Inflammation, DIC, and Shock Flashcards

1
Q

What is the definition of Shock?

A

State in which diminshed cardiac output or reduced effective circulating blood volume impairs tissue perfusion and leads to cellular hypoxia

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2
Q

What are the three common classifications of shock?

A

Cardiogenic, Hypovolemic, and Septic

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3
Q

What is the non-progressive phase of shock?

A

Initial stage which reflex compensatory mechanisms are activated and perfusion of vital organs is maintagened. This is sometimes called the reversible stage of shock

  • peripheral vasocontriction due to ANS stimulus and adrenal catecholamines (try to drive up BP)
  • AV shunts open to redistribute blood from splanchnic circulation to the heart and brain, so renal function will decrease due to decreased glomerular filtration (no more urine output)
  • decreased pH across capillary beds

Hemodilution of interstitial fluids move into vascular spaces to replace blood loss

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4
Q

What is the progressive stage of shock?

A

Increasing tissue hypoxia (hypoperfusion) and the beginning of lactic acidosis, due to anaerobic metabolism in the tissues

  • critical phase of shock
  • continued decrease in blood volume and pressure
  • maximal peripheral vasocontriction
  • lactic acidosis
  • decreased capillary perfusion - endothelial hypoxia
  • sludging and clotting begin
  • the patient can still be saved but you are nearing the end of the golden hour
  • see image: shunt diverts blood from the organs, preserving flow to the heart and CNS. There is intensive vasocontriction in an attempt to keep BP within normal limits
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5
Q

What is the irreverisble stage of shock?

A

The stagnant phase that sets in after the body has incurred cellular and tissue injury so severe that even if the hemodynamic defect are corrected, survival is not possible

  • arteriolar vasodilation leads to pooling and stagnation
  • increased capillary hydrostatic pressure leads to interstitial edema
  • decreased function of vital organs
  • sever metabolic lactic acidosis

leads to death

-at this point you have DIC, clotting is now massive in the capillar beds and multi-organ failure

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6
Q

What is normal circulation?

A

Capillary beds are perfused, sphincters controlled, AV shunts controlled, minimal hypoxia and drop of pH across the capillarhy beds

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7
Q

What causes bleeding associated with DIC?

A

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

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8
Q

What is the most frequent cause of Septic Shock?

A

Gram-positive bacterial infections

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9
Q

What are the 5 factors involved in the pathogenesis of shock?

A
  1. Inflammatory and Counter-inflammatory responses
  2. Endothelial cell activation and injury
  3. induction of pro-coagulative state
  4. metabolic abnormalities (acidosis)
  5. Organ dysfunction (due to hypoxia from low BP, and clotting of capillary blood suuply due to disseminated intravascular coagulopathy DIC)
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10
Q

What is the standard of treatment for sepsis?

A

Treat underlying infection with antibiotics, give intraveous fluids, pressors, and supplemental oxygen to maintain blood pressure and limit tissue hypoxia.

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11
Q

What is SIRS

A

Systemic Inflammatory Response Syndrome, thought to be the result of a cytokine storm, resulting in multiple organ dysfunction. 20% mortality rate.

-Infection organisms are isolated from the blood in only about 20% of cases of septic shock, so SIRS is the rule.

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12
Q

What is DIC?

A

Disseminated Intravascular Coagulation (consumption coagulopathy) is a dangerous acquired disorder where platelets and clotting factors are consumed by massive intravascular coagulation, often within capillar beds. Conversely, this leads to uncontrollable hemorrhage in other ares of the body. This is what produces the hemorrhage in hemorrhagic fevers like Ebola.

  • DIC is not a specific disease, but rather a complication of a large number of conditions associated with systemic activation of thrombin.
  • central event in the initiation of DIC is the activation of the clotting cascades within the vascular compartment by tissue injury, damage to endothelium or both. Thrmoboplastin from amniotic fluid embolism can also initiate the clottinc cascade during certain obstetrical emergencies.
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13
Q

Where is fibrin/platelet thrombi normally found and what happens to it in DIC?

A

Normally it is found in many venules, capillaries and arterioles.

-they are consumed in DIC and clot and thrombose leading to organ dysfunction

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14
Q

What is this?

A

Diffuse alveolar damage due to DIC. (so called shock lung)

-this is rare in hypovalemic shock becasue the lungs are somewhat resistant to hypoxic injury. But in spesis or trauma diffuse alveolar damage may develop. DIC leads to widespread deposition of firbin-rich microthrombi

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15
Q

What is Waterhouse-Friderirchson Syndrome?

A

Infarted adrenal galnds due to DIC. So you can no longer produce cortisol and other hormons so they must be replaced by giveing them as corticosteroids.

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16
Q

What is this?

A

These are Schistocytes (fragmented RBC) in a peripheral smear. Also called helmet cells

-caused by fibrin meshwork fragmenting normal RBCs due to DIC

17
Q

What is hypovolemic shock?

A

Results from low cardiac output due to low blood volume, and or bleeding

18
Q

What is FactorXII (Hageman’s factor)?

A

Microbial compoenents can activate coagulation in affected tissues directly through Factor XII

19
Q

What is the role of PDGF as a tissue mediator?

A

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

20
Q

What is this?

A

Nutmeg Liver (centri-lobular congestation)

-shows RBC congested around the central vein

21
Q

What are some cytokines and signals in inflammatory response of septic shock?

A

TNF, IL-1, and other cytokines trigger downstream evens and hyper inflammatory state

22
Q

What is this?

A

Waterhouse-Friderichson Syndrome (infarction of adrenal glands) need steroids!

23
Q

What is the role of EGF as a tissue mediator?

A

Stimulate cell growth via tyrosine kinases

24
Q

What is the role of FGF as a tissue mediator?

A

Stimulate angiogenesis

25
Q

What is the role of endothelial activation in septic shock

A

Leads to widespread leakage and tissue edema which decreases nutrient delivery and waste removal

26
Q

What is this an image of?

A

Nutmeg liver- from passigve congestion as a result of right-sided heart failure. Blood in the centrilobular are of the liver

27
Q

What is this?

A

Fibrin thrombi in the glomerulus caused by DIC

-the black is unwanted fibrin that is preventing glomerulus filtration

28
Q

What is this?

A

Microthrombi in the glomerulus caused by DIC

29
Q

Anaerorib metabolism in tissues leads to what?

A

Lactic Acidosis

30
Q

What is this an image of?

A

Shock liver with cell dropout (necrosis) of hepatocytes. Liver enzyme would be moderately increased in this patient, a condition known as shock liver.

31
Q

How to manage septic shock?

A

Pressors (dopamine, to support BP), IV fluid, antibiotics, gotta remove the cause.