Term
| What are the 6 causes of inflammation? |
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Definition
Infection
Tissue Necrosis
Immune Reaction
Trauma
Foreign bodies
Physical/Chemical Agents
NOTE- nonspecific reaction |
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Term
| What are the 4 cardinal manifestations of acute inflammation? |
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Definition
1) Redness
2) Swelling
3) Heat
4) Pain |
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Term
| What are the 5 forms that inflammation can take? |
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Definition
1) Purulent (Suppurative) (Acute response with pus containing neutrophils, necrotic debris and edema fluid that is commonly caused by infection with pyogenic bacteria.
2) Abscessing (Necrotizing) (Acute response with localized, liquefactive necrosis packed with neutrophils and debris- must be drained surgically).
3) Fibrinous (Acute response with deposition of fibrin-rich exudate on pleura, pericardium and interstitial tissues with SG >1.020)
4) Serous (acute response with thin fluid transudate from vessels, skin blister or chest/abdominal mesothelium)
5) Granulomatous (consisting of immune cells and debris) |
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Term
| What are the 3 components of the inflammatory response? |
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Definition
1) Vascular (Dilation and increased permeability, allowing outflow of fluid, leukocytes and plasma proteins from blood into ECM)
2) Leukocyte (WBC)
3) Systemic |
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Term
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Definition
| Adolescent Neutrophils (0.5 % of blood leukocytes) with bi-lobed nucleus. |
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Term
| How does Histamine act in the Vascular component of inflammation? |
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Definition
Binds H1 endothelial receptors to cause vasodilation of arterioles and increased permeability of venules.
Released from mast cells, basophils and platelets during trauma, cold, heat , immune reactions, anaphylatoxins, IL-1 and IL-8. |
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Term
| Where are Mast cells found and how are they activated? |
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Definition
Tissue counterpart to blood basophils found around blood vessels, nerves and skin. They attract neutrophils, eosinophils and platelet activating factor.
They are activated by cross-linking of IgE Fc receptors, complement C5a and C3a (anaphylatoxins) some drugs (codeine and morphine), adenosine, bee venom, heat, cold and sunlight! |
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Term
| How does NO relate to hypertension and atherosclerosis |
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Definition
| Vasodilator and Platelet inhibitor produced by endothelial cells, that is deficient in these conditions, as well as in Diabetes Mellitus. |
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Term
True or False
Edema fluid can be considered "exudate" |
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Definition
False!
Exudate in inflammatory extracellular fluid with high protein content and cellular debris.
You find "Transudate," the thin, acellular serous edema fluid. |
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Term
| What are the 5 steps of the leukocyte response component of inflammation? |
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Definition
1) Margination (hemodynamic forces push leukocytes toward blood vessel periphery following dilatation of venules)
2) Rolling (Marginalized leukocytes transiently adhere to endothelium)
3) Adhesion (Leukocytes stop and firmly adhere)
4) Diapedesis (Push through pseudopods and squeeze into extravascular space)
5) Chemotaxis (Histamine, Cytokines and receptors draw leukocytes to target) |
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Term
1) How does Histamine mediate Leukocyte "Rolling" at endothelial inner surfaces?
2) How does E-selectin relate to P-selectin? |
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Definition
1) Stimulates endothelial cells to move P-selectin molecules from Webel-Palade bodies (storage granules) to their surfaces, where they receive P-selectin glycoprotein ligand-1 (PSGL-1) on the surface of leukocytes.
2) TNF and IL-1 induce E-seelctin expression on endothelial surfaces. E-selectin binds leukocytes more tightly than P-selectin and mediates both rolling and adhesion. |
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Term
| What portion of Leukocyte migration are L-selectin, VCAM-1 and VLA-4 integrin all involved in? |
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Definition
Adhesion (Only).
L-selectin expressed on leukocyte surfaces binds all 3
VCAM-1 on endothelial cells binds lymphocytes and monocytes but DOES NOT bind neutrophils
VLA-4 integrin ispresent on lymphocytes and monocytes but NOT Neutrophils (late response). |
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Term
| What processes are the inflammation receptors ICAM-1 and PECAM involved in? |
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Definition
ICAM-1 Mediates adhesion and diapedesis of lymphocytes, monocytes and neutrophils on endothelial cells
PECAM mediates ONLY DIAPEDESIS |
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Term
| What is the general course of the Leukocyte response in inflammation? |
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Definition
1) Cytokines activate Leukocytes
2) Leukocytes release pro-inflammatory Cytokines resulting in phagocytosis of inflammatory agents. |
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Term
| What are the 5 steps of phagocytosis? |
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Definition
1) Recognition
2) Attachment (enhanced by Opsonins)
3) Engulfment (in Lysosomes)
4) Killing (H2O2 and ROS/ Myeloperoxidase takes H2O2 and Cl- to make HOCL for lipid peroxidation and halogenation)
5) Degradation |
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Term
| What are the most important Systemic Effects of Acute Inflammation? |
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Definition
1) Fever (hypothermia)
2) Tachycardia
3) Hyperventilation (tachypnea)
4) Leukocytosis |
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Term
| What types of inflammatory responses do Neutrophils, Lymphocytes and Eosinophils deal with, respectively? |
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Definition
1) Neutrophilia- Bacterial
2) Lymphocytosis- Viral
3) Eosinophilia- Allergy and Parasitic |
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Term
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Definition
| Coat and target molecules for phagocytosis |
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Term
| Why might a pathologist tell you that he observes a "Left Shift" in a patient's blood serum? |
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Definition
| Release of immature neutrophils from bone marrow (adolescent "bands"). Usually less severe inflammation |
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Term
| What is the ESR and how can it be used to detect occult inflammation? |
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Definition
Erythrocyte Sedimentation Rate is a measure of how "sticky" Fibrinogen has made erythrocytes. Higher ESR means more fibrinogen and more inflammation.
Remember, Fibrinogen is an "Acute Phase Reactant" |
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Term
| What are the 4 Major Plasma Protein Systems that mediate Inflammation? |
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Definition
1) Kinin
2) Coagulation
3) Fibrinolytic System
4) Complement System (increased vascular permeability and chemotaxis, and "Opsonize" stuff.
** There is a great deal of cross-talk ** |
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Term
1) How can Arachadonic Acid act in Inflammation?
2) How do Corticosteroids relate? |
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Definition
1) Cell membrane FA whose metabolites are short-acting Intracellular agents or short-range extracellular mediators.
Lioxygenases convert AA into precursors for leukotrienes and lipoxins.
Cyclooxygenase convertes AA into prostaglandins
2) Corticosteroids block AA production and all things made from it, masking signs and symptoms of inflammation (opportunist infections occur here) |
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Term
| Why might you use Non-steroidal anti-inflammatory drugs instead of Corticosteroids to treat inflammation? |
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Definition
| Non-steroidal anti-inflammatory drugs only block prostaglandin production, instead of ALL arachadonic acid functions, and are therefore associated with fewer side-effects. |
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Term
| Why is NSAID use sometimes associated with gastric bleeding? |
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Definition
| NSAIDS inhibit prostaglandins, causing analgesic (pain) and antipyretic (fever) effects, but also interfering with prostaglandin-mediated gastric mucosal protection. |
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Term
| How is Aspirin different than generic NSAIDS? |
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Definition
Aspirin is an irreversible innactivatior of Cyclooxygenases.
In response to Aspirin,
Endothelia make more enzyme, which makes more prostacyclin, leading to vasodilation and platelet aggregation
Platelets lack DNA and cannot make more enzyme, so they are "zapped"
NET EFFECT- vasodilation and platelet aggregation inhibition. |
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Term
| How is Cyclooxygenase action different in endothelial cells and Platelets? |
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Definition
OPPOSITE EFFECTS!
1) In endothelial cells, it makes prostacyclin for vasodilation and inhibition of platelet aggregation
2) In Platelets, it makes thromboxane, which is a vasoconstrictor and platelet aggregation promotor.
NOTE- Aspirin is an irreversible inhibitor |
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Term
1) What is the difference between Cyclooxygenase-1 and Cyclooxygenase-2?
2) How does this difference relate to COX-2 inhibitors? |
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Definition
1) COX-1 is constitutively expressed and COX-2 is inducible
2) COX-2 inhibitors may prevent gastric bleeding associated with induced response (BUT, causes heart attacks, perhaps through prostacyclin inhibition). |
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Term
1) A patient presents with a temperate > 100.4, with increased heart rate, RR > 20/min and WBC count >12,000/cu mm. Whats going on?
2) A patient presents with Temperature < 96.8 and pCO2 <32mm Hg. Whats going on? |
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Definition
1) Systemic Inflammatory Response Syndrome (SIRS).
2) ALSO SIRS!
** Sepsis is SIRS due to infection, it is NOT a (+) blood test! ** |
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