Deep Dive Questions Flashcards

1
Q

What role does nitric oxide play in septic shock pathophysiology?

A

Inflammatory cytokines upregulate inducible nitric oxide synthase (iNOS), leading to excess nitric oxide → systemic vasodilation and decreased SVR.

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2
Q

How does lactic acidosis develop in septic shock?

A

Hypoperfusion and mitochondrial dysfunction cause cells to shift to anaerobic metabolism, producing lactate as a byproduct.

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3
Q

Why does ARDS cause decreased lung compliance?

A

Inflammatory damage leads to alveolar edema, surfactant inactivation, and hyaline membrane formation → stiff lungs.

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4
Q

How does systemic inflammation in sepsis affect the coagulation system?

A

Activation of coagulation cascade + suppression of fibrinolysis → microthrombi, DIC, and organ dysfunction.

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5
Q

What is the mechanism behind refractory hypoxemia in ARDS?

A

Intrapulmonary shunting — blood passes through non-aerated alveoli, bypassing gas exchange despite high FiO₂.

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6
Q

How does Preload, Afterload, and Contractility change in septic shock?

A

↓ Preload (vasodilation & capillary leak), ↓ Afterload (vasodilation), ↓ Contractility (myocardial depression from cytokines).

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7
Q

What receptor does ketamine act on, and how does it cause dissociative anesthesia?

A

NMDA receptor antagonist → disrupts thalamocortical pathways, leading to dissociation of sensory input from consciousness.

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8
Q

How does dexmedetomidine (Precedex) produce sedation and analgesia?

A

Alpha-2 receptor agonist in the CNS → ↓ norepinephrine release → sedation, anxiolysis, and mild analgesia.

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9
Q

What is the primary mechanism of action of benzodiazepines like midazolam (Versed)?

A

Binds GABA-A receptor → increases frequency of chloride channel opening → hyperpolarization → CNS depression.

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10
Q

Why does propofol cause hypotension?

A

Decreases systemic vascular resistance through vasodilation and directly depresses myocardial contractility.

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11
Q

What is the mechanism by which norepinephrine increases blood pressure?

A

Alpha-1 agonism → vasoconstriction ↑ SVR; beta-1 agonism → ↑ HR and contractility.

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12
Q

How does vasopressin work in vasodilatory shock?

A

Binds V1 receptors on vascular smooth muscle → vasoconstriction independent of adrenergic receptors.

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13
Q

Why might epinephrine cause hyperglycemia in septic patients?

A

Beta-2 receptor stimulation → glycogenolysis and gluconeogenesis; also inhibits insulin secretion.

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14
Q

What is the effect of prolonged high-dose fentanyl on the endocrine system?

A

Suppresses ACTH and cortisol → may contribute to adrenal insufficiency in critical illness.

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