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Normal body
composition
Water composes about 60% of total body
mass
3 body compartments containing H2O:
Intracellular
Interstitial
Plasma
= 70%
= 25%
= 5%
Edema
The term edema signifies increased fluid in
Pathophysiology of
Edema
Anatomic
structures which
drain excess
interstitial fluid
into venous blood:
Lymphatics
Hydrostatic
pressure
Plasma colloid
oncotic pressure
Two opposing
major factors
governing fluid
movement between
vascular and
interstitial space:
Edema
Exudate - increased vascular permeability,
inflammatory edema is a protein-rich exudate
with a specific gravity that is usually greater
than 1.020
Transudate- volume or pressure overload, or
Increased Hydrostatic
Pressure
Localized increases in intravascular pressure
Clinical manifestations of
edema
Clinical Signs
Increased hydrostatic
pressure in veins due to
congestive heart failure
Lymphatic obstruction
Lymphatic Obstruction
Impaired lymphatic drainage and consequent
Inflammatory Lymphatic
Obstruction
Filariasis
A parasitic infection
EDEMA INCREASED
HYDROSTATIC
PRESSURE
CongestiveHeartFailure
Ascites
VenousObstruction
INCREASED
PERMEABILITY
Inflammation
Summary
HEART
LIVER
KIDNEY
DECREASED
ONCOTIC
PRESSURE
NephroticSyndrome
Cirrhosis
ProteinMalnutrition
LYMPHATIC
OBSTRUCTION
Inflammatory
Neoplastic
Edema Fluid
Exudate
Inflammatory
Transudate
High hydrostatic Cause
pr.
High
Low
Protein content
>1.020)
<1.012)
Specific gravity
Rich
Absent
Inflammatory
cells
Summary
Edema is extravasation of fluid from vessels into
Subcutaneous Edema
Edema of the
subcutaneous tissue is
most easily detected
Grossly (not
microscopically)
and a depression
remains
pitting edema
Edema
Pulmonary Edema
is most frequently seen in Congestive Heart
Failure
May also be present in renal failure, adult
Pulmonary Edema
The Lungs are
Normal lung
Pulmonary Edema
Pulmonary Edema
Clinical Correlation
May cause death by interfering with Oxygen
and Carbon Dioxide exchange
Creates a favorable environment for
infection
Brain Edema
Trauma, Abscess, Neoplasm, Infection
(Encephalitis)
Brain Edema
Clinical Correlation
foramen magnum
leads to death
condition.
It usually points to an underlying disease.
However, it can impair wound healing or clearance
of infection.
Creates a favorable environment for infection.
May cause death by interfering with Oxygen and
Hemodynamic
terminology
Hyperemia : locally increased blood
Hemostasis overview
Normal hemostasis
Maintain blood fluid within vessels
Induce rapid localized plug at injury site
Thrombosis
Formation of blood clot within vessel
(appropriately or inappropriately)
Three components which regulate normal
hemostasis / thrombosis:
Vascular wall, Platelets, Coagulation cascade
Hyperemia
Hyperemia and congestion:
Both indicate a local increased volume of blood
in a particular tissue
Hyperemia:
an active process resulting from augmented
blood flow due to arteriolar dilation
Examples:
sites of inflammation
skeletal muscle during exercise
Congestion:
a passive process resulting from impaired
venous return out of a tissue
It may occur:
systemically, as in cardiac failure
locally, resulting from an isolated venous obstruction
Congestion (continued):
Chronic passive congestion:
Is a long-standing congestion
The stasis of poorly oxygenated blood causes:
Chronic hypoxia degeneration or death of
parenchymal cells subsequent tissue fibrosis
Capillary rupture small foci of hemorrhage
phagocytosis and catabolism of the erythrocyte
debris accumulations of hemosiderin-laden
macrophages
Hemorrhage
Extravasation of blood from vessels into the
extravascular space
Hemorrhagic diatheses :
increased tendency to hemorrhage (usually
Hematoma:
any accumulation within tissue that results
from a hemorrhage
Large accumulations of blood in body cavities
Causes:
Trauma
Atherosclerosis
Inflammatory erosion of vessels wall
Neoplastic erosion of the vessel wall
Purpura :
Slightly larger (3- to 5-mm) hemorrhages
can be associated with:
many of the same disorders that cause petechiae
Trauma
vasculitis
increased vascular fragility
Ecchymoses:
Larger (1- to 2-cm) subcutaneous hematomas (bruises)
Vasoconstriction
Hemostasis sequence 1
Hemostasis sequence 2
Secondary Hemostasis (fibrin clot)
Green
molecule?
Anticoagulant (inhibits
thrombosis)
vWF
Orange
molecul
e?
AT III
2 =
Aggregation
3 =
Coagulation Cascade: 3
component
Fibrinolytic system:
restriction of clotting to local
site of injury
Application: Lab
evidence of DIC?
(3 nonmorphologic
abnormalities)
1) prolonged PT
2) elevated D-dimer
3) thrombocytopenia
One RBC
morphologic
abnormality?
(not sensitive or
specific)
histocytes
Fig. 4-12, Pathologic Basis of
Trauma,
atherosclerosis,
vasculitis
Atherosclerosis,
aneurysms,
valvular heart
disease
Abnormal
blood flow
Hypercoagulability
Inherited or
acquired
Blood clot
Venous thrombosis
Most common location?
Most serious complication?
Disseminated intravascular
coagulation (DIC)
Not a primary disease, but complication of
Morphology
Thrombi can develop anywhere in the cardiovascular
system
The size and shape of a thrombus depend on the site
of origin and the cause.
Arterial or cardiac thrombi typically begin at sites of
endothelial injury or turbulence; venous thrombi
characteristically occur at sites of stasis.
Thrombi are focally attached to the underlying
vascular surface; arterial thrombi tend to grow in a
retrograde direction from the point of attachment,
while venous thrombi extend in the direction of blood
flow (thus both tend to propagate toward the heart).
The propagating portion of a thrombus tends to be
poorly attached and therefore prone to fragmentation,
generating an embolus.
Clinical Correlations
Venous versus Arterial Thrombosis
Thrombi are significant because they cause
Embolism
Definition: detached intravascular solid,
Pulmonary thromboembolism
Occlusion of
small artery
results in
what type of
infarction?
Occlusion large pulmonary artery
hemorrhagic
Pulmonary thromboembolism
200,000 deaths/year in US
Many are clinically silent if small
Saddle: thrombus occluding main p. artery at bifurcation
Paradoxical : thromboembolus originating in veins, passing
arterioles
Systemic Thromboembolism
Systemic thromboembolism refers to emboli in the arterial
circulation.
Most (80%) arise from intracardiac mural thrombi, most are
associated with left ventricular wall infarcts
The remainder originate from aortic aneurysms, thrombi on
ulcerated atherosclerotic plaques, or fragmentation of valvular
vegetations.
A very small fraction of systemic emboli appear to arise in veins
but end up in the arterial circulation, through interventricular
defects. These are called paradoxical emboli.
In contrast to venous emboli, which tend to lodge primarily in one
vascular bed (the lung), arterial emboli can travel to a wide
variety of sites; the site of arrest depends on the point of origin of
the thromboembolus and the relative blood flow through the
downstream tissues.
The major sites for arteriolar embolization are the lower
extremities (75%) and the brain (10%),
Fat Embolism
Microscopic fat globules can be found in the
Air Embolism
Gas bubbles within the circulation can
Infarction
An infarct is an area of ischemic necrosis caused by
Morphology
Infarcts are classified on the basis of their
Red infarcts
Occur
1. with venous occlusions (such as in ovarian torsion);
2. in loose tissues (such as lung) that allow blood to collect
White infarcts
occur with arterial occlusions or in solid
Spleen
Septic infarctions
occur when bacterial vegetations from a heart
important determinant.
For example, as mentioned above, lungs have a dual
pulmonary and bronchial artery blood supply; thus,
obstruction of small pulmonary arterioles does not cause
infarction in an otherwise healthy individual with an intact
bronchial circulation.
Similarly, the liver, with its dual hepatic artery and portal
vein circulation, and the hand and forearm, with their dual
radial and ulnar arterial supply, are all relatively resistant to
infarction.
In contrast, renal and splenic circulations are end-arterial,
and obstruction of such vessels generally causes infarction.
Vulnerability to Hypoxia
The susceptibility of a tissue to hypoxia
Infarction, gross
features
Shock
Def.: systemic hypoperfusion due to reduced
Septic shock
25-50% mortality rate, >100,000 deaths/yr.
Increasing incidence (intensive care,
macrophages
Produced by:
macrophages
Produced by:
macrophages
Stages of shock
Nonprogressive phase
Reflex mechanisms activated and perfusion of
vital organs maintained
Progressive stage
Persistent tissue hypoperfusion leads to
widespread hypoxic cell damage, metabolic
acidosis, prolonged vasodilation
Irreversible stage
Severe cellular injury with multiorgan failure,
dominated by renal, lungs, heart