CLASS: 11:00 – 12:00
DATE: November 8, 2010
PROFESSOR: Anderson
I.
CELL ADAPTATION (IP LAB)
Scribe: Adam Baird
Proof:
Page 1 of 4
INTRODUCTION
a. These are the same sort of pictures that we looked at during the last IP lab.
b. The exact same cases that we used in today’s lecture (11-08-10-1) will be used here too.
c. Myocardial hypertrophy is a typical scenario. But for people who don’t get their blood pressure checked, for
people who don’t go to the doctor and get examined for a heart murmur, it’s difficult to determine whether or
not they have cardiac hypertrophy.
II.
HEART: MYOCARDIAL HYPERTROPHY
a. This patient had symptoms of exercise intolerance. He began to get occasionally peripheral edema. He also
mentioned that he was diagnosed with a heart murmur 25 years ago, but apparently felt fine, so he wasn’t too
concerned about it.
b. He had an aortic valve problem.
c. Eventually, the heart gets very big.
d. People with cardiac hypertrophy are more prone to die of sudden death. The cells are so big, and the heart is
working so hard, that these patients are more likely to get a bad arrhythmia (abnormal electric activity of the
heart) and suddenly die.
e. If the hypertrophy caused by hypertension, these patients tend to have more severe coronary artery disease.
(Recall: Hypertension is a risk factor for coronary artery disease.)
1.
1st IMAGE REFERENCED
a. Here is a normal heart (right). Here is a hypertrophied heart (left).
b. In addition to the cells of the heart getting bigger, adequate oxygen supply for the cells
becomes more difficult. Even though the heart tries to grow new blood vessels and
capillaries, the oxygenation inside the heart isn’t as good as it should be.
c. The pressure inside the heart becomes very great as well, making it hard for blood to flow.
d. The end result: cell injury and possible cell death.
e. So, the cells aren’t getting enough oxygen to stay alive, so they die. This, in turn, results in
fibrosis, specifically interstitial fibrosis (meaning that fibrous tissue forms between heart
muscle cells). This, too, is irreversible. Even if the patient’s aortic valve is surgically replaced,
the fibrosis is still present. Even though these cells may, in time, go back to normal size, the
fibrosis will never go away.
f. Eventually, the heart has trouble producing the high pressure needed for heartbeat. The
heart muscle cells push against the fibrous tissue (which acts like a girdle), preventing the
heart from contracting completely. Heart cells are strong though, so they can still contract,
even with all of the fibrous tissue surrounding it. The problem is that the heart cells can’t relax
though. Think about a heartbeat: the heart has to relax and refill before it can beat again. So
the common observation for patients like this is a diastolic dysfunction. During diastole (when
the heart should be filling), the heart just can’t fill properly because it is too rigid. This in turn,
doesn’t allow for enough blood to be pumped out.
g. Eventually, the heart will fail.
2.
2nd IMAGE REFERENCED
a. This picture is “turned around”. Notice the left ventricle though. Notice the right ventricle as
well. Notice how big and dilated the left ventricle is. Notice how thin the left ventricle is too.
The left ventricle started out looking like the right ventricle, but over time, it ends up looks like
this (shown in the picture). This is a “classic” congestive heart failure picture.
b. If a patient develops pulmonary disease, the pulmonary pressure goes up and the right
ventricle has to work harder to pump blood into the lungs (deoxygenated blood). This leads to
hypertrophy of the right ventricle. In a normal heart, the right ventricle just isn’t as strong as
the left ventricle, so the right ventricle can fail even earlier (and with less stress) than the left
ventricle. Right ventricular failure, then, tends to be more common than left ventricular failure.
3.
3rd IMAGE REFERENCED
a. Here is the picture of the postpartum uterus (showing hypertrophy of the uterus due to the
increase in size in order to carry the child).
III. PROSTATE: NODULAR HYPERPLASIA
1.
1st IMAGE REFERENCED
a. Here is a patient from autopsy with prostatic hyperplasia.
b. Notice the bladder. The wall of this bladder is much thicker than it should be.
c. It may be difficult to see, but there are trabeculae on the inner surface of the bladder. This is
a “classic” observation seen in over-distended bladders (it’s like hypertrophy of the bladder).
The proliferation of the cells inside the prostate
CLASS: 11:00 – 12:00
Scribe: Adam Baird
DATE: November 8, 2010
Proof:
PROFESSOR: Anderson
CELL ADAPTATION (IP LAB)
Page 2 of 4
d. Recall: The prostate surrounds the urethra. So if the prostate proliferates, it constricts the
urethra too, resulting in too much urine in the bladder. Example: older men who can’t “fully
empty” their bladders. More urine is produced then, and the bladder actually hypertrophies
and forms trabeculae in order to hold the extra urine.
e. The ureter is usually has a very small, very fine lumen. Here, the lumen of the ureter is
swollen, because the kidneys are producing urine, which is directed to the bladder. If the
bladder is already full though, there’s no room for extra urine. So the ureter dilates (and so
does the renal pelvis). The system is simply getting “backed up”. The kidneys, the ureter, and
the bladder are all affected because of constriction of the prostate (due to prostatic
hyperplasia).
2.
2nd IMAGE REFERENCED
a. Here is a normal prostate shown at low magnification.
b. Notice the glands (there are not many of them though). These glands are needed for
secretions from the prostate. Now compare this to the previous picture (4th image
referenced), which shows prostatic hyperplasia with many glands.
3.
3rd IMAGE REFERENCED
a. This is a different case, but somewhat similar. If a patient has prostatic hyperplasia, and the
urine can’t be fully emptied, the urine builds up inside the renal pelvis. Because the urine
can’t flow out, it just remains there.
b. Example: A patient has a blood pressure reading of 120 mmHg coming into the kidney. The
blood is trying to force through the capillaries (that are inside the glomeruli) so that the fluid
can go out and into the urinary space. (Recall: This is, in essence, how urine is made. Blood
serum is filtered through the glomeruli membranes, into the renal space of Bowman’s
capsule, then down through the collecting ducts, and finally into the renal pelvis.) The blood
flow can’t be forced into the kidney because of the subsequent pressure from the urine
collection, so the blood flow must be stopped. In order for the high pressure of blood flow to
be stopped, the pressure inside the kidney must eventually equal the pressure outside the
kidney. This results in atrophy in the wall of the kidney. The whole kidney becomes thick
because of the pressure buildup. This is also known as hydronephrosis – “hydro” meaning
water and “phrosis” meaning damage to the kidney. So hydronephrosis is fluid inside the
renal pelvis that causes atrophy of the wall of the kidney, meaning that this kidney doesn’t
work very well.
c. This is sometimes seen in patients who have a stone lodged in their ureter. Again, the
pressure builds up so much that it eventually causes hydronephrosis.
IV.
KIDNEY: SQUAMOUS METAPLASIA
1. 7th IMAGE REFERENCED
a. Here is the histology section of the kidney. Notice the renal pelvis, which has blood in it due
to the kidney stone destroying the surrounding lining.
b. Notice the area with “normal” transitional epithelium, but also notice that it gradually gets
thicker, to the point that is begins to form squamous cells. Notice the inflammatory cells in the
wall too.
2. 8th IMAGE REFERENCED
a. Notice the other area with “normal” transitional epithelium, but again, notice that it gradually
gets thicker. This is hyperplasia that eventually leads into metaplasia (where keratin is laid
down by squamous epithelial cells).
3. 9th IMAGE REFERENCE
a. Squamous metaplasia in the bronchus of a chronic smoker. Notice the mitotic figure here.
b. The irritation of the smoke causes the cells at the surface to look funny (i.e., the nuclei look
large and dark).
c. The irritation of the smoke causes squamous metaplasia, which is a normal process. The
problem: cigarette smoke also contains carcinogens. The normal metaplastic process,
combined with carcinogens from the smoke, leads to the beginning stages of dysplasia.
Dysplasia is similar to metaplasia, because the cells change from one cell type to another cell
type; specifically though, dysplasia causes cells to change from one cell type to neoplastic
cell. This picture is “halfway in between” dysplasia and metaplasia. It could be considered
dysplasia because the cells at the surface look odd (due to the carcinogens from the chronic
smoking) and it seems to be forming dysplasia and possibly neoplasia.
V.
TESTES: ATROPHY
1. 1st IMAGE REFERENCED
CLASS: 11:00 – 12:00
Scribe: Adam Baird
DATE: November 8, 2010
Proof:
PROFESSOR: Anderson
CELL ADAPTATION (IP LAB)
Page 3 of 4
a. Typical case of a patient with prostate cancer.
b. Prostate cancer can be very painful, especially when there are metastases forming in the
bones.
c. Orchiectomy (removal of the testicles) is a common treatment, as it removes the hormone
stimulation of the metastatic tumor.
d. Another treatment option: leave the testicles, but give the patient estrogen.
e. Another treatment option: newly developed drugs that are designed to block the testosterone
receptors (called androgen depravation therapy).
f. The development and growth of new cells causes extremely painful bone pain. So with any
treatment, it’s important to stop the hormone from stimulating the prostate cells in the tumor,
which will stop the growth of new cells.
2. 2nd IMAGE REFERENCED
a. This is an example of a patient who had estrogen therapy (before androgen depravation
therapy was developed).
b. Estrogen causes atrophy of the testicles.
c. Notice that this testicle is much smaller than a normal testicle.
d. When observed from a low power, very few nuclei are seen. Many of the nuclei have gone
away.
3. 3rd IMAGE REFERENCED
a. These are normal seminiferous tubules.
b. Notice the area where the cells are gone (atrophy of the cells due to a lack of hormone
stimulation). The tropic stimulus is decreased, telling the cells to grow, but the cells actually
stop growing and some of them even die (apoptosis).
4. 4th IMAGE REFERENCED
a. Here is an example of a different kind of apoptosis. This is a patient with atherosclerosis in
his aorta. We are looking at the inner surface of the aorta. Notice the kidneys. Notice the
clump of atherosclerotic lesion (atheroma) that is formed at the ostium for the renal artery.
This stops a portion of the blood flow to this kidney. This kidney is smaller than normal
because it’s atrophied due to a lack of blood flow.
b. The other kidney, then, must work harder and is larger than normal as a result. This is
identified as “compensatory hypertrophy”. Renal cells can divide and make more cells, but
they can also get bigger. (Compare this to heart cells, which can only get bigger.) In this
example, specifically, the renal cells have both divided and produced more and gotten bigger.
5. 5th IMAGE REFERENCED
a. Renal stone has blocked the ureter, resulting in hydronephrosis.
b. So the urine flow is blocked, the renal pelvis gets filled with urine, causing pressure atrophy in
the kidney wall.
c. This kidney is bigger than the other as well (as it “picks up the slack” from the other kidney).
d. Another example of compensatory hypertrophy due to decreased renal function.
6. 6th IMAGE REFERENCED
a. A kidney that has decreased in size due to poor blood supply or hydronephrosis.
7. 7th IMAGE REFERENCED
a. A kidney that did not develop properly.
b. Atrophy is when something is “normal size” and then it shrinks.
c. Hypoplasia is when something “just doesn’t grow big enough”.
d. How can we know that this kidney didn’t atrophy though? Look at it. Notice that the only thing
in the kidney is the ureter, which looks about the right size in some areas; other areas of the
ureter look too small.
8. 8th IMAGE REFERENCED
a. An example of senile atrophy. This is true atrophy because it used to be “normal” size, but it
has shrunk.
VI. LUNG: METASTATIC CALCIFICATION
1. 1st IMAGE REFERENCED
a. It is metastatic because this patient had a carcinoma.
b. Some carcinomas can produce abnormal hormones (called “paraneoplastic hormones”). In
this case, it produced parathyroid-like proteins that caused hypercalcemia, where each
alveolus is held open by calcium.
2. 2nd IMAGE REFERENCED
a. Low-powered photomicrograph of the patient’s lung.
CLASS: 11:00 – 12:00
Scribe: Adam Baird
DATE: November 8, 2010
Proof:
PROFESSOR: Anderson
CELL ADAPTATION (IP LAB)
Page 4 of 4
b. In histology sections, alveoli usually collapse, but here, they are all wide open because of the
surrounding calcium.
c. Notice the pink areas inside the alveoli. This is pulmonary edema. This affects the blood flow
through the lungs. It slows down the blood flow. It’s hard for the blood to get through the lung
tissue due to the calcium, so the blood tends to get slowed down, causing capillary fluid to
leak out into alveolar space.
3. 3rd IMAGE REFERENCED
a. Compare the metastatic calcification of the previous picture to the dystrophic calcification of
this picture.
b. Here is a heart autopsy. We are looking down on the aortic valve. Notice the calcification.
c. This is damaged heart tissue that has been calcified as a result.
d. Normal calcium level = dystrophic calcification
e. High calcium level = metastatic calcification
VII. LIVER: FATTY CHANGE AND CIRRHOSIS
1. 1st IMAGE REFERENCED
a. Here is another example of a patient with pneumonia. Sickness can lead to a decreased
appetite, which alters the metabolism. This can result in a fatty liver.
b. Notice that the picture looks “greasy”.
2. 2nd IMAGE REFERENCED
a. Low-powered photomicrograph of liver.
b. Notice that there is very little normal tissue left. All of the hepatocytes are full of fat.
3. 3rd IMAGE REFERENCED
a. Notice that the fat globules are round. The liver is primarily made of water, which is why these
fat globules form in a sphere-like shape.
4. 4th IMAGE REFERENCED
a. Notice the nucleus of the hepatocyte. The nucleus looks fine. They are just deformed by the
fat. Eventually, once the metabolism is balanced, the fat can be reabsorbed and transported
out of the cell, restoring normalcy to the cells and the tissue.
b. Notice the cytoplasm of the hepatocyte. It’s pushed off to the side by the fat.
5. 5th IMAGE REFERENCED
a. Notice the apoptotic cell (shown by the arrow). If the cells only went through the apoptotic
cycle, not inflammation or fibrosis would be expected. If, however, someone drinks alcohol
and doesn’t eat properly, they may lose some hepatocytes (they would die). If there is dead
tissue, the inflammatory cascade is triggered (to clean up the mess of the dead cells). The
end result: the laying down of fibrous connective tissue.
6. 6th IMAGE REFERENCED
a. Notice the area of inflammation.
b. Notice all the fibrosis here.
7. 7th IMAGE REFERENCED
a. Here is what the liver looks like grossly.
b. Notice the white areas (containing dead liver tissue that has been replaced fibrous connective
tissue).
c. Notice the nodules too. They are proliferation nodules of the residual hepatocytes that are
going through hyperplasia (in hopes to replenish the tissue).
[End 31:59 mins]