9/4/13 Flashcards

1
Q

When there is a vascular injury, what is the first response and what is secreted

A

neurogenic arteriolar vasonconstriction, endthelin is secreted

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2
Q

what activates platelets during a vascular injury

A

exposure to ECM

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3
Q

What are three ways that the endothelium prevents platelet aggregation

A
  1. Prevent contact with matrix,
  2. thrombin and cytokines bind to endothelial cells and release NO and PGI-2 which vasodilate and inhibit aggregation
  3. ADPase degrades ADP
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4
Q

What are three ways that the endothelium prevents coagulation factors

A
  1. antithrombin III binds to heparin like molecules and inactivates thrombin and factors XII,XI,X, and IX
  2. Thrombin binds to thrombomodulin which leads to Protein C inactivating factor V and VIII in the presence of Protein S
  3. tPA activates plasmin which cleaves fibrin
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5
Q

What promotes platelet adherence to the collagen of the ECM

A

von willebrand factor

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6
Q

What are the two specific granule types found in platelets

A

Alpha-granules (contain factor V and VIII), dense core granules (these contain histamin, serotonin, epinephrine, ADP, ATP, Ca2+)

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7
Q

During the secretion phase of prothrombotic activity, what is released and what happens

A

Ca2+ and ADP released, as granules released phospholipid surfaces of the platelet membrane become available to factors of the intrinsic pathway

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8
Q

During the aggregation phase of prothrombotic activity, what is released in addition to ADP

A

TXA2

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9
Q

What attracts macrophages and neutrophils to the site of coagulation?

A

Fibrin split products

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10
Q

Describe the intrinsic pathway of the coagulation cascade

A

Kallikrein activates XII–> activates XI–> activates IX–> activates X in the presence of VIII, Ca2+ and phospholipid surface–> common pathway

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11
Q

Describe the extrinsic pathway of the coagulation cascade

A

Tissue factor activates VII–> activates X–> common pathway

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12
Q

Describe the common pathway of the coagulation cascade

A

X activate thrombin from prothrombin in the presence of V–> thrombin cleaves fibrinogen to fibrin–> factor XIII helps stabilize the fibrin clot

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13
Q

Tissue factor pathway inhibtor inhibts which to coagulation factors

A

VII, X

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14
Q

Virchow’s triad of thrombosis formation include

A
  1. Endothelial injury
  2. Abnormal blood flow
  3. Hypercoagulability
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15
Q

Leiden factor is a mutation for which coagulation factor?

A

V, Protein C resistance

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16
Q

Lines of Zahn are typically more visible in this type of vessel

A

Artery, rapid blood flow

17
Q

Thrombus growth is (opposite/same) direction as the direction of flow in arteries

18
Q

Thrombus growth is (opposite/same) direction as the direction of flow in veins

19
Q

Describe the effects found in disseminated intravascular coagulation

A

Small thrombi formation in many tissues and organs–> coagulation proteins are used up–> fibrinolytic mechanisms are activates–> bleeding disorders evolves

20
Q

Where do most pulmonary thromboembolism originated

21
Q

Emboli that get stuck at the bifurcation of the pulmonary trunk

A

Saddle embolus

22
Q

What percentage of obstruction in the pulmonary vasculature could cause sudden death

23
Q

Why are pulmonary emboli not always fatal?

A

The lung has dual blood supply and bronchial arteries from the aorta can pick up the slack (except in the case of left-sided heart failure)

24
Q

Systemic thromboembolism arises from the (arterial/venous) system

25
Most systemic thromboembolism originate from
cardiac mural thrombi
26
How does paradoxical emboli occur
A thrombus in the vein becomes an embolus--> right atrium--> right ventricle--> left ventricle via an interventricular septal defect--> systemic distribution
27
The pathogenesis of the syndrome include mechanical obstruction as well as the release of inflammatory in response to free fatty acids and endothelial cell injury
Fat embolism syndrome
28
Amniotic fluid embolism can lead to this because of the presence of fetal substances
Disseminated intravascular coagulation
29
What are the two types of infarcts
Red (soft tissue, secondary blood supply), White (solid organs, single arterial supply)
30
Infarcts leads to mostly this type of necrosis
Coagulative necrosis
31
Systemic hypoperfusion is a common outcome in
shock
32
Cardiogenic shock can result from
MI, Ventricular rupture, arrhythmia
33
Obstructive shock can result from
pulmonary embolism, cardiac tamponade
34
Describe the process of Endotoxic shock
LPS binds to LPS binding proteins--> complex binds to CD14 (TLR4) on monocyts, macrophages, and neutrophils--> acute inflammation followed by acute phase reaction (IL-1,6, TNF)--> stimulates synthesis of coagulation proteins
35
What are the three stages of shock
1. Non-progressive--> tries to maintain CO, renin angiotensin 2. Progressive-->widespread hypoxia, anaerobic metabolism leads to lower pH 3. Irreversible stage--> further damage proceeds due to necrosis and leads to total organ failure