CIRCULATORY DISTURBANCE Flashcards
distribution of fluid is a carefully controlled
HOMEOSTATIC MECHANISM
It play an important role in fluid distribution, hemostasis,
inflammation and healing.
ENDOTHELIAL CELLS
60% of the total lean body weight is composed of
WATER
40% of this is in the
INTRACELLULAR SPACE
15% in the
EXTRACELLULAR COMPARTMENT
5% in the
PLASMID
the accumulation of an excessive amount of extracellular water in the
interstitial fluid spaces
EDEMA
edema may be a:
TRANSUDATE or EXUDATE
The relationship between the various forces at work in the microcirculatory
bed is described by what is known as the
STARLING EQUILIBRIUM
balance exists between the?
NET FILTRATION & NET ABSORPTION PRESSURE
The changes associated with edema are dependent on:
- the severity of edema
- the rapidity of onset,
- the extent,
- the anatomic location, and
- the underlying cause of edema.
often more evident in the:
- subcutaneous tissue,
- lungs
- brain.
– fixative of choice to retain edema lesion.
BOUINS FLUID
an inflammatory effusion or edema characterized
by, high protein content, increased specific gravity
& increased number of inflammatory cells
EXUDATE,
exudate is a type of ?
ACTIVE PROCESS
-a non-inflammatory effusion or edema
characterized by:
* Low protein content
* Low specific gravity
* Low or absence on inflammatory cells
TRANSUDATE
what type of process is transudate?
PASSIVE PROCESS
refers to a local increase in the volume of blood in
tissues due to dilation of the small blood vessels,
HYPEREMIA
occurs following an increase in demand for more blood as
in the stomach and intestines during digestion, in the stimulation of erectile
tissues, and in the fleeting and pleasing neurovascular dilatation called blushing.
PHYSIOLOGICAL HYPEREMIA
on the other hand occurs as a manifestation of some
alterations in blood flow characteristics. These
include those observed during inflammation, in cardiac failure, and obstructive
venous diseases.
PATHOLOGICAL HYPEREMIA
Three factors are considered in the classification of pathological hyperemia, and
includes the following:
- Duration of hyperemia (acute or chronic)
- Extent of hyperemia (general or local)
- The underlying mechanism (active or passive)
Occurs in inflammation, and is due to
engorgement of the vascular bed following an increase in arteriolar flow into the area. Characterized by bright color of tissue due to well oxygenated blood
Acute Local Active Hyperemia.
This refers to passive engorgement of
the drainage area due to obstruction in the venous drainage.
ACUTE LOCAL PASSIVE HYPEREMIA
organ system develops chronic inflammatory lesions which progress to fibrosis and therefore, obstruction or impediment in the tissue’s venous drainage, chronic local passive hyperemia occurs.
CHRONIC GENERAL PASSIVE HYPEREMIA or
CONGESTIVE HEARTH FAILURE
major site of CHRONIC GENERAL PASSIVE HYPEREMIA
HEART & LUNGS
the liver will show generalized
congestion and could result to necrosis of periacinar (or centrilobular) hepatocytes, in a characteristic gross appearance as “nutmeg liver”.
RIGHT SIDE CHF
the lungs will show
severe congestion and edema, and in some, hydrothorax could be seen.
LEFT SIDE CHF
The term hemorrhage obviously implies rupture of a blood vessel
HEMORRHAGE BY RHEXIS
Yet, blood could also be lost from the blood vessels
through a passive process known as
HEMORRHAGE by DIAPEDESIS
usual cause of hemorrhage, where blood vessels are
ruptured or a rant is created.
TRAUMA
Deficiencies in blood coagulation factors
such as prothrombin following vitamin K deficiency and in liver disease cause a
condition called
HEMORRHAGIC DIATHESIS
clinical significance of hemorrhage depends on:
location of hemorrhage
volume of blood lost
rate of blood lost
is the formation of ante mortem clot within the blood vessels,
THROMBOSIS
clot form is called
thrombus
plural of thrombus
thrombi
or the arrest of hemorrhage by clot formation involves five
essential steps:
- vascular contraction,
- stasis of blood,
- endothelial adhesion,
- blood coagulation, and
- platelet aggregation.
This mechanism involves the components normally present in the plasma,
INTRINSIC CLOTTING FACTORS
this mechanism that involves tissue component in
addition to the components from the blood.
EXTRINSIC CLOTTING FACTOR
These two systems have a
pathway centering on the activation of Factor X (Stuart-Prower factor) into
a common pathway that leads to fibrin formation
intrinsic & extrinsic clotting factors
Central to both intrinsic and extrinsic pathways, its activation marks the point of convergence and initiation of the common pathway
Factor X (Stuart-Prower Factor):
The end product of the coagulation cascade, it forms a clot by intertwining with blood cells, plugging the wound and stopping bleeding
FIBRIN
the non-thrombogenic properties of intact
endothelial lining cells is due to the carbohydrate-rich cell coat (glycocalyx) that prevents circulating cells from adhering to the surface.
Glycocalyx Theory
the negatively-charged surface of
endothelial lining lead to a mutual electrostatic repulsion between two sets
of negatively charged cells (endothelia and blood cells).
Surface Negativity Theory
– Endothelial cells have the ability to
synthesize prostacyclin (PGI2), a prostaglandin that prevent platelet aggregation by converting platelet aggregation factors (endoperoxidase and thromboxane A2) into unstable substances.
Surveillance System Theory
a prostaglandin that prevent platelet
aggregation by converting platelet aggregation factors (endoperoxidase
and thromboxane A2) into unstable substances.
prostacylin
are three major determinants in the pathogenesis of thrombosis and are traditionally called the
Virchow’s triad
Injury to the vessel wall triggers reactions involving endothelial cells, platelets, coagulation factors, and fibrin, leading to vasoconstriction and the formation of blood clots.
vascular damage
alters blood rheology and favor thrombosis.
Venous stasis
commonly known as serotonin
5-hydroxytryptamine
norm blood pH is maintained between
7.35 and 7.45
main buffer system
bicarbonate and carbonic acid.
Excess of bicarbonate, or a deficiency of carbonic acid, leads to severe
alkylosis at a blood pH of about
7.8 pH
occurs following prolonged vomiting with loss of acid.
Metabolic alkylosis
