Module 3 Flashcards

Question

What does it mean when you find a large number of neutrophils at a site of injury? - Acute reactions? - After 2-3 days - Normal life span of macrophages? pH?

Answer 1

It is a major histological feature of acute inflammation In most acute reactions, neutrophils appear first and are followed by macrophages - This is due to their greater mobility and also because there are many more neutrophils than monocytes in the circulation After two or three days, macrophages begin to outnumber neutrophils in most inflammatory reaction sites (an exception to this would be in those instances in which the injurious stimulus continues to operate) The normal life span of macrophages is much greater (months to years) versus the life span of an average neutrophil (2-4 days) - Also, macrophages are relatively resistant to the lower pH (acidity) which is found at inflammatory sites.

Answer 2

The process of ingestion of particulate matter, i.e., bacteria, foreign debris, by the cell - It literally means "cell eating" - It may be regarded as the culmination of an inflammatory reaction

Answer 3

Neutrophils and macrophages | - Eosinophils

Answer 4

Lymphocytes and plasma cells

Answer 5

1) Debris 2) Inflammatory 3) Site 4) Removed 5) Macrophages 6) Lymphatics

Answer 6

1. Recognition and attachment (may be mediated by opsonins). 2. Engulfment (pseudopods flow around organisms/particle with complete enclosure followed by fusion with lysosomal granules resulting in a phagolysosome; requires the presence of calcium and magnesium). 3. Killing and/or degradation (Lysosomes then fuse to the sack and release their enzymes directly into this sack or vacuole).

Answer 7

Most micro-organisms are not recognized until they are coated by naturally occurring serum factors called opsonins. These are substances which coat bacteria and render them more susceptible to phagocytosis. They are usually immunoglobulins (e.g., IgG) or complement fractions (e.g., C3b). The opsonized particles attach to two receptors or PMNs or macrophages: - a receptor for the Fc fragment of IgG (to react with the IgG opsonin) and - a receptor to C3b (to react with C3b opsonin)

Answer 8

Pseudopods flow around organisms with complete enclosure followed by fusion with lysosomal granules resulting in a phagolysosome - While this takes place, leakage of enzymes and metabolic products (H2O2) from the leukocyte into the extracellular space occurs, thus increasing the tissue damage - This process of engulfment requires the presence of calcium and magnesium and is associated with calcium transport across the plasma membranes - The Ca acts as a second messenger to initiate the cell events in the microfilaments and microtubules, culminating with engulfment - The biochemical events involved in phagocytosis are somewhat similar to those of chemotaxis; it is associated with receptor-ligand binding, phospholipase with activation and there is an eventual increase in Ca in the cytosol

Answer 9

The killing of microbes and the destruction of ingested materials are accomplished by reactive oxygen species (ROS, also called reactive oxygen intermediates), reactive nitrogen species, mainly derived from nitric oxide (NO), and lysosomal enzymes. this is the final step in the elimination of infectious agents and necrotic cells

Answer 10

With phagocytosis, there is a burst in oxygen use - The surge of oxygen consumption results in production of ROS (reactive oxygen species) such as H2O2 - Hydrogen peroxide is inefficient at killing microbes by itself but can be converted to OCl● (hypochlorite) via the enzyme MPO (myeloperoxidase) - Hypochlorite is a very efficient killer of microbes. It can also be converted to ●OH (hydroxyl radical) via an MPO-independent reaction - The hydroxyl radical is also a powerful destructive agent

Answer 11

H+ ion from increased lactate and from action of carbonic anhydrase produces a marked reduction of intravacuolar pH, which is bactericidal - Substances from leukocyte granules are also bactericidal (e.g., BPI, lysozyme, lactoferrin, major basic protein, defensins, granules with enzymes); most of these substances induce injury by increasing the membrane permeability of the microbe

Answer 12

1. In most instances, the material is destroyed - For example, bacteria may be destroyed and digested by the lysosomal enzymes within the neutrophil or macrophage 2. However, in some cases, it is the white blood cell that may be destroyed by the foreign particle - For example, a particularly virulent bacteria may cause death of the ingesting cell 3. A third possibility is that the organisms may survive for some time within the macrophages - For example, this occurs in cases of tuberculosis in which the tuberculous bacillus remains viable within macrophages for many months or even years and movement of the macrophage through the lymphatics to the lymph nodes actually results in the spread of infection

Answer 13

Chemical mediators direct the vascular and cellular events in acute inflammation. General principles are as follows: a. Mediators are produced locally by cells at the site of injury (cell-derived vasoactive mediators), or may be circulating within the plasma (plasma derived vasoactive mediators). b. Most mediators induce their effects by binding to specific receptors on target cells. c. Mediators may stimulate target cells to release secondary effector molecules. d. Mediators may act on only one or a very few targets, or they may have widespread activity; there may be widely differing outcomes depending on which cell type they affect. e. Mediator function is generally tightly regulated. f. A major reason for the checks and balances is that most mediators have the potential to have harmful effects.

Answer 14

a) This is the major mediator in the early phases of the acute inflammatory reaction. Histamine acts via H-1 type receptors present in vascular endothelium. Effect is short- lived (< 60 minutes) - Major source is mast cells - these are ubiquitous throughout the body and occur in connective tissue often adjacent to blood vessels - Histamine is contained within granules of the mast cell (and also found in granules of basophils and platelets). - When mast cells are injured or appropriately activated, they degranulate, i.e. contents of the granules are released - Serotonin is present in platelets only - In humans, serotonin probably has little role. Mast cells degranulate in response to: 1. Physical injury - trauma, cold, heat, irradiation. 2. Immunological process - immune complexes, via receptors for IgE 3. Fragments of the complement system - C3a and C5a (anaphylatoxins) 4. histamine releasing factors from PMNs, monocytes and platelets. 5. interleukin-1 Has two major functions: 1) Dilatation of arterioles (vasodilatation). 2) Increased vascular permeability in venules.

Answer 15

b) They are derived from cell membrane phospholipids. - Release of arachidonic acid by phospholipase (lysosomes) is induced by mechanical, chemical and physical stimuli - The end products are prostaglandins and leukotrienes - Prostaglandins produce vasodilatation and increased permeability - Leukotrienes increase permeability and have chemotactic activity

Answer 16

is generated by stimulation of practically all inflammatory cells, endothelial cells and damaged tissue cells. In addition to being a powerful vasodilator, it also increases permeability. Other functions include: stimulation of platelets, inflammatory cells and endothelial cells. It is best known for its ability to produce aggregation of platelets at the site of injury. It also has chemotactic functions.

Answer 17

Kinin system - is activated by stimulation of the plasma kinin cascade from precursor (high molecular weight kininogen) - The ultimate result is bradykinin which is the active kinin. Bradykinin when released: - Increases vascular permeability - Produces contraction of smooth muscle - Vasodilatation - Produces pain It acts on endothelial cells to increase gaps and it is inactivated by kininases (in plasma and tissue) - Like histamine, the effects of bradykinin are transitory and are most important during the early phases of inflammation

Answer 18

In brief, complement consists of at least 20 different proteins (including their cleavage products) circulating in the blood - Upon activation of the system - for example, by contact with antigen-antibody complexes (classic pathway) or by- products released by bacteria or by components of other plasma protein systems (alternative pathway) various by-products of complement are released - The complement system is a non-specific self defense mechanism - The complement system is the most important of the plasma protein systems of inflammation; its components participate in practically every aspect of the inflammatory response. Activation of components C1 --> C5 produces subunits that enhance inflammation by - opsonizing bacteria (C3b) - attracting leukocytes (chemotaxis) - C5b, 6, 7 complex, C5a - by acting as mast cell activators causing degranulation and histamine release (C3a, C5a) - Components C6-->C9 create pores in the bacterial walls producing an influx of ions and fluid into bacteria which subsequently bursts.

Answer 19

The clotting (coagulation) system forms a fibrinous exudate or meshwork at the inflamed site to trap cells, microorganisms and foreign bodies - This prevents the spread of infection and inflammation into the surrounding tissues; keeps cell debris, bacteria and foreign bodies at the site of greatest phagocytic activity; and forms a clot that stops the bleeding and provides a framework for repair and healing - The main substance of this mesh is an insoluble protein called fibrin which is the end product of the coagulation cascade

Answer 20

1. Redness or rubor - vasodilatation and congestion of blood vessels by chemical mediators (PGs). 2. Swelling or tumor - exudation of fluid / edema (increased vascular permeability) and cells. Mediated by vasoactive amines: C3a and C5a, bradykinin, leukotriene C, D, E 3. Heat or calor - mechanisms for this are poorly understood; however, greater blood flow to the region may be a contributing factor. increased metabolic rate? 4. Pain or dolor - direct pressure upon nerves by the edema fluid. Also signaling of the neural system by chemical mediators (bradykinins, histamine, serotonin, and prostaglandins). 5. Loss of function (functio laesa) - secondary to reflex inhibition of muscular movements associated with pain. Also, mechanical disability may be produced by the swelling and pain.

Answer 21

To this point, only the local changes at the site of an injury have been discussed. In severe inflammatory reactions, however, there may be changes that involve the entire body. 1. Fever - this is probably the result of release of factors from white blood cells or from microorganisms (pyrogens) that act directly on the temperature regulating centre in the hypothalamus. - Examples: bacterial, chemical, endogenous (from PMN and Examples: bacterial, chemical, endogenous (from PMN and other phagocytes). Now there is evidence that prostaglandins are mediators of fever - Fever increases the metabolic rate and theoretically has a beneficial effect - Extreme high temperatures are lethal (denature proteins). 2. Leukocytosis - an increase in the white blood cell count above normal levels (i.e. greater than 10,000 per mm). Increased production and release of WBC from and by the bone marrow - In acute inflammatory responses, the leukocytosis is the result generally of an increase in the number of neutrophils - In addition, one will see increased numbers of immature neutrophils in the circulating blood - In a chronic inflammatory reaction, one is more likely to have a lymphocytosis (i.e. absolute increase in numbers of lymphocytes) - In allergic conditions, an eosinophilia is frequently seen 3. Other - malaise, anorexia, sleepiness, etc.

Answer 22

The basic pathophysiologic and morphologic changes follow a fairly regular progression and occur in a predictable sequence in inflammation; the ultimate character, extent, severity and duration of the tissue changes are dependent upon many factors relating to the host, the injurious agent and the clinical intervention. - Accordingly, certain inflammations are short-lived or protracted, they may be characterized by an exudate reflecting the etiological agent or they may be of a certain special form because of the location. Thus, inflammations are usually classified according to: • Duration • Predominant type of the exudate formed • Location in which they take place, and special forms.

Answer 23

All three categories are descriptive of every inflammatory reaction, since all have in common: duration, some type of exudation and location - Therefore, inflammations do not fall into only one of these categories, but rather can be described fairly specifically in all three terms.

Answer 24

No sharp line of division exists between these forms - An acute inflammation may subside or may persist and become chronic - Not all chronic inflammation begins as an acute inflammation - A low- grade stimuli or organisms of low toxicity may incite a chronic reaction without ever arousing a full blown acute response - Clinically the difference between acute and chronic inflammation is purely one of duration; chronic inflammation lasts two weeks or longer, regardless of the etiology - Chronic inflammation is sometimes preceded by an unsuccessful acute inflammatory response (i.e. foreign bodies) - Chronic inflammation can also occur without evidence of preceding acute inflammation (i.e. tuberculosis)

Answer 25

- In a clinical sense, acute inflammation is usually of sudden onset and accompanied by one or more of the cardinal signs. It also generally lasts a matter of hours or days; Acute reactions occur when the injury is transient, e.g. physical trauma, burn, or an infection in which the organism is rapidly eradicated by the body's defense mechanisms. - In a pathological sense, acute inflammation has, as its dominant morphological changes, the vascular and exudative changes described, i.e. exudation of fluid and accumulation of cells; The cellular infiltrate contains numerous neutrophils = exudative inflammation.

Answer 26

Chronic Inflammation: This results from an injurious agent which persists in the tissues and continues to cause damage often for weeks or months, e.g. foreign body (wood splinter) which remains in the tissue, organisms which are not eradicated.

Answer 27

1) Evolution of acute to chronic inflammation: This occurs characteristically in certain infections - An acute inflammation becomes chronic when it can not be resolved (etiologic agent persists, impairment in normal healing, etc.) So, there are chronic inflammations with persisting acute disease (peptic ulcer disease) The inflammatory reaction with chronicity takes on two new facets: i. A proliferation of connective tissue (predominantly fibroblasts) and vessels (angiogenesis) . ii. Local increase in macrophages, lymphocytes and plasma cells. Chronic inflammation without any recognizable acute phase: - This occurs with low grade injuries, such as with organisms of relatively low virulence - An example of this is the inflammatory reaction to the tubercle bacillus which rapidly passes through an acute pattern; exposure to non-degradable material (dusts); autoimmune reactions (rheumatoid arthritis) - While the acute inflammation was characterized by vascular and exudative features (microscopic) and cardinal signs grossly, in chronic inflammation there is great amount of proliferation of cells and connective tissue, while exudation is less conspicuous (lymphocytes, plasma cells)

Answer 28

The chronic inflammatory pattern described above (mononuclear cell infiltrate, connective tissue response) is described as being of a non-specific pattern - A special form of chronic inflammation is granulomatous inflammation: - This is a characteristic response seen in some infections such as tuberculosis, syphilis and some fungi, as well as in foreign body inflammatory reactions - This form of chronic inflammation is characterized by the presence of granulomas (a nodule, a grain- like body or a tiny 'tumor') - A granuloma may perhaps be best described as a well-circumscribed collection of epithelioid macrophages - They are termed epithelioid because they resemble epithelial cells, i.e. they have abundant eosinophilic cytoplasm - In addition to the collection of these cells, other elements are usually present in a granuloma - There may or may not be a central focus of necrotic debris (this feature is especially prominent in tuberculosis). - Often multinucleated giant cells are present and these are very helpful in recognizing a granuloma - The giant cells represent epithelioid macrophages which have fused their cell borders resulting in one large multinucleated cell. - Often, giant cells form around foreign bodies when the foreign particles are too large to be engulfed (phagocytosis) by a single macrophage - An outer rim of lymphocytes and plasma cells is also frequently seen around many granulomas. Granulomatous inflammations - characteristic tissue reactions in some infections (tuberculosis; syphilis; cat-scratch disease; fungal; protozoan); in persistent foreign body inflammations (foreign body granuloma; pneumoconioses), in rheumatic fever (Aschoff body); in rheumatoid arthritis (subcutaneous nodules) and in some diseases of unknown etiology (sarcoidosis, granuloma annular of skin). - Some granulomatous inflammations are sufficiently characteristic for a consideration of a given disease, but the demonstration of the specific agent is necessary for the ultimate diagnosis.

Answer 29

1) Serous: usually due to mild injuries - characteristically derived from secretions of serosal mesothelial cells (pleural, peritoneal, pericardial and synovial) - Examples: blister from burns of skin; pulmonary TB (effusion into pleural space = pleuritis, serous); in early phase of bacterial infections. In tissues: identified with difficulty (abnormally dilated spaces; fine precipitate of protein). 2) Firbrinous: characterized by the presence of fibrin (derived from leakage of fibrinogen from blood vessels) - seen in more severe inflammations in which the greater degree of increased vascular permeability allows the escape of larger plasma proteins such as fibrinogen - Examples: in rheumatic fever ("bread and butter" pericarditis) in pneumococcal pneumonias. In tissues: easily identifiable because the precipitated fibrin is deeply acidophilic; in strands and bands, in part fibrillar - Observed in acute inflammatory but also in active zones of chronic inflammatory process - Fibrin can be removed (fibrinolysis) or may get replaced by fibrous tissue scar 3) Suppurtive/Purulent: a type of liquefactive necrosis caused by pyogens (pus-producing bacteria); large amount of pus, i.e. fluid containing neutrophils and liquefied tissue debris and bacteria is seen. Pus = protein-rich fluid containing viable and necrotic neutrophils and tissue debris partially liquefied by proteolytic enzymes. Also see abscess and empyema - characteristically seen in certain infections, e.g. staphylococcus, pneumococcus, meningococcus, gonococcus, E coli, some non-hemolytic streptococcus. - Example: acute appendicitis (see Case Study) In tissue: recognized by pools of numerous PMNs (viable and dead).

Answer 30

1) Abscess: Is a localized collection of pus caused by suppuration (= formation of visible pus) in a tissue or organ - It is caused by an irritant of great intensity (staphylococcus; turpentine) that characteristically remains localized leads to outpouring of great numbers or polys; the locally liberated large amounts of trypsin overcome the tryptic inhibitor of the serum (difficulty in permeating solid tissues); the trypsin digests damaged and dead tissues and converts it into a semisolid mass 2) Empyema: is a localized collection of pus in the pleural cavity. 3) Ulcer: is a local defect or excavation of the surface of an organ covered or lined by an epithelium (mucous membrane; epidermis); produced by sloughing of inflammatory necrotic tissue on or near the surface.

Answer 31

1. Complete resolution. 2. Healing by connective tissue replacement (scarring, fibrosis). 3. Progression to chronic inflammation.

Answer 32

The components of the reaction that tend to neutralize, destroy and eliminate the injurious agent 1) removal of exudate - Removal of exudate and cellular/tissue debris were discussed at various points in the inflammatory process (e.g. phagocytosis). 2) removal of cellular and tissue debris 3) replacement of cells and tissues lost

Answer 33

a. Regeneration: Term used if the cells (or tissue) replacing those lost in inflammation are identical or very similar. b. Repair: is a broader term; it includes the process of replacement by cells and tissues, either of the same kind as those lost, or of a different and often simpler type.

Answer 34

Is much better developed in lower animals, and in protozoa and metazoa represents the major feature of reaction to injury Physiological regeneration (replacement) in humans: - epidermis - blood - uterine mucosa - glandular epithelium There is great variation in the ability of different kinds of cells and tissues to regenerate: - supporting tissue regenerates best (connective tissue - fibrous, osseous, cartilage, blood vessels; epithelium - epidermis, renal tubular, glandular, intestinal, uterine); epithelial usually regenerate well. - other cells lose their ability to regenerate in postnatal life (muscle, nerve require replacement by simpler tissue). Atypical regeneration of an organ - in an organ, restoration depends not only upon the parenchymal tissue's ability to regenerate, but also whether or not the framework was destroyed (e.g. in the skin: no sweat + sebaceous glands or hair; in liver: when architectural skeleton destroyed regeneration is irregular producing afunctional tissue - cirrhosis). Regeneration of organs in mammals - liver and lung best - also kidney and spleen (accessory splenic tissue)

Answer 35

Repair may begin shortly after injury and overlap with the vascular and cellular phenomena of inflammation. Repair often consists of variable proportions of 2 distinct processes: regeneration and scarring (i.e. laying down of fibrous tissue), the latter occurring because the extracellular matrix has been damaged by the inciting injury Components of the extracellular matrix (ECM): a) Structural proteins (e.g. Collagen, elastin) - E.g. Collagen: 18 types. Of the five major types, types I, II, and III are fibrillary while types IV and V are amorphous. Digested by collagenases and metalloproteins - E.g. elastic fibers: Consist of two components, elastin (amorphous) and elastic microfibril (fibrillary). Digested by elastases. b) Adhesive glycoproteins - Mediate cell attachment to the matrix - E.g. fibronectin: Gylocoprotein which associates with cell surfaces, basement membrane, matrix - E.g. laminin: Glycoprotein which is a component of the basement membrane and mediates attachment of epithelial cells to type IV collagen. c) Glycosaminoglycans, proteoglycans and hyaluronic acid - Possibly responsible for orientation of collagen fibers

Answer 36

1. Control of cell proliferation | 2. Collagenization and acquisition of wound strength

Answer 37

The cells of the body are divided into three groups on the basis of their regenerative capacity: 1) Labile: continue to proliferate throughout life (e.g. epithelium, blood cells). Follow cell cycle from one mitosis to the next. 2) Stable: low normal level of replication but able to divide in response to stimuli (e.g. parenchymal cells of glandular organs, mesenchymal cells, hepatocytes, etc.). Considered to be on G0 but recruited to G1. 3) Permanent: cannot divide in postnatal life (e.g. neurons of CNS). Have left the cell cycle. Growth is best accomplished by recruitment of G0 cells into the cell cycle. This takes place by the action of:  Growth or stimulatory factors  Loss of a growth inhibitor normally present (negative feedback)  Cell-cell or cell-matrix interactions All three are probably in effect at any given time.

Answer 38

Well-known hormones: estrogens, progesterone, somatotropin, insulin. Current areas of research in circulating growth factor include a variety of polypeptides: epidermal growth factor (EGF), fibroblast growth factor(bFGF), platelet-derived growth factor (PDGF), vascular endothelial growth factor (VEGF), interleukins I and II (lymphocyte proliferating factors), TNF, tumour- induced growth factors (sarcoma growth factor), nerve growth factors, macrophage-derived growth factors. - Essentially they are all mitogenic

Answer 39

Tissue culture experiments with cessation of proliferation most likely due to "contact inhibition". - This also is now known to be "density dependent".

Answer 40

Cells have receptors that recognize extracellular matrix. - These receptors (transmembrane glycoproteins) interact with cell cytoskeleton. One group of such receptors is called "integrins". - They are a large family and include: Fibronectin receptor, platelet surface receptors, and leukocyte adhesion molecules. - Integrins recognize specific AA sequence.

Answer 41

It involves the proliferation of endothelial cells, fibroblasts and deposition of collagen in wounds. When the injury is severe or persistent and there is damage of parenchymal cells and stromal framework, healing cannot occur by regeneration alone. - Non-regenerated parenchymal cells are initially replaced by proliferating fibroblasts and endothelial cells. - By 3-5 days, granulation tissue is established. - Granulation tissue is pink, soft, granular and painless. - Histologically, it is a mesh of capillaries, fibroblasts, inflammatory cells and extracellular matrix (ECM). - This tissue acts like a scaffold on which the final scar will form. - With time, the cells will diminish, the capillaries will disappear and an increasing amount of connective tissue (scar) will be laid down.

Answer 42

1. Angiogenesis: new vessels form by budding from pre-existing vessels - These newly formed vessels are immature and therefore leaky (incompletely formed intercellular junctions), thus the edematous appearance - Chemical mediators responsible for angiogenesis include: VEGF and bFGF - They bind to the proteoglycans of the basement membranes and are released when they are damaged. 2. Fibrosis: by proliferation of site fibroblasts and deposition of ECM by these cells. - Again, this process is dependent on various growth factors released by inflammatory cells. 3. Maturation and organization of the scar (remodeling): collagen and other ECM are degraded by a family of metalloproteinases (zinc-dependent). - They cleave fibrillar collagen types I, II and III as well as collagen IV and fibronectin. - They are produced by inflammatory cells as well as by some epithelial cells. - They aid in the debridement of the injured site and the remodeling of the connective tissue.

Answer 43

Is the most common protein in animal world - Is a family of molecules (18 types) There are five major types of collagen according to biochemical composition: - types I, II & III are fibrillary - types IV & V are amorphous Collagenases (produced by fibroblasts, macrophages, PMN, synovial cells, some epithelial cells) - metalloproteins Types IV and V collagen, along with laminin, fibronectin and heparin sulfate proteoglycan are components of the basement membranes.

Answer 44

"Most wounds involving skin, fascia or tendon never regain initial strength of tissue derived." (70-80% of tensile strength achieved at 3 months). - Why? Probably related to the type of collagen laid down and its organization. Adult skin -- collagen type I Granulation tissue -- collagen type III Cicatrization -- replacement of type III by type I

Answer 45

Repair of dermal wounds is a good example of a repair process; similar events take place in the healing of ulcers; repair in tuberculous cavities of lung; repair of abscesses in liver and kidneys; following trauma, etc.

Answer 46

Provides a quick provisional closure to the wound - after hemorrhage has ceased, the wound is covered by coagulated blood which dries and hardens = crust or scab It is useful in two ways: - it stops further leaking of blood - it is a barrier to infection Thus, the crust effects a provisional closure of the wound; it forms only if: - blood is available (i.e. if vessels present and damaged) - conditions permit drying There is no crust formation in the cornea (why?) and uterine mucosa (why?)

Answer 47

Following injury, a large mass of dead tissue remains in contact with living parts; the dead tissue may be removed by sloughing (falling-off): the inflammatory response of the surrounding living tissue initiates the process of repair ---> a zone of demarcation being formed ---> slough loses continuity with living tissue. 23 - small amounts of dead tissue, debris and exudate are removed by liquefaction and phagocytosis (discussed in previous module - Inflammation) and by lymphatics.

Answer 48

takes place largely by two processes: - cell migration - cell division (proliferation) the cells swell and reassume embryonal properties in skin wounds, three kinds of cells proliferate and migrate: - fibroblasts - endothelium (migrates in arcs and after a lag period = angiogenesis) - epithelium (migrates in sheets) - the direction of fibres formed is determined by tissue tension new tissue containing proliferating cellular and extracellular components is thus formed to replace the loss; it is termed: granulation tissue (N.B.: Quite different from granuloma!) To the naked eye it appears as an aggregation of tiny pink granules; these consist of: - newly formed capillaries - fibroblasts elaborating connective tissue (extracellular) - many macrophages the granulation tissue has the following properties: - it bleeds freely (if slightly touched) - it is insensitive to pain (no nerves are present)  it is quite resistant to infections.

Answer 49

- in order to migrate (in sheets) it requires a substratum (granulation tissue/fibronectin). - when there is no defect in the underlying mesenchyme, migration is immediate (in cornea, completion in 6 hrs) - in larger skin wounds, it passes between the scab (crust) and the granulation tissue - the scab then drops off

Answer 50

Is the conversion of granulation tissue to scar (via gradual closing of small vessels)

Answer 51

May form in repair following injury and inflammation of serous membranes (fibrous "connections" between two serosal surfaces) i.e. after abdominal surgery.

Answer 52

Tepresents a post-traumatic repair / connective tissue proliferation in the dermis that exceeds "above and beyond" the amounts necessary - Grossly, it is a red (or pigmented), raised and firm lesion with sharp, often irregular outline and a smooth, shiny surface. - Microscopically, the epidermis and the subjacent dermis are normal but there are no skin appendages - The actual lesion consists of irregularly arranged, broad, homogenous, hyalinized and, at times, basophilic collagen fibres - There is a moderate increase in the number of fibroblasts and capillaries; both "disappear" in an "aging" lesion - About 10% of normal people develop keloid scars.

Answer 53

- the "type" of repair that follows when the edges of the wound are in apposition - the wound is superficial, involving only the epidermis and the dermis remains intact; there will be no bleeding; the repair takes place actually via regeneration of the epithelium; the epithelial cells migrate across the cut (wound) and may replace it in one day. - when cut deeper into the dermis, with a few capillaries cut ---> few drops of blood which "cement" the edges of the wound, thus, no wound retraction; a few fibroblasts and endothelial cells migrate ---> practically no scar. - in deeper cuts when retraction present: surgeon may approximate the edges with sutures.

Answer 54

when there is a considerable loss of tissue and the edges of wound cannot be approximated. - this kind of healing proceeds through replacement of the lost tissue by granulation tissue ---> scar - we distinguish several stages of wound closure (rate of wound closure): - latent period (size of wound does not change; one to several days) - period of contraction (probably results from shrinkage of the granulation tissue ---> edges are pulled together) - epidermization (later in the process than contraction). - When wound edges are apart more than 20-25 mm, migration of epithelial cells ceases; it requires skin grafting.

Answer 55

Local - Decreased blood supply - Denervation - Local infection - Foreign bodies - Necrotic tissue - Mechanical stress - Hematoma - Increased size of the wound Systemic - Decreased blood supply - Age - Anemia - Malignancy - Malnutrition - dietary status (Vit C, Vit D, protein intake) - Obesity - Presence of diabetes - Infection - Organ failure

Answer 56

- Protect the wound. - Prompt irrigation. - Immobilize the injured area (rest + immobilization). - Avoid manipulation. - Drainage of exudate and pus. - Administration of antibiotics in infections. - Noxious materials removed (excision of devitalized tissues = debridement). - Control of bleeding and removal of excessively clotted blood. - Judicious use of suture material. - Preserve blood supply; no tight dressing. - Elevate affected parts to help drain. - Apply appropriate thermal modification (be certain when cold and when heat application) . - Maintain optimal nutritional status for a given age.