Pathophysiology of Sepsis Flashcards

1
Q

What is sepsis according to Sepsis-3?

A

Life-threatening organ dysfunction caused by a dysregulated host response to infection.

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2
Q

What do Pattern Recognition Receptors (PRRs) detect?

A

PAMPs (pathogen-associated molecular patterns) on pathogens.

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3
Q

What are common PAMPs involved in sepsis?

A

LPS (Gram-negative), peptidoglycan, flagellin, lipoteichoic acid, bacterial DNA.

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4
Q

Which immune receptors recognise PAMPs in sepsis?

A

Toll-like receptors (TLRs).

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5
Q

Which cytokines initiate the SIRS response?

A

TNF-α, IL-1, IL-6.

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6
Q

What is the role of IL-10 and TNF-β in sepsis?

A

They contribute to the compensatory anti-inflammatory response (CARS).

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7
Q

What is the gut hypothesis of sepsis?

A

Reduced gut perfusion increases permeability, allowing bacteria to translocate into the bloodstream.

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8
Q

What is the endotoxin-macrophage hypothesis?

A

Endotoxins trigger macrophages to release cytokines causing systemic inflammation.

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9
Q

What is the tissue hypoxia-microvascular hypothesis?

A

Microvascular damage leads to poor oxygen delivery, causing cell death and organ dysfunction.

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10
Q

What is the mitochondrial DNA hypothesis in sepsis?

A

Cell death releases mtDNA, triggering NET formation and immune overactivation.

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11
Q

What is the integrated hypothesis of sepsis?

A

Combines multiple mechanisms including gut leak, endotoxin, and mitochondrial pathways.

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12
Q

Which pathogens commonly cause sepsis?

A

S. pneumoniae, S. aureus, E. coli, Klebsiella spp., Pseudomonas aeruginosa.

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13
Q

What vascular changes occur during sepsis?

A

Vasodilation, capillary leak, and hypotension.

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14
Q

How do free radicals contribute to sepsis damage?

A

Produced by immune cells, they cause oxidative stress and tissue injury.

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15
Q

What is the role of endothelial cells in sepsis?

A

They release inflammatory mediators, increase permeability, and promote leukocyte adhesion.

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16
Q

What causes hypotension in sepsis?

A

Capillary leak and sustained vasodilation reduce blood volume and pressure.

17
Q

What is the first stage of coagulation in sepsis?

A

Activation of complement, coagulation, and fibrinolysis systems.

18
Q

What is the role of PAI-1 in sepsis?

A

It inhibits fibrinolysis, promoting thrombotic coagulopathy.

19
Q

What is Disseminated Intravascular Coagulation (DIC)?

A

Widespread microthrombi block capillaries and use up clotting factors, leading to bleeding.

20
Q

What leads to multiple organ failure in sepsis?

A

Tissue hypoxia, inflammation, and microvascular occlusion cause irreversible damage.

21
Q

What early signs may indicate sepsis?

A

Fever, tachycardia, tachypnea, confusion, decreased urine output.

22
Q

Who is at high risk for sepsis?

A

Elderly, neonates (babies in their first 28 days of life), immunocompromised, recent surgery, pregnant women.

23
Q

How are dental infections linked to sepsis?

A

Severe infections may allow oral bacteria to enter the bloodstream and trigger sepsis.

24
Q

What is the clinical definition of septic shock?

A

Persistent hypotension with high lactate despite fluid resuscitation.

25
Q

How does sepsis lead to organ damage?

A

Reduced perfusion, inflammation, and oxygen depletion damage tissues.

26
Q

How is sepsis managed in hospital?

A

IV fluids, antibiotics, vasopressors, and critical care support.

27
Q

What is the role of antibiotic stewardship in sepsis?

A

Preserving antibiotic effectiveness for severe infections like sepsis.

28
Q

What is the estimated annual death toll due to AMR by 2050?

A

10 million globally according to WHO projections.

29
Q

Why is early recognition of sepsis crucial?

A

It significantly improves survival outcomes.