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Edema Thrombosis Hemostasis Embolism Infarction Hemorrhage Shock
Edema
abnormal increase in interstitial fluid within tissues caused by either increased capillary pressure or diminished colloid osmotic pressure mostly seen in subcutaneous tissues, lungs and brain. Type of edema: exudate in inflammatory and transudate in non inflammatory conditions
Edema - Pathogenesis
Constrictive Pericarditis
Venous Obstruction
Hyperemia
Locally increased blood volumes Active Process
Arteriolar dilation leads to increased blood flow
Erythema
Congestion
locally increased blood volumes Passive process
resulting from reduced outflow of blood from a tissue. can be systemic or local
Cyanosis
Capillary rupture
Microscopically:
Central vein is congested as well as the hepatic sinusoids centrilobular hemorrhage hemosiderin-laden macrophages degeneration of hepatocytes
Microscopically:
Sinusoids of red pulp are dilated and engorged with blood Hemorrhage may occur
Hemostasis
Vasoconstriction
Reflex neurogenic mechanism; endothelin
Primary hemostasis
Platelet adhesion and aggregation
Secondary hemostasis
Thrombin activation; fibrinogen to fibrin; fibrin deposition
Hemorrhage
Hemorrhage
Extravasation of blood into the extravascular space. Hemorrhagic Diathesis
increased tendency to hemorrhage that occurs in a variety of clinical disorders
Hemorrhage sequelae
Loss volume
>20% - hemorrhagic shock
Loss rate
Acute - hemorrhagic shock Chronic - peptic ulcer, menstrual bleeding
Iron deficiency anemia
Site of hemorrhage
Subcutaneous tissues - fatal in brain
Thrombosis
Thrombosis
The formation of a blood clot (thrombus) in an uninjured vessel after an injury. The THROMBUS is formed of blood elements essentially platelets.
3 Primary abnormalities
Virchows triad
Endothelial injury Stasis or turbulence of blood flow Blood hypercoagulability
Types of Thrombi
Pale Thrombus
In a flowing blood as in cardiac chambers or in arteries. Formed mainly of platelets FIRM PALE REDDISH G RE Y
Red Thrombus
In a stagnant blood adjacent to complete vascular occlusion Formed of fibrin platelets SOFT DARK RED & G ELATI N O U S
Mixed Thrombus
In a slowly flowing blood usually in veins & arteries. Formed of alternating layers of platelets and fibrin ALTER N ATI N G RED & PALE LAY ERS
Pale Thrombus
Site: heart valve, artery Component: Platelet, fibrin
Red Thrombus
Mixed Thrombus
Site: heart chamber, vein Component: Platelet, fibrin, R B C
Mural thrombosis
Thrombi occurring in heart chambers or in the aortic lumen.
Mural thrombosis
Pathogenesis
Pathogenesis
Pathogenesis
Fate of Thrombus
Propagation
Thrombi accumulate additional platelets and fibrin.
Embolization
Thrombi dislodge and travel to other sites in the vasculature
Dissolution
the result of fibrinolysis, which can lead to the rapid shrinkage and total disappearance of recent thrombi.
Morphology
Thrombi may develop anywhere inside the C V S. They are variable in size and shape depending on its site of origin and the causes of their development. Thrombi are significant because they cause obstruction of arteries and veins, and are sources of emboli.
Venous Thrombi
Arterial/Cardiac Thrombosis
Atherosclerosis major cause.
Loss of endothelial integrity with abnormal vascular flow
Superficially,
venous thrombi typically occur in the saphenous veins in the setting of varicosities.
Gross: firm, red, attached to wall Microscopically: RBC + fibrin known as red, or stasis.
Embolism
Embolus
An embolus is a detached intravascular solid, liquid, or gaseous mass that is carried by the blood to a site distant from its point of origin. Coined by Rudolf Virchow in 1848.
fat droplets, nitrogen bubbles, atherosclerotic debris (cholesterol emboli), tumor fragments, bone marrow, or even foreign bodies.
Types of Embolism
Pulmonary embolism
95% venous emboli from deep leg veins Depending on the size may lodge pulmonary artery bifurcation (saddle embolus) or in the small arterioles. Most pulmonary emboli are clinically silent (small) Sudden death, right heart failure (cor pulmonale) occurs when more 60% or more of the pulmonary circulation is obstructed by emboli
Types of Embolism
Systemic thromboembolism
Emboli traveling in arterial circulation 80% from intracardiac mural thrombi Aortic aneurysm, thrombi, atherosclerotic plaques, paradoxical thrombi Lower extremities (75%); brain (10%)
Types of Embolism
Fat embolism
Microscopic fat globules seen in circulation 90% with severe skeletal injuries Pulmonary insufficiency, neurologic symptoms, anemia and thrombocytopenia (1-3 days after injury)
Types of Embolism
Air embolism
Excess of more than 100cc is required to have clinical effect Decompression sickness- sudden change in atmospheric pressure Bends (gas bubbles within skeletal muscles) (caissons disease)
Types of Embolism
Amniotic fluid embolism
1 in 50,000 deliveries Infusion of amniotic fluid or fetal tissue into the maternal circulation via tear in the placenta or rupture of uterine veins.
Infarction
Infarction
Ischemic necrosis caused by occlusion of either arterial supply or the venous drainage 99% of all infarcts results from thrombotic episodes Almost all result from arterial occlusion
Infarction
Red infarct venous occlusion, loose tissues, tissue with dual circulation White infarct arterial occlusions solid organs Mostly ischemic coagulative necrosis Brain-liquefactive necrosis
Infarction Factors
NATURE of VASCULAR SUPPLY RATE of DEVELOPMENT
SLOW (BETTER) FAST (WORSE)
VULNERABILITY to HYPOXIA
MYOCYTE vs. FIBROBLAST
Morphology
1. red infarcts
venous occlusion loose tissue (lung) blood collection dual circulation lung + bowel previously congested organs reperfusion (angioplasty, drug-induced thrombolysis)
2. white infarcts
arterial occlusion solid organs heart (yellow), spleen, kidney
Morphology
wedge shape
apex to occluded artery base to organ periphery + fibrinous exsudate (pleuritis, pericarditis epistenocardiaca)
WEDGE SHAPED SCARRED INFARCT following the distribution of an end artery branch of the renal artery. FIBROSIS implies that it is old (months to years)
2. partial necrosis
some cells survive inflammation (neutrophils) 1-2 days degradation of dead tissue
healing
granulation tissue (5-7 day) fibrous scar (6-8 weeks) In brain liquefactive necrosis pseudocyst
Septic infarctions
occur when infected cardiac valve vegetations embolize or when microbes seed necrotic tissue. the infarct is converted into an abscess, with a correspondingly greater inflammatory response.
Shock
Shock
characterized by systemic hypotension due either to reduced cardiac output or to reduced effective circulating blood volume. Consequences:
impaired tissue perfusion cellular hypoxia
Shock
the final common pathway for several potentially lethal clinical events:
severe hemorrhage, extensive trauma or burns, large myocardial infarction, massive pulmonary embolism, and microbial sepsis.
Shock
Features:
hypotension, tachycardia, tachypnea, cool cyanotic skin
Causes:
Cardiogenic Septic Hypovolemic
Cardiogenic Shock
results from low cardiac output due to myocardial pump failure. This can be due to intrinsic myocardial damage (infarction), ventricular arrhythmias, extrinsic compression, or outflow obstruction.
MI Ventricular rupture Arrythmia Cardiac tamponade Pulmonary embolism
Hypovolemic Shock
results from low cardiac output due to the loss of blood or plasma volume
Hemorrhage Fluid loss (e.g. vomiting, diarrhea, burns)
Septic Shock
results from vasodilation and peripheral pooling of blood as part of a systemic immune reaction to bacterial or fungal infection.
Overwhelming microbial infection Endotoxic shock Gram positive septicemia Fungal sepsis Superantigens
Shock
Neurogenic Shock
loss of vascular tone e.g. spinal cord injury
Shock
Anaphylactic Shock
denotes systemic vasodilation and increased vascular permeability caused by an IgEmediated hypersensitivity reaction. acute widespread vasodilation results in tissue hypoperfusion and hypoxia.
Clinical Stages
Nonprogressive
Progressive
Irreversible
Morphology
brain - ischemic encephalopathy
tiny ischemic infarctions (border zones)
heart
subendocardial hemorrhage + necroses, contr. bands
Morphology
adrenal gland
lipid depletion
liver
fatty change, central necrosis
Clinical Stages
1. nonprogressive
Compensatory mechanism (neurohumoral) activation centralization of blood circulation
2. progressive
tissue hypoperfussion metabolic dysbalancies
3. irreversible
incurred cellular damage + tissue injury
Tachycardia
Tachypnea
Obtundance
Death