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72 Cards in this Set

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Q: What is inflammation?
-a complex reaction to injurious agents such as microbes and damaged, usually necrotic, cells that consists of vascular responses, migration and activation of leukocytes, and systemic reactions
-it is unique in that there is a reaction of blood vessels, leading to the accumulation of fluid and leukocytes in extravascular tissues
Q: What is the purpose of inflammation?
-is closely intertwined with the process of repair, serves to destroy, dilute or wall of the injurious agent and it sets into motion a series of events that try to heal and reconstitute the damaged tissue
-is a protective response, the ultimate goal of which is to rid the organism of both the initial cause of cell injury and the consequences of such injury, without inflammation, infectious would go unchecked
Q: What are the main components of the inflammatory response?
-a vascular reaction and a cellular reaction, circulating cells include neutrophils, monocytes, eosinophils, lymphocytes, basophils and platelets
-the vascular and cellular reactions of both acute and chronic inflammation are mediated by chemical factors that are derived from plasma proteins or cells and are produced in response to or activated by the inflammatory stimulus
Q: What medications are given to patients with inflammation?
-For pain relief from various mild injuries you will give some of your patients Advil and Aspirin. These are anti-inflammatory drugs and work, in part, because inflammation is a part of trauma and almost any cell injury.
Q: What are the different types of inflammation?
-Usually, inflammation is broken down into acute and chronic. Many conditions show both acute and chronic inflammation occurring together.
Q: Describe acute inflammation.
-is rapid in onset (seconds or minutes) and is of relatively short duration, lasting for minutes, hours or a few days
-main characteristics are the exudation of fluid and plasma proteins (edema) and the emigration of leukocytes, predominately neutrophils
Q: What cell types are associated with acute inflammation.
-Histologically, acute appendicitis shows neutrophils in the mucosa, the wall (submucosa and muscularis), and the serosa. So, neutrophils are usually the predominate inflammatory cell during the first 6 to 24 hours. After this they are gradually replaced by monocytes (histiocytes or macrophages) and lymphocytes in 24 to 48 hours.
Q: Describe chronic inflammation.
-is of longer duration and is associated with lymphocytes, proliferation of blood vessels, fibrosis and tissue necrosis
-This is considered to be inflammation of prolonged duration (weeks or months). In active chronic inflammation, tissue destruction (the DOWN side of chronic inflammation) and attempts at repair are all simultaneously happening.
Q: What cell types are associated with chronic inflammation.
-an inflammatory reaction may continue the process and turn into chronic inflammation. Here, the predominate cell is the lymphocyte. For example, histologically in rheumatoid arthritis, a chronic inflammatory disease, there are numerous lymphocytes in the synovium.
Q: What are the characteristics of chronic inflammation?
1. Mononuclear cells, which include macrophages, lymphocytes and plasma cells.
2. Tissue destruction. This is caused by the persistent inflammatory cells, lymphocytes and macrophages. Although neutrophils are not the predominate cell in chronic inflammation, they can be present and they can contribute to the destruction. Macrophages are going to directly or indirectly contribute to the tissue destruction.
3. Attempts at healing by scarring and fibrosis.
Q: Are there exceptions to the classification of acute or chronic inflammation?
-There are exceptions to these generalizations. For example, in many acute viral infections the predominate cell is the lymphocyte. In cases of acute viral encephalitis lymphocytes are the predominate cell. One reason is that there is a major immunoloical response to many viral infections.
Q: Case #1. A patient sustains a cut on her arm. A few days later it is red, swollen, painful and tender. She gently squeezes this wound and a little purulent fluid (pus) oozes from the wound. So, this is an infected wound. Culture may show bacteria such as streptococcus or staphylococcus. What would a biopsy of this wound show?
-Lots of neutrophils in the dermis. Blood vessels would be dilated and this is the reason for the redness. It’s also the reason why the wound is warm to your touch. This vasodilation leads to increased vascular permeability, which allows a protein-rich fluid to flow between the cells and the collagen fibers of the dermis. This is called edema fluid and is present in almost every inflammatory process.
Q: Is this patient in pain? Is there swelling?
-With this increased amount of fluid, dilated blood vessels and increased numbers of neutrophils, this area of inflammation is swollen. It is PAINFUL because the nerves in this area are stimulated by the swelling and the inflammatory cells and their products.
Q: What made the neutrophils migrate to this area of infection?
-If there are no defenses, the bacteria would proliferate and cause lots of cellular injury and tissue damage. Cells are needed to ingest these bacteria, kill them, degrade the necrotic tissue and begin tissue repair. Neutrophils can do all of this. When the bacteria first invade the local tissues the resident cells secrete chemokines, which are a type of cytokine. These help activate local endothelial cells.
Q: What is the purpose of endothelial cells in this migration?
-The endothelial cells then express, on their surface, adhesion molecules called E-selectin. Neutrophils are already flowing in the blood and are displaced by erythrocytes to the sides of blood vessels. This is called margination.
Q: What types of proteins do neutrophils express that help in their migration?
-Neutrophils constitutively express L-selectin (L for leukocyte). When L-selectin interacts with E-selectin, the neutrophil slows and begins “rolling” along the endothelial cell lining. The selectin to selectin interaction and secreted chemokines from endothelial cells stimulate the neutrophil to express another adhesion molecule called an integrin. Specifically, it is LFA-1 and this interacts with intercellular adhesion molecule-1 (ICAM-1) on the endothelial cell and this “firmly” attaches the neutrophil to the endothelium. Now the neutrophil is ready for transmigration.
Q: Describe transmigration.
-Most of the time this happens near an endothelial-endothelial junction. Using an adhesion molecule called PECAM (platelet endothelial cell adhesion molecule) which is expressed along the junction—pore channel, the neutrophil squeezes between the endothelial cells and into the extracellular space. This takes about 15 seconds. Then, by a process called chemotaxis, the neutrophil moves to the bacteria.
Q: What happens in leukocyte adhesion deficiency type 1?
-In leukocyte adhesion deficiency type 1 there is a congenital defect in the synthesis of LFA-1 molecules. What may be a clinical consequence of this? There would be impaired neutrophil adhesion to blood vessels with recurrent bacterial infections. There is also impaired wound healing.
Q: What happens after the neutrophil arrives at the site of bacterial infection?
-Once the neutrophil arrives at the bacterial in the above infection, it has to engulf them to kill them. This process is called phagocytosis. The neutrophil needs to recognize the bacteria to make an attachment. Host molecules, called opsonins, facilitate this.
Q: What are the two important opsonins?
-Two important opsonins are IgG antibodies (the Fc portion) and complement (the C3b fragment). Both of these attach to the outer bacterial wall. The neutrophil then attaches to these.
Q: What happens to the neutrophils after they attach to the outer bacterial wall?
-Cytoplasmic pseudopods flow around the bacterium creating a vacuole (a sac) called the phagosome. This is engulfed into the cytoplasm. Next, specific or azurophil granules of the neutrophil fuse with the phagosome (forming a phagolysosome) and release their contents, one of which is myeloperoxidase (MPO). Hydrogen peroxide is made within the phagolysosome. H2O2 plus the MPO plus a chloride ion combine to form HOCl (a compound found in household bleach). This kills the bacteria by halogenation or oxidation of its proteins and lipids.
Q: What is another important killer compound in the phagolysosome?
-Another important killer compound with the phagolysosome is the free radical superoxide. O2*(superoxide) is generated by NADPH. After the organism is killed it is degraded by phagolysosomal hydrolases. Once neutrophils complete phagocytosis they undergo apoptosis and are ingested by macrophages or cleared by the lymphatics.
Q: What else is found in phagolysosomes?
-Within the phagocysosome are some potent compounds-hydrolases, H2 O2¬, oxygen free radicals, etc. If these react with the surrounding cells, tissue damage will occur. And this is what occurs if the inflammation is unchecked or persistent. “Regurgitation during feeding” occurs when the phagosome does not completely close and some of its contents spill outside the cell.
Q: Describe frustrated phagocytosis.
-“Frustrated phagocytosis” occurs when the phagosome membranes cannot physically close around the material to be engulfed with release of its contents to the outside. One example of this is when immune complexes attach to the glomerular basement membrane this stimulates neutrophils to try and engulf them. But the membrane is a flat surface, the pseudopodia cannot extend around the complexes and the phagosome releases its contents outside the neutrophil and local tissue damage occurs.
Q: What are some examples of inherited defects in the phagocytic process?
-There are many inherited defects in the phagocytic process. Two better-known diseases are the Chediak-Higashi syndrome (CHS) and chronic granulomatous disease (CGD).
Q: Describe Chediak-Higashi syndrome.
-In CHS the neutrophils have giant granules, which appear to be created through aberrant fusion of the neutrophil granules with the phagosome. This leads to reduced lysosomal enzymes to the phagosome resulting in delayed bacterial killing (within the phagolysosome) and subsequent recurrent infections.
Q: Describe Chronic granulomatous disease.
-In CGD there are inherited defects in the genes encoding components of the NADPH system, which generates superoxide (O2*) as above. Thus, there is impaired bacterial killing and so there are recurrent bacterial infections. When you get on Pediatrics you will be shown how to rule these diseases in or out in kids with recurrent infections.
Q: What causes the vasodilation (vascular change) associated with acute inflammation?
-The vasodilation, which we discussed in the above case, is caused by a number of compounds activated by the inflammatory process. One of these is histamine. It is stored in mast cells which normally reside in connective tissue adjacent to blood vessels. The mast cells degranulate releasing histamine when activated by complement components, which also have become activated by the inflammatory process.
-Another potent vasodilator is bradykinin, which is produced through the kinin system.
-Some components of the clotting system are also activated and these help in the vasodilatation, vascular permeability, increased neutrophil adhesion and chemotaxis.
Q: Describe the arachidonic acid (AA) cascade-type pathway that is activated during inflammation.
-Another cascade-type pathway to become activated during inflammation [and almost all types of cell injury] is that started by Arachidonic acid (AA). AA is formed when a phospholipase attacks the phospholipids of the plasma membranes. AA is released from cellular membranes and is metabolized, by two pathways, into eicosanoids.
Q: What are the two pathways that metabolize AA into eicosanoids?
-One pathway (found in almost all cells), using enzymes called cyclooxygenases (COX), produces prostaglandins and thromboxanes. The other pathway uses enzymes called lipoxygenases and this produces leukotrienes and lipoxins.
Q: What role do prostaglandins have on inflammation?
-The prostaglandins are involved with producing the pain and fever that typically occur with inflammatory processes. Anti-inflammatory drugs such as aspirin and ibuprofen inhibit the COX, which helps reduce the pain and fever. A quick sidelight. COX has two isoforms, COX-1 and COX-2.
Q: What is the mechanism of action for the older anti-inflammatory drugs (aspirin, advil)?
-The older anti-inflammatory drugs (aspirin, advil) inhibited both COX-1 and COX-2. Inhibition of COX-1 (within the stomach and duodenum) can lead to duodenal and gastric ulcers with bleeding and perforation.
Q: What are the advantages of the new COX-2 inhibitors?
-New COX-2 inhibitors, such as Vioxx (robecoxib) and Celebrex relieve the pain and fever but don’t appear to produce the GI problems. This was a big step forward in pain management but Vioxx was removed from the commercial market because of the severe side effects in some patients.
Q: What role do cytokines have on inflammation?
-Cytokines are generated by activated lymphocytes and macrophages and they can influence other cells in many different ways. Interleukins (IL) are a type of cytokine, which act on leukocytes. Chemokines are also a type of cytokine that can attract and activate leukocytes (chemotaxis). Chemokine receptors are important in the attachment of the AIDS virus to CD4 lymphocytes.
Q: Describe the secretion and stimulation of IL-1 and TNF-alpha?
-IL-1 and tumor necrosis factor-alpha (TNF-alpha) are two important cytokines involved with inflammation. Both are produced by activated macrophages. Their secretion can be stimulated by endotoxin, immune complexes, toxins, physical injury and a variety of inflammatory processes. They can have three general effects.
Q: What are the functions of IL-1 and TNF-alpha?
-An autocrine effect is when they act on the same cell, which produced them. A paracrine effect is when they act on the cells in the immediate vicinity. An endocrine effect is a systemic (the whole body) effect. IL-1 and TNF can activate endothelial cells to express adhesion molecules, other cytokines, and nitric oxide (NO), etc. TNF also causes aggregation and priming of neutrophils. IL-1 and TNF can induced the usual systemic effects of infection and injury. These would include fever, loss of appetite, release of neutrophils into the circulation, the release of ACTH and corticosteroids. TNF can also cause hypotension, decreased vascular resistance, increased heart rate and decreased blood pH. All of these effects of TNF can have serious detrimental clinical effects on sick patients.
Q: What role does NO have as a mediator of inflammation?
-Nitric oxide (NO) is another mediator of inflammation, playing an important role in vascular function. NO is a gas, produced by endothelial cells, macrophages and neurons in the brain. It is a potent vasodilator because it relaxes smooth muscle in blood vessel walls. NO acts in the host’s response to infection. Reactive NO species possess antimicrobial acitivity. Interactions between NO and oxygen free radicals produce antimicrobial metabolites such as peroxynitrite. Genetic inactivation of nitric oxide synthase in experimental animals enhances microbial replication.
Q: Case #2 – A 55-year-old chronic alcoholic male develops acute bacterial pneumonia in the lower lobe (lobar pneumonia) of his right lung. Antibiotics are given but they fail to eradicate this pneumonia and it develops into an abscess. What is the fate of the abscess?
-Unless he dramatically responds to other antibiotics they may have to surgically drain this area of the right lung. Remember from cell injury that this abscess is from liquefactive necrosis. This is one of the bad outcomes to acute inflammation
Q: What are the four outcomes to acute inflammation?
1. Complete resolution. This would be perfect recovery from an inflammatory process. This can occur if the inflammation is small in area and easy to resolve.
2. Abscess formation. Can occur if the infection/inflammation is severe and diffuse and if the infection/inflammation is not treated with antibiotics or resolves very slowly.
3. Healing by connective tissue replacement. This is equivalent to scarring or fibrosis. This is a very common outcome.
4. Progression of the acute inflammation to chronic inflammation. In inflammation there is a delicate balance between mediators which initiate and maintain inflammation and those mediators which shut the process down. When the balance shifts to mediators which initiate and maintain inflammation, then chronic inflammation occurs. Usually cellular damage and tissue destruction occur.
Q: Under what settings does chronic inflammation occur?
1. Persistent infection by certain microorganisms, such as TB (Mycobacterium tuberculosis) or certain fungi. In both of these infections there is granuloma formation. Surrounded by active scarring.
2. Prolonged exposure to toxic substances. Silicosis, a chronic inflammatory disease of the lungs results from prolonged inhalation of silica. Scarring of the lungs results with possible lung cancer development.
3. Autoimmune reactions occur when the body produces an immune attack on its own cells and tissues. One example is autoimmune thyroiditis. T lymphocytes and antibodies attack thyroid cells. The thyroid is constantly damaged.
Q: What are the cells and mechanisms involved in chronic inflammation?
-Macrophages are tissue monocytes recruited from the blood. They begin migrating to the inflamed area immediately but are the minority cell until after 48 hours when they progressively become a major cell along with lymphocytes. In addition to performing phagocytosis, macrophages can become activated to secrete a number of biologically active products. All of these products contribute to eliminating bacteria and other invaders. This weaponry can also produce tissue destruction. Macrophage products recruit lymphocytes to the inflammation. Lymphocytes also secrete inflammatory mediators, which contribute to the chronic inflammation. Eosinophils are present in significant numbers if there is an allergic etiology for the inflammation or there is a parasitic infection.
Q: Describe granulomatous inflammation.
-When you studied “necrosis” you learned that TB (tuberculosis) can cause caseous necrosis. Surrounding this necrosis is a specific type of chronic inflammation called granulomatous consisting of macrophages and lymphocytes. The macrophages enlarge and appear like epithelial cells and these are called epithelioid macrophages. Some of these latter cells fuse to form giant cells, which is a large cell with multiple nuclei. This collection of cells is called a “granuloma”. It can form a small to moderate sized mass.
Q: Where can granulomas be seen?
-Granulomas can be seen in many organs such as the liver, spleen and bone marrow. Other processes besides TB can cause granulomatous inflammation, including many fungi and foreign material. When you attend the “lumps and bumps” surgery clinic many patients show foreign body granulomas in their subcutaneous fat. For example, a patient gets a large wood splinter jammed into his arm. He thinks he has pulled it all out, but a month later he gets a tender bump in this area. You take it out, send it to a pathologist and the path report reads “foreign body granuloma”.
Q: Case #4 A veterinarian sustains a cat bite, a penetrating puncture wound, on his right hand. He thoroughly washes it. 24 hours later the bite area is red, swollen and painful. He goes to his doctor who sees “red streaks” on the anterior right forearm and enlarged lymph nodes in his right axilla. The bite area looks inflamed. What initiates the inflammation?
-A bacteria. Probably Pasteurella multocida, which is common after a cat bite. Why are there red streaks up his arms? The lymphatic channels are draining the lymph and edema fluid from around the inflamed area. Some of the bacteria probably are being transported and the lymphatics are secondarily inflamed and they appear red and swollen. Why are the lymph nodes enlarged? The lymphatics drain into these lymph nodes. So the cytokines, bacteria, etc. activate the germinal centers and there is an inflammatory response. The lymph node enlarges from this “lymphadenitis”.
Q: Give a case concerning ulcers.
-Case #5 A person sustains a brown recluse spider bite on the leg. After 8 hours it becomes red and swollen. It stays red and swollen for a few days, and then the central skin turns brownish, becomes necrotic and ulcerates. This is a typical picture of an ulcer. Peptic ulcers in the stomach and duodenum show a central, necrotic area surrounded by inflamed GI mucosa. Ulcers can be painful, become secondarily infected with bacteria and if there is enough mucosal erosion, they can erode into a blood vessel and hemorrhage.
Q: Define edema.
-Edema is the accumulation of fluid within the extravascular compartment and the interstitium.
Q: Define effusion.
-An effusion is excess fluid in the cavities of the body. A pleural effusion is fluid within the pleural cavity.
Q: What is the difference between transudate and exudate?
-A transudate is edema fluid with a low protein content.
-An exudate is edema fluid with a high protein content, which frequently contains inflammatory cells.
Q: Define a purulent exudate.
-A purulent exudate or effusion is one, which contains prominent cellular components. Purulent exudates (pus) associated with bacterial infections contain neutrophils.
Q: Define a serosanguineous effusion.
A serosanguineous effusion contains edema fluid with erythrocytes. So it would have a red tinge. This is very common after trauma.
Q: What things cause inflammation?
-anoxia, trauma, biologic agents (bacteria), physical agents (heat and cold), metabolic injury (chemicals/drugs), immunologic reactions
Q: What is the purpose of inflammation?
-repair (heal and reconstitute damaged tissue), disease (rheumatoid arthritis, IBD), protect (destroy, dilute or remove injurious agent
Q: What are the vascular changes involved with inflammation?
-changes in vascular flow and caliber, INC vascular permeability (vascular leakage)
Q: Describe changes in vascular flow and caliber.
-begin early after injury and devlop at varying rates depending on the severity of the injury, changes occur in the following order
-vasodilation -> INC permeability of the microvasculature -> loss of fluid concentrating the red cells -> stasis
Q: Describe vasodilation associated with inflammation.
-follows a transient constriction of arterioles, first involves the arterioles and then results in opening of new capillary beds in the area, get INC blood flow (causes heat and redness)
-vasodilation is induced by the action of several mediators (histamine and NO) on vascular smooth muscle
Q: Describe the INC permeability associated with inflammation.
-get outpouring of protein-rich fluid into the extravascular tissue, this reduces the intravascular osmotic pressure and INC the osmotic pressure of the interstitial fluid, leads to a marked outflow of fluid and its accumulation in the interstitial fluid leading to edema, the endothelium then becomes leaky via unknown mechanisms
Q: What are some proposed mechanisms of how the endothelium becomes leaky?
-formation of endothelial gaps in venuls (immediate transient response), this type of leake affects venules 20-60 um in diameter leaving capillaries and arterioles unaffected, allows for release of cytokines (IL-1, TNF alpha, gamma-interferon)
-driect endothelial injury, resulting in endothelial cell necrosis and detachment (immediate sustained response), all levels of the microcirculation are affected including the venules, capillaries and arterioles
-delayed prolonged leakage, begins after a delay of 2 to 12 hours, lasts for several hours or even days and involves venules as well as capillaries
-leukocyte-mediated endothelial injury
-INC transcytosis across the endothelial cytoplasm
-leakage from new blood vessels
Q: Describe gaps due to endothelial contraction.
-affects venules, initateid by vasoactive mediators (histamine, leukotries), the most common, fast and short-lived (minutes)
Q: Describe direct injury.
-affects arterioles, capillaries and venules, activated by toxins, burns, and chemicals, is fast and may be long-lived (hours to days)
Q: Describe leukocyte-dependent injury.
-affect mostly venules and pulmonary capillaries, is a late response that is long-lived (hours)
Q: Describe the INC transcytosis.
-affects venules, initiated by vascular endothelium-derived growth factor
Q: Describe new blood vessel formation.
-affects sites of angiogenesis, persists until intercellular junctions form
Q: Give a summary of fluid loss from vessels with INC permeability during acute inflammation.
-occurs in distinct phases
1. an immediate transient response lasting for 30 minutes or less, mediated mainly by the actions of histamine and leukotries on endothelium
2. a delayed reponse starting at about 2 hours and lasting for about 8 hours, mediated by kinins, complement and other factors
3. a prolonged response that is most noticeable after direct endothelial injury (after burns)
Q: What are the plasma derived sources of INC vascular permeability (and edema)?
-Hagemna factor activation leads to activation of clotting/fibrinolytic system which leads to fibrin split products and kinins (bradykinin) that leads to INC vascular permeability
-also get complement activation (C3a and C5a) which leads to INC vascular permeability
Q: What are the cell-derived sources of INC vascular permeability (and edema)?
-mast cell/basophile degranulation -> histamine
-platelets (serotonin)
-inflammatory cells -> platelet activation factor, prostaglandins, leukotrienecs
-endothelium -> NO, platelet activation factor, prostaglandins
Q: Describe the evolution of an abscess.
1. bacteria cause tissue damage and necrosis
2. bacteria multipley, polymorphs pack the central zone, get swelling (edema) and hyperaemia)
3. delineation of abscess by pyogenic membrane, get new capillaries, polymorphs and a few fibroblasts, pus forms in the center then starts to track towards the surface which has a thinning epithelium
4. abscess points and ruptures discharging pus, pyogenic membrane more pronounced
5. swelling subsides, cavity collapses, organization and fibrosis proceed
6. final small scar
Q: What are the major local manifestations of acute inflammation?
1. vascular dilation and INC blood flow (causing erythema and warmth)
2. extravasation and deposition of plasma fluid and proteins (edema)
3. leukocyte emigration and accumulation in the site of injury
Q: What are the mechanisms for extracellular release of leukocyte products?
-regurgitation during feeding (phagocytic lysosome remains transiently open to extracellular environment
-reverse endocytosis (frustrated or unsuccessful phagocytosis)
-cytotoxic release of intracellular products due to disruption of the integrity of the neutrophils
Q: What are the problems with liquefactive necrosis and abscesses?
-several tissue destruction, no blood vessels so antibiotics cannot get into abscess and kill bacteria, usually abscesses have to be drained
Q: What are the functions of the activated macrophage?
-tissue injury via toxic oxygen metabolites, proteases, neutrophil chemotactic factors, coagulation factors, AA metabolites, NO
-fibrosis via growth factors, fibrogenic cytokines, angiogenesis factors (FGF), and remodeling collagenases
Q: Give a summary to what causes a granuloma.
-starts with injury (bacterium (Mycobacterium tuberculosis), fungus (Histoplasma capsulatum), or foreign partical (suture)) -> inability to digest inciting agent
-if you can’t digest inciting agent, get failure of acute inflammatory response, if get a persistent injurious agent then get cell-mediated immune response and sequestration within macrophages
-these two lead to recruitment of macrophages, with epithelioid and giant-cell formation leading to granuloma
Q: Case #6 A 40-year-old male develops acute bacteria prostatitis. In the ER his temperature is 103 (98.6 normal), his pulse and respirations are rapid, he cannot stop shivering (chills) and his teeth are chattering. He says he feels weak and tired. Why would a local infection cause systemic effects?
-Many local bacterial infections trigger this acute-phase reaction. The development of fever is complex but cytokines (IL-1 & 6 and TNF), produced in the inflamed prostate, stimulate the hypothalamus to start the fever causing cascade. So this is a type of “endocrine” effect. Gram negative septic shock can result in a dramatic acute phase reaction with hypotension, shock and death.