Anatomy
1 questionsWhich muscle receives a muscular branch from the ulnar nerve?
NEET-PG 2013 - Anatomy NEET-PG Practice Questions and MCQs
Question 371: Which muscle receives a muscular branch from the ulnar nerve?
- A. Both FCU and FDP (Correct Answer)
- B. FCU
- C. None of the options
- D. FDP
Explanation: ***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.
Biochemistry
1 questionsGlucagon stimulates
NEET-PG 2013 - Biochemistry NEET-PG Practice Questions and MCQs
Question 371: Glucagon stimulates
- A. Gluconeogenesis (Correct Answer)
- B. Glycogenesis
- C. Fatty acid synthesis
- D. Glycolysis
Explanation: ***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.
Internal Medicine
1 questionsChronic atrophy of adrenal gland will result in which hormone deficiency ?
NEET-PG 2013 - Internal Medicine NEET-PG Practice Questions and MCQs
Question 371: Chronic atrophy of adrenal gland will result in which hormone deficiency ?
- A. Aldosterone
- B. Dehydroepiandrosterone (DHEA)
- C. Epinephrine
- D. Cortisol (Correct Answer)
Explanation: ***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.
Obstetrics and Gynecology
1 questionsOvulation occurs how long after the LH surge peak?
NEET-PG 2013 - Obstetrics and Gynecology NEET-PG Practice Questions and MCQs
Question 371: Ovulation occurs how long after the LH surge peak?
- A. 48-72 hours
- B. 72-96 hours
- C. 24-48 hours
- D. 12-24 hours (Correct Answer)
Explanation: ***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.
Pathology
3 questionsIn which condition are Pseudo-Pelger-Huët cells typically seen?
Peliosis hepatis is caused by all except?
In which condition are Michaelis Gutmann bodies typically seen?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 371: In which condition are Pseudo-Pelger-Huët cells typically seen?
- A. Hairy cell leukemia
- B. Multiple myeloma
- C. Hodgkin's lymphoma
- D. Myelodysplastic syndrome (Correct Answer)
Explanation: ***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.
Question 372: Peliosis hepatis is caused by all except?
- A. OC pills
- B. Danazol
- C. Anabolic steroids
- D. Analgesics (Correct Answer)
Explanation: ***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.
Question 373: In which condition are Michaelis Gutmann bodies typically seen?
- A. Xanthogranulomatous
- B. Pyelonephritis
- C. Malakoplakia (Correct Answer)
- D. Nail patella syndrome
Explanation: ***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.
Physiology
3 questionsWhich of the following hormones is not stored in cells?
LH surge is associated with?
Which of the following statements about thyroid hormone receptors is correct?
NEET-PG 2013 - Physiology NEET-PG Practice Questions and MCQs
Question 371: Which of the following hormones is not stored in cells?
- A. Thyroxin
- B. Renin
- C. Insulin
- D. Cortisol (Correct Answer)
Explanation: ***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.
Question 372: LH surge is associated with?
- A. Increased estrogen & decreased progesterone (Correct Answer)
- B. Increased estrogen & increased progesterone
- C. Decreased estrogen & increased progesterone
- D. Decreased estrogen & decreased progesterone
Explanation: ***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 373: Which of the following statements about thyroid hormone receptors is correct?
- A. They directly bind to thyrotropin-releasing hormone (TRH)
- B. They directly bind to thyroid-stimulating hormone (TSH)
- C. They cause nuclear transcription after binding with T4
- D. They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3. (Correct Answer)
Explanation: ***They are intracellular receptors that mediate gene transcription after binding with T3 or T4, but their primary action is through T3.*** - **Thyroid hormone receptors** are indeed **intracellular** and act as **ligand-activated transcription factors**, regulating gene expression. - While both **T3** and **T4** can bind, **T3 (triiodothyronine)** is the more potent and active form, binding with much higher affinity to the receptors to exert its primary metabolic effects. *They directly bind to thyrotropin-releasing hormone (TRH)* - **TRH (thyrotropin-releasing hormone)** is produced by the hypothalamus and acts on the **pituitary gland** to stimulate TSH release, not directly on thyroid hormone receptors. - Thyroid hormone receptors bind to thyroid hormones (**T3 and T4**), not to the hypothalamic releasing hormones like TRH. *They directly bind to thyroid-stimulating hormone (TSH)* - **TSH (thyroid-stimulating hormone)** is produced by the pituitary gland and primarily acts on receptors located on the **thyroid gland cells** to stimulate thyroid hormone synthesis and release. - Thyroid hormone receptors are distinct from TSH receptors and bind to the hormones themselves (**T3/T4**), not the stimulating hormone TSH. *Causes nuclear transcription after binding with T4* - While **T4 (thyroxine)** can bind to thyroid hormone receptors, it is primarily a **prohormone**. - T4 is largely converted to the more active **T3** within target cells, and **T3** is the main mediator of nuclear transcription through these receptors.