Hyperemia and Congestion
By Dr. Eric Po Lasala
Hyperemia
n Increased volume of blood in a particular tissue
n Active process due to augmented tissue outflow because of arteriolar dilatation resulting to bright red color
n Examples
u Exercise
u Inflammation
Congestion
n A passive process, that results from impaired outflow from tissues
n May occur systemically as in cardiac failure or localized as in isolated venous obstruction
n The accumulation of deoxygenated blood will cause blue red color
n When present in the capillary beds may also result to edema
n Chronic passive congestion
o Long standing poorly oxygenated blood causes hypoxia resulting to parenchymal cell degeneration and death
o The breakdown and phagocytosis of red cells results to hemosiderin laden macrophages, aka. Heart failure cells
n It gives a characteristic appearance of nutmeg liver under the microscope
n This arise as a result of alternating centrilobular necrosis and fibrosis
Hemorrhage
n Extravasation of blood
n Maybe external or internal
n Maybe enclosed within tissues, thus arising to hematoma
n Hemorrhagic diathesis is a condition that arise from a variety of other conditions increasing capillary bleeding that may arise from chronic congestion
n Forms of hemorrhage
o Hematoma
o Petechiae
o Purpura
o Ecchymosis
o Hemothorax
o Hemopericardium
o Hemopertoneum
o Hemarthrosis
n Clinical significance:
o Depends on the volume and rate of loss
o May result to hemorrhagic shock if excessive
o Other consequences:
Ø Iron loss
Ø Damage to tissues
Thrombosis
n Hemostasis is a result of a regulated process that:
o Maintain blood in a fluid clot free state
o Induce rapid localized hemostatic plug at a site of injury
n This is the pathologic opposite of hemostasis
n 3 general components of hemostasis and thrombosis
o Vascular wall
o Platelets
o Coagulation cascade
n Virchow’s triad ( 3 primary factors that leads to thrombus formation):
o Endothelial injury
o Stasis or turbulence of flow
o Blood hypercoagulability
n Genetic causes of hypercoagulability:
o Mutations
in factor V gene called
o Inherited lack of AT-III, Protein C and Protein S
o Release of PGI2 in the elderly causes increased thrombus formation in this age group
n Acquired causes of hypercoagulability:
o Endothelial injury to arteries
o Stasis of flow in veins
n Events that follow thrombosis:
o Propagation-leads to vessel obstruction
o Embolization- the thrombus fragments to several pieces and distributed along the flow of the blood stream
o Dissolution
o Organization and recanalization
n Clinical Significance
o Obstructs veins and arteries
o Possible sources of emboli
Disseminated Intravascular Coagulation (DIC)
n Sudden, insidious onset of widespread thrombi in the microcirculation
n Not usually visible on gross inspection but easily apparent under the microscope
n Causes diffused circulatory insufficiency:
v Brain, heart, lungs and kidneys
n Platelets are consumed along with the coagulation proteins and fibrinolytic enzymes that results to initial thrombotic disorder that ends in a serious bleeding disorder
n Not a primary disease
n Associated only with any condition that activates thrombin
Infarction
n An area of ischemic necrosis caused by the occlusion of the arterial supply or venous drainage of a particular site
n 99% of all infarcts are results of thrombotic or embolic events and almost all results to arterial occlusion
n Other causes:
o Local vasospasm
o Expansion of atheroma owing to hemorrhage within a plaque
o Extrinsic compression of vessels
o Twisting of vessels
o Compression of blood supply by edema
o Traumatic rupture of the vessels
n Types of infarcts:
o Red infarct-occurs in venous occlusions
o White Infarct-occurs in arterial occlusions
n Factors that influence development of infarcts:
o Nature of vascular supply
o Rate of development of the occlusion
o Vulnerability of the given tissue to hypoxia
o Blood oxygen content
Shock
n Aka, cardiovascular collapse
n Final common pathway for several potentially lethal events
n Shock is a result of systemic hypoperfusion as a result of
o Reduced cardiac output
o Inefficient circulation of blood
n End results of shock:
o Hypotension
o Hypoxia
o Impaired tissue perfusion
n General categories of shock:
o Cardiogenic shock
o Hypovolemic shock
o Septic shock
o Neurogenic shock
o Anaphylactic shock
n Stages of shock:
o Non-progressive phase-reflex compensatory mechanisms are activated
o Progressive Stage-tissue hypoperfusion
o Irreversible stage- tissue damage and necrosis, survival is impossible