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Metabolic Response to Injury & Shock
Q1. Counter regulatory hormones in response to metabolic response to injury are all except
Answer: C. Thyroid hormones
In response to injury, the body releases counter-regulatory hormones to mobilize energy substrates and promote healing. These include glucocorticoids (e.g., cortisol), catecholamines (e.g., epinephrine, norepinephrine), and glucagon, which increase blood glucose levels and support metabolic adaptation.
Thyroid hormones, while essential for metabolic regulation, are not considered primary counter-regulatory hormones in the acute metabolic response to injury.
In response to injury, the body releases counter-regulatory hormones to mobilize energy substrates and promote healing. These include glucocorticoids (e.g., cortisol), catecholamines (e.g., epinephrine, norepinephrine), and glucagon, which increase blood glucose levels and support metabolic adaptation.
Thyroid hormones, while essential for metabolic regulation, are not considered primary counter-regulatory hormones in the acute metabolic response to injury.
Q2. Direct effects of GH in metabolic response to injury are all except:
Answer: B. Insulin agonist
Growth hormone (GH) is lipolytic, promoting fat breakdown, and acts as an insulin antagonist, decreasing tissue sensitivity to insulin, leading to hyperglycemia. GH also has proinflammatory effects by stimulating immune and inflammatory responses during injury.
GH is not an insulin agonist; rather, it promotes gluconeogenesis and lipolysis, counteracting insulin's effects.
Growth hormone (GH) is lipolytic, promoting fat breakdown, and acts as an insulin antagonist, decreasing tissue sensitivity to insulin, leading to hyperglycemia. GH also has proinflammatory effects by stimulating immune and inflammatory responses during injury.
GH is not an insulin agonist; rather, it promotes gluconeogenesis and lipolysis, counteracting insulin's effects.
Q3. What is not seen in Distributive Shock?
Answer: A. High central venous pressure
In distributive shock (e.g., septic, neurogenic), vasodilation leads to low CVP due to reduced preload.
Other features:
• High cardiac output (e.g., septic shock)
• High base deficit (metabolic acidosis)
• High mixed venous saturation (due to reduced oxygen extraction by tissues)
Causes: Anaphylaxis, high spinal cord injury, septic shock, toxic shock syndrome.
In distributive shock (e.g., septic, neurogenic), vasodilation leads to low CVP due to reduced preload.
Other features:
• High cardiac output (e.g., septic shock)
• High base deficit (metabolic acidosis)
• High mixed venous saturation (due to reduced oxygen extraction by tissues)
Causes: Anaphylaxis, high spinal cord injury, septic shock, toxic shock syndrome.