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147 Cards in this Set
- Front
- Back
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Proteins can move laterally, but generally do not _________ in the phospholipid bilayer - if they do it's an indication something has gone wrong
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flip over
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In cell injury when you deplete the oxidative pathway you start using the _________ pathway. Oxidative stress is when you have more _______ than _______. Intracellular calcium causes _______ activation. MPTP is the ________, if it stays open it is bad for the cell, ______ can leak out and active apoptosis
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- glycolytic
- free radicals than scavengers - enzyme - mitochondrial permeability transition pore - cyt c |
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What is the difference between ischemia & hypoxia? A blood clot is an example of which of these? What is a reperfusion injury?
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- ischemia: cut off of blood supply (nutrients in addition to oxygen, etc.)
- hypoxia is decreased oxygen - blood clot is ischemia - reperfusion injury is when blood flows back & more cells die after ischemia |
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In a reversible cell injury there is a temporary loss of volume & energy regulation. There are change in membrane permeability, influx of _____, ____ & ____, efflux of _____ & _______. Changes in dry weight to _____ weight ratio. Leakage of ______ molecules from the cell.
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- sodium, water, calcium
- potassium, magnesium - wet - small |
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What happens to the anaerobic pathway when you start depleting the aerobic pathway? What happens to the glycogen stores? The pH? To protein synthesis (specifically what happens to the ribosomes)?
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- start using the anaerobic pathway
- glycogen stores deplete - pH decreases due to increase in lactic acid - protein synthesis decreases - detachment of ribosomes & polyribosomes |
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In reversible cell injury: what do you see on the LM (hydropic/nuclear)? The EM (ER/glycogen/mito/membrane)?
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- LM: hydropic changes - slight clumping of chromatin
- EM: dilation of ER, glycogen stores decrease, mitochondria condenses, blebbing of membrane/blunting of microvilli |
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What happens to the H&E staining in reversible cell injury? What do the nuclei look like?
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- stain much lighter b/c of hydropic changes due to dilution defect
- nuclei are still ok - this is IMPORTANT |
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What condition does cold mimic? Why? Is it reversible?
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- ischemia b/c ATP decreases, Na+ & H20 flow in
- reversible if don't leave it for too long |
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In irreversible cell injury there is a permanent loss of selective permeability. There is leakage of ______ molecules out of the cell. You ______ oxidative phosphorylation. Glycolysis ______ & pH ______. Mitochondrial _______ experiences permeability changes. The calcium leaking out of the mito activates enzymes that damage the membrane through ______, cytoskeleton through ______ & DNA through _______.
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- large
- uncouple - increases - decreases -MPTP - lipases - proteases - nucleases |
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Cardiac markers in serum are an indication of _______ cell injury
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irreversible
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In irreversible cell injury: the LM cytoplasm stains more _______ (loss of differential staining), and the nuclei can either exhibit ______, ______ or ________. The EM shows ________ problems (matrix granules, flocculent densities, swelling/rupturing).
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- eosinophilic
- pyknosis, karyolysis, karyorrhexis - mitochondrial |
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In irreversible cell injury: ________ is complete dissaperance of the nuclei, _______ is shrinking of the nuclei, ______ is fragmentation of nuclei
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- karyolysis
- pyknosis - karyorrhexis |
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Increased cytosolic Ca & ROS, lipid peroxidation lead to mitochondrial injury which decreases _____ production. This can affect the _________ which allows leakage of molecules such as ______ which trigger apoptosis.
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- ATP
- mitochondrial transition pore - cyt c |
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What is the main morphological change you see in a dead cell?
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NUCLEAR CHANGES
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Why is the liver less susceptible to injury (ischemia)? Why are brain/retina not?
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- liver has lots of glycogen & dual blood supply
- brain & retina are too metabolic they cannot deal with ischemia |
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What do phospholipases, mercurial compounds, immune-mediated injury/MAC & killer T-cell perforin all have in common in terms of the plasma membrane?
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- all result in colloid osmotic lysis (aka punch hole in membrane)
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What does clostridium perfringens do to the cell?
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- releases lipases that can destroy membranes & destroy cells in the process
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What does mercurial compounds do to the cell?
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- hurt the membrane - will rupture cell fast due to changes in volume regulation
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what do MAC & Perforin both do to cell?
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- similar mechanism - punch hole in membrane & mess up osmotic gradient
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What does cyanide do (aka which vunerable inracellular system does it mess up)?
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- messed up oxidative phosphorylation
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Which intracellular vulnerable intracellular system does ricin effect?
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- protein synthesis - ribosomes are detached
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Which intracellular vulnerable intracellular system do free radicals effect?
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- effect DNA
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name an example of a compound that affects each of the following vulnerable intracellular systems:
1) membranes 2) aeorbic respiration 3) protein synthesis 4) genetic apparatus integrity |
1) membranes: clostridium perfringes/mercuy/MAC/perforin
2) aeorbic respiration: cyanide 3) protein synthesis: ricin 4) genetic apparatus integrity: free radicals |
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Given the choice, mitochondria would rather take up calcium or do oxidative phosphorylation?
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- take up calcium
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calcium can trigger increased _________ which leads to loss of membrane potential & a decrease in ____ production, which eventually leads to _______.
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- mitochondrial permeability transition
- ATP - necrosis |
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There is no clear point of no return but a good biochemical indication of ___ depletion, while an unequivocal morphological indication is ______ changes.
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- ATP
- nuclear |
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As the amount of ATP depletes, the population of ______ cells increases
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necrotic
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Free radicals cause lipid ______ of membranes by attacking _____ bonds. The reaction propagates in an _______ reaction. Free radicals may be captured by _______.
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- peroxidation
- double - autolytic - scavengers |
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How do free radicals affect proteins? DNA? calcium?
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- proteins: cross link & break & hurt proteasome complex
- DNA: break strands - calcium: oxidative stress & influx of calcium |
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What does oxidative stress mean?
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- there are more free radicals then mechanisms of fighting against them
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Which antioxidants can protect against free radicals?
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- A C E
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What do transferrins, ferritin, lactoferrin, etc. all have in common?
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- all metal binding proteins to help defend against free radicals
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What do the enzymes catalse, SOD & glutathione peroxidase all have in common?
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- all cellular defense mechanism against free radicals
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What does carbon tetrachloride do? What are EM changes that occur (important: what accumulates in cytoplasm)?
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- causes lipid peroxidation by generation of free radicals - autolytic rxn
- water accumulation in ER, mito change shape, lipid droplets accumulate in cytoplasm |
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Towards the central vein in the liver there is more p450 which activates _____ to a more active form causing more lipid peroxidation. This kills the cells & they lose _______ staining (turn more eosinophilic) & end up dying due to lipid _______
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- carbon tetrachloride
- differential - peroxidation |
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There is a role of ___________ & ________ in reperfusion injury
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- free radicals
- calcium |
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Free radicals can be formed during _____ of bacteria or cellular debris
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- phagocytosis
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necrosis/oncosis are greek for _______. It refers to spectrum of morphological changes that follow cell death in living tissue, resulting from preogressive degradative action of enzymes on lethally injured cell.
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swelling
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The most common form of necrosis is _______ necrosis. Here you see eosinophilia & nuclear changes. The 2 concurrent processes are _____________ & ___________. After necrosis there is an _________ response.
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- coagulative
- enzymatic digestion & denaturation of proteins - inflammatory |
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In necrosis: Cell death characterized by cell and organelle ______, ____ depletion, increased plasma membrane permeability, release of ________ coming out in blood, autolysis and inflammation.Involves a number of cells, a _______’ in the tissue
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- swelling
- ATP - macromolecules - ‘geographical area |
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Ghost town is a classic example of ____________, architecture is there but nobody is home - know cell is dead b/c of _______ changes
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- coagulative necrosis
- nuclear |
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In the beginning of coagulative necrosis you see ______ changes & lighter staining, then you see darker staining & _______ infiltration.
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- hydropic
- inflammatory |
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______ necrosis looks like cheese, common in TB leads to calcificaiton
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- caseous
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In a _______ granuloma, there is a center, common in ____
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- caseous
- TB |
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_______ necrosis occurs commonly in the CNS. It gets washed away & is absorbed
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- liquefactive
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______ necrosis happens in tissues like the pancreas. If you damage it the tissue can die for whatever reason, the enzymes get let out activated by calcium start eating up everything, if _____ & _______ together make soap, the _____ white spots
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- Fat
- calcium - FAs - chalky |
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In apoptosis, Cell deletion by ___________ into membrane-bound particles that are _________ by other cells.An energy-dependent process involving activation of a coordinated, internally programmed series of events effected by a dedicated set of gene products.
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- fragmentation
- phagocytosed |
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In apoptosis there is cell _____, chromatin ______, cytoplasmic blebs & apoptotic bodies, Phagocytosis of apoptotic cells and bodies & little ________
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- shrinkage
- condensation - inflammation |
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_______ body are cells in the liver undergoing apoptosis usually b/c of viral infection
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counsilmans body
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What are counsilmans body?
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cells in the liver represents cell undergoing apoptosis, usually when cells infected by viruses
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In apoptosis there is formation of __________, ________ activation & protein cleavage, protein cross-linking, ___ fragmentation & phagocytic recognition
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- mitochondrial permeatiblity transition
- caspace - DNA |
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In apoptosis who can engulf the apoptotic fragments?
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- macrophages & non-professional phagocytes
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What's the difference b/w apoptotic & necrosis DNA ladders? Who cleaves the apoptotic one?
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- apoptotic has DNA ladder & necrosis does not
- caspaces do the DNA ladder for apoptosis |
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What is a signal that triggers other cell to phagocytose apoptotic bodies?
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- phosphatidyl serine flips out & is recognized
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The two pathways for signaling apoptosis are: _______ & ________ signals
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transmembrane & mitochondrial (intrinsic)
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TNF & Fas are examples of the ______ apoptotic pathway. Leakage of Cyt C from the mito is an example of the ______ apoptotic pathway.
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- transmembrane (extrinsic)
- mitochondrial (intrinsic) |
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BCL-2 family members are part of which apoptotic family? Which ones are Bax & Bad/ Bcl-2 & Bcl-XL?
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- mitochondrial
- Bax & Bad are pro apoptosis, Bcl-2 & Bcl-XL are anti apoptosis |
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How doGranzyme released by cytotoxic lymphocytes causes apoptosis
es p53 fit into apoptosis? |
- P53 can induce apoptosis if the cell has damaged DNA
- p53 mutations are linked to cancer |
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Granzyme released by cytotoxic lymphocytes causes __________
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apoptosis
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In apoptosis there is death of ____ cell vs. necrosis where there is death of _____ cells. What's the difference in cell size? Organelles? energy usage? inflammation?
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- one vs. multiple
- shrinking vs. swelling - intact vs. broken down - energy dependent vs. no energy needed - no inflammation vs. inflammation |
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What is the difference between primary, secondary & tertiary lysosomes?
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Primary: package with lysosomal enzymes, secondary is the one that discharged into autophagic vacule, tertiary is when they can’t degrade the material
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What is autophagy? Heterophagy? Which one is removal of apoptotic bodies & bacteria?
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- eating up own tissue, normal
- hetero is someones elses - removal of apoptotic bodies, bacteria |
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What does cholchazine do?
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- is what you give to people with gout because breaks up the cytoskeletal elements & keeps the lysosomes from moving to other areas
- can cut down inflammation by stabilizing lysosomes |
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What are lipofuscin pigment granules?
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Sometimes lipids cannot be degraded & they stay in cell & they’re called lipofuscin pigment granules: sign of wear & tear – older age of cell, more of these accumlate with age
You can find these in myocardialcytes b/c over normal circumstances cardiac myocytes do not turn over |
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What happens in Chediak-Higashi Disease? What do you see on the EM?
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- Lysosomes will fuse with phagositic vacule, lysosomes move & fuse & this becomes phagolysosome – lysosomal enzymes will degrade things via number of mechanisms
- see huge polys - giant lysosomes with the disease When you put white blood cells in culture (messed up ones) it takes longer time for cell to recognize bacteria, then takes longer time to phagocytose them & takes a long time for lysosomes to migrate/fuse Bacteria can start dividing inside phagosomes & killer mechanism not very effective |
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Accumulation of metabolites – lack of _______ & substrate will accumulate inside cell. What is a good example (i.e. what type of storage diseases)? What part of the body does it normally effect?
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- enzymes
- LSDs are good examples - mental state |
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Gaucher disease is a deficiency in _______ leading to the accumulation of ________ in cells. What characteristic do the cells have (spleen macrophages that accumulate it)?
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- glucocerebrosidase
- glucosylceramide - tissue paper like cells - mental state affected |
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______ comes in two forms, cells become smaller (sometimes happens first), then can be the loss of cells – one way body responds to stress. If you put more load on the tissue or organ they change by undergoing _____ – organ becomes bigger b/c cells themselves become bigger (can have physiological or pathological). Other way to response in hormonal stimulation is _______– increasing number of cells that carry out a job (can have physiological or pathological). ______ is changing the cell type – replace one differentiated cell with a new differentiated cell type
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- Atrophy
- hypertrophy - hyperplasia - Metaplasia |
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________: increase in the size of a cell accompanied by and augmented functional capacity, by either hormone stimulation or increased functional demand._______ and ________frequently occur together, and they may be triggered by the same mechanism
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Hypertrophy
hypertrophy & hyperplasia |
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Mediterranean Salad
M |
Mixed field greens, romaine hearts tossed with artichoke hearts, chopped pepperocini, kalamata olives, red onion, fennel and roma tomatoes, tossed in our pesto vinaigrette (pesto:vinaigrette, 2:1)
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What cell changes occur in the uterus during pregnancy? What triggers this (i.e. what stimulation)?
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- hyperplasia & hypertrophy
- this is HORMONAL stimulation |
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_________ decrease in the size and function of a cell, and eventually, the affected organ due to reduced functional demand, inadequate supply of _____, insufficient nutrients, interruption of signals, persistent injury, aging.
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- ATROPHY
- oxygen |
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Denervation _____ in Skeletal Muscle happens when neuron gets severed from muscle & cannot find original myelin sheath
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Atrophy
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In older individuals, the brain ______ due to reduction in blood & oxygen supply
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atrophies
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When you castrate an animal the tissue ________ because you do not have the hormonal signal anymore
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atrophies
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What is barretts esophagus?
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SSNKE all the way to the stomach – a person with acid reflux doesn’t have good protection with squamous cells – certain area can be replaced with intestinal epithelium like cells to protect
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What is the connection b/w smoking & metaplasia (also happen in cervix with repeated infection)?
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Smoking causes metaplasia: columnar to squamous
Start losing the mucus so when you stop you start coughing a lot, start producing a lot of mucus – metaplasia going back in other direction |
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__________ is Disordered growth and maturation of the cellular component of a tissue. Response to the persistence of injurious influence.Results from sequential mutation in a proliferating cell population. Morphological expression of the disturbance in growth regulation . Shares many cytological features with _____
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- dysplasia
- cancer |
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What happens in cervical dysplasia? What is carcinoma insitu?
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Promoting grade 1 to grade 5, they should not be there, lack of maturation closer to the top layer
When you do papsmear you only look at top layer and if it’s messed up they you need to byopsy it Carcinoma insitu means no one looks mature when this happens the next step they go down, penetrate basal lamina and become invasive cancer More dysplastic the tissue, more red flags for cancer are being waved |
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What happens in fatty liver? What do you see in the EM? What can cause this?
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Defects in any of these steps of uptake, catabolism, or secretion of FAs can result in lipid accumulation
- see lipid droplets - ethanol can cause this |
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What happens in cholesterolosis?
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Cholesterolosis: cholesterol-laden macrophages in a focus of gallbladder cholesterolosis
- macrophages loaded with cholesterol = accumulation of material |
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What happens in an atherosclerotic plaque with cholesterol clefts?
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have cracks, narrowed blood vessel, cracks called cholesterol clefts, accumulation of cholesterol in the artery
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Accumulation of excessive amount by normal proteins (_______ bodies in plasma cells). Defects in intracellular transport and secretion (____________ deficiency). Accumulation of cytoskeletal proteins/beta amyloid (_________ disease)
Accumulation of abnormal proteins (_________) |
- Russell
- alpha-1-antritrypsin - Alzheimer - amyloidosis |
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What is alcoholic hyaline?
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- accumulation of keratin intermediate filaments in hepatocytes
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You can also accumulate exogenous particles that you cannot digest such as macrophages do in the lung with ______
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carbon
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_________--- hemoglobin-derived, golden yellow-to-brown, granular or crystalline pigment. One of the major storage forms of _____. Ferritin forms hemosiderin granules when there is a local or systemic excess of iron. (endogenous pigment)
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- Hemosiderin
-iron Lung macrophages happens during heart failure cells, happens when macrophages eat Find it in spleen a lot b/c spleen degrades red blood cells |
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in ______ calcification, Calcium metabolism is normal.Serum level of calcium is normal. Found in ______ tissues.Examples: atheromas, damaged heart valves, TB lymph nodes etc (caseous necrosis). Macroscopic: fine, ____ granules. Microscopic: ________ amorphous granules
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- dystrophic
- nonviable/dying - white - basophilic/dark purple |
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In ______ calcification Calcium metabolism is abnormal. Serum calcium is high (hypercalcemia). May occur in ______ tissues.Principal causes:Hyperparathyroidism, Destruction of bone tissues,Vitamin-D related disorders, Renal failure. Generally does not cause clinical dysfunctions.
Morphology similar to that in __________ calcification |
- metastatic
- normal - dystrophic |
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Hyaline changes look
Homogeneous (no ______), glassy, ____ appearance in routine H&E stained section. Intracellular --- _____bodies, alcoholic hyaline. Extracellular --- walls of _____ |
- nuclei
- pink - Russell - arterioles |
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Pancreas: ______ Islets in Type II Diabetes
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Hyalinized
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Inflammation is the response of a ______ tissue and its ________ to injury.
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- living
- microcirculation |
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What are the 5 cardinal signs of inflammation?
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1) Calor (heat)
2) Rubor (redness) 3) Dolor (pain) 4) Tumor (swelling) 5) Functio lasesa (loss of function) |
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The 3 main characteristics of inflammation are: ________ Reaction of vessels and movements of fluids from blood into the extravascular tissues. ________ Including movements of leukocytes from blood vessels into the tissues and participation of other cells. ________ Elaboration of inflammatory mediators derived from plasma and from cells
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- vascular
- cellular - chemical |
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What are the 3 tissue responses to injury?
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1) Scar
2) Resolution 3) Chronic |
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A persistent inflammatory response, usually associated with the inability to eliminate the offending agent and clear the injured tissue, is known as ______ inflammation. This condition often has an _______ component.
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- chronic
- immune |
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In acute inflammation there is a transient _______ first then _______ of ______ arterioles --- increase blood flow to the tissue (________), caused by specific mediators such as histamine, prostacyclin, and nitric oxide. Accounts for redness (________) and warmth at the site of tissue injury.
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- vasoconstriction
- Vasodilation - precapillary - hyperemia - erythema |
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After vasodilation, Vasoactive mediators from plasma and cells are generated at the site of injury. Mediators (e.g. ______) bind to specific receptors on _______ cells, causing contraction an gap formations, increase in endothelial cell permeability, --- leakage of fluid into ________ space. Short lived, ‘immediate transient response”. This leads to ______loss of fluid from vessel into tissue, local stasis of blood, lasts minutes to hours. Next, ________ marginate.
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- histamine
- endothelial - extravascular - Edema - Leukoycytes |
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For a mild injury there are two different increases in permeability (one within 30 mins, second within 3-5 hours: _____ response). In severe injury there is an _____________ response, steady leakage & persists for hrs or days
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- delayed
- immediate sustained |
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_______ edema has low protein content, __________ edema has high protein content - there can be _______ (with large amounts of fibrin) or _______ (prominent cellular component) exudate.
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- transudate
- exudate - fibrinous - purulent (pus) |
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Transudate edema occurs because of an increased ________ pressure and a decreased _______ pressure. An exudate is formed in ________ because vascular permeability increases as a result of increated interendothelial spaces.
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- hydrostatic
- colloid osmotic - inflammation |
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Endothelial cells are activated by products of tissue injury & _______. They change shape & increase their synthesis of ____________ (binding molecule). They secrete mediators & there are changes on their surface adhesion molecules.
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- cytokines
- platelet activating factor (PAF) |
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The neutrophil (poly) are from precursor cells in the ____________. They increase in acute inflammation - arrive early & have a _____ lifespan. Their nuclei is _______ (i.e. jelly beans).
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- bone marrow
- short - lobular |
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Tissue macrophages are derived from blood _______. They have a _______ lifespan than neutrophils & arrive later (2-3 days). They are important in the ______ phase & in _______.
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- monocytes
- longer - chronic - repair |
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The mas cell (basophil) is an important source of ______ which vasodilates. ________ are found in parasitic reactions & antibody antigen complexes. _______ are involved in acute inflammation & blood clotting. ________ are prominent in viral infections & chronic inflammation
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- histamine
- eosinophils - platlets - lymphocytes |
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In acute inflammation, leukocytes, particularly PMNs, accumulate in the affected tissues. Leukocytes in the blood first adhere to the endothelium and become activated (________, adhesion). They then migrate through the endothelial cell layer into the surrounding tissue (________, chemotaxis). The PMNs _____ foreign materials, microbes and debris in the extravascular tissue.
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- margination
- transmigration - ingest |
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Leukocyte recruitment: in response to histamine & thrombin, endothelial cells redistribute ________. In response to chemokines leukocytes have increased avidity of ______. In response to ____ & IL-1 (cytokines), endothelial cells with express adhesion molecules. CD31(PECAM-1) is involved in _________ then at the end there is chemotaxis.
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- p-selectin
- integrins - TNF - transmigration |
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In acute inflammation the predominant cell type is ______ (jelly bean nuclei) & in later stages the predominant cell type is _______ (round nuclei). _______ predominate in the inflammatory infiltrate during the first 6 to 24 hours and are replaced by _______ in 24 to 48 hours.
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- polys (neutrophils)
- mononuclear cells (macrophges) - Neutrophils - monocytes |
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In order for a leukocyte to phagocytose an agent the agent needs to be _______. It then engulfs it and destroys it in an ______ dependent & non- ______ dependent manner.
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- opsonized
- oxygen - oxygen |
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NADPH oxidase, Superoxide anion, Hydrogen Peroxide, Hypochlorous Acid, Hydroxyl radicals, Nitric oxide are all examples of ______ mechanisms of leukocyte killing. Lysosomal hydrolases
Bactericidal / permeability increasing proteins, Defensins, Lactoferrin,, Lysozyme, Bactericidal proteins of eosinophils are _______ mechanisms of killing. |
- oxidative
- non-oxidative |
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The mechanisms involved in eliminating microbes and cellular debris (the physiologic role of inflammation) are also capable of damaging normal tissues (the pathologic consequences of inflammation, “_______ damage”)Examples include acute respiratory distress syndrome, acute transplant rejection, asthma, arthritis, pulmonary fibrosis etc.
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- collateral
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Defects in leukocyte function can lead to severe and _______ infections.Defects can involve inadequate number of leukocytes, as in bone marrow suppression in chemotherapy or radiation.
Defects can involve any step in the sequence of adherence, emigration, chemotaxis, phagocytosis and the killing mechanisms etc. Some of the defects are congenital while others are acquired. |
- frequent
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Congenital defects in phagocytic function include: chediak-hagashi syndrome, chronic granulomatous disease, myeloperoxidase deficiency & LAD --- what do all of these do? Aquired defects of phagocytic function include: chemo, diabetes, leukemia, malnutrition, sepsis, viruses
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- Chediak-Higashi Syndrome
Poor chemotaxis, defective lysosomal granules - Chronic granulomatous disease: Deficient NADPH oxidase, no H2O2 production - Myeloperoxidase deficiency Deficient HOCl generation - LAD --- leukocyte adhesion deficiency --- defective integrin expression/function, defective selectin binding |
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_______ --- restoration of normal tissue architecture and physiological function.
_____ --- replacement of injured tissue by connective tissue, normal architecture and function not restored Persistent inflammation --- prolonged acute response or ______ inflammation |
- Resolution
- Scar - chronic |
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MORPHOLOGICAL PATTERNS OF ACUTE INFLAMMATION: ______ Inflammation --- with outpouring of a thin, protein-poor fluid from the plasma or from mesothelial cells lining the body cavities. Accumulation of fluid in these cavities is called _____. Ex = skin blister
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- Serous
- effusion |
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MORPHOLOGICAL PATTERNS OF ACUTE INFLAMMATION: _________ inflammation, exit of fibrin from blood vessels, Fibrinous exudate is characteristic of inflammation in the lining of body cavities, such as the meninges, pericardium, and pleura.
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- fibrinous
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MORPHOLOGICAL PATTERNS OF ACUTE INFLAMMATION: __________ Inflammation, Production of large amount of purulent exudate (pus) containing neutrophils, necrotic cells, and edema fluid.Abscesses are localized collection of purulent inflammatory tissue caused by suppuration buried in a tissue, an organ, or a confined space.
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- Suppurative (Purulent)
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MORPHOLOGICAL PATTERNS OF ACUTE INFLAMMATION: _______ is a local defect, or excavation, of the surface of an organ or tissue that is produced by sloughing of inflamed necrotic tissue. Ex = in stomach where something ate through mucosa layer
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- ulcers
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____________ is a key source of vasoactive mediators. It triggers intrinsic coagulation cascade, complement pathway, kallikrein-kinin system - the resulting products increase vascular permeability & lead to _______. It is a _______ derived mediator.
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- Hageman Factor (Clotting Factor XII)
- emema - plasma |
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The __________ pathway converts arachidonic acid to prostaglandins and thromboxanes.The __________ pathway converts arachidonic acid to leukotrienes and lipoxins.
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- cyclooxygenase
- lipoxygenase |
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_______ cells – actually performs the function of the organ. _______ cells – support cells where you suspend the parenchymal cells
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- Parenchymal
- Stromal |
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______ --- fibrosis that develops in a tissue space occupied by an inflammatory exudate
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- Organization
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Epithelial & hematopoietic cells are considered ______ cells b/c they're continuously dividing. Liver, kidney, fibroblasts, smooth muscle, mesenchymal tissues are considered ______ cells b/c they're quiescent (i.e. low level of replication unless called upon). Neurons, skeletal muscle & cardiac muscles are ______ cells b/c they do not divide ever.
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- labile
- stable - permanent |
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Epidermal growth factor (EGF), transforming growth factor-α (TGF-α), vascular endothelial growth factor (VEGF), fibroblast growth factor (FGF), hepatocyte growth factor (HGF), platelet-derived growth factor (PDGF) all have ___________ activity.
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intrinsic tyrosine kinase
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__________ Activation triggers a cascade of phosphorylating events through MAP kinases (mitogen-activated protein), or phosphoinositide-3 (PI-3) kinase pathways, resulting in transcription factor activation and DNA replication
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intrinsic tyrosine kinase growth factor
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Cytokines, interferons, colony-stimulating factors, growth hormones and erythropoietin are all growth factor receptors without ___________ activity
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- intrinsic tyrosine kinase
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________________ Activation leads to an association with intracellular protein kinases, Janus kinases (JAKs), resultant activation of cytoplasmic transcription factors (STATs, signal transducers and activators of transcription) move into the nucleus and activate gene transcription
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- growth factor receptors without tyrosine kinase activity
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Epinephrine, vasopressin, serotonin, histamine, glucagon and the chemokines are all growth receptors coupled to _________
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G- proteins
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seven transmembrane ____________ --- activation triggers the cAMP pathway with multiple effects. Can also activate the PI3 pathway.
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G-protein-coupled receptors
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The two components of the ECM are the ________ matrix & _________ membrane
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- interstitial
- basement |
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________ & _______ are both fibrous structural proteins that are a part of the ECM
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- collagen
- elastin |
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Proteoglycans & hyaluronan are examples of ___________ gels that are components of the ECM
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- water-hydrated gels
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Fibronectin, laminin & adhesion receptors are ____________ & adhesion receptors that are components of the ECM. They are involved in cell-to-cell adhesion, linkage b/w ECM & cells, and binding between ECM components.
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- adhesive glycoproteins
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The residual tissue must be structurally and functionally intact for regeneration to be successful. The integrity of the _____ is important. Liver is really the only tissue that can regenerate.
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- stroma
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Healing by ________ example = uncomplicated pneumonia. First inflammation in aveoli (exudate with polys & fibrin), appearance of macrophages to remove debris, removal of exudate, epithelial regeneration & minimal damage to tissue, stroma intact, successful removal of inflammatory products
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- resolution
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Repair by connective tissue: starts early in __________ (within 24 hr) with the proliferation and migration of fibroblasts, vascular EC leading to the formation of _________ tissue by 3-5 days.
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- inflammation
- granulation |
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Repair by connective tissue: _______ occurs first forming granulation tissue.
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- angiogenesis
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____, FGF-2 and _______ (Ang) are the most important factors in angiogenesis
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- VEGF
- Angiopoietins |
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_______ makes Mobilization of EPC from bone marrow, enhancement of their proliferation / differentiation at sites of angiogenesis
Stimulate proliferation and motility of existing ECs, promoting capillary sprouting |
- VEGF
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_______ binds to member receptor with tyrosine kinase activity, Enhances endothelial cell proliferation
Enhances EC differentiation Enhances EC motility Promotes migration of macrophages and fibroblasts to the damaged area Stimulates epithelial cell migration |
- FGF (basic fibroblast growth factor)
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_________ Involves in stabilizing newly formed vessels
Recruits pericytes (capillaries) and smooth muscle cells (large vessels) Enhances deposit of ECM Mediates vessel maturation from simple tubes into more elaborate vascular structures Helps maintain EC quiescence (Ang 1) Processes also involve PDGF and TGF-β |
Angiopoietins 1 and 2 (Ang 1, Ang 2)
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During repair by connective tissue, _______ under the influence of growth factors migrate to & proliferate at the site of repair. Then ECM gets deposited - ECM degredation diminished, Granulation tissue scaffold converted into a scar composed of fibroblasts and _________.
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- fibroblasts
- collagen |
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The ECM initially laid down in the scar undergo changes
Growth factors modulate the synthesis and activation of _______________ These proteinases modify the ECM The net effect of ECM synthesis vs. degradation results in debridement of injured sites and remodeling of the connective tissue framework |
matrix metalloproteinases
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In _______________, Epithelial regeneration predominates over fibrosis. Small scar, Minimal wound contraction.
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healing by first intention
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In _______________, there is more extensive tissue loss, larger clot/scab, more granulation tissue, larger scar, wound contraction
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- healing by second intention
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Wound strength depends on suturing, _______ after surgery, suture removal, wound strength is about 10% of normal
Wound strength increases rapidly over next _______ Tensile strength eventually plateaus at 70-80% within ________ |
- one week
- 4 weeks - 3 months |
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Deficient ________: inadequate granulation tissue or collagen deposition and remodeling. Wound dehiscence or ulceration. _________ : excessive granulation (exuberant granulation/proud flesh) can protrude above the skin and block reepithelialization. ______: excessive collagen accumulation forming a raised hypertrophic car, progression beyond the original area of injury without subsequent regression. Formation of ______: excessive wound contraction, can cause deformity or limits joint mobility
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- scar formation
- Excessive Repair - Keloid - contractures |
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________ --- formation of fibrous tissue as a reparative or reactive process.. is associated with chronic inflammatory diseases such as rheumatid arthritis and cirrhosis. Lymphocyte-macrophage interactions sustain the synthesis and secretion of __________ and fibrogenic _______ and other biologically active molecules that lead to fibrosis.
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- Fibrosis
- growth factors - cytokines |
