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Dr Chacko again.
We have a two hour lab today. a lot of the stuff he's going to talk about 
we will appreciate more in the lab.

so we'll have a quick overview here then go there.
it's important to understand different terminologies and processes in 
circulatory disturbances. it's not really a big deal or very complex, but 
there are situations where things are not like in biochem or 
anatomy...things may vary widely from specimen to specimen. eg, you've 
heard the term ischemia and infarction. what does it really mean? does 
ischemia always lead to infarction? no. you can have decreased blood 
supply due to arterial or venous occlusion....you could have  a stenotic 
eg atherosclerotic lesion...sometimes, tissue dies and undergoes necrosis 
- that's infarction. other times, tissue will just atrophy, or a couple 
of cells will die but not many....then there is no infarction. eg, if 
blood supply to heart or brain is reduced, there may be ischemic changes 
- eg atrophy, very small foci of cell death - but no real infarct. also, 
how tissue responds depends on the blood supply. some tissues have double 
blood supply - eg lung (bronchial and pulmonary) so infarct is rare 
there, and liver (hepatic and portal) as well. for infarct to occur in 
lung, occlusion must be massive - eg, HW dz.  if there is thrombosis in 
the PA of a lung already affected by other circulatory disturbances, then 
there is a problem. Also in liver, COULD see infarct, but is more rare. 
some tissues have parallel blood supplies. eg, forearm, has radial and 
ulnar supply. also in brain, the circle of willis - but infarct in brain 
is common - it depends on degree of occlusion. sometimes you just see 
atrophy, not full infarct.

end arteries - artery that is the end of the line, supplying to one area 
of cells. eg, in the kidney - the end arteries become occluded, you get a 
wedge shaped infarct.

type of tissue - solid organs eg kidney, liver, myocardium - infarct 
looks one way....looser organs like lung, may appear differently. also 
the brain - infarcts look different - tend to see liquefactive necrosis 
sometimes due to nature of tissue (fatty).

red infarct: looks red, due to hemorrhage - common in organs with lots of 
blood supply eg lung, w/double circulation. you get a lot of hemorrhage 
with an infarct. never see white infarct in the lung. reason for red 
color is because of collateral circulation, blood flows into artery 
that's dying and bursts...


white infarct: blood supply cut off, area dies, it looks white - seen in 
kidney. but even in this case, initially, there may be a slight reddening 
because there is some anastomosis of collateral circulation, and if blood 
goes into some of the branches can rupture arterial wall. but eventually 
looks white.
also in heart, if you have infarct, initially looks red but becomes 
white. spleen is another area...may see raised white area after infarct - 
more of a solid organ, blood supply is cut down, tissue turns white.
in healing stage, will see hyperemia around the white part.

Congestion and hyperemia:

congestion/hyperemia can be confusing. basically, both terms mean there 
is a lot of blood in the area. but generally - some people say hyperemia 
involves arterial blood, congestion involves venous blood - but that's 
less important. Dr. Chacko uses the terms interchangeably. 

so, you see a reddened area. you say the area is congested/hyperemic. 
what caused it? that's where the rest of this comes in...
two kinds of hyperemia:

ACTIVE HYPEREMIA:
Dr weber talked about active hyperemia, when he talked about 
inflammation. the first sign of inflammation is hyperemia, 
reddening...that's active, caused by active process - release of 
vasoactive amines, dilation of capillaries. this means more arterial 
blood is in the area. Two kinds of active hyperemia:
PHYSIOLOGICAL: if animal has just eaten meal, mucosa will be really red, 
because animal needs lot of blood for digestion. also, during exercise, 
muscles are redder, need more blood. that's physiological.
PATHOLOGICAL: associated with acute inflammation. Pathological active 
hyperemia is always an acute process, always associated with acute 
inflammation. where do you see the blood in active hyperemia? You see 
capillaries dilated and full of blood, and the arterioles. we're talking 
about end of vascular tree - capillaries, arterioles, maybe a very very 
small artery...but not big arteries. we're talking about arterial blood 
with this kind of hyperemia. another thing about acute inflammation - how 
do we know it is really a pathological active hyperemia? well, we see the 
vasodilation...to know if it is pathological, we look for other signs of 
inflammation. if there are no other signs of inflammation, it's not a 
pathological hyperemia. if it is, you will see edema, inflammatory cells 
eg PMNs, etc. always associated with inflammatory exudate, influx of 
inflammatory cells. it's always acute, always associated with 
inflammation.

PASSIVE HYPEREMIA:
you see that for example if you have a weak heart, the animal is in CHF, 
the pump isn't working well, and the blood coming into R side of heart 
starts to back up in the venous side. there is more blood on this side. 
again, we see capillaries, and now venules, become full of blood. a 
generalized passive congestion is seen in CHF patients.  This is a more 
chronic thing. It *could* also be acute. passive hyperemia can be acute 
or chronic, unlike active hyperemia. a venous thrombosis could cause an 
acute passive hyperemia.
the main thing is, it's more the venous blood. if you have a tumor 
developing somewhere, the tumor could put pressure on the vein, and cause 
passive hyperemia distal to the tumor. in pregnancy, may see passive 
hyperemia due to pressure of fetus on vein. this can be local process eg 
secondary to thrombosis, tumor, pregnancy; or generalized eg due to CHF. 


so, an active hyperemic lesion would look more purple/red, due to 
arterial blood. a passive hyperemic lesion will look more bluish/red - 
since it is venous. sometimes esp w/fixed tissue this is really hard to 
tell :)

also, grossly, we will see swelling of affected tissue. another term to 
know is called HYPOSTATIC CONGESTION. In necropsy room, if animal dies an 
is placed on right side, right lung is redder, that's hypostatic 
congestion - positional, postmortem. but if patient has CHF, and is lying 
on right side, will also have hypostatic congestion of the right lung. so 
this is mainly due to gravity. 

what are the effects of congestion? lets look at liver and lung.

if you have poor circulation in an area, there is less oxygenation. how 
does liver respond? you have central vein, hepatocytes, sinusoids. you 
have chronic passive congestion of liver due to heart problem. blood 
backs up in vena cava, enters hepatic vein - so central vein is 
completely full of blood, and we also see sinusoids in central area 
totally full of blood. so histologically, we see engorgement of central 
vein and sinusoids. this is poorly oxygenated blood. so hepatocytes will 
start to undergo necrosis. we'll see fatty change occuring due to cell 
injury - will start looking yellowish. so histologically we have the 
engorgement of vein and sinusoids, and the central area of hepatocytes 
starting to undergo necrosis and showing ischemic changes (fatty 
degeneration) - note that at periphery, hepatocytes are getting some 
oxygenated blood from portal system, so not as affected. this liver 
grossly will have "nutmeg" appearance. a dark red color with intermingled 
yellow areas of fatty change/necrosis. tend to call this a "nutmeg liver" 
even though technically, nutmeg is food. this is appearance of liver due 
to chronic passive congestion. thinking further, hepatocytes necrose, get 
eaten by mphages. some regeneration occurs, there's proliferation of 
hepatocytes in portal region...lots of times whne you have regeneration, 
the new tissue doesn't have normal architecture so it will end up 
undergoing necrosis as well. but grossly, early stages of chronic passive 
congestion in liver will look swollen, purple red, firm with sharp edges. 
as time goes by, will see fibrosis, firmness, shrinkage of liver, nodular 
hyperplasia. also may see icterus in the animal - hepatogenous jaundice 
(note: so far, we all did well on exam :)).

think of the lung. if animal has lesion on L heart so L heart isn't 
putting all blood out - decreased CO. blood backs up in lung, so we see 
congestion - passive congestion in the lung. so we'll see the lung 
looking red. if you cut lung, lots of blood oozes out. histologically, 
we'll see full capillaries, and eventually with this poorer oxygenation 
there may be some damage to endothelium, and we may see some fluid in the 
alveoli - maybe some edema. we'll discuss edema tomorrow. also may see 
some rupture of capillaries secondary to blood stagnation and poor 
oxygenation. may see RBC...may see macrophages filled with hemosiderin 
(heart failure cells?). long standing congestion will stimulate 
fibroblasts to proliferate, will see fibrosis, loss of alveoli. this 
makes lung feel firm, makes lung less compliant. if you have mphages with 
lots of hemosiderin, will have brown color. they call this "brown 
induration of the lung" - induration means fibrosis. brown is because of 
hemosiderin. that's the gross appearance of the lung in chronic passive 
congestion.

hemorrhage: we should see red blood cells outside the vascular system to 
call it hemorrhage. can occur by breaking the vascular system (eg cut 
artery or something) which is called RHEXIS. another way is if capillary 
walls are weak, or extreme vasodilation, can have diapedesis. hemorrhage 
can be local or generalized.

SLIDES:

[] heart - lots of fat marks the AV junction. normal muscle is nice 
pinkish brown color. then there is a whitish area with dark red edges. 
this is a recent infarct, a white infarct with hyperemia at the 
periphery.

[]another heart in cross section. an infarct in an area with more 
collateral circulation producing a red lesion - later, looks white.

[] kidney showing white lesion on surface - white infarct. don't have to 
use terms "white" and "red" infarct, though. just describe lesion as an 
infarct.

kidney is solid organ. you expect to see white infarct. but if infarct is 
due to septic embolism, you may get abscess, lots of inflammation, may 
look red. 

[]paw of animal with infection. skin is hyperemic - a bright pink color. 
this is an active hyperemia, if you look at it histologically, but you 
can't say that from just looking without knowing about the infection. you 
could do a scraping to look for infection, or take a biopsy, or 
something.

[]mast cell tumor on dog skin. we see swelling and bright red area 
surrounding a skin erosion. this is also an active hyperemia.

[] section of a bladder, histological section - the bladder was grossly  
containing several raised whitish nodules in the mucosa, but generally 
was hyperemic as well. the raised areas are full of lymphocytic 
infiltrate on histology. we also see the capillaries are all full of 
blood. we call this a follicular cystitis, because you see development of 
lymphoid follicle type structures. we see lots of mphages and neutrophils 
as well.

[] cow lung. the pleura kind of septates through it. the pleura 
penetrates through lung normally. here, we see that there are many 
engorged capillaries in the pleura. we can tell it isn't hemorrhage 
because the RBCs are in the shape of capillaries. also in lung proper we 
see hyperemia, and inflammatory cells. this animal had pneumonia.

[]liver. enlarged, dark red/purplish red. edge is very sharp from 
swelling.  chronic, passive congestion.

[]histology of above liver. can see sinusoids full of RBCs. in liver can 
be hard to tell hemorrhage from hyperemia b/c of sinusoids, but here we 
can see is really w/in sinusoids, not obscuring hepatocytes. 

[] gross appearance of liver and gross appearance of nutmeg. the mottled 
dark red/whitish yellow pattern really does resemble a nutmeg. the red is 
the blood in sinusoids, the white/yellow is necrosis/fatty change of 
hepatocytes. this is chronic, passive congestion again.

[]later stage of above - liver is more shrunken, more yellow, much more 
firm
more fibrosis has occured, still see dark red areas.

can also see chronic passive congestion with intussusception where part 
of intestine telescopes into proximal part carrying with it arteries and 
veins, causing veins to collapse - arteries don't,b ut veins do, leading 
to passive congestion.





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