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ASF Block 1, MUSC '13 > 9/4/13 > Flashcards

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

A

opposite

18
Q

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

A

same

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

A

DVT

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

A

60%

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

A

arterial

25
Q

Most systemic thromboembolism originate from

A

cardiac mural thrombi

26
Q

How does paradoxical emboli occur

A

A thrombus in the vein becomes an embolus–> right atrium–> right ventricle–> left ventricle via an interventricular septal defect–> systemic distribution

27
Q

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

A

Fat embolism syndrome

28
Q

Amniotic fluid embolism can lead to this because of the presence of fetal substances

A

Disseminated intravascular coagulation

29
Q

What are the two types of infarcts

A

Red (soft tissue, secondary blood supply), White (solid organs, single arterial supply)

30
Q

Infarcts leads to mostly this type of necrosis

A

Coagulative necrosis

31
Q

Systemic hypoperfusion is a common outcome in

A

shock

32
Q

Cardiogenic shock can result from

A

MI, Ventricular rupture, arrhythmia

33
Q

Obstructive shock can result from

A

pulmonary embolism, cardiac tamponade

34
Q

Describe the process of Endotoxic shock

A

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
Q

What are the three stages of shock

A
  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

ASF Block 1, MUSC '13 (9 decks)

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