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Biology of Disease I

General pathology and principles

Objective description: CLASS-C Color, location, appearance, size, shape, consistency
Process: -itis Inflammatory
Process: -osis, -opathy Degenerative
Process: -trophy, -plasia, -oma Disorders of growth
Degree types mild, moderate, marked, severe (subjective)
Duration types peracute, acute, subacute, chronic
Distribution types focal, multifocal, locally or regionally extensive, disseminated, diffuse
Mild degree mild exudative changes, little discerible tissue destruction (high likelihood of restitution)
Moderate degree prominent vascular and cellular exudative changes, moderate tissue destruction
Severe degree Substantial tissue destruction
Minimal degree change not clinically detectable
Peracute rapid onset, lasts hours, exudative, few cells
Acute onset in few hours, can last days, primarily neutrophils
subacute onset days to weeks, exudative changes diminished, cell infiltrate evolves from neutrophilic to mononuclear
chronic onset days to weeks following injury; can last years; mononuclear infiltration, tissue regeneration, neovasculatization and fibrosis
chronic-active recurrent bouts of active inflammation superimposed on chronic inflammation
etiologic diagnosis a diagnosis denoting cause: cause and tissue process
morphologic dx "3D ATP" tissue, process, adjective, degree, duration, distribution
Players in cell injury ATP depletion, calcium, membrane permeability, mitochondrial damage, oxygen and reactive oxygen species
Effects of ATP depletion membrane transport, protein synthesis, lipogenesis, phospholipid turnover
cytoplasmic calcium activates: phospholipases, proteases, ATPases, endonucleases
Effects of mitochondrial damage increased Ca, oxidative stress, phospholipid breakdown and breakdown products. Results in Mitochondrial Permeability Transition (MPT), cytochrome C leakage, loss of membrane potential
Effects of oxygen and ROS damage damage to membranes, proteins, nucleic acids
Reversible hypoxia steps 1. ATP depletion: anaerobic glyclysis 2. Na:K:ATPase pump shuts down 3. intracellular Na accumulation 4. intracellular water accumulation via osmotic mechanisms 5. swelling of organelles
Transition to irreversible injury 1. Degranulation of RER (loss of ribosomes) 2. Moderate to severe mitochondrial swelling
Irreversible ischemic injury steps 1. Severe mitochondrial swelling 2. massive Ca influx 3. increased membrane permeability 4. lysosomes leak 5. cellular enzymes leak into extra-cellular space
Irreversible injury: pyknosis condensation of molecular material (calcium sink in mitochondria leads to mineralization and dissolution)
Irreversible injury: karyorrhexis destructive fragmentation of nucleus
karyolysis dissolution of cell nucleus
Ischemia/reperfusion injury continued cell death following reperfusion. 1. cells are structurally intact but have lethal functional changes; 2. new injuring processes are initiated; perhaps elaboration of ROS
Reactive Oxygen Species (5) Superoxide anion (O2-); singlet oxygen (O); hydroxyl radical (OH); nitric oxide (NO); hydrogen peroxide (H2O2)
Fenton Reaction Pro-oxidative: transition metals (Fe or Cu) catalyze reactions generating reactive oxygen species (OH. and OH-) (hemostasis during surgery can increase Fe in tissue and cause oxidative injury)
Haber-Weiss Reaction Pro-oxidative: antioxidant defenses are overwhelmed, superoxide and hydrogen peroxide interact to form hydroxyl radical (OH.) and hydroxide (OH-)
Superoxide Dismutase Inactivates superoxide (forming H2O2 + O2), preventing ROS damage. 1. Mg SO in mitochondria; 2. Cu Zn SOD in cytosol
Specific antioxidant: Catalase Inactivates H2O2 --> O2 + 2H2O
Specific antioxidant: Glutathione Peroxidase Inactivates H2O2 and hydroxyl radical (GSSG (disulfide bond) + 2H2O) - can measure glutathione to assess oxidative stress
***Non-specific cellular antioxidant defenses Vitamin A, E (membrane antioxidant - prevents lipid peroxidation), C (water soluble); Caeruloplasmin (binds Cu2+); transferrin, lactoferrin, ferritin, hemosiderin (iron bound by protein prevents Fenton Rxn)
4 morphologic patterns of necrosis 1. coagulative 2. liquefactive 3. caseous 4. "special cases" - fat necrosis, gangrene
Coagulative necrosis: gross "cooked"
Coagulative necrosis: histo hypereosinophilic "ghost cells" (tissue architecture intact)
Coagulative necrosis: cause usually ischemia (or occur in tissues with few proteases)
Liquefactive necrosis: gross "liquid"
Liquefactive necrosis: histo usually neutrophils (granulation tissue)
Liquefactive necrosis: cause usually bacterial, or tissues with little stoma (e.g. CNS)
Caseous necrosis: gross "cheese" (can be mineralized - "gritty")
Caseous necrosis: histo sheets of macrophages (granulomatous) surrounding an amorphous center of debris
Caseous necrosis: cause specific immuno-pathologic phenomenon; mycobacterial cell walls
Fat necrosis: gross chalky or mineralized
Fat necrosis: histo lightly basophilic, smudgy saponified material, sometimes with granulomatous inflammation
Fat necrosis: cause ischemia, toxins, lipases
Gangrene: cause ischemia
Gangrene: typical location distal extremity or GI tract
"dry" gangrene: pattern of necrosis coagulative
"wet" gangrene: pattern of necrosis liquefactive, with tissue digestion by opportunistic bacteria (often w/ gas production)
Autolysis: process "rotting"- enzymatic degradation and protein denaturation by host enzymes (typically w/ microbial enzyme involvement)
4 tissue types which undergo rapid autolytic change adrenal, CNS, liver, gut
Rigor mortis: influencing factors temperature, glycogen stores, pH of muscle
"hyaline" definition microscopic appearance = eosinophilic, homogeneous, glassy material (intracellular or extracellular)
Extracellular protein deposits: three examples edema fluid, fibrin, amyloid
amyloid: definition any protein with fibrils measuring 7.5-10.0nm with a beta-pleated sheet configuration will take on the histologic appearance referred to as "amyloid" (aka "beta-fibrilloses")
amyloid: morphology amorphous, hyaline, extracellular (red-orange or apple green depending on stain)
AL amyloid formed from Ig light chains
AA amyloid formed from serum amyloid A (SAA), an acute phase reactavt stains blue-black w/ iodine followed by sulfuric acid (typically follows chronic inflammation)
AF amyloid usually prealbumin; named for its presence in human familial amyloidoses
Endocrine amyloid formed from a variety of hormone and hormone-like receptors
Lipofuscin (pigment) lipid breakdown product; "wear and tear" pigment w/in lysosomes. granular golden-brown
carbon (pigment) "antracosis" - lung, urban environments, incidental
biological pigments certain fungi, protozoa, etc. are pigmented (e.g. blue-green algae)
acid-hematin (pigment) artifact of tissue processing (blackish - can resemble hemosiderin)
***Melanosis incidental pigmentation of tissues in pigmented animals; pleura and meninges most commonly infected
***Reactive melanosis/hyperpigmentation chronically inflamed skin
***Pseudomelanosis postmortem artifact: production of hydrogen sulfide by bacteria with subsequent reaction with iron in hemoglobin to form insoluble iron sulfide (particularly seen in peritoneal and retroperitoneal cavity due to high levels of bacteria in gut)
hemosiderin (pigment) lighter brown granular pigment; represents large accumulations of iron and apoferritin (together called ferritin)
hematoidin (pigment) light yellow variant of hemosiderin that occurs during wound resolution as iron is removed from hemosiderin by macrophages
bilirubin (pigment) greenish yellow pigment, usually not granular; seen within hepatocytes, bile canaliculi, and renal tubular epithelium
dystrophic calcification mineralization of dead or dying cells; membrane vesicles form as cell membranes break down and these serve as a nidus for mineral deposition (often seen w/ granulomatous inflammation w/ casseation, e.g. TB)
metastatic calcification mineralization in living tissue; excess Ca and P in the blood precipitate (exceed max saturation); commonly seen in gastric mucosa, blood vessels, basement membranes in the lungs and kidney (i.e. sites of acid exchange)
metastatic calcification: causes hypervitaminosis D, renal disease, primary hyperparathyroidism hyperadrenocorticism, paraneoplastic syndrome (PTH-like related protein released by tumors)
necrosis passive, degradative, from fatal cell injury
apoptosis, pyroptosis, pyronecrosis, autophagy, and oncosis programmed cell death
cell death producing inflammation necrosis, oncosis, pyroptosis, pyronecrosis
cell death without inflammation apoptosis, autophagy
In which tissues does apoptosis normally occur? tissues undergoing physiologic or post-pathologic atrophy; embryonic tissues
What cells are typically subject to apoptosis? hematopoietic cell lines (termination of inflammation, self-reactive T cells), cells killed by T cells (AI, viral infection, cells with DNA damage, cells injured by hypoxia, irradiation, hyperthermia, toxins, and drugs
necrosis vs. apoptosis: which has mitochondrial and ER changes? necrosis
necrosis vs. apoptosis: which has membrane alterations? necrosis (apoptosis has blebbing only)
necrosis vs. apoptosis: which is active? apoptosis
necrosis vs. apoptosis: which has DNA damage? apoptosis
necrosis vs. apoptosis: which has membrane injury? necrosis
necrosis vs. apoptosis: which undergoes karyolysis? necrosis
necrosis vs. apoptosis: which appears as cytoplasmic eosinophilia? BOTH
3 types of initiation phase of apoptosis 1. extrinsic pathway 2. intrinsic pathway (mitochondria) 3. perforin/granzyme pathway (activate T cells)
Final result of all three types of initiation phase of apoptosis Execution pathway: caspase 3 activation leading to cellular degradation and formation of apoptotic bodies
apoptosis intrinsic pathway: intracellular signals - negative factors absence of growth factors, hormones, or cytokines; loss of apoptotic suppression
apoptosis intrinsic pathway: intracellular signals - positive factors radiation, toxins, hypoxia, hyperthermia, viral infections, free radicals
apoptotic changes in mitochondrial membrane Mitochondrial Permeability Transmission (MPT) - release of pro-apoptotic proteins from intermembrane space (including CYTOCHROME C) into cytosol - initiation of caspase cascade
apoptosis - perforin/granzyme pathway 1. CD8 T cell recognizes foreign antigen on cell surface 2. secretion of perforin forming pore in target cell surface 3. secretion of Granzyme B which activates caspases
apoptosis: DNA damage-mediated 1. damage to DNA results in elaboration of p53 (proofreading enzyme) 2. p53 stops cell cycles to allow DNA repair 4. if DNA damage is too great, p53 initiates apoptosis
p53 DNA proofreading enzyme. Can initiate apoptosis in event of irreparable DNA damage (prevention of neoplastic cell proliferation)
Executioner caspases point where initiation pathways (w/ initiator caspases 8, 9, 10) converge; activation of ENDONUCLEASES AND PROTEASES
phosphatidylserine externalized to apoptotic cell surface - signal non-inflammatory phagocytic recognition and phagocytosis
pyroptosis caspase-1 dependent cell death (active cell deletion); results in swelling and lysis of cell - cytokine release causes inflammation (desired for scarring and tissue repair)
autophagy Double membraned lysosomal digestion of cell components (autophagosome) - characterized by vacuolization, degradation of cell components, lack of chromatin condensation; results in non-inflammatory phagocytosis
two disorders associated with decreased apoptosis 1. neoplasia 2. autoimmune disease - insufficient apoptosis of auto-reactive cells
three disorders associated with increased apoptosis 1. neurodegenerative disorders 2. exacerbation of damage in ischemic injury (e.g. ischemia-reperfusion) 3. virus-induced lymphocyte depletion in acquired immune deficiency syndromes
Created by: Chovenga



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