GP 32 - Hemodynamic Disorders 4 Flashcards

1
Q

List the key differences between a clot and a thrombus.

A
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2
Q

What are lines of Zahn?

A

Alternating pale and dark lines

Light lines - platelets and fibrin

Dark Lines - RBCs

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3
Q

T/F - anti-coagulants are the apropriate treatment for thrombi

A

Partly True

Arterial thrombi are mostly platelets so anti-coagulants are useful for dissolving them. However, after some time, the fibrin in these thrombi begin to cross-link and it becomes less susceptible to anti-coagulants.

Venous thrombi are mostly RBCs so anti-coagulants are not useful for dissolving them

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4
Q

Describe the possible fates of a thrombus

A
  1. Resolution - thrombus is dissolved
  2. Embolization - thrombus breaks off and lodges somewhere else
  3. Organization - the endothelium, fibroblasts, and smooth muscle cells begin to grow around the thrombus causing:
    1. First - recanalization
    2. Second - incorporation into vessel wall
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5
Q

List the most commonly seen arterial thrombi in order

A
  1. Coronaries
  2. Carotids, cerebral
  3. Femoral
  4. Mesenteric
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6
Q

List the special thrombi names we need to know and where they’re found?

A

Mural Thrombi - thrombi that form in cavities like a heart chamber or aneurysm

Occlusive - thrombi that form in smaller arteries and cause occlusions

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7
Q

How can venous thrombi be distinguished from arterial thrombi? Where do venous thrombi typically form and how often do they embolize?

A
  • Venous thrombi take the shape of the vessels in which they form, arterial thrombi do not
  • Redder than arterial thrombi

Most venous thrombi form in the deep veins of the legs and often embolize due to muscle contractions

Some thrombi form in the superficial veins of the legs, forming varicosities. These rarely embolize

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8
Q

What percentage of thrombi formations are asymptomatic?

A

50%

due to collaterals

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9
Q

What is Trousseau’s Syndrome? What is it indicative of?

A

Unexplained and recurrent thrombophlebitis. This is a common feature of thrombus and is often indicative of an underlying abdominal malignancy, like pancreatic cancer.

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10
Q

What are the general effects of thrombi on organs?

A

For arterial thrombi, it depends on the thrombus progression:

  • If acute (or it embolizes), it will cause an infarct and necrosis
  • If slow, it will cause atrophy and fibrosis

For Venous thrombi

  • It will cause edema and congestion which, if bad enough, can cause occlusion of a nearby artery
  • If it embolizes, it will most likely end up in the lungs
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11
Q

What are the commonest forms of embolism?

A
  • Deep leg vein thromboembolism to the lungs. However, most of these are asymptomatic.
  • The most common clinically significant embolism is a thromboembolism from the heart to the legs or brain
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12
Q

Describe the severity classification system for pulmonary embolisms.

A
  • Massive - sudden obstruction of 60% of pulmonary vasculature causing sudden death. No time to develop infarction
  • Major - multiple medium sized vessels occuled causing dyspnea and pain, Infarction in only 10% of tissues due to collateral circulation
  • Minor - small vessels obstructed. Embolism will get lysed as treatment. Asymptomatic
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13
Q

What is a fat embolism and what usually cause it? What are the general symptoms?

A

A fat embolism is when fat globules enter the circulation, aggregate with platelets, and then lodge themselves somewhere.

Usually caused by bone trauma rupturing the marrow vascular sinusoids or venules, releasing fat globules. Also caused by damage to subcutaneous tissue and burns

Usually asymptomatic

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14
Q

What is fat embolism syndrome?

A

While fat embolisms are typically asymptomatic, if the embolism is large and widespread enough, fat embolism syndrome can appear 1 to 3 days after the injury. It is characterized by:

  • Pulmonary Insufficiency
  • Neurologic Symptoms
  • Anemia (RBCs get trapped in embolism)
  • Thrombocytopenia (WBCs get trapped in embolism)

All of this causes tachypnea, dyspnea, tachycardia, petechiae, irritability, restlessness, and/or delirium/coma

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15
Q

How are fat emboli diagnosed?

A
  • Fat globules in sputum or urine
  • Postmortem - H&E slide wil show round empty spaces in the thrombus (where the fat cells were washed out during prep). Refer to image.
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16
Q

What is Caisson’s disease and how is it treated?

A

Caisson’s disease is more chronic form of a nitrogen embolism where persistent gas emboli form in the bones, leading to necrosis of the femur, tibia, and humerus. It is treated with a pressure chamber and slow decompression.

17
Q

What is a bone marrow embolism?

A

Similar to a fat embolism. Typically seen in small pulmonary vessels and is usually caused by vigorous cardiac resuscitation. Is usually an incidental finding at autopsy, not a cause of death.

18
Q

What is the cause of an amniotic fluid embolism?

A

Amniotic fluid, squames (flakes of skin), hair, or meconium entering the venous circulation of the mother during childbirth.

19
Q

What is an infarction and what are the major causes?

A

An infarction is an area of ischmic necrosis caused by occlusion of either the arterial suppy or venous drainage.

  • 99% are caused by thrombotic or embolic events
  • Hemorrhage in atherosclerotic plaque
  • Torsion of vessels
  • Hypoperfusion
  • Vasculitis
20
Q

List and describe the two major types of infarcts. In which situations are these infarcts seen?

A
  • White Infarcts (pale) - infarcts with very little bleeding. Usually seen in the solid organs (kidney, spleen, heart) when an artery is occluded and there are no collaterals
  • Red Infarcts - infarcts with a large amount of bleeding. Usually seen in soft organs with tissue spaces (lungs), when there are anastomosing vessels, when it’s a venous infarct, and/or when flow is reestablished after arterial occlusion and necrosis.
21
Q

Describe the morphology of infarcts.

A
  • Gross
    • Wedge shaped with occluded vessel at apex
    • Initially congested with ill defined margins but will develop a rim of hyperemia
    • Later brown due to hemosiderin
  • Micro
    • Ischemic coagulation necrosis

If it becomes septic an abscess will form

22
Q

Describe the evolution of a cerebral infarct

A
  • 12 hours - coagulation necrosis starts
  • 48 hours - edema of the infarcted region causes increased ICP
    • Microglia engulf necrotic material, becoming Gitter Cells
    • Further breakdown leads to liquefactive necrosis, cyst formation, and the thickening of the overlying meninges called gliosis.
23
Q

What is the type of necrosis seen with MI?

A

Coagulative