Showing posts with label pathology I and II. Show all posts
Showing posts with label pathology I and II. Show all posts
Friday, December 11, 2009
Thursday, April 30, 2009
pathology: cellular growth and differentiation
this pathology lecture covered some basic concepts about normal and abnormal cell growth and differentiation. there are several categories of such processes: first is "acquired benign changes", which includes hyperplasia- the increase in the number of cells in a tissue or organ, as well as hypertrophy, which is an increase in the size of the cells. atrophy is the opposite; the decrease in cellular substance and therefore size, due to aging or decreased workload/innervation/nutrients/blood supply/endocrine stimulation. the next category is "congenital/developmental changes", and includes hypoplasia- the defective formation or incomplete development of a part, and agenesis- the absence or failure of formation of an organ or tissue.
the next categories are acquired pre-malignant and acquired malignant. metaplasia is the abnormal transformation of fully differentiated cells into another type of cell; for example, the transition from columnar to squamous cells in a smoker's larynx, or the transition from squamous to columnar cells in a lower esophagus damaged by acid reflux. dysplasia is a partial "de-differentiation" of cells which causes them to lose their functionality, adhesions to neighboring cells, and causes their nuclei to enlarge. anaplasia is an acquired malignant change which is a complete loss of differentiation of cells, as in oat cell carcinoma.
questions
1. define "differentiation" with respect to cell development.
2. what is hyperplasia?
3. what is hypertrophy?
4. what is atrophy?
5. what can cause cell atrophy?
6. what is hypoplasia?
7. what is agenesis?
8. what is metaplasia?
9. what are some examples of metaplasia?
10. what is dysplasia?
11. what is anaplasia?
answers
1. development of specialized morphology and function in cells.
2. increase in the number of cells in an organ or tissue.
3. increase in size of cells in an organ or tissue.
4. decrease in cell size by loss of cell substance.
5. aging, or decreased workload, blood supply innervation, nutrition, endocrine stimulation.
6. defective formation or incomplete development of a tissue or organ.
7. absence or failure of formation of a tissue or organ.
8. the abnormal transformation of one differentiated tissue into another.
9. columnar cells changing into squamous cells in the smoker's larynx, and chronic acid irritation in the lower esophagus changing squamous to columnar cells.
10. an abnormal de-differentiation of tissue. cells lose adhesions, nucleus grows bigger, becomes like a stem cell.
11. a total loss of differentiation as in oat cell carcinoma.
the next categories are acquired pre-malignant and acquired malignant. metaplasia is the abnormal transformation of fully differentiated cells into another type of cell; for example, the transition from columnar to squamous cells in a smoker's larynx, or the transition from squamous to columnar cells in a lower esophagus damaged by acid reflux. dysplasia is a partial "de-differentiation" of cells which causes them to lose their functionality, adhesions to neighboring cells, and causes their nuclei to enlarge. anaplasia is an acquired malignant change which is a complete loss of differentiation of cells, as in oat cell carcinoma.
questions
1. define "differentiation" with respect to cell development.
2. what is hyperplasia?
3. what is hypertrophy?
4. what is atrophy?
5. what can cause cell atrophy?
6. what is hypoplasia?
7. what is agenesis?
8. what is metaplasia?
9. what are some examples of metaplasia?
10. what is dysplasia?
11. what is anaplasia?
answers
1. development of specialized morphology and function in cells.
2. increase in the number of cells in an organ or tissue.
3. increase in size of cells in an organ or tissue.
4. decrease in cell size by loss of cell substance.
5. aging, or decreased workload, blood supply innervation, nutrition, endocrine stimulation.
6. defective formation or incomplete development of a tissue or organ.
7. absence or failure of formation of a tissue or organ.
8. the abnormal transformation of one differentiated tissue into another.
9. columnar cells changing into squamous cells in the smoker's larynx, and chronic acid irritation in the lower esophagus changing squamous to columnar cells.
10. an abnormal de-differentiation of tissue. cells lose adhesions, nucleus grows bigger, becomes like a stem cell.
11. a total loss of differentiation as in oat cell carcinoma.
Saturday, April 25, 2009
pathology I: cellular injury and death
this was the first pathology lecture (besides the introductory pathology lecture that defined some general terms used in pathology) and introduced some key concepts in cell injury and death. the first section gave a broad overview of the variety of injurious influences on cells: physiological agents, chemical agents, immunological agents, nutritional imbalances, stress. some physiological agents include mechanical trauma, temperature excess, pressure changes, radiation, electric shock, etc. chemical agents can include environmental toxins, poisons, alcohol, tobacco, synthetic drugs.
one area of injurious chemical agents is the oxygen derived free radicals. these are highly reactive molecules such as superoxide anion, hydroxide ion (recall the production of hydroxide ion via the fenton reaction from biochemistry), hydrogen peroxide, which have a single electron in their outer orbitals, allowing them to cause damage in a variety of cellular components such as lipid membranes, membrane proteins, DNA, and mitochondria. the body is equipped with antioxidant enzymes which counteract the action of oxygen-derived free radicals, such vitamin E, glutathione peroxidase, superoxide dismutase, and catalase.
another type of common cellular damage is "cloudy swelling", which is a loss of fluid and ionic homeostasis which leads to cellular swelling and other metabolic dysfunction. cloudy swelling is generally caused by a lack of blood supply, which cuts of oxygen and glucose supplies, and causes a whole host of other effects; decreased ATP concentration, intracellular accumulation of sodium (and thus water) and calcium, increased anaerobic respiration and thus lower pH, swelling of mitochondria and ER, and membrane damage. the increased calcium levels alone have an injurious effect on the cell, activating protein kinases, phospholipases, and proteases which damage cellular components.
there are many different types of cellular degeneration. fatty degeneration, or steatosis, is characterized by excess lipid accumulation in cells and can be caused by excess released of lipids from the liver, excess fatty acid synthesis or dysfunctional fatty acid oxidation, etc. steatosis can cause accumulation of fat in the liver in particular and cause it to grow up to 4 times normal liver mass. hyaline degeneration is a type of degeneration that shows abnormal, intracellular protein that stains pink with the H+E stain. this is seen in some viral infections, in the liver of alcoholics, scar tissue, and sometimes in proximal tubule epithelial cells, among other instances. myxomatous degeneration is a type of degeneration in which increased ground substance damages connective tissue fibers, as in the mitral valve, or cystic medial necrosis.
calcification is another type of degeneration or damage that can occur with cells. normal calcification is the process by which insoluble calcium deposits accumulate in tissues; this process can occur naturally in the pineal gland, the tunica media of large arteries, the annulus of the mitral valve, and tracheal cartilage. dystrophic or abnormal calcification when calcium starts depositing in "non-viable" tissues such as in atheroma, tuberculosis, psammoma bodies, or hyperparathyroidism. metastatic calcification results from highly elevated serum calcium that can result from destruction of bone by cancer, abuse of milk or antacids, or parathyroid adenoma.
there are many other types of pathologies that result from high accumulations of various material in different tissues or organs. for example, amyloidosis is accumulation of amyloid protein. fatty infiltration is the abnormal accumulation of fat in the pancreas, lymph nodes, right heart, and muscles (in cystic fibrosis). iatrogenic accumulations can include talc, silicon, myelogram dyes in tissues. anthracosis is the accumulation of carbon deposits within tissues. finally, hemosiderin is an iron storage molecule that can accumulate within the liver.
there are many other types of pathologies that result from high accumulations of various material in different tissues or organs. for example, amyloidosis is accumulation of amyloid protein. fatty infiltration is the abnormal accumulation of fat in the pancreas, lymph nodes, right heart, and muscles (in cystic fibrosis). iatrogenic accumulations can include talc, silicon, myelogram dyes in tissues. anthracosis is the accumulation of carbon deposits within tissues. finally, hemosiderin is an iron storage molecule that can accumulate within the liver.
the last topic in this lecture is the two different ways in which cells can die: necrosis (which is considered homicide) and apoptosis (considered suicide). necrosis is a messy cell death caused by external factors such as ischemia, toxins, infections, trauma, extreme temperature. there are several different types, such as coagulation necrosis, in which denatured coagulated cytoplasmic proteins accumulate, caseous necrosis, and liquefaction necrosis, which involves enzymatic digestion via leukocytes. in contrast, apoptosis is an orderly cell death, where the apoptodic cell loses cell adhesions, divides into apoptodic bodies, which are then phagocytosed by immune cells. apoptosis can be intrinsically mediated by release of pro-apoptodic proteins from the mitochondrial or extrinsically mediated by receptor-ligand interactions.
questions
etiology...
1. what are some etiologic agents that can cause cell death?
2. what are some physiologic agents that are injurious to cells?
3. what are some chemical agents that are injurious to cells?
4. what are examples of infectious agents that are injurious to cells?
5. what are examples of immunologic reactions that can be injurious to cells?
oxygen derived free radicals...
6. describe the effect of oxygen derived free radicals on cells.
7. what are some methods of oxygen derived free radical production?
8. what are some of the free radical scavengers present in the body?
9. what are some examples of oxygen derived free radicals?
cloudy swelling...
10. what is cloudy swelling?
11. describe the swelling mechanism.
12. how is cloudy swelling detected?
13. what is cloudy swelling caused by?
14. what goes on inside the cell as a result of cloudy swelling?
15. what does cellular injury induce in mitochondria?
16. what effects does high intracellular calcium levels have on the cell?
degeneration...
17. what is fatty degeneration / steatosis and what is it caused by?
18. what are some possible mechanisms of steatosis?
19. how much does a normal liver weigh and how much does a liver from a person with steatosis weigh?
20. what is hyaline degeneration?
21. what are some examples of proteins that qualify for hyaline degeneration?
22. what is myxomatous degeneration?
23. which conditions is myxomatous degeneration seen in?
calcification...
24. describe the normal process of calcification.
25. what are structures that normally calcify with age?
26. what is dystrophic calcification and what are some examples where this occurs?
27. what is metastatic calcification?
28. what are some examples in which metastatic calcification occurs?
other accumulations...
29. what is amyloidosis?
30. which pathologies are associated with abnormal levels of amyloid protein?
31. what is fatty infiltration?
32. gaucher, hurler, and tay sachs are all examples of diseases in which...
33. what are some examples of iatrogenic accumulations?
34. what is anthracosis?
35. what is hemosiderin?
necrosis and apoptosis...
36. what can necrosis be caused by?
37. what is coagulation necrosis?
38. what is liquefaction necrosis?
39. what is fat necrosis?
40. what is gangrene? what are the different types?
41. what is apoptosis?
42. describe what happens during apoptosis.
43. what are the intrinsic and extrinsic pathways for apoptosis?
answers
1. hypoxia, ischemia, physiological agents, chemical agents, immunological agents, genetic factors, nutritional imbalances, stress.
2. mechanical trauma, temperature extremes, pressure changes, radiation, electric shock.
3. environmental toxins, poisons, alcohol, tobacco, synthetic drugs.
4. viruses, rickettsiae, bacteria, fungi, helminthes, arthropods
5. allergy/hypersensitivity, anaphalaxis, autoimmunity.
6. oxygen derived free radicals have a single electron in an outer orbital which can react strongly with various cellular components such as proteins, lipids, carbohydrates, nucleic acids.
7. redox reactions, xanthine oxidase, free iron, neutrophils/macrophages, oxygen therapy, drugs/irradiation.
8. vitamin E, glutathione peroxidase, superoxide dismutase,
9. superoxide anion, hydrogen peroxide, hydroxide ion.
10. a cellular swelling due to loss of fluid and ionic homeostasis.
11. decreased ATP concentration reduces sodium ATPase pump, causing Na to accumulate in cells and draw water in osmotically.
12. the detection of intracellular proteins that have accumulated in the serum, such as AST, ALT in liver degeneration or CK-MB, LDH, and troponin T in cardiac degeneration.
13. blockage in blood flow, which causes a whole host of effects due to the resulting decrease of glucose and oxygen.
14. increased intracellular Ca2+ and Na+ concentrations, swelling of mitochondria and endoplasmic reticulum, membrane damage, and a switch to anaerobic respiration, which lowers the intracellular pH.
15. formation of non selective pores; leakage of apoptotic proteins.
16. activation of protein kinases which phosphorylate proteins, phospholipases which can cause membrane damage, and proteases which can dissassemble proteins and the cytoskeleton.
17. abnormal accumulation of triglycerides due to cellular metabolic damage and increased lipids.
18. excess free fat coming from the liver; due to overactive fatty acid synthesis, dysfunctional fatty acid oxidation, excess esterification of fatty acids to triglycerides, apoprotein or lipoprotein dysfunction.
19. 1500g, 4500g.
20. cells with intracellular protein that stain pink with the H+E stain.
21. viral inclusions, deposits in alcoholic hepatocytes, keloid collagen (aggressive scar tissue).
22. increased ground substance with damage to connective tissue fibers.
23. cystic medial necrosis, mitral valve prolapse.
24. the hardening of tissue or non-cellular material as a result of calcium deposits.
25. pineal gland, tunica media of large arteries, mitral valve annulus, and tracheal cartilage.
26. abnormal calcification of non-viable tissues. occurs in atheroma, tuberculosis (lymph nodes calcify), psammoma bodies, heart valves, hyperparathyroidism.
27. occurs when there is highly elevated calcium or phosphate levels in serum.
28. breakdown of bone by cancer, milk abuse, antacid abuse, parathyroid adenoma.
29. an idiopathic disease in which amyoid protein accumulates extracellularly in organs and tissues.
30. b cell proliferations, chronic inflammation, chronic renal failure, alzheimer's, type II diabetes, prion disease.
31. high deposits of fat, most often occurs in pancreas, lymph nodes, right heart, muscles.
32. there is a high level of complex lipid and carbohydrate deposition in tissues and organs.
33. talc, silicon, myelogram dyes.
34. accumulation of carbon deposits.
35. an iron storage complex that can form in large deposits and cause organ damage.
36. ischemia, infection, toxins, hyperimmune reactions, hypoxia, trauma, temperature extremes.
37. cell death similar in appearance to cloudy swelling, involving denatured, coagulated cytoplasmic proteins.
38. necrosis that results from enzymatic digestion by leukocytes-- common in brain and lipid rich tissues.
39. destruction of fat in certain tissues or organs such as the pancreas or breast.
40. death of a body part with putrification. dry gangrene involves an area with little or no blood supply, no sepsis. wet gangrene is bacterial infection on top of coagulative necrosis. gas gangrene is specific to clostridium perfringens.
41. an orderly, programmed cell death without inflammation.
42. apoptodic cells lose their cell adhesions, divide into apoptotic bodies, which are phagocytosed.
43. intrinsic is triggered by release of apoptodic mitochondrial proteins and extrinsic is triggered by receptor-ligand interactions.
one area of injurious chemical agents is the oxygen derived free radicals. these are highly reactive molecules such as superoxide anion, hydroxide ion (recall the production of hydroxide ion via the fenton reaction from biochemistry), hydrogen peroxide, which have a single electron in their outer orbitals, allowing them to cause damage in a variety of cellular components such as lipid membranes, membrane proteins, DNA, and mitochondria. the body is equipped with antioxidant enzymes which counteract the action of oxygen-derived free radicals, such vitamin E, glutathione peroxidase, superoxide dismutase, and catalase.
another type of common cellular damage is "cloudy swelling", which is a loss of fluid and ionic homeostasis which leads to cellular swelling and other metabolic dysfunction. cloudy swelling is generally caused by a lack of blood supply, which cuts of oxygen and glucose supplies, and causes a whole host of other effects; decreased ATP concentration, intracellular accumulation of sodium (and thus water) and calcium, increased anaerobic respiration and thus lower pH, swelling of mitochondria and ER, and membrane damage. the increased calcium levels alone have an injurious effect on the cell, activating protein kinases, phospholipases, and proteases which damage cellular components.
there are many different types of cellular degeneration. fatty degeneration, or steatosis, is characterized by excess lipid accumulation in cells and can be caused by excess released of lipids from the liver, excess fatty acid synthesis or dysfunctional fatty acid oxidation, etc. steatosis can cause accumulation of fat in the liver in particular and cause it to grow up to 4 times normal liver mass. hyaline degeneration is a type of degeneration that shows abnormal, intracellular protein that stains pink with the H+E stain. this is seen in some viral infections, in the liver of alcoholics, scar tissue, and sometimes in proximal tubule epithelial cells, among other instances. myxomatous degeneration is a type of degeneration in which increased ground substance damages connective tissue fibers, as in the mitral valve, or cystic medial necrosis.
calcification is another type of degeneration or damage that can occur with cells. normal calcification is the process by which insoluble calcium deposits accumulate in tissues; this process can occur naturally in the pineal gland, the tunica media of large arteries, the annulus of the mitral valve, and tracheal cartilage. dystrophic or abnormal calcification when calcium starts depositing in "non-viable" tissues such as in atheroma, tuberculosis, psammoma bodies, or hyperparathyroidism. metastatic calcification results from highly elevated serum calcium that can result from destruction of bone by cancer, abuse of milk or antacids, or parathyroid adenoma.
there are many other types of pathologies that result from high accumulations of various material in different tissues or organs. for example, amyloidosis is accumulation of amyloid protein. fatty infiltration is the abnormal accumulation of fat in the pancreas, lymph nodes, right heart, and muscles (in cystic fibrosis). iatrogenic accumulations can include talc, silicon, myelogram dyes in tissues. anthracosis is the accumulation of carbon deposits within tissues. finally, hemosiderin is an iron storage molecule that can accumulate within the liver.
there are many other types of pathologies that result from high accumulations of various material in different tissues or organs. for example, amyloidosis is accumulation of amyloid protein. fatty infiltration is the abnormal accumulation of fat in the pancreas, lymph nodes, right heart, and muscles (in cystic fibrosis). iatrogenic accumulations can include talc, silicon, myelogram dyes in tissues. anthracosis is the accumulation of carbon deposits within tissues. finally, hemosiderin is an iron storage molecule that can accumulate within the liver.
the last topic in this lecture is the two different ways in which cells can die: necrosis (which is considered homicide) and apoptosis (considered suicide). necrosis is a messy cell death caused by external factors such as ischemia, toxins, infections, trauma, extreme temperature. there are several different types, such as coagulation necrosis, in which denatured coagulated cytoplasmic proteins accumulate, caseous necrosis, and liquefaction necrosis, which involves enzymatic digestion via leukocytes. in contrast, apoptosis is an orderly cell death, where the apoptodic cell loses cell adhesions, divides into apoptodic bodies, which are then phagocytosed by immune cells. apoptosis can be intrinsically mediated by release of pro-apoptodic proteins from the mitochondrial or extrinsically mediated by receptor-ligand interactions.
questions
etiology...
1. what are some etiologic agents that can cause cell death?
2. what are some physiologic agents that are injurious to cells?
3. what are some chemical agents that are injurious to cells?
4. what are examples of infectious agents that are injurious to cells?
5. what are examples of immunologic reactions that can be injurious to cells?
oxygen derived free radicals...
6. describe the effect of oxygen derived free radicals on cells.
7. what are some methods of oxygen derived free radical production?
8. what are some of the free radical scavengers present in the body?
9. what are some examples of oxygen derived free radicals?
cloudy swelling...
10. what is cloudy swelling?
11. describe the swelling mechanism.
12. how is cloudy swelling detected?
13. what is cloudy swelling caused by?
14. what goes on inside the cell as a result of cloudy swelling?
15. what does cellular injury induce in mitochondria?
16. what effects does high intracellular calcium levels have on the cell?
degeneration...
17. what is fatty degeneration / steatosis and what is it caused by?
18. what are some possible mechanisms of steatosis?
19. how much does a normal liver weigh and how much does a liver from a person with steatosis weigh?
20. what is hyaline degeneration?
21. what are some examples of proteins that qualify for hyaline degeneration?
22. what is myxomatous degeneration?
23. which conditions is myxomatous degeneration seen in?
calcification...
24. describe the normal process of calcification.
25. what are structures that normally calcify with age?
26. what is dystrophic calcification and what are some examples where this occurs?
27. what is metastatic calcification?
28. what are some examples in which metastatic calcification occurs?
other accumulations...
29. what is amyloidosis?
30. which pathologies are associated with abnormal levels of amyloid protein?
31. what is fatty infiltration?
32. gaucher, hurler, and tay sachs are all examples of diseases in which...
33. what are some examples of iatrogenic accumulations?
34. what is anthracosis?
35. what is hemosiderin?
necrosis and apoptosis...
36. what can necrosis be caused by?
37. what is coagulation necrosis?
38. what is liquefaction necrosis?
39. what is fat necrosis?
40. what is gangrene? what are the different types?
41. what is apoptosis?
42. describe what happens during apoptosis.
43. what are the intrinsic and extrinsic pathways for apoptosis?
answers
1. hypoxia, ischemia, physiological agents, chemical agents, immunological agents, genetic factors, nutritional imbalances, stress.
2. mechanical trauma, temperature extremes, pressure changes, radiation, electric shock.
3. environmental toxins, poisons, alcohol, tobacco, synthetic drugs.
4. viruses, rickettsiae, bacteria, fungi, helminthes, arthropods
5. allergy/hypersensitivity, anaphalaxis, autoimmunity.
6. oxygen derived free radicals have a single electron in an outer orbital which can react strongly with various cellular components such as proteins, lipids, carbohydrates, nucleic acids.
7. redox reactions, xanthine oxidase, free iron, neutrophils/macrophages, oxygen therapy, drugs/irradiation.
8. vitamin E, glutathione peroxidase, superoxide dismutase,
9. superoxide anion, hydrogen peroxide, hydroxide ion.
10. a cellular swelling due to loss of fluid and ionic homeostasis.
11. decreased ATP concentration reduces sodium ATPase pump, causing Na to accumulate in cells and draw water in osmotically.
12. the detection of intracellular proteins that have accumulated in the serum, such as AST, ALT in liver degeneration or CK-MB, LDH, and troponin T in cardiac degeneration.
13. blockage in blood flow, which causes a whole host of effects due to the resulting decrease of glucose and oxygen.
14. increased intracellular Ca2+ and Na+ concentrations, swelling of mitochondria and endoplasmic reticulum, membrane damage, and a switch to anaerobic respiration, which lowers the intracellular pH.
15. formation of non selective pores; leakage of apoptotic proteins.
16. activation of protein kinases which phosphorylate proteins, phospholipases which can cause membrane damage, and proteases which can dissassemble proteins and the cytoskeleton.
17. abnormal accumulation of triglycerides due to cellular metabolic damage and increased lipids.
18. excess free fat coming from the liver; due to overactive fatty acid synthesis, dysfunctional fatty acid oxidation, excess esterification of fatty acids to triglycerides, apoprotein or lipoprotein dysfunction.
19. 1500g, 4500g.
20. cells with intracellular protein that stain pink with the H+E stain.
21. viral inclusions, deposits in alcoholic hepatocytes, keloid collagen (aggressive scar tissue).
22. increased ground substance with damage to connective tissue fibers.
23. cystic medial necrosis, mitral valve prolapse.
24. the hardening of tissue or non-cellular material as a result of calcium deposits.
25. pineal gland, tunica media of large arteries, mitral valve annulus, and tracheal cartilage.
26. abnormal calcification of non-viable tissues. occurs in atheroma, tuberculosis (lymph nodes calcify), psammoma bodies, heart valves, hyperparathyroidism.
27. occurs when there is highly elevated calcium or phosphate levels in serum.
28. breakdown of bone by cancer, milk abuse, antacid abuse, parathyroid adenoma.
29. an idiopathic disease in which amyoid protein accumulates extracellularly in organs and tissues.
30. b cell proliferations, chronic inflammation, chronic renal failure, alzheimer's, type II diabetes, prion disease.
31. high deposits of fat, most often occurs in pancreas, lymph nodes, right heart, muscles.
32. there is a high level of complex lipid and carbohydrate deposition in tissues and organs.
33. talc, silicon, myelogram dyes.
34. accumulation of carbon deposits.
35. an iron storage complex that can form in large deposits and cause organ damage.
36. ischemia, infection, toxins, hyperimmune reactions, hypoxia, trauma, temperature extremes.
37. cell death similar in appearance to cloudy swelling, involving denatured, coagulated cytoplasmic proteins.
38. necrosis that results from enzymatic digestion by leukocytes-- common in brain and lipid rich tissues.
39. destruction of fat in certain tissues or organs such as the pancreas or breast.
40. death of a body part with putrification. dry gangrene involves an area with little or no blood supply, no sepsis. wet gangrene is bacterial infection on top of coagulative necrosis. gas gangrene is specific to clostridium perfringens.
41. an orderly, programmed cell death without inflammation.
42. apoptodic cells lose their cell adhesions, divide into apoptotic bodies, which are phagocytosed.
43. intrinsic is triggered by release of apoptodic mitochondrial proteins and extrinsic is triggered by receptor-ligand interactions.
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