Block 1 Adaptation & Necrosis Flashcards
Causes of atrophy
Physiologic: thymus, tonsils
Pathologic: decreased workload, denervation, ischemia, inadequate nutrition, decreased endocrine stimulation, aging, pressure
Causes of hypertrophy
Physiologic: hormones
Pathologic: increased workload, hormonal stimulation, growth factors, switch to adult gene/protein
Causes of hyperplasia
Physiologic: hormonal, compensatory
Pathologic: increased hormonal stimulation, growth factors, viral infections (HPV)
Causes of metaplasia
Cytokines, growth factors, ECM components, environmental
Hallmark of reversible cell injury
decreased oxidative phosphorylation –> decreased ATP –> cell swelling & fatty change (lipid vacuoles)
Gross: pallor, turgor, weight, greasy, larger
Hallmark of irreversible cell injury
Mito swelling, PM damage, lysosomal swelling
Features of necrosis
Group of cells, inflammation, cytoplasm and mito swelling, loss of PM integrity, Ca2+ overload
Coagulative necrosis
Infarcts, firm tissue, cell outlines preserved, general red appearance, inflammation, leuko lysosomes remove dead cells
Liquefactive necrosis
Bacterial & fungal infections, brain infarcts; microbial cell, inflammatory cells, cell debris
Caseous necrosis
TB; cheese-like, amorphous debris in granuloma with lympho border and macrophages
Fat necrosis
Acute pancreatitis, white areas from new FFAs with Ca2+, shadowy outline of cells with bluish cast (Ca), b/c damaged cells release lipases
Fibrinoid necrosis
Vasculitis, bright pink amorphous area around vessel, immune complexes in artery walls
Gangrene
Loss of blood supply (DM) –> black decomposing skin
Dry: coagulative necrosis
Wet: liquefactive due to superimposed bacterial infection
Apoptosis features
Singe cells, no inflam, shrinking cyto and mito, blebbing w/o loss of integrity, fragmented and hyperchromatic nuclei, ATP-dep
Physiologic vs. pathologic apoptosis
Phy: embryogenesis, menses, lymphocyte selection
Path: DNA or protein damage, GF deprivation, infection, atrophy
Intrinsic & extrinsic apoptosis pathway proteins
I: Bcl-2, Bax, Bak, Bcl-x, cyt C
E: Fas, TNF-R, caspases
Bcl-2
Anti-apoptotic important in cancer, inhibit Bax and Bak from opening pore in mito –> apoptosis
Bak, Bax
Pro-apoptotic, open pore in mito to release cyt C and pro-apoptotic proteins
Substances accumulated intracellularly
Fat, cholesterol, protein, glycogen, pigment, calcification
Foam cell
Oxidative LDL cholesterol ingested by MFs –> atherosclerotic plaque
Protein accumulation
AD neurofibrillary tangles of hyper-P Tau
Pigment accumulation
Carbon (pollution -> anthracosis), lipofuscin (ROS damage; heart, liver, brain), melanin, hemosiderin (excess iron)
Anthracosis
Benign deposition of coal dust in lungs from inhalation of sooty air
Calcifications
Ca salts, iron, Mg
Dystrophic: dying/dead cells secondary to injury/necrosis (heart valves) with normal serum Ca level
Metastatic: normal cells, hypercalcemia (PTH-sec tumor, Paget’s, vit D disorders, renal failure)
Icterus
Yellow appearance (bilirubin)
