Download Cell Inflammation IP Lab - UAB School of Optometry

CLASS: 10:00 – 11:00
DATE: November 10, 2010
PROFESSOR:
I.
II.
INFLAMMATION (IP LAB)
Scribe: Adam Baird
Proof:
Page 1 of 7
INTRODUCTION
a. This lecture will cover case studies that give examples of acute and chronic inflammation.
b. These examples will relate to the subjects that Dr. Anderson discussed in his recent lectures (on acute and
inflammatory responses).
c. A lot of the cases that we’ll look at today are applicable to the information that we previously covered on
microbiology and infectious disease.
d. In upcoming lectures, we’ll review pathology of infection, because inflammation is an important aspect of
infection. It’s important to note that inflammation can be seen in non-infectious conditions as well (as in the
first case of today’s lab, for example).
e. We’ll look at the histological findings and the mechanisms causing them, in hopes to understand the clinical
manifestations of the disease.
f. Note: It’s important that you study these IP labs on your own (through the website). The lectures are only to
acquaint you with the material.
g. Much of the information in these IP labs is simply vocabulary though; understanding the terminology and the
definitions of this material is an important element to this course.
APPENDIX: ACUTE APPENDICITIS
a. This patient is an 11-year-old male. He was hospitalized with a complaint of 8 hours of sever pain in the right
lower quadrant of the abdomen accompanied by nausea, vomiting, and diarrhea.
b. He had a temperature of 101 degrees Fahrenheit.
c. He had leukocytosis (increase of leukocytes) of 21,200 cells/cmm with a “shift to the left”. A normal white
blood cell count is about 6,000 – 10,000 cells/cmm. (Recall: WBC counts are measured in thousands. RBC
counts are measured in millions.) But what is a “shift to the left”? When there is an acute inflammatory
reaction, the bone marrow (the site of neutrophil production and maturation) is signaled (by chemotatic
factors) to make many more neutrophils. In an effort to provide as many neutrophils as possible, the bone
marrow actually releases neutrophils before they are mature. On a peripheral blood smear, these immature
neutrophils have just one lobe (rather than the normal 3 -5 lobes that mature neutrophils have), and they are
accordingly called “band forms” (because the one lobe looks like a band). The clinical machine that is used to
manually count cells has several “keys” designated for the type of cell that you are observing (there are keys
for monocytes, lymphocytes, mature neutrophils, and immature neutrophils, for example). The immature
neutrophil key on the machine is to the “left” of the mature neutrophil key, which is why it is clinically called a
“shift to the left”.
d. An exploratory laparotomy (a surgical incision into the abdominal cavity) revealed an inflamed appendix,
retocecal in location, which was adherent to the wall of the colon. Cases like this usually require an
immediate CT scan, which would show whether the appendix was enlarged or inflamed (if it were, the
appendix would need to be surgically removed). That is what was done in this case.
1. 1st Image Referenced
a. You can actually see acute inflammatory process. Notice that the appendix is swollen; it’s
very edematous and red, indicating the acute inflammatory response.
2. 2nd Image Referenced
a. Here is a normal appendix and an inflamed appendix. Notice the differences.
b. Look at the size. The inflamed appendix is much bigger; it’s swollen. Why? Because swelling
is part of the acute inflammatory response.
c. Look at the wall of the appendix. Notice the edema. Notice the WBC. Even in normal
appendix, there are collections of lymphoid cells (sometimes called lymphoid follicles), which
are normal parts of the reticuloid epithelial system (immune system).
d. Notice the amount of inflammatory cells. When many of these inflammatory cells are seen,
it’s evident that it’s an acute inflammatory process. How can you tell? Look at the cross
section of the appendix. Notice the purple areas, which are probably lymphoid cells or
neutrophils (which have completely taken over and caused swelling and acute inflammation
in the wall of the appendix).
3. 3rd Image Referenced
a. Notice the ulceration.
b. Most of the epithelium has been lost, but some of it can still be seen. Notice the crypts.
c. Notice the purple areas. These are inflammatory cells (most of which will be neutrophils).
4. 4th Image Referenced
a. Notice the epithelium in some areas, but the loss of epithelium in other areas (which have
been filled with neutrophils now).
5. 5th Image Referenced
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: November 10, 2010
Proof:
PROFESSOR:
INFLAMMATION (IP LAB)
Page 2 of 7
a. One concern in cases like these: a ruptured appendix (which can be seen here).
b. Notice the fibrinous material over the surface of the appendix (indicated by the redness).
c. When the appendix gets occluded and has a severe inflammatory response, it can result in
peritonitis. You can feel this on a patient’s abdomen by “rebound tenderness”. “Rebound
tenderness” is determined when you press on the patient’s abdomen, release, and the patient
feels more pain on the release than when you initially press on the abdomen. This indicates
inflammation of the peritoneal wall and possibly a ruptured appendix.
d. When the contents (bacteria) of the GI tract (which is normally a closed system) gets into the
abdominal cavity, it can results in life-threatening peritonitis.
6. 6th Image Referenced
a. Here is an example of peritonitis. Notice the inflammation in the areas of the omentum and
the mesentery.
e. The study questions will not be reviewed right now, but they are questions that you need to look at when you
study. The answers are given to help you review.
III.
LUNG: LOBAR PNEUMONIA
a. This patient is a 41-year-old man who was brought to the hospital in a comatose state. He had a history of
heavy alcohol intake. No additional information was known about him.
b. When he got to the hospital, he had a temperature of 104 degrees Fahrenheit, a WBC count of 22,700
cells/cmm (meaning he probably has a “shift to the left” like the previous patient), nuchal rigidity (meaning he
had a stiff neck), elevated spinal fluid pressure, and the presence of Gram-positive diplococci on a smear of
spinal fluid (meaning he grew streptococcus pneumoniae from his blood and spinal fluid).
c. He had a pneumonia that had become bacteremic and had spread to his spinal fluid; he had pneumonia,
bacterimia, and meningitis.
d. Recall: Streptococcus pneumoniae is the most common cause of community-acquired pneumonia, lobar
pneumonia, and is an important cause of meningitis too. Meningitis almost always happens because of
bacteremic spread of microorganisms that cross the blood-brain barrier. About 1 in 4 people with
pneumococcal pneumonia may develop bacterimia (and some may develop meningitis too).
e. The main thing here: the pneumonia.
f. Recall: When pneumococci are inhaled, it goes down to the lung, stimulating the acute inflammatory
response; it will be chemotactic for neutrophils. The neutrophils, then, will come into the lung. The vastitude of
the lung will become more permeable and the alveoli will be filled with protein and fluid (as a response to the
inflammatory stimulus). The fluid (a very good culture medium for the pneumococcus) increases the amount
of pneumococcus in the blood. Lots of fluid, then, fills the lungs and lots of neutrophils fills the alveolar
spaces. When all of this happens, an x-ray will show consolidation (because the lung is usually full of air and
you can see through it, but when it has inflammatory processes in it, it becomes opaque and you can’t see
through it). Typically, pneumococcal pneumonia is called lobar pneumonia because it occurs in large
segments of the lung simultaneously (and more than one lobe may be involved).
1. 1st Image Referenced
a. This is a lung affected by pneumonia.
b. Normally, the lung will feel spongy (if you were to touch it). Notice that it is swollen and tense
(because it is full of inflammatory processes). Notice the unaffected area of the lung. Now
notice the affected area of the lung.
2. 2nd Image Referenced
a. Notice the consolidation and infiltration here.
b. Notice the outside section of the lung. Notice the septa too (which separates the segments
and lobes of the lung).
c. Recall from some of the histology sections: If you look at the lung, you should be able to see
the alveolar walls. The alveolar spaces should be clear too.
d. The main thing here: notice that it is uniformly pink (because of the fluid and protein in the
alveolar spaces). The protein is eosinophilic and it stains pink. It’s evident that there is an
infiltrate present.
3. 3rd Image Referenced
a. With higher magnification power, it’s apparent that the alveoli are filled with inflammatory
cells.
b. This picture shows what is typical in a lung with acute bacterial pneumonia. Notice the outline
of the alveolus. Notice the congested blood vessels.
c. Notice that the alveolus is packed with neutrophils. Look closely. Notice that there are
polymorphonuclear leukocytes.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: November 10, 2010
Proof:
PROFESSOR:
INFLAMMATION (IP LAB)
Page 3 of 7
d. Notice the background of proteinaceous material, evidence of the leakage of capillaries into
the lung.
e. A Gram stain on this would make the bacteria more evident (Gram-positive diplococci).
f. When a patient has diplococcal pneumonia, they will cough (among other symptoms). They
are coughing up “rusty sputum”, as it might have streaks of blood in it (due to the
inflammatory process). It will be purulent too, because it consists of WBC, pus, bacteria, and
necrotic tissue.
g. In most cases, someone with lobar pneumonia would be treated with antibiotics. Unless the patient has a
severe case of lobar pneumonia, or unless their immune system is compromised, the patient will likely
recover. The infected lung will eventually return to its normal state too, because it’s not a bad necrotizing
pneumonia (like in Gram-negative bacteria or staphylococcus where abscesses are in the lung resulting in
the loss of the lung structure.
IV.
LUNG: BROCHOPNEUMONIA
a. Bronchopneumonia is another way that pneumonia can be classified.
b. There are many ways that pneumonia can be classified though. Pneumonia can be classified according to the
organism; bacterial pneumonia due to pneumococcus or bacterial pneumonia due to mycoplasm or a viral
pneumonia, for example, all of which are different classifications of pneumonia.
c. Pneumonia can also be classified anatomically; lobar pneumonia or bronchopneumonia, for example. Recall:
Lobar pneumonia uniformly involves the bacterial process of the entire lung. In some cases,
bronchopneumonia is a more localized bacterial process that only involves one part of the lobe of the lung
and the inflammation is mainly at the individual airway (seen here).
1. 1st Image Referenced
a. Bronchopneumonia is seen here.
b. Notice that it is localized to one particular area of the lung. It doesn’t involve the entire lung.
c. In some cases, this localized infection can produce abscessing (focal abscesses of the lung).
d. At a higher power, the abscess is evident. Compare this to lobar pneumonia (which was nonnecrotizing). Bronchopneumonia shows a liquefaction-type necrosis, because the
preservation of the outside lines of the alveoli is not seen.
e. Notice the sack of pus.
f. Lung abscesses are more difficult to treat than pneumonia. The sack of pus shown in lung
abscesses can be very large; because the bacteria that are growing in the middle of it (the
bacteria that are causing it) and because the pH of it is very low (it is very acidic), antibiotics
have a hard time penetrating the abscess, and thus, have a hard time killing the harmful
bacteria. Because there is such a necrotic process, and because there is so much damage to
the tissue due to the toxins of the bacteria and the enzymes of the neutrophils, treatment can
be even more complicated. The best way to treat an abscess is to drain it (sucking the pus of
it with a needle) and then giving attacking it with antibiotics.
2. 2nd Image Referenced
a. Notice that the architecture of the lung has been lost.
3. 3rd Image Referenced
a. A higher magnification, again showing that the architecture of the lung has been lost.
b. Notice that the alveoli are filled with neutrophils.
c. Notice the edge of the abscess. Notice that there is more bleeding and more congestion
here.
d. Notice that the alveoli walls are beginning to be destroyed.
e. Notice that this is a liquefaction-type necrosis.
f. Notices that the white cells have seemingly dominated the lung tissue; there is just too much
necrosis, bacteria, and inflammation.
V. LUNG: SARCOIDOSIS
a. Another disease is sarcoidosis, which is a chronic inflammatory condition that is not associated with a
particular type of microorganism (although viral etiology has been suspected).
b. Optometry students: Why is it important for you to know about sarcoidosis? Sarcoidosis is a glaucomatous
disease that produces granulomas that can affect many parts of the body, but especially in the eye, possibly
leading to ocular damage. It’s a condition that may show “raised things” on the conjunctiva.
c. In this case, the patient is a 33-year-old woman admitted for evaluation of an abnormal chest x-ray (because
sarcoidosis usually produces abnormal findings in the lung, although it can be found in other parts of the
body, particularly the eye). She was asymptomatic. Lab results indicated hypocalcaemia (which is important
because elevated calcium levels can be associated with sarcoidosis). She also had elevated gamma globulin
(which is a marker of chronic inflammation). She had enlarged lymph nodes too. In the lung, these sarcoid
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: November 10, 2010
Proof:
PROFESSOR:
INFLAMMATION (IP LAB)
Page 4 of 7
granulomas are typically in the lymph nodes and when the lymph nodes are replaced with granulomas, it
enlarges. Many time, people may be asymptomatic, but have abnormal chest x-rays, prompting further testing
(biopsies, usually) to determine what’s going on (because these same abnormalities can resemble cancer).
The biopsy can then be stained to look for tuberculosis and for fungi (because they can cause granuloma
disease too). In this case, the diagnosis was sarcoidosis.
1. 1st Image Referenced
a. This is a lymph node. Notice the abnormal nodules (non-caseating granulomas). With a
bacterial disease, like tuberculosis, where a chronic inflammatory response results in
granulomas, which break down in the middle and leads to caseating necrosis. With
sarcoidosis, the cells are usually preserved.
b. We know that this is a granuloma because we can see the lymphoid cells (the purple areas
around the middle).
c. Notice the epithelial cells and macrophages encircling the lymphocytes.
d. This particular lymph node is filled up with granulomas.
e. This same type of appearance may be seen in the conjunctiva of the eye.
2. 2nd Image Referenced
a. Here is a close view.
b. Notice the lymphoid cells (purple areas).
c. Notice the epithelial cells. Notice the macrophages.
d. Notice the giant cell. Notice the coalescence of the cell here too.
VI.
LUNG: TUBERCULOSIS (TB)
a. Recall: Mycobacteria causes of tuberculosis.
b. In this case, the patient is a 57-year-old man. During a routine physical examination, a lesion was found in the
upper lobe of his right lung. He was treated with ampicillin for a bacterial infection. He was later admitted to
the hospital. Additional studies for tubercle bacilli, bronchial washings, and bronchoscopy were negative and
he was released from the hospital. He was re-admitted to the hospital later on though. Upon being readmitted, he had a positive PPD test (PPD tests measure delayed hypersensitivity, so it’s important in
determining if someone has/had tuberculosis). Over the past 4 to 5 years, he has had positive PPD test, but it
had never been evaluated. A CT scan revealed several small cavities in his right lower lung field. He
underwent a thoracotomy (a procedure in which an opening is made in the chest wall).
1. 1st Image Referenced
a. Notice the old TB lesions. This patient probably has secondary TB.
b. Notice that TB lesions are usually found in the upper lobes of the lung. Why? Because this is
an aerobic bacteria and the oxygen concentrations are highest in the upper parts of the lung.
2. 2nd Image Referenced
a. Notice the “cheesy appearance”.
b. Someone might actual test negative for TB even if they have it though (which is why it’s
important to look at the patient’s lung).
3. 3rd Image Referenced
a. This is not a normal lung. There aren’t any nice, clean alveoli present. Instead, notice the
circumscribed lesions.
4. 4th Image Referenced
a. This is a granuloma.
b. Notice that the lymphocytes here aren’t as rounded as the lymphocytes seen in sarcoidosis.
c. Notice the giant cell (where the macrophages coalesce and share their nuclei).
d. Notice that the cellular architecture is lost though. This is called a caseating granuloma,
because there aren’t any cells present.
5. 5th Image Referenced
a. Notice the multinucleated giant cells.
b. Notice the lymphocytes surrounding the granuloma.
c. Notice the necrosis and that there isn’t any cellular lining of the lungs (caseating
granulomas).
6. 6th Image Referenced
a. This is an acid-fast smear (with a carbofuscion stain and a methylene blue counterstain).
Notice the acid-fast rods (red), which is typical of tubercle bacillus.
b. Question from student: Inaudible. Answer: You might see that if the patient has miliary
disease, but patients can have granulomas and caseastion without the widespread miliary
lesions. Miliary lesions are punctuate, little spots on the lung (usually white). Depending on
the size of the granuloma, it may or not be viewable to the human eye. There are multiple
CLASS: 10:00 – 11:00
DATE: November 10, 2010
PROFESSOR:
VII.
VIII.
IX.
Scribe: Adam Baird
Proof:
INFLAMMATION (IP LAB)
Page 5 of 7
different causes of granulomas. We discussed sarcoidosis, bacteria, and fungi. Foreign
bodies can cause granulomas too. People who work in coal mines, for example, may develop
black lung. The silica particles of the coal puncture the macrophages, resulting in fibrotic
areas of the lung and granulomas, leading to severe lung dysfunction. Anytime a foreign body
is inhaled and it works its way into the lung, a potential granuloma may result (as protection
for the lung).
LUNG: FOREIGN BODY GRANULOMA
a. In this case, the patient is a 21-year-old man who suffered a gunshot wound to his right chest. Several
operations were needed. Results showed that he had Gram-negative pneumonia. (It’s not unusual to have an
infection after trauma to the lung.) He also had neurologic dysfunction, apparently as a result of emboli from
iliofemoral venous thrombosis.
1. 1st Image Referenced
a. Notice the hemorrhaging in the lung (possibly from the surgery).
b. Notice the granulomas, which were probably from gunshot particles. It’s very difficult to get
them all removed though.
c. Every gunshot particle will lead to a granuloma surrounding it (which is seen here).
d. Notice the alveoli that have air space. Notice the little granulomas surrounding it.
2. 2nd Image Referenced
a. Here is a close-up view.
b. Notice the RBCs.
c. Viewed under polarized light, small birefringent particles can be seen, indicating foreign
bodies.
HEART: FIBRINOUS PERICARDITIS
a. In this case, a 36-year-old man with renal disease who present end-stage kidney disease. His BUN (blood
urea nitrogen) was 112 mg/dL, which is about ten times the normal level. He also had a pericardial friction rub
and pericardial and pleural effusions. A semi-elective pericardiectomy was performed.
b. Creatinine goes up. (Creatinine is one way to measure kidney function.)
c. With kidney failure, BUN goes up. BUN is the byproduct of transamination. When amino acids are broken
down in the body, urea is produced (as it is a byproduct of protein metabolism).
d. Urea circulates throughout the body and is usually filtered out and removed by the kidney. This is why
measuring the amount of urea in the body is a way to evaluate kidney function.
e. Elevated urea and nitrogen is called “azotemia” (elevated ammonia and urea).
f. Urea is an irritant, and when there is an elevated amount of urea, it can affect the pericardium (thin, sack-like
layer that encloses the heart and the chest), leading to inflammation. The pericardium will subsequently get
thicker and stiffer as it develops a fibrin coating over it.
g. Pericardial fluid cushions the heart, allowing it to pump without friction. But this fibrin coating “sticks” to the
heart. So, if you listen to someone’s chest who has pericarditis, you won’t hear the distinct “lub-dub” of a
normal heartbeat, but will instead hear a “sliding noise” or “friction rub” of the heartbeat (because the heart is
sticky as it expands/contracts).
1. 1st Image Referenced
a. Normally, the heart has a smooth, clean surface.
b. The pericardium in this case has “sticky stuff” on it due to uremic pericarditis.
2. 2nd Image Referenced
a. Here is the heart shown with pericardium. Notice the thicker areas. Notice the projections
(called the fibrinous pericarditis). It is called the “fronds of fibrin”. It looks like fronds of a fern.
b. Normally, the pericardium is very thin. In this case, it is much thicker. Notice the red fibrin that
causes it to stick to the heart.
c. Cardia tamponode can sometimes result from pericarditis. This can be a life-threatening
problem.
3. 3rd Image Referenced
a. Notice the inflammatory cells.
b. Notice the fibrin.
STOMACH: CHRONIC PEPTIC ULCER
a. Note: some of these cases are old. They are still very good for teaching, but we have learned a lot since
some of these cases too. When this case, in particular, was initially presented, it was not known that chronic
peptic ulcers are due to heliobacter pylori. It was thought that they were due to stress, lack of sleep, etc. We
now know that ulcers are infectious.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: November 10, 2010
Proof:
PROFESSOR:
INFLAMMATION (IP LAB)
Page 6 of 7
b. In this case, a 56-year-old woman had a history of epigastric pain and burning, which was worse at night or
on an empty stomach; drinking milk relieved it. She had episodes of hematemesis (vomiting blood) and
melena (passing bloody stools). She had colicky pain too.
c. She had an abdominal exploration and a partial gastrectomy.
1. 1st Image Referenced
a. Notice the stomach and the ulcer cavity. (The actual ulcer has been removed.)
b. Recall: an ulcer is just a loss of epithelium.
2. 2nd Image Referenced
a. This is the abdominal epithelium.
b. Notice the ulcer cavity, where there isn’t an epithelium.
c. We know this is a chronic and healing ulcer because inflammatory cells are not seen at the
base. If this were an acute or active ulcer, many inflammatory cells would be seen. What is
seen here, instead, is a healing ulcer, made up of mainly scar tissue.
d. Notice the acute inflammation is some areas though. Notice the epithelium. Notice the ulcer.
e. There may be some more acute areas and there may be some chronic areas as well.
3. 3rd Image Refrerenced
a. Notice the ulcer. Notice the inflammation. Notice the granulation tissue, which is an important
part of the wound healing process. The wound healing process happens as the body tries to
heal an ulcer by sending blood vessels into the area. There is collagen and fibroblast
proliferation.
b. Notice the highly vascularized tissue area. Notice the blood vessels that are present too.
c. Notice the area with inflammatory cells and epithelium lining loss. This is a more acute
process.
4. 4th Image Referenced
a. Notice the granulation tissue. Notice the inflammatory cells and the fibroblasts.
b. Notice the blood vessels too.
c. Notice the lymphocytes as well.
5. 5th Image Referenced
a. Here is the healing reaction at the base of the ulcer.
b. Notice the muscle and the scar tissue. Not many cells are seen here.
c. Notice the granulation tissue. Notice the fibroblasts and the blood vessels. Inflammatory cells
may sometimes be present too. This is the process of healing.
6. 6th Image Referenced
a. This is a trichrome stain, showing collagen and scar tissue (shown in blue).
X.
BRAIN: HEALED INFARCTION
a. What would cause a brain infarction? Any interruption of blood flow to the brain can result in a loss of
neurological function (motor or sensory, or both). There can actually be infarction and damage to the brain
too. Any interruption of oxygen to the brain can result in cell death. Recall: no scar tissue is formed in the
brain, because neurons don’t make scars. Instead, the cells undergo liquefaction necrosis (they simply
breakdown and die), resulting in fluid-filled areas. The fluid will usually get absorbed, leaving “clear spaces” in
the brain. This is usually is seen in patients that have had strokes too.
b. In this case, a 48-year-old man had a dissecting aortic aneurysm with an associated aortic valve insufficiency.
He had a stroke with left hemiparesis and obtundation. He ended up dying from complications.
1. 1st Image Referenced
a. This is his brain. Notice how it looks after the liquefying necrosis and the inflammatory
response (that helps to clean up brain tissue).
b. Notice the large areas over the cerebrum where there is loss of brain tissue. This is just fluid,
instead. Notice the meninges too.
c. Anytime there is an infarction (in any organ), one of the first processes that it stimulates is
part of an inflammatory response where neutrophils are replaced by macrophages, which
then engulf tissue.
2. 2nd Image Referenced
a. Here is a cross section. Here is the normal brain. Notice the multifocal areas. There were
probably several branches of blood vessels that were occluded (called “watershed areas”).
b. Notice that brain tissue is lost in the infarction area.
c. Notice the liquefied material. Notice that the structure of the brain has broken down.
3. 3rd Image Referenced
a. Notice the macrophages (which are “eating” the tissue).
b. There will be a “nice, little, clean area” that will be filled with fluid.
CLASS: 10:00 – 11:00
Scribe: Adam Baird
DATE: November 10, 2010
Proof:
PROFESSOR:
INFLAMMATION (IP LAB)
Page 7 of 7
c. Notice the “glitter cells”. These are just the macrophages that are seen.
XI.
HEART: ACUTE MYOCARDIAL INFARCTION & HEART: HEALED MYOCARDIAL INFARCTION
a. The last two cases will be combined so that we can compare and contrast them.
b. In the first case (acute myocardial infarction), the patient is a 78-year-old man experiencing posterior
myocardial infarction over the past 6 years. He has begun to experience angina. Just before he died, he had
chest discomfort. The patient deteriorated with left ventricular failure and died with arrhythmia and pulmonary
edema. The most common reason that people die from heart attacks is because of arrhythmias, as it
damages the heart and the heart can no longer pump in sync.
c. The second case (healed myocardial infarction), the patient is a 37-year-old woman with a history of diabetes.
She had chest pain and shortness of breath. 3 months before, she had weakness; 3 weeks before she had
increasing dyspnea on exertion and worsening of a chronic cough.
d. The common underlying fact: there is a lesion in one of the coronary arteries, usually preceded by
atherosclerosis. There will usually be a clot in the coronary artery, disrupting blood circulation to the part of
the heart that the coronary artery divides. Soon after that, the acute inflammatory process beings (or death).
e. One way to measure if a heart attack has occurred: measure the enzymes (creatine phosphokinase,
troponins, etc.) that leak out of the cells as the cells die.
f. Ultimately, neutrophils will start to come too, which invade the heart. The dead tissue is usually digested by
macrophages, leaving only a scar.
g. You can determine the date of someone’s death by what the heart looks like. If someone dies immediately
after a heart attack, the heart will appear relatively normal, for example.
1. 1st Image Referenced
a. Notice the areas of hemorrhaging. This is typically seen in recent infarctions.
b. Notice the wavy line of neutrophils.
2. 2nd Image Referenced
a. Notice the inflammatory cells.
b. Notice the heart cells.
c. Notice the coagulation necrosis, because the cells have lost their structure. The cells will be
hyper-eosinophilic instead.
3. 3rd Image Referenced
a. Compare the normal heart to the heart with the infarction.
4. 4th Image Referenced
a. Notice the thrombosis of the heart.
b. Notice the neutrophils, RBCs, and fibrin (all shown in red), called the “lines of Zahn”.
5. 5th Image Referenced
a. This is the chronic infarction case.
b. We know it is chronic because of the evident scar tissue (white). This is where all of the lines
of Zahn have already come and gone. The neutrophils and macrophages have already
cleaned up the dead material at this point. Scar tissue and fibroblasts form as a result. This is
why patients who have heart infarctions usually have arrythmias. When the impulses of the
SA node to the Purkinje fibers, etc., they hit the scar tissue and they stop; hopefully they will
take a detour and move on. Scar tissue cannot conduct heart electrical impulses. This is why
patients may experience heart failure.
6. 6th Image Referenced
a. Here is some of the scar tissue (dead myocardium).
b. Notice the fibrous structure.
7. 7th Image Referenced
a. Here is a healed myocardium, showing scar tissue in between the myocardial fibers. Some
scar tissue can be seen here too.
8. 8th Image Referenced
a. Here is the trichrome stain showing all of the collagen fibers present.
b. Notice the scar tissue.
c. Normally, the heart should be good muscle, not scar tissue. This is where the problem lies.
h. Know some of the diseases that are examples of acute and chronic inflammation. Be able to relate everything
together (lectures, IP labs, definitions, clinical manifestations, etc.).
[End 51:05 mins]