Pathology Lab - Angelfire



Adaptation, Necrosis and Inflammation CPC-1, Cases

During lab, we went through the cases. We are not expected to know anything clinical at this point, although some clinical scenarios may be obvious. They are just ways to discuss some of the ideas we’ve been talking about and to give more examples of processes covered in class.

Robbin’s Review of Pathology is a good book to go over.

Student Questions:

1. Describe and show the differences between a granuloma and granulation tissue.

2. Various kinds of necrosis - how can you identify one versus another, and versus apoptosis (in an H + E stain)?

3. What is a Mallory body?

Clinical Scenarios:

I. A 55 year-old man presents with symptoms of hepatic failure after a long history of diabetes mellitus.

A. He might appear gray-skinned.

B. He could be a drinker with diabetes, but suppose he has a disease that affects both organ systems. Try to come up with one diagnosis that explains all presenting symptoms (doesn’t always work, but will here.)

C. Clinical signs that he has hepatic failure:

1. Jaundice (icterus).

2. Ascites.

a. Could be caused by portal hypertension (that led to his hepatic failure)

b. Functional changes:

1. Low albumin leads to decreased oncotic pressure.

2. Clotting factors (also made by liver) cause the patient to bleed easily.

a. Simply

b. Complexly

3. Can also measure PT + PTT in the serum. (Prothrombin time, partial thromboplastin time)

4. Ammonias in blood lead to a change in behavior.

a. Clouding of their sensorium.

D. In diabetes the major thing he will present with (if uncontrolled) is hyperglycemia.

E. Things to consider:

1. He denies ever drinking.

2. His hepatitis panels are completely negative.

F. Liver biopsy:

1. Whole liver section. Stain: Prussian blue – shows that this liver has too much iron.

G. Iron deposition can occur in the liver

1. Classically as a secondary process in people who have chronic transfusions. (In people with aplastic anemias, chronic blood loss, others)

2. Genetic predisposition with hemochromatosis.

H. Why does iron produce injury in this case

1. Free radicals lead to local problems associated with fibrosis, scarring, change in function, liver failure over time.

2. Increased incidence of hepatocellular carcinomas due to repeated repair over time.

I. Why does he have problems with diabetes?

1. Iron deposition occurs not only in the liver, but can happen in other tissues like the epithelial cells in the pancreas.

2. Leads to pancreatic damage that looks similar to liver slide only in a pancreatic fibrosing pattern with evidence of diabetes mellitus.

J. Hemochromatosis is notable for multi-organ system problems.

K. Remember, Fe deposition occurs in everyone and does not always lead to damage if it is not overwhelming for the anti-oxidant systems of the tissue.

II. A 30 pack-year smoker is hit by the Graham ambulance service walking across Slide road. He is found to have emphysematous lung change and a dark discoloration in his lung.

A. An emphysematous lung change is permanent loss of some lung because of inequities in the

elastases in the lung because of alpha-1-antitrypsin deficiency (too little of that) and/or injury

from the outside, classically cigarette smoke. You end up with holes in the lung.

B. There is low grade injury associated initial damage, so low that really only see a few increased inflammatory cells around the areas of injury. Nothing that shows up in chest x-rays or that causes problems due to the inflammatory changes systemically. Only shows up when you have enough scarring or holes in the lung to produce functional changes. (More about that at another time).

C. To note here is that in these areas of change (usually at the areas of low-grade chronic changes in the lung) where you can collect anything that comes into the lung. One of these is pigment of all kinds, usually carbon.

1. Carbon deposition in lung = anthracosis.

2. Occurs without producing any reaction to injury.

3. Will see in patients with emphysema, chronic obstructive pulmonary disease, old scar

diseases (old TB).

4. Marks old scarring, doesn’t mean much. If see it there is something else going on in lung.

5. When we talk about pneumoconiosis, will see massive amount of carbon deposition. Is

seen usually in coal miners. It usually has some other substances in it, e.g. silicates. Black

lung disease. Much worse that even a heavy smoker.

6. Remember, almost everyone has at least some carbon in their lungs.

III. A 35 year-old female complains of RUQ pain worse after eating for 5 months.

A. Gall bladder problems. Is a classical scenario. Women tend to have gall bladder disease more. (Fat Fertile Female over Forty.) More extensively seen in Hispanics, and so forth.

B. A person suspected of gall bladder disease is given an ultra sound and gallstones are

discovered. Based on clinical history and finding of stones, a cholecystectomy is performed.

C. Shows slide of gall bladder opened to reveal its contents.

1. Strawberry gallbladder- yellow with a background of red.

2. This is cholesterolosis. Each yellow dot is a tiny little polyp of cholesterol.

D. New slide – shows the smooth muscle wall and mucosa. Shown are cholesterol laden

macrophages aka “foamy” macrophages.

1. Normally, in this mucosa, the only thing seen would be a few blood vessels, a few

strands of pink fibrous stromal stuff, maybe a few inflammatory cells.

2. You would not see the lipid laden macrophages. Can see foamy macrophages

anywhere there is cholesterol breakdown, eg arteriosclerosis.

3. Normal = simple columnar epithelium of the mucosa. Normally would have small

little fingers of the epithelium, plicae.

4. Shown is not normal, too many cells. Hyperplasia. Labile cells line gall bladder.

5. Complexity of this mucosa has to do with the healing that goes on.

E. Shown is a lower power slide of the same gallbladder.

1. Wall is hypertrophied. Is thicker than normal, muscle is lumpy and nodular.

2. Wall is made up of smooth muscle so could be both hyperplastic and hypertrophic. Is

a mixture of the two- mostly hypertrophy because cell division takes longer.

3. Stress turns on hypertrophy. In gallbladder is pressure from obstruction (work stress

leads to hypertrophy of the wall).

F. May get inflammation and infection with obstruction. It is easier to get infected due to stagnation.

G. Could also get pancreatitis (infected or enzymatic) because stone may obstruct the common

duct. If you obstruct the acini draining down the duct in the pancreas, the acini will eventually

end up with fibrosis and atrophy because they are turned off due to the pressure. Also

possible are hyperplasia and metaplasia.

IV. A 25 year-old man is in a MVA with a loss of 4 units (4*500cc) of blood. He is resuscitated but

develops a rapid “white out” of his chest x-ray, as well as severe SOB which is not helped by O2.

A. “White out” describes a reaction in which, in an hour or so, the lung goes from being a normal

chest x-ray to being all white, increased radio densities.

1. It means that something is filling up the alveolar space with something that is

radiodense.

2. It happens very rapidly.

3. Is not a pneumothorax or a hemothorax because both sides of the lung are now white.

B. Since both lungs “white out” and O2 doesn’t help at all means that it is probably acute

respiratory distress syndrome (ARDS).

1. Is an example of inflammatory change.

2. Can be caused by multiple injurious agents, from infections to shock and infinite

others.

3. Alveolar walls normally show little. Normally they are made up of epithelial cells and

capillaries.

4. Now the capillary is stuffed with red cells. Is at least congestion.

(Remember vascular congestion in lecture, leaks in vessel allows leaking out of fluid and/or cells, depending upon the injury. Could end up with fluid outside and sludging inside the capillary.)

5. The pink stuff outside the capillary is hyaline material (amorphous red stuff).

Includes protein, fibrin and necrotic debris. (Red is dead).

6. Produces all kinds of clinical symptoms.

C. Exudate (mostly cellular matter) vs transudate (mostly fluid).

Question: What is the connection between the trauma and white out lung? Tried to avoid that because didn’t want to go into lung now. Is all sorts of chemokines, cytokines and other toxic substances that are not well understood in many injuries that produce that injury. Sometimes can be caused by a local bug . No obvious anatomical correlate. Not necessary to know diseases presented here.

V. A 28 year medical student complains of mid epigastric pain which is worse on an empty stomach and exacerbated by Pathology lectures in the early afternoon. One day he vomits up a small amount of coffee ground material, which scares him to death and sends him to the ER.

A. An ulcer.

Pain plus blood limits the diagnosis.

B. Shown fundus of stomach at real low power.

1. What is abnormal is the lymphoid aggregates, with pseudofollicle center. Is not a

granuloma. Therefore is chronic due to build up of lymphoid tissue.

2. Therefore think that it is some kind of chronic gastritis, continuing injury.

3. (Don’t see signs of an ulcer on the slide.)

4. Every instance of injury produces more acute inflammatory change, which is why can

see pictures with acute changes, means that it is an ongoing injury.

C. H. pylori is the usual cause of gastritis, ulcers. It has a urease , which allows it to dive into the

cell.

Until bacterial infection is treated, the injury will remain.

D. Two new slides of the pylorus, higher power..

1.Glandular cells are shown.

2. There are too many of the inflammatory cells in the walls of these glands.

3. Too many blue cells (plasma cells and lymphocytes) in the lamina propia.

4. The glands are “ratty”. Neutrophils are eating up the glands.

5. Signs of acute inflammation.

E. Stomach will respond to this injury by:

1. Proliferating (preferred response – maintains functionality). Cells are labile and can

regenerate unless stroma damaged. If treated soon enough can end up with a return to

normal.

2. Metaplasia (not necessarily a permanent change) and hyperplasia possible. Still not

necessarily a stromal or an architectural change. But would be a loss of function

(maybe a decrease in acid production)

3. Also possible is fibrous tissue if stromal damage occurs.

F. Erosion versus ulcer.

1. Erosion used often to mean some superficial necrosis of the mucosa (GI lined

surfaces). Have not destroyed the wall of the organ you are talking about. Less

scarring/ less functional change.

2. Ulcer is deep necrosis of the epithelium.

G. Show a slide of the stomach that underwent metaplasia since this looks like the alternating

goblet cell pattern of small intestine.

H. Shown another slide of an ulcer, a duodenal ulcer in which the ulcer has penetrated deeply (it

bleed enough to require its surgical removal.)

VI. Granulation tissue versus fibrous tissue.

A. Scar is the end stage healing process of a variety of repair mechanisms, one of which is granulation tissue. A scar means you’ve got mostly fibrous tissue.

B. Granulation tissue have blood vessels (occur early on, within hours) come in with endothelium proliferating making tubes, that whole VGEF system. They provide nutrition (O2, chemicals, others) and cells- especially monocytes, the main cell in repair and healing. Become macrophages after migration (also called a histiocyte).

C. Fibroblasts along with some perivascular cells (like pericytes and so forth) are also developing. After injury is gone, the fibroblasts will proliferate in order to make a scar. Fibroblasts make collagen as an extracellular matrix.

D. Will eventually need less energy and the blood vessels are no longer required.

E. Early on you will have very vascular granulation tissue which will be lumpy, bumpy, red, bright and will bleed easily.

- Continued next hour -

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