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42 Cards in this Set
- Front
- Back
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4 aspect of disease process within the scope of pathology.
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- etiology
- pathogenesis - pathologic anatomy: structural alterations both gross and microscopic. - pathophysiology: functional consequence. |
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3 general response to cellular injury.
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1. adaptation
- hypertrophy, atrophy - hyperplasia, hypoplasia - metaplasia 2. injury - reversible vs irreversible - causes: ischemia, hypoxia - mechanisms: ATP deprivation, membrane damage, Ca influx, oxygen reactive species. 3. death - necrosis vs. apoptosis |
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5 major types of cellular adaptations.
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1. hyperplasia:
- physiological: hormonal vs compensatory - pathological: excess hormonal stimulation -> dysfunction 2. hypoplasia - normal: hormonal removal response - path: chemo 3. hypertrophy - normal: uterine smooth muscle during pregnancy - path: left ventricle hypertrophy (up regulation of myosin, actin, ANP) 4. atrophy - disuse - denervation - decreased blood supply - mal nutrition - lost endocrine stimulation 5. metaplasia |
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Effect of upregulation of myosin, actin, ANP during cardio myocyte hypertrophy.
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- myosin, action: increase muscle actiivity
- ANP: increase renal Na excretion -> less blood volume -> less work load |
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Five pathological causes of atrophy.
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- disuse
- denervation - mal nutrition - decreased blood supply - reduced hormone stimulation |
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Mechanisms of atrophy.
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- protein degradation: lysosomal, ubiquitin-proteasome pathway.
- autophagic vacuoles: lipofuscin granules. |
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What type of cellular adaptation is this?
- myositis ossificans |
metaplasia
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What is the most significant potential adverse coutome of metaplasia?
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Dysplasia/carcinoma
- columnar -> squamous (brochi): smokers - squamous -> columnar (esophagus): acid reflux |
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What etiology/cellular adaptation?
columnar eqithelium changed to squamous epithelium in bronchi. |
smokers (metaplasia)
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What etiology/cellular adaptation?
squamous eqithelium changed to columnar epithelium in lower esophagus. |
acid reflux (metaplasia)
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Sequential morphologic changes in nuclei of cells undergoing necrosis.
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- pyknosis: nuclear condensation
- karyorrhexis: nuclear fragmentation - karyolysis: nuclear dissolution |
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Differences between hypoxia and ischemia.
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ischemia: reduced blood supply that consequently cause oxygen depreivation in tissue.
hypoxia: O2 deprivation in organ and tissue. hypoxemia: O2 deprivation in blood. |
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4 mechanisms of cellular injury.
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1. ATP deprivation:
- acidosis (glycolysis) - cellular swelling (Na/K pump, Na/Ca pump) - lipid deposition(ribosome detachment) 2. membrane damage: - apoptosis due to cytochrome c leakage in mitochondria - Ca influx: protein degradation - perforins due to CD8 T cell 3. Ca influx: - protein degradation 4. oxigen reactive species due to inadequate scavenge system (SOD, catalase, glutathione peroxidase, vitaminesE,A,C, ferrtin, ceruloplasmin): - lipid peroxidation - oxidative modification of proteins - react with thymine in DNA -> ssDNA breaks |
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Five adverse effects of ATP depletion to 10% of normal.
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- compromised plamsa membrane Na+ pump
- anaerobic glycolysis: acidosis - compromised Ca pump - ribosome damage - failure to maintain intact mitochondrial and lysosomal membrane |
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Process of mitochondrial membrane damage causing apoptosis.
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membrane damage -> high ocnductance channels -> membrane permeability transition -> cytochrome c leakage -> apoptosis
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Four enzymes activated by Ca2+ influx.
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- ATPase
- phospholipase - protease - endonuclease |
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How are reactive oxygen species activated?
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- by products of oxidative phosphorylation
- radiation - drug metabolism - transition metals |
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Three antioxidant enzymes and two storage proteins.
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- SOD (mitochondria, cytosol)
- catalase (peroxisome) - glutathione peroxidase (mitochondria, cytosol) - vitamie E,A,C - ferritin: minimize OH ion. - ceruloplasmin: minimize OH ion. |
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2 functional defects in irreversible cell injury.
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- inability to fix or reverse mitochondrial dysfunction
- severely disrupted membrane function |
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3 morphologic defects in irreversible cell injury.
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- disrupted cell membranes
- swollen mitochondria - nuclear pyknosis |
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2 morphologic changes of reversible injury in hepatocytes.
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- hydropic degeneration: cell taking in water
- macrovesicular steatosis: fatty change |
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Compare necrosis with autolysis.
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- Necrosis: progressive degradation of cells due to external factors (infection, toxins, or trauma).
- Autolysis: enzymatic degrations of cells caused by release of dead cell's own lysosomal enzymes. |
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What the most common type of necrosis?
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Coagulative necrosis:
- denaturation of structural and enzymic proteins - gradual nuclear degeneration - ghost cell outlines - typical in ischemia (except in the brain) |
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Microscopic features and clinical settings of liquection necrosis.
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Microscopic:
- complete acellular necrotic debris - surrounding zone of inflammatory cells Clinical setting: - severe inflammtion, toxin elaboration as in bacterial infections. - hypoxia in CNS |
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Microscopic features and clinical settings of caseous necrosis.
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Microscopic:
- central acellular necrosis - surrounding zone of histiocytes, lymphocytes Clinical setting: - TB (acid fast bacilli) - fungal infection |
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What type of necrosis?
- dry gangreenous necrosis - wet gangreenous necrosis |
- dry gangreenous necrosis: coagulative
- wet gangreenous necrosis: liquifective |
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Causes of non-caseating granulomas.
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- foreign material: pneumoconpisis
- hypersensitivity - sarcoidosis - leprosy - cat-scratch disease |
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Name an etiology of fat necrosis.
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Pancreatitis
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Morphology of fat necrosis.
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- chalky white areas: fatty acids combined with calcium
- necrotic cells without nuclei. |
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Why do ischemia tissues injure faster than isolated hypoxia?
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Ischemia deprives tissues of both oxygen(hypoxia) and nutrients.
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3 mechanisms of ischemia-reperfusion injury.
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1. reactive oxygen species -> mitochondrial permeability transition
2. inflammation exacerbated by restoration of blood flow 3. complement activation by IgM antibodies |
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How do indirectly injuring chemicals become toxic withi nhepatocytes?
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P450 in smooth ER
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2 mechanisms of chemical injury.
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- direct: eg mercuric chloride binds to sulfhydryl groups on cell membrane in the kidney ane small intestines.
- indirect: through P450 |
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Compare necrosis with apoptosis.
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Necrosis:
- cell enlarged - pyknosis->karyorrhexis->kartylysis - enyzmes leak into ECM - always pathologic Apoptosis: - cells shrink - nucleosomes - apoptotic bodies - often physiologic, may be pathologic |
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2 pathways of initiating apoptosis
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- intrinsic: withdrawl of growth factors/hormone -> BCL2 dysregulation.
- extrinsic: death receptor activated(FAS, TNFR1 perforins[granzyme])-> caspases |
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Name the family of intracellular proteins that regulates rate of apoptosis.
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Bcl-2: inhibits apoptosis
- prevent cytochrome c release - sequester Apaf-1 |
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Name the enzyme family which executes the "death program" of apoptosis.
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caspases
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Name 4 disease groups associated with dysregulated apoptosis.
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1. atrophy of target organ: loss of trophic hormone -> mitochondrial pathway
2. neoplasia: p53 mutation 3. autoimmune disease: mutated Fas or FasL -> self-reactive T cell not eliminated. 4. cytotoxic T cell mediated: perforins -> granzyme-> caspases |
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4 cytoplasmic structures that are altered in non-lethal injuries and give an example for each of them.
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1. lysosome: lysosomal storage disease, drug induced lysosomal disease (antimalarial chloroquine)
2. smooth ER: ethanol/barbituates -> SER hypertrophy, P450 induction -> tolerance of other drugs, oxygen reactive species 3. mitochondria: - ethanol, nutritional deficiency: megamitochondria 4. cytoskeletal: - infection -> immotile cilia -> sperm inmotility - cytochalasin B -> actin -> defective leukocytes - alcohol: keratin intermediate filament accumulation(mallory bodies, hyaline change) - alzheimers: microtubule, neutofillament -> neurofibrillary tangles |
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3 categories of substances that may accumulate intracellularly.
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1. excess normal cellular constituents:H2O, lipid, CHO
- steatosis: ethanol, protein malnutrition, obesity, DM. - cholesterol: atherosclerosis, xanthoma, cholesterosis - proteins: nephrotic syndrome, bonemarrow neoplasm(Igs) 2. Abnormal substance - endogenous: protein misfolding -> low serum alpha-1 antitrypsin -> emphysema - exogenous 3. pigment - endogenous: lipofuscin, melanin, iron, bilirubin(hemosiderin), homogentisic acid(alkaptouria). - exogenous: carbon(anthracosis), ink. |
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2 forms of pathologic calcifications.
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1. dystrophic: normal serum calcium level
2. metastatic: secondary to hypercalcemia. - excess of PTH: parathyroid neoplasm, renal failure - destruction of bone: Paget's disease - vitD disorder:vitamien toxicity, sarcoidosis |
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Explain molecular basis for senescence in normal somatic cells.
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lack of telemerase -> pregressive shortening of DNA
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