Path Block 1
1. Atrophy:
Decrease in size, cell # Physiologic or pathologic Often reversibleMechanism:
decrease metabolic activity decrease protein synthesisIf caused by decrease
blood flow apoptosis Brown Atrophy: due to accumulations of lipofuscin
2. Hypertrophy: Increase in size Common in: heart kidney striated muscle and
smooth muscle Subcellular Hypertrophy due to P450
3. Hyperplasia: Increase number of cells Traction on bone or skin
Physiologic=Hormonal or Compensatory
Pathologic: XS hormones of GFs viral infections chronic renal failure
4. Metaplasia: Change of one mature cell to another (reversible) Retinoic Acid
plays a role in transcriptionMechanism: reprogramming stem cells
5. Squamous metaplasia: the transformation of a less resistant mucinous or
glandular epithelium to a more resistant stratified squamous type. For example,
squamous metaplasia of bronchus due to cigarette smoke. Also squamous
metaplasia of urinary bladder, pancreatic duct, gallbladder. Caused by chronic
mechanical irritation, parasites, inflammation, chemicals, malnutrition. May give
rise to squamous cell carcinoma in tissue where squamous epithelium does not
normally exist. Reversible on tissue level.
6. Autophagy: Self/ auto digestion
7. Aplasia: Failure of development of primordium
8. Hypoplasia: Incomplete development
9. Atresia: Absence of an opening
10. Dysplasia: Abnormal cell growth
11. Hypoxia: Decrease in O2; can cause cell injury
12. Ischemia: Decrease in blood flow and therefore O2 and nutrients; can cause
cell injury
13. Hyperemia: Increase blood flow
14. Reversible Cell Injury: Decrease phosphorylation decrease ATP (exaggerated
by increase cytoslic Ca++) Changes in [ion] increase in H20 ("cloudy swelling")
Cellular and fatty changes
15. Irreversible Cell Injury: Defect in membrane permeability increase intracellular
[Ca++] activate phospholipases mt membrane damage more Ca++ Longer
duration of injury
Cell Death
, .
Ultrastructural Changes
Light microscopic changes
Gross morphologic changes (take the longest to become irreversible)
16. Oncosis: Cell Death due to irreversible injury
17 Apoptosis: Oncosis w/ no inflammation (pathologic or physiologic)
Intact cell membrane
No leakage
Activation of proteases/ endonucleases
Intrinsic: withdrawal of growth factors/ hormones
Extrinsic: Receptor-ligand interaction (FAS and TNF receptor)
Anti-apoptotic= Bcl-2
18. Necrosis: Oncosis with inflammation (pathologic) Disrupted cell membrane
Leakage
Determinants: Protein denaturation and Enzymatic digestion
19. Coagulative Necrosis: Denaturation of cellular proteins
Cellular outlines preserved
Pale/White vs. Hemorrhagic/ Red (dual blood supply)
e.g. Myocardial Infarction
20. Liquefactive Necrosis: Digestion of cells and tissue predominates Loss of
structure due to PMN enzymes e.g. Abscess (Pus, bacterial infection)
21. Caseous Necrosis: Due to Mycobacteria or fungal infection Granular, cheesy
material surrounded by macrophages, giant cells, and fibrosis
Granuloma
e.g. Tuberculosis
22. Fibrinoid Necrosis: In Arteriolar walls due to leakage of fibrin and other
plasma proteins following damage
Fibrinoid= fibrin + other compounds
e.g. Hypertension/ immunocomplex disease
23. Fat Necrosis: Of Pancreatic cells containing lipase and amylase
Saponification:
FAs+ Ca++
Calcium deposits (basophilic)
e.g. Acute Pancreatitis
24. Steatosis: "fatty" e.g. Steatosis of liver due to diabetes; starvation; ethanol;
hypoxia - triglyceride accumulation
, .
25. Karyolysis: Nuclear Death: nucleus broken down into little pieces and fades
away
26. Pyknosis: Nuclear Death: hard and dark nucleus heavily stained (basophillia)
27. Karyorrhexis: Random break up of nucleus (seen in apoptosis)
28. Pyroptosis: Cell death from S. enterica replication in macrophages
29. Paraptosis: Cell death triggered by Caspase 9
30 Polyploidy: Large cells with large nuclei Accompanies hypertrophy but also
seen in normal cells
Increase in number with increase in age
31. p450: Detoxifier in liver Subcellular hypertrophy
32. Reperfusion: Resumption of blood supply and oxygenation to ischemic tissue
may cause further tissue injury/ destruction
33. Councilman Bodies: Describe anything that looks viral in infection
34. Mallory Bodies: In alcoholics, due to hyaline degeneration
35. Foam Cells: Macrophages that have taken up cholesterol disrupt membrane
36. Iron Molecules: Transferrin: transports Ferritin: stores Ferritin: stores
Hemosiderin: brown pigment, dead end product from local or systemic excess of
ferritin
37. Anthracosis: Dark pigments distribute along lymphatics
38. Dystrophic Calcification: Deposition of calcium in damaged tissue
39. Metastatic Calcification: Deposition of calcium in tissue due to hi serum
calcium (hypercalcemia)
40. Senescence: Decline in cell function due to lifespan of cell Telomere
shortening,
environmental insults, DNA repair, and abnormal growth affect cell aging
Clk-1: gene controls rate and timing of aging
41. Hyaline: Adjective: Describes homogeneous glassy pink appearance
42. Hyalin: Noun: Refers to substance with hyaline appearance
43. Acute Inflammation: Rubor (redness); Calor (heat); Tumor (swelling); Dolor
Rapid delivery to site of injury; More neutrophils, less mononuclear cells
Increase vascular permeability and vasodilation due to retraction of endothelial
cells, endothelial injury, leukocyte-mediated vascular injury, increased transcytosis
Lewis Triple Response: Red Line and Flare (vasodilation), Wheal (vascular
leakage) Arterioles involved first
1. Atrophy:
Decrease in size, cell # Physiologic or pathologic Often reversibleMechanism:
decrease metabolic activity decrease protein synthesisIf caused by decrease
blood flow apoptosis Brown Atrophy: due to accumulations of lipofuscin
2. Hypertrophy: Increase in size Common in: heart kidney striated muscle and
smooth muscle Subcellular Hypertrophy due to P450
3. Hyperplasia: Increase number of cells Traction on bone or skin
Physiologic=Hormonal or Compensatory
Pathologic: XS hormones of GFs viral infections chronic renal failure
4. Metaplasia: Change of one mature cell to another (reversible) Retinoic Acid
plays a role in transcriptionMechanism: reprogramming stem cells
5. Squamous metaplasia: the transformation of a less resistant mucinous or
glandular epithelium to a more resistant stratified squamous type. For example,
squamous metaplasia of bronchus due to cigarette smoke. Also squamous
metaplasia of urinary bladder, pancreatic duct, gallbladder. Caused by chronic
mechanical irritation, parasites, inflammation, chemicals, malnutrition. May give
rise to squamous cell carcinoma in tissue where squamous epithelium does not
normally exist. Reversible on tissue level.
6. Autophagy: Self/ auto digestion
7. Aplasia: Failure of development of primordium
8. Hypoplasia: Incomplete development
9. Atresia: Absence of an opening
10. Dysplasia: Abnormal cell growth
11. Hypoxia: Decrease in O2; can cause cell injury
12. Ischemia: Decrease in blood flow and therefore O2 and nutrients; can cause
cell injury
13. Hyperemia: Increase blood flow
14. Reversible Cell Injury: Decrease phosphorylation decrease ATP (exaggerated
by increase cytoslic Ca++) Changes in [ion] increase in H20 ("cloudy swelling")
Cellular and fatty changes
15. Irreversible Cell Injury: Defect in membrane permeability increase intracellular
[Ca++] activate phospholipases mt membrane damage more Ca++ Longer
duration of injury
Cell Death
, .
Ultrastructural Changes
Light microscopic changes
Gross morphologic changes (take the longest to become irreversible)
16. Oncosis: Cell Death due to irreversible injury
17 Apoptosis: Oncosis w/ no inflammation (pathologic or physiologic)
Intact cell membrane
No leakage
Activation of proteases/ endonucleases
Intrinsic: withdrawal of growth factors/ hormones
Extrinsic: Receptor-ligand interaction (FAS and TNF receptor)
Anti-apoptotic= Bcl-2
18. Necrosis: Oncosis with inflammation (pathologic) Disrupted cell membrane
Leakage
Determinants: Protein denaturation and Enzymatic digestion
19. Coagulative Necrosis: Denaturation of cellular proteins
Cellular outlines preserved
Pale/White vs. Hemorrhagic/ Red (dual blood supply)
e.g. Myocardial Infarction
20. Liquefactive Necrosis: Digestion of cells and tissue predominates Loss of
structure due to PMN enzymes e.g. Abscess (Pus, bacterial infection)
21. Caseous Necrosis: Due to Mycobacteria or fungal infection Granular, cheesy
material surrounded by macrophages, giant cells, and fibrosis
Granuloma
e.g. Tuberculosis
22. Fibrinoid Necrosis: In Arteriolar walls due to leakage of fibrin and other
plasma proteins following damage
Fibrinoid= fibrin + other compounds
e.g. Hypertension/ immunocomplex disease
23. Fat Necrosis: Of Pancreatic cells containing lipase and amylase
Saponification:
FAs+ Ca++
Calcium deposits (basophilic)
e.g. Acute Pancreatitis
24. Steatosis: "fatty" e.g. Steatosis of liver due to diabetes; starvation; ethanol;
hypoxia - triglyceride accumulation
, .
25. Karyolysis: Nuclear Death: nucleus broken down into little pieces and fades
away
26. Pyknosis: Nuclear Death: hard and dark nucleus heavily stained (basophillia)
27. Karyorrhexis: Random break up of nucleus (seen in apoptosis)
28. Pyroptosis: Cell death from S. enterica replication in macrophages
29. Paraptosis: Cell death triggered by Caspase 9
30 Polyploidy: Large cells with large nuclei Accompanies hypertrophy but also
seen in normal cells
Increase in number with increase in age
31. p450: Detoxifier in liver Subcellular hypertrophy
32. Reperfusion: Resumption of blood supply and oxygenation to ischemic tissue
may cause further tissue injury/ destruction
33. Councilman Bodies: Describe anything that looks viral in infection
34. Mallory Bodies: In alcoholics, due to hyaline degeneration
35. Foam Cells: Macrophages that have taken up cholesterol disrupt membrane
36. Iron Molecules: Transferrin: transports Ferritin: stores Ferritin: stores
Hemosiderin: brown pigment, dead end product from local or systemic excess of
ferritin
37. Anthracosis: Dark pigments distribute along lymphatics
38. Dystrophic Calcification: Deposition of calcium in damaged tissue
39. Metastatic Calcification: Deposition of calcium in tissue due to hi serum
calcium (hypercalcemia)
40. Senescence: Decline in cell function due to lifespan of cell Telomere
shortening,
environmental insults, DNA repair, and abnormal growth affect cell aging
Clk-1: gene controls rate and timing of aging
41. Hyaline: Adjective: Describes homogeneous glassy pink appearance
42. Hyalin: Noun: Refers to substance with hyaline appearance
43. Acute Inflammation: Rubor (redness); Calor (heat); Tumor (swelling); Dolor
Rapid delivery to site of injury; More neutrophils, less mononuclear cells
Increase vascular permeability and vasodilation due to retraction of endothelial
cells, endothelial injury, leukocyte-mediated vascular injury, increased transcytosis
Lewis Triple Response: Red Line and Flare (vasodilation), Wheal (vascular
leakage) Arterioles involved first
