Pathology

Question 1

Characteristics of coagulative necrosis

Answer 1

The tissues affected are firm and the cells do not have a nucleus.
Localized area of coagulative
Cell swelling will make the cells look more pink. (Cytoplasm more pink)
Lose membrane

Question 2

Characteristics of Liquefactive necrosis

Answer 2

Affects the brain and CNS mostly.
No nucleus present
The dead cells are digested and it makes the Tissue turn into a liquid (enzymatic lysis of cells)
The necrotic material looks like a creamy yellow (pus=dead leukocytes)
Phagocytes will be present to clean up
No cell border

Question 3

Characteristics of Caseous Necrosis

Answer 3

Mostly in the lungs because of tb infections.
Cheese like
Combination of coagulative and liquefactive
Inflammation will take on the appearance of a granuloma
The cells look like they radiate out.
Distinctive inflammatory border.
Macrophage will clean in up

Question 4

Characteristics of fat necrosis

Answer 4

Chalky white
No specific pattern
Fat destruction typically caused by active pancreatic lipases 
Shadow outlines of necrotic fat cells
Basophils could calcium deposits
Inflammatory reaction
Nuclear moves to the center
Cytoplasm becomes more granular

Question 5

Characteristics of fibrinoid necrosis

Answer 5

Immune reactions involving blood leak
Happens with a complex of antigens and antibodies and inserted into the walls of arteries
Bright pink on H&E stains and look amorphous and this is called fibrinoid
Happens mostly because of malignant hypertension or vasculitis
Neutrophils will come and destroy

Question 6

Characteristics of gangrenous necrosis

Answer 6

No specific pattern of cell death
Coagulation of the limbs look mummified
Mostly lower limb
Happens because of decrease in blood supply
If it happens with a superimposed infection then it is liquefactive necrosis or wet gangrene

Question 7

What is steatosis?

Type of Accumulation?

Answer 7

Reversible change until it’s not
Build up of triglycerides in parenchyma, cells and it happens mostly in the liver.
Heart and kidney are also common
Caused by alcoholic liver disease, non alcoholic liver disease like diabetes and obesity
On slides it looks like a fat cell and the fat is usually washed out of tissue during slide preparation.
Lipid Accumulation

Question 8

What is xanthoma and what type of Accumulation?

Answer 8

Build of macrophage that have cholesterol. Groups of foamy macrophages found in the connective Tissue of the skin and tendons that form masses
Mostly seen in people with hyperlipidemia
GASTRIC XANTHOMA is an example and on slides they have foamy macrophages in the lamina propriety beneath the epithelial surface and they have high amounts of cholesterol.
Location dependent, we learned stomach.
Lipid Accumulation

Question 9

What is atherosclerosis and what is the Accumulation?

Answer 9

It is caused by plaques found in the smooth muscle cells and macrophages are found in the walls of arteries and they are often with lipid vacuoles.
Foam cells in the surface of wall of the vessel look yellow
The vacuoles could release lipids into the extracellular space and they could in turn make cholesterol clefts which look like lingo needles.
Lipid Accumulation. Location dependent, arteries.

Question 10

What is cholesterolsis and type of accumulation?

Answer 10

It is an accumulation of cholesterol that have macrophages in the lamina propriety of the GALLBLADDER.
On slides they look grainy and have a glomerization.
Lipid Accumulation

Question 11

What are renal tubule resorption droplets and accumulation?

Answer 11

It is often reversible and it is a protein loss in the urine.
With heavy protein Uris there is an increased resorption of proteins into vesicles
Protein has appearance of pink hyaline droplets in the cytoplasm.
High protein absorption in the cytoplasm=high accumulation.
On slides they have eosinophils droplets
Lipid Accumulation

Question 12

What are Russel Bodies?

Answer 12

Plasma that is actively making immunoglobulins.

The ER becomes distended and there are large eosinophilia cytoplasmic inclusions.

Question 13

How can glycogen be related to an accumulation in abnormal proteins?

Answer 13

There is glycogen storage disease and it has a defect in the enzyme that breaks down glycogen so in turn there is a build up of glycogen and this build up can cause Cell death or injury.n

Question 14

What are protein accumulations?

What are the characteristics of alpha-1 anti-tripsin deficiency?

Answer 14

It is caused when there is a protein build up around eosinophilia droplets, vacuoles, aggregates in the cytoplasm and often cause a defect in folding, packing, and transport of the protein and since they are essentially broken then they can accumulate.
Alpha-1 anti-tripsin deficiency is caused by a mutation that decreases folding which leads to the build up of partially folded intermediates that aggregate in the ER of liver cells and are not secreted.
Could cause emphysema of the long
Damage the ET because of the stress of misfolded proteins.
On a slide t hey have magenta colored cytoplasmic inclusions and they show misfolded A1AT protein.

Question 15

What are the characteristics of a lack of enzyme?

What is Niemann-Pick Disease, Type C.

Answer 15

It is the failure of the breakdown of a metabolite because of an inherited deficiency. Like a lysosomal storage disease.
Niemann-Pick Disease Type C is a lysosomal storage disease that is caused by mutations that affect the enzymes involved in cholesterol trafficking. This causes a cholesterol backup in many organs. No lysosomes can’t get rid of stuff.

Question 16

What happens when you ingest some indigestible materials?

Answer 16

Drop off and build up of abnormal exogenous substance and the cell doesn’t have the stuff needed to break down the substance or the ability to move it to sites that can digest it.

Question 17

Is carbon an exogenous pigment and if so why?

Answer 17

Yes, it is an exogenous pigment since it comes from outside of the body. Carbon is usually inhaled in the form of coal dust especially in urban areas.the carbon blackens the lung and node tissues and this process is called anthracisis and coal miners have an increased chance of lung disease

Question 18

Are tattoos exogenous and if so why?

Answer 18

Yes, it is the localized pigment of the skin or bowel and when in the skin it is phagocytosis by dermal macrophages, typically inert with no inflammation and pigment will stay for a long time. In surgery doctors will put it there so that they can go back to the area and it is taken up my macrophages. Stain the suspected tumor site and go back to it later.

Question 19

Is lipofuscin and exogenous pigment and if not why not?

Answer 19

Lipofuscin is not an exogenous pigment instead it is ENDOGENOUS. It usually happens with typical wear and tear and it is seen in slow regressive change. They are insoluble polymers of lipids and phospholipids and they look yellow and brown in color and we often granular. They are not harmful to the cell and thy show the cell exposure to free radical injury

Question 20

Why is melanin an endogenous pigment?

Answer 20

Melanin is an endogenous pigment because the body makes it and it looks like a brown or black pigment to it. It is formed when enzyme tyrosine she catalyze seems the oxidation of tyrosine to dihydroxyphenylalanine in melanocytes. Mostly epithelial , but could be found deeper.

Question 21

What is hemosiderin and what type of pigment is it?

Answer 21

Hemosiderin is made from hemoglobin and it stores iron. It is often seen in bruises and it often looks yellow, brown and granular or crystalline
HEMOSIDEROSIS is too much iron and they put halo glob in back into the Tissue. And the type of pigment is endogenous
On the slides they have cytoplasm that look granular and some stains show the iron as a blue color

Question 22

What are is dystrophic calcifications?

Answer 22

It is when calcium is put locally in dying or necrotic tissues. Usually happens in atheroma and atherosclerosis and if feels crunchy to the touch. It is basophilic meaning it has epithelial and a stroma. It looks granular and clumped no an H&E stain.
Often coincides with the presence of psammoma bodies which are are deposition and layers of calcium depositions, they make concentric circles.
There can also be a bestows bodies which is caused by the deposition of calcium, iron salt on Barstow fibers and they look like a dumbbell or beaded

Question 23

What is metastatic calcification?

Answer 23

It usually happens wherever hypercalcemia occurs.
Looks dystrophic under microscope, but has no clinical dysfunction unless calcium is put on the lung or kidney. It is characterized by the deposition of calcium on healthy tissue, usually benign with no cancer.

Question 24

What are examples of benign mesenchlymal tissues?

Answer 24

Fibroma
Lipoma
Leiomyoma
Rhabomyoma

Question 25

What are examples of malignant mesenchymal Tissue?

Answer 25

Fibrosarcoma
Liposarcoma
Leiomyosarcoma
Rhabdomyosarcoma

Question 26

What are examples of benign epithelial neoplasms and where do they come from?

Answer 26

Adenoma-glands
Papilloma-producing fingerlike, wart projections—urinary bladder
Cystadenoma-forming large cystic masses
Polyp-forming visible projections above mucosal surface

Question 27

What are examples of malignant epithelial neoplasm. Where do they come from?

Answer 27

Adenocarcinoma-tumor from gland or columnar mucosa
Squamous Cell Carcinoma-squamous epithelium
Renal cell carcinoma-kidney
Hepatocellular carcinoma-liver cell

Question 28

What is a fibroadenoma?

Answer 28

Benign neoplasm of breast. It is biphasic so it is made from a fibroblast and a granular epithelium. Basically epithelium and soft tissue.

Question 29

How can we tell benign from malignant?

Answer 29

1. Organ is invaded locally
2. Degree of Differentiation, so if it looks like the organ then well differentiated and most likely benign. If it looks whack then malignant (anaplasia)
3. distant spread or metastasis, if it spreads then most likely malignant
4. Rates of growth and proliferation, malignant usually grows fast and can undergo necrosis because it ran out of blood supply.

Question 30

Describe how sustaining proliferation signaling is a hallmark of cancer
Describe in lung, colon, breast

Answer 30

Cancer typically doesn’t need External stimuli usually because of oncogene activation. Oncogenes promote cell growth and they happen because of mutations in the proto oncogene which is the wild type mutation oncogene
LUNG: gefitinib are tyrosine kinase inhibitors and they stop the egfr when it is mutated or the tks will always be on.
COLON: activate KRAS mostly but can also activate BRAF and you treat the mutations if the mutation is a wild type.
BREAST: ERBB2(HER) ERBB2 has a HER2 receptor and is part of the EGFR family so there is gene amplification because of the overexpression of the HER2 receptor and herceptin will bind to HER2 and arrest the cell Cycle

Question 31

Describe how inducing angiogenesis is a Hall mark of cancer

Answer 31

Angiogenesis is a process by which the cancer makes new blood vessels to keep up with it’s needed supply in order to get more nutrients and to transport waste. If VEGF is active then angiogenesis will occur, but if made inactive by bevacizumab then no new blood vessels and treated mostly in colon patients.

Question 32

Describe how enabling replication immunity is a hallmark of cancer

Answer 32

Cancer stem cells are essentially immortal because they have unlimited replicated potential. Most normal chromosomes will degrade over each replication so we add telomeres to them to protect the ends so that we don’t degrade the important information. Cancer cells have telomerase which can keep adding more and more telomeres to the cancer cells which allow for more division and more protection from degradation.

Question 33

Describe how activating invasion and metastasis is a Hall mark of cancer

Answer 33

Cancer cells invade other normal tissue via travel through the blood to different areas and they colonize it. It has to be the right fit or else the tumor will not plant. Once it fits then it starts angiogenesis and will grow in a new area.
Initially cancer cells loosen the cell to cell adhesion and they let the protease break down the ECM and they use adhesion molecules to get through ECM.

Question 34

Describe how resisting cell death is a hallmark of cancer

Answer 34

Cancer cells that avoid or evade apoptosis. There can be mutations in P53 which keeps cell cycle going and apoptosis from not happening. There can also be other mutations in genes that regulate apoptosis and cancer cells overexpress anti apoptotic signaling molecules like BCL2 which deals with membrane integrity.

Question 35

Describe how evading growth suppressors is considered a hallmark of cancer

Answer 35

In cancer cells there can be mutated tumor suppressor genes that fail to inhibit growth and lead to uncontrolled proliferation. Most tumor suppressor genes deals with transcription factors, cell Cycle inhibitors, etc.
If P53 is mutated then there will be no cell cycle attest and then the DNA damage will go unprepared and it allows for the growth of damaged cells (cancer) and this can lead to a malignant tumor.
If RB is mutated then it will always be off and will allow for the continuation of the cell Cycle and lead to uncontrolled proliferation.