Circulatory Disturbances (Ex2) Flashcards

(32 cards)

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
Explain the resolution of hematoma (colors)
Hemoglobin (dark red/blue) is enzymatically converted to bilirubin (blue/green) and eventually into hemosiderin (gold-brown)
26
What are the components necessary for normal hemostasis or thrombosis to occur?
- vascular wall (endothelium) - platelets - coagulation cascade
27
Describe normal Hemostasis
- 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
What is a thrombus?
- 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
What is the pathogenesis of thrombosis?
- endothelial injury - alterations in blood flow - hypercoagulability (increase in coagulation factors)
30
What is an embolism? | What is an embolus?
Embolism: process of pieces of a thrombus breaking off the mass and lodging at distant sites Embolus: the mass that breaks off
31
What is Disseminated Intravascular Coagulation?
systemic reaction in which there is generalized activation of the blood coagulation system
32
What is infarction?
localized area of ischemic necrosis in a tissue or organ caused by occlusion of either the arterial supply or the venus drainage