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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 2
◼ Congestion
◼ Hemorrhage
◼ Thrombosis
◼ Embolism
◼ Infarction
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 3
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 4
SECTION 1
HYPEREMIA & CONGESTION
A local increased volume of blood in a
particular tissue
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 5
Hyperemia
Congestion
An active process
A passive process
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 6
Hyperemia
an active process
resulting from augmented tissue inflow
because of arteriolar dilation
◆ Skeletal muscle during exercise
◆ Sites of inflammation
redder
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 7
Congestion
a passive process
resulting from impaired outflow from a tissue
◆ a blue-red color (cyanosis)
◆ cut surfaces: hemorrhagic and wet
◆ capillaries engorged with blood
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 8
◆ Systemical Congestion
◆ Local Congestion
Etiology
Cardiac failure
An isolated venous obstruction
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 9
◆ Edema
◆ Parenchymal cell degeneration or death
◆ Small foci of hemorrhage
◆ Fibrosis
◆ Infection
OUTCOME
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 10
e.g. Pulmonary Congestion
⚫ alveolar capillaries engorged with blood
⚫ alveolar septal edema
⚫ focal intra-alveolar hemorrhage
ACUTE
(1)
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 11
e.g. Pulmonary Congestion
CHRONIC
(2)
⚫ Thickened and fibrotic septa
⚫ Numerous hemosiderin-laden macrophages
in the alveolar spaces (heart failure cells)
⚫ Brown induration
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 12
e.g. Hepatic Congestion
⚫ Distended central vein and sinusoids
with blood
⚫ Hepatocyte degeneration
ACUTE
(1)
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 13
e.g. Hepatic Congestion
⚫ Central regions: red-brown
⚫ Surrounding zones: tan /or yellow
CHRONIC
(2)
Nutmeg Liver
Hepatic Lobules
Necrosis & hemorrhage
Fatty change
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 14
e.g. Hepatic Congestion
CHRONIC
(3)
Hepatic Fibrosis (cardiac cirrhosis)
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 15
SECTION 2
HEMORRHAGE
Extravasation of blood due to vessel rupture
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 16
◆ Capillary bleeding: chronic congestion
◆ Rupture of a large artery or vein:
vascular injury
ETIOLOGY
⚫ Trauma
⚫ Atherosclerosis
⚫ Inflammatory or neoplastic erosion
of the vessel wall
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 17
Hematoma: accumulation of blood
within tissue
PATTERNS
Depending on the size, extent,
and location of bleeding
Petechiae: 1- to 2-mm hemorrhages
into skin, mucous membranes,
or serosal surfaces
(1)
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 18
PATTERNS
Purpura: slightly larger (≥3 mm)
hemorrhages
Ecchymoses: larger (>1 to 2 cm)
subcutaneous hematomas (i.e., bruises)
(2)
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 19
◆ Hemothorax
◆ Hemopericardium
◆ Hemoperitoneum
◆ Hemarthrosis
…
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 20
Depending on the volume
the rate of bleeding
the site
CLINICAL SIGNIFICANCE
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 21
SECTION 3
THROMBOSIS
Process of formation of a solid mass
from the constituents of the blood
within the heart or the vascular system
in a living organism
A thrombus
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 22
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 23
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 24
PATHOGENESIS
Virchow’s Triad
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 25
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 26
ENDOTHELIAL INJURY
◆ Exposure of subendothelial collagen
◆ Adherence of platelets
◆ Release of tissue factor
◆ Depletion of PGI2 & PA
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 27
ENDOTHELIAL INJURY
◆ Exposure of subendothelial collagen
◆ Adherence of platelets
◆ Release of tissue factor
◆ Depletion of PGI2 & PA
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 28
Activation of platelets
◆ Adhesion and shape change
◆ Secretion (release reaction)
◆ Aggregation
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 29
Virchow’s Triad
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 30
ABNORMAL BLOOD FLOW
◆ Turbulence
◆ Stasis
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 31
Virchow’s Triad
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 32
HYPERCOAGULABILITY
◆ Genetic (primary)
◆ Acquired (secondary)
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Pathology
12/1/2019 PATHOLOGY (reform)-DH 33
Genetic (Primary)
Common
Mutation in factor V gene (factor V
Leiden)
Mutation in prothrombin gene
Mutation in methyltetrahydrofolate gene
Rare
Antithrombin III deficiency
Protein C deficiency
Protein S deficiency
Very rare
Fibrinolysis defects
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Pathology
12/1/2019 PATHOLOGY (reform)-DH 34
Secondary (Acquired) (1)
High risk for thrombosis
Prolonged bed rest or immobilization
Myocardial infarction
Atrial fibrillation
Tissue damage (surgery, fracture, burns)
Cancer
Prosthetic cardiac valves
Disseminated intravascular coagulation
Heparin-induced thrombocytopenia
Antiphospholipid antibody syndrome
(lupus anticoagulant syndrome)
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Pathology
12/1/2019 PATHOLOGY (reform)-DH 35
Secondary (Acquired) (2)
Lower risk for thrombosis
Cardiomyopathy
Nephrotic syndrome
Hyperestrogenic states
(pregnancy)
Oral contraceptive use
Sickle cell anemia
Smoking
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 36
Virchow’s Triad
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 37
PROCESS OF THROMBOSIS
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 38
TYPES OF THROMBUS
◆ Pale Thrombus
◆ Red Thrombus
◆ Mixed Thrombus
◆ Hyaline Thrombus
or Microthrombus
Vegetations
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 39
SITES OF THROMBOSIS
◆ Arterial Thrombosis
◆ Cardiac Thrombosis
◆ Venous Thrombosis
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 40
FATE OF THE THROMBUS
◆ Dissolution
◆ Propagation
◆ Embolization
◆ Organization and Recanalization
◆ Calcification (phlebolith)
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 41
Potential outcomes of venous thrombosis.
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 42
SIGNIFICANCE OF THE THROMBUS
◆ Prevention of excessive bleeding
◆ Obstruction of arteries and veins
◆ Possible sources of emboli
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 43
SIGNIFICANCE OF THE THROMBUS
◆ Venous Thrombosis (Phlebothrombosis)
◆ Arterial and Cardiac Thrombosis
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 44
SECTION 4 EMBOLISM
Occlusion or obstruction of a vessel
by an abnormal mass (solid, liquid, or gaseous)
transported from a different site by the circulation
An Embolus Thromboembolism
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 45
Moving Pathway of An Embolus
The same direction as the blood
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 46
Types & Sequences
◆ Thromboembolism
◆ Fat embolism
◆ Air embolism
◆ Amniotic fluid embolism
◆ Others
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 47
Types & Sequences
◆ Thromboembolism
1. Pulmonary Thromoembolism
2. Systemic Thromboembolism
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 48
➢ Small &/or a few
--- clinical silent
infarction, if left cardiac failure
➢ Small & massive /or large
--- sudden death
1. Pulmonary Thromoembolism
Sites of Originthe large deep veins of the lower leg
Effects Emboli
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CHAPTER 3
12/1/2019 PATHOLOGY (reform)-DH 49
Pulmonary embolism
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CHAPTER 3
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2. Systemic Thromoembolism
Sites of OriginLeft cardiac thrombi(85%), arterial thrombi
Effects
➢the size
➢the lodged vessel
➢the collateral blood supply in the tissue
➢the vulnerability of the tissue to ischemia
Depending on
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Types & Sequences
◆ Thromboembolism
◆ Fat embolism
◆ Air embolism
◆ Amniotic fluid embolism
◆ Others
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SECTION 5
INFARCTION
Ischemic Necrosis
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Etiology
◆ Thrombosis
◆ Embolism
Arterial occlusion
◆ Local vasospasm
◆ Twisting of the vessels
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Morphology
◆ Red (hemorrhagic) infarcts
◆ White (anemic) infarcts
◆ Septic infarcts
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Morphology
◆ Red (hemorrhagic) infarcts
◆ White (anemic) infarcts
◆ Septic infarcts
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Morphology
◆ Red (hemorrhagic) infarcts
◆ White (anemic) infarcts
◆ Septic infarcts
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Morphology
◆ Red (hemorrhagic) infarcts
◆ White (anemic) infarcts
◆ Septic infarcts
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Sequences
◆ Nature of the vascular supply
◆ Rate of development of occlusion
◆ Vulnerability to hypoxia
◆ Oxygen content of blood
Site & Size