Cellular Responses To Stress Flashcards
Hypertrophy involves growth of which cellular structure
Cytoskeleton, plus extra organelles
Hypertrophy, hyperplasia, or both
- Uterus
- Cardiac Myocytes
- Skeletal Muscle
- Nerve
- Both
2,3,4 - hypertrophy only (permanent cells no stem cell)
Physiologic vs pathologic hyperplasia
Physio - pregnancy
Pathologic - cancer precursor (except BPH)
Stimulus for atrophy
Decrease in organ stress
Mechanisms of atrophy
- Apoptosis - decrease cell number
2. Decrease in cell size - degradation of cytoskeleton, autophagy
Mechanism of degradation of cytoskeleton (name)
Ubiquitin-proteosome degradation
Ubiquitin - marker
Proteosome - destroyes proteins
TRUE OR FALSE
Metaplasia is reversible?
TRUE - remove driving force to return cell growth type to normal. Reprogramming of stem cells
TRUE OR FALSE
All metaplasia progress to cancer if left untreated
FALSE - exception is Apocrine Metaplasia (breast)
Deficiency of which vitamin can cause metaplasia
Vitamin A - keratomalacia
Metaplasia of conjunctiva – thickening
Mesenchymal tissue undergoing metaplasia
Myositis ossificans - production of bone in skeletal muscle
TRUE OR FALSE Dysplasia is reversible
TRUE
Carcinoma is the one which is ireeversible
Aplasia vs Hypoplasia
Aplasia - failure of development
Hypoplasia - decrease cell production, small organ
Classic finding of exposure to this poison is cherry red skin with headache in early exposure
Carbon Monoxide
Condition when iron is oxidized to ferric ion Fe3+, which cannot.bind O2, leading to cyanosis with chocolate colored blood
Methemoglobinemia
Cellular findings in reversible injury
Cellular swelling - hallmark (failure of Na K pump)
Loss of microvilli, blebbing, RER swellimg
Cellular features of irreversible cellular injury
Membrane damage (hallmark)
Plasma membrane, leak of intracellular content
Mitochondrial membrane - inefficient O2 use
Lysosome membrane
What substance in the mitochondria when released triggers apoptosis?
Cytochrome C
Morphologic hallmark of cell death
Loss of nucleus
Nucleus shrinks
Pyknosis
Breaking up of nucleus into small pieces
Karyorrhexis
Breaking down of nuclear fragments to basic building blocks
Karyolysis
TRUE OR FALSE
Necrosis is always pathologic
True
Necrosis where tissue remains firm, and cell retains shape and organ structure is preserved, but nuclei disappear
Coagulative Necrosis
Ischemic infarction of organs except brain is what type of necrosis
Coagulative
TRUE OR FALSE
All infarcts are pale colored
FALSE
Red infarction can happen (when vein is blocked but not artery.) Ex. Testis
Necrosis with enzymatic lysis of cells
Liquefactive necrosis
Three major examples of liquefactive necrosis
Brain infarct
Absess
Pancreatitis (of panc tissue)
Logic behind liquefactive necrosis of brain
Microglial cells contain enzymes which destroy brain tissue when they die
Necrosis resembling mummified tissue
Gangrenous necrosis
What is wet gangrene
Gangrenous necrosis with superimposed infection, making it liquefactive
Necrosis which is combination of coagulative and liquefactive, characteristic of granulomatous infection
Caseous necrosis
Necrosis of adipose tissue with chalky white apperance from deposition of calcium. What is process of deposition
Fat necrosis
Saponification
Dystrophic calcification vs metastatic calcification
Dystrophic - normal serum Ca, reacts with dead tissue
Metastatic -high serum Ca and PO4 3-, deposits in tissue
Necrotic damage to blood vessel wall
Fibrinoid necrosis
Three conditions associated with fibrinoid necrosis
Malignant hypertension
Vasculitis
Preeclampsia
Morphological changes in apoptosis
Nucleus shrinks, apoptotic bodies fall off from cell, no inflammation
Enzymes that mediate apoptosis
Caspases
Activate protease(cytoskeleton) and endonuclease (DNA)
Three pathways of apoptosis
Intrinsic mitochondrial pathway - cell damage, dna damage, decreased hormones, cytochrome C leaks
Extrinsic receptor-ligand pathway - ligand binds to cell and activate apoptosis
Cytotoxic CD8 T cell pathway - through perforins and granzymes
Molecule which stabilizes mitochondrial membrane. This is knocked out during apoptosis
Bcl2
Most damaging free radical
OH.
Hydroxyl ion
Reaction name where ion generates free radicals
Fenton reaction
Mechanisms of free radical damage
Peroxidation of lipids
Oxidation of dna and proteins
Mechanisms of eliminating free radicals
Antioxidants
Metal carrier proteins - bind metals to prevent reactions
Free radical scavenging enzymes
Three enzymes in charge of destroying reactive oxygen species
Superoxide dismutase - superoxide
Catalase - peroxide
Glutathione peroxidase - hydroxyl
Mechanism of free radical injury of carbon tetrachloride
Breakdown to free radical CCl3. – attack liver cells and disrupts protein synthesis
Mechanism of reperfusion injury
Infarction –> cell membrane damage –> enzyme leakage,
Return of blood brings inflammatory cells and Oxygen in contact with dead tissue, and this creates free radicals and do more damage
Intracellular Ca overload, complement activation
Misfolded proteins that deposit in extracellular space
Amyloid
Stains which detect amyloid
Congo red
Apple green birefringence
Primary vs secondary amyloidosis
Primary - systemic deposition of AL amyloid from Ig light chain
Secondary - systemic deposition of AA amyloid from SAA (which is an acute phase reactant)
Plasma cell dyscrasia is associated with which amyloidosis
Primary
Most commonly involved organ in amyloidosis and classic presentation
Kidney - nephrotic syndrome