Download PATHOLOGY

PATHOLOGY
周
韧
ZHOU REN
Prof., M.D.,Ph.D.
Institute of Pathology & Forensic Medicine
Department of Pathology & Patho-physiology,
Zhejiang University Judicial Evidence & Evaluation Center
Zhejiang University School of Medicine
Chapter 3.
Disorder of vascular flow
Disorder of vascular flow may be divided
into general and local categories.
The local disorders contain:
①Derangement of local blood volume:
hyperemia and ischemia,
②Derangement of blood properties and
content: thrombosis, embolism and
infarction.
③Derangements of vascular permeability
and anatomic integrity:
edema, hemorrhage.
Hyperemia
Def. Hyperemia refers to a local
increased volume of blood caused by
dilatation of the small vessels.
1. Arterial hyperemia (active hyperemia)
It results from an augmented arterial
inflow, such as occurs in the muscles
during exercise, at sites of inflammation,
and in the pleasing neurovascular
dilatation termed blushing.
Active hyperemia causes increase of the
volume of local tissue, of the
metabolism and function of the organ.
It is beneficial to the organism. Active
hyperemia of body surface shows red in
color and increase in local temperature.
2. Venous hyperemia (passive
hyperemia, congestion)
It results from diminished venous flow
such as follows cardiac failure or
obstructive venous disease.
Etiology
(1)Compression on vein
(2)Intravenous obstruction
(3)Cardiac failure
Morphology
Congested organ increases in size and
weight, solidifies in consistence, and
shows dark color and capsular stiffness.
Chronic congestion of lung
Chronic congestion of liver
Chronic congestion of liver
Hemorrhage
Def. Hemorrhage refers to
extravasation of blood caused by
rupture of blood vessel.
Hematoma: Accumulation of large
amount of blood within the tissue of the
body.
Hemothorax, hemopericardium,
hemoperitoneum, hemarthrosis:
blood accumulation in body cavities as
thoracic cavity, pericardial cavity,
Peritoneal cavity and arthritic cavity
respectively.
Petechiae: Minute hemorrhage into
skin, mucous membrane or serosal
surface.
Purpura: Slight larger hemorrhage.
Ecchymosis: A large subcutaneous
hematoma.
Thrombosis
Def. Thrombosis refers to the process of
formation of an adherent clotted mass
of blood within the cardiovascular
system in a living body.
1. Factors and mechanism of thrombosis
(1)Endothelial injury
On the one hand, endothelial cells possess
antiplatelet, anticoagulant, and fibrinolytic
properties; on the other hand they exert
procogulant functions.
Intact endothelium insulates the blood
platelets and coagulation proteins from
the highly thrombogenic subendothelial
components, principally collagen.
Damage to vascular endothelium is the
dominant influence thrombogenesis,
and the only one which, by and of itself,
may lead to thrombus formation. It may
occur in the following situations:
ulcerated atherosclerotic plaques;
vascular traumatic or inflammatory
injury; endocardium in the site of
myocardial infarction or myocarditis.
(2)Alteration of blood flow (stasis and
turbulence)
In normal laminar blood flow, all of the
formed elements are separated from the
endothelial surface by a clear plasmatic
zone.
①disrupt laminar flow and permit
platelets to come into contact with the
endothelium;
②prevent dilution of activated clotting
factors to subcritical concentrations;
③retard the inflow of clotting factor
inhibitors;
④permit the build-up of platelets aggregates
and nascent fibrin either in the sluggish
stream or in the pockets of stasis;
⑤promote endothelial cell hypoxia and injury,
predisposing to platelet and fibrin deposition
as well as reducing release of TPA;
⑥the turbulence is a mechanism for endothelial
injury.
(3)Hypercoagulability
Hypercoagulability can be defined as an
alteration of the blood or , specifically, the
clotting mechanism that in some way
predisposes to thrombosis.
Hypercoagulability can be seen in many
clinical settings such as severe trauma, burns,
disseminated cancer, long term use of oral
contraceptives.
Morphogenesis of thrombi
①Endotbelial injury→platelets adhesion
and aggregation. Platelets
activation→release reaction (ADP,
TxA2, 5-HT)→platelet aggregation.
②Intrinsic and extrinsic coagulation
sequence:
prothrombin→thrombin
↓
fibrinogen ———→fibrin
White thrombus (head of thrombus):
dry, friable gray mass
transection: darker gray lines of platelets
(Zahn’s line)
H. Platelet trabeculae formation
z
mixed thrombus (body)
White thrombus intermingled with red
thrombus
z
Dark red in color, laminations are not
well developed and composed of RBC
and fibrin
z red thrombus (tail) :
3. Types of thrombi
(1)Arterial thrombi
①Mural thrombi
②Ball thrombi
③Occlusive thrombus
(2)Venous thrombus
(3)Vegetations
The potential outcomes of thrombus:
(1)Softening, liquefaction and absorption
(2)Detachment of thrombus followed by
thromboembolism
(3) Organization and recanalization
(3) Organization and recanalization
(4)Calcification
Microcirculatory Thrombosis(DIC)
Def. Widespread thrombosis in the
microcirculation is referred to
disseminated intravascular
coagulation(DIC).
Etiology and mechanism DIC is not a
primary disease, rather, it is a
complication of some underlying
diseases (trauma, severe infection,
shock, carcinoma etc.) which activate
the processes involved in blood
clotting.
The simplest mechanism involves the
release of tissue factor into the
circulation, for example, from the
placenta in obstetric complication.
Carcinomas may also release other
thromboplastic substances such as
proteolytic enzymes etc.
Morphology The microthrombi are
composed of platelets and fibrin and
are found principally in the arterioles
and capillaries of the kidney, adrenals,
brain and heart.
The bleeding tendency is probably
attributable to the rapid consumption of
platelets and clotting factors; hence DIC
is sometimes also referred to
defibrillation syndrome or consumption
coagulopathy.
Embolism
Def. Embolism refers to occlusion of
some part of the cardiovascular system
by any foreign mass carried there in the
blood stream. The transported mass is
called as embolus.
1. Routes of embolus transportation
(1)Arterial emboli induce embolism in
brain, kiney, spleen and lower limbs.
(2)Venous emboli usually lodge in the
lung.
(3)Paradoxical embolism: In case of
congenital septum defect of the heart,
venous emboli may enter from the right
into the left heart chambers.
(4)Retrograde embolism: Emboli
occasionally may travel against the
direction of blood flow.
2. Types of emboli
(1)Thromboembolism
①Pulmonary embolism most
commonly originates from thrombus of
lower limb. The prognosis depends on
the size of the occluded vessel and the
status of the patient’s cardiovascular
system.
Large embolus: fatal.
Mechanical obstruction + severe strain
on the right side of the heart (acute cor
pulmonale) + reflexive vascular and
bronchial spasm.
Small emboli obstruct small branches of
pulmonary artery: The thrombi can be
resolved and so of little significance.
If bronchial circulation is insufficiency
(chronic passive congestion of lung),
small emboli may produce either
pulmonary hemorrhage or infarction
②Arterial embolism
Origin: Emboli usually arise from
mural thrombi in the left ventricle or
atrium, from vegetations on the left side
valves, and occasionally from thrombi
on the aorta.
Morphology: They produce occlusion of
blood stream most frequently in the
spleen, the kidneys, the brain, and
lower extremities, often with resultant
infarcts in the organs and gangrene in
the limbs.
(2)Fat embolism
Etiology: Fracture of the shafts of long
bones, soft tissue trauma, burns.
Morphology:
Sequences: The prognosis of fat
embolism depends on the quantity and
site of embolism.
①Pulmonary fat embolism:
9～20g fat→75% pulmonary arteries
are occluded→pulmonary edema,
hemorrhage, atelectasis→asphyxia,
right sided heart failure.
②Lung-brain-kidney-skin embolism
syndrome
(3)Gas embolism
①Air embolism
Etiology: As a complication of trauma
(chest), cardio-thoracic surgery, various
diagnostic or therapeutic procedures, or
rupture of veins during delivery.
Sequences:
Small volume: absorbed
>100ml: acute distress.
>300ml: fatal due to pulmonary
embolism.
②Decompression sickness (cassion disease)
Etiology and mechanism: Decompressed
rapidly from high atmospheric pressure to a
normal level of pressure (in deep sea divers,
in underwater construction workers) or from
normal atmospheric pressure to a low
pressure (in aviators)→Gas comes out of
solution in the blood, tissue fluid, and fat, in
the form of minute bubbles which are
composed of O2, CO2 and nitrogen. The
nitrogen is of low solubility and persists as
minute bubbles.
(4)Amniotic fluid embolism
Etiology and mechanism: After rupture of
membranes, some of the amniotic fluid
may be forced by vigorous uterine
contractions between the membranes
and the uterine wall and then up to the
placentar margin to enter the uterine
sinusoids.
It is now suspected that vasoactive
substances within the amniotic fluid
such as prostaglandins may be the
cause of pulmonary vasoconstriction.
Morphology: The classic findings in the
pulmonary arteries and capillaries at
autopsy are epithelial squames from
fetal skin, lanugo hairs, fat from vernix
caseosa, and mucin, presumed to be
from the fetal GIT.
Infarction
Def. Ischemic necrosis of tissue or organ
caused by occlusion of either its arterial
supply or its venous drainage is
referred to infarct, the process of infarct
formation is called as infarction.
1. Causes and factors that condition
the development of an infarct
(1)Nature of vascular supply
①Effective anastomosis
②Double blood supply (liver, lung etc)
(2)Rate of development of occlusion
(3)Vulnerability of the organ or tissue to
hypoxia
(nerve cells, myocardial muscle>fibroblasts)
(4)Oxygen carrying capacity of blood:
The anemia or cyanotic patient tolerates
arterial insufficiency less well than does
the normal person.
2. Types
(1)White infarct: It result of arterial
occlusion, commonly seen in compact,
solid organs with less collateral
circulation, such as the kidneys, spleen
and heart.
(2)Red infarct:
Red infarct of intestine: Limited venous
outflow due to vascular obstruction +
by pass channels can’t develop.
3. Morphology
G. All infarcts, red and white, tend to be
wedge shape, the occluded vessel at the
apex and the periphery of the organ
forming the base.
Shortly after the vascular obstruction,
the area involved becomes red and
congested as a result of dilatation of the
vessels and flowing of blood into the
part from adjacent vessels. Hemorrhage
occurs as a result of ischemic damage to
vessel wall.
Compact organs have relative little
hemorrhage, the necrotic area is
gradually decolorized (rbc are lysed
and removed from the area), and
appears pale or yellow-white (white
infarct).
Organs of soft, loose tissue with double
supply, infarcts tend to remain
hemorrhagic (Red infarct)
Pulmonary hemorrhagic infarct
H. Necrotic tissue surrounding with
hyperemic and hemorrhagic zone.
* Septic infarct: When an infarct is
produced by a septic embolus, the
infarct is converted to an abscess.
4. Fate of infarct
(1)Small infarct: softened, absorbed
(2)Large infarct: organization and scar
formation
(3)Septic infarct: abscess formation
(4)Infarction of brain, myocardium or
lung: sometimes may cause sudden
death.