Exam 1; Edema/Congestion/Hemostasis Flashcards

1
Q

This causative agent of edema can be caused by impaired venous return (mechanical obstruction, congestive heart failure)

A

increased hydrostatic pressure

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2
Q

This causative agent of edema can be caused by reduced protein synthesis (cirrhosis) and and increased loss of protein (nephrotic syndrome)

A

reduced plasma osmotic pressure

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3
Q

This causative agent of edema can be caused by fibrosis, parasites, cancer, and compression

A

lymphatic obstruction

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4
Q

This causative agent of edema can be caused by acute impairment of renal function and decreased renal perfusion with release of renin (CHF)

A

sodium and water retention

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5
Q

This causative agent of edema can be caused by increased vascular permeability, necrosis, or angiogenesis

A

inflammation

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6
Q

This term refers to generalized and usually severe increase in fluid

A

anasarca

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7
Q

This type of edema impairs gas exchange

A

pulmonary edema

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8
Q

This type of edema causes compression and herniation of critical areas, decreases blood flow

A

cerebral

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9
Q

This is the collection of fluid in a body cavity or space

A

effusion

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10
Q

This is an increased tissue blood volume secondary to neurogenic mechanisms or inflammation (active)

A

hyperemia

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11
Q

This is the increased tissue blood volume secondary to improved venous return (passive)

A

congestion

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12
Q

What are some examples of congestion

A

acute pulmonary congestion
chronic pulmonary congestion with hemosiderin; laden macrophages
chronic hepatic congestion produces the gross appearance of “nutmeg” pattern due to blood in the centrizonal sinusoids
acute hepatic congestion can lead to ischemic necrosis of centrizonal hepatocytes

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13
Q

This is the loss of blood secondary to vessels injury or physical disruption

A

hemorrhage

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14
Q

This type of hemorrhage is a large mass (tumor) of blood

A

hematoma

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15
Q

What are the measurements of ecchymosis, purport, petechia

A

ecchymosis; ≥1 cm (bruise)
purpura; 0.3-0.9 cm (3-9mm)
petechia; 1-2 mm (pinpoint)

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16
Q

This can lead to shock

A

acute hemorrhage of >20% of blood volume

17
Q

Chronic blood loss can lead to what

A

iron deficiency anemia

18
Q

This is the rapid arrest of blood loss at the site of injury

A

hemostasis

19
Q

What are the three properties of the endothelium component of hemostasis

A

anticoagulant
antithrombotic
prothrombic

20
Q

What are the characteristics of the anti-thrombotic properties of endothelium

A

barrier from ECM

prostacyclin inhibits platelet adhesion

21
Q

What are the characteristics of the anti-coagulant properties of endothelium

A

heparin-like molecules allows anti-thrombin III to inactivate thrombin, Xa, and other factors
thromomodulin binds to thrombin and this complex activates protein C
synthesis of protein S
synthesis of tissue plasminogen activator

22
Q

What are the characteristics of the pro-thrombic properties of endothelium

A

von Willebrand factor is a cofactor for binding platelets to collagen
tissue factor is secreted after exposure to cytokines (referred to endothelial activation) and initiates the extrinsic clotting pathway
inhibits plasminogen activity

23
Q

What are the three phases of the platelet characteristic of homestasis

A

adhesion
secretion
aggregaition

24
Q

This phase is mediated by von Willebrand factor which bridges collagen and a surface platelet receptor (glycoprotein Ib)

25
This phase is when there is the release of contents from both types of granules.
secretion
26
This mediates platelet aggregation and Ca is required for the coagulation cascade
ADP
27
There is surface expression of this which is a binding site for calcium and coagulation factors
phospholipid complex
28
This is stimulated by ADP and thromboxane A2; thrombin derived from the coagulation cascade binds to a platelet surface receptor enhancing this property and platelet contraction
aggregation
29
This binds the platelet surface receptor GP IIb-IIIa and the platelet plus becomes cemented by fibrin
fibrinogen
30
This is a series of enzymatic conversion of inactive proenzymes to activated enzymes
coagulation cascade
31
The binding of calcium, active enzyme cofactor and substrate (the proenzyme) occurs where
at the phospholipid complex on platelet membranes
32
This is activated by tissue factor
extrinsic system
33
This is activated by factor XII
intrinsic system
34
What are the final products to the extrinsic and intrinsic systems
thrombin and fibrin
35
What controls excess coagulation
anti-thrombins, they inhibit the activity of thrombin and other coagulation factors, and protein C and S which inactivate factors Va and VIIIa
36
This occurs by the activation of plasmin from plasminogen by TPA
fibrinolysis
37
This breaks down fibrin to form fibrin split products
plasmin