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Cell Injury & Death


8 major pathologic processes of disease [INVEGE] Inflammation; Neoplasia; Vascular; Environmental/Nutritional; Genetic/developmental; Endocrine/metabolic
3 main mechanisms of cell injury Deficiency; intoxication; trauma
6 ways cells respond to non-lethal injury Atrophy; Hypertrophy; Hyperplasia; Metaplasia; Dysplasia; Intracellular Storage
Lack of vitamin B12 (in vegans), or pernicious anemia, are examples of: Deficiency
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)
Trauma may be (4): Hypothermia (causing ice crystal formation); Hyperthermia (=> denaturation or oxidation of proteins); Mechanical pressure; Infxs (=> cell rupture or lysis)
Decrease in size & fn of cells, assoc w/decrease in size/function of a tissue or organ = Atrophy
Increase in size of cells, 2/2 increase in amount of protein a& organelles, which => increase in size of tissue or organ = Hypertrophy
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)
Increase in the number of cells in an organ or tissue, often resulting in an increase in size of the tissue or organ = Hyperplasia
Causes of hyperplasia (3) Growth factor stimulation (endocrine or stress-induced); callus formation during bone healing; erythroid hyperplasia under chronic hypoxic conditions
Warts (viral-induced) are an example of which cellular response to injury? Hyperplasia
Replacement of one differentiated cell type with another = Metaplasia
Main cause of metaplasia Irritation
Common sites of metaplasia (3) Respiratory tract of smokers; Cervix of sexually active females; Esophagus in response to gastric acid
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
Examples of Intracellular Storage (3) Lipid accumulation (fatty change) in hepatocytes; Anthracotic pigment in alveolar macrophages; Lipofuscin
Morphologic expression of cell death; progressive disintegration of cellular structure; generally initiated by overwhelming stress; generally elicits acute inflammatory cell response = Necrosis
An alternate pathway of cell death, called "programmed cell death" or "physiologic cell death" = Apoptosis
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
Consequences of Necrosis (2) Loss of functional tissue; Impaired organ function, transient or permanent
Consequences of Apoptosis Removal of damaged or unnecessary cells
PHYSIOLOGIC States Where Apoptosis May Be Important (3) Embryogenesis; development; Withdrawal of trophic hormones, growth factors
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)
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
Viruses that encode proteins that can block apoptosis Adenoviruses; human papilloma virus (HPV)
How is apoptosis important in HIV? Loss of CD4+ T lymphocytes may be mediated in part by apoptosis
_______ can kill target cells by inducing apoptosis Cytotoxic T lymphocytes
Study of disease, focusing on physiologic, gross, and microscopic morphologic changes in cells reacting to injury Pathology
Definition of etiology The cause of diseases
Definition of Iatrogenic Provider induced
Definition of Idiopathic Unknown etiology
Description of the mechanisms by which diseases develop Pathogenesis
Objective evidence (a perceptible change) that signals disease Sign
A patient’s subjective experience or interpretation of the disease Symptom
A sign, symptom or characteristic of a disease that leads to its accurate diagnosis Pathognomonic
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
The functional elements of an organ, e.g., myocardial cell (myocyte) of the heart; neuron of the brain Parenchyma
The framework or support elements of an organ, e.g., the connective tissue (interstitium) of the heart surrounding the myocyte Stroma
Any pathological abnormality of tissue structure or function Lesion
Necrosis or Apoptosis? Usually affects large areas (contiguous cells) Necrosis
Necrosis or Apoptosis? Control of intracellular environment lost early Necrosis
Necrosis or Apoptosis? Cells swell and organelles swell Necrosis
Necrosis or Apoptosis? Nuclear chromatin marginates early, while injury is still reversible Necrosis
Necrosis or Apoptosis? When DNA is cleaved (usually a late event) fragments are random in size Necrosis
Necrosis or Apoptosis? Cell membrane ruptures as terminal event and cell contents are released, which are chemotactic Necrosis
Necrosis or Apoptosis? Chemotactic factors lead to neutrophil infiltration to degrade dead cells Necrosis
A smear pattern is seen in gels in Necrosis or Apoptosis? Necrosis
Necrosis or Apoptosis? Usually affects scattered individual cells Apoptosis
Necrosis or Apoptosis? Control of intracellular environment maintained in early stages Apoptosis
Necrosis or Apoptosis? Cells contract (“implode”) Apoptosis
Necrosis or Apoptosis? Nuclear chromatin marginates and chromatin condenses, becoming very compact Apoptosis
Necrosis or Apoptosis? Chromatin condensation and DNA fragmentation occur together; DNA cleaved into multiples of 200 base pair units Apoptosis
Necrosis or Apoptosis? Blebs form and apoptotic bodies containing nuclear fragments are shed Apoptosis
Necrosis or Apoptosis? Phagocytosis of intact apoptotic bodies, no chemotactic factors are generated Apoptosis
A ladder pattern is seen in gels in Necrosis or Apoptosis? Apoptosis
Morphologic Patterns of Lethal Cell Injury (5 types of necrosis) Coagulative Necrosis; Liquefactive Necrosis; Fat Necrosis; Caseous Necrosis; Fibrinoid Necrosis
Similar to autolysis Coagulative Necrosis
Pattern of cell death characterized by progressive loss of cell structure Coagulative necrosis
In ______ necrosis, cytoplasm becomes more eosinophilic Coagulative necrosis
Nucleus shrinks and chromatin condenses; nucleus becomes deeply basophilic (very dark blue with H&E stain) Pyknosis
Nucleus breaks up into small pieces Karyorrhexis
Nucleus becomes progressively paler staining and eventually disappears Karyolysis
Pattern of cell death characterized by dissolution of necrotic cells Liquefactive Necrosis
Pattern of cell death typically seen in an abscess, with pus formation Liquefactive Necrosis
Pattern of cell death that results from release of lipases into adipose tissue Fat Necrosis
Pattern of cell death in which fatty acids binds and precipitate calcium ions, forming insoluble salts; chalky white on gross examination Fat Necrosis
Pattern of cell injury that occurs with granulomatous inflammation in response to certain microorganisms (e.g. tuberculosis) Caseous necrosis
Pattern of cell injury that evokes a chronic inflammatory response Caseous necrosis
Forms with a center of cellular debris that grossly has the appearance and consistency of cottage cheese Caseating granuloma
Pattern of cell injury occurs in the wall of arteries in cases of vasculitis Fibrinoid Necrosis
Pattern of cell injury in which plasma proteins, primarily fibrin, are deposited in the area of medial necrosis Fibrinoid Necrosis
Definition of Infarction Cell death and coagulative necrosis due to prolonged ischemia
These infarcts are typically wedge-shaped Renal and splenic
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
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
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
Other Manifestations of Ischemic Injury Enzyme release; Cardiac specific protein release; Arrhythmias; Permanent ECG changes; Heart failure; Tissue rupture, aneurysm, mural thrombi
Indicators of functional loss in cell injury Decreased oxygenation, decreased mobility, increased bilirubin
Cell constitutents released in cell injury K+ from RBC, troponin or CPK from heart
Change in electrical activity in cell injury EKG, EEG, EMG
Created by: Abarnard
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