Circulatory Disturbances (Ex2) Flashcards

1
Q

What are the roles of Vascular Endothelium in hemostasis?

A
  • anti-thrombotic and pro-fibrinolytic when normal

- pro-thrombotic and anti-fibrinolytic during injury

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2
Q

What are the roles of Vascular Endothelium in inflammation?

A
  • regulates the traffic of inflammatory cells
  • produces pro-inflammatory cytokines
  • controls angiogenesis and tissue repair
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3
Q

What are the pathomechanisms of Edema?

A
  • increased blood hydrostatic pressure
  • decreased plasma colloidal osmotic pressure
  • lymphatic obstruction
  • increased vascular permeability
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4
Q

Type of fluid in Inflammatory Edema

A

Exudate - protein rich

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5
Q

Type of fluid in Non-inflammatory Edema

A

Transudate - protein poor

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6
Q

Gross appearance of Edema

A
  • wet
  • gelatinous and heavy
  • swollen organs
  • fluid weeps from cut surfaces
  • may be yellow
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7
Q

Histological appearance of Edema

A
  • clear/pale eosinophilic staining
  • spaces are distended
  • blood vessels may be filled with RBCs
  • lymphatics are dilated
  • collagen bundles separated
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8
Q

What is Pitting Edema?

A

When pressure is applied to an area of edema, a depression or dent results as excessive fluid is forced to adjacent areas

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9
Q

What is Anasarca?

A

generalized edema with profuse accumulation of fluid within the subcutaneous tissue

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10
Q

What are the usual causes of Pulmonary non-inflammatory and inflammatory edema?

A

Non: left-sided congestive heart failure
Inflam: damage to pulmonary capillary endothelium

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11
Q

What happens in chronic pulmonary edema?

A
  • commonly associated with cardiac failure
  • alveolar walls become thickened, may lead to fibrosis
  • congestion, microhemorrhages, and accumulation of heart failure cells
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12
Q

What is Hyperemia?

A

increase of arteriole-mediated engorgement of the vascular bed
- blood is oxygenated

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13
Q

What is Congestion?

A
  • passive, venous engorgement caused by decreased outflow of blood
  • blood is not oxygenated
  • tissues dark red to blue
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14
Q

What are examples of Physiological Hyperemia?

A
  • increase blood flow to GI tract during digestion
  • increase blood flow to muscles during exercise
  • increase blood flow to skin to dissipate heat
  • involuntary increased blood flow to the face
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15
Q

What is Pathological Hyperemia?

A
  • caused by underlying pathological process, usually inflammation
  • arteriolar dilatation secondary to inflammation
  • reddening
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16
Q

What is the cause of “Nutmeg Liver”?

A
  • subacute to chronic hepatic congestion

- low-grade hypoxia and increased pressure of hepatocytes, leading to atrophy and necrosis

17
Q

What is hemorrhage by rhexis?

A

due to a substantial rent or tear in the vascular wall

18
Q

What is hemorrhage by diapedesis?

A

due to a small defect in the vessel wall or RBCs passing through the vessel wall in cases of inflammation or congestion

19
Q

What is hemorrhagic diathesis?

A

increased tendency to hemorrhage from usually insignificant injuries

20
Q

What is Hemoptysis?

A

coughing up of blood or blood-stained sputum from the lungs or airways

21
Q

What is Epistaxis?

A

bleeding from the nose

22
Q

What are agonal hemorrhages?

A

petechiae and ecchymoses associated with terminal hypoxia

- results from slaughter

23
Q

What is suffusive hemorrhage?

A

larger than ecchymosis and contiguous

24
Q

What is an organizing hematoma?

A

a central mass of fibrin and RBCs surrounded by supportive vascular connective tissue
- will eventually be phagocytosed

25
Q

Explain the resolution of hematoma (colors)

A

Hemoglobin (dark red/blue) is enzymatically converted to bilirubin (blue/green) and eventually into hemosiderin (gold-brown)

26
Q

What are the components necessary for normal hemostasis or thrombosis to occur?

A
  • vascular wall (endothelium)
  • platelets
  • coagulation cascade
27
Q

Describe normal Hemostasis

A
  • after initial injury, a brief period of arteriolar constriction occurs (augmented by endothelin)
  • platelets adhere and activate
  • activated platelets change shape (round to flat) and release secretory granules attracting more platelets and form hemostatic plug (primary)
  • tissue factor leads to activation of coagulation cascade, culminating in thrombin
  • thrombin cleaves fibrinogen to fibrin
  • fibrin and platelets form permanent plug
28
Q

What is a thrombus?

A
  • aggregate of platelets, fibrin, and entrapped blood cells
  • can result in occlusion of the vascular lumen ad embolism
  • is adhered to the vascular wall (opposite of blood clot)
29
Q

What is the pathogenesis of thrombosis?

A
  • endothelial injury
  • alterations in blood flow
  • hypercoagulability (increase in coagulation factors)
30
Q

What is an embolism?

What is an embolus?

A

Embolism: process of pieces of a thrombus breaking off the mass and lodging at distant sites
Embolus: the mass that breaks off

31
Q

What is Disseminated Intravascular Coagulation?

A

systemic reaction in which there is generalized activation of the blood coagulation system

32
Q

What is infarction?

A

localized area of ischemic necrosis in a tissue or organ caused by occlusion of either the arterial supply or the venus drainage