What 2 conditions create increase in volume of blood in tissues/organs?
Hyperemia and congestion
Hyperemia
active arteriolar dilation and increased blood inflow
Congestion
passive process resulting from impaired outflow of venous blood from a tissue
Congested tissue is
stiff, cold, cyanotic
Hyperemia can be either _________ or ___________
neurogenic or myogenic
Hyperemic tissues are
red, swollen, warm, white upon pressure
General congestion - causes
heart failure, respiratory movement restrictions, vena cava compression
Regional congestion - causes
cirrhosis, limbs
Local congestion - causes
obstruction of vein or pulmonary artery, hypostasis, limb paralysis
Chronic congestion may cause
fibrosis, thrombosis
pulmonary congestion leads to _________ while hepatic congestion leads to _______
right, left ventricular failure
chronic pulmonary congestion
brown induration
acute hepatic congestion
central vein and sinusoids are distended
chronic hepatic congestion
red-brown and slightly depressed, nutmeg
Spleen or skin with cyanotic induration and atrophy may cause
hepatic congestion
Hepatic congestion may be caused by congestive serous inflammation of the
GI tract
Hepatic congestion may be caused by a kidney with
albuminuria
Infarction
ischemic necrosis caused by vascular occlusion in vitro
Ischemia
inadequate arterial blood supply to tissue/organ
Relative ischemia may cause
distrophy, atroophy or sclerosis
General ischemia
decrease in arterial perfusion pressure (left heart failure)
Local ischemia
artery obstruction
Collateral ischemia
of the brain, episodic
End-arterial circulation by
intercapillary anastomosis
Functional end-arterial circulation by
small interarterial anastamosis
Arteries with collateral branches circulation by
large arterial anastamosis
Dual artery blood supply by
lungs and liver
Collaterla circulation occurs in __________ or __________
congestion (venous), ischemia (arterial)
Causes of infarction
Arterial thrombosis or arterial embolism, tumour, vasospasm, twisting
Red infarctions occur at
lungs and intestines
White infarcations occur at
myocardium, spleen, kidney, brain, liver, limbs
Infarction - appearance
triangular, tip at occluded vessel, hyperemic narrow rim
liquefactive necrosis
ischemic tissue injury in the central nervous system; brain infarction
ischemic coagulative necrosis
inflammatory response of white infarction
3 variables of infarction development
type of vascular supply, rate of occlusion, tissue vulnerability to hypoxia
5 steps of necrotic area replaced by scar tissue
1 organization 2 capsuling 3 liquefaction 4 superinfection 5 autoamputation (gangrene)
The brain may be deprived of oxygen by two general mechanisms
functional hypoxia or ischemia
thrombosis
formation of blood clot (thrombus) within non-traumatized, intact vessels in vivo
Virchow triad of thrombosis
endothelial injury, abnormal blood flow, hypercoagulability
prothrombotic alterations by endothelial cells (thrombosis)
downregulate the expression of thrombomodulin
secrete Plasminogen activator inhibitors (PAI), which limit fibrinolysis
Stasis and turbulence promote thrombosis by
endothelial cell activation + procoagulant activity
platelets and leukocytes come into contact with endothelium
slows the washout of activated clotting factors
Turbulence contributes to arterial and cardiac thrombosis by causing _____________ ____________, as well as by forming ___________ and local pockets of ________
endothelial injury, countercurrents, stasis
Abnormalities of vessel wall in thrombosis causes
atherosclerosis
inflammations
Disorders of blood flow in thrombosis causes
slowed/stopped flow, turbulence
Abnormalities of blood components in thrombosis causes
increase in platelet #
platelet clumping
hyperviscosity
coagulation cascade activation
Hypercoagulability is typically caused by alterations in _______ __________ and is a risk factor for _____ _________
coagulation factors, venous thrombosis
Primary (inherited) hypercoagulability is most often caused by mutations in
the factor V and prothrombin genes
Arterial or cardiac thrombi occur at sites of_________ or ____________; venous thrombi occur at sites of _______
endothelial injury, stasis
Lines of Zahn
Alternating layers of platelets/fibrin and RBCs
What promote cardiac mural thrombi
Abnormal myocardial contraction or endomyocardial injury
Types of venous thrombi
mural (cardiac), occlusive (vascular)
Evolution of thrombus - propagation
thrombus enlarges through the accretion of additional platelets and fibrin
Evolution of thrombus - embolization
Part or all of the thrombus is dislodged and transported elsewhere in the vasculature
Evolution of thrombus - dissolution
new thrombi - fibrinolytic factors may lead to its rapid shrinkage and complete dissolution lysis of old thrombi
Evolution of thrombus - Organization and recanalization
organized by the ingrowth of endothelial cells, smooth muscle cells, and fibroblasts, reestablishing the continuity of the original lumen
Most venous thrombi occur in and are associated with
deep veins of leg (DVT), stasis and hypercoagulable states (immobilization)
Arterial and Cardiac Thrombosis occur in and are associated with
Brain kidney and spleen, loss of endothelial integrity and with abnormal blood flow
Disseminated Intravascular Coagulation (DIC)
onset of widespread fibrin thrombi in the microcirculation
DIC usually is triggered by either (1) ___________ or (2) _____________
release of tissue factor or thromboplastic substances into the circulation
widespread endothelial cell damage
DIC is most often associated with
sepsis, obstetric complications, malignancy, and major trauma (especially to the brain)
DIC causes (2)
widespread fibrin deposition
bleeding tendency (activation of blood-thrombin)
Embolus
migration of a liquid, solid or gaseous mass into the blood stream, causing tissue dysfunction or infarction
Consequence of embolism
ischemic necrosis of downstream tissue
Pulmonary emboli originate from
deep venous thromboses
Pulmonary emboli cause
hypoxia, hypotension, and right-sided heart failure
Most systemic emboli arise from
intracardiac mural thrombi, or aortic aneurysms
Systemic emboli location
lower extremities and CNS
Causes of fat embolism (2)
Soft tissue crush injury or injection with oil drugs
amniotic fluid embolism can cause
fatal pulmonary and cerebral manifestations
Air embolism is caused by
rapid decompression (sudden bubbling of nitrogen dissolved in blood at higher pressures)
amniotic fluid embolism
amniotic fluid and fetal cells enter the pregnant woman's pulmonary and circulatory system
Hemorrhage
extravasation of blood from vessels in vivo
Causes of hemorrhage
Rupture of vessel wall, erosion of vessel wall or diapedesis
Hematoma
hemorrhage that accumulates within a tissue
Three types of hemorrages (smallest to biggest)
Petechiae, Purpura, Ecchymoses
Physiological hyperemia is due to ________ while pathologic hyperemia is due to ___________
digestion or activity, inflammation
Congestion may cause (5)
tissue lesions, fibrosis, increase in capillary permeability, collateral circulation and thrombosis
cause of acute pulmonary congestion is
alveolar and septal edema
Systemic circulation congestion - spleen
cyanotic induration and atrophy
Systemic circulation congestion - GI tract
congestive serous inflammation
Systemic circulation congestion - kidney
cyanotic induration and atrophy (albuminuria)
Systemic circulation congestion - skin
cyanosis, atrophy, dermatosclerosis, ulceration
Zahn infarctions occur at
liver (portal vein)
Fibrin thrombi are in ______
microcirculation (Disseminated Intravascular Coagulation - DIC)
what is White thrombi (ARTERIAL) made of
platelets in keeping circulation, lines of Zhan
Red thrombi (VENOUS) in
fibrin, erythrocytes, leukocytes in vessel obstruction
Mixed thrombi in
platelet clumping, erythrocytes
Composed thrombi (composition)
head - white thrombus body - mixed thrombus tail - red thrombus
types of arterial thrombi
broken or continuous (uninterrupted)
consequences of venous thrombus
congestion, edema, variceal ulcers embolism
consequences of arterial thrombus
ischemia, atrophy, sclerosis, infarction (total occlusion)
DIC is followed by the consumption of
platelets and coagulation proteins
Difference bw disseminated microthrombosis and consumptive coagulopathy
both cause fibrin activation and platelet clumping; consumptive coagulopathy happens when coag factors are consumed
consumptive coagulopathy causes
hemorrhages
2 origins of emboli
endogenous (thrombi, tissue) or exogenous (foreign matter)
anterograde embolism migration - into
pulmonary artery and diff organs
paradoxical embolism migration - into
venous embolism into arterial embolism
retrograde embolism migration - into
suprahepatic vein, renal vein, Batson's veins
3 steps of pathomechanism of thromboembolism
Thrombus detachment 2. Migration 3. Lodge (fixation)
consequences of fat embolism
right heart failure or fat globules in systemic arterial circulation