Path Block 1 Lecture 1

Front 2

What are the 3 types of tissues classified based on their proliferative capacities?

Back 2

Labile (continuously replicating)
Stable (quiescent - normally replicate minimally but proliferate in response to injury)
Permanent tissues (non proliferative)

Front 3

What are labile tissues? What are some examples of labile tissues?

Back 3

Labile tissues divide continuously.
Examples are hematopoetic cells and surface epithelia (skin, gi, and lining of upper respiratory airways)

Front 4

What are stable tissues? What are some examples of stable tissues?

Back 4

Stable tissues are those that replicate minimally under normal conditions but proliferate following injury. The examples include parenchyma of solid organs (pancreas, liver, kidney) and various cells (fibroblasts, SMC, and endothelial)

Front 5

What are permanent tissues? What are some examples of permanent tissues?

Back 5

Permanent tissues are non-proliferative. These include neurons and cardiac muscle cells.

Front 6

An increase in the size of cells = increase in the size of organs is called?

Back 6

Hypertrophy

Front 7

What causes the increase in the size of cells in hypertrophy?

Back 7

Increased amount of proteins and organelles due to trophic or mechanical triggers to the cell.

Front 8

In hypertrophy, do cells divide?

Back 8

In hypertrophy, cells have no capacity to divide or a minimal one.

Front 9

What is the example of physiologic hypertrophy given? What is the example of pathological hypertrophy given?

Back 9

Physiological hypertrophy- skeletal muscle hypertrophy in weight lifting athlete.

Pathological hypertrophy: cardiac muscle hypertrophy in hypertension.

Front 10

T/F The adaption to higher loads is hypertrophy but the adaption to severe cell injury is cell death

Back 10

True.

Front 11

What are some of the findings in pathologic hypertrophy in the heart?

Back 11

Increased heart weight. Increased left ventricular thickness in response to higher workloads (hypertension/valvular stenosis)
Histologically, we see larger nuclei and wider myofibers.

Front 12

What is the definition of hyperplasia? In what type of cells does it occur?

Back 12

In hyperplasia, there is an increase in cell number. This occurs in cells capable of cell division - stabile and labile cells.

Front 13

Give 2 examples of physiological hyperplasia. Give 2 examples of pathological hyperplasia after defining the cause.

Back 13

Physiological hyperplasia - female breast at puberty and in pregnancy. Hyperplasia of liver after partial resection.

Pathological hyperplasia is caused by excessive stimulation of growth factors or hormones. HPV virus causing squamous hyperplasia is an example. Hormonal imbalance stimulating endometrial hyperplasia is another example.

Front 14

Is hyperplasia reversible or irreversible? What is the clinical significance of hyperplasia?

Back 14

Hyperplasia is reversible. Hyperplasia is associated with an increased risk for cancer.

Front 15

What is atrophy?

Back 15

Atrophy refers to the decrease in a size of a cell due to loss of a cell substance. If it is severe, this leads to decreased organ size.

Front 16

What are some characteristics of the cell in atrophy.

Back 16

Decreased protein synthesis
Increased protein degradation
Decreased function but not death

Front 17

What are the causes of physiologic and pathological atrophy?

Back 17

Physiological - Loss of hormonal stimulation
Pathological - decreased functional demand, loss of innervation, inadequate nutrition

Front 18

What is unique about skeletal muscle myopathy?

Back 18

There is hypertrophy and atrophy in the fibers.

Front 19

Is metaplasia reversible or irreversible? Why is metaplasia clinically significant?

Back 19

Metaplasia is reversible. Metaplasia may be associated with increased cancer risk.

Front 20

What is the definition of metaplasia?

Back 20

In metaplasia, one cell type is replaced by another. This is an adaptive response to chronic stress and or persistent cell injury (smoking, acid reflux).

Front 21

What is epithelial metaplasia?

Back 21

Ciliated columnar epithelium becomes squamous epithelium.
Squamous epithelium becomes gastric/intestinal.

Front 22

What is mesenchymal metaplasia?

Back 22

At sites of injury, you get bone formation in soft tissue (muscle or connective tissue).

Front 23

What kind of metaplasia would you expect to see in smokers?

Back 23

Respiratory tissue is epithelium. You would expect to see a type of epithelial metaplasia. In fact, smokers have conversion of ciliated columnar epithelia to squamous epithelia.

Front 24

What kind of metaplasia would you expect to see in the endocervix?

Back 24

In the endocervix, which is again an epithelia, you would see the ciliated columnar epithelia become squamous epithelia. This increases the risk for HPV infection.

Front 25

What happens in Barrett esophagus?

Back 25

In Barrett esophagus, the squamous epithelia becomes gastric epithelia to protect reflux. This is epithelial metaplasia.

Front 26

In irreversible cell injury, what causes the cell death?

Back 26

Inability to reverse mitochondrial dysfunction (lack of oxidative phosphorylation and ATP generation). There is also a disturbance in membrane function.

Front 27

What are the two outcomes of irreversible cell injury.

Back 27

Irreversible cell injury always leads to cell death. Necrosis or apoptosis are the only two outcomes.

Front 28

Compare the size of the cell in necrosis vs apoptosis?

Back 28

Necrosis has an enlarged cell size, apoptosis has a reduced cell size.

Front 29

Compare the nucleus dismantling in necrosis vs apoptosis.

Back 29

Necrosis involves pyknosis (chromatin condensation), karyorrhexis (fragmentation of the nucleus), followed by karyolysis.

In apoptosis, the nucleus is fragmented into nucleosome sized fragments.

Front 30

What are the some of the causes of cell injury?

Back 30

Oxygen deprivation, physical agents, chemical agents, infectious agents, immunological reactions, genetic derangements, nutritional imbalances, aging.

Front 31

Differentiate between hypoxia and ischemia.

Back 31

Hypoxia (inadequate oxygenation of blood such as in lung disease, lack of oxygen in air, or reduced carrying capacity of blood)

Ischemia involves lack of blood supply to the site.

Front 32

What are the physical agents that cause cell injury?

Back 32

Trauma, temperature extremes, and radiation

Front 33

What are the chemical agents that cause cell injury?

Back 33

Chemicals (Na, glucose), poison, asbestos.

Front 34

What are some infectious agents that cause cell injury?

Back 34

Viruses, fungi, bacteria, parasites

Front 35

What are some immunologic reactions that cause cell injury?

Back 35

Autoimmune diseases, hypersensitivity

Front 36

What are some genetic derangements that cause cell injury?

Back 36

Point mutations, polymorphisms,

Front 37

Why does aging cause cell damage?

Back 37

Decreased ability to repair damage as you get older.

Front 38

What are some morphology changes you observe during reversible cell injury?

Back 38

Cellular swelling- hydropic change or vacuolar degeneration. This is due to membrane pumps failing to maintain homeostasis- membrane blebs. Vacuoles appear in cells corresponding to a distended ER.

You also will see lipid vacuoles in the cytoplasm. This occurs with toxic and hypoxic injury, primarily in cells dependent on fat metabolism.

Front 39

What are some of the morphological features of necrosis?

Back 39

Increased eosinophilia, nuclear shrinkage, fragmentation, breakdown of plasma membranes and organelle membranes.

Front 40

What is coagulative necrosis? What are the causes of coagulative necrosis? Where does coagulative necrosis occur?

Back 40

In coagulative necrosis, you have intact outlines, but loss of cellular details. This means that the injury denatures proteins and enzymes but no proteolysis occurs. This is caused by hypoxic or anoxic injury due to ischemia (infarct). This occurs in all tissues but the brain. In the brain infarcts do not result in coagulative necrosis but liquefactive necrosis.

Front 41

What is liquefactive necrosis? What are the causes of liquefactive necrosis? Where does liquefactive necrosis occur?

Back 41

In liquefactive necrosis, dead cells are completely digested. This is commonly seen in bacterial and fungal infections. Microbes stimulate accumulation of WBC, which release digestive enzymes. The collection of necrotic cells with acute inflammatory cells = pus.

Front 42

What is unique about brain liquefactive necrosis?

Back 42

The first unique part is that we would expect an infarct injury to give a coagulative necrosis rather than a liquefactive necrosis. The other unique aspect is that brain liquefactive necrosis does not have pus.

Front 43

What is caseous necrosis? What are the causes of caseous necrosis? Where does caseous necrosis occur?

Back 43

In caseous necrosis, there is a gross resemblance to cheese. There is a loss of cell outlines. Cells are fragmented and coagulated. There is a border of inflammatory cells that surrounds the necrosis called a granuloma. Usually, caseous necrosis is associated with TB.

Front 44

What is gangrenous necrosis?

Back 44

Gangrenous necrosis is not a specific type of necrosis but is used to refer to ischemic coagulative necrosis of lower or upper extremities. It can also refer to severe necrosis of some organs (bowel, gallbladder, appendix)

Front 45

What is the difference between dry and wet gangrene?

Back 45

When a bacterial infection is also present in addition to the ischemia, the necrosis has liquefactive characteristics (wet gangrene)

Front 46

What is fibrinoid necrosis? In what diseases does it occur?

Back 46

Fibrinoid necrosis involves the deposition of immune complexes (antigens/antibodies) in vascular wall. This occurs in vasculitis syndromes It is fibrin like because it has a bright pink appearance.

Front 47

What is fat necrosis? Where is it typically seen?

Back 47

Fat necrosis is typically seen in acute pancreatitis in the pancreas. Injury to the pancreas releases lipase which liquefies fat and splits triglycerides. Fatty acids combine with calcium to form white chalky material (saponification).

It can also be seen in fatty tissue such as in the breast following trauma.

Front 48

Compare the plasma membrane in necrosis vs apoptosis

Back 48

NEcrosis plasma membrane is disrupted. In Apoptosis its intact

Front 49

comopare cellular contents in necrosis vs apoptosis

Back 49

NEcrosis has frequent enzymes that leak out of the cell. Apoptosis the cell contents are usually intact but may be released in apoptotic bodies

Front 50

Compare inflammation in necrosis and apoptosis

Back 50

Necrosis has inflammation and apoptosis does not

Front 51

Is necrosis physiological or pathological. What about apoptosis?

Back 51

Necrosis is pathologic. Apoptosis is physiological or pathological