Systems Physiology Approach — MCQs
Following pathogenetic mechanisms operate in septic shock except -
Some cells secrete chemicals into the extracellular fluid that act on cells in the same tissue. Which of the following refers to this type of regulation?
What is the primary cardiovascular compensatory mechanism in acute hemorrhage?
Which of the following physiological changes occur during fever?
In surgical stress all hormones are increased except:
All of the following are increased in Acute stress except
When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?
Which of the following can cause delirium?
Risk Scoring System which can be used postoperatively is:
When two different chemicals act on two different receptors and their responses are opposite to each other on the same cell, this phenomenon is called?
Systems Physiology Approach Indian Medical PG Practice Questions and MCQs
Question 1: Following pathogenetic mechanisms operate in septic shock except -
- A. Direct toxic endothelial injury
- B. Veno constriction
- C. Increased peripheral vascular resistance (Correct Answer)
- D. Activation of complement
Explanation: Following pathogenetic mechanisms operate in septic shock except - ***Increased peripheral vascular resistance*** - Septic shock is characterized by profound **vasodilation** and a subsequent **decrease in systemic vascular resistance (SVR)**, leading to hypoperfusion. - The body's compensatory mechanisms attempt to increase cardiac output rather than constrict peripheral vessels, making increased PVR an unlikely finding in established septic shock. [1] *Direct toxic endothelial injury* - **Bacterial products** (e.g., endotoxins from Gram-negative bacteria) and inflammatory mediators directly damage the **endothelium**, leading to capillary leak and microvascular dysfunction. - This endothelial damage contributes significantly to the widespread organ damage seen in sepsis. *Veno constriction* - While initial compensatory mechanisms might involve elements of vasoconstriction to maintain blood pressure, the hallmark of septic shock is widespread **vasodilation**, which includes both arterial and venous beds. - Early, fleeting venoconstriction is overshadowed by the profound venodilation and loss of venous tone that ultimately contributes to reduced preload and distributive shock. *Activation of complement* - The innate immune response in sepsis triggers the **complement cascade**, leading to the generation of potent inflammatory mediators. - Complement activation contributes to endothelial damage, leukocyte recruitment, and further amplification of the systemic inflammatory response.
Question 2: Some cells secrete chemicals into the extracellular fluid that act on cells in the same tissue. Which of the following refers to this type of regulation?
- A. Neural
- B. Endocrine
- C. Neuroendocrine
- D. Paracrine (Correct Answer)
Explanation: ***Paracrine*** - **Paracrine signaling** involves chemical messengers, or **paracrine factors**, that act on **neighboring cells** within the **same tissue** without entering the bloodstream. - This type of regulation is crucial for local communication and coordination, such as in wound healing or immune responses. *Neural* - **Neural regulation** involves communication via **neurons** that transmit **electrical signals** (action potentials) and release **neurotransmitters** at synapses. - Neurotransmitters act on target cells, which can be distant from the neuron, for rapid and precise responses throughout the body. *Endocrine* - **Endocrine regulation** involves glands that secrete **hormones** directly into the **bloodstream**, which then travel to distant target cells in other tissues or organs. - This form of signaling leads to widespread and long-lasting effects, such as growth regulation or metabolic control. *Neuroendocrine* - **Neuroendocrine regulation** is a hybrid system where specialized **neurons** (neurosecretory cells) release **hormones** into the **bloodstream**, rather than releasing neurotransmitters into a synapse. - An example is the hypothalamus secreting ADH and oxytocin, which act on distant target organs.
Question 3: What is the primary cardiovascular compensatory mechanism in acute hemorrhage?
- A. Decreased myocardial contractility
- B. Increased respiratory rate
- C. Decreased heart rate
- D. Increased heart rate (Correct Answer)
Explanation: ***Increased heart rate*** - In acute hemorrhage, the body senses a decrease in **blood volume** and **blood pressure**, triggering the **baroreceptor reflex**. - This reflex leads to increased sympathetic nervous system activity, causing an immediate compensatory **increase in heart rate** to maintain **cardiac output** and tissue perfusion. *Decreased myocardial contractility* - A decrease in myocardial contractility would worsen the situation in hemorrhage by further reducing **cardiac output** and is not a primary compensatory mechanism. - While prolonged severe hemorrhage can lead to myocardial depression due to ischemia, it is a pathological consequence, not a compensatory response. *Decreased heart rate* - A decrease in heart rate would reduce **cardiac output** and further compromise blood flow to vital organs during hemorrhage, which is precisely the opposite of what the body needs. - This response is usually seen with vagal stimulation, not in response to hypovolemic shock. *Increased respiratory rate* - An **increased respiratory rate** is a compensatory mechanism for conditions like **metabolic acidosis** (which can occur in severe shock due to lactic acid accumulation) or to improve oxygenation, but it is not the primary cardiovascular compensatory mechanism for maintaining blood pressure and cardiac output in acute hemorrhage. - While it often accompanies hemorrhage, it acts to regulate oxygen and CO2 levels, not directly blood volume or pressure.
Question 4: Which of the following physiological changes occur during fever?
- A. Resetting of skin temperature
- B. Thermoregulatory centre to shift to new level (Correct Answer)
- C. Both of the above
- D. None of the above
Explanation: ***Thermoregulatory centre to shift to new level*** - During a fever, **pyrogens** (e.g., interleukins, prostaglandins) act on the **hypothalamus**, which is the thermoregulatory center. - This action causes the hypothalamus to **reset its set point** to a higher temperature. The body then works to raise its core temperature to this new, elevated set point. *Resetting of skin temperature* - The **skin temperature** is a result of the body trying to achieve the new set point, but it's not the primary physiological change that *initiates* the fever. - Changes in skin temperature, like **vasoconstriction** leading to cold skin or **vasodilation** leading to warm skin, are mechanisms for heat retention or dissipation, driven by the change in the hypothalamic set point. *Both of the above* - While skin temperature does change, the fundamental physiological event driving fever is the **resetting of the hypothalamic thermoregulatory set point**. - Skin temperature changes are a **consequence** of the body's efforts to reach this new set point, not a primary cause or an independent "resetting" event itself. *None of the above* - This option is incorrect because the **thermoregulatory center** indeed shifts to a new, higher set point during fever. - This shift is the hallmark physiological response to pyrogens.
Question 5: In surgical stress all hormones are increased except:
- A. Insulin (Correct Answer)
- B. Epinephrine
- C. ACTH
- D. Cortisol
Explanation: ***Insulin*** - While other **stress hormones** increase, **insulin** levels typically **decrease** or remain stable due to increased **insulin resistance** during surgical stress. - This physiological response aims to maintain **blood glucose** levels for energy during heightened metabolic demands. *Epinephrine* - **Epinephrine** (adrenaline) is a key **catecholamine** released during surgical stress, leading to a "fight or flight" response. - It increases **heart rate**, **blood pressure**, and promotes **gluconeogenesis** to supply quick energy. *ACTH* - **Adrenocorticotropic hormone (ACTH)** is released from the **pituitary gland** in response to surgical stress. - **ACTH** stimulates the adrenal cortex to produce **cortisol**, a critical stress hormone. *Cortisol* - **Cortisol** levels significantly rise during surgical stress, mediated by **ACTH** release. - It plays a crucial role in **modulating inflammation**, **glucose metabolism**, and maintaining **hemodynamic stability**.
Question 6: All of the following are increased in Acute stress except
- A. Growth hormone
- B. Epinephrine
- C. Glucagon
- D. Insulin (Correct Answer)
Explanation: ***Insulin*** - During acute stress, **insulin secretion is actively suppressed** by catecholamines (epinephrine and norepinephrine) acting on **alpha-2 adrenergic receptors** on pancreatic beta cells. - This suppression is crucial for the stress response, as it allows **unopposed action of counter-regulatory hormones** to mobilize glucose and raise blood glucose levels. - The body prioritizes **immediate energy availability** (high blood glucose) over storage, making insulin the hormone that is **decreased, not increased**, during acute stress. *Growth hormone* - **Growth hormone** is a counter-regulatory hormone that **increases during acute stress** to mobilize energy stores, particularly by promoting lipolysis and gluconeogenesis. - Its actions contribute to the stress-induced elevation of **blood glucose levels**. *Epinephrine* - **Epinephrine** (adrenaline) is a primary catecholamine released during acute stress, leading to a rapid **fight or flight response**. - It significantly **increases heart rate**, blood pressure, and **glucose mobilization** through glycogenolysis and gluconeogenesis. *Glucagon* - **Glucagon** is a key hormone involved in **maintaining glucose homeostasis** and is significantly **increased during acute stress**. - It primarily acts on the liver to **stimulate glycogenolysis** and **gluconeogenesis**, thereby raising blood glucose levels to provide energy.
Question 7: When blood pressure falls below 40 mm Hg, which mechanism of regulation is working?
- A. CNS ischemic reflex (Correct Answer)
- B. Chemoreceptor response
- C. Baroreceptor response
- D. None of the options
Explanation: ***CNS ischemic reflex*** - The **CNS ischemic reflex** is activated when blood pressure falls below 60 mmHg, with maximal activation below 40 mmHg, indicating severe ischemia in the brain's vasomotor center. - This reflex elicits an intense **sympathetic vasoconstriction** and cardiac stimulation to prioritize blood flow to the brain even at the expense of other organs. *Chemoreceptor response* - The chemoreceptor reflex is primarily activated by a decrease in **arterial pO2**, an increase in **pCO2**, or a decrease in **pH**. - While it can increase blood pressure, it is not the primary or most profound regulatory mechanism specifically triggered by extremely low blood pressure (below 40 mmHg) to prevent brain ischemia. *Baroreceptor response* - **Baroreceptors** are most sensitive to changes in blood pressure within the normal to moderately hypotensive range (e.g., 60-180 mmHg). - At very low pressures (below 40-50 mmHg), baroreceptors become **less sensitive** or "saturated," and their effectiveness in raising blood pressure significantly diminishes. *None of the options* - This option is incorrect because the **CNS ischemic reflex** specifically functions as a powerful, last-ditch mechanism to maintain cerebral blood flow during severe hypotension which is a life saving reflex during conditions like hemorrhage.
Question 8: Which of the following can cause delirium?
- A. Barbiturates
- B. Hypoxia
- C. Alcohol withdrawal
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Barbiturates**, **hypoxia**, and **alcohol withdrawal** are all well-established causes of delirium, affecting the brain's cognitive function. - Delirium is a state of **acute brain failure** characterized by fluctuating attention, altered consciousness, and cognitive dysfunction, often *multifactorial*. *Barbiturates* - These drugs are **CNS depressants** and can cause delirium, especially in susceptible individuals or with overdose. - They can lead to **sedation**, confusion, and a paradoxical agitated state, contributing to delirium. *Hypoxia* - **Lack of oxygen to the brain** is a significant cause of delirium as neurons are highly sensitive to oxygen deprivation. - This can result from various conditions such as **respiratory failure**, anemia, or circulatory compromise, directly impairing brain function. *Alcohol withdrawal* - Abrupt cessation of alcohol in dependent individuals causes severe **CNS hyper-excitability**, leading to delirium tremens. - Symptoms include **agitation**, hallucinations, confusion, and autonomic instability characteristic of delirium.
Question 9: Risk Scoring System which can be used postoperatively is:
- A. ASA American Society of Anaesthesiologist
- B. MET Metabolic Equivalent Task
- C. POSSUM Physiologic and Operative Severity Score for Enumeration of Mortality and Morbidity (Correct Answer)
- D. RCRI Revised Cardiac Risk Index
Explanation: ***POSSUM (Physiologic and Operative Severity Score for enUmeration of Mortality and Morbidity)*** - **POSSUM** is a risk scoring system specifically designed to predict **postoperative mortality and morbidity** based on physiological and operative factors. - It includes both **preoperative physiological variables** and **intraoperative findings** to provide a comprehensive risk assessment after surgery. *ASA (American Society of Anesthesiologists)* - The **ASA physical status classification system** is used to assess a patient's **preoperative health status** and predict anesthetic risk, not directly postoperative outcomes. - It is determined **before surgery** to categorize patients into different classes based on their overall health and presence of co-morbidities. *MET (Metabolic Equivalent Task)* - **METs** are a measure of **exercise capacity** and reflect a person's functional status, often used in preoperative cardiac risk assessment. - They are used to gauge a patient's ability to perform physical tasks, not as a direct predictor of postoperative complications. *RCRI (Revised Cardiac Risk Index)* - The **RCRI** is used to predict the risk of **major cardiac events** in patients undergoing non-cardiac surgery. - It is primarily a **preoperative tool** focused on cardiac risks, not a general predictor of all postoperative morbidity and mortality.
Question 10: When two different chemicals act on two different receptors and their responses are opposite to each other on the same cell, this phenomenon is called?
- A. Physiological antagonism (Correct Answer)
- B. Chemical antagonism
- C. Reversible antagonism
- D. Competitive antagonism
Explanation: ***Physiological antagonism*** - This occurs when two drugs act on **different receptors** to produce **opposite physiological effects** within the same system or cell, effectively canceling each other out [1]. - A classic example is the opposing actions of **histamine** (causing bronchoconstriction) and **adrenaline** (causing bronchodilation) on the bronchi [1]. *Chemical antagonism* - This involves a direct **chemical interaction** between two drugs that results in the **inactivation of one or both** of them. - An example is the binding of **chelating agents** to heavy metals, forming an inert complex. *Reversible antagonism* - This describes antagonism where the antagonist binds to the receptor and can be **displaced by a higher concentration of the agonist**. - It does not specifically describe antagonists acting on different receptors or producing opposing physiological effects. *Competitive antagonism* - This occurs when an antagonist directly **competes with an agonist for the same binding site** on a receptor [1]. - The antagonist, while not producing a response itself, prevents the agonist from binding and activating the receptor.
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free