Consider the following hemodynamic changes occurring during pregnancy:
1. Increase in cardiac output
2. Increase in stroke volume
3. Increase in colloid oncotic pressure
4. Increase in pulse rate
Which of the statements given above are correct?
Q2
Which of the following statements regarding β-Human chorionic Gonadotropin are NOT correct?
1. It is a glycoprotein hormone.
2. Serum levels increase in pregnancy, germ cell tumors and gestational trophoblastic disease
3. Its levels are same in single and multiple pregnancy
4. Both alpha and beta subunits are unique and not shared with other hormones
Select the correct answer using the codes given below:
Q3
Which one of the following factors is NOT involved in the pathogenesis of Systemic inflammatory response syndrome (SIRS)?
UPSC-CMS 2018 - Physiology UPSC-CMS Practice Questions and MCQs
Question 1: Consider the following hemodynamic changes occurring during pregnancy:
1. Increase in cardiac output
2. Increase in stroke volume
3. Increase in colloid oncotic pressure
4. Increase in pulse rate
Which of the statements given above are correct?
A. 1, 3 and 4
B. 1, 2 and 4 (Correct Answer)
C. 2, 3 and 4
D. 1, 2 and 3
Explanation: ***Correct Answer: 1, 2 and 4***
**Statement 1: Increase in cardiac output** - CORRECT
- Cardiac output increases by **30-50% during pregnancy**, peaking at 28-32 weeks
- This increase is driven by increased blood volume (40-50% increase), higher metabolic demands, and the need to perfuse the uteroplacental unit
**Statement 2: Increase in stroke volume** - CORRECT
- Stroke volume increases by **20-30% during pregnancy**, particularly in the first and second trimesters
- This contributes significantly to the overall increase in cardiac output alongside increased heart rate
**Statement 3: Increase in colloid oncotic pressure** - INCORRECT
- Colloid oncotic pressure actually **decreases during pregnancy** from normal values of 25-28 mmHg to approximately 22-24 mmHg
- This occurs due to **hemodilution** (plasma volume increases more than red cell mass) and **decreased serum albumin concentration** (dilutional hypoalbuminemia)
- The reduced oncotic pressure contributes to the **increased tendency for peripheral edema** in pregnant women
**Statement 4: Increase in pulse rate** - CORRECT
- Heart rate increases by **10-20 beats per minute** during pregnancy
- This tachycardia helps maintain adequate cardiac output to meet the increased circulatory demands of pregnancy
*Incorrect Options:*
*1, 3 and 4* - Statement 3 is incorrect as colloid oncotic pressure decreases, not increases
*2, 3 and 4* - Statement 3 is incorrect as colloid oncotic pressure decreases during pregnancy
*1, 2 and 3* - Statement 3 is incorrect; colloid oncotic pressure falls due to hemodilution and hypoalbuminemia
Question 2: Which of the following statements regarding β-Human chorionic Gonadotropin are NOT correct?
1. It is a glycoprotein hormone.
2. Serum levels increase in pregnancy, germ cell tumors and gestational trophoblastic disease
3. Its levels are same in single and multiple pregnancy
4. Both alpha and beta subunits are unique and not shared with other hormones
Select the correct answer using the codes given below:
A. 1, 3 and 4
B. 2, 3 and 4
C. 1, 2 and 3
D. 1, 2 and 4
E. 3 only
F. 3 and 4 (Correct Answer)
Explanation: ***3 and 4***
* Statements 3 and 4 are both **incorrect** regarding β-hCG.
* **Statement 3 is incorrect:** β-hCG levels are **significantly higher** in multiple pregnancies compared to singleton pregnancies. Twin pregnancies typically show 30-50% higher β-hCG levels.
* **Statement 4 is incorrect:** β-hCG shares a **common alpha subunit** with FSH, LH, and TSH. Only the **beta subunit is unique** and provides diagnostic specificity. This is a key concept in understanding glycoprotein hormone structure.
*1, 3 and 4*
* This option incorrectly includes statement 1 as incorrect.
* Statement 1 is **correct** - β-hCG is a well-established glycoprotein hormone with carbohydrate moieties attached to a protein core.
* While statements 3 and 4 are indeed incorrect, including the correct statement 1 makes this option wrong.
*2, 3 and 4*
* This option incorrectly includes statement 2 as incorrect.
* Statement 2 is **correct** - serum β-hCG levels are markedly elevated in normal pregnancy, germ cell tumors (seminomas, choriocarcinomas), and gestational trophoblastic disease (molar pregnancy).
*1, 2 and 3*
* This option incorrectly identifies statements 1 and 2 as incorrect when both are correct.
* It also omits statement 4, which is incorrect regarding the subunit structure of β-hCG.
Question 3: Which one of the following factors is NOT involved in the pathogenesis of Systemic inflammatory response syndrome (SIRS)?
A. Free radical production
B. Increased cytokine production
C. Abnormal nitric oxide synthesis
D. Microvascular occlusion (Correct Answer)
Explanation: ***Microvascular occlusion***
- While microvascular occlusion (including microthrombi formation) does occur in SIRS, it is generally considered a **secondary phenomenon or consequence** rather than a **primary initiating pathogenic mechanism**.
- It develops as a result of **endothelial dysfunction, platelet activation, and coagulation cascade activation** triggered by the primary inflammatory mediators.
- More characteristically associated with **disseminated intravascular coagulation (DIC)**, which is a complication of severe SIRS/sepsis rather than an initiating factor.
- The primary pathogenic drivers initiate the cascade, while microvascular occlusion represents a downstream effect contributing to organ dysfunction.
*Free radical production*
- **Free radicals** (reactive oxygen species and reactive nitrogen species) are directly produced by activated inflammatory cells and damaged tissues.
- They cause **oxidative stress**, leading to direct cellular damage, lipid peroxidation, and increased vascular permeability.
- Free radical production is a **key pathogenic mechanism** amplifying the inflammatory response and tissue injury in SIRS.
*Increased cytokine production*
- **Pro-inflammatory cytokines** (TNF-α, IL-1, IL-6, IL-8) are the **central mediators** of SIRS pathogenesis.
- They are released early in response to inflammatory stimuli (infection, trauma, burns, pancreatitis).
- These cytokines trigger the **systemic inflammatory cascade**, causing fever, vasodilation, capillary leak, leukocyte activation, and acute phase response.
- Represent the **primary pathogenic mechanism** driving SIRS.
*Abnormal nitric oxide synthesis*
- **Excessive nitric oxide (NO) production** by inducible nitric oxide synthase (iNOS) is a **direct pathogenic mechanism** in SIRS.
- Leads to **inappropriate vasodilation**, contributing to the **distributive shock** and **refractory hypotension** seen in severe SIRS and septic shock.
- NO also impairs vascular responsiveness to vasoconstrictors and contributes to **myocardial depression**.
- This abnormal synthesis is a **primary factor** in the hemodynamic instability of SIRS.