Hemodynamic Disorders

and Thrombosis
Lucy Xu
 Contents
 Congestion
 Thrombosis
 Embolism
 Infarction
 Hyperemia and congestion
 A local increased volume of blood in a
particular tissue.
 Arterial hyperemia (hyperemia) :
 active
 Hyperemia
 Result from: augmented blood flow due to
arteriolar dilation.
 Inflammation
 Post-ischemic
 Blush

 Red, warm and large

 Not last long time
What is congestion?
 Congestion
 The dilation of veins and capillaries due to
impaired venous drainage results in passive
venous hyperemia, commonly referred to as
congestion.
 Congestion
 Local congestion: obstruction
 External pressure
 Intraluminal occlusion

 Systemic congestion
 Heart failures
 Diseases of lungs
 Congestion
 Bloody and wet
 The affected part is red-blue color owing to d
eoxgenation of impounded red cells—cyanosi
s.

Normal kidney Nephritic congestion

 Chronic congestion
 The stasis of poorly oxygenated blood
 Chronic hypoxia
 Parenchymal cells’ degeneration or death

 Capillary rupture
 Small foci of hemorrhage
 Hemosiderin-laden macrophages
 Chronic congestion
degeneration
(fatty change)

hemorrhage

atrophy or death
Hemosiderin-laden macrophages

Red cells
Hemosiderin-laden
macrophages
Macrophage
Chronic congestion

Hemosiderin-laden macrophages
 Chronic pulmonary congestion

Left ventricular failure

Brown induaration of lungs

pigmentation and fibrosis
 Chronic pulmonary congestion
 Alveolar spaces are not empty
 Edema
 Red blood cell
 Hemosiderin-laden

macrophages
(heart failure cell)
 Chronic pulmonary congestion
 Septa thickened and fibrotic
Dilation and
Normal congestion
structure of capillary Fibrosis of alveolar septa

Sketch map of alveolar septa capillary congestion

 Chronic pulmonary congestion

Dilation and congestion

of alveolar septa
capillary, alveolar spaces
contain exudation and
edema liquid

The septa have become thicke

ned and fibrotic, and the alveol
ar spaces contain hemosiderin
pigment
 Chronic congestion of liver
 Right ventricular failure
 Veins and sinusoids
 Distend
 Full of blood

 Liver cells
 Degeneration
 Death
Chronic congestion of liver

Vein and sinusoids distend and full of blood

Chronic congestion of liver

Central hepatocytes show atrophy or death; Th

e peri portal hepatocytes experience less severe
hypoxia and may only develop fatty change. (be
tter oxygenated because of their proximity to he
patic arterioles)
Chronic congestion of liver

red

yellow
 Chronic congestion of liver
 Nutmeg liver

Blood cells: red/black; Fatty change: yellow

Yellow stripes alternated with red stripes on
the section surface of the liver
 Hepatic fibrosis

In severe and long-standi

ng hepatic congestion there m
ay even be grossly evident he
patic fibrosis.

Congestive hepatic cirrhosis

 Chronic congestion of liver

Macroscopic
Nodular on liver surface

Microscopic
Fibrosis of liver tissue
Thrombosis
 Thrombosis
 Thrombosis is a pathologic process
 which represents the formation of a blood cl
ot (thrombus)
 within the unruptured cardiovascular system
.
 Virchow’s triad
 Endothelial injury (most important).
 Alterations in normal flow.
 Hypercoagulability.
 Endothelial injury
 Exposure of subendothelial collagen
 Adherence of platelets
 Release of tissue factor
 Elaborate greater amounts of procoagulant f
actors and smaller amounts of anticoagulant
effectors
Endothelial injury
 Alterations in normal flow
Normal flow Disrupt laminar flow and
bring platelets into contact
with the endothelium
Axial flow

Plasma

Endothelium

Plasma and platelet

elements mixed
 Alterations in normal flow
 Platelets activated by contact with endotheli
um.
 Turbulence may induce endothelial injury
 Arterial or cardial thrombi : turbulence
 Venous thrombi : stasis
 Hypercoagulability
 Definition: Alteration in the hemostatic bala
nce between blood fluidity and clot formatio
n.
 This is acquired disorders which shift this ba
lance toward excessive or inappropriate plat
elet aggregation and fibrin formation and pr
edispose to thrombosis.
 Hypercoagulability
 Prolonged bed rest or immobilization.
 Myocardial infarction. Cardiac failure.
 Tissue damage (surgery, fractures, burns).
 Cancer.
 DIC.
 Fibronolysis is not enough.
Forming process of thrombi

Endothelial injury
Platelets adhered and aggregated
Fibrin / leucocytes / red cells
The vessel is obstructed
Blood coagulation
 Thrombus
 Thrombus may develop anywhere in the
cardiovascular system:
 Veins
 Arteries
 Within the cardiac chambers
 On valve cusps
 Capillaries
DVT
Varicose veins
Atherosclerosis
Aneurysm
Heart infarction
 Heart failure

Mural thrombus
Mitral valves
Infection
 Types of thrombus
 White thrombus
 Mixed thrombus
 Red thrombus
 Hyaline thrombus
 White thrombus
 White thrombus (rapid moving blood flow)
 Vegetations
 Arterial thrombus

 Head of thrombus
 Firm and pale
 Platelets and fibrin meshwork
Vegatations

Rheumatic valve vegetation

Small white and line up
Arterial thrombus

Arterial thrombus
Usually begin at a site of endothelial injury
Tend to grow in a retrograde direction
from the point of attachment
White thrombus

Mesh of platelets and fibrin

 Mixed thrombus
 Mixed thrombus (slowly moving blood flow)
 Venous thrombus (low extremities)
 Propagating thrombus

 Body of thrombus
 Lines of Zahn
 Platelets and fibrin meshwork
 Blood cells
 Mixed thrombus

Venous thrombus extend in the direction of blood flow

Mixed thrombus
Mixed thrombus
Mixed thrombus

Lines of Zahn
Light-staining: aggregated platelets admixed
with fibrin meshwork
Dark-staining: red cells
Mixed thrombus (leg vein)
 Red thrombus
 Red thrombus (slowly moving blood flow)
 Venous thrombus
 Tail of thrombus
 Red, soft, and gelatious – dry and fragile
 Abundant red cells entrapped in fibrin mesh
work
Red thrombus

Close to blood clot

Abundant red cells, leucocytes and platelets
entrapped in fibrin meshwork
 Hyaline thrombus
 Minute thrombus (capillaries)
 Fibrinous
 DIC
 Fate of the thrombus
 Resolution
 Organization

recanalisation
 Propagation
 Embolization
 Resolution
 Thrombi activate the fibrinolytic system
 Organization
 Phagocytic cells (neutrophils and macrophag
es) appear and begin to phagocytose fibrin a
nd cell debris.
 Capillaries grow into the thrombus from the
site of its attachment.
 Fibrovascular granulation tissue is formed.
Organization
Recanalization
 Recanalisation
 The fibrovascular granulation is covered ove
r by endothelial cells.
 The thrombus is excluded from the vascular
lumen and becomes part of vessel wall.
 The new vascular channels may be able to re
-establish the blood flow, called recanalisatio
n.
Recanalisation
Recanalisation
 Propagation
 The thrombi may enlarge in size due to more
and more deposition from the constituents of
flowing blood.
 Consequence: obstruction.
Propagation
 Embolization
 Thrombi (red or mixed) may get detached.
 Released in part of completely in bloodstrea
m as emboli.
 May produce ill-effects at the site of their lod
gement.
Effects of thrombosis on the body
 Stop bleeding
 Bad effects
 Obstruction/congestion
 Infarction
 Valvular disease
 Serious bleeding / DIC