NEET-PG 2020 - Physiology Practice Questions

Q: Identify the sleep stage marked in the EEG during the sleep-wake cycle?

REM sleep. ***REM sleep*** - The marked EEG pattern shows **low-amplitude, mixed-frequency waves** which are characteristic of REM sleep, often resembling an awake state. - This stage is associated with **rapid eye movements**, vivid dreams, and muscle atonias. *Stage 1 sleep* - Characterized by a transition from alpha waves to **theta waves**, which are slightly slower than alpha waves and have a higher amplitude than the waves shown. - This is the **lightest stage of sleep**, with the person easily aroused. *Stage 2 sleep* - Marked by the presence of **sleep spindles** (bursts of high-frequency waves) and **K-complexes** (large, slow waves), which are not visible in the image. - The background activity consists of **theta waves,** which are slower and higher amplitude than the waves present in the image. *Stage 3 sleep* - This is **deep non-REM sleep**, also known as slow-wave sleep, characterized by **delta waves** (high-amplitude, low-frequency waves). - The waves in the image are much faster and lower amplitude than delta waves characteristic of Stage 3 sleep.

Q: Where does meiosis occur in human females?

In the adult ovary. ***In the adult ovary*** - **Meiosis I** in oocytes starts during fetal development but arrests in prophase I. It resumes and completes in the **adult ovary** just before ovulation in response to hormonal signals. - **Meiosis II** begins after the completion of Meiosis I and arrests in metaphase II. It is only completed upon **fertilization** by a sperm, also occurring within the adult reproductive tract. *At birth in the ovary* - At birth, female ovaries contain primary oocytes that have entered **meiosis I** but are arrested in prophase I; actual meiotic divisions promoting maturation do not occur at this stage. - The completion of meiosis I and the initiation of meiosis II are processes that are **post-puberty** and occur in response to hormonal changes leading to ovulation. *In the adult testis* - The testis is the male gonad, and it is the site of **spermatogenesis**, the process of sperm production involving meiosis in males. - **Oogenesis**, the formation of female gametes, occurs exclusively in the **ovaries** of females. *In the prepubertal testis* - In the prepubertal testis, spermatogenesis has not yet begun, and thus **meiosis does not occur** at this stage in males. - Meiosis in males usually begins during **puberty** under the influence of hormones like testosterone.

Q: Cerebral blood flow is regulated by all of the following except:

Calcium ions. ***Calcium ions*** - While **calcium ions (Ca²⁺)** are mechanistically essential for vascular smooth muscle contraction and relaxation, they are **not considered a primary regulatory signal** for cerebral blood flow (CBF) in the same way as the other factors listed. - Ca²⁺ acts as an **intracellular second messenger** that mediates the effects of other regulatory factors (like PCO2, K⁺, and vasoactive substances), rather than being a direct extracellular regulatory signal itself. - The question refers to primary regulatory factors that directly modulate CBF, not the intracellular mechanisms by which vascular smooth muscle responds. *Blood pressure* - **Cerebral autoregulation** maintains relatively constant CBF despite changes in **mean arterial pressure (MAP)** between approximately 60-150 mmHg. - Blood pressure is a **key regulatory factor** - when MAP falls below or exceeds this range, CBF becomes pressure-dependent. - This protective mechanism prevents cerebral ischemia or hyperemia with systemic blood pressure fluctuations. *Arterial PCO2* - **Arterial partial pressure of carbon dioxide (PaCO2)** is one of the **most potent direct regulators** of CBF. - **Hypercapnia** (increased PaCO2) causes cerebral vasodilation and increased CBF (approximately 1-2 mL/100g/min increase per 1 mmHg rise in PaCO2). - **Hypocapnia** (decreased PaCO2) causes vasoconstriction and reduced CBF, utilized therapeutically in managing elevated intracranial pressure. *Potassium ions* - **Increased extracellular K⁺** in the perivascular space causes **direct vasodilation** of cerebral arterioles. - This mechanism is crucial for **neurovascular coupling** (functional hyperemia) - when neurons are active, they release K⁺, which dilates nearby vessels to increase local blood flow. - K⁺-mediated vasodilation helps match cerebral perfusion to metabolic demand during neuronal activity.

Q: A patient with pH of 7, pCO2 of 30 mmHg and Bicarbonate levels of 10 meq. What is the acid base abnormality?

Metabolic Acidosis. ***Metabolic Acidosis*** - The pH is 7, which is severely **acidotic** (normal range 7.35-7.45). This indicates an acid-base disorder where the body is too acidic. - The **bicarbonate level is 10 mEq/L** (normal range 22-26 mEq/L), which is significantly low, directly contributing to the acidosis and pointing towards a metabolic origin. *Respiratory alkalosis* - This condition involves an **elevated pH** (alkalosis) due to a primary decrease in pCO2. - In this case, the pH is acidic, not alkaline. *Metabolic alkalosis* - This condition involves an **elevated pH** (alkalosis) due to a primary increase in bicarbonate levels. - Here, the pH is acidic and bicarbonate is low, directly contradicting metabolic alkalosis. *Respiratory Acidosis* - This condition involves a **decreased pH** (acidosis) due to a primary increase in pCO2. - Although the pH is acidotic, the pCO2 is 30 mmHg (normal range 35-45 mmHg), which is low, indicating a respiratory compensation rather than the primary cause.

Q: In a preterm baby with respiratory distress syndrome, which type of cell is deficient?

Type 2 alveolar cell. ***Type 2 alveolar cell*** - **Type 2 alveolar cells** (pneumocytes) are responsible for producing and secreting **surfactant**. - A deficiency in these cells, common in preterm infants, leads to insufficient surfactant, causing alveolar collapse and respiratory distress syndrome. *Type 1 alveolar cell* - **Type 1 alveolar cells** are primarily involved in **gas exchange** due to their thin, flat structure. - While essential for respiration, their deficiency is not the primary cause of respiratory distress syndrome in preterm infants. *Alveolar capillary endothelial cell* - **Alveolar capillary endothelial cells** form the walls of the capillaries surrounding the alveoli, facilitating the transfer of gases between the alveoli and blood. - They do not produce surfactant, and their deficiency is not the direct cause of respiratory distress syndrome. *Bronchial mucosal epithelial cell* - **Bronchial mucosal epithelial cells** line the airways and are involved in mucus production and ciliary clearance. - While important for respiratory function, their primary role is not in preventing alveolar collapse in respiratory distress syndrome.

Q: The lab reports of a patient given below: pH = 7.2, HCO3 = 10 mEq/L, PCO2 = 30 mmHg. This exemplifies which of the following disorders?

Metabolic acidosis. ***Metabolic acidosis*** - The pH of 7.2 is acidic, and the **bicarbonate (HCO3) of 10 mEq/L** is significantly low (normal: 22-28 mEq/L), indicating a primary metabolic disturbance causing acidosis. - The **PCO2 of 30 mmHg** is also low (normal: 35-45 mmHg), which represents **partial respiratory compensation** through hyperventilation to blow off CO2 and raise pH. - This is a classic example of **metabolic acidosis with respiratory compensation**. *Metabolic alkalosis* - This condition would be characterized by a **high pH** and a **high bicarbonate (HCO3)** level, which is the opposite of the given values. - The body would attempt to compensate by increasing PCO2 through hypoventilation. *Respiratory acidosis* - This would present with a **low pH** and a **high PCO2** (>45 mmHg), indicating a primary respiratory problem leading to CO2 retention and acid accumulation. - Metabolic compensation would show elevated HCO3, not the low HCO3 (10 mEq/L) seen here. *Respiratory alkalosis* - This condition is characterized by a **high pH** (>7.45) and a **low PCO2**, due to excessive ventilation causing CO2 elimination. - While PCO2 is low in the given scenario, the pH is acidic (7.2), not alkalotic, ruling out this diagnosis.

Q: Serum prolactin levels are highest

During third trimester of pregnancy. ***Correct: During third trimester of pregnancy*** - **Serum prolactin levels reach their absolute highest** during the **third trimester of pregnancy**, rising progressively from normal levels (5-25 ng/mL) to peak values of **200-400 ng/mL** near term. - This represents the **highest physiological prolactin levels** observed in humans. - Despite these high levels, **lactation does not occur** during pregnancy because **estrogen and progesterone** block prolactin's action on mammary tissue. - The high prolactin prepares the breast for lactation but milk secretion is inhibited until delivery. *Incorrect: 24 hrs after parturition* - After delivery, prolactin levels actually begin to **decline** from their pregnancy peak, though they remain elevated (around 200 ng/mL). - While **lactogenesis II** (copious milk production) begins 24-72 hours postpartum, this is due to the **removal of estrogen/progesterone inhibition**, not because prolactin levels peak at this time. - The confusion arises from conflating **functional milk production** with **peak hormone levels**. *Incorrect: REM sleep* - Prolactin exhibits **circadian variation** with nocturnal rise during sleep, peaking in early morning hours. - However, these sleep-related peaks (typically 25-40 ng/mL) are **much lower** than pregnancy levels. - This physiological variation is unrelated to reproductive function. *Incorrect: In actively lactating mothers* - During established lactation, basal prolactin levels gradually decline over weeks to months. - Each **suckling episode** causes transient prolactin surges (2-10 fold increase), but these peaks are still **lower than third trimester levels**. - By 6 months postpartum, basal prolactin may return near pre-pregnancy levels despite continued lactation.

Q: Prolactin levels are highest in which of the following?

After nipple stimulation. ***After nipple stimulation*** - Nipple stimulation is a powerful physiological stimulus for **prolactin release** from the anterior pituitary. - This reflex is essential for **lactation** and milk let-down, as suckling signals directly enhance prolactin secretion. *After 24 hrs of ovulation* - Prolactin levels do not peak significantly 24 hours after ovulation; while some fluctuation occurs during the menstrual cycle, the highest levels are not seen at this time. - **Luteinizing hormone (LH)** and **follicle-stimulating hormone (FSH)** are the primary hormones exhibiting surges related to ovulation. *After 24 hours of parturition* - While prolactin levels are elevated throughout the third trimester and immediately postpartum, they tend to **decline somewhat** if breastfeeding is not initiated within the first 24-48 hours. - Post-partum, prolactin levels are primarily sustained by **frequent nipple stimulation** from breastfeeding. *Just before parturition* - Prolactin levels are **chronically elevated** during the third trimester of pregnancy, but the **acute highest surge** or peak is typically in response to specific triggers like nipple stimulation, rather than just the state of being immediately pre-partum. - High prolactin during late pregnancy prepares the breasts for lactation but is not necessarily the **absolute peak** that nipple stimulation can elicit.

Q: In a fetus highest oxygen concentration is found in?

Umbilical vein. ***Umbilical vein*** - The **umbilical vein** carries oxygenated blood from the **placenta**, which serves as the site of gas exchange, making its oxygen concentration the highest in the fetal circulation. - This highly oxygenated blood bypasses the fetal lungs via shunts such as the **ductus venosus** and **foramen ovale** to supply vital organs. *Superior vena cava* - The **superior vena cava** carries deoxygenated blood from the upper body and head back to the heart, mixing with oxygenated blood in the right atrium. - Its blood has a relatively **low oxygen saturation** compared to the umbilical vein. *Left ventricle* - The **left ventricle** receives blood that has already mixed in the atria and passed through the foramen ovale, then the left atrium. - While relatively oxygen-rich for systemic circulation, its oxygen concentration is lower than that in the umbilical vein due to **mixing with deoxygenated blood**. *Ascending aorta* - The **ascending aorta** receives blood from the left ventricle, which has a moderate oxygen content. - The blood in the ascending aorta feeds the upper body, but its oxygen saturation is lower than that in the umbilical vein due to the **physiological shunts** and mixing of blood.

Q: What does aquaporin deficiency cause?

Nephrogenic diabetes insipidus. ***Nephrogenic diabetes insipidus*** - Aquaporins, specifically **aquaporin-2**, are crucial for **water reabsorption** in the renal collecting ducts in response to ADH. - A deficiency or dysfunction of aquaporins leads to the kidneys being unable to concentrate urine, resulting in **excessive dilute urine production** and **polydipsia**, characteristic of nephrogenic diabetes insipidus. *Liddle syndrome* - This is an **autosomal dominant** disorder caused by a **gain-of-function mutation** in the **epithelial sodium channel (ENaC)**, leading to increased sodium reabsorption and hypertension. - It does not involve aquaporin deficiency but rather an overactive sodium channel. *Bartter syndrome* - Characterized by mutations in the **Na-K-2Cl cotransporter (NKCC2)** in the thick ascending limb of the loop of Henle, leading to impaired reabsorption of sodium, potassium, and chloride. - It results in **hypokalemia**, **metabolic alkalosis**, and **hypotension**, and is not directly caused by aquaporin deficiency. *Gitelman syndrome* - Caused by mutations in the **thiazide-sensitive Na–Cl cotransporter (NCC)** in the distal convoluted tubule, impairing sodium and chloride reabsorption. - It presents with symptoms similar to thiazide diuretic use, including **hypokalemia**, **hypomagnesemia**, and **metabolic alkalosis**, and is distinct from aquaporin-related disorders.

Question 1

Identify the sleep stage marked in the EEG during the sleep-wake cycle?

Accepted Answer

REM sleep

Answer

Stage 1 sleep

Answer

Stage 2 sleep

Answer

Stage 3 sleep

Question 2

Where does meiosis occur in human females?

Accepted Answer

In the adult ovary

Answer

At birth in the ovary

Answer

In the adult testis

Answer

In the prepubertal testis

Question 3

Cerebral blood flow is regulated by all of the following except:

Accepted Answer

Calcium ions

Answer

Blood pressure

Answer

Arterial PCO2

Answer

Potassium ions

Question 4

A patient with pH of 7, pCO2 of 30 mmHg and Bicarbonate levels of 10 meq. What is the acid base abnormality?

Accepted Answer

Metabolic Acidosis

Answer

Respiratory alkalosis

Answer

Metabolic alkalosis

Answer

Respiratory Acidosis

Question 5

In a preterm baby with respiratory distress syndrome, which type of cell is deficient?

Accepted Answer

Type 2 alveolar cell

Answer

Type 1 alveolar cell

Answer

Alveolar capillary endothelial cell

Answer

Bronchial mucosal epithelial cell

Question 6

The lab reports of a patient given below: pH = 7.2, HCO3 = 10 mEq/L, PCO2 = 30 mmHg. This exemplifies which of the following disorders?

Accepted Answer

Metabolic acidosis

Answer

Metabolic alkalosis

Answer

Respiratory acidosis

Answer

Respiratory alkalosis

Question 7

Serum prolactin levels are highest

Accepted Answer

During third trimester of pregnancy

Answer

24 hrs after parturition

Answer

REM sleep

Answer

In actively lactating mothers

Question 8

Prolactin levels are highest in which of the following?

Accepted Answer

After nipple stimulation

Answer

After 24 hrs of ovulation

Answer

After 24 hours of parturition

Answer

Just before parturition

Question 9

In a fetus highest oxygen concentration is found in?

Accepted Answer

Umbilical vein

Answer

Superior vena cava

Answer

Left ventricle

Answer

Ascending aorta

Question 10

What does aquaporin deficiency cause?

Accepted Answer

Nephrogenic diabetes insipidus

Answer

Liddle syndrome

Answer

Bartter syndrome

Answer

Gitelman syndrome

NEET-PG 2020 — Physiology