Disorders of Blood Circulation

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126 Terms

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