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General Pathology > Fluid & Hemodynamic disorders 2 > Flashcards

Fluid & Hemodynamic disorders 2 Flashcards

0
Q

Fibrin

A

A polymerized fibrinogen

Forms mesh network of thin filaments biding blood cells to form thrombus or hemostatic plug

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1
Q

Thrombosis

A

Transformation of a fluid into a solid

Clotting of whole blood into an aggregate of blood cells and fibrin

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2
Q

Thrombus pathogenesis

A

Thrombi from only in living organisms
End products of the coagulation sequence
Normally activated to prevent blood loss from disrupted vessels
If coagulation sequence activated in intact vessels pathological thromboses develop

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3
Q

what will promote thrombosis and what will counteract it

A

Clotting factors and platelets promote thrombosis
Endothelial cells and plasmin counter act it
Under normal conditions, clotting and anti-clotting are in balance.

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4
Q

Intravascluar coagulation is the result of interaction between:

A
  1. Coagulation proteins
  2. Endothelial cells
  3. platelets
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5
Q

Coagulation proteins

A

Cascade sequence of activation culminates in thrombin
Thrombin is catalyst, promoting polymerization of fibrinogen into fibrin
Meshwork of fibrin is the frame work for the clot which includes blood cells and proteins

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6
Q

Thrombin promotes

A

Polymerization of fibrinogen into fibrin

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7
Q

Endothelial cells

A

Normal resting endothelial cells have antihromboti function, but if activated, will initiate coagulation
Can initiate thrombosis
E.g. IL-1 and TNF

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8
Q

What will activate Endothelial cells to coagulate?

A

Inflammation or trauma

Cytokines also activate endothelial cells

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9
Q

Patelets

A

Neutralize heparin and other anticoagulation factors
Secrete thromboxane
Coagulation stimulation

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10
Q

What will degrade thrombi

A

Thrombolytic chemicals like plasmin

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11
Q

Pathologic thrombus formation

A

Virchow’s Triad (predisposing factors)

  1. Endothelial cell injury
  2. Hemodynamic changes
  3. Hypercoagulability of whole blood
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12
Q

Virchow’s triad 1:

A

Endothelial cell injury
Intact endothelium has anticoagulant properties
Under influence of inflammatory mediators, endothelium loses antithrombotic properties

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13
Q

Virchow’s Triad 2

A

Hemodynamic change

  • Disturb noral laminar flow resulting in turbulence and margination
  • slow blood flow results in sedimantation and blood eddies
  • small thrombi no dissolved by thrombolytic substance tend to persist or even grow in sluggish blood stream
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14
Q

Virchow’s Triad 3

A

Hypercoagulability

  • blood is hypercoagulable in severe burn victims probably due to severe fluid loss and hemoconcentration
  • also in cancer, chronic cardiac failure and pregnancy
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15
Q

Intramural thrombi

A

mural endocardium - attached to wall of heart chambers and commonly found overlying myocardial infarction

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16
Q

Thrombi attached to wall of heart chambers

A

Intramural thrombi

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17
Q

Fibrinous growths in debilitated persons, mimics endocarditis

A

Valvular thrombi

AKA non-bacterial (marantic) or sterile thrombotic endocarditis

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18
Q

Attached to arterial wall

A

Arterial thrombi cover ulcerated atheromas in aorta or coronary arteries

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19
Q

Arterial thrombi cuases

A

Atherosclerosis/aneurysms

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20
Q

Thrombi attached to veins

A

Venous thrombi, common in varicose veins

Chronic may lead to organized granulation tissue and inflammation (thrombophlebitis)

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21
Q

Thrombi in arterioles, capillaries, venules

A

Microvascular thrombi

Typical of Disseminated Intravascular Coagulation (DIC)

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22
Q

Thrombi in small vessels are red

Composed of tightly intermixed RBC and fibrin

A

Red (conglutination) thrombi

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23
Q

Distinct layering of cellular elements and fibrin (white line), in large arteries, veins, mural thrombi

A

Layered (sedimentation) thrombi

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24
Q

What does white lines in Layered thrombi

A

Lines of Zahn

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25
Q

Why is Red thrombi red?

A

Because intermixed with RBC

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26
Q

What is kind of thrombi seen in varicose veins?

A

Venous thrombi

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27
Q

Thrombi mimics endocarditis

A

Valvular thrombi

28
Q

Fate of thrombi depends on

A

Size, location, hemodynamics of vessel
Most small thrombi lysed without consequence
Larger thrombi remain attached to surface of vessel wall or endocardium

29
Q

Stages of fate of thrombi 1

A

Attachment initially mediated by adhesion molecules such as fibronectin or fibrin
Eventually thrombus can stimulate ingrowth of inflammatory cells and vessels
Granulation tissue forms firmer anchorage - organization

30
Q

Stage of thrombi 2

A

Inflammatory cells of granulation tissue dissolve the thrombus
Granulation tissue replaced by collagenous fibrous tissue
Occlusive thrombi can be recanalized
Can become break off and become emboli
Can block blood vessel leading to infarction

31
Q

Clinical correlations

A

Thrombotic occlusions of cardiac and cerebral arteries are a major cause of death in US
Clinical symptoms depend on site, extent of thrombi, rapidity with which they form, duration of thrombosis, widespread nature of disease complications

32
Q

Thromboi clinical correlations: occlusion of lumen of blood vessel causes

A

Ischemia

33
Q

Clinical correlations of thrombi: Sudden thrombotic occlusion of coronary arteries most common cause of

A

Myocardial infarction

34
Q

Clinical correlations of Thrombi: Slowly narrowing of lumen of blood vessel and decrease in blood flow results in

A

Hypoxia and reduced function of affected organ over time (Chronic heart failure)

35
Q

Thrombus detached and free flowing in blood is called

A

Embolus

36
Q

Emboli can become lodged in arteries and lead to

A

Infarct

37
Q

Cerebral infarct

A

Stroke

38
Q

Thrombus can accelerate the development of

A

atherosclerosis

39
Q

Thrombus can become infected and break off

A

Septic emboli

40
Q

A freely movable intravascular mass that is carried from one anatomical site to another by blood

A

Embolus

41
Q

Plural of embolus

A

Emboli

42
Q

Infarct caused by embolus

A

Emoblism

43
Q

Thrombi carried by venous or arterial blood

A

Thromboemboli

44
Q

fat emboli following bone fracture (femur), amniotic fluid emboli in veins

A

Liquid emboli

45
Q

Air injected into veins, air liberated under decreased pressure (caisson disease or decompression sickness)

A

Gaseous emboli

46
Q

Cholesterol, tumour cells, bone marrow

A

Solid particle emboli

47
Q

All emboli can

A

occlude blood vessels resulting in decreased blood supply to organ (ischemia)

48
Q

Only clinically significant emboli

A

Thromboemboli all others are rare

49
Q

Where does venous emboli typically lodge and cause

A

Typically lodge in pulmonary artery and cause pulmonary embolism
Smaller emboli cause pulmonary infarcts - subpleural pain

50
Q

What does arterial emboli cause

A

Common cause of ischemia in spleen, kidney, intestines
Usually originate from cardiac mural or valvular thrombi
Can also originate from aorta

51
Q

Characteristics of arterial emboli

A

Mechanically fragmented inside vessels because arterial blood flows fast and disrupts them
Therefore tend to lodge in small and medium-sized arteries
Greatest risk in cerebral circulations

52
Q

What does emboli lodge in middle cerebral artery cause

A

infarcts of basal ganglia, associated with high mortality and neurological defects

53
Q

What kind of emboli cause infarcts with sharp subcostal pain?

A

splenic emboli

54
Q

What kind of emboli causes infarcts with subpleural pain

A

smaller venous emboli cause pulmonary infarcts

55
Q

Painful and associated with hematuria

A

Renal infarcts

56
Q

Medical emergency, can cause gangrene of intestines

A

Intestinal infarct

57
Q

infarcts of basal ganglia

A

emboli in middle cerebral artery, associated with high mortality and neurological defects

58
Q

Intestinal infarct

A

Medical emergency, can cause gangrene of intestines

59
Q

Renal infarcts

A

Painful and associated with hematuria

60
Q

Splenic emboli

A

cause sharp subcostal pain

61
Q

Infarction

A

sudden insufficiency of blood supply resulting in an area of necrosis
most are caused by thrombi or thromboemboli
May be classified by origin as arterial or venous
Can be further classified by appearance as white or red

62
Q

White or pale infarcts

A

typical of solid organs
E.g. heart, kidney, spleen
Ischemic necrosis paler than surrounding tissue
Blood may infiltrate from collateral arteries resulting in mottled appearance

63
Q

Red infarcts

A

Typical of venous infarction
E.g. particulary of intestines or testes
Circulation can be interrupted by twisting organ
E.g. torsion of testes

64
Q

Fate of infarcts depends on

A

Anatomic site
Circulatory status
Capacity for repair

65
Q

Ischemic necrosis of Post mitotic cells

A

ischemic necrosis of post-mitotic cells (e.g. heart) can not be repaired -only replaced with fibrous tissue (scarring).

66
Q

Necrotic brain cells

A

can not be repaired, but liquefactive necrotic tissue resorbed. Leaves clear fluid filled cyst

67
Q

Mitotic tissues and facultative (occurring optionally in response of circumstances, but not of nature) mitotic tissue

A

heal with relatively few defects - e.g. liver, however large infarcts may be impossible to regenerate completely - leaves scarring and loss of function

General Pathology (12 decks)

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