1. Cellular Pathology - BP

Question 1

What is the mechanism by which hyperplasia and hypertrophy can occur?

Answer 1

1. Up regulation or down regulation of receptors.

2. Induction of new protein synthesis.

Question 2

What are the 4 main cellular systems that are especially vulnerable to cellular injury?

Answer 2

1. DNA
2. Cell membranes
3. Protein generation
4. ATP production

Question 3

What damage do the free radicals do especially?

Answer 3

1. Lipid peroxidation
2. DNA fragmentation
3. Protein cross-linking –> incr. degradation and decr. activity.

Question 4

What happens when there is an increased mt cytosolic calcium?

Answer 4

Incr. Ca –> Lipid peroxidation –> formation of mt permeability transition (a non selective pore that dissipates the protein gradient) + release of cytochrome c –> apoptosis.

Question 5

What are the 2 most important factors determining irreversible damage?

Answer 5

1. Membrane disturbances

2. Inability to reverse the mt dysfunction

Question 6

What morphologic changes of cellular injury do we see under light microscope?

Answer 6

Reversible injury : Cellular swelling and fatty change.

Irreversible injury : Nuclear karyolysis - pyknosis - karyorrhexis.

Question 7

What morphologic changes in cellular injury do we see under electron microscope?

Answer 7

Reversible injury : Cellular blebs and small mt densities.
Irreversible injury : Ruptured lysosomes, myelin figures, lysis of endoplasmic reticulum + large calcium rich mitochondrial densities

Question 8

What organs are affected by coagulative necrosis?

Answer 8

May occur in any organ –> in organs with high LIPID content (brain), coagulative necrosis is rapidly followed by liquefactive necrosis.

Question 9

What is the basic description of coagulative necrosis?

Answer 9

Protein denaturation is more prominent than enzymatic breakdown.

Question 10

What is the basic description of liquefactive necrosis?

Answer 10

Occurs in situations in which enzymatic breakdown is more prominent than protein denaturation.

Question 11

What organs are affected in liquefactive necrosis?

Answer 11

Organs with high fat and low protein content (brain), or those with high enzymatic content (pancreas).

Question 12

What is the mechanism that leads to lipofuscin accumulation?

Answer 12

Lipofuscin is a product of lipid peroxidation, which accumulates in the LYSOSOMES as the cell ages.

Question 13

What are the 2 organs where lipofuscin most commonly accumulates?

Answer 13

1. Heart

2. Liver

Question 14

What is the gross morphology of lipofuscin accumulation?

Answer 14

Brown discoloration to organ –> such organs may be atrophic hence the term , brown atrophy.

Question 15

What is the microscopic morphology of lipofuscin accumulation?

Answer 15

Finely granular yellow-brown pigment, which often surrounds the nucleus.

Question 16

Mention 2 examples of protein accumulation.

Answer 16

Involve intermediate filaments :

1. Mallory hyaline in the liver.
2. Alzheimer’s - neurofibrillary tangles.

Question 17

What is hemosiderosis?

Answer 17

Accumulation of iron in organs without resultant side effects –> Iron pigment is frequently within the macrophages.

Question 18

What are the 4 most common organs affected by fat accumulations

Answer 18

1. Liver
2. Kidney
3. Heart
4. Skeletal muscle

Question 19

Mention one important point about steatosis (fat accumulation).

Answer 19

Can indicate reversible damage or may be the sign of an intrinsic abnormality in fat metabolism.

Question 20

What is the most commonly affected organ by cholesterol accumulation?

Answer 20

Blood vessels - by atherosclerosis or at the site of hemorrhage (cholesterol accumulates within phagocytic cells).

Question 21

What are the 2 most commonly affected organs of glycogen accumulation?

Answer 21

1. Liver

2. Skeletal muscle

Question 22

What happens in Werner syndrome?

Answer 22

Premature aging due to a defective DNA helicase.

Question 23

What are the basic types of cellular adaptation?

Answer 23

1. Hyperplasia
2. Hypertrophy
3. Atrophy
4. Metaplasia