1.2.2 Inflammation, DIC and Shock Flashcards Preview

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Flashcards in 1.2.2 Inflammation, DIC and Shock Deck (36)
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1
Q

Stage in which compensatory physiologic mechanisms may allow survival (reversible)

A

Non-progressive stage

2
Q

What causes bleeding associated with DIC?

A

Central event is the activation of the intrinsic or extrinsic clotting cascade within the vascular compartment by tissue injury. Platelets and clotting factors are consumed by massive intravascular coagulation, often in the capillary beds.

3
Q

What is this an image of?

A

Diffuse alveolar damage - so called shock lung

4
Q

What is significant about Waterhouse-Friderichson syndrome?

A

infarcted adrenal glands due to DIC. Need to used corticosteroids because fluid and pressors will not be enough

5
Q

What is the arrow pointing to?

A

Schistocytes which are caused by the fibrin meshwork fragmenting normal RBCs

6
Q

What is hypovolemic shock?

A

results from low cardiac output due to low blood volume; bleeding

7
Q

What is shock?

A

a state in which diminished cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia

8
Q

Capillary bed perfused, sphincters controlled, AV shunts controlled, minimal hypoxia and drop of pH across capillary beds are characteristic of what stage?

A

Normal stage

9
Q

What is the importance of factor XII (Hageman’s Factor)

A

Microbial components can activate coagulation in affected tissues directly through factor XII

10
Q

What is the role of PDGF as a tissue mediator?

A

Secreted by activated platelets and macrophages. Induces vascular remodeling and smooth muscle cell migration. Stimulates fibroblast growth and collagen synthesis

11
Q

What is this?

A

Nutmeg liver - centri-lobular congestion

12
Q

What are some roles of inflammatory responses in septic shock?

A

TNF, IL-1, and other cytokines will trigger downstream events leading to a hyper inflammatory state

13
Q

What is this an image of?

A

Waterhouse-Friderichson syndrome (NEEDS CORTICOSTEROIDS!)

14
Q

Arteriolar vasodilation (pooling of blood), increased capillary hydrostatic pressure, decreased function of vital organ, and severe metabolic lactic acidosis are characteristics of what stage?

A

Irreversible stage

15
Q

What is the role of organ dysfunction in septic shock?

A

Systemic hypotension, interstitial edema, and small vessel thrombosis all decrease the delivery of oxygen and nutrients to tissues

16
Q

Stage in which increasing tissue hypoxia and beginning of lactic acidosis due to anaerobic metabolism in the tissues

A

Progressive

17
Q

Peripheral vasoconstriction, AV shunts open (redistributing blood to heart and brain), decreased pH across capillary beds, hemodilution (interstitial fluid moves into vascular spaces) are characteristics of what stage?

A

Reversible or non-progressive stage

18
Q

What is the role of EGF as a tissue mediator?

A

Stimulates cell growth via tyrosine kinases

19
Q

What is the role of induction of a pro-coagulative state in septic shock?

A

Sepsis alters the expression of many factors to favor coagulation by decrease of endothelial anti-coagulant factors. Can lead to DIC

20
Q

What is the role of FGF as a tissue mediator?

A

Stimulates angiogenesis

21
Q

What is the role of endothelial activation in septic shock?

A

activation leads to widespread leakage and tissue edema which has deleterious effects on nutrient delivery and waste removal

22
Q

What is this an image of?

A

Nutmeg Liver - from passive congestion, this was a result of right-sided heart failure

23
Q

What is the arrow pointing to?

A

Fibrin thrombi in the glomerulus caused by DIC

24
Q

Decreased blood volume, maximum peripheral vasoconstriction, lactic acidosis, decreased capillary perfusion, sludging and clotting begin are characteristics of what stage?

A

Progressive stage

25
Q

Stage that even if the hemodynamic defects are corrected tissue survival is not possible

A

Irreversible

26
Q

What is the arrow pointing to?

A

Microthrombi in the glomerulus caused by DIC.

27
Q

What percent of patients survive hypovolemic shock?

A

90% survival with appropriate management

28
Q

Anaerobic metabolism in tissues leads to what?

A

Lactic acidosis

29
Q

What is the role of TGF-beta as a tissue mediator?

A

Angiogenesis, fibrosis, and cell cycle arrest

30
Q

What is this an image of?

A

Shock liver, with cell dropout - prolonged hypoxia produces “cell dropout” (necrosis) of hepatocytes. Liver enzymes would be moderately increased

31
Q

What percent of patients survive septic or cadiogenic shock?

A

50-80% range

32
Q

How to manage septic shock?

A

pressors (dopamine) and IV fluid to manage until the underlying cause is discovered

33
Q

What is cardiogenic shock?

A

results from low cardiac output due to myocardial pump failure

34
Q

What is the role of VEGF as a tissue mediator?

A

Stimulates angiogenesis

35
Q

What is systemic inflammation shock?

A

inflammatory mediators lead to vascular leakage and blood pooling

36
Q

What is the presentation of DIC in the clinic?

A

Massive bleeding

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