Term
| Define hypertrophy and discern between hormonal and compensatory types. |
|
Definition
| Increase in the size of cells. Hormonal is caused by hormones (like in the uterus during pregnancy), compensatory is caused by an increase in the demand of the tissue types of interest (as in the heart during hypertension) |
|
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Term
|
Definition
| Increase in the number of cells. This usually increases the volume of the organ where the cells reside. |
|
|
Term
| Define squamus metaplasia |
|
Definition
| Metaplasia is when a cell turns into another type. An example is when cells of the lungs change from gladular to squamus to prevent them from being damaged when exposed to cigarette smoke. |
|
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Term
|
Definition
| This is like an early neoplasm. The cells freak out and change their shape or organize themselves differently. |
|
|
Term
|
Definition
| A special type of cell death where cells die after becoming detatched from their matrix. This prevents metastasis. |
|
|
Term
|
Definition
| Cells dying from degradative enzymes. Always pathologic. During this process it will swell, then its lysozomes will rupture causing digestion and membrane blebbing. |
|
|
Term
| What is hydropic swelling? |
|
Definition
| A symptom of acute cell injury that may be caused by infetions, ischemia, heat or toxins that causes blebs, chromatin clumping. Most of this is caused by lots of Na in the cell which causes influx of water. |
|
|
Term
| What are the 5 types of necrosis? |
|
Definition
| 1. Coagulative (proteolysis stops and it dies in its own waste), 2. Liquefactive (accelerated lysis of adjacent cells), 3. Fat (chalky areas in fat), 4. Caseous (tuberculosis), 5. Fibrinoid (in Blood vessels) |
|
|
Term
| How does apoptosis progress initially? |
|
Definition
| Cells shrink and detatch, DNA is fragmented, cell surface blebs and apoptotic bodies form. |
|
|
Term
| Microscopically, what distinguishes necrosis from apoptosis? |
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Definition
| In necrosis you will see a significant swelling of the cell unlike apoptosis. Apoptotic bodies would come from apoptotic cells. Also, the necrotic cells would break apart themselves and later be scavenged, whereas the apoptotic bodies would be phagocytized. |
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|
Term
| What are occurs in apoptosis after apoptotic bodies form? |
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Definition
| Healthy cells will phagocytize them, they will be degraded in the lysozomes. |
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Term
| You build a perfect cell but insert a cytoplasmic protein that neutralizes cytochrome C. What effect may this have on apoptosis rates? |
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Definition
| This would decrease apoptotic rates since the cytochrome C help to form the apoptosome. |
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Term
| What would happen to cell death if you increased the translation of functional p53 and simultaneously exposed the cell to UV rays causing Thymidine dimers? |
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Definition
| You would increase the cell death rate. P53 recognizes errors in DNA and initiates apoptotic responses. |
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Term
|
Definition
| The cell will lyse its own organelles. It is a mechanism of programmed cell death distinct from apoptosis. You want this when you won't be able to have phagocytes digest apoptotic cells. |
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|
Term
| What distinguishes entosis from apoptosis? |
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Definition
| The cell will first be internalized into another cell not by phagocytosis but by cell invasion. This occurs in epithelial cells frequently. The cell won't be dead at the time it is internalized and the process is reversible. |
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|
Term
| What are the three types of calcification? |
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Definition
| Dystrophic (usually in necrotic or messed up tissues), metastatic (calcium salts in normal tissue, because high Ca in serum), calcium stones (CaCO3, in gallbladder, kidney (ouch!)) |
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Term
|
Definition
| It is a mixture of genetic and environmental factors including REACTIVE OXYGEN SPECIES, DNA repair defects, abnormal cell signalling, inability to make new cells (telomeres) and proteasome malfunctions |
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Term
| You invent a telomere polymerase (TPOL) that makes telomeres really long. How will this affect the amount of divisions you'll get from TPOL active cells? |
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Definition
| You will have increased number of generations. Cancer cells, for example have lots of telomerase. |
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Term
|
Definition
| They can neutralize toxoids and bacteria. They can also opsonize and function in the complement cascade. |
|
|
Term
| What percentage of White blood cells do lymphocytes compose? |
|
Definition
| 25% (80% of which are T cells) |
|
|
Term
| Phagocytes can kill cells by |
|
Definition
| ROS, swallowing, cytokines |
|
|
Term
| What are some differences between CD 4 and 8 cells |
|
Definition
| 4= helper, 8= suppressor. 4 will promote antibody and inflammation. These are type Th1, but 8 cells inhibit immune response and are type Th2 |
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|
Term
|
Definition
| Target tumurs and virally infected cells. They will cause apoptosis. They do not recognize cells from antigen, but other means. |
|
|
Term
|
Definition
| Vaccines will expose us to integral parts of an organism. We will catalogue these agents as harmful and we will be able to combat insults of the same variety much quicker |
|
|
Term
| What are the two grand errors in immunity |
|
Definition
| 1 Our immune system doesn't recognize or clear foreign insults. 2. When our immune system considers our own cells foreign and starts attacking the hosts own cells. |
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Term
| Anemia, splenomegaly (big spleen), fatigue, weakness caused by and attack on your own red blood cells is what? |
|
Definition
| Autoimmune hemolytic anemia |
|
|
Term
| An autoimmune infection on lungs and kidneys causing coughing of blood is what? |
|
Definition
|
|
Term
| What is the organ affected in Grave's disease? |
|
Definition
| The tyroid. This would cause hyperthyroidism. This could cause increased heart rate, weight loss and nervousness |
|
|
Term
| antibodies attacking the Beta cells in the pancrease causing reduction in insulin is which autoimmune disease? |
|
Definition
| Diabetes mellitus (type 1). This also causes thirst and frequent yrination. |
|
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Term
|
Definition
| Lots of collagen deposited in the skin. This can cause edema, ishema of fingers amongst other things. |
|
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Term
| Which organs are affected by SLE (lupus) |
|
Definition
| The joints, kidneys, skin, lungs, heart brain, or blood cells. This can cause anemia and other issues with lack of function of the affected organs. The tell-tale sign is the malar rash which looks like a butterfly on the face. |
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|
Term
| What may occur that will cause us to develop an autoimmune disease? |
|
Definition
| A foreign substance that causes an immune reaction is similar in composition to self proteins, altered self substance (by a virus, drug, sunlight) or a substance in the body that is not normally seen by the immune cells that is suddenly released into the bloodstream. |
|
|
Term
| Which factors cause sjogren's? |
|
Definition
| Lacrimal and salivary glands gland is infiltrated by lymphocytes, which will cause atrophy in these glands leading to less tears and saliva. |
|
|
Term
| Why does HiV need a host? Which cells do they hijack? |
|
Definition
| Because it is an RNA virus (a retrovirus), and needs the host cells to use the host's DNA with REVERSE TRANSCRIPTASE to replicate ourselves. In this way, it integrates it's gemone with our own. It uses our CD4 cells becaues these have a receptor on them that HIV uses to get inside. |
|
|
Term
| When will symptoms of Aids begin? |
|
Definition
| After latent phase, when the rate of destruction of CD4 cells rises above the rate of CD4 replication |
|
|
Term
| CD4 counts that are important to aids are 500 and 200 per ml. What do each of these signify? |
|
Definition
| 500=HIV is defined at this amount. 200=level where HIV related infections will ensue |
|
|
Term
| What is the karposi sarcoma? |
|
Definition
| HIV related blood vessel cancer that causes purple lesion on the skin. |
|
|
Term
| Which of these isn't a classic infection associated with HIV: Candidiasis, Mycobacterium Avium, Rickettsia or TB? |
|
Definition
|
|
Term
| Which isn't a symptom of candidiasis: Thrush, xerostomia, angular chelitis or erythematous? |
|
Definition
|
|
Term
| What is inflammation and what five insults is it usually aimed at? |
|
Definition
Body's attempt to get rid of noxious stimuli or injury
Microbial, mechanical, chemical, foreign materials, neoplasia |
|
|
Term
| What are the two major concepts that differentiate acute inflammation from chronic inflammation? |
|
Definition
Duration of inflammation
Nature of response |
|
|
Term
| Describe the time period and particular reaction that can occur with acute inflammation. |
|
Definition
Usually onset is abrupt and short duration, associated with sudden injuries
Exudative reaction = fluid, serum proteins, and leukocytes arrive from vasculature |
|
|
Term
| Can acute inflammation become chronic inflammation? |
|
Definition
|
|
Term
| You were silly in Sim Lab and you've cut yourself with your handpiece. Now you've got some acute inflammation; what are ALL the possible outcomes of this?? |
|
Definition
Complete resolution (heals and we're all good)
Abscess formation (gets wall off with tons of leukocytes)
Resolution with sequalae (you get a lovely battle scar)
Chronic (becomes WORSE) |
|
|
Term
| Describe the time period of chronic inflammation, the particular reaction associated with it, and the only way to cause resolution. |
|
Definition
Tissue injury continues (can be weeks, months, etc.)
Proliferative reaction = fibroblasts, endothelial cells mass proliferate and chronic inflammatory cells (think macrophages) parade in
Only end with the PERSISTENT SOURCE is REMOVED |
|
|
Term
| Which is more important in acute inflammation: severity of injury or cause of injury? |
|
Definition
|
|
Term
| Acute inflammation can be broken into two major event categories. Name them and give a brief description of each. |
|
Definition
Vascular events = think increase permeability of fluids and plasma pieces and increased blood flow
Cellular Events = think calling the troops to battle (PMNs, platelets, macrophages) |
|
|
Term
| Walk through a basic cycle of acute inflammation as if you have just gotten a cut. |
|
Definition
1. Bacteria/pathogens invade wound!
2. Platelets release blood-clotting factors at wound
3. Mast cells start dumping out histamine, seratonin, and bradykinin to increase blood and plasma to wound
4. Neutrophils chomp on pathogens
5. Macrophages dump cytokines for chemotaxis (see more with chronic)
6. Keep going until remove material or repair wound! |
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|
Term
| The vascular response of acute inflammation is like an EMT; why is this? |
|
Definition
| It acts as a delivery system for inflammation and helps bring the life-saving materials to the wound |
|
|
Term
| Describe the basic components of the vascular response. |
|
Definition
Rapid and transient vasoconstriction followed by vasodilation (hyperemia)
Increased vascular permability
System slows down in a progression to concentrate cellular supplies causing statis and leukocyte margination |
|
|
Term
| What are the four classic signs of acute inflammation and what is the extra special fifth one? |
|
Definition
Redness/erythema
Heat
Swelling
Pain
**Loss of function** |
|
|
Term
| Vasodilation is associated with which cardinal signs of inflammation? |
|
Definition
|
|
Term
| Swelling is caused by what response? |
|
Definition
| Vascular response = exudation of fluid, plasma proteins and leukocytes |
|
|
Term
| Pain in acute inflammation is caused by what? |
|
Definition
Tissue distension
Nerve ending compression |
|
|
Term
| What are the three systemic signs of acute inflammation? |
|
Definition
Fever = endogenous pyrogens (injured cells OR microorganisms)
Leukocytosis = increase in WBC (neutrophils = neutrophilia)
Lymphadenopathy = swelling of lymph nodes |
|
|
Term
| When we say that vessels are getting 'leaky' during acute inflammation, what are we talking about? |
|
Definition
| Endothelial cells have retracted from each other and made gaps so fluid can leak from intravascular compartment into extracellular compartment |
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|
Term
| In acute inflammation, the vascular response produces a 'triple response of the skin' and goes through all signs of inflammation. Name the three steps and the signs associated. |
|
Definition
Immediate injury = vasodilation with dull redness (rubor and calor)
Wait a few seconds = vasodilation with red flare (rubor and calor)
About a minute =swelling with wheal and edema (tumor and dolor) |
|
|
Term
| Which cells most likely cause the red flare seen in acute inflammation? |
|
Definition
|
|
Term
| What is vascular stasis and why does it help in the delivery system? |
|
Definition
Fluid loss from vessels without blood cell loss
Causes increased viscosity of blood, decreasing flow so more concentration of materials |
|
|
Term
| What is leukocyte margination and what happens as this occurs? |
|
Definition
WBC stick together
Intravascular hydrostatic pressure increases, causing more fluid loss and cells to enter extravascular space |
|
|
Term
| Edema is swelling because fluid leaked into tissues. This escape is also called exudate. What are the two types of exudate and how are they different? |
|
Definition
Serous exudate = thin clear fluid, usually plasma fluids (low protein and cells) in mild inflammation
Purulent exudate = suppration with nasty pus, rich in neutrophils and cell debris, plasma fluids/protein from pyogenic bacterial infections |
|
|
Term
|
Definition
| A canal for drainage of purulent exudate that the body produces itself |
|
|
Term
| Did you know that having edema and nasty swelling is actually protective to your body??? What does edema do for the body? |
|
Definition
Diluate toxins in tissues
Inactive those toxins via proteases
Give nutrients to inflammatory cells
Concentrate antibodies/complement
Have fibrinogen --> to fibrin for movement of inflammatory cells |
|
|
Term
| Let's review immunology! What is chemotaxis? |
|
Definition
| Directed movement of WBCs to area of injury stimulated by factors (Like C5a and cytokines!) |
|
|
Term
| Let's review immunology! What is phagocytosis? |
|
Definition
| cells engulfing and ingesting foreign substances from injured site; involves neutrophils and macrophages |
|
|
Term
| Neutrophils are pretty awesome. What is their purpose and what is so special about them? |
|
Definition
Hallmark of acute inflammation, first on the job!
Phagocytose nasty things
Multilobular nucleus and granular cytoplasm with lysosomes |
|
|
Term
| Monocytes are pivotal cells in regulating chronic inflammation. Describe them and their functions. |
|
Definition
Part of WBCs, second line of defense!
Large, mononuclear and phagocytose nasty stuff with lysozymes
Can migrate out of bloodstream to become tissue macrophages |
|
|
Term
| What are the sequence of microscropic events that occur during the inflammatory response? |
|
Definition
1.) Injury
2.) Constriction of microcirculation
3.) Dilation of small blood vessels
4.) Increase in permeability of small blood vessels
5.) Exudate leaves small blood vessels |
|
|
Term
| We can classify inflammatory mediators into two broad categories; what are these and what do each of these categories lead to? |
|
Definition
Vasoactive factors (think histamine) increase vascular permeability and cause edema
Chemotactic factors (think C5a) call up inflammatory cells to cause either acute or chronic inflammation |
|
|
Term
| What are formylated peptides? |
|
Definition
| Peptides that have formylated Met as their first amino acid (hallmark of bacterial proteins!) |
|
|
Term
| When you compare vasoactive factors to direct vascular injury, what will you notice about the time period for the change in permeability? |
|
Definition
Vasoactive factors change permeability within a hour but then go back to normal
Injury will cause slower change but will last longer (think burn victims) |
|
|
Term
| Let's review immunology! What is emigration? |
|
Definition
| Passage of white blood cells through endothelium/microcirculation into injured tissue |
|
|
Term
| In acute inflammation, neutrophils come out first to help deal with the insults. What are the steps in the process of exudation? |
|
Definition
Margination - short vasoconstriction then vasodilation (think bradykinin, PAF)
Adhesion - stimulated by adhesion factors and cytokines
Emigration and chemotaxis- go towards stimulus!!
Phagocytosis and degranulation (oxygen dependent/independent killing)
Extracellular release of leukocyte products |
|
|
Term
| Chemical mediators come in a variety of flavors. Name the two big categories we can divide them into and the three subdivisions of each. |
|
Definition
Cells = cytokines, prostaglandins, and histamine
Plasma = complement, kinins, and clotting |
|
|
Term
| Describe in a general sense where cell mediators are made and what each class does. |
|
Definition
Cytokines made in cells = cause more inflammation (attract cells) and systemic effects (think fever)
Prostaglandins made in cells = cause more inflammation and pain
Histamine released from granules = cause vasodilation and increase permeability |
|
|
Term
| Describe in a general sense what plasma mediators do. |
|
Definition
Complement = increase permeability, attract inflammatory cells, and attack microorganisms
Kinins = increase permeability and cause pain
Clotting = coagulation |
|
|
Term
| Resolution of acute inflammation depends on what factors? |
|
Definition
Injury is limited or brief
Minimal tissue destruction
Tissue can regenerate |
|
|
Term
| How does resolution of acute inflammation occur? |
|
Definition
Remove/neutralize chemical mediators
Normalize vascular permeability
Stop leukocyte emigration
Clear edema, inflammatory cells, and debris via lymphatic drainage and macrophage digesting |
|
|
Term
| Sometimes you get a nasty scar after you've cut yourself. Why is this and what does it involve during the acute inflammation process? |
|
Definition
Tissue could NOT regenerate or there was tons of tissue destruction
Massive amounts of fibrinous exudates couldn't be absorbed so lots of connective tissue elements were laid down |
|
|
Term
| We get abscess formation when what infects us? |
|
Definition
| Pyogenic (pus-forming) bacteria or fungi |
|
|
Term
| What are three hallmarks of chronic inflammation? |
|
Definition
Mononuclear cells invade! (macrophages, etc)
Tissue is destroyed (inflammatory cells do this!)
Repair via new vessel proliferation and scarring |
|
|
Term
| What three general situations would you expect to find chronic inflammation in? |
|
Definition
Persistent infection of organisms with LOW pathogenicity causing delayed hypersensitivity (think TB)
Prolonged exposure to toxic agents (asbestos skank)
Autoimmune diseases (since body keeps making the antigens) |
|
|
Term
| What four cells would you expect to find in a wound that is chronically infected? |
|
Definition
Tissue macrophages- trying to chomp on debris and spewing out cytokines
T-Lymphocytes- stimulating more macrophages
Plasma cells- making antibodies
Eosinphils- dealing with nasty parasites and allergies (IgE response!) |
|
|
Term
| What steps occur during macrophage activation? |
|
Definition
1.) Chemokines are secreted by smooth muscle, monocytes, and fibroblasts (RANTES, MCP-1, MIP-1)
2.) Chemokines recruit and activate monocytes so they bind to VCAMS and ICAMS to migrate
3.) Lymphokines recruit and activate macrophages to increase their size, make them produce enzymes, and spew cytokines for local healing |
|
|
Term
| An activated macrophage spits out tons of IL-1 and TNF-alpha. What are some of the effects of doing this? |
|
Definition
Acute phase = fever, increase sleep, decrease appetite, cause muscle wasting, increase acute phase proteins, cause hemodynamic effects and neutrophilia
Endothelial effects = increase leukocyte adherence, PGI synthesis, PAF, pro-coagulant activity, and decrease anti-coagulant activity
Fibroblast effects = increase proliferation, collagen synthesis, collagenase, protease, and pGE synthesis |
|
|
Term
| Macrophages can also cause some nasty tissue damage. How do they do it? |
|
Definition
| Toxic oxygen metabolites, proteases, neutrophil chemotactic factors, coagulation factors, amino acid metabolites, and nitric oxide |
|
|
Term
| What things do activated macrophages deal with to cause fibrosis? |
|
Definition
| Increase growth factors (think TGF-beta), fibrogenic cytokines, angiogenesis factors, and remodeling via collagenases |
|
|
Term
| What are the three systemic manifestations of chronic inflammation? |
|
Definition
Fever- endogenous pyogens (IL-1 and TNF-alpha)
Leukocytosis- increase number of leukocytes
Acute Phase response- that feeling that you are sick (weakness, don't want to eat...) releasing C-protein and lectins from liver to start up complement |
|
|
Term
| What do eosinphil granules contain? |
|
Definition
| Major basic protein (MBP)- highly charged catonic protein that is deadly to parasites BUT also causes epithelial damage |
|
|
Term
| What are the two types of chronic inflammation? |
|
Definition
Non-specific inflammation- mononuclear cell infiltrate and proliferate fibroblasts and new blood vessels
Granulomatous inflammation- get collections of activated macrophages |
|
|
Term
| What basic things can cause granulomatous inflammation? |
|
Definition
Bacterial infection
Fungal infection
Parasitic infection
Inorganic metals/dust
Foreign body reactions
Diseases with unknown cause (think Crohn's disease) |
|
|
Term
| There are different flavors of granulomas. Name them and give a brief description. |
|
Definition
Epitheloid cells- in center with long, stringy nulcei
Giant cells- macrophages have fused together and now multinucleated
Caseating- epitheloid cells in center are all irregular and amorphous
Foreign body giant cells- near foreign materials in body with nuclei scattered haphazardly |
|
|
Term
| What is orofacial granulomatosis and what would you possibly see clinically? |
|
Definition
Non-specific granulomatous inflammation in orofacial tissue - diagnose via EXCLUSION
Possibly see chelitis granulomatosa (swollen lips), Melkersson-Rosenthal syndrome (swollen lips, fissured tongue, and facial palsy), or Intraoral sites with swelling, erythema, erosins, paresthesia, or pain |
|
|
Term
| When cells get hit with stress, they have to adapt in one of four ways. What are they? |
|
Definition
Atrophy
Hypertrophy
Hyperplasia
Metaplasia |
|
|
Term
| What two processes does the body use for tissue repair? |
|
Definition
Regeneration- use parenchymal cells
Replacement with scar- use connective tissue |
|
|
Term
| What are the three types of cells and which are able to renew? |
|
Definition
Labile cells- always renewing (think epithelium)
Stable cells- can renew if needed (think hepatocytes)
Permanent cells- NO RENEW (think neurons) |
|
|
Term
| In tissues with stable cells, what determines whether or not the tissue with regenerate? |
|
Definition
| Depends on potential to replicate NOT actual number of stead-state mitoses |
|
|
Term
| What two factors influence regeneration and what responses do they modify? |
|
Definition
Soluble factors (growth factors)
Insoluble factors (Laminin, fibronectin, collagens)
Influence cell growth, locomotion, contractility, and differentiation |
|
|
Term
| What do growth factors basically do? |
|
Definition
| Cause fibroblast proliferation, collagen synthesis, and provide blood and nutrients |
|
|
Term
| Let's review cell bio! What is the extracellular matrix (ECM) and why is it so important? |
|
Definition
| Network of crosslinked fibrous structural proteins and interstitial ground substance (remember collagens, elastins, and proteoglycans) to provide a substrate so cells can adhere, regulates movement, growth, and differentiation of cells in it --> MUST BE INTACT TO REPAIR INJURED TISSUE |
|
|
Term
| Let's review cell bio! What is the basement membrane, collagen, glycoproteins, and proteoglycans? |
|
Definition
Basement membrane- separated epithelial from endothelial and provides polarity
Collagen- give strength and support (triple helix!)
Glycoproteins- Linking ECM to cells and together (laminin, fibronectin, thrombospondins)
Proteoglycans- maintain ECM structure and permeability (bottle brush like) |
|
|
Term
| Let's review more cell bio! Name the five types of collagen discussed in Dr. Basile's lecture. |
|
Definition
Type I- principle in bone, skin, tendons, mature scars
Type II- cartilage
Type III- embryonic tissues, GI, blood vessels
Type IV- ONLY basement membranes
Types V-XXII- more basement membranes |
|
|
Term
| Which protein is the most abundant in the basement membrane? |
|
Definition
|
|
Term
| What are the four steps to scar formation/fibrosis? |
|
Definition
1.) Angiogenesis- make new but leaky vessels (always see edema)
2.) Migration and proliferation of fibroblasts- GFs control and promote
3.) Deposit ECM- at first only proteoglycans then only collagen (depends on tensile strength of wound)
4.) Maturation and organization of scar- make metalloproteinases and serine proteases to regulate (originally made as zymogens) |
|
|
Term
| What are the changes that occur in angiogenesis? |
|
Definition
1.) Basement membrane and ECM degradation and remodeling
2.) Cell migration
3.) Mitosis
4.) Capillary differentiation and anastomosis |
|
|
Term
| What are the steps in wound healing? |
|
Definition
1.) Induction of acute inflammation (after initial injury)
2.) Parenchymal cell regeneration (if possible)
3.) Migration and proliferation of parenchyma and CT
4.) Synthesis of ECM Components
5.) Remodeling of parenchyma and ECM to restore function and increase wound strength |
|
|
Term
| Over the course of two weeks, describe the typical wound healing process. |
|
Definition
Day of injury= make clot and increase fibrin, RBCS, and platlets
Day one= neutrophils come and phagocytosis happens
Day two= macrophages, lymphocytes, plasma cells, fibroblasts, and epithelial cells come
Up to a week = fibrin digestion of initial repair and inflammation complete *granulation tissue formed and epithelial proliferation and migration*
Two weeks= SCAR |
|
|
Term
| What are the phases of cutaneous wound healing? |
|
Definition
1.) Injury --> increase permeability to allow inflammatory cells to invade and then vasoconstriction follows
2.) Coagulation as platelets spew fibrin in wound
3.) Platelets attract PMNs and commence inflammation
4.) After 48 hrs, macrophages replace PMNs and release GFs to make collagen
5.) After 72 hrs, proliferation to make collagen
6.) After 3 wks, slow down collagen synthesis but continue crosslinking |
|
|
Term
| What happens in healing by primary intention? |
|
Definition
| Clean incision with approximated ends so more epithelial regeneration over fibrosis and LESS scar tissue |
|
|
Term
| What happens in healing by secondary intention? |
|
Definition
| Cell or tissue loss is massive so lots of granulation tissue and scarring with wound contraction (via myofibroblasts) |
|
|
Term
| What happens in healing by tertiary intention? |
|
Definition
| Must wait until an infection is resolved before performing tissue repair |
|
|
Term
| What factors influence wound healing? |
|
Definition
Local factors = wound type (size and location), vascular supply, infection, movement
Systemic factors = circulatory status, infection, metabolic status, malnutrition |
|
|
Term
| What complications can arise from wound healing? |
|
Definition
Deficient scar formation - leads to dehiscence and incisional hernias or ulceration
Excessive scar formation
Excessive contraction |
|
|
Term
|
Definition
Firm, rubbery lesions that are usually darkly colored
Occur after trauma and may be itchy
Can be on earlobes after piercing |
|
|
