phathology-3(disorders of blood circulation)
TRANSCRIPT
Chapter 3Chapter 3
Disorders of Vascular FlowDisorders of Vascular Flow
DURGE RAJ GHALANDURGE RAJ GHALAN Department of Pathology, The First Affiliated HospitDepartment of Pathology, The First Affiliated Hospit
al of Sun Yat-sen Universtyal of Sun Yat-sen Universty
Contents:Contents:
11 .. Hyperemia Hyperemia
2 2 . . ThrombosisThrombosis
3. Embolism 3. Embolism
4. Infarction 4. Infarction
11 . . HyperemiaHyperemia
Hyperemia means an increased volume of bHyperemia means an increased volume of b
lood in an affected tissue or organ. Capillarlood in an affected tissue or organ. Capillar
y beds are extended y beds are extended (( dilatation and opendilatation and open
ing of capillaries & venules closed in non-hing of capillaries & venules closed in non-h
yperemia stateyperemia state ))
1.1 Arterial Hyperemia1.1 Arterial Hyperemia
Arterial or active hyperemia is caused Arterial or active hyperemia is caused
by increased arterial inflow of tissues or by increased arterial inflow of tissues or
organs. organs.
Physiological: blushing for shyness, Physiological: blushing for shyness,
muscular exercisemuscular exercise
Pathological: at the beginning of the Pathological: at the beginning of the
inflammationinflammation
Inflammation inducing factorsInflammation inducing factors
( Bacterial, chemical, mechanical......etc)( Bacterial, chemical, mechanical......etc)
sympathetic neurogenic reflex (axial reflex)sympathetic neurogenic reflex (axial reflex)
& Vasoactive substances& Vasoactive substances
arteriolararteriolar dilatation dilatation
The organ in hyperemia is swollen and redder tThe organ in hyperemia is swollen and redder than in normal statehan in normal state
1.2 Venous Hyperemia 1.2 Venous Hyperemia (Congestion)(Congestion)
Venous or passive hyperemia or congestion Venous or passive hyperemia or congestion
results from block (obstruction) of venousresults from block (obstruction) of venous
drainage (outflow)drainage (outflow)
Occur systemically: in cardiac failureOccur systemically: in cardiac failure
Occur locally because the vein is blocked by the Occur locally because the vein is blocked by the
obstructionobstruction
more common and important than arterial more common and important than arterial
hyperemiahyperemia
1. Causes:1. Causes:
1) Compression of veins1) Compression of veins
• pregnant uterus — iliac vein hyperemiapregnant uterus — iliac vein hyperemia
• expansile tumors or scar tissue — leg vein hyperemiexpansile tumors or scar tissue — leg vein hyperemi
aa
• intussusception / volvulus / hernia / fibrous adhesiointussusception / volvulus / hernia / fibrous adhesio
n of intestine — mesenteric veins congestionn of intestine — mesenteric veins congestion
• cirrhosis (disturbance of lobular circulation) —portcirrhosis (disturbance of lobular circulation) —port
al vein hyperemia — gastrointestinal and spleen coal vein hyperemia — gastrointestinal and spleen co
ngestionngestion
2) Obstruction of venous lumen: venous thrombi2) Obstruction of venous lumen: venous thrombi
3) Heart failure3) Heart failure
The heart fails to expel the normal amount of The heart fails to expel the normal amount of
blood, the blood accumulate in venous systemblood, the blood accumulate in venous system
left heart failure —pulmonary congestionleft heart failure —pulmonary congestion
right heart failure —systemic venous congestionright heart failure —systemic venous congestion
Venous HyperemiaVenous HyperemiaVenule outflow decreaseVenule outflow decreaseContent of oxygen decreaseContent of oxygen decrease
Arterial HyperemiaArterial HyperemiaArteriole inflow increaseArteriole inflow increaseContent of oxygen increaseContent of oxygen increase
Normal stateNormal state
2. General features of venous hyperemia2. General features of venous hyperemia
1) Morphology1) Morphology
Grossly (macroscopically) : swollen, heavier, bluGrossly (macroscopically) : swollen, heavier, blu
e-red color (increased of deoxygenated hemogloe-red color (increased of deoxygenated hemoglo
bin), cut surface: excessively bloodybin), cut surface: excessively bloody
Body surface: cyanosis (nail, lip), lower temperaBody surface: cyanosis (nail, lip), lower tempera
tureture
Microscopically: engorgement of capillaries & veMicroscopically: engorgement of capillaries & ve
nules, minute hemorrhage; nules, minute hemorrhage;
Edema: in loose tissues or organsEdema: in loose tissues or organs
(hydrostatic pressure↑and permeability↑of capil(hydrostatic pressure↑and permeability↑of capil
laries & venules)laries & venules)
2) Chronic (long-standing) congestion may lead to 2) Chronic (long-standing) congestion may lead to
degeneration or death of parenchymal cells (livedegeneration or death of parenchymal cells (live
r) and fibrosis and hemosiderin (product of degr) and fibrosis and hemosiderin (product of deg
radation of hemoglobin) deposition. radation of hemoglobin) deposition.
3. Congestion of important organs3. Congestion of important organs
1) congestion of the lung1) congestion of the lung
Causes: Causes: left heart failure (mitral stenosis or heart infaleft heart failure (mitral stenosis or heart infa
rct, etc) —pulmonary congestionrct, etc) —pulmonary congestion
Acute pulmonary congestion: congestion of alveolar cAcute pulmonary congestion: congestion of alveolar c
apillaries, edema, minute hemorrhage apillaries, edema, minute hemorrhage
heart failure cellsheart failure cells (hemosiderin-laden macrophages) in (hemosiderin-laden macrophages) in
alveolar spacealveolar space
Symptoms: Symptoms:
Dyspnea:Dyspnea: difficult or labored breathing difficult or labored breathing
Hypoxia:Hypoxia: absent or decrease of oxygen absent or decrease of oxygen
Cyanosis:Cyanosis: A bluish or purplish discoloration of the skin and A bluish or purplish discoloration of the skin and
mucous membranes due to an increase in the amount of deoxygmucous membranes due to an increase in the amount of deoxyg
enated hemoglobin in the bloodenated hemoglobin in the blood
Bloody or tinged rusty sputum:Bloody or tinged rusty sputum: there are many red cellthere are many red cell
s in the alveolar spaces in the alveolar space
Chronic pulmonary congestion:Chronic pulmonary congestion:
congestioncongestion
fibrosis fibrosis
hemosiderin deposition (brown induration) hemosiderin deposition (brown induration)
pulmonary hypertension (fibrous thickening pulmonary hypertension (fibrous thickening
of pulmonary arterioles and arteries ) of pulmonary arterioles and arteries )
2) congestion of the Liver2) congestion of the Liver
Causes: Causes:
right heart failure —systemic congestion (pulmonaright heart failure —systemic congestion (pulmona
ry heart diseases and congenital pulmonary stenosry heart diseases and congenital pulmonary stenos
is) , such as liver congestion is) , such as liver congestion
left heart failure can lead to right heart failure (lefleft heart failure can lead to right heart failure (lef
t heart failure→pulmonary congestion →pulmont heart failure→pulmonary congestion →pulmon
ary hypertension→right heart failure) ary hypertension→right heart failure)
Morphology of Liver congestionMorphology of Liver congestion
1) central region of lobules (red-blue):1) central region of lobules (red-blue):
engorgement of central veins and blood engorgement of central veins and blood
sinusoids nearby (dilatation ) , minute sinusoids nearby (dilatation ) , minute
hemorrhage (bleeding) , atrophy and hemorrhage (bleeding) , atrophy and
necrosis of liver cellsnecrosis of liver cells
2)2) peripheral region of lobules (yellow- peripheral region of lobules (yellow-
brown)brown)
peripheral sinusoids slight congestionperipheral sinusoids slight congestion
fatty degeneration of liver cellsfatty degeneration of liver cells
Nutmeg LiverNutmeg Liver
central region dilatation, bleeding, atrophy and necrosis of central region dilatation, bleeding, atrophy and necrosis of liver cells; liver cells; peripheral sinusoids slight congestion, fatty peripheral sinusoids slight congestion, fatty degeneration of liver cellsdegeneration of liver cells
liver sinusoids dilatation, blood cells aggregateliver sinusoids dilatation, blood cells aggregate
Kupper cells laden with hemosiderin in liver sinusoidsKupper cells laden with hemosiderin in liver sinusoids
3) longstanding chronic congestion of the 3) longstanding chronic congestion of the
liver— liver— cardiac cirrhosiscardiac cirrhosis
fibrosis of center of liver lobules, extension fibrosis of center of liver lobules, extension
of fibrous tissue into peripheral of lobules of fibrous tissue into peripheral of lobules
and connection with portal areas leads to and connection with portal areas leads to
reconstruction of normal lobular reconstruction of normal lobular
structure (cardiac cirrhosis) structure (cardiac cirrhosis)
22 . . ThrombosisThrombosis
Thrombosis is the process of formation of a sThrombosis is the process of formation of a s
olid mass from constituents of the blood within volid mass from constituents of the blood within v
essels or the heart in a essels or the heart in a livingliving body body .. The solid The solid
mass is termed a thrombusmass is termed a thrombus ..
The composition of a thrombus is similar to The composition of a thrombus is similar to
the blood clot, but different in proportion of the blood clot, but different in proportion of
various componentsvarious components .. Thrombus contains Thrombus contains
more platelets and fibrin than blood more platelets and fibrin than blood
clotclot .. Thrombus forms in Thrombus forms in moving moving bloodblood ..
Vascular and cardiac endothelial injury
Slowing and turbulence of blood flow
Hypercoagulability of blood
2.1 Predisposing factors of thrombosis2.1 Predisposing factors of thrombosis
ThrombosisThrombosis
Vascular and cardiac endothelial injuryVascular and cardiac endothelial injury
It is particularly improtantIt is particularly improtant in thrombus formatioin thrombus formatio
n in the heart and arterial circulation, for example, n in the heart and arterial circulation, for example,
within the cardiac chambers when there has endocawithin the cardiac chambers when there has endoca
rdial injury (rheumatic or bacterial endocarditis, etrdial injury (rheumatic or bacterial endocarditis, et
c); over ulaerated of plaques in severely atherosclerc); over ulaerated of plaques in severely atheroscler
otic arteries; or at the site of traumatic or imflammotic arteries; or at the site of traumatic or imflamm
atory vascular injury. atory vascular injury.
Exposure of subendothelial collagens will lead to the rExposure of subendothelial collagens will lead to the r
elease of platelets activators, and consequently PL agelease of platelets activators, and consequently PL ag
gregation initiate thrombosis.gregation initiate thrombosis.
There are coagulation and fibrinolytic systems in bloThere are coagulation and fibrinolytic systems in blo
od. The balance between these two systems is very finod. The balance between these two systems is very fin
ely regulated. Exposure of subendothelial collagens wiely regulated. Exposure of subendothelial collagens wi
ll also activate the coagulative system and make the sll also activate the coagulative system and make the s
oluble fibrinogen become insoluble fibrin.oluble fibrinogen become insoluble fibrin.
Slowing and turbulence of blood flowSlowing and turbulence of blood flow
Normal blood flow in vessels Normal blood flow in vessels central stream: white, red cells central stream: white, red cells laminar stream: platelets laminar stream: platelets peripheral stream: plasmaperipheral stream: plasma Slowing and turbulence of blood flow Slowing and turbulence of blood flow · · bring platelets into contact with endotheliumbring platelets into contact with endothelium · · cause mild injury of endothelium, and collagen cause mild injury of endothelium, and collagen exposure, the collagen prevents dilution and clearance exposure, the collagen prevents dilution and clearance
of blood clotting factors in locationof blood clotting factors in location
A. VeinsA. VeinsThrombi are most commonly located in veinsThrombi are most commonly located in veinsThrombi in Low extremities accounts for 90%Thrombi in Low extremities accounts for 90%
B. Arteries and the heart B. Arteries and the heart Arteries: occur in aneurysm Arteries: occur in aneurysm Heart: Heart: Mural thrombi in Mural thrombi in left atrialeft atria occur in case of mit occur in case of mitral stenosis in rheumatic heart diseaseral stenosis in rheumatic heart disease Mural thrombi in Mural thrombi in left ventricleleft ventricle occur on the en occur on the endocardium overlying an infarct docardium overlying an infarct
Hypercoagulability of bloodHypercoagulability of blood
Increase in amount and viscosity of platelets (postpaIncrease in amount and viscosity of platelets (postpa
rtum, postoperation, post-trauma high lipid diet, cigarrtum, postoperation, post-trauma high lipid diet, cigar
ette smoking, atherosclerosis, and the release of procoaette smoking, atherosclerosis, and the release of procoa
gulant tumor product in disseminated cancers) gulant tumor product in disseminated cancers)
Increase in amount and viscosity of platelets will be seIncrease in amount and viscosity of platelets will be se
en in DIC (Disseminated Intravascular Coagulation)en in DIC (Disseminated Intravascular Coagulation)
2.2 The process of thrombosis & types of 2.2 The process of thrombosis & types of
thrombithrombi
(1)(1) TThe process of thrombosishe process of thrombosis
1)1) It initiates from adhesion of PL to exposed sub- It initiates from adhesion of PL to exposed sub-
endothelial collagens and subsequent PL endothelial collagens and subsequent PL
aggregate.aggregate. Then they develop in different ways, Then they develop in different ways,
their composition, size and shape are dependent their composition, size and shape are dependent
on their locations and speed of local blood flow.on their locations and speed of local blood flow.
Platelets adhere to the subendothelial collagens, and leaPlatelets adhere to the subendothelial collagens, and leads to degranulation, releasing serotonin, ADP,ATPds to degranulation, releasing serotonin, ADP,ATP
ADP is a powerful platelet aggregator, and will cause ADP is a powerful platelet aggregator, and will cause further accumulation of plateletsfurther accumulation of platelets
2)2) Activation of Activation of intrinsic and extrinsic blood intrinsic and extrinsic blood
coagulation cascade, soluble fibrinogen coagulation cascade, soluble fibrinogen
become insoluble Fibrin; While the become insoluble Fibrin; While the
fibrinolytic activity are preventedfibrinolytic activity are prevented
3)3) The head of thrombus is mainly composed of platelet The head of thrombus is mainly composed of platelet
trabecula with less fibrin network between PL trabecula trabecula with less fibrin network between PL trabecula
4)4) red ,white cells are trapped and form a blood plugred ,white cells are trapped and form a blood plug
5) 5) Development of thrombus Development of thrombus
(2) Types of thrombus(2) Types of thrombus
Pale (white) thrombus Pale (white) thrombus
Mixed thrombus Mixed thrombus
Red thrombus Red thrombus
Hyaline thrombus (microthrombus)Hyaline thrombus (microthrombus)
1) White thrombus : 1) White thrombus :
White thrombus is formed under high speed of bloWhite thrombus is formed under high speed of blo
od flow in arteries & heart (in heart chamber , on heod flow in arteries & heart (in heart chamber , on he
art valves). art valves).
White thrombus is mainly composed of platelet traWhite thrombus is mainly composed of platelet tra
becula with less fibrin network between PL trabeculbecula with less fibrin network between PL trabecul
a, and red and white cells trapped.a, and red and white cells trapped.
Thrombi lined on the heart Mitral valve, be gray-white and small, granulo-like. Firmly adherent to the valve. Firmly adherent to the valve.
Thrombi lined on the heart Aortic valve
White thrombus composed by platelets trabecula with less fibrin network, they are pink with pale lines in HE stained slides.
2) Mixed thrombus2) Mixed thrombus : :
Mixed thrombus is formed under slower-moMixed thrombus is formed under slower-mo
ving blood in veins and arteries (aneurysm) and ving blood in veins and arteries (aneurysm) and
heart (left atria dilated with mitral stenosis).heart (left atria dilated with mitral stenosis).
Mixed thrombus in veins can be divided intoMixed thrombus in veins can be divided into 3 3 parts parts
Head:Head: initial PL aggregate initial PL aggregate
Body:Body: platelet trabecula (gray layers, called zahn lines platelet trabecula (gray layers, called zahn lines
) and alternately separated blood clot layers) and alternately separated blood clot layers
Tail:Tail: The tail is at down stream of the thrombus body The tail is at down stream of the thrombus body
under very slow-moving blood or blood stasis, which iunder very slow-moving blood or blood stasis, which i
s composed by blood coagulates, so it can also be nams composed by blood coagulates, so it can also be nam
ed Red thrombus. The red thrombus almost or compled Red thrombus. The red thrombus almost or compl
etely occlude the venous lumen.etely occlude the venous lumen.
left ventricleleft ventricle dilate filled with mixed thrombusdilate filled with mixed thrombus
aneurysmaneurysm
platelet trabecul
platelet trabecul
aa
blood blood clotclot
3) Red thrombus: 3) Red thrombus:
red thrombus closely resembles to blood clotred thrombus closely resembles to blood clot
Mixed thrombus, especially it’s tail part (red thrombMixed thrombus, especially it’s tail part (red thromb
us) is readily to shed off (dislodge) and be carried by us) is readily to shed off (dislodge) and be carried by
blood flow to impact vessels in a distal organ (blood flow to impact vessels in a distal organ (thrombthromb
oembolismoembolism))
Thrombi in systemic veins - Pulmonary embolismThrombi in systemic veins - Pulmonary embolism
Thrombi in portal veins – Liver embolismThrombi in portal veins – Liver embolism
Thrombi in heart & aorta - spleen , kidneys, Thrombi in heart & aorta - spleen , kidneys,
brain embolism, etcbrain embolism, etc
4) Hyaline thrombus (microthrombus)4) Hyaline thrombus (microthrombus)
occur in DIC ( Disseminated Intravascular Coaoccur in DIC ( Disseminated Intravascular Coa
gulation)gulation)
microscopically , occur in microcirculation, maimicroscopically , occur in microcirculation, mai
nly composed of fibrinnly composed of fibrin
There are numerous microthrombi in the glomerular capillariesThere are numerous microthrombi in the glomerular capillaries
There are microthrombi in the alveolar capillaries. They are There are microthrombi in the alveolar capillaries. They are pink, and uniformly stainedpink, and uniformly stained
(3) The fate of thrombi(3) The fate of thrombi
softening, dissolving softening, dissolving ( in newly formed thrombi)( in newly formed thrombi)
and the vascular lumen is reestablished, it is the and the vascular lumen is reestablished, it is the
ideal end result;ideal end result;
Organization: the thrombus is displaced by Organization: the thrombus is displaced by
granulation tissue and collagen. granulation tissue and collagen.
Recanalization: the new small vessels in the granulRecanalization: the new small vessels in the granul
ation tissue proliferate and enlarge, and may establisation tissue proliferate and enlarge, and may establis
h new channels across the thrombus.h new channels across the thrombus. (in large throm(in large throm
bi)bi)
Organization and Recanalization may slightly improve tissue peOrganization and Recanalization may slightly improve tissue pe
rfusion over the long term.rfusion over the long term.
Calcification:Calcification: Calcium salt deposite in the thrombus Calcium salt deposite in the thrombus
DislodgeDislodge
Vascular wall and collagen area
out-of –date granulation tissue
a part of the thrombus
(4) The effects of thrombi to the body(4) The effects of thrombi to the body
Occlusion of vessels Occlusion of vessels
Thromboembolism Thromboembolism
Distorted cardiac valvesDistorted cardiac valves
Hemorrhage (occur in DIC)Hemorrhage (occur in DIC)
DIC DIC (Disseminated Intravascular Coagulation)(Disseminated Intravascular Coagulation)
A kind of clinical syndrome caused by multiple factorsA kind of clinical syndrome caused by multiple factors
Formation of hyaline thrombi throughout theFormation of hyaline thrombi throughout the
microcirculation.microcirculation.
Consumption of platelets and coagulation factors, Consumption of platelets and coagulation factors,
bleeding tendency bleeding tendency
3. Embolism3. Embolism
Embolism is the occlusion or obstruction of a Embolism is the occlusion or obstruction of a
vessel by an abnormal mass transported from a vessel by an abnormal mass transported from a
different site by the circulation.different site by the circulation.
An An embolus embolus is a detached intravascular solid, is a detached intravascular solid,
liquid, gaseous, or tumor cell mass.liquid, gaseous, or tumor cell mass.
3.1 Possible moving pathways of an embolus 3.1 Possible moving pathways of an embolus
depends on the sites of its origindepends on the sites of its origin
A.A. The emboli originateing from systemic vein The emboli originateing from systemic vein
entering right heart entering right heart pulmonary pulmonary
Emboli in right heart Emboli in right heart
arterial system arterial system pulmonary embolism pulmonary embolism
B.B. The emboli from left heart or main artery The emboli from left heart or main artery
entering systemic arteries entering systemic arteries lodging in lodging in
a distal systemic artery a distal systemic artery such as brain such as brain
arteriole, heart arteriole, kidney arteriole, arteriole, heart arteriole, kidney arteriole,
extremity arteriole, intestine arteriole, etc.extremity arteriole, intestine arteriole, etc.
especially in the extremity arteriole.especially in the extremity arteriole.
C.C. The emboli from mesenteric vein or portal vein The emboli from mesenteric vein or portal vein
liver embolism (rarely occur)liver embolism (rarely occur)
D.D. Crossed embolism: occur uncommonly. There is a Crossed embolism: occur uncommonly. There is a
defect in the wall between the right and the left heart defect in the wall between the right and the left heart
lumen, the thrombus in right heart lumen go directly lumen, the thrombus in right heart lumen go directly
into the left heart lumen, and consequently cause the into the left heart lumen, and consequently cause the
embolism in distant systemic organs. embolism in distant systemic organs.
There is a defect iThere is a defect i
n the interatrial sn the interatrial s
eptum, so the emeptum, so the em
bolus in right heabolus in right hea
rt go directly into rt go directly into
the left heart, and the left heart, and
consequentlyconsequently CrCr
ossed embolisossed embolis
mm formationformation
3.2 Types of Embolism3.2 Types of Embolism
(1) Thromboembolism(1) Thromboembolism
Obstruction of a vessel by a disloged thrombi thObstruction of a vessel by a disloged thrombi th
at has been transported from a distant site by the bloat has been transported from a distant site by the blo
od stream. od stream.
1) Pulmonary embolism1) Pulmonary embolism
The origin of emboli: The origin of emboli: >> 90%90% from deep leg veinfrom deep leg vein
The sequel of pulmonary embolism:The sequel of pulmonary embolism:
LargeLarge emboliemboli (several centimeters long and of the (several centimeters long and of the
same diameter as the femoral vein) may lodge in same diameter as the femoral vein) may lodge in
the outflow of the right heart ventricle or in the the outflow of the right heart ventricle or in the
main pulmonary artery , and cause circulatory main pulmonary artery , and cause circulatory
obstruction and sudden death. obstruction and sudden death.
Lodgment in a large branch of pulmonary artery Lodgment in a large branch of pulmonary artery
may also cause sudden death by severe may also cause sudden death by severe
vasoconstriction of the entire pulmonary arterial vasoconstriction of the entire pulmonary arterial
circulation. circulation.
Pulmonary embolism. The pulmonary artery has been opened Pulmonary embolism. The pulmonary artery has been opened to reveal a large thromboembolus within it.to reveal a large thromboembolus within it.
In healthy individuals, the bronchial artery In healthy individuals, the bronchial artery
supplies blood and oxygen to the lung, and the supplies blood and oxygen to the lung, and the
function of pulmonary artery is mainly gas function of pulmonary artery is mainly gas
exchange.exchange.
Medium-size emboli: Medium-size emboli: often lodge in a major often lodge in a major
branch of the pulmonary artery.branch of the pulmonary artery.
In In a normala normal person, a moderate-sized pulmonary e person, a moderate-sized pulmonary e
mbolus creates an area of lung having no gas exchmbolus creates an area of lung having no gas exch
ange function, but infarction of the lung does not oange function, but infarction of the lung does not o
ccur.ccur.
In a patient In a patient with severe pulmonay hyperemiawith severe pulmonay hyperemia, the p, the p
ulmonary blood and oxygen supplies dependent oulmonary blood and oxygen supplies dependent o
n both bronchial artery and pulmonary artery. In n both bronchial artery and pulmonary artery. In
these patients, obstruction of pulmonary artery bthese patients, obstruction of pulmonary artery b
y a moderate-sized embolus results in pulmonary iy a moderate-sized embolus results in pulmonary i
nfarction.nfarction.
SSmall embolimall emboli may lodge in minor branchs of th may lodge in minor branchs of th
e pulmonary artery, and usually be clinical silee pulmonary artery, and usually be clinical sile
ntnt
However,However, if numerous small emboli occur for a if numerous small emboli occur for a
long period, the pulmonary microcirculation mlong period, the pulmonary microcirculation m
ay be so severely compromised that pulmonary ay be so severely compromised that pulmonary
hypertension results.hypertension results.
Pulmonary thromboembolusPulmonary thromboembolus occluding a small branch of toccluding a small branch of the pulmonary artery in the lunghe pulmonary artery in the lung
2) Systemic embolism2) Systemic embolism
The origin of emboli:The origin of emboli:
Most emboli arise from intracardiac mural thromMost emboli arise from intracardiac mural throm
bi bi (infective endocarditis with vegetations on (infective endocarditis with vegetations on
the valves, mural thrombosis occurred in myocardial infarctithe valves, mural thrombosis occurred in myocardial infarcti
on, etc. )on, etc. )
The remainder emboli may originate from ulceratThe remainder emboli may originate from ulcerat
ed atherosclerotic plaquesed atherosclerotic plaques
The sequel: The sequel:
The clinical effects is govened by the size of the obstrThe clinical effects is govened by the size of the obstr
ucted vessel, the availability of collateral arterial circucted vessel, the availability of collateral arterial circ
ulation, and the susceptibility of the tissue to ischemiulation, and the susceptibility of the tissue to ischemi
a. a.
Necrosis is common when arteriolar embolization ocNecrosis is common when arteriolar embolization oc
cur in the brain, kidneys , spleen and intestines, etc.cur in the brain, kidneys , spleen and intestines, etc.
Arterial embolization of brainArterial embolization of brain, shows impacted throm, shows impacted thromboemboli at the orifice of cerebral middle arteryboemboli at the orifice of cerebral middle artery
The brain tissue suplied by the obstructed vessel necrosThe brain tissue suplied by the obstructed vessel necros
e for ischemia and hypoxiae for ischemia and hypoxia
Arteriolar embolization of kidneyArteriolar embolization of kidneythe kidney tissue supplieded by the obstructed arteriole necrothe kidney tissue supplieded by the obstructed arteriole necro
se for ischemia and hypoxiase for ischemia and hypoxia
Arteriolar embolization of spleen by tumor embolusArteriolar embolization of spleen by tumor embolus
Arteriolar embolization of intestineArteriolar embolization of intestine because of volvulus because of volvulus
Intestin tissue necrose for ischemia and hypoxiaIntestin tissue necrose for ischemia and hypoxia
(( 22 )) Fat embolismFat embolism
The origin of emboli: The origin of emboli:
Fat globules in the circulation after fractures Fat globules in the circulation after fractures
of long bone, trauma of sofe tissue and a liver with of long bone, trauma of sofe tissue and a liver with
fatty change.fatty change.
• Fat globules at trauma sites can enter the circulFat globules at trauma sites can enter the circul
ation, and the catecholamines due to the stress ation, and the catecholamines due to the stress
of trauma mobilizes free fatty acids to form proof trauma mobilizes free fatty acids to form pro
gressively enlarging fat globules.gressively enlarging fat globules.
• Adhesion of platelets to fat globules further incAdhesion of platelets to fat globules further inc
reases their size and causes thrombosis. reases their size and causes thrombosis.
• The sequel:The sequel:
depends on the size and the number of fat globulesdepends on the size and the number of fat globules
• Circulating fat globules first enter the capillary netCirculating fat globules first enter the capillary net
work of the lung.work of the lung.
>20μm>20μm in diameter: be arrested in the lung and occl in diameter: be arrested in the lung and occl
usion of the branching arterioles of pulmonary arteusion of the branching arterioles of pulmonary arte
ry formation (dyspnea and normal gas exchange)ry formation (dyspnea and normal gas exchange)
< 20μm< 20μm in diameter: pass through the pulmonary in diameter: pass through the pulmonary
circulation and enter left heart, and consequently circulation and enter left heart, and consequently
obstruct small systemic arteries.obstruct small systemic arteries.
Typical clinical features of fat embolism include a Typical clinical features of fat embolism include a
hemorrhagic skin rash and brain involvement for hemorrhagic skin rash and brain involvement for
embolism of cerebral microvasculatureembolism of cerebral microvasculature
formation.formation.
Pulmonary fat embolus: occluding a small branch of the Pulmonary fat embolus: occluding a small branch of the pulmonary arteriole by a piece of Bone marrowpulmonary arteriole by a piece of Bone marrow
Fat bubbles in the lumen of vessels stained by Sudan III Fat bubbles in the lumen of vessels stained by Sudan III ,,Showing brilliant red colorShowing brilliant red color
Fat emboli in the pulmonary arterioles stained by Sudan IIIFat emboli in the pulmonary arterioles stained by Sudan III
Fat emboli in Fat emboli in the brain the brain arterioles arterioles stained by stained by Sudan IIISudan III
Necrosis of the Necrosis of the area occluded area occluded by the fat by the fat emboli in the emboli in the brainbrain
(( 33 ) ) Air embolismAir embolism
Gas bubbles within the circulation can obstruct Gas bubbles within the circulation can obstruct
cardio-vascular flow. Generally, in excess of 100ml ocardio-vascular flow. Generally, in excess of 100ml o
f air is required to produce a clinical effect.f air is required to produce a clinical effect.
The origin of gas:The origin of gas: Air may enter the circulation Air may enter the circulation
during obstetric procedures or as a result of chest during obstetric procedures or as a result of chest
wall injury. Occur in caisson workers and under-sea wall injury. Occur in caisson workers and under-sea
divers, occasionally occur in the injury of chest or divers, occasionally occur in the injury of chest or
making a mistake to inject air into vessel lumen.making a mistake to inject air into vessel lumen.
The sequel: The sequel:
• The gas bubbles may form frothy masses with The gas bubbles may form frothy masses with
blood in right heart, and then act like physical blood in right heart, and then act like physical
obstructions to occlude major vessels.obstructions to occlude major vessels.
• Platelets adhere to air bubbles in the Platelets adhere to air bubbles in the
circulation and active coagulation cascade.circulation and active coagulation cascade.
Decompression sickness:Decompression sickness:
Occur in caisson workers and under-sea divers. Occur in caisson workers and under-sea divers.
When air is breathed at high underwater pressure, When air is breathed at high underwater pressure,
an increased volume of air (mainly nitrogen) become an increased volume of air (mainly nitrogen) become
dissolved in the blood and tissues. If the diver then dissolved in the blood and tissues. If the diver then
ascends too rapidly, the nitrogen come out of solution ascends too rapidly, the nitrogen come out of solution
and form bubbles in the tissues and bloodstream that and form bubbles in the tissues and bloodstream that
act as gas emboli.act as gas emboli.
(( 44 ) ) Amniotic fluid embolismAmniotic fluid embolism
The amniotic fluid and its component are iThe amniotic fluid and its component are i
nfusednfused into the maternal circulation via a tear in tinto the maternal circulation via a tear in t
he placental membranes and rupture of the uterine he placental membranes and rupture of the uterine
veins. The onset is characterized by sudden severe veins. The onset is characterized by sudden severe
dyspnea, cyanosis, DIC and shock, followed by seizdyspnea, cyanosis, DIC and shock, followed by seiz
ures and coma.ures and coma.
• Amniotic fluid contains fetalAmniotic fluid contains fetal squamous epithelisquamous epitheli
um, fetal hair, fetal fat, mucin, etc. All of them um, fetal hair, fetal fat, mucin, etc. All of them
may lodge in the pulmonary capillaries, and mamay lodge in the pulmonary capillaries, and ma
y cause disseminated intravascular coagulation.y cause disseminated intravascular coagulation.
Several pieces of fetal hair in the alveolar space
( 5( 5 ) ) Tumor embolismTumor embolism
Cancer cellsCancer cells often enter the circulation durinoften enter the circulation durin
g metatasis of malignant tumors. And this typg metatasis of malignant tumors. And this typ
e of embolus is tumor embolus.e of embolus is tumor embolus.
4.4. InfarctionInfarction
Tissue necrosis resulting from extreme Tissue necrosis resulting from extreme
reduction or loss of blood supply (vascular reduction or loss of blood supply (vascular
occlusion) is referred to as occlusion) is referred to as infarctioninfarction. .
The necrotic tissues are called The necrotic tissues are called infarctinfarct..
1. Causes:1. Causes:
Thrombosis:Thrombosis: the most common causethe most common cause
Embolism of arteriesEmbolism of arteries
Compression and obstruction of vessels Compression and obstruction of vessels
Arterial spasmArterial spasm
2. General morphology of infarcts2. General morphology of infarcts
(1) Shape:(1) Shape: depend on vascular distribution of depend on vascular distribution of
the organ the organ
Wedge orWedge or pyramid shaped infarct: kidney, lungs, pyramid shaped infarct: kidney, lungs,
and spleen and spleen
irregular, map shaped infarct: heart, brainirregular, map shaped infarct: heart, brain
The arterial system in kindey is branching pattern, liThe arterial system in kindey is branching pattern, like wedge or pyramid shape ke wedge or pyramid shape
When the branch of the arterioles are obstructed, the tWhen the branch of the arterioles are obstructed, the tissue supplied by the arterioles necrose. The necrotic fissue supplied by the arterioles necrose. The necrotic foci are also wedge oroci are also wedge or pyramid shaped pyramid shaped
(2)(2) Color:Color: depends on the amount of the blood in tdepends on the amount of the blood in t
he infarct focihe infarct foci
(3)(3) Texture: Texture: depends on pathological changes in ddepends on pathological changes in d
ifferent organsifferent organs
Coagulative necrosis – solid organs (kidenys, spleCoagulative necrosis – solid organs (kidenys, sple
en), lungs and intestine etcen), lungs and intestine etc
Liquefactive necrosis – brain(cerebral malacia)-cLiquefactive necrosis – brain(cerebral malacia)-c
yst formationyst formation
3. Types of infarcts3. Types of infarcts
3.1 Anemic infarcts (White infarcts)3.1 Anemic infarcts (White infarcts)
Organ involved:Organ involved: solid organs with deficient solid organs with deficient
collateral circulation of arteries (heart, kidneys, collateral circulation of arteries (heart, kidneys,
spleen, etc.) spleen, etc.)
Grossly:Grossly: wedge-like or triangular necrotic foci with wedge-like or triangular necrotic foci with
peripheral hemorrhagic zone peripheral hemorrhagic zone
Anemic infarcts of spleen: Anemic infarcts of spleen: wedge shaped infarct, the top wedge shaped infarct, the top
of the wedge directe to the hilum of the spleenof the wedge directe to the hilum of the spleen
Anemic infarcts of kidney:Anemic infarcts of kidney: wedge shaped infarct, thwedge shaped infarct, the top of the wedge directe to the hilum of the kidneye top of the wedge directe to the hilum of the kidney
• The shapeThe shape of cerebralof cerebral and myocardialand myocardial
infarcts is irregular. It is determined by infarcts is irregular. It is determined by
the distribution of the occluded artery, the distribution of the occluded artery,
and limits of collateral arterial supply.and limits of collateral arterial supply.
Anemic infarcts in Anemic infarcts in heart:heart: irregular, map irregular, map shapedshaped infarctinfarct
Anemic infarcts Anemic infarcts of brain: of brain: irregular, irregular, map shapedmap shaped infarctinfarct
And And cyst formationcyst formation
Microscopically:Microscopically: ischemic coagulative necrosis ischemic coagulative necrosis
The outline of tissue structure remains The outline of tissue structure remains
Nuclear changes: pyknosis, karyorrhesix, or Nuclear changes: pyknosis, karyorrhesix, or
karyolysis karyolysis
Leucocytic reaction at peripheral marginLeucocytic reaction at peripheral margin
Anemic infarcts of kidney:Anemic infarcts of kidney: wedge shaped foci wedge shaped foci
keeping the outline of tissue structure, hyperemia and leucocytic rkeeping the outline of tissue structure, hyperemia and leucocytic reaction at peripheral margineaction at peripheral margin
Coagulative necrosis, the tissue Coagulative necrosis, the tissue contour is kept, but the is kept, but the cell died with the changes of the nucli. cell died with the changes of the nucli.
Anemic infarcts of spleenAnemic infarcts of spleen
Anemic infarcts of heart muscleAnemic infarcts of heart muscle
Anemic infarcts of brainAnemic infarcts of brain
Irregular shaped fociIrregular shaped foci
Liquefactive necrosisLiquefactive necrosis
- cerebral malacia- cerebral malacia
- cyst formation- cyst formation
Cerebral liquefactive necrosisCerebral liquefactive necrosis
3.2 Hemorrhagic infarcts (Red infarcts)3.2 Hemorrhagic infarcts (Red infarcts)
occur in an organ:occur in an organ:
composed of loose tissue, such as the lungscomposed of loose tissue, such as the lungs
with double circulation (lungs) and rich with double circulation (lungs) and rich
collateral circulation (small intestine) collateral circulation (small intestine)
associated with congestionassociated with congestion
Capillary Capillary networknetwork
bronchia
PAPA
BABA
PVPV
BVBV
The changes of the blood circulation when The changes of the blood circulation when embolism of pulmonary arteries occurembolism of pulmonary arteries occur
hydrostatic pressure increased dramatically
Pulmonary hemorrhagic infarctsPulmonary hemorrhagic infarcts
Conditions:Conditions:
serious pulmonary congestion before infarctionserious pulmonary congestion before infarction
the organs are composed of loose tisssuethe organs are composed of loose tisssue
Grossly:Grossly: wedge-like or triangular necrotic foci, red wedge-like or triangular necrotic foci, red
Microscopically:Microscopically: coagulative necrosis plus with lar coagulative necrosis plus with lar
ge amount of hemorrhagege amount of hemorrhage
Lung Lung wedge-like or triangular necrotic foci, red color
Cut surface featrue: necrosis plus with large amount of hemorrhage
Microscopical
feature in the
lowest amplifi
ed: necrosis pl
us with large
amount of he
morrhage
necrosis plus with large amount of hemorrhage
Intestine hemorrhagic infarcts (causing by volvulus) Intestine hemorrhagic infarcts (causing by volvulus)
Intestine hemorrhagic infarcts (causing by embolism) Intestine hemorrhagic infarcts (causing by embolism)
Intestinal necrosis plus with large amount of hemorrhage
Cerebral hemorrhagic infarcts: coagulative necrosis Cerebral hemorrhagic infarcts: coagulative necrosis plus with large amount of hemorrageplus with large amount of hemorrage
Cerebellum hemorrhagic infarcts: coagulative necrosis Cerebellum hemorrhagic infarcts: coagulative necrosis plus with large amount of hemorrageplus with large amount of hemorrage
4. Influence to the body and the sequal of 4. Influence to the body and the sequal of
the infarction the infarction
Influence Influence :: decided by the organ or the size decided by the organ or the size
The sequel:The sequel:
Orgnization and eventually form a scarOrgnization and eventually form a scar CalcificationCalcification
Cystic cavity formationCystic cavity formation