Fluid & Hemodynamic disorders 2

Question 0

Fibrin

Answer 0

A polymerized fibrinogen

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

Question 1

Thrombosis

Answer 1

Transformation of a fluid into a solid

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

Question 2

Thrombus pathogenesis

Answer 2

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

Question 3

what will promote thrombosis and what will counteract it

Answer 3

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

Question 4

Intravascluar coagulation is the result of interaction between:

Answer 4

1. Coagulation proteins
2. Endothelial cells
3. platelets

Question 5

Coagulation proteins

Answer 5

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

Question 6

Thrombin promotes

Answer 6

Polymerization of fibrinogen into fibrin

Question 7

Endothelial cells

Answer 7

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

Question 8

What will activate Endothelial cells to coagulate?

Answer 8

Inflammation or trauma

Cytokines also activate endothelial cells

Question 9

Patelets

Answer 9

Neutralize heparin and other anticoagulation factors
Secrete thromboxane
Coagulation stimulation

Question 10

What will degrade thrombi

Answer 10

Thrombolytic chemicals like plasmin

Question 11

Pathologic thrombus formation

Answer 11

Virchow’s Triad (predisposing factors)

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

Question 12

Virchow’s triad 1:

Answer 12

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

Question 13

Virchow’s Triad 2

Answer 13

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

Question 14

Virchow’s Triad 3

Answer 14

Hypercoagulability

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

Question 15

Intramural thrombi

Answer 15

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

Question 16

Thrombi attached to wall of heart chambers

Answer 16

Intramural thrombi

Question 17

Fibrinous growths in debilitated persons, mimics endocarditis

Answer 17

Valvular thrombi

AKA non-bacterial (marantic) or sterile thrombotic endocarditis

Question 18

Attached to arterial wall

Answer 18

Arterial thrombi cover ulcerated atheromas in aorta or coronary arteries

Question 19

Arterial thrombi cuases

Answer 19

Atherosclerosis/aneurysms

Question 20

Thrombi attached to veins

Answer 20

Venous thrombi, common in varicose veins

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

Question 21

Thrombi in arterioles, capillaries, venules

Answer 21

Microvascular thrombi

Typical of Disseminated Intravascular Coagulation (DIC)

Question 22

Thrombi in small vessels are red

Composed of tightly intermixed RBC and fibrin

Answer 22

Red (conglutination) thrombi

Question 23

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

Answer 23

Layered (sedimentation) thrombi

Question 24

What does white lines in Layered thrombi

Answer 24

Lines of Zahn

Question 25

Why is Red thrombi red?

Answer 25

Because intermixed with RBC

Question 26

What is kind of thrombi seen in varicose veins?

Answer 26

Venous thrombi

Question 27

Thrombi mimics endocarditis

Answer 27

Valvular thrombi

Question 28

Fate of thrombi depends on

Answer 28

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

Question 29

Stages of fate of thrombi 1

Answer 29

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

Question 30

Stage of thrombi 2

Answer 30

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

Question 31

Clinical correlations

Answer 31

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

Question 32

Thromboi clinical correlations: occlusion of lumen of blood vessel causes

Answer 32

Ischemia

Question 33

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

Answer 33

Myocardial infarction

Question 34

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

Answer 34

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

Question 35

Thrombus detached and free flowing in blood is called

Answer 35

Embolus

Question 36

Emboli can become lodged in arteries and lead to

Answer 36

Infarct

Question 37

Cerebral infarct

Answer 37

Stroke

Question 38

Thrombus can accelerate the development of

Answer 38

atherosclerosis

Question 39

Thrombus can become infected and break off

Answer 39

Septic emboli

Question 40

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

Answer 40

Embolus

Question 41

Plural of embolus

Answer 41

Emboli

Question 42

Infarct caused by embolus

Answer 42

Emoblism

Question 43

Thrombi carried by venous or arterial blood

Answer 43

Thromboemboli

Question 44

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

Answer 44

Liquid emboli

Question 45

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

Answer 45

Gaseous emboli

Question 46

Cholesterol, tumour cells, bone marrow

Answer 46

Solid particle emboli

Question 47

All emboli can

Answer 47

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

Question 48

Only clinically significant emboli

Answer 48

Thromboemboli all others are rare

Question 49

Where does venous emboli typically lodge and cause

Answer 49

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

Question 50

What does arterial emboli cause

Answer 50

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

Question 51

Characteristics of arterial emboli

Answer 51

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

Question 52

What does emboli lodge in middle cerebral artery cause

Answer 52

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

Question 53

What kind of emboli cause infarcts with sharp subcostal pain?

Answer 53

splenic emboli

Question 54

What kind of emboli causes infarcts with subpleural pain

Answer 54

smaller venous emboli cause pulmonary infarcts

Question 55

Painful and associated with hematuria

Answer 55

Renal infarcts

Question 56

Medical emergency, can cause gangrene of intestines

Answer 56

Intestinal infarct

Question 57

infarcts of basal ganglia

Answer 57

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

Question 58

Intestinal infarct

Answer 58

Medical emergency, can cause gangrene of intestines

Question 59

Renal infarcts

Answer 59

Painful and associated with hematuria

Question 60

Splenic emboli

Answer 60

cause sharp subcostal pain

Question 61

Infarction

Answer 61

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

Question 62

White or pale infarcts

Answer 62

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

Question 63

Red infarcts

Answer 63

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

Question 64

Fate of infarcts depends on

Answer 64

Anatomic site Circulatory status Capacity for repair

Question 65

Ischemic necrosis of Post mitotic cells

Answer 65

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

Question 66

Necrotic brain cells

Answer 66

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

Question 67

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

Answer 67

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