Pathology
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| 8 major pathologic processes of disease [INVEGE] | Inflammation; Neoplasia; Vascular; Environmental/Nutritional; Genetic/developmental; Endocrine/metabolic
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| 3 main mechanisms of cell injury | Deficiency; intoxication; trauma
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| 6 ways cells respond to non-lethal injury | Atrophy; Hypertrophy; Hyperplasia; Metaplasia; Dysplasia; Intracellular Storage
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| Lack of vitamin B12 (in vegans), or pernicious anemia, are examples of: | Deficiency
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| Intoxication (leading to cell injury) may be (2): | Endogenous (genetic defect or accumulation of metabolite due to poor circulation) or Exogenous (infxs agents, chemicals, drugs)
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| Trauma may be (4): | Hypothermia (causing ice crystal formation); Hyperthermia (=> denaturation or oxidation of proteins); Mechanical pressure; Infxs (=> cell rupture or lysis)
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| Decrease in size & fn of cells, assoc w/decrease in size/function of a tissue or organ = | Atrophy
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| Increase in size of cells, 2/2 increase in amount of protein a& organelles, which => increase in size of tissue or organ = | Hypertrophy
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| Causes of hypertrophy | Mechanical stimulus (e.g., cardiac and skeletal muscle hypertrophy); Growth factor stimulation (e.g., endocrine stimulation at puberty, pregnancy); Increased functional demand (e.g., unilateral nephrectomy)
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| Increase in the number of cells in an organ or tissue, often resulting in an increase in size of the tissue or organ = | Hyperplasia
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| Causes of hyperplasia (3) | Growth factor stimulation (endocrine or stress-induced); callus formation during bone healing; erythroid hyperplasia under chronic hypoxic conditions
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| Warts (viral-induced) are an example of which cellular response to injury? | Hyperplasia
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| Replacement of one differentiated cell type with another = | Metaplasia
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| Main cause of metaplasia | Irritation
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| Common sites of metaplasia (3) | Respiratory tract of smokers; Cervix of sexually active females; Esophagus in response to gastric acid
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| Abnormal or disorderly growth, recognized by a change in size, shape, and/or organization of cells within a tissue; can be a precursor to cancer = | Dysplasia
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| Examples of Intracellular Storage (3) | Lipid accumulation (fatty change) in hepatocytes; Anthracotic pigment in alveolar macrophages; Lipofuscin
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| Morphologic expression of cell death; progressive disintegration of cellular structure; generally initiated by overwhelming stress; generally elicits acute inflammatory cell response = | Necrosis
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| An alternate pathway of cell death, called "programmed cell death" or "physiologic cell death" = | Apoptosis
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| Characteristics of apoptosis (4) | Controlled by specific genes; fragmentation of DNA, fragmentation of nucleus; Blebs form and "apoptotic bodies" are released; "Apoptotic bodies" phagocytized, no neutrophils
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| Consequences of Necrosis (2) | Loss of functional tissue; Impaired organ function, transient or permanent
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| Consequences of Apoptosis | Removal of damaged or unnecessary cells
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| PHYSIOLOGIC States Where Apoptosis May Be Important (3) | Embryogenesis; development; Withdrawal of trophic hormones, growth factors
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| Examples of trophic hormone/growth factor withdrawal | Prostate glandular epithelium after castration; Regression of lactating breast after weaning; Withdrawal of interleukin-2 results in apoptosis of stimulated T lymphocytes)
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| Pathologic states where apoptosis may be important | Ionizing radiation; Conditions assoc. with free radical generation; MILD thermal injury; Steroids (GCs induce lymphocyte apoptosis); viral infection; cell-mediated immunity; autoimmune diseases; degenerative diseases of the CNS; neoplasia
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| Viruses that encode proteins that can block apoptosis | Adenoviruses; human papilloma virus (HPV)
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| How is apoptosis important in HIV? | Loss of CD4+ T lymphocytes may be mediated in part by apoptosis
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| _______ can kill target cells by inducing apoptosis | Cytotoxic T lymphocytes
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| Study of disease, focusing on physiologic, gross, and microscopic morphologic changes in cells reacting to injury | Pathology
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| Definition of etiology | The cause of diseases
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| Definition of Iatrogenic | Provider induced
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| Definition of Idiopathic | Unknown etiology
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| Description of the mechanisms by which diseases develop | Pathogenesis
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| Objective evidence (a perceptible change) that signals disease | Sign
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| A patient’s subjective experience or interpretation of the disease | Symptom
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| A sign, symptom or characteristic of a disease that leads to its accurate diagnosis | Pathognomonic
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| Reasonable predictions about the course of a disease or process taking into account the natural history, the expected effects of therapy and particular factors specific for the individual case | Prognosis
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| The functional elements of an organ, e.g., myocardial cell (myocyte) of the heart; neuron of the brain | Parenchyma
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| The framework or support elements of an organ, e.g., the connective tissue (interstitium) of the heart surrounding the myocyte | Stroma
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| Any pathological abnormality of tissue structure or function | Lesion
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| Necrosis or Apoptosis? Usually affects large areas (contiguous cells) | Necrosis
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| Necrosis or Apoptosis? Control of intracellular environment lost early | Necrosis
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| Necrosis or Apoptosis? Cells swell and organelles swell | Necrosis
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| Necrosis or Apoptosis? Nuclear chromatin marginates early, while injury is still reversible | Necrosis
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| Necrosis or Apoptosis? When DNA is cleaved (usually a late event) fragments are random in size | Necrosis
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| Necrosis or Apoptosis? Cell membrane ruptures as terminal event and cell contents are released, which are chemotactic | Necrosis
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| Necrosis or Apoptosis? Chemotactic factors lead to neutrophil infiltration to degrade dead cells | Necrosis
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| A smear pattern is seen in gels in Necrosis or Apoptosis? | Necrosis
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| Necrosis or Apoptosis? Usually affects scattered individual cells | Apoptosis
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| Necrosis or Apoptosis? Control of intracellular environment maintained in early stages | Apoptosis
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| Necrosis or Apoptosis? Cells contract (“implode”) | Apoptosis
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| Necrosis or Apoptosis? Nuclear chromatin marginates and chromatin condenses, becoming very compact | Apoptosis
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| Necrosis or Apoptosis? Chromatin condensation and DNA fragmentation occur together; DNA cleaved into multiples of 200 base pair units | Apoptosis
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| Necrosis or Apoptosis? Blebs form and apoptotic bodies containing nuclear fragments are shed | Apoptosis
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| Necrosis or Apoptosis? Phagocytosis of intact apoptotic bodies, no chemotactic factors are generated | Apoptosis
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| A ladder pattern is seen in gels in Necrosis or Apoptosis? | Apoptosis
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| Morphologic Patterns of Lethal Cell Injury (5 types of necrosis) | Coagulative Necrosis; Liquefactive Necrosis; Fat Necrosis; Caseous Necrosis; Fibrinoid Necrosis
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| Similar to autolysis | Coagulative Necrosis
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| Pattern of cell death characterized by progressive loss of cell structure | Coagulative necrosis
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| In ______ necrosis, cytoplasm becomes more eosinophilic | Coagulative necrosis
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| Nucleus shrinks and chromatin condenses; nucleus becomes deeply basophilic (very dark blue with H&E stain) | Pyknosis
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| Nucleus breaks up into small pieces | Karyorrhexis
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| Nucleus becomes progressively paler staining and eventually disappears | Karyolysis
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| Pattern of cell death characterized by dissolution of necrotic cells | Liquefactive Necrosis
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| Pattern of cell death typically seen in an abscess, with pus formation | Liquefactive Necrosis
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| Pattern of cell death that results from release of lipases into adipose tissue | Fat Necrosis
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| Pattern of cell death in which fatty acids binds and precipitate calcium ions, forming insoluble salts; chalky white on gross examination | Fat Necrosis
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| Pattern of cell injury that occurs with granulomatous inflammation in response to certain microorganisms (e.g. tuberculosis) | Caseous necrosis
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| Pattern of cell injury that evokes a chronic inflammatory response | Caseous necrosis
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| Forms with a center of cellular debris that grossly has the appearance and consistency of cottage cheese | Caseating granuloma
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| Pattern of cell injury occurs in the wall of arteries in cases of vasculitis | Fibrinoid Necrosis
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| Pattern of cell injury in which plasma proteins, primarily fibrin, are deposited in the area of medial necrosis | Fibrinoid Necrosis
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| Definition of Infarction | Cell death and coagulative necrosis due to prolonged ischemia
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| These infarcts are typically wedge-shaped | Renal and splenic
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| Histologic Changes in Infarcts | Cytoplasmic hyper-eosinophilia; Karyolysis is complete at 2 days; Acute inflammatory cell infiltration begins at 12 hours after coronary occlusion and peaks at 2-3 days
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| Late Histologic Changes in Infarcts (Permanent Occlusion) | Karyorrhectic debris from neutrophils becomes prominent at 3-4 days; neutrophil infiltrate abates by day 5; around day 5, sprouting of new capillaries and phagocytosis of dead myocytes begin at periphery of infarct
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| Healing Phase of Infarction | Sprouting of new capillaries; Fibroblast proliferation; Collagen synthesis; Highly vascularized cellular connective tissue termed “granulation tissue”; Replacement of dead myocytes by mature scar tissue
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| Other Manifestations of Ischemic Injury | Enzyme release; Cardiac specific protein release; Arrhythmias; Permanent ECG changes; Heart failure; Tissue rupture, aneurysm, mural thrombi
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| Indicators of functional loss in cell injury | Decreased oxygenation, decreased mobility, increased bilirubin
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| Cell constitutents released in cell injury | K+ from RBC, troponin or CPK from heart
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| Change in electrical activity in cell injury | EKG, EEG, EMG
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