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Homeostasis
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EDEMA
Increased fluid in the interstitial tissue spaces
Massive edema is calledAnasarca.
Fluid may also accumulate in body cavities
These collections of fluid are referred to based on
location as:
Hydrothorax, hydropericardium, hydroperitoneum (Ascites
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maintained by opposing effects of vascular hydrostatic
pressure and plasma colloid osmatic pressure
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Homeostasis ismaintained by the
opposing effects of
vascular hydrostatic
pressure and plasma
colloid osmoticpressure
Fluid Homeostasis
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Edema
Development
Picture
Fig 2.2
Either increased
vascular hydrostatic
pressure or decreased
plasma colloidosmotic pressure can
lead to EDEMA
Inflammatory
mediators can alter
vascular permeability
causing local
EDEMA
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Edema Fluid = TRANSUDATE
A transudate is protein-poor (specific gravity
1.020)
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Pathophysiologic Categories of Edema
I. Increased Hydrostatic Pressure
II. Reduced Plasma Oncotic PressureIII. Inflammation
IV. Other
I. Increased Hydrostatic Pressure
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I. Increased Hydrostatic Pressure:
Generalized increases in venous pressure, with
resultant SYSTEMIC EDEMA, occur MOSTCOMMONLY in CONGESTIVE HEARTFAILURE
Thus, Congestive Heart Failure is the most
common cause of EDEMA due to IncreasedHydrostatic Pressure
Types of disease causing Edema:
A. Congestive Heart Failure
B. Portal HypertensionC. Venous Thrombosis
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Congestive Heart Failure
The Pump is FAILING!!! (All the bloodgoing in IS NOT going out!)
Blood backs up, first into the lungs, then into the venous circulation - increasing
Central Venous Pressure (CVP)
Increased CVP leads to increased capillarypressure (Hydrostatic Pressure) leading to Edema
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Congestive Heart Failure
Overall, there are TWO main effects..
1. Increased Central Venous Pressure
(we just talked about this one)
2. Decreased Renal Perfusion
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Congestive Heart Failure
Decreased Renal Perfusion Decreased Cardiac Output
Leads to decreased ARTERIAL blood volume Activates the Renal Defense Mechanisms:
Renin-Angiotensin-Aldosterone Axis
Renal VasoconstrictionIncreased Renal Anti-diuretic Hormone (ADH)
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Congestive Heart Failure
Decreased Renal Perfusion Decreased Renal Perfusion activates the Renal
Defense Mechanisms:Renin-Angiotensin-Aldosterone Axis
Renal Vasoconstriction
Increased Renal Anti-diuretic Hormone (ADH)
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Congestive Heart FailureRenin-Angiotensin-Aldosterone Axis
Renin AldosteroneRenal Na
reabsorption
Renal retention of
Na + H2OPlasma volume
Transudation
EDEMA
Decreased Renal Perfusion
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Congestive Heart FailureRenal Vasoconstriction
Renal
Vasoconstriction
Glomerular Filtration
Rate (GFR)
Tubular
reabsorption of
Na + H2O
Plasma volume
Transudation
EDEMA
Decreased Renal Perfusion
Renal retention of
Na + H2O
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Congestive Heart FailureRenal Vasoconstriction
Anti-Diuretic
Hormone (ADH)
Renal retention of
H2O
Plasma volume
Transudation
EDEMA
Decreased Renal Perfusion
Renal retention of
Na + H2O
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Congestive Heart Failure
CentralVenous
Pressure
RenalPerfusion
Renin Renal
Vasoconstriction
ADH
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Portal Hypertension
Portal Hypertension is Increased resistance to portal bloodflow
The most common cause of Portal Hypertension is
CIRRHOSIS. Pathogenesis of Ascites is complex
Increased Portal Pressure (hydrostatic pressure) leads to increasedliver sinusoidal hypertension. Fluid moves into the Space of Dissethen into lymphatics
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Pathogenesis of Ascites is
complex Cirrhosis leads to hypoalbuminemia sneaking
into the next category And ultimately, there is decreased renal
perfusion leading to secondary
hyperaldosteronism (increased renin etc.)
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Portal Hypertension
Sinusoidal
HypertensionRenal
Perfusion
Hepatic LymphOverwhelms
Thoracic Duct
Aldostero
ASCITES
Cirrhosi
Serum
Albumin
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Venous Thrombosis
Impaired venous outflow increases hydrostatic
pressure
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Pathophysiologic Categories of Edema
I. Increased Hydrostatic Pressure
II. Reduced Plasma Oncotic PressureIII. Inflammation
IV. Other
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Reduced Plasma Osmotic Pressure
Albumin is the serum protein MOST responsible forthe maintenance of colloid osmotic pressure.
A decrease in osmotic pressure can result fromincreased protein loss or decreased protein synthesis.
Increased albumin Loss: Nephrotic SyndromeIncreased protein permeability of the glomerular basement
membrane
Reduced albumin synthesis
CirrhosisProtein malnutrition
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Pathophysiologic Categories
of EdemaI. Increased Hydrostatic Pressure
II. Reduced Plasma Oncotic PressureIII. Inflammation
IV. Other
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Inflammation
Both Acute and Chronic Inflammation are
associated with EDEMA
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Pathophysiologic Categories
of EdemaI. Increased Hydrostatic Pressure
II. Reduced Plasma Oncotic PressureIII. Inflammation
IV. Other
Lymphatic Obstruction
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Lymphatic Obstruction
Impaired lymphatic drainage with resultantlymphedema, usually localized
Usually due to INFLAMMATION orNEOPLASTIC OBSTRUCTION
Inflammatory (Filariasis - A parasitic infection
affecting inguinal lymphatics resulting inelephantiasis
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Picture of Elephantiasis
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Resection and/or radiation to auxiliary lymphatic
can lead to arm edema
Carcinoma of breast with obstruction of superficia
lymphatic can lead to an unusual appearance of th
breast - peau dorange (orange peel)
Neoplastic
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GENERALIZED EDEMA
(Walkers Law) HEART
LIVER KIDNEY
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Edema
Morphology Edema of the Subcutaneous
Tissue is most easily detected
Grossly (not microscopically)
Push your finger into it and a
depression remains
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Dependent Edema is a prominent feature of
Congestive Heart Failure
Facial edema is often the initial manifestation of
Nephrotic Syndrome
Edema
Morphology
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Pulmonary Edema is mostfrequently seen in CongestiveHeart FailureMay also be present in Renal
failure, Adult RespiratoryDistress Syndrome (ARDS),Pulmonary Infections andHypersensitivity Reactions.
The Lungs are typically 2-3times normal weight
Cross sectioning causes anoutpouring of frothy,
sometimes blood-tinged fluid
Normal Pulmonary Edema
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Normal Pulmonary Edema
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Edema of the Brain :
Trauma, Abscess, Neoplasm, Infection (Encephalitis), etc.
The big problem is: There is no place for the fluid to go!!! The skull is
the limit. Herniation into the foramen ovale will kill
Subcutaneous Edema :
Annoying but Points to Underlying Disease However, it can impair wound healing or clearance of Infection.
Pulmonary Edema :
May cause death by interfering with Oxygen and Carbon Dioxideexchange
Creates a favorable environment for infection
Culture Media
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Hyperemia and Congestion
Hyperemia : is an active process resulting from
augmented tissue inflow due to arteriolar dilation
(e.g. acute inflammation).
Congestion is a passive process resulting from
impaired outflows from a tissue
(e.g. cardiac failure or venous obstruction)
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Hyperemia in PneumoniaHyperemiaInfection
(Pneumonia)
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Hemorrhage
extravasation of blood due to rupture of blood vessels
Rupture of a large vessel: Trauma, Atherosclerosis, Inflammatory orNeoplastic Erosion
Rupture of small vessels: hemorrhagic diathesis. May be external, into a body cavity or into a tissue
hematoma: accumulation of blood enclosed or confined withintissue
petechiae: minute hemorrhages into skin or lining surface
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Hemorrhage Purpura (slightly larger hemorrhages than petechia) Ecchymoses (over 1-2 cm subcutaneous hematoma aka bruise).
Accumulation of blood in a body cavity: Hemothorax
Hemopericardium
Hemoperitoneum
Hemarthrosis
The RBCs in a hemorrhage are broken down: hemoglobin (red) bilirubin (blue-green) hemosiderin (golden-brown)
Thats why bruises change color as they resolve
Cli i l Eff t f
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Clinical Effects of
Hemorrhage
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Clinical Effects of
Hemorrhage >20% blood loss, hemorrhagic shock
Bleeding into the brainstem is fatal while sameblood loss from a finger cut is trivial
Chronic recurrent bleeding can lead iron
deficiency anemia!
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Anemia from Blood Loss
This may be the only hint of Occult Cancer
Carcinoma of the Colon
Gastric Carcinoma (less common)
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Hemostasis & Thrombosis
Hemostasis is the normal, rapid formation of
a localized plug at the site of vascular
injury Thrombosis is thepathologic formation of a
blood clot within the non-interrupted
vascular system in a living person
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Hemostasis
Normal - blood is flowing and not clotting
Injury - blood is clotting and not flowing This works due to a daily interaction between the
vascular wall, platelets and the coagulation
cascade
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Thrombosis
Abnormal activation of the normal hemostatic
process
Thrombosis is Pathologic
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Hemostasis
after initial injury, there is a brief period of
arteriolar vasoconstriction (neurogenic
reflex augmented by local factors such as
endothelin)
Vasoconstriction A transient effect
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Vasoconstriction A transient effect
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Hemostasis
Endothelial injury exposes the blood to the
extracellular matrix (ECM)
The ECM is highly thrombogenic
Platelets adhere, flatten and then activate
To form hemostatic plug (primary hemostasis)
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vWF = von Willebrand Factor
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summary
Adhere
FlattenActivate
Recruit
HemostaticPlug
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Secondary Hemostasis
Tissue factor together with platelet factors
activate the coagulation cascade with fibrin
deposition. Thrombin activation induces further
platelet recruitment and granule release
(secondary hemostasis)
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Secondary Hemostasis
Polymerized fibrin and platelet aggregates to
form permanent plug
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Secondary Hemostasis Pic
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Anti-thrombotic Regulation
Components of Normal
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Components of Normal
Hemostasis
Endothelium
Platelets
Coagulation Cascade
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Endothelium
Anti-thrombotic and Procoagulant Properties
Anti-thrombotic - Anti-platelet, anti-coagulant and
fibrinolytic effects
Procoagulant - Tissue Factor, vWF attachment
Figure 4-5 pro- anti coag
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Figure 4 5 pro anti coag
effects of endothelium
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Endothelial Anti-platelet Effects
Physical Barrier
prevent platelet contact with ECM;
Endothelial production of prostacyclin and nitric
oxide inhibits platelet adhesion to normal
endothelium
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Endothelial Anticoagulant Effects
Mediated by membrane-associated, heparin-like
molecules and thrombomodulin and anti-
thrombin III
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Endothelial Fibrinolytic Effects
Synthesize tissue type plasminogen activation
(t-PA) promoting fibrinolytic activity
Pro-thrombotic Properties
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Pro-thrombotic Properties
- Normal endothelium produces : von Willebrandfactor (vWF) facilitates adhesion of platelets to ECM
- Tissue Factor secretion by endothelium is induced by
cytokines or bacterial endotoxin
Tissue Factor activates the extrinsic clotting pathway.
- Endothelial cells secrete plasminogen activator
inhibitors (PAIs) which depress fibrinolysis thus
promoting thrombosis
Pl t l t
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Platelets
When circulating are (membrane-bound smooth discs)
They contain two specific types of granules:
alpha granules and delta granules.
1- Alpha: contain fibrinogen, fibronectin, factors V andVIII, platelet factor 4, platelet-derived growth factor(PDGF), and transforming growth factor (TGF- ) .
2- Delata: contain adenine nucleotides (ADP and ATP),
ionized calcium, histamine, serotonin and epinephrine
Pl t l t A ti ti
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Platelet Activation
On contact with ECM, platelets undergo:
(1) Adhesion and shape change
(2) Secretion (release reaction)
(3) Aggregation
Pl t l t Adh i
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Platelet Adhesion
Adhesion to ECM is mediated largely via
interactions with vWF which acts as a bridge
between platelet surface receptors and exposedcollagen.
Platelet Secretion
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Platelet Secretion
Both granules Explode soon after adhesion Calcium and ADP: potent mediators of
coagulation and platelet aggregation
Platelet Aggregation
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Platelet Aggregation
ADP and thromboxane A2 (TXA2) stimulate further
platelet adhesion
This sets up an autocatalytic reaction leading to anenlarging platelet mass(the primary hemostatic plug)
This is a reversible collection of platelets
Platelet Aggregation
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Platelet Aggregation
With activation of the coagulation cascade, thrombin is
generated, causing further aggregation then platelet
contraction constituting the secondary hemostatic plug This is an irreversible fusion of platelets
Prostaglandin Balancing Act
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Prostaglandin Balancing Act
PG12 (endothelium)
vasodilator
inhibits platelet aggregation TXA2 (platelets)
vasoconstriction
Stimulates platelet aggregation
Clinical Use of ASPIRIN in
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Cardiac Patients
Inhibits TXA2 Synthesis by platelets
Benefits Patients at risk for Coronary Artery
Thrombosis
New
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New
CoagulationCascadeFactor XII Tissue
Factor
X
Prothrombin
Fibrinogen
Fibrin
Thrombin
Activates Activates
Activates Activates
Xa
Coagulation Cascade
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Conversion of Pro-Factors to Activated Factors , ending in the
formation ofThrombin, Thrombin converts Fibrinogen toFibrin, Fibrin is critical for hemostasis.
Each reaction is the result of the assembly of:
Enzyme (activated) coagulation factor
Substrate (pro-enzyme form of a coagulation factor)
Co-Factor (reaction accelerator).
Occurs on a phospholipid substrate
Such as on the surface of activated platelets
Held together by calcium ions
This helps to Localize the thrombus To sites of platelet aggregation
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Fig 4-7 Thrombosison a phospholipid
surface
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Thrombosis
Pathogenesis Of Thrombosis
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Pathogenesis Of Thrombosis
Virchows triad
endothelial injury
stasis or turbulence of blood flow
blood hypercoagulability
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Endothelial Injury
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Endothelial Injury
exposure of subendothelial collagen and other
platelet activators
adherence of platelets release of tissue factor
local depletion of postacyclin (prostaglandin)
and plasminogen activator (PA)
ALTERATIONS IN
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NORMAL BLOOD FLOW
turbulence of blood flow (arterial and cardiac
thrombosis); stasis of blood flow (venous
thrombosis)
disrupt laminar flow and brings platelet in
contact with endothelium
prevent dilution of activated clotting factors
ALTERATIONS IN NORMAL BLOOD FLOW
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ALTERATIONS IN NORMAL BLOOD FLOW
Retard the inflow of clotting factor inhibitors
and permit thrombi build-up
Promote endothelial cell activation Aneurysms, mitral valve stenosis, hyperviscosity
syndromes (e.g. polycythemia)
HYPERCOAGULABILITY
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HYPERCOAGULABILITY
any alterations of the coagulation pathways that
predispose to thrombosis primary (genetic) or secondary (acquired)
disorders
HYPERCOAGULABILITY
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(contd)
mutation of factor V gene with functional
deficiency of protein C, and other anticoagulants
(protein S, antithrombin III). Patient will havevenous thrombosis and recurrent
thromboembolism
smoking, obesity, lupus anticoagulant with lupuserythematosis (arterial and venous thrombosis)
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Arterial thrombi
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Arterial thrombi
Usually begin at site of endothelial injury and
grow along flow of blood
Typically are firmly adherent to the injured
arterial wall (atherosclerotic plaque)
Clinical Settings for Cardiac/arteria
Th b F ti
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Thombus Formation
Myocardial Infarction (MI)
Rheumatic Heart Disease
Atherosclerosis
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Morphology of Thrombi
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p gy
Arterial Thrombi Are Usually Occlusive
Venous Thrombi Are Almost Always Occlusive
85-90% of Venous Thrombi Form in Lower
Extremities
Walkers Law :-)
VENOUS THROMBOSIS (PHLEBOTHROMBOSIS
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Superficial venous thrombi, usually occur in
saphenous system, may cause local congestion,
swelling, and pain; rarely embolize
Deep thrombi, usually in large leg veins at or
above knee joint (e.g. popliteal, femoral, and
iliac veins); cause edema of foot and ankle; may
embolize
Ch i i ll
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Characteristically occur at
site of stasis and extend inthe direction of blood
flow (towards heart);
contains more enmeshederythrocytes (red)
Superficial Veins of the Lower Extremities
Cause Pain, Swelling - Rarely with emobolization
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Cause Pain, Swelling Rarely with emobolization
Associated With Varicosities
Varicose Veins - Abnormally Dilated, Tortuous Veins
Increased Risk of Infections
Increased Risk of Varicose Ulcers.
Thrombi in Deep Veins (Femoral, Iliac)More Likelyto show emobolization
About 50% Are Asymptomatic (Formation of
Collaterals)
May Produce Edema, Pain and Tenderness
Clinical Settings for Venous Thrombus Formation
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Cardiac Failure (CHF)
Trauma
Surgery
Burns. 3rd Term Pregnancy and Postpartum
Cancer
Migratory Thrombophlebitis (Trousseaus Syndrome)
Bed Rest Immobilization
Valvular Thrombi
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Infective Endocarditis
Non-bacterial Thrombotic Endocarditis
Verrucous Endocarditis (Libman-sacks)
Lupus Related
FATE OF THROMBOSIS
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Propagation and obstruction
Embolization
Dissolution
Organization and recanalization
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Dissolution of Thrombi
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Recent Thrombi Can Undergo Total Lysis
After the First 2-3 h, Thrombi wont undergo
Lysis
Thus the Use of TPa Is Only Effective in the First 1-
3 Hours
Organization/Recanalization
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Granulation Tissue Followed by Capillary
Channel Formation or may heal so totally As to
Leave Only a Small Fibrous Lump AsEvidence of a Previous Thrombus
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EMBOLISM
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An embolus is a detached intravascular solid, liquid
or gaseous mass that is carried by the blood to a sit
distant from its point of origin 99% are dislodged thrombus
potential consequence: ischemic necrosis (infarctio
PULMONARY THROMBOEMBOLISM
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Generally originates from deep leg veins
Usually pass through the right heart into
pulmonary vasculature and may occlude main
pulmonary artery, across the bifurcation (saddle
embolus) or pass into the smaller, branching
arterioles; multiple emboli may occur
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Paradoxical Embolism
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Paradoxical Embolism
An embolus pass through an interarterial or
intraventricular defect to gain access to the
systemic circulation( from vein to artery)
Most pulmonary emboli (60-80%) are clinically
silent because of small size
PULMONARY THROMBOEMBOLISM
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When 60% or more of the pulmonary circulation isobstructed, sudden death may occur as caused by right
heart failure .
Embolic obstruction of medium-sized arteries may
result in hemorrhage without infarction because ofintact bronchial circulation (unless bronchial
circulation is compromised - left heart failure).
multiple pulmonary emboli over time may causepulmonary hypertension and right heart failure
SYSTEMIC THROMBOEMBOLISM
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emboli traveling within the arterial circulation
80% arise from intracardiac mural thrombi, others
from ulcerated atherosclerotic plaques, aortic
aneurysm, or from fragmentation of valvularvegetation
major sites are lower extremities (75%), brain
(10%), intestines and kidneys
FAT EMBOLISM SYNDROME
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characterized by pulmonary insufficiency,
neurologic symptoms, anemia, and
thrombocytopenia. 10% of cases are fatal
typically are caused by microscopic fat globules
derived from long bone fractures (fatty marrow),
or rarely from soft tissue trauma and burns
AIR EMBOLISM
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gas bubbles within the circulation can obstruct
vascular flow to cause distal ischemic injury
air may enter circulation in chest wall injury or
in individuals exposed to sudden atmospheric
pressure changes (decompression sickness)
AIR EMBOLISM (contd)
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Caisson Disease: chronic form of decompression
sickness in which persistent of gas emboli in the
bones (heads of femora, tibia, and humera) leadsto multiple foci of ischemic necrosis
Amniotic Fluid Embolism
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Torn placental membrane - amniotic fluid
release
Rupture of uterine veins
Infusion of amniotic fluid into maternal venous
circulation
Amniotic Fluid Embolism
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Lungs show squamous cells, lanugo hair, fat
from vernix caseosa
Pulmonary edema, diffuse alveolar damage
DIC
Amniotic Fluid Embolism
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Present with dyspnea, cyanosis, shock, seizures
and coma
Mortality of 80% Walkers Law :-)
Embolism
Potential Consequences
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Potential Consequences
Ischemic Necrosis (Infarction)
Though Pulmonary Emboli Are Common and
Important, Secondary Pulmonary Infarction Is Not
CommonLung Is Protected by a Dual Blood Supply
The Brain Is Not So Protected and Gets Infarcts
(Stroke) LIQUEFACTIVE NECROSIS
INFARCTION
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An infarct is an area of ischemic necrosis caused
by occlusion of either the arterial supply or
venous drainage in a particular tissue
nearly 90% of all infarcts result from thrombotic
or embolic events in arterial vasculatures
Venous infarcts are more
likely in organs with a
single venous outflow
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single venous outflow
channel (testis, ovary)
All infarcts tend to be
wedge-shaped, with theoccluded vessel at the
apex
RED INFARCTSO
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Occur:
with venous occlusions (e.g. ovarian torsion)
in loose (spongy) tissues (e.g. lung) that allow blood
to collect in the infarcted zone
in tissues with dual circulations (e.g. lung and small
intestines)
in tissues that were previously congested
when the occluded site is re-perfused
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FACTORS THAT INFLUENCE
DEVELOPMENT OF AN
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INFARCT
nature of the vascular supply (dual arterial
supply?)
rate of development of occlusion
vulnerability of the tissue to hypoxia
oxygen content of blood
SHOCK
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Constitutes systemic hypoperfusion due to reductioneither in cardiac output or in the effective circulatingblood volume. The end results are hypotension,followed by impaired tissue perfusion and cellular
hypoxia Three main categories: cardiogenic, hypovolemic, and
septic
Others: neurogenic shock and anaphylactic shock
CARDIOGENIC SHOCK
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Results from myocardial failure (infarction),
ventricular arrhythmia, extrinsic compression
[cardiac tamponade, or outflow obstructionpulmonary embolism)]
HYPOVOLEMIC SHOCK
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Results from loss of blood or plasma volume
(hemorrhage, fluid loss from severe burns or
trauma)
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SEPTIC SHOCK
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Caused by systemic microbial infection, most
often by gram-negative infection (endotoxic
shock) but can also occur with gram-positive and
fungal infections
PATHOGENESIS OF
SEPTIC SHOCK
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Endotoxic shock: endotoxins are bacterial wall
lipopolysaccharides (LPS) which consists of atoxic fatty acid (lipid A) core and a complex
polyssacharide cost (including O antigen)
PATHOGENESIS OF
SEPTIC SHOCK (contd)
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LPS TNF (macrophages) 1L-1
1L6/1L8
systemic vasodilation (hypotension), diminishedcardiac contractility, endothelial injury and
activation (alveolar capillary damage), activation
of coagulation system
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ANAPHYLATIC SHOCK
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IgE mediated hypersensitivity response
associated with systemic vasodilatation andincreased vascular permeability
NEUROGENIC SHOCK
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Occur in esthetic accident or spinal cord injury
with loss of vascular tone and peripheral pool ofblood
STAGES OF SHOCK
1- Initial non-progressive stage: compensatory
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1 Initial non progressive stage: compensatory
reflex, perfusion of vital organs maintained
2- Progressive stage: characterized by tissue
hypoperfusion and onset of circulatory and
metabolic imbalance
3- Irreversible stage: tissue and organ damage