine* - Epinephrine is produced by the **adrenal medulla**, which is distinct from the adrenal cortex where atrophy typically occurs in conditions causing hormone deficiencies. - Therefore, **adrenal gland atrophy** primarily affecting the cortex would not lead to **epinephrine deficiency** as the medulla usually remains functional.

Q: Ovulation occurs how long after the LH surge peak?

12-24 hours. ***12-24 hours*** - Ovulation, the release of a mature egg from the **ovary**, typically occurs within **12 to 24 hours after the peak of the luteinizing hormone (LH) surge**. - The LH surge itself usually lasts 24 to 48 hours and is a critical signal for the final maturation and release of the oocyte. *24-48 hours* - While the **LH surge** can last up to 48 hours, **ovulation** (the actual release of the egg) generally happens more rapidly, usually within 12-24 hours of the *peak* of this surge. - This timeframe is a common misconception, as it refers more to the duration of the surge rather than the precise timing of ovulation post-peak. *48-72 hours* - Ovulation rarely occurs this late after the peak of the **LH surge**; if it does, it suggests a potential delay or irregularity in the **ovulatory process**. - The window for successful fertilization is relatively narrow and aligns with the more immediate post-surge timing. *72-96 hours* - This time frame is significantly beyond the typical window for **ovulation** following the **LH surge**. - By this point, the egg would have either been released or the ovulatory event would have passed without the egg releasing.

Q: In which condition are Pseudo-Pelger-Huët cells typically seen?

Myelodysplastic syndrome. ***Mylodysplastic syndrome*** - Pseudo-Pelger-Huet cells are characteristic and often observed in myelodysplastic syndromes, indicating an ineffective hematopoiesis [1]. - These cells appear as **hyposegmented neutrophils** and are associated with dysplastic changes in the bone marrow [1]. *Hairy cell leukemia* - Typically presents with **hairy cells** in peripheral blood and often involves splenomegaly; pseudo-Pelger-Huet cells are not usual in this condition. - Associated with **PANCYTOPENIA** and reticulin fibrosis, differing from myelodysplastic syndrome. *Hodgkin's lymphoma* - Characterized by the presence of **Reed-Sternberg cells** and typically involves lymphadenopathy. - Peripheral blood findings generally do not include pseudo-Pelger-Huet cells; the focus is on lymphatic tissue. *Multiple myeloma* - Commonly presents with **plasma cells** and related symptoms like bone pain and renal failure, not associated with pseudo-Pelger-Huet cells. - It primarily causes an increase in monoclonal proteins rather than dysplastic changes seen in myelodysplastic syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.

Q: Peliosis hepatis is caused by all except?

Analgesics. ***Analgesics*** - While various drugs can cause liver injury, **analgesics** are not typically associated with the development of **peliosis hepatis**. [1] - **Peliosis hepatis** involves blood-filled cysts in the liver and is linked to specific agents, not common pain relievers. *Anabolic steroids* - **Anabolic steroids** are a well-known cause of **peliosis hepatis**, especially with prolonged high-dose use. - They can induce sinusoidal dilation and hemorrhage, leading to **blood-filled cysts** in the liver. *OC pills* - **Oral contraceptive pills** (OCPs) containing estrogen have been implicated in the development of **peliosis hepatis**, though it is rare. - The estrogen component is thought to affect the **vascular endothelium** and sinusoidal integrity of the liver. *Danazol* - **Danazol**, an attenuated androgen, is strongly associated with **peliosis hepatis** and other liver complications. - It can cause severe damage to the **hepatic sinusoids**, leading to the characteristic blood-filled cavities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 847-848.

Q: In which condition are Michaelis Gutmann bodies typically seen?

Malakoplakia. ***Malakoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic histological features of malakoplakia, representing calcified concretions containing **iron and calcium** within macrophages. - These are formed around **partially digested bacteria** within defective macrophages, appearing as basophilic inclusions with a "target-like" or "owl's eye" appearance. - Malakoplakia is a chronic granulomatous inflammatory condition most commonly affecting the **urinary tract** (bladder, kidney), but can occur in other organs. *Xanthogranulomatous* - This condition is characterized by an infiltrate of **lipid-laden macrophages** (xanthoma cells, foam cells) and occasional giant cells, but **not** Michaelis-Gutmann bodies. - It most commonly affects the kidney (**xanthogranulomatous pyelonephritis**) and is a destructive inflammatory process with a mass-like appearance. *Pyelonephritis* - Refers to **inflammation of the kidney and renal pelvis**, usually due to bacterial infection (commonly E. coli). - Histologically, it is characterized by acute or chronic inflammatory cells, neutrophil infiltration, and potential abscess formation, **without** Michaelis-Gutmann bodies. *Nail patella syndrome* - This is a **genetic disorder** (autosomal dominant) affecting primarily the **nails, bones** (absent/hypoplastic patella, elbow dysplasia), and sometimes the kidneys (glomerular disease). - It is associated with developmental abnormalities and has **no association** with Michaelis-Gutmann bodies or malakoplakia.

Q: Which of the following hormones is not stored in cells?

Cortisol. ***Cortisol*** - Cortisol is a **steroid hormone** that is synthesized from **cholesterol** on demand and is **not stored** in secretory vesicles or elsewhere within cells. - Being **lipophilic**, it diffuses freely across cell membranes immediately after synthesis. - Its release is regulated by the **hypothalamic-pituitary-adrenal (HPA) axis**, with synthesis and immediate secretion occurring upon stimulation. *Insulin* - Insulin is a **peptide hormone** synthesized as **proinsulin** and then cleaved into active insulin. - It is **stored in secretory granules** within pancreatic beta cells, allowing for rapid release in response to elevated blood glucose. *Thyroxine* - Thyroxine (T4) is a **thyroid hormone** that is synthesized from tyrosine and iodine. - It is **stored extracellularly** within the thyroid gland's follicles as part of a large protein called **thyroglobulin**. - Unlike cortisol (which is never stored), thyroxine has a **substantial storage pool** that can last weeks, though the storage is extracellular rather than intracellular. *Renin* - Renin is an **enzyme** produced by the **juxtaglomerular cells** of the kidney. - It is **stored in secretory granules** within these cells and released in response to decreased renal perfusion pressure or sympathetic stimulation.

Q: LH surge is associated with?

Increased estrogen & decreased progesterone. ***Increased estrogen & decreased progesterone*** - The **LH surge** is triggered by a significant rise in **estrogen** levels from the dominant follicle, indicating ovarian readiness. - At the time of the LH surge, **progesterone** levels remain low; they only begin to rise significantly after ovulation, when the corpus luteum forms. *Increased estrogen & increased progesterone* - While **estrogen** levels are high, **progesterone** only significantly increases *after* ovulation, as the corpus luteum develops. - High estrogen *and* high progesterone together are typically seen in the **luteal phase**, not at the peak of the LH surge. *Decreased estrogen & increased progesterone* - A decrease in **estrogen** would suppress LH, not trigger a surge. - Increased **progesterone** would also inhibit LH release via negative feedback in the follicular phase if it were to occur pre-ovulation. *Decreased estrogen & decreased progesterone* - Both **decreased estrogen** and **decreased progesterone** would lead to low FSH/LH levels and would not promote an LH surge or ovulation. - This hormonal profile is more characteristic of the very early follicular phase or menopause.

Question 1

Which muscle receives a muscular branch from the ulnar nerve?

Accepted Answer

Both FCU and FDP

Answer

FCU

Answer

None of the options

Answer

FDP

Question 2

Glucagon stimulates

Accepted Answer

Gluconeogenesis

Answer

Glycogenesis

Answer

Fatty acid synthesis

Answer

Glycolysis

Question 3

Chronic atrophy of adrenal gland will result in which hormone deficiency ?

Accepted Answer

Cortisol

Answer

Aldosterone

Answer

Dehydroepiandrosterone (DHEA)

Answer

Epinephrine

Question 4

Ovulation occurs how long after the LH surge peak?

Accepted Answer

12-24 hours

Answer

48-72 hours

Answer

72-96 hours

Answer

24-48 hours

Question 5

In which condition are Pseudo-Pelger-Huët cells typically seen?

Accepted Answer

Myelodysplastic syndrome

Answer

Hairy cell leukemia

Answer

Multiple myeloma

Answer

Hodgkin's lymphoma

Question 6

Peliosis hepatis is caused by all except?

Accepted Answer

Analgesics

Answer

OC pills

Answer

Danazol

Answer

Anabolic steroids

Question 7

In which condition are Michaelis Gutmann bodies typically seen?

Accepted Answer

Malakoplakia

Answer

Xanthogranulomatous

Answer

Pyelonephritis

Answer

Nail patella syndrome

Question 8

Which of the following hormones is not stored in cells?

Accepted Answer

Cortisol

Answer

Thyroxin

Answer

Renin

Answer

Insulin

Question 9

LH surge is associated with?

Accepted Answer

Increased estrogen & decreased progesterone

Answer

Increased estrogen & increased progesterone

Answer

Decreased estrogen & increased progesterone

Answer

Decreased estrogen & decreased progesterone

Question 10

Which of the following statements about thyroid hormone receptors is correct?

Accepted Answer

They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.

Answer

They directly bind to thyrotropin-releasing hormone (TRH)

Answer

They directly bind to thyroid-stimulating hormone (TSH)

Answer

They cause nuclear transcription after binding with T4

NEET-PG 2013

Anatomy

Biochemistry

Internal Medicine

Obstetrics and Gynecology

Pathology

Physiology