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I.Edema
accumulation of abnormal amounts of fluid in the
interstitial tissue spaces or body cavities
*Effusion = edema in body cavities
Two Major Types of Edema
1. Inflammatory Edema due to increased
vascular permeability (exudate)
*TUMOR in inflammation
2. Non-inflammatory Edema (Hemodynamic
Edema) due to hemodynamic alterations
(transudate)
Factors that Maintain Normal Fluid Exchange
1. Plasma important factors; major
y Hydrostatic Pressure
y Colloid osmotic Pressure
2. Interstitial Tissue minor role in
maintaining fluid balance
y Interstitial Colloid Osmotic Pressure
y Interstitial Tissue Hydrostatic
Pressure
3. Lymphatic Drainage important since it
drains any accumulation of fluid in the
interstitial tissue and drains it into the
Thoracic Duct
DIAGRAM ABOVE:
*Microcirculation arterioles, capillaries and
venules.
*In the arteriolar end:
y Hydrostatic pressure is 32mmHg
y Interstitial Pressure is 12mmHg
*In the venular end:y Osmotic Pressure is 20mmHg
*Whatever fluid that comes out from the arteriolar
end is absorbed in the venular end; it is almost zero.
Pathophysiologic Classification of Hemodynamic
Edema
A. Increased hydrostatic pressure
y CHF
y Liver cirrhosis
B. Reduced plasma osmotic pressurey Nephrotic syndrome
y Liver cirrhosis
y Malnutrition
C. Sodium retention
y Excess salt intake with reduced
renal function
y Increased tubular reabsorption of
sodium
Reduced renal perfusion
Increased renin
angiotensin-aldosterone
secretion
D. Lymphatic obstruction Localized edema
y Inflammatory disease
Filariasis
y Post-mastectomy
*A, B, and C = GENERALIZED EDEMA
Subject: PathologyTopic: Hemodynamics 1Lecturer: Dr. Ignacio De GuzmanDate of Lecture: 08/02/2011Transcriptionist: BellasPages: 12 S
Y
2011-2012
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Difference between Exudate and Transudate
*Malignant Effusion
y Exudate
y Bloody, high SG, high protein concetration
Ascites accumulation of fluid in the peritoneal
cavity
*OVARIAN Cancer *
Hydrothorax pleural effusion; fluid accumulation
in the pleural cavity
Hydropericardium pericardial effusion
*if clear and yellowish = hemodynamic cause
*bloody and cloudy = inflammation or malignancy
Anasarca (Generalized Edema)
*maybe due to Rh incompatibility
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Periorbital Edema (in renal disease)
Bipedal Edema (in CHF)
Localized Edema (Filariasis)
*due to obstruction of the lymphatics secondary to
infectious agent
Lymphedema (Post-Mastectomy)
Pulmonary Edema - fatal
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*fluids in the alveolar spaces
*causes: Left Ventricular Failure, Infection,
Hypersensitivity Reaction, Renal Failure, etc.
Cerebral Edema fatal due to brain herniation that
can compression of the vital center of the brain
*bubbles or holes indicating edema
Cerebral Edema with Herniation
*affected side RIGHT (bigger)
*Tonsilar Herniation due to edema
*Tx/Prevention = DIURETICS
II. Hyperemia and Congestion
- Increased volume of blood in affected
tissues
Hyperemia
- arterial and arteriolar dilation with
increased capillary blood flow due to
sympathetic-neurogenic factors- ACTIVE process
- e.g: muscular exercise, febrile state, early
acute inflammation
- Color: Bright red (oxygenated blood)
Congestion
- Due to impaired venous outflow
- PASSIVE process
- Related to edema
- e.g: CHF, cirrhosis (portal hypertension)- Color: Blue-red (unoxygenated blood)
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*LUNGS
-induration/firmness due to fibrosis of the
interstitium
-brown due to hemosiderin
*Hemosiderin particles
*LIVER
-centrilobular congetion
-mottled appearance
*CARDIACCIRRHOSIS
-due to fibrosis in severe and long-standing
congestion
-liver is cirrhotic, not the heart
III.Hemorrhage
rupture of blood vessels due to trauma, surgery,
vascular disease or diseases of the blood factors
Types of Hemorrhages
1. Hematoma collection of blood in the skin
or subcutaneous tissues or even within
visceral organs
2. Ecchymoses collection of blood within
subcutaneous tissues
3. Petechiae capillary bleeding
4. Purpura larger petechiae
5. Hemothorax
6. Hemopericardium
7. Hemoperitoneum
Three Factors that Determine the Significance of
Any Type of Hemorrhage
1. Amount of blood loss
2. Rate of blood loss sudden or slow
3. Site of haemorrhage brain, pericardial,
external
Hematoma
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Ecchymoses
Petechiae
Purpura
Hemothorax
Hemopericardium
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Hemoperitoneum
*ruptured ectopic pregnancy
Hemorrhage
*most likely cause is hypertensive hemorrhage
IV. Hemostasisand Thrombosis
Hemostasis
factors that control excessive bleeding by forming
a solid plug of blood to close ruptured blood vessels
(physiologic)
Three Factors involved in Hemostasis1. Vascular wall
2. Platelets
3. Coagulation system
Events in the Formation of Hemostatic Plug
1. vessel injury vasoconstriction (transcient)
2. adherence of platelets to subendothelial
collagen activation of platelets release
of ADP, thromboxane A2 recruit
additional platelets platelet aggregation hemostatic plug (primary hemostasis)
3. release of tissue factors and platelet factors
activates plasma coagulation thrombin
converts fibrinogen to fibrin and induces
further platelet release and aggregation
(secondary hemostasis)
4. polymerized fibrin and platelets aggregate
to form solid mass (permanent plug)
Thrombosis
pathologic process characterized by formation of
a clotted mass of blood within intact vascular
system
Pathogenesis
1. Endothelial Injury
y Platelets gain access to the
subendothelial collagen
y Mural thrombi overlying areas of
myocardial infarction
y Ulcerated plaques of
atherosclerotic aorta
y Inflamed heart valves
2. Alterations in normal blood flow (stasis or
turbulence)
y Atrial fibrillation in RHD
y Aneurysms
y Sites of myocardial infarction
y Varicose veins
3. Alterations in the blood inducing
hypercoagulability
y Genetic
Common: mutations in
Factor V gene, prothrombin
gene,
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methyltetrahydrofolate
gene
Rare: antithrombin
deficiency, protein C
deficiency, protein S
deficiency, fibrinolysis
defects
y Acquired Prolonged immobilization,
DIC, APAS, contraceptive
pill, postpartum state, NS,
severe burns, disseminated
cancer
AtheroscletoricPlaque
Aortic Aneurysm
Morphology
1. Mural thrombi thrombi applied to one
wall of a capacious underlying structure
(heart, aorta)
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2. Vegetations thrombi deposited in heart
valves (infective and non-infective
endocarditis)
3. Arterial thrombi occlusive thrombi in
coronary, cerebral and femoral artery
*important factor = ENDOTHELIAL INJURY
4. Venous thrombi (phlebothrombosis)
invariably occlusive; most affect lowerextremities (90%), deep calf; femoral,
popliteal; ileal
*important factor = STASIS
Mural thrombi
(Left Ventricle)
*INFARCTION
- potential area for thrombosis due to:
a. endothelial injury
b. stasis
(Left Atrium)
*Rheumatic Heart Disease (RHD)
-most commonly affected valve is MITRAL VALVE
resulting in fibrosis of the valve, causing dilation of
the Left Atrium resulting to atrial fibrillation
Vegetations
(Infective Endocarditis)
-gross: large and bulky
Mitral Valve
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Aortic and Pulmonic Valves
(Non-Infective Endocarditis)
-gross: small and uniform in size
(Non-Infective Libman-Sacks Endocarditis in SLE)
Arterial Thrombi
(Coronary Artery Thrombosis)
(Cerebral Artery Thrombosis)
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Venous thrombi
(Femoral Vein Thrombosis)
Fate of Thrombosis
1. Propagation
-enlarge depending on the site
-arterial = retrograde
-venous = towards the blood flow
2. Embolization
- Fragmentation of the thrombus
- Depend on the localition
- If in the lower ex = LUNGS
- If in the heart/valves = depending on the
blood flow
3.
Dissolution (Resolution)-if the thrombus is small
4. Organization and Recanalization
-organization invasion by capillaries,
fibroblast, endothelial cell and smooth
muscles
-recanalization - channels are formed by
the capillaries which can retain some
degree of blood flow
Propagation
Embolization
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Organization
Recanalization
Clinical Significance of Thrombosis
1. Obstruction of arteries (INFARCTION)
2. Obstruction of veins
y Congestion and edema
y Will NOT cause Infarction except for
organs that have a single VENOUS
DRAINAGE such as TESTES and
OVARIES3. Provide possible source of emboli if
fragmented
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