Hemodynamic Disorders Flashcards

(13 cards)

1
Q

He most asks

A

Hemostasis is a precisely orchestrated process involving platelets, clotting factors, and endothelium that occurs at the site of vascular injury and culminates in the formation of a blood clot, which serves to prevent or limit the extent of bleeding

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2
Q

Hemorrhagic disorders

A

Disorders associated with abnormal bleeding from primary or secondary defects in vessel walls, platelets, or coagulation factors, all of which must function properly to ensure hemostasis. The presentation of abnormal bleeding varies widely.

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3
Q

Thrombi

A

Thrombi can develop anywhere in the cardiovascular system and vary in size and shape depending on the involved site and the underlying cause. Arterial or cardiac thrombi usually begin at sites of turbulence or endothelial injury, whereas venous thrombi characteristically occur at sites of stasis. Thrombi are focally attached to the underlying vascular surface, particularly at the point of initiation. From here, arterial thrombi tend to grow retrograde, while venous thrombi extend in the direction of blood ow; thus both propagate toward the heart. The propa- gating portion of a thrombus is often poorly attached and there- fore prone to fragmentation and embolization.

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4
Q

Thrombi appearance

A

grossly and microscopically apparent laminations called lines of Zahn, which are pale platelet and brin deposits alternating with darker red cell–rich layers. Such laminations signify that a thrombus has formed in owing blood; their presence can therefore distinguish antemortem clots from the bland nonlaminated clots that occur postmortem

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5
Q

Mural thrombi

A

Occurring in heart chambers or aortic lumen. Abnormal myocardial contrac- tion (arrhythmias, dilated cardiomyopathy, or myocardial infarc- tion) or endomyocardial injury (myocarditis or catheter trauma) promotes cardiac mural thrombi (Fig. 4-13A), while ulcerated atherosclerotic plaque and aneurysmal dilation are the precur- sors of aortic thrombi

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6
Q

Arterial thrombi

A

frequently occlusive; the most common sites in decreasing order of frequency are the coro- nary, cerebral, and femoral arteries. They typically consist of a friable meshwork of platelets, brin, red cells, and degenerating leukocytes. Although these are usually superimposed on a rup- tured atherosclerotic plaque, other vascular injuries (vasculitis, trauma) may be the underlying cause.

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7
Q

Vegetations

A

Thrombi on heart VALVES. Bloodborne bacteria or fungi can adhere to previously damaged valves (e.g., due to rheumatic heart disease) or can directly cause valve damage; in either case, endothelial injury and disturbed blood ow can induce the formation of large thrombotic masses (infective endocarditis; Chapter 12). Sterile vegetations can also develop on noninfected valves in persons with hypercoagulable states, so-called nonbacterial thrombotic endocarditis (Chapter 12). Less commonly, sterile verrucous endocarditis (Libman-Sacks endocarditis) can occur in the setting of systemic lupus erythematosus

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8
Q

Venous thrombosis

A

phlebothrombosis) is almost invari- ably occlusive, with the thrombus forming a long luminal cast. Because these thrombi form in the sluggish venous circulation,they tend to contain more enmeshed red cells (and relatively few platelets) and are therefore known as red, or stasis, thrombi. Venous thrombi are rm, are focally attached to the vessel wall, and contain lines of Zahn, features that help distin- guish them from postmortem clots (see later). The veins of the lower extremities are most commonly involved (90% of cases); however, upper extremities, periprostatic plexus, or the ovarian and periuterine veins can also develop venous thrombi. Under special circumstances, they can also occur in the dural sinuses, portal vein, or hepatic vein.

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9
Q

Fates of thrombi 3

A

Propagation, embolization, dissolution

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10
Q

Thrombi come to clinical attention when

A

when they obstruct arteries or veins, or give rise to emboli

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11
Q

Infarction

A

An infarct is an area of ischemic necrosis caused by occlusion of either the arterial supply or the venous drainage. Tissue infarction is a common and extremely important cause of clinical illness.

Arterial thrombosis or arterial embolism underlies the vast majority of infarctions.

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12
Q

White infarcts

A

White infarcts occur with arterial occlusions in solid organs with end-arterial circulation (e.g., heart, spleen, and kidney), and where tissue density limits the seepage of blood from adjoining capillary beds into the necrotic area.

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13
Q

Red infarcts

A

occur (1) with venous occlusions
(e.g., testicular torsion, Chapter 19), (2) in loose, spongy tissues (e.g., lung) where blood can collect in the infarcted zone, (3) in tissues with dual circulations (e.g., lung and small intestine) that allow blood to ow from an unobstructed parallel supply into a necrotic zone, (4) in tissues previously congested by sluggish venous out ow, and (5) when ow is reestablished to a site of previous arterial occlusion and necrosis (e.g., following angioplasty of an arterial obstruction).

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