Disorders of Blood Circulation

What 2 conditions create increase in volume of blood in tissues/organs?

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

1. Thrombus detachment 2. Migration 3. Lodge (fixation)

consequences of fat embolism

right heart failure or fat globules in systemic arterial circulation