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Pathology #1 > Trombosis, Embolism, infarction and Shock #4 (1/25/16) > Flashcards

Trombosis, Embolism, infarction and Shock #4 (1/25/16) Flashcards

1
Q

What is a Thrombus?

What is Thrombosis?

A

Thrombus = An intravascular clot often impeding or preventing blood flow.

Thrombosis = Formation or presence of thrombus that may result in an infarction.

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2
Q

What is Virchow’s Triad?

A

3 factors that can lead to a thrombus/thrombosis:

  1. Endothelial injury
  2. Alterations in blood flow = like turbulence or stasis (both lead to endothelial activation)
  3. Hyper-coagulability
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3
Q

What conditions cause Hyper-coagulability?

A
  1. Inherited Conditions
    - Factor V leiden (Va cannot be cleaved)
    - AT III deficiency
    - Prothrombin Mutation
  2. Acquired conditions
    - prolonged bed rest
    - extensive tissue injury
    - pregnancy
    - cancer
    - anti-PL ab
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4
Q

Describe arterial Thrombosis….

A
  • White (Because of fibrin)
  • Often at sites of turbulence/endothelial injury
  • Occlusive or mural
  • Distinct lines of Zahn
  • on heart valves (NBTE)
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5
Q

Describe venous thrombosis….

A
  • Red
  • Often at sites of stasis (Where blood slowed down) such as deep leg veins.
  • Indistinct lines of Zahn
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6
Q

What are the 4 possible fates of Thrombi?

A
  1. Propagation - whole thrombus moves.
  2. Embolization - piece of thrombus breaks off and goes elsewhere.
  3. Dissolution (resolution) - thrombus gets resorbed by body.
  4. Organization/recanalization - thrombus gets holes in it so blood flow can be restored THROUGH thrombus.
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7
Q

What is DIC?

A

Disseminated Intravascular Coagulation

  • Widespread activation of the coagulation cascade and fibrinolytic factors.
  • Depletion of coagulation factors and platelets
  • Elevation of fibrin spilt products
  • Micro thrombi and hemorrhage
  • Consumptive coagulopathy
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8
Q

What are the Etiologies of DIC? (7)

A
  • Infection (gram negatives)
  • Obstetric complications
  • Placental abruption
  • Retained dead fetus
  • Neoplasm
  • Shock
  • Massive tissue injury.
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9
Q

Describe treatment for DIC….

A

Treatment is highly variable and dependent on management of underlying disorder. (Can be potentially life threatening)

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10
Q

What is an Embolus?

A

An intravascular solid, liquid or gaseous mass carried by the blood to a site distant from its point of origin. *The vast majority of Emboli are dislodged thrombus material.

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11
Q

Describe a Pulmonary Thromboembolism - Origin? Consequences?

A 
Origin = Deep leg veins
Clinical consequences:
- No manifestations
- pulmonary hemorrhage
- Pulmonary infarction
- Sudden death
- Pulmonary Hypertension
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12
Q

Describe Systemic Embolization - Origin?

A

Origin = left atrium, left ventricle, atherosclerotic plaque.
*Paradoxical embolus = arises in a vein (Often leg vein) then crosses into the arterial side, often through patent foramen ovale.

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13
Q

What are the 5 types of Embolism?

A
  1. Thrombus = most common by far
  2. Fat
  3. Air (“Bends” and caisson disease)
  4. Amniotic fluid
  5. Atherosclerotic plaque material
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14
Q

What is an Infarction?

A

Area of Ischemic Necrosis, secondary to occlusion of arterial supply or venous drainage.
*Major contributor to mortality associated with cardiovascular disease.

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15
Q

What are the 2 types of infarctions?

A

Red = hemorrhagic

  • venous occlusion
  • loose tissue
  • dual blood supply
  • previous congestion
  • reflow of blood to infarcted area

White = pale
- Arterial occlusion in solid organ.

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16
Q

What factors influence Infarct development?

A
  • Nature of vascular supply (Multiples, loose tissue)
  • Rate of occlusion
  • Vulnerability to hypoxia
  • Oxygen carrying capacity of cardiovascular system
17
Q

What is shock? What are the types of shock? (5)

A

Systemic Hypoperfusion (Not moving blood so well)

  • Cariogenic shock
  • Hypovolemic shock
  • Septic shock (#1 cause of death in intensive care units)
  • Anaphylactic shock
  • Neurogenic shock
18
Q

What is the most common cause of septic shock?

A

Gram + or Gram - Bacteria

  • Activation of TLR on monocytes and neutrophils with release of IL-1, TNF and other mediators.
  • Dose dependent effects, DIC in 50% of patients.
19
Q

What are the stages of Shock?

A
  1. Non-progressive = compensatory mechanism maintain perfusion.
  2. Progressive = Inadequate perfusion, anaerobic metabolism, lactic acidosis, DIC.
  3. Irreversible = Tissue injury unrecoverable, multiple organ failure, death.
20
Q

What are the clinical manifestations of Shock?

A
  • Tachycardia
  • Tachypena
  • Hypotension
  • Cool clammy skin (septic may be warm)
  • Pallor/cyanosis
  • Confusion
  • Low urine output
  • Acidosis
  • High lactic acid

Pathology #1 (9 decks)

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