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31 Cards in this Set
- Front
- Back
- 3rd side (hint)
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What's Etiology |
Causes of diseases might be genetic or environmental |
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What is pathogenesis |
This is the temporal sequence and patterns of cellular injury that leads to disease |
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What is Morphology |
These are changes of the disease process including gross and microscopic changes |
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What is Clinical Significance? |
These are the signs and symptoms, disease course including complications and prognosis |
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Hematoxylin stains ? |
1. Nuclei 2. Nucleoli 3. Bacteria 4. Calcuim |
Stains blue to purple |
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Eosin stains? |
1. Cytoplasm 2. Collagen 3. Fibrin 4. RBCs 5. Thyroid colloid |
Stains pink to red |
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Prussian blue stains? |
Iron |
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Congo Red stains? |
Amyloid |
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Acid fast (Ziehl-Neelsen, fite) Stains? |
Acid-fast bacilli |
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Periodic acid-sniff PAS stains |
High carbohydrate content molecules |
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Gram stain, stains? |
Bacteria |
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Trichrome stains? |
Connective tissue |
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Reticulin stains? |
Collagen type III molecules |
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Cytokeratin Stains? |
Epithelial cells |
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Vimentin stains? |
Mesenchymal orgin except 3 muscle types stains most sacromas |
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Destination stains? |
Smooth, Cardiac and skeletal myosin and prostrate specific antigen |
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Ancillary techniques and thier common uses? |
1. Immunofluorescence microscopy(IFM): renal and autoimmune disease 2. Transmission Electron Microscopy(EM): renal disease, neoplasms, infections&genetic disorders |
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Types of Molecular techniques? |
Protein electrophoresis, southern and western blots, polymerase chain reaction (PCR) and cytogenetic analysis(karyotyping, in situations hybridization) |
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What is the most common cause of hypoxia, what causes it and examples? |
Ishemia, due to loss of blood supply as a result of decreased arterial flow or no venous outflow of blood eg. Atherosclerosis, thrombus, thromboembolus |
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What are the causes of cellular injury? |
1. Hypoxia 2. Pathogens 3. Chemical injury 4. Immunological Dysfunction 5. Nutrition or vitamin imbalance 6. Physical forms of injury 7. Congenital disorders |
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What the cellular response to injury? |
1. Adaptation( hypertrophy, atrophy, hyperplasia, metaplasia ) 2. Reversible injury 3. Irreversible injury 4. Cell death( apotosis, necrosis, necroptosis ) |
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Features of reversible cell injury? |
1. Decreased synthesis of ATP 2. Decreased function of Na+K+ATPase membrane pump 3. Switch to anaerobic glycolysis 4. Decreased protein synthesis 5. Plasma membrane bless and myelin figures may be seen |
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Features of irreversible cell injury? |
1. Severe membrane damage 2. Marked mitochondria dysfunction 3. Rupture of the lysosomes 4. Nuclear changes( pyknosis= degeneration and condensation of nuclear chromatin, karyorrhexis= nuclear fragmentation and karyolysis= dissolution of nucleus |
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Clinical correlate of loss of membrane integrity after cell injury? |
When intracellular enzymes leak out as a result of cellular injury they can be measured in the blood as a marker of cell death or injury e.g 1. Myocardial injury: troponin( most specific ), CPK-MB, lactate dehydogenase(LDH) 2. Hepatitis: transaminase 3. Pancreatitis: amylase&Lipase 4. Biliary tract obstruction: alkaline phosphatase |
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Morphologic types of necrosis and brief description of each? |
1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. 1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. 1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. 1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. 1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. 1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. 1. Coagulative Necrosis: most common often due to ischemic injury(infarct), caused by denaturing of protein within cytoplasm, microscopic examination shows loss of nucleus but preservation of cellular shape, it's common in most organs including heart, liver&kidney but not brain.2. Liquefaction Necrosis: as a result of cellular destruction by hydrolytic enzymes, leading to autolysis(release of proteolytic enzymes from injured cells) and heterolysis(release of proteolytic enzymes from inflammatory cells) occurs in abscesses, brain infarcts, pancreatic necrosis.3. Caseous Necrosis: combination of coagulation and liquefaction necrosis, gross appearance is soft, friable, and "cheese-like". Characteristics of granulomatous disease, eg tuberculosis 4. Fat Necrosis: caused by action of lipase on adipocytes characteristic of acute pancreatitis, chalky white appearance.5. Fibrinoid necrosis: necrosis of connective tissue histologically resembles fibrin, eosiniphilic(pink) homogeneous appearance, often due to acute immunologic injury(e.g hypersensitivity type rxn II&rxn III) and hypertensive damage.6 Gangrenous Necrosis: dry gangrene has coagulative necrosis, while wet gangrene has liquefactive necrosis. |
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Difference between necrosis and apotosis? |
Necrosis: death of living tissue with an inflammatory response Apotosis: death of living tissue with no inflammatory response |
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What is Hemosiderosis? |
Increase in total body iron without tissue injury. |
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What is Hemochromatosis? |
Increase in total body iron with tissue injury. |
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What is Hyaline change? |
Nonspecific term used to describe any intracellular or extracellular alteration that's has a pink homogeneous appearance (protien) on H&E stains Examples: 1. Intracellular=renal proximal tubule protein reabsorption droplets, Russell bodies and alcoholic hyaline 2. Extracellular=hyaline arteriosclerosis, amyloid, hyaline membrane disease of the newborn |
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Examples of Dystrophic calcification? |
Fat Necrosis (saponification), psammoma bodies(laminated calcification occurs in meningiomas and papillary carcinomas of thyroid&ovary), Monckberg medial calcific sclerosis in arterial walls and atherosclerotic plaque |
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Examples of metastatic calcification? |
Hyperparathyroidism, parathyroid adenomas, renal failure, paraneoplastic syndrome, vitamin D intoxication, milk-alkali syndrome, sarcoidosis, Paget disease, multiple myeloma, matastatic cancer of the bone, they are located in the interstitial tissues of the stomach, kidney, lungs and blood vessels |
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