FLUID AND HEMODYNAMICS DERANGEMENTS

TERMINAL OBJECTIVES
Once this section is completed, each student should be able to perform the
following tasks.
1. Give the identifying feature and distinguish between active hyperemia,
congestion and hemorrhage on the basis of causative mechanisms, gross
lesions, microscopic findings and prognosis.
2. Briefly outline the manner in which heart lesions may lead to passive
congestion of the lungs, passive congestion of the liver, lung infarction, kidney
infarction, ischemia or the myocardium, generalized edema and shock.
. !iscuss the causes, types, significance and fate of hemorrhage.
". !iscuss the interrelationship between thrombi, emboli and ischemia in the
formation of renal infarction, beginning with a lesion in the left atrium of the
heart.
#. !iscuss the role of platelets, components of the blood vessel wall and the
clotting se$uence in normal hemostasis.
%. &ist and describe the factor which predisposes to thrombosis. !ifferentiate
between a thrombus and a postmortem clot on the basis of gross and
microscopic findings.
'. Give the identifying feature of "disseminated intraas!"#ar !$a%"#ati$n"
and e(plain why bleeding tendencies are induced by this condition.
). Briefly discuss the causes and effects of pulmonary and systemic
embolism.
*. Briefly outline the manner in which red and pale infarcts develop in various
organs and+or tissues.
1,. !iscuss the causative mechanisms of generalized and localized edema.
11. !iscuss the manner by which a loss of blood volume and the pooling of
blood in capillary beds may induce shock
12. -rovide appropriate answers for the post.instructional self.e(amination
$uestions outlined at the end of this section.
AN OVERVIE&
/t this point, the student understands the ways in which normal and abnormal
cells accumulate a variety of products.
Remember, the gamut of cellular changes discussed in the
preceding sections will be encountered over and over again
throughout all subsequent considerations of disease states.
0n this section, lesions related to circulatory disturbances are considered. 1ost
lesions that develop in the body are influenced directly or indirectly by the blood
and+or blood vessels. 2hose circulatory disturbances common to many types of
lesions include hemorrhage, hyperemia, congestion, ischemia, thrombosis,
embolism, infarction, edema, shock and disseminated intravascular coagulation.
TERMINAL OBJECTIVES
Once this section is completed, each student should be able to perform the
following tasks.
1. Give the identifying feature and distinguish between active hyperemia,
congestion and hemorrhage on the basis of causative mechanisms, gross
lesions, microscopic findings and prognosis.
2. Briefly outline the manner in which heart lesions may lead to passive
congestion of the lungs, passive congestion of the liver, lung infarction,
kidney infarction, ischemia or the myocardium, generalized edema and
shock.
. !iscuss the causes, types, significance and fate of hemorrhage.
". !iscuss the interrelationship between thrombi, emboli and ischemia in
the formation of renal infarction, beginning with a lesion in the left atrium of
the heart.
#. !iscuss the role of platelets, components of the blood vessel wall and
the clotting se$uence in normal hemostasis.
%. &ist and describe the factor which predisposes an animal to thrombosis.
!ifferentiate between a thrombus and a postmortem clot on the basis of
gross and microscopic findings.
'. Give the identifying feature of 3disseminated intravascular coagulation3
and e(plain why bleeding tendencies are induced by this condition.
). Briefly discuss the causes and effects of pulmonary and systemic
embolism.
*. Briefly outline the manner in which red and pale infarcts develop in
various organs and+or tissues.
1,. !iscuss the causative mechanisms of generalized and localized
edema.
11. !iscuss the manner by which a loss of blood volume and the pooling
of blood in capillary beds may induce shock in an animal.
12. -rovide appropriate answers for the post.instructional self.e(amination
$uestions outlined at the end of this section.
'EY &ORDS
2he student should attempt to define, spell and use the following terms prior to
and after embarking on a study of circulatory disturbances.
.. /ctive hyperemia .. !iapedesis
.. -assive congestion .. 4emostasis
.. 5enous congestion .. 4ypostatic congestion
.. Generalized passive congestion .. 6ludged blood
.. 7yanosis .. 4emorrhage
.. Brown induration of the lungs .. -etechiae
.. 4eart failure cells .. 8cchymoses
.. 7ardiac compensation .. -urpura
.. 7ongestive heart failure .. /gonal
.. 7ardiac decompensation .. 8(travasation
.. &eft.sided heart failure .. 4emothora(
.. 9ight.sided heart failure .. 4emoperitoneum
.. -hagocytosis .. 4emopericardium
.. /no(ia .. 8pista(is
.. 0schemia .. 4emoptysis
.. 4ypo(ia .. 4ematemesis
.. 4emorrhage by rhe(is .. 4ypercoagulability
.. 4emorrhage by diapedesis .. /rterial thrombi
.. 4ematuria .. 1ural thrombi
.. 1etorrhagia .. 5enous thrombi
.. 8nterorrhagia .. 5alvular thrombi
.. &inear hemorrhages .. /septic thrombi
.. -aint.brush hemorrhages .. 6eptic thrombi
.. /gonal hemorrhages .. 7analized thrombi
.. 0ntercellular spaces .. 6addle thrombi
.. 0nterstitial spaces .. Occluding thrombi
.. Bruise .. 7hicken fat clots
.. 4ematocyst .. 7urrent :elly clots
.. 4emorrhagic shock .. -ostmortem clots
.. 1elena .. !isseminated intravascular
.. 6uffusion .. coagulation
.. 38nd artery3 .. -arado(ical embolism
.. 7ollateral circulation .. 9ed infarct
.. /nemia .. 4emorrhagic infarct
.. 2hrombosis .. /nasarca
.. 2hrombi .. 4ydropericardium
.. 2hrombus .. /scites
.. 8mbolism .. 4ydrothrora(
.. 8mboli .. 8(udate
.. 8mbolus .. 2ransudate
.. 0nfarction .. 0nflammatory edema
.. 0nfarct .. ;on.inflammatory edema
.. 2hromboembolism .. 4ydrostatic pressure
.. 2hrombocytes .. Osmotic pressure
.. -latelets .. 4ypoproteinemia
.. 8ndothelial cells .. 4ypovolemic shock
.. 7oagulation system .. 6eptic shock
.. <ibrin .. 8(trinsic clotting pathway
.. <ibrinolysis .. 0ntrinsic clotting pathway
.. 7ardiogenic shock .. <at embolus
.. ;eurogenic shock .. 1etastasis
HY(EREMIA AND CONGESTION
2he terms hyperemia and congestion refer to an increased volume of blood in an
affected tissue or part. 4yperemia =a#s$ !a##ed "a!tie )*+eremia"> occurs
when arterial and arteriolar dilatation produces and increased flow of blood into
capillary beds =ina!tie !a+i##aries are $+ened>. 7ongestion ,a#s$ re-erred t$
as +assie !$n%esti$n $r en$"s !$n%esti$n> results from impaired venous
drainage. 9emember, in both hyperemia and congestion, blood is retained within
the vascular system? whereas in hemorrhage, blood is found outside of the
vascular system.
ACTIVE HY(EREMIA
Occurs when too much arterial blood is brought to an organ or tissue by dilated
arterioles and capillaries. 2he arteriolar dilatation is brought about by sympathetic
neurogenic mechanisms or by the release of vasoactive substances. 0n most
instances, active hyperemia occurs subse$uent to an inflammatory reaction =it is
t)e -irst sta%e $- in-#ammati$n>. Other situations characterized by active
hyperemia include@
=1> heat applied locally to a part and
=2> increased physiological activity.
1icroscopically, the capillaries are dilated and filled with blood. Grossly, the
involved organ+part takes on the bright red color of arterial blood =de+endin% $n
t)e $ri%ina# !$#$r.. 7linically, the organ+part is warmer than normal.
Remember, active hyperemia is usually localized (if it was
generalized, there would be insufficient blood in major
vessels to maintain systemic blood pressure and shock
would occur).
(ASSIVE CONGESTION
,C$n%esti$n> occurs when the flow of blood leaving an organ or part is impeded
=impaired venous drainage>. 1icroscopically, congestion is similar to hyperemia
=!a+i##aries and eins are di#ated and -i##ed /it) 0#$$d>. Grossly, the involved
tissues appear bluish.red because of the poorly o(ygenated venous blood.
Remember, congestion of capillary beds is closely related to the
development of edema thus, passive congestion and edema
commonly occur together.
&ocalized -assive 7ongestion is usually caused by pressure placed on veins
leaving an organ or part ,ia 0anda%e1 r"00er 0and1 t$rsi$n1 et!2>. Oftentimes,
the compression on vessels is such that blood still gets in through thick.walled,
muscular arteries but pressure on thinner.walled veins restrict the outflow and
venous blood accumulates.
Generalized -assive 7ongestion is associated with impediment of blood flow in
the central circulation =)eart1 #"n%s1 ma3$r esse#s1 et!2>. 0t may be acute or
chronic. /cute generalized passive congestion is usually associated with a failing
heart. 7hronic generalized passive congestion is most obviously manifested in
the lungs, liver and spleen.
7hronic Generalized -assive 7ongestion of the &ungs is encountered in all forms
of cardiac decompensation that occurs subse$uent to reduced left ventricular
output =#e-t4sided )eart -ai#"re.. /n accumulation of blood and increased
hydrostatic pressure occurs in the lungs. 6ome of the distended lung capillaries
may rupture or hemorrhage per diapedesis may occur. 8ventually, the
breakdown and phagocytosis of erythrocyte debris leads to the appearance of
hemosiderin.laden macrophages =)eart4-ai#"re !e##s> in the alveolar spaces. 0n
time, the alveolar walls become fibrotic. 2hus, the fibrosis and hemosiderin
pigmentation constitute the basis for the designation "0r$/n ind"rati$n $- t)e
#"n%2"
7hronic -assive 7ongestion of the &iver results from right.sided heart failure
=rare#* -r$m $0str"!ti$n $- t)e +$steri$r ena !aa..
HEMORRHAGE
4emorrhage refers to the presence of erythrocytes outside the blood vessels.
2he vessel may be physically damaged so that erythrocytes flow out through a
break in the wall or the erythrocytes may pass through an intact vascular wall by
a process called diapedesis. 2he various etiologic agents that play a role in the
development of hemorrhage are discussed in your te(tbook =pages !""#!"!>.
2he following are some of the terms used to denote hemorrhage.
.. -etechiae5 re-er to very tiny hemorrhages which occur as "tin* +in
+$ints3 up to 1.2 mm in diameter. 6uch hemorrhages occur in the skin,
mucous membranes and serosal surfaces. -etechiae are commonly
observed in septicemia where the endothelium is damaged or destroyed.
.. 8cchymoses@ re-er to larger hemorrhagic areas up to 2. cm in size
=#ar%e 0r"ises are e!!)*m$ses>.
.. -urpura@ re-er to hemorrhages which are slightly larger than petechiae.
6uch hemorrhages are associated most commonly with disturbances of
the clotting mechanism.
.. /gonal hemorrhages@ re-er to small hemorrhages the size of petechiae
and ecchymoses that arise :ust prior to death ,ass$!iated /it) t)e deat)
str"%%#e..
.. &inear hemorrhages@ re-er to hemorrhages which appear as lines.
.. -aint.brush hemorrhages@ re-ers to e(tensive streaking with
hemorrhages =seera# #inear )em$rr)a%es /)i!) a++ear side 0* side.2
.. 8(travasation@ re-ers to hemorrhages in tissues spread over
considerable areas. 6uffusions are diffuse, flat, often irregular.shaped
areas of bleeding. 4ematocyst re-ers to more or less spherical shaped
collection of blood in tissues =si6e /i## ar*.2
.. 4emothora(@ re-ers to hemorrhage into the thoracic cavity.
.. 4emopericardium@ re-ers to hemorrhage into the pericardial sac.
.. 8pista(is@ re-ers to hemorrhage from the nostrils.
.. 4emoptysis@ re-ers to the e(pectoration of blood that originates from the
respiratory tract.
.. 8nterorrhagia@ re-ers to intestinal bleeding.
.. 1etorrhagia@ re-ers to uterine bleeding.
.. 4ematuria@ re-ers to blood in the urine.
.. 4emorrhage by rhe(is@ re-ers to hemorrhage that occurs subse$uent to
a break in the wall of a vessel ,a## !$nstit"ents $- t)e 0#$$d es!a+es.2
.. 4emorrhage by diapedesis@ re-ers to hemorrhage that occurs when
erythrocytes escape through an apparently intact vessel wall.
2he significance of hemorrhage depends on@
=1> the volume of blood loss,
=2> the rate of blood loss and
=> the site of hemorrhage.
/bout ,A of the total blood volume is the ma(imum which can be lost and the
animal still recover. 0f more is lost, death is likely to occur subse$uent to
hypovolemic shock. 4owever, the amount of blood which can be lost depends
upon the rapidity with which it leaves the vascular system. $or e%ample, when
the rate of hemorrhage is slow ,st$ma!) /$rm in-e!ti$ns>, fluid can be added
to the blood rapid enough to maintain near normal blood pressure? thus, the loss
of large amounts may have little clinical significance. /lso, the site of hemorrhage
will influence its effect on the host. / hemorrhage which would be trivial in the
subcutaneous tissues may cause death when located in the brain stem.
9epeated or chronic e(ternal hemorrhages ,i2e21 /)en 0#$$d is s)ed -r$m t)e
s7in1 G2I2 tra!t1 et!2. represent losses not only of blood volume but also of
valuable iron. Bsually, the small but repeated volume losses are rapidly corrected
by movement of water from the interstitial spaces into the vascular compartment,
but the chronic losses or iron may lead to iron deficiency anemia. 0n contrast,
when erythrocytes are retained, as occurs with hemorrhages into the body
cavities, :oints or tissues, the iron can be recaptured for synthesis of hemoglobin.
2he fate of an area of hemorrhage depends upon the amount of blood that has
escaped from the vascular system. 0f the hemorrhage is relatively small, the fluid
portion of the blood is absorbed, the leukocytes move back into the vascular
system and the erythrocytes are phagocytized. 0n a larger hemorrhage, there is
disintegration and breakdown of erythrocytes with the formation of hematoidin
and hemosiderin. 7holesterol may also be seen in the tissues. 2he escaped
blood also clots with the formation of fibrin and this fibrin and the remaining
leukocytes may eventually be phagocytized. 0n still larger areas of hemorrhage,
fibroblasts and new capillaries may proliferate into the area of clotted blood. 2his
process is known as organization of the area of hemorrhage.
SLUDGED BLOOD
6ludged blood refers to the conglutination or sticking together of erythrocytes
within blood vessels and should be distinguished from simple rouleau( formation
in which erythrocytes merely stack one on top of another. 0n the formation of
sludged blood, large masses of erythrocytes adhere to each other and may settle
to the lower portion of large vessels or even block smaller vessels. 2he etiologic
mechanism is uncertain, but for some reason the erythrocytes lose their ability to
repel each other and conglutinate. 2his condition has been studied e(tensively in
man by microscopic e(amination of vessels in the con:uctiva during life and has
also been reported in swine infected with hog cholera virus. 0t is postulated that
sludged blood flows more slowly, may give rise to blood clots within the vessel
and may cause hypo(ia of the tissues involved.
ISCHEMIA
0schemia refers to local anemia or a deficiency of arterial blood to a portion of an
organ or part. 2he chief causes of ischemia are
=1> e(ternal pressure upon an artery,
=2> narrowing of the lumen of an artery and
=> a thrombus or embolus.
4owever, ischemia may be caused by vasoconstriction as observed in ergot
poisoning. 2he effects of ischemia are dependent on the organ involved, the size
of the vessel, the degree of occlusion and the degree of collateral circulation. 0f
ischemia occurs in an "end arter*1" as in the kidneys, the result is likely to be
acute necrosis of tissue supplied by the vessel. 0f the obstruction to blood flow is
gradual, atrophy may occur.
THROMBOSIS
2hrombosis refers to the formation of a clot from elements of the circulating blood
within the vascular system during life. 2his clot is known as a thrombus ,+#"ra#1
t)r$m0i.2 2he development of a clot is life.saving when a large vessel ruptures
or is severed. 4owever, when a thrombus develops within the vascular system, it
may be life.threatening because@
.. 0t may decrease of obstruct vascular flow causing ischemic+hypo(ic
in:ury to cells, tissues and organs.
.. 0t may become dislodged or fragmented to create emboli =an em0$#"s
is an intraas!"#ar mass !arried in t)e 0#$$dstream t$ s$me site
rem$ed -r$m its $ri%in..
2he ischemic necrosis created by a thrombus ,em0$#"s. is referred to as an
infarct ,t)r$m0$sis and em0$#ism are s$ !#$se#* interre#ated as t$ %ie rise
t$ t)e term t)r$m0$em0$#ism.. 2o a considerable e(tent, thrombosis is the
conse$uence of inappropriate activation of the processes of normal hemostasis.
2herefore, the student should review normal hemostasis as outlined in the
te(tbook before considering the pathogenesis of thrombosis.
"N$rma# Hem$stasis" is influenced by components of the blood vessel wall,
platelets and the clotting se$uence. 2he integrity of the blood vessel wall is
crucial in normal hemostasis as well as in thrombosis. 2he lining endothelium
provides a nonreactive interface between the underlying reactive element of the
vessel wall and the fluid blood. 0n addition, the endothelial cells serve to protect
against thrombi formation by@
=1> releasing plasminogen activator which initiates fibrinolysis and
=2> degrading platelet.aggregating agents such as adenosine phosphate
and certain forms of prostaglandins. Bnderlying the endothelial layer is the
subendothelial connective tissue which contains collagen fibrils. 2hese
collagen fibrils are potent activators of clotting factors, and they promote
platelet adhesion. 0n summary, the endothelial cells of the vessel wall are
crucial in the maintenance of normal blood flow. 0f the endothelial layer is
damaged, the subendothelial collagen fibrils will release 3tissue factors3
that activate the coagulation system.
-latelets are assigned a central role in normal hemostasis and thrombosis. 2hey
adhere to sites of endothelial in:ury, aggregate to form platelet masses, release
granules rich in a variety of secretory products and synthesize several types of
prostaglandins. 0n normal hemostasis, platelets adhere to the severed margins of
a vessel within seconds to a few minutes. 2he most important stimulus to such
adherence is the e(posure of collagen fibrils. Once adhered, platelets release
two types of granules@
=1> alpha granules which contain fibrinogen, beta thromboglobulin, cationic
protein and platelet factor " =a )e+arin ne"tra#i6in% +r$tein> and
=2> dense bodies, which are rich in serotonin, /!-, /2- and ionized
calcium.
2he release of platelet granules is triggered by a number of substances,
including collagen fibrils, thrombin, plasmin, trypsin, endoto(in and antigen.
antibody comple(es. 0t is believed that these stimuli to platelet activation inhibit
membrane.bound adenyl cyclase ,de!reased am$"nts $- !*!#i! AM( are
-$"nd in a%%re%ated +#ate#ets.. Cithin aggregated platelets, there is increased
concentration of calcium ,t)is !ati$n is a +$tent stim"#"s t$ +#ate#et
a!tiati$n.2 0n addition, platelet factor , which participates in the intrinsic
pathway of the clotting se$uence, becomes activated. 0nitially, the platelet
aggregation forms a temporary hemostatic plug which is friable and easily
dislocated in rapidly flowing bloodstreams ,)$/eer1 at t)is time1 t)e !#$ttin%
se8"en!e #eads t$ t)e -$rmati$n $- t)r$m0in /)i!) is t)e m$st +$/er-"#
+#ate#et a%%re%at$r *et identi-ied.. 0n summary, platelets@
=1> provide a temporary plug capable of controlling blood flow in small
vessels in low pressure systems,
=2> initiate the development of a permanent plug composed of aggregated
platelets and fibrin,
=> release serotonin which augments vasoconstriction and
="> contributes to the coagulation mechanism.
2he coagulation system plays a ma:or role in normal hemostasis. 1aintenance of
normal fluidity of blood involves the interplay between procoagulants and
anticoagulants. Chen the procoagulants dominate and clotting is triggered
inappropriately in the intact cardiovascular system, thrombi result. 7oncurrent
with the formation of the platelet plug, the coagulation system is activated =the
clotting factors involved are listed on page 1,# of your te(tbook>. 2he critical
events in blood clotting are the conversion of prothrombin to thrombin and the
subse$uent conversion of soluble fibrinogen into the stable fibrin polymer ,t)e
se8"en!e $- intera!ti$ns am$n% t)e !#$ttin% -a!t$rs is +resent in *$"r
te9t0$$7.2 9emember, clotting may be initiated by the intrinsic pathway when
blood is e(posed to a negatively charged surface, such as collagen. 2he e(trinsic
pathway initiates clotting when in:ury e(poses the blood to factors derived from
in:ured cells and tissues. 2hus, the evolution of a thrombus begins with the
adherence of platelets at sites of vascular in:ury followed by the build.up, first of a
temporary aggregation of platelets, and then the formation of a more permanent
platelet mass which in turn leads to the standard clotting se$uence, possibly
involving both the intrinsic and e(trinsic pathways.
2hrombosis is influenced by three ma:or factors@
=1> in:ury to vascular endothelium,
=2> alterations in normal blood flow and
=> alterations in the blood =)*+er!$a%"#a0i#it*>.
8ndothelial in:ury plays a dominant role in the formation of thrombi in arteries and
in the heart. Once the endothelium is damaged, subendothelial collagen may be
e(posed and tissue thromboplastic, etc., is released and the se$uence of platelet
adherence and activation of the clotting se$uence follows.
/lterations in ;ormal <low as encountered with stasis and turbulence of blood
contributes to the development of arterial and cardiac thrombi and are probably
re$uisite for venous thrombosis. 0n the normal flowing bloodstream, the larger
particles, such as erythrocytes and leukocytes, occupy the central or more
rapidly moving a(ial stream. 2he smaller platelets are carried in the more slowly
moving laminar stream outside the central column. 2he periphery of the
bloodstream ad:acent to the endothelial layer moves more slowly and is free of
all formed blood elements. 0f stasis or turbulence occurs, this laminar flow is
disrupted and platelets are brought in contact with the endothelium. 8vidence
suggests that stasis and turbulence assume the greatest degree of importance in
the formation of venous thrombi.
/lterations in blood that induce hypercoagulability have been proposed to e(plain
the increased incidence of thrombosis encountered in certain clinical states
,-$##$/in% s"r%i!a# +r$!ed"res1 +art"riti$n1 a!!identa# tra"ma1 et!2. 4yper.
coagulability has been defined as "an a#tered state $- !ir!"#atin% 0#$$d t)at
re8"ires a sma##er 8"antit* $- !#$t4+r$m$tin% s"0stan!es t$ ind"!e
intraas!"#ar !$a%"#ati$n t)an is re8"ired t$ +r$d"!e !$m+ara0#e
t)r$m0$sis in a n$rma# )$st2" 0ncreased numbers of platelets, increased
platelet stickiness, elevated levels of fibrinogen, increased generation of
thrombin, etc., have been identified as causing hypercoagulability in various
clinical conditions.
Grossly, thrombi are friable, a mi(ture of red and gray in irregular layers, dull, and
attached to the endothelium. /rterial thrombi formed in a rapidly flowing
bloodstream are usually dry, friable gray masses composed of almost regularly
arranged layers of platelets and fibrin, irregularly mi(ed with small amounts of
darker red coagulated blood. 2he resulting laminations are known as the "#ines
$- :a)n2" /rterial thrombi are referred to as white or conglutination thrombi.
5enous thrombi, formed in a slow.moving bloodstream, appear as an
intravascular clot that closely resembles the clotting of blood in a test tube. 6uch
thrombi are red, gelatinous, and they are referred to as stasis or red coagulation
thrombi. 2he following terms are used to describe thrombi@
.. 1ural thrombi . are attached to the wall of the heart or blood vessel.
.. Occluding thrombi . are attached to the entire circumference of the
vessel.
.. 5alvular thrombi . are attached to the heart valves.
.. 7analized thrombi . occur when new blood channels form in an
organized thrombus.
.. 6addle thrombi . straddle the bifurcation of blood vessels.
.. 6eptic thrombi . are those which contain bacteria.
.. /septic thrombi . are those that do not contain bacteria, etc.
1icroscopically, thrombi are eosinophilic masses in which leukocytes and
erythrocytes may be seen. <ibrin is usually obvious, but it is seldom possible to
identify platelets.
2he significance, effects and outcome of thrombi should be reviewed in your
te(tbook. 0f an animal survives the immediate ischemic effects of a newly
developed thrombus, one of several pathways may be followed. 2he thrombus
may
=1> increase in size and, by its enlargement, eventually cause obstruction
of some critical vessel,
=2> give rise to emboli =t$ 0e dis!"ssed.,
=> be removed by fibrinolytic action or
="> become organized.
(OSTMORTEM CLOTS5
/ thrombus must not be confused with postmortem clotting of blood within the
vascular system. 2he two types of postmortem clots are@
=1> red or current :elly clots and
=2> yellow or chicken fat clots.
9ed or 7urrent Delly 7lots occur when the components of the blood are evenly
distributed throughout the clot. 2his type develops when there is rapid clotting of
blood.
Eellow or 7hicken <at 7lots result from a settling and separation of erythrocytes
from the fluid phase of the blood. 6uch clots occur when postmortem clotting is
delayed.
2he following table gives the characteristic features of a thrombus and a
postmortem clot.
DISSEMINATED INTRAVASCULAR COAGULATION
!isseminated intravascular coagulation ,DIC. refers to widespread microthrombi
formation in capillaries, arterioles and venules. 2he thrombi are composed
largely of fibrin and aggregated platelets. 2he disorder may be a complication of
a diverse group of clinical diseases in which there is activation of the intrinsic
pathway of blood clotting. !uring the widespread intravascular coagulation, fibrin
is deposited throughout the vascular tree resulting in microthrombi. /lthough the
fibrinolytic system is activated, it cannot effectively deal with the large deposits of
fibrin. /s a result, there is rapid consumption and eventually a deficiency of
clotting factors, including fibrinogen, platelets, prothrombin and factor 5, 500, and
F =a de-i!ien!* $- -i0rin$%en1 +#ate#ets and +r$t)r$m0in is re8"ired -$r t)e
dia%n$sis $- DIC.2 2herefore, animals with !07 have bleeding tendencies on
hemorrhagic diathesis. /lso the widespread occlusion of the microcirculation may
induce signs of shock, acute respiratory distress, central nervous system
depression, heart failure or renal failure. 9emember, affected tissues may not
necessarily disclose the microthrombi because of prompt activation of the
fibrinolytic system.
EMBOLISM
8mbolism refers to the process of a foreign body moving through the circulatory
system and becoming lodged in a vessel causing obstruction. /n embolus
,+#"ra#4 em0$#i. is a detached intravascular solid, li$uid or gaseous mass that is
carried by the blood to a site distant from its point of origin. 0nevitably, emboli
lodge in vessels too small to permit their further passage resulting in partial or
complete occlusion of the vessel. 2he ma:ority of all emboli arise from thrombi
,t)r$m0$em0$#ism.. 2hese are pieces of thrombi which have been broken
loose by the force of the bloodstream. &ess common forms of emboli include fat
emboli, gas emboli, bacterial emboli, tumor emboli and parasitic emboli (see
your te%tbook).
!epending on their site of origin, emboli may come to rest anywhere within the
cardiovascular system. ,Un#ess $t)er/ise 8"a#i-ied1 t)e term "em0$#"s"
im+#ies t)r$m0$em0$#ism t)r$"%)$"t t)is dis!"ssi$n.2
(ULMONARY EMBOLISM5
-ulmonary emboli usually originate from thrombi in veins or in the
right heart. !islodgement of venous thrombi, in part or whole,
produces an embolus which flows with the venous drainage
through progressively larger vessels to the right heart. Bnless the
embolus is very large, it passes through the spacious chambers
and valve openings of the right heart and enters the pulmonary
arterial circulation. &odgement of emboli in ma:or pulmonary
vessels is commonly fatal, resulting in sudden death. Chen
pulmonary emboli occlude smaller vessels, they usually cause lung
hemorrhage or infarcts. 4owever, in animals without cardiac or
circulatory insufficiency, the bronchial circulation suffices to
substain the vitality of lung tissue. 9emember, pulmonary infarction
results only when the bronchial circulation is inade$uate to
compensate, which is common in animals with impaired
cardiovascular function.
SYSTEMIC EMBOLISM5
6ystemic embolism re-ers to emboli which travel through the
arterial circulation. 6uch emboli usually arise from thrombi within
the left heart. 0n contrast to venous embolism, arterial emboli travel
through vessels of progressively diminishing caliber. 2he
myocardium, spleen, kidneys, brain and lower e(tremities are
commonly the victims of arterial embolism.
-arado(ical embolism refers to emboli which enters the right side of
the heart and pass through interatrial or interventricular septal
defects to gain access to the arterial side of the circulation.
INFARCTION
/n infarct is a localized area of ischemic necrosis in an organ or tissue resulting
from occlusion of either its arterial supply or venous drainage. 2he vascular
occlusion is usually caused by thrombosis and+or embolism of the arterial blood
supply. 1ore rarely, e(ternal compression of vessels by e(panding tumors, etc.,
may result in infarction.
0nfarcts are classified on the basis of their color =red $r +a#e in-ar!ts> and on the
presence or absence of bacterial contamination ,se+ti! $r ase+ti! in-ar!ts.2
-ale or anemic infarcts are encountered with arterial occlusion and in solid
tissue. Chen a solid tissue is deprived of its arterial circulation, the infarct may be
transiently hemorrhagic, but most become pale in a very short time. 2he reasons
for the development of pale infarcts are as follows@
"T)e arteria# !ir!"#ati$n t$ an area is $!!#"ded2 Vesse#s1 +arti!"#ar#*
!a+i##aries1 as /e## as +aren!)*ma# !e##s are destr$*ed2 At t)e m$ment $-
as!"#ar $!!#"si$n1 0#$$d -r$m anast$m$ti! +eri+)era# esse#s -#$/s int$
t)e -$!"s $- in3"r*1 +r$d"!in% t)e initia# )em$rr)a%i! a++earan!e2 I- t)e
a--e!ted tiss"e is s$#id1 see+a%e $- 0#$$d -r$m t)e anast$m$ti! esse#s is
minima#2 S$$n a-ter t)e initia# 0#$$d see+a%e1 t)e er*t)r$!*tes are #*sed
and t)e re#eased )em$%#$0in +i%ment eit)er di--"ses $"t $r is !$nerted t$
)em$siderin2 T)ere-$re1 in s$#id $r%ans1 t)e arteria# in-ar!t /i## s$$n ,;< t$
<= )$"rs. 0e!$me +a#e $r anemi!2 T)e )eart and 7idne*s are re+resentatie
$- s$#id1 !$m+a!t $r%ans /)i!) tend t$ )ae +a#e in-ar!ts2"
9ed or 4emorrhagic 0nfarcts are encountered usually under the following
circumstances@
=1> with venous occlusion,
=2> in loose tissue,
=> in tissue with a dual circulation and
="> in tissues previously congested.
9ed or hemorrhagic infarcts develops in loose tissue subse$uent to arterial
obstruction in the following manner.
2he arterial circulation to an area is obstructed. 0f the tissue is loose ,#"n%1 et!2>,
large amounts of blood collect in the spongy, loose tissue at the moment of
vascular occlusion. 2his blood remains for long periods? thus, the arterial infarct
remains red. 2he lungs and intestine are sites where red infarcts tend to occur.
Remember, red infarcts may occasionally be encountered in solid
tissue or white infarcts in loose tissue.
<actors that influence the severity of damage resulting from infarction include the
following@
1.General 6tatus of the Blood and 7ardiovascular 6ystem@ /ny alteration
in the systemic circulation that reduces the o(ygen.carrying capacity of the
blood or the velocity and volume of blood flow through the tissues
predisposes to infarction.
2./natomic -attern of /rterial Blood 6upply@ 2he various tissues and
organs of the body receive their arterial supply through one of several
patterns@
o =1> a dual arterial blood supply,
o =2> a "sin%#e" arterial blood supply with few anastomoses
,ins"--i!ient t$ +r$ide ade8"ate 0*+ass !)anne#s., so.called
3end arteries,3
o => a "sin%#e" arterial blood supply with rich interarterial
anastomoses and
o ="> parallel arterial systems.
/ dual blood supply is received by the lungs and liver. 0n animals with normal
cardiac and cardiovascular status, the bronchial circulation is capable of
preventing ischemic necrosis of the lungs when a branch of the pulmonary artery
is obstructed. 6imilarly, infarction is uncommon in the liver because the portal
supply of blood may be ade$uate, even when the hepatic arterial supply is
compromised. 4owever, in the presence of cardiac failure, severe anemia, or
reduced o(ygenation of the blood, occlusion of one system may precipitate
ischemic necrosis.
/n arterial blood supply with rich interarterial anastomoses is found in the small
intestine. 4ere, blood is able to bypass focal areas of occlusion.
/n arterial blood supply with so.called "end arteries" is found in the kidneys, for
e(ample. 2he ma:or branches of the renal artery supply well.defined segments of
the kidneys. Occlusion of one of the ma:or branches, or of the main renal artery,
is invariably followed by ischemic necrosis. 4owever, if the occlusion occurs at
the terminal ramification and involves subcapsular parenchyma, there may be
sufficient blood flow from capsular vessels to prevent tissue damage.
-arallel arterial system is encountered in the forelimbs. 8ither the radial or the
ulnar artery is sufficient to sustain the vitality of the tissues when one or the other
is occluded.
.9ate of !evelopment of Occlusion@ 6lowly developing occlusions are
better tolerated than those occurring suddenly since they provide an
opportunity for alternative pathways and collateral circulation to become
activated.
1icroscopically, all areas of infarction undergo coagulative necrosis and
resorption as discussed in 6ection
(Remember, central nervous tissue undergoes liquefactive rather
than coagulative type necrosis).
2he typical coagulative appearance may be modified by e(tensive hemorrhage in
red infarcts and by bacterial suppuration in septic infarcts. Cithin a few days after
an infarct is initiated, an inflammatory reaction becomes well.defined. &ater, a
reparative process begins.
Grossly, both red and pale infarcts tend to be wedged.shaped, with the ape( of
the wedge pointing toward the focus of vascular occlusion.
EDEMA
8dema refers to an abnormal accumulation of fluid ,/ater. in the intercellular
tissue spaces or body cavities. 0t may occur as a localized ,e2%2 $0str"!ti$n $-
en$"s $"t-#$/ -r$m t)e #e%., or it may be generalized in distribution ,e2%21 in
!)r$ni! !$n%estie )eart -ai#"re.. 2he following terms are used to describe
edema@
../nasarca@ re-ers to generalized edema in which fluid in subcutaneous
tissues is especially prominent.
../scites@ re-ers to a collection of edematous fluid in the peritoneal cavity.
..4ydrothora(@ re-ers to a collection of edematous fluid in the thoracic
cavity.
..4ydropericardium or -ericardial 8ffusion@ re-ers to a collection of
edematous fluid in the pericardial sac.
8dematous fluid may be inflammatory or non.inflammatory. 0nflammatory edema
is referred to as an e(udate and it is associated with an inflammatory reaction.
;on.inflammatory edema is referred to as a transudate.
2he term "edema" refers to non.inflammatory edema throughout this discussion,
unless otherwise $ualified.
;on.inflammatory edema =trans"date. can be distinguished from an
inflammatory edema ,e9"date. on the basis of the following features.

Me!)anisms $- Edema F$rmati$n5
Before embarking on a study of the pathogenic mechanisms of edema, the
normal control and relationships of tissue fluid must be clearly understood.
Bnder normal physiologic conditions, the main filtration force that e(pels fluid
from the vessel is the hydrostatic pressure at the arterial end of the capillary
minus the osmotic pressure of the blood. 2he main absorption force that draws
fluid into the vessel is the osmotic pressure of the blood minus the hydrostatic
pressure at the venous end of the capillary. 0n the normal animal, there is a
continuous circulation of fluid from the arterial end of the capillary through the
tissues and back into the venous end of the capillary.
-hysiologically, blood enters the arterial end of a capillary with a hydrostatic
pressure =0#$$d +ress"re. of about "# millimeters of mercury, which e(pels fluid
and smaller dissolved molecules into the intercellular spaces. 4owever, this
hydrostatic pressure ,e9+"#sie -$r!e. is opposed by the osmotic pressure of
blood e(erted by such molecules as albumin and globulin. 2he osmotic pressure
is about , mm of mercury. 2herefore, at the arterial end of the capillary,
hydrostatic pressure at "# mm of mercury is overcoming the , mm osmotic
pressure of the blood plasma, and fluid is forced into the intercellular spaces at
the rate of 1# mm of mercury. /s blood travels through capillaries, its hydrostatic
pressure decreases rapidly to about 1# mm of mercury. 2herefore, at the venous
end of the capillary, hydrostatic pressure at 1# mm of mercury cannot overcome
, mm osmotic pressure of the blood, and fluid flows from the intercellular
spaces into the bloodstream at the rate of 1# mm of mercury. 6ince fluid enters
tissues at about the same rate as it leaves, there is no accumulation of fluid in
the intercellular spaces in the normal animal. 4owever, edema occurs if there is
any interference with this normal flow.
Basi!a##*1 edema is !a"sed 0*5
=1> decreased plasma osmotic pressure,
=2> increased hydrostatic pressure,
=> increased permeability of vascular endothelium and
="> lymphatic obstruction.
DECREASED (LASMA OSMOTIC (RESSURE5
Occurs when there is a deficiency of blood proteins ,)*+$+r$teinemia.2
2hus, hypoproteinemia may result from decreased formation or e(cessive
loss from the blood. /lbumin is most important in maintaining osmotic
pressure and it e(erts four times the osmotic pressure of globulin. / low
osmotic pressure in the blood increases the pressure differential at the
arterial end of the capillary so that more fluid is pushed into the
intercellular spaces. /lso, the force available to pull fluid into the
bloodstream at the venous end of the capillary is reduced. 2hus, there is
an accumulation of fluid in intercellular spaces and+or body cavities.
/ failure to form blood proteins results from malnutrition ,starati$n1
ema!iati$n> in which the "0"i#din% 0#$!7s" for blood protein formation
are not available. 6evere or advanced liver diseases ,!irr)$sis1 et!.> may
lead to hypoproteinemia since this is the site in which blood proteins
=a#0"min and %#$0"#in> are synthesized. 2he loss of plasma proteins
from the blood occurs through the intestine and kidneys. 0n the intestine,
blood protein loss is usually the result of hemorrhage over a long period of
time ,st$ma!) /$rms in s)ee+ and !att#e1 s#$/#* 0#eedin% st$ma!)
"#!ers in +i%s and d$%s1 et!2>. 0n the kidneys, renal amyloidosis is the
only fre$uently encountered condition in animals in which large volumes of
blood protein are lost through the urine.
Remember, decreased plasma osmotic pressure always
leads to generalized edema.
INCREASED HYDROSTATIC (RESSURE5
0s influenced mainly at the venous end of the capillary and it usually
results from venous stasis =severe passive congestion that results in
increased back pressure in the venous circulation>. 2he increased
hydrostatic pressure at the venous end of the capillary which pushed fluid
out of the bloodstream counterbalances the osmotic pressure which pulls
fluids into the bloodstream. 2herefore, fluid fails to return to the vessel
from the intercellular tissue. 6ubse$uent to venous stasis, the capillaries
become more permeable to large molecules ,a#0"min and %#$0"#in.,
since they are deprived of their normal supply of o(ygen and other
nutrients.
Remember, the usual causes of venous stasis and
subsequent increased hydrostatic pressure are impaired
heart function or a lesion in which the venous flow is
obstructed.
INCREASED (ERMEABILITY OF CA(ILLARY ENDOTHELIUM5
Occurs subse$uent to venous stasis ,res"#tin% in in!reased )*dr$stati!
+ress"re.1 as well as from direct damage, as in inflammation. 0ncreased
vascular permeability is the most important mechanism in the formation of
inflammatory edema ,e9"date.2
LYM(HATIC OBSTRUCTION5
Occurs when any lesion impedes normal lymphatic drainage by pressure
or obstruction. Bnder normal conditions, the lymphatics constantly drain
small amounts of fluid from the intercellular spaces. 2hus, in the absence
of lymphatic drainage from a area, fluid accumulates.
0n summary, decreased plasma osmotic pressure produces generalized
edema, whereas increased hydrostatic pressure may induce either
localized or generalized edema. 0ncreased permeability of capillary
endothelium and lymphatic obstruction almost always lead to localized
edema.
1icroscopically, when well.defined, edema appears as a granular,
eosinophilic interstitial precipitate that separates the cellular and fibrillar
elements of tissue ,t)e +in74stainin% a++earan!e is d"e +rimari#* t$
t)e +resen!e $- a#0"min in t)e edemat$"s -#"id.. 0n the absence of
albuminous precipitate, edema is represented by empty spaces in the
interstitial areas.
Grossly, edematous tissues are swollen, firm, doughy and pit on pressure.
2here is no redness and not sign of pain. 0f the edematous part is e(ternal,
it is cool to the touch.
8dema of the brain and lungs is the most life.threatening form of abnormal
fluid retention. 0n animals, edema is almost always parasitic, nutritional,
cardiac or renal in origin. 0f the cause is removed, edematous fluid
disappears $uickly, leaving no permanent defect in the area. 4owever, if
edematous fluid persists, it acts as a tissue irritant.
SHOC'
6hock is a clinical term which refers to peripheral circulatory failure with pooling
of the blood in the terminal circulatory beds =sma## !a+i##aries>. 2he fundamental
disturbance is that blood volume is too small to fill the vascular system, resulting
in a fall of blood pressure and cell damage due to ano(ia.
&'()*+f all capillary beds in the body were to open up, there would
not be enough blood to fill the major vessels and,or heart
thus, blood pressure falls and the flow of blood is decreased.
-lso, the loss of massive amounts of blood via hemorrhage,
etc., would have a similar effect. .ubsequently, o%ygen and
nutrient delivery to cells and removal of waste products are
decreased. (herefore, depending on the severity and
duration of the shock state, the cells of many vital organs
suffer injury and even death.
2he clinical signs of shock are inconsistent and vary with the precipitating cause.
4owever, animals with shock are usually inactive and unresponsive to e(ternal
stimuli. 1uscle weakness is prominent and there is pallor and coolness of the
skin. Body temperature is subnormal and the heart rate is increased in most
types of shock ,0"t it ma* 0e s#$/ and irre%"#ar.. !epression of renal function
and urine production often occur.
2he causes of shock may be classified as hypovolemic, septic, cardiogenic and
neurogenic.
HY(OVOLEMIC SHOC'5
0s due to loss of blood volume =)em$rr)a%e1 tra"ma1 #$ss $-
-#"ids in 0"rns1 et!2. which directly induces inade$uate perfusion
of organs and tissues.
Remember, e%tensive blood loss is required before
animals develop hypovolemic shock. (he following
sequence of changes is associated with hypovolemic
shock (as well as other forms).
6evere blood loss occurs. 2he arterial blood pressure drops and
venous return to the heart decreases. 2he heart rate may increase
but stroke volume and cardiac output are decreased. /rterial
vasoconstriction occurs rapidly with the drop in blood pressure and
increased peripheral resistance is produced which shunts blood
from the skin and viscera to the heart and brain. 0n the kidneys,
vasoconstriction reduces perfusion and causes activation of the
:u(taglomerular apparatus with the release of the enzyme renin into
the plasma. 9enin acts on an unidentified plasma protein substrate
converting it to a polypeptide angiotensin 0. /ngiotensin 0 is
converted to the potent vasoactive polypeptide angiotensin 00 by
another converting enzyme. /lso, the pituitary gland is stimulated to
release the antidiuretic hormone ,as$+ressin> which acts to
conserve water normally lost from the lower nephrons. /ldosterone
secretion by the adrenal corte( is augmented which leads to
increased resorption of salt and water by the renal tubules. /ll of
the above mechanisms conserve fluid and support blood volume.
Remember, progressive deterioration of the circulatory
system may occur despite the above compensatory
mechanisms. (he term /irreversible shock/ implies the
refractory state of circulatory failure with inability to
clinically control the condition.

SE(TIC SHOC'5
0mplies septicemia or an overwhelming infection with gram.negative
,end$t$9i! s)$!7> or gram.positive =e9$t$9i! s)$!7. organisms.
0n to(ic and septicemic conditions, there is oftentimes peripheral
dilatation of the capillary beds which subse$uently lead to shock.
Chen capillary beds are fully dilated ,as$di#ati$n>, they have the
capacity to accommodate nearly the total blood volume. 0f this
occurred, blood pressure would drop to zero =n$rma##*1 !$ntin"a#
as$!$nstri!ti$n $- t)e termina# arteri$#es +reents t)is -r$m
)a++enin%.2
CARDIOGENIC ,CARDIAC. SHOC'5
7an be viewed as "+"m+ -ai#"re23 0t occurs subse$uent to the
sudden decrease in cardiac output which accompanies sudden
e(tensive damage to the heart. 4owever, most animals succumb
directly to the myocardial failure. 0n those animals that do not,
shock may ensue because of the pooling of the blood.
NEUROGENIC SHOC'5
0mplies a shock state mediated by the nervous system which
induces peripheral dilatation ,di#atati$n $- t)e !a+i##ar* 0ed.. 0t
occurs in animals with severe fright, pain and trauma =/it)$"t
)em$rr)a%e.2
2he manifestations of shock involve many vital organs =de+endin%
$n t)e seerit* and d"rati$n $- t)e s)$!7 state>. 2he se$uence
of changes at the cellular and subcellular levels are those
described for hypo(ic in:ury ,re-er t$ se!ti$n > $- t)is s*##a0"s..
0n general, the brain and heart are highly susceptible to hypo(ia
generated by the shock state.
(OST4INSTRUCTIONAL SELF4E?AMINATION
/fter completing this section, each student should be in a position
to provide appropriate answers for the following $uestions.
-lease complete the following statements@
@"esti$ns
AAAAAAAAAAAAAAAAis t)e t*+e $- s)$!7 !a"sed 0* massie )em$rr)a%e -r$m
a %"ns)$t /$"nd2
AAAAAAAAAAAAAAAAis t)e t*+e $- s)$!7 t)at ma* dee#$+ -r$m massie
%an%rene $- t)e #$/er e9tremities 2
AAAAAAAAAAAAAAAAis t)e t*+e $- s)$!7 e9+e!ted in a +9 /it) -$"rt) de%ree
0"rns2
AAAAAAAAAAAAAAAAis t)e t*+e $- s)$!7 mediated 0* t)e ner$"s s*stem2
AAAAAAAAAAAAAAAAis t)e -"ndamenta# !a"se $- edema in a B4*ear4$#d +9 /it)
seere ne+)riti! s*ndr$me 2
AAAAAAAAAAAAAAAAis t)e -"ndamenta# !a"se $- edema in a BC *r $#d +9 /it)
!$n%estie )eart -ai#"re 2
AAAAAAAAAAAAAAAAis t)e -"ndamenta# !a"se $- edema in a CB *ear4$#d ma#e
/it) a#!$)$#i! !irr)$sis 2
AAAAAAAAAAAAAAAAre-ers t$ an a0n$rma# a!!"m"#ati$n $- -#"id in tiss"e t)at
is ass$!iated /it) an in-#ammat$r* rea!ti$n2
AAAAAAAAAAAAAAAAre-ers t$ an a!!"m"#ati$n $- a trans"date in t)e s!r$ta#
sa!2
AAAAAAAAAAAAAAAAis t)e +r$tein /)i!) e9erts a++r$9imate#* =DE $- t)e
$sm$ti! +ress"re in t)e 0#$$dstream2
AAAAAAAAAAAAAAAAre-ers t$ a !$##e!ti$n $- -#"id in t)e t)$ra!i! !ait*2
AAAAAAAAAAAAAAAAre-ers t$ #$!a# anemia in an $r%an $r +art2
AAAAAAAAAAAAAAAAre-ers t$ a #$!a#i6ed area $- is!)emi! ne!r$sis in an $r%an
t)at dee#$+s s"0se8"ent t$ $!!#"si$n $- its arteria# 0#$$d s"++#* 0* a
t)r$m0"s2
AAAAAAAAAAAAAAAAre-ers t$ t)e +r$!ess $- a -$rei%n 0$d* m$in% in t)e
0#$$dstream and s"0se8"ent#* 0e!$min% #$d%ed in a esse# !a"sin%
is!)emia and in-ar!ti$n2
AAAAAAAAAAAAAAAAre-ers t$ !#$ttin% /)i!) is tri%%ered ina++r$+riate#* in t)e
inta!t !ardi$as!"#ar s*stem $- a #iin% +atient 2
AAAAAAAAAAAAAAAAre-ers t$ t)e !$n%#"tinati$n $- er*t)r$!*tes /it)in 0#$$d
esse#s $- a #iin% anima#2
AAAAAAAAAAAAAAAAre-ers t$ )em$siderin #aden ma!r$+)a%es -$"nd in t)e
#"n% $- a CB4*ear4$#d -ema#e /it) CHF 2
AAAAAAAAAAAAAAAAre-ers t$ )em$rr)a%e t)at $!!"rs s"0se8"ent t$ a 0rea7
in t)e /a## $- a 0#$$d esse#2
;2H$/ /$"#d *$" distin%"is) a!tie )*+eremia -r$m +assie !$n%esti$nF
>2Distin%"is) )em$rr)a%e -r$m )*+eremia and !$n%esti$n $n t)e 0asis $-
%r$ss -indin%s2
<2Under /)at !ir!"mstan!es /$"#d *$" e9+e!t a!tie )*+eremia and
+assie !$n%esti$n t$ $!!"r in a d$%F
C2&)* /$"#d *$" e9+e!t edema t$ a!!$m+an* +assie !$n%esti$n $- t)e
#ierF
B2&)* /$"#d *$" e9+e!t +assie )*+eremia t$ 0e t)e d$minant -eat"re in a
t/isted +$rti$n $- t)e intestineF
G2Under /)at !ir!"mstan!es /$"#d *$" e9+e!t %enera# +assie !$n%esti$n
t$ dee#$+ in a H4*ear4$#d C$$n)$"ndF
=2Brie-#* $"t#ine t)e eents t)at #ead t$ "0r$/n ind"rati$n $- t)e #"n%" t)at
dee#$+s s"0se8"ent t$ a$rti! sten$sis2
H2&)* /$"#d #"n% edema $!!"r in a d$% /it) seere a$rti! sten$sisF
ID2Brie-#* $"t#ine t)e +at)$%enesis $- !)r$ni! +assie !$n%esti$n $- t)e
#ier t)at dee#$+s s"0se8"ent t$ sten$sis $- t)e +"#m$nar* a#e2
II2Distin%"is) )em$rr)a%e 0* r)e9is -r$m )em$rr)a%e 0* dia+edesis $n t)e
0asis $- !a"satie me!)anisms2
I;2On t)e 0asis $- %r$ss -indin%s1 )$/ /$"#d *$" distin%"is) +ete!)ia# -r$m
e!!)*m$ti! )em$rr)a%esF
I>2Distin%"is) s"--"si$n )em$rr)a%e -r$m a )emat$!*st2
I<2Distin%"is) )em$t)$ra9 -r$m )*dr$t)$ra9 $n t)e 0asis $- %r$ss -indin%s2
IC2&)* /$"#d *$" e9+e!t a sma## )emat$!*st in t)e 0rain stem t$ 0e m$re
#i-e4t)reatenin% t)an a simi#ar #esi$n in t)e s"0!"tane$"s tiss"eF
IB2&)at !$m+#i!ati$ns /$"#d *$" e9+e!t t$ $!!"r in a d$% t)at #$st
a++r$9imate#* <CE $- its t$ta# 0#$$d $#"me at a er* ra+id rateF
IG2&)at !$m+#i!ati$ns /$"#d *$" e9+e!t t$ $!!"r in a +i% /it) a s#$/#*
0#eedin% %astri! "#!erF
I=2&)at are t)e m$st !$mm$n !a"ses $- is!)emiaF
IH2&)at is t)e interre#ati$ns)i+ 0et/een an $!!#"din% t)r$m0"s1 is!)emia1
)*+$9ia and in-ar!ti$nF
;D2&)at e--e!t,s. /$"#d is!)emia d"e t$ s#$/#* +r$%ressie e9terna#
+ress"re $n t)e rena# arter* )ae $n t)e 7idne*F
;I2&)at is a t)r$m0"sF Under /)at !ir!"mstan!es is t)e dee#$+ment $- a
!#$t in t)e as!"#ar s*stem #i-e4sain%F
;;2&)* /$"#d *$" e9+e!t t)e dee#$+ment $- a t)r$m0"s in t)e -#$/in%
0#$$dstream t$ 0e #i-e4t)reatenin%F
;>2E9+#ain )$/ a t)r$m0"s ma* #ead t$ in-ar!ti$n2
;<2&)at t)ree ,>. -a!t$rs e9ert t)e ma3$r in-#"en!e $n n$rma# )em$stasisF
;C2&)* is t)e inta!t end$t)e#i"m t)at #ines t)e 0#$$d esse#s im+$rtant in
+reentin% t)r$m0$sisF
;B2&)* /$"#d *$" e9+e!t t)r$m0$sis t$ dee#$+ s"0se8"ent t$ in3"r* t$
as!"#ar end$t)e#i"mF
;G2&)* is t)e r$te $- s"0end$t)e#ia# !$nne!tie tiss"e in t)r$m0"s
-$rmati$nF
;=2Brie-#* $"t#ine t)e r$#e $- +#ate#ets in t)r$m0"s -$rmati$n2
;H2O"t#ine t)e se8"en!e $- eents t)at $!!"r in t)e dee#$+ment $- a
tem+$rar* )em$stati! +#"%2 &)at is a +ermanent )em$stati! +#"%F
>D2List t)e t)irteen ,I>. 0#$$d !#$ttin% -a!t$rs 0* t)eir R$man N"mera#
termin$#$%* as /e## as 0* a!!e+ta0#e s*n$n*ms2
>I2O"t#ine t)e se8"en!e $- eents t)at $!!"r in t)e intrinsi! !#$ttin%
+at)/a*1 0e%innin% /it) a!tiati$n $- Ha%eman -a!t$r and endin% /it) t)e
-$rmati$n $- ins$#"0#e -i0rin +$#*mers2
>;2O"t#ine t)e se8"en!e $- eents t)at $!!"r in t)e e9trinsi! !#$ttin%
+at)/a*1 0e%innin% /it) e9+$s"re $- -#$/in% 0#$$d t$ s"0end$t)e#ia#
!$nne!tie tiss"e and endin% /it) t)e -$rmati$n $- ins$#"0#e -i0rin
+$#*mers2
>>2&)at t)ree ,>. -a!t$rs e9ert t)e ma3$r in-#"en!e $n t)r$m0"s -$rmati$n in
t)e -#$/in% 0#$$dstreamF
><2&)at is +r$0a0#* t)e m$st im+$rtant +redis+$sin% -a!t$r t)at #eads t$
t)r$m0"s -$rmati$n in arteriesF
>C2&)at is +r$0a0#* t)e m$st im+$rtant +redis+$sin% -a!t$r t)at #eads t$
t)r$m0$sis in einsF
>B2&)at is t)e distri0"ti$n $- !e##"#ar e#ements in t)e n$rma# -#$/in%
0#$$dstreamF
>G2&)at is )*+er!$a%"#a0i#it*F &)* /$"#d *$" e9+e!t )*+er!$a%"#a0i#it* t$
#ead t$ t)r$m0i -$rmati$nF
>=2On t)e 0asis $- %r$ss a++earan!e1 )$/ /$"#d *$" distin%"is) an arteria#
t)r$m0"s -r$m a en$"s t)r$m0"sF
>H2Distin%"is) a !)i!7en -at !#$t -r$m a !"rrent 3e##* !#$t $n t)e 0asis $-
!a"satie me!)anisms and %r$ss a++earan!e2
<D2/)* is it im+$rtant -$r t)e +at)$#$%ist t$ distin%"is) a +$stm$rtem !#$t
-r$m an antem$rtem !#$t at t)e time $- ne!r$+s*F
<I2&)at is a +$stm$rtem !#$tF &)at is an antem$rtem !#$tF
<;2Distin%"is) a +$stm$rtem !#$t -r$m an antem$rtem !#$t $n t)e 0asis $-
!$nsisten!*1 !$#$r1 s"r-a!e a++earan!e1 atta!)ment t$ t)e "nder#*in%
end$t)e#i"m1 et!2
<>2&)at is disseminated intraas!"#ar !$a%"#ati$nF
<<2H$/ /$"#d *$" distin%"is) disseminated intraas!"#ar !$a%"#ati$n -r$m
a t)r$m0"sF
<C2O"t#ine t)e se8"en!e $- eents t)at #eads t$ 0#eedin% tenden!ies in a d$%
/it) disseminated intraas!"#ar !$a%"#ati$n2
<B2&)at is an em0$#"sF &)* /$"#d *$" e9+e!t em0$#i t$ 0e #i-e4
t)reatenin%F
<G2Under /)at !ir!"mstan!es /$"#d *$" e9+e!t -att* em0$#i t$ $!!"r in
anima#sF
<=2&)at is s$4!a##ed "!aiss$n diseaseF" Under /)at !ir!"mstan!es /$"#d
*$" e9+e!t t)is !$nditi$n t$ $!!"rF
<H2E9+#ain t)e manner in /)i!) 0a!teria# em0$#i #ead t$ metastasis $-
in-e!ti$n2
CD2O"t#ine t)e se8"en!e $- eents t)at $!!"r in t)e dee#$+ment $- #"n%
in-ar!ts -r$m a t)r$m0"s #$!ated in t)e "terine ein2
CI2Under /)at !ir!"mstan!es /$"#d *$" e9+e!t s$4!a##ed +arad$9i!a#
em0$#ism t$ $!!"rF
C;2O"t#ine t)e +at)$%enesis $- an in-ar!t t)at dee#$+s s"0se8"ent t$
t)r$m0$sis1 0e%innin% /it) 7e* 0i$!)emi!a# !)an%es and +r$%ressin%
t)r$"%) t)e "#trastr"!t"ra#1 #i%)t mi!r$s!$+i! and %r$ss a#terati$ns2
C>H$/ /$"#d *$" distin%"is) a +a#e in-ar!t -r$m a red in-ar!tF
C<2List and des!ri0e t)e -a!t$rs t)at in-#"en!e t)e seerit* $- dama%e
res"#tin% -r$m in-ar!ti$n2
CC2Under /)at !ir!"mstan!es /$"#d *$" e9+e!t in-ar!ts t$ dee#$+ in t)e
#ierF
CB2&)at t*+e ne!r$sis is ass$!iated /it) in-ar!ti$n $- t)e m*$!ardi"mF
CG2&)at t*+e ne!r$sis is ass$!iated /it) in-ar!ti$n $- t)e !ere0r"mF
C=2Distin%"is) 0et/een in-#ammat$r* and n$n4in-#ammat$r* edema $n t)e
0asis $- +r$tein !$ntent1 en6*me !$ntent1 !e## !$"nt1 s+e!i-i! %rait*1 +H1
$d$r1 !$nsisten!* and !$#$r $- t)e -#"id2
CH2H$/ /$"#d *$" distin%"is) 0et/een as!ites and )*dr$+erit$ne"mF
BD2&)at is a trans"dateF &)at is an e9"dateF
BI2E9+#ain /)* a trans"date d$es n$t dee#$+ in t)e inter!e##"#ar s+a!es
"nder n$rma# +)*si$#$%i! !$nditi$ns2
B;2&)at are t)e -$"r ,<. 0asi! !a"ses $- edemaF &)i!) $ne $- t)ese is
a#/a*s ass$!iated /it) %enera#i6ed edemaF &)i!) $ne is ass$!iated /it)
0$t) %enera#i6ed and #$!a#i6ed edemaF
B>2&)* /$"#d *$" e9+e!t edema t$ $!!"r s"0se8"ent t$ )*+$+r$teinemiaF
B<2Gie an a!!e+ta0#e de-initi$n $- s)$!72
BC2Brie-#* des!ri0e t)e si%ni-i!ant 0i$!)emi!a# and "#trastr"!t"ra# !)an%es
e9+e!ted in t)e m*$!ardia# !e##s $- d$% in a s)$!7 stateF
BB2&)at are t)e !$mm$n !#ini!a# si%ns e9+e!ted in s)$!7 stateF
BG2&)at is "irreersi0#e s)$!7F"
B= 2E9+#ain t)e manner in /)i!) 0a!teria# t$9ins are a0#e t$ +r$d"!e s)$!7
in a +9 /it) "rinar* tra!t in-e!ti$n 2
BH2H$/ /$"#d *$" distin%"is) 0et/een !ardi$%eni! s)$!7 and ne"r$%eni!
s)$!7F