Download Cell Injury IP Lab

CLASS: 11:00 – 12:00
DATE: November 5, 2010
PROFESSOR: Anderson
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CELL INJURY (IP LAB)
Scribe: Adam Baird
Proof:
Page 1 of 2
INTRODUCTION
a. The pictures shown in the previous lecture (11-05-10-1) will be the same pictures shown here in today’s IP
lab.
b. We’ll look at coagulative necrosis (in the heart and the kidney, for example), lung abscess, pancreatic fat
necrosis, apoptosis of the prostate, and one other form of necrosis.
HEART: MYOCARDIAL INFARCTION (COAGULATIVE NECROSIS)
a. The blue links on this page are definitions that you may want to look up.
b. A normal heart should not weigh more than 360 grams. This patient’s heart weighed 410 grams. So, the
patient had a big heart, meaning that he had hypertension, which is a risk factor for atherosclerosis.
1. 1st Image Referenced
a. The normal heart is “out here”. The necrotic heart is “in here”.
b. Along the border zone is hydropic degeneration (that is seen with reversible cell injury).
c. Notice the area of infarction.
d. What type of necrosis is this myocardial tissue? Coagulative necrosis.
c. Some of the exam questions will have a picture with a question. Example: Picture of myocardial infarction
with a question about the type of necrosis present, or what the main cause of cell death is (which would be
the stoppage of oxidative phosphorylation and ATP production, in this example).
KIDNEY: INFARCTION (COGULATIVE NECROSIS)
1. 1st Image Referenced
a. Here is a thrombus in a kidney, leading to an infarction.
b. Notice the shape of the kidney. It looks different than normal. Why? There is a branch point in
the interlobular arteries, right at the corticomedullary junction. (You don’t have to know this
though.)
c. Notice the junction between the cortex and the medulla. The blood vessels come up from the
medulla and then make a 90-degree turn to form interlobular arteries. When this happens, the
thrombus can get stuck. This is why thrombi leading to infarcts are commonly seen at the
corticomedullary junction.
2. 2nd Image Referenced
3. 3rd Image Referenced
LUNG: ABSCESS (LIQUEFACTIVE NECROSIS)
1. 1st Image Referenced
a. Autopsy of the central slice of a lung.
b. Notice the fluid (that has poured out of the abscesses). How can the fluid remain during the
autopsy process though? The front and the back of the lung (not shown because they have
been cut off) can be put in formaline, fixing them, allowing you to go back later and cut it
again. The liquefied material (the liquefactive necrosis) actually gets solidified by the
formaline. This is why an autopsy slice can be taken and the fluid doesn’t pour out. So, in
summary, the liquid doesn’t pour out because it is fixed in the formaline.
c. The hallmark of liquefaction necrosis: all of the underlying tissue is broken down and turned
into “mush” (free chunks of protein floating around in the liquefied pus).
d. It’s called liquefaction necrosis because it’s considered “pure liquid”.
e. Next week, when we talk about inflammation and wound healing (coagulation necrosis versus
liquefaction versus granuloma). The question we’ll discuss later: how does the body heal?
PANCREAS: FAT NECROSIS (ENZYMATIC NECROSIS)
1. 1st Image Referenced
a. Shown at a higher power.
b. Notice the fat (adjacent to the pancreas). Notice the red and blue material, showing the
saponification nodules (partially calcified). These saponified nodules form from free fatty
acids (in the local fat globule) reacting to the calcium, ultimately leading to calcified soap.
LUNG: TUBERCULOSIS (CASEOUS NECROSIS)
1. 1st Image Referenced
a. This is actually a different picture than the one shown in the previous lecture.
b. This is a patient with miliary tuberculosis.
c. When autopsied, this looks like bird food. Each of the little dots looks like a little birdseed.
Each of these dots is a tuberculoid granuloma. At the center of each of these dots is an area
of caseous necrosis (it’s a granuloma with a caseous granuloma).
d. All of the organs will look like this.
2. 2nd Image Referenced
CLASS: 11:00 – 12:00
Scribe: Adam Baird
DATE: November 5, 2010
Proof:
PROFESSOR: Anderson
CELL INJURY (IP LAB)
Page 2 of 2
a. Here is an example of hilar lymph nodes. Notice the aorta/aortic arch. Right where the aortic
arch and the bifurcation of the trachea and the bronchi is the hilar lymph node (which has
been cut open in this picture).
b. Notice the granulomas with the caseous necrosis inside (in the hilar lymph node).
c. This patient was probably a coal miner or a smoker – or possibly both. This is why everything
looks black.
d. Specifically, the nodules are the caseous necrosis.
3. 3rd Image Referenced
a. Notice the multinucleated giant cells (a trademark of tuberculoid granuloma).
b. Notice the rim of tissue too (which has macrophages and lymphocytes).
c. We’ll discuss granulomas more when we talk about inflammation.
d. One thing to remember: not every patient looks like the book; not every granuloma will have a
perfect caseous center (some will be very cellular, others will be “burned out” and have fiber
tissue instead). There is a continuum of changes. This can make it difficult to identify. On the
exam, however, the only pictures that will be shown are the “classic” examples.
VII.
PROSTATE: APOPTOSIS
a. Recall: there are many reasons a cell may enter apoptosis.
1. 1st Image Referenced
a. In this case, the patient is a male with prostate cancer, and with that prostate cancer included
metastatic areas. It must have been very painful.
b. Possible treatment: orchiectomy (removal of the testicles), reducing hormonal stimulation.
The tumor, remember, responds to hormones. So if the hormones are reduced, the tumor
cells won’t grow.
c. Another possible treatment: estrogen (estradiol) therapy, blocking the testosterone effect.
d. Today’s most common treatment: androgen depravation therapy, which binds the
testosterone receptors, keeping testosterone from stimulating the tumor cells. Some areas of
the patient’s prostate may still be functionally normal, meaning that those areas still need to
be stimulated by the hormone in order to grow. (This is discussed in more detail in the
lecture.) Because the testosterone is blocked, the tumor cells don’t have the trophic stimuli
anymore, so they turn on their apoptotic cascade.
2. 2nd Image Referenced
a. When endonucleases are activated, they begin “chewing up” the DNA into 180 – 200 base
pair fragments. The end of the DNA has a specific morphology and a specific antigenicity.
They’ve made antibodies that bind to the end of the DNA. This is called a tunnel reaction.
b. An antibody, then, will only bind to the ends of DNA that has been “chewed up” by
endonucleases. If it finds them, then a color reaction can be added to result in brown nuclei
(shown here). These cells (with the brown nuclei) have started the apoptotic cascade
(because they are “tunnel positive”).
c. There are other cells that aren’t “tunnel positive” though (because they haven’t turned on the
apoptotic cascade.
[END 16:18 mins]