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Immuno - PCC
Immunology - first lecture exam
| Question | Answer |
|---|---|
| 2 types of human defenses | 1. Innate resistance 2. Acquired (adaptive immune system |
| What are pathogen-associated molecular patterns or PAMPs | Cells that are common among microbes that innate resistance recognizes |
| Does innate resistance recognize every possible anitgen? | Hell no! PAMPs dude |
| Are PAMPs associated with mamillian cells? | Nope, just trying to beat a concept to death |
| 8 examples of PAMPs | 1. LPS 2. Mannose 3. Bacterial and viral DNA 4. Amino acid N-Formylmethionine 5. Double stranded and single stranded RNA 6. Endotoxins 7. Peptidoglycans 8. Bacterial flagellin |
| What is LPS and what does it do? | Lipo Polysacharide.... forms gram negative cell wall endotoxin |
| LPS is from _____. Lipotechoic acid is from _____. | 1. Gram negative cell wall (endotoxin) 2. Gram postive cell wall |
| Terminal sugar common in microbial glycolipids and glycoproteins | Mannose |
| Endotoxins are part of what? | Outer membrane of cell walls of gram negative bacteria |
| Endotoxin is invariably associated with ___ bacteria weather the organism is pathogenic or not. | Gram negative |
| Endotoxin is the ____ complex associated with outer membrane of ____ pathogens | 1. LPS 2. Gram negative |
| Innate vs Acquired immunity: 1. Evolutionary origin 2. Type of response 3. Timing of response 4. Examples | 1. Early - Late 2. General response - Targeted response antigen-specific 3. Early line of defence (unchanging - Slow developpement (has a memory) 4. Complement, Inflammation, NK cells, Interferon --- Antibodies, cell mediated attack |
| The thick rigid layer composed of overlapping lattice of 2 sugars, N-Acetyl, etc | Peptidoglycans |
| The exact molecular make-up of peptidoglycans is ____ | Species-specific |
| 1. NAM is only found where? 2. NAM???? | 1. In cell walls of bacteria 2. N-Acetyl Muramic Acid |
| T or F : PAMPs distinguish between benign and pathogenic organisms | False! |
| PAMPs simply ID what? | Foreigness!! |
| What else can act as PAMPs? | Unique molecules displayed on stressed, injured, infected or transformed human cells |
| Because all microbes, not just pathogenic microbes possess PAMPs, they are sometimes refered to as what? | MAMPs : Microbe Associated MOlecular Patterns |
| What is needed in order to recognize PAMPs? | Pattern Recognition Receptors (PRR) |
| What are PRRs? | Receptors capable of binding specifically to conserved portions of pamps |
| 5 types of cells that possess PRRs? | 1. Macrophages 2. Dendritic cells 3. Endothelial cells 4. Mucosal epithelial cells 5. Lymphocytes |
| 1. Subclass of PRRs 2. What do they do? | 1. Toll-Like Receptors (TLRs) 2. Recognize molecules that are shared by pathogens but distinguishable from host molecules |
| TLRs ID possible ____ but nothing ____ | 1. Danger 2. Specific |
| Total WBCs | 4500-10,000 per micro liter |
| 2 parts of innate immunity | 1. Cellular 2. Humeral |
| 2 subclasses in cellular portion of innate immunity | 1. Granulocytes 2. Agranulocytes |
| Most common WBC in circulation? | Neutrophils |
| 3 cells associated with granulocytes | 1. Neutrophils 2. Eosinophils 3. Basophils |
| Inapropriate activity of what cells indicate allergies? | 1. Eosinophils 2. Basophils |
| 2 types of agranulocytes | 1. Monocytes 2. NK cells |
| What are monocytes? | Immature WBC (maybe, not sure) |
| 1. Humoral portion of innate resistance represents ___ factors 2. 3 things associated with humoral portion | 1. Soluble factors 2. Complement, Interferon, Lysozyme |
| 2 Components of aquired immunity | 1. Cellular 2. Humoral |
| Agranulocytes found in cellular portion of aquired immunity? | Lymphocytes |
| 2 examples of lymphocytes? | 1. T-cells (t-helper cells and t-cytotoxic cells) 2. B cells |
| How many lymphocytes in aquired immunity? | 1700-3500 |
| What is in the humoral portion of aquired immunity? | Immunoglobins |
| Site of all WBC formation | Bone marrow |
| What is the pluri potential? | Depending on signal, cells will differentiate into desired cell |
| Do mast cells circulate? | Nope |
| Viruses = ? | Tropism |
| 1. Rapid, nonspecific, stereotypical 2. Slow, highly-specific, memory | 1. Innate 2. Acquired |
| 2 basic types of cells associated with innate response | 1. Neutrophils 2. Macrophages |
| Neutrophils and Macrophages: 1. Which one is in circulation? 2. Which one is a sentinal? | 1. Neutrophils 2. Macrophages |
| 2 types of cytokines associated with innate response | 1. Interleukine - 1 2. TNF - alpha |
| First line of defense to prevent damage or invasion of pattogens | Physical and mechanical barriers |
| 4 things that provide biochemical barriers against pathogens? | 1. Antibacterial peptides 2. Perspiration 3. Saliva 4. Tears |
| The normal bacteria flors provides protection by relasing chemicals that prevent what? | Colonization of pathogenic organisms |
| Time line for inflammation : ? --- ? --- ? | Edema --- Neutrophils - Macrophages / Monocytes |
| What is the second line of denfense for injury and pathogens? | Inflammation |
| 1. Rapid, non-specific protective response to cellular injury from any cause? 2. Where can it only occur? | 1. Inflammation 2. Vascular tissue |
| Macroscopic hallmarks of inflammation | 1. Calor 2. Rubor 3. Tumor 4. Dolar |
| What is the microscopic hallmarks of inflammation? | Accumulation of fluid and cells at inflammatory site |
| 1. Inflammation is designed to respond to ___ 2. Activation of inflammatory response leads to 3 things | 1. Tissue injury 2. Attempt to neutrolize injurious agents, Remove debris, Stimulate repair / healing |
| What cells attempt to neutrolize injurious agents? | Macrophages |
| 1. Inflammation has the same response to ___ or ____ 2. What is this response? | 1. Tissue injury, Infection 2. Release of cytokines |
| Inflammatory response is a vascular response that allows what? | Allows ellements confined in vascular compartements to leave and enter parenchymal tissues where injury occurs |
| 2 things that are associated with vascular response | 1. Vasodilation 2. Increase in vascular wall permeability |
| Inflammation is designed to respond to tissue injury ____ and then ____ | 1. Quickly 2. Terminate |
| Chronic inflammation may become a source of what? | Tissue injury that may exceed the injurious potential of initiating event |
| 1. Specific cells are imported in to do what during inflammation? 2. This is done through what? | 1. to attack and destroy injurious agents or remove tramatized tissue 2. Enzymatic digestion and physical isolation of offending agent |
| During the process of enzymatic digestion or physical isolation, what happens to damaged cells and tissues? | They are digested and removed to allow repair to take place |
| The response to many damaging agents is ___ and ____ | Immediate and Sterotypic |
| The inflammatory response is modulated by 4 things | 1. Nature of offending agent 2. Duration of insult 3. Extent of tissue dammage 4. Micro environment |
| Describe chronic inflammation | Injurues that trigger a sustained immune response with the inability to clear injured tissue and foreign agents |
| 3 cells chronic inflammatory infiltrates are composed of | 1. Lymphocytes 2. Plasam cells 3. Macrophages |
| T or F: Accute and chronic inflammatory infiltrates can often co-exist | True |
| Inflammation usually works to defend the body. When can it be harmful? | When it is chronic |
| 2 examples of inflammation that is detrimental | 1. Bacterial pneumonia 2. Joint destruction in septic arthritis |
| ___ may also damage tissue and lead to scarring and loss of function | Chronic inflammation |
| Chronic inflammation may also damage tissue leading to ___ and loss of ____ | 1. Scarring 2. Loss of function |
| Chronic inflammation is the basis for many ___ | Degenerative diseases |
| Impaired inflammatory response may lead to uncontrolled ____ as in ___ hosts | 1. Infection 2. Immunocomprimised |
| Sevral ___ disease are characterized by a deficient inflammatory response due to deffects in inflammatory cell function or immunity | Congenital |
| 1. Sentinals are like _____ 2. 2 examples | 1. Lookuts 2. Macrophages and dendritic cells |
| 1. Both macrophages and dendritic cells function via ____ 2. What are their individual unique function? | 1. Phagositosis 2. Macrophages = stays and fights Dendritic cells = takes foreign material to nearest lymph node |
| The 3 major components of the accute inflmmatory response acount for what 3 classic signs of inflammation? | Calor, Rubor, Tumor |
| 1. What are the 3 major components of acute inflammation? | 1. Local increase in blood flow via vasodilation 2. Increase in microvascular permiability 3. Passage of fluid and leucocytes from vasculature to site of injury |
| In acute inflmmation, what is responsible for : 1. Tumor 2. Calor and Rubor | 1. Increase in microvascular permeability 2. Local increase in blood flow via vasodilation |
| The acute inflammatory response begins with ____ or ____ | Direct injury or stimulation of parenchyma or stroma |
| 1. Parenchyma = ? 2. Stroma = ? | 1. Cells that do the job of particular tissue 2. Everything else! CT, Nerves, Vessels, etc |
| Increase in blood vessel permiability usually occurs in what? | Fuckin microvasculature |
| 3 vascular changes in acute inflammation | 1. Vasodilation leads to increase in capillary flow 2. Leakage of protein-rich fluid into extravascular space leading to blood stasis 3. Neutrophils and leukocytes go to area of injury (leaves blood vessels) |
| What is blood stasis? | Slowing of blood flow |
| 1. Margination = ? 2. Emigration = ? | 1. Neutrophil adherence to endothelium 2. Penetration of endothelium by leukocytes |
| 1. What is released by damaged cells? 2. What does this do ? | 1. Interleukine - 1 2. Sends an SOS signal to blood vessels to undergo changes to let neutrophils and leukocytes out of vessels to the localized area of injury |
| What 2 cells in vessel wall respond to IL-1? | Endothelium and Smooth muscle cells |
| ISF is continously being produced... what is the source? | Process of vascular filtration |
| ISF is ultimatly returned to the vasculature vua what? | Lymphtic drainage |
| What causes edema? | Accumulation of ISF because lymphatic drainage cannot keep up |
| 1. ___ results from blood flow and plasma volume. 2. What happens when this is increased? | 1. Hydrostatic pressure 2. Fluid is forced out of vasculature |
| 1. What is oncotic pressure? 2. What does it do? | 1. Reflects plasma protein concentration 2. Draws fluid into vessels |
| Osmotic pressure is determined by relative amounts of ___ and ___ in vascular and tissue spaces | Na and Water |
| What happens as blood stasis develops? | Neutrophils settle out and adhere to endothelium (margination) and leukocytes penetrate endothelium (emmigration) |
| 1. Where is flow quickest in vessel for particles? 2. What happens because of this? | 1. In the middle 2. Particles line up in the middle and are kept appart from each other |
| Why is it very important for particles, especially platelets to be kept appart? | If platelets hit each other, they activate and form a clot |
| Absence of ordered flow | Turbulence |
| _______ promote inappropriate clotting | Eddy currents (form of turbulance) |
| Eddy currents (turbulance) happens due to ____ | Arterosclerosis |
| 1. 2 vascular changes that occur in imflammation 2. What signals this to happen? | 1. Vasodilation and increase in wall permiability 2. IL-1 |
| 1. When vascular wall permiability increses, what happens to water and proteins? 2. What is the result of this? | 1. Water leaves and proteins are left behind 2. Increase in blood viscosity |
| What happens to neutrophils when there is an increase in blood viscosity | They slow down via rolling and eventually become attached to endothelium (margination) |
| Among the earliest response of tissue injury is change in microvascular activity which results in ____ | Inflammatory edema |
| What is edema? | Accumulation of fluid in extravascular compartments and interstial tissues |
| What is effusion? | Excess fluid in body cavities |
| How long does it take for vascular permiability changes? | 15-30 mins |
| 1. Vascular permiability changes affect only _____ IMMEDIATLY 2. Mediated by what chemicals? (3) | 1. Venules 2. Histamine, Bradykinin, Leukotrienes |
| 1. In a sustained vascular permiability response, what parts of vessel is affected? 2. Results in what? | 1. All vascular elements 2. Endothelial cell detachement |
| 1. Tranducate = ? 2. Exudate = ? | 1. Edema composed of water and solutes 2. Edema composed of water, solutes AND proteins |
| In rolling of neutrophils, what protein extends from the neutrophils and endothelium which atcually slows it down? | EéC selectins (chris drew a picture here) |
| IL - 1 signals ____ to attract neutrophils to surface | I-CANS (yet another picture) |
| 3 terms used to describe the process of neutrophils penetrating endothelium of vessel | 1. Diapadesis 2. Emmigration 3. Transmigration |
| In diapedes, emmigration and transmigration, what is the process by which neutrophils travel to site of injury? | Chemotaxis |
| How does the soldier, the neutrophil, hack its way through the jungle of collagen to get to the site of injury | Collagenase enzyme |
| ____ allows neutrophils and leukocytes to begin rolling and margination? | Blood stasis |
| Adhesion molecules, I-CANs, are stimulated by what? | IL-1 and TNF |
| How long do leukocytes survive in extravascular spaces? | 24-48 hrs |
| Examples of chemotctic factors (2) | Cytokines and leukotrienes |
| 1. Gradient of chemotactic factors affects the leukocytes forming what? 2. Activation involves the release of _____ and ____ | 1. Pseudopodia 2. Arachadonic acid metabolites and Lysosomal enzymes |
| 1. Draws fluid into vessel? 2. Forces fluid out of vessel | 1. Oncotic pressure 2. Hydrostatic pressure |
| Onctic pressure is determined by levels of ____ | Protein |
| Phagocytosis is triggered by what? | The coating of microorganisms by serum proteins called opsonins |
| Outer serum protein coat of microorganisms? | Opsonins |
| 2 major opsonins | IgG and Complement factors |
| Microbial killing results from the production of what? (4) These are all weapons systems neutrophils have? | 1. ROS 2. Lysozyme 3. Lactoferrin 4. Defensins |
| Describe leukocyte induced tissue injury | The release of activated axygen species, proteolytic enzymes and other substances by leukocytes into : interstitium (leads to damaged tissue in local area) |
| People with defects in leukocytes are at higher risk of infection by microorganisms.... major defect sites include whatÉ (3) | 1. Adhesion 2. Chemotaxis\phagocytosis 3. Microbial killing |
| 1. Edema with protein 2. Edema without protein | 1. Exudate 2. Transdusate |
| ____ and ____ derived mediators work in concert to activate inflammation | Cell and Plasma |
| 1. These plasma derived mediators are short lived and are inhibited by ___. 2. This does what to the response? | 1. Intrinsic mechanism 2. Turns it off |
| Important ''on-off'' switches in mechanisms of inflammation | Plasma derived mediators |
| Three enzymatic cascades that plasma contains...plasma protease systems | 1. Coagulation cascade 2. Kinin generation 3. Complement system |
| 1. Hageman factor aka? 2. Where is it generated? | 1. Clotting factor 12 2. Plasma |
| How is hageman factor 12 activated into factor 12a? | Factor 12 leaks out as transdusate. As soon as it is exposed to collagen it becomes activated but it needs to be exposed to a NEGATIVE environement |
| Collagen has a ____ environement which activated hageman factor 12 | Negative |
| What other negative environments besides collagen will activate factor 12? (4) | 1. Basement membranes 2. Proteolytic enzymes 3. Bacterial lipopolysacharides 4. Foreign material |
| Many factors are activated by exposure of collagen...then what happens? Thrombin does what? | Turns fibrinogin into fibrin and fibrinopeptides |
| What is the glue that holds the colts together? | Fibrin |
| Chemotactic substance that promotes vascular permeability? | Fibrinopeptide |
| Clotting cascade key features: 1. 2 things the generation of thrombin will produce 2. 2 things fibrinopeptides will do | 1. Produces fibrin and promotes leukocyte adhesion 2. Increase vascular permeability acts as chemotactic factor |
| Intrinsic or extrinsic activation of clotting? : 1. Production of tissue factors via damage to cell membrane 2. Activation of factor 12 via contact with subendothelial collagen | 1. Extrinsic 2. Intrinsic |
| T or F In vivo there is no real distinction between intrinsic and extrinsic activation | True |
| Clotting tests : 1. Measures intrinsic clottin using kaolin as stimulant. 2. Meaures extrinsic clotting using thromboplastin (tissue factor) as stimulant. 3. Measures circulating fibrinogen levels using activated thrombin kinin system activation | 1. aPTT (activated partial thromboplastin time 2. PT (Prothrombin time) 3. TT (thrombin time) |
| 1. Plasma kallikrein is generated by activated ____ 2. It (kallikrein) cleaves high-molecular weight ____ | 1. Hageman factor 2. Kininogen |
| After Kininogen is cleaved via kallikerin, sevral vasoactive low molecular weight peptides called ___ are produced | Kinins |
| Function of kinin (4) | 1. Increased blood flow 2. Makes it easier for fluid to pass through caps 3. Stimulates pain receptors 4. Helps repain damaged tissues |
| 1. What does the biological glue do? 2. When is it produced? | 1. Traps bacteria 2. As soon as factor 12 comes in contact with collagen |
| What can bacteria do about the biological glue? | They can anticipate it and produce enzymes that combat it |
| Phospholipids, cell membrane, fragments and platelets is pavlof for what? | Extrinsic clotting |
| What converts plasminogen to plasmin? | kallikrein |
| 1. What is fibrinolysis? 2. What makes it possile? | 1. Degredation of fibrin 2. Plasmin |
| For intrinsic clotting, factor 12 must come in contact with what? | Collagen |
| 1. 2 things used as clot busters 2. What is not used so much anymore? why? | 1. tPA and Streptokinase 2. Streptokinase -- because it is obtained from bacteria |
| 1. What releases tPA? 2. What is tPA? | 1. Endothelium 2. Tissue plasminogin activator... intiates breakdown of clots |
| Itch is pavlov for what? | Bradykinin |
| Regulates multiple physiological processes including : BP, Contracts/relaxes smooth muscle, Plasma extravasation, Cell migration, Inflammatory cell activation, Inflammatory mediated pain response | Bradykinin |
| Fibrin-split products augment ___ in skin and ____ | Vascular permeability in skin and lungs |
| 1. Plasmin cleaves components of the ___ system 2. This generates biologically active products such as what? | 1. Complement systems 2. Anaphylatoxins C3a and C5a |
| 1. C3b forms what? 2. C3a-C5a forms what? 3. MAC stands for what? | 1. Opsonin 2. Analyticaltoxins 3. Membrane attack complex |
| C3a and C5a keeps the war going. They are said to be what? | Proinflammatory |
| Targetting system | Opsonin (C3b) |
| What do MACs do? | Punches holes in the cell |
| Group of proteins found in plasma and on cell surfaces, in whose primary function is defence against microbes | Complement system |
| 3 physiologic activities of the complement system | 1. Defense against pyogenic bacterial infection 2. Bridges innate and adaptive immunity for defense against microbes 3. Disposal of immune and inflammatory products |
| How does the compliment system defend us against pyogenic bacterial infections? (4) | 1. Opsonization 2. Chemotaxis 3. Activation of leukocytes 4. Lysis of bacteria |
| Describe the process of opsonization? | Process by which a special molecule (IgG or C3b) binds to the surface of bacterium. This enhances phagocytosis by enabling receptors on phagocytic cell membranes to recognize and bind the opsonized bacterium and eat it! |
| How does the completement system bridge innate and adaptive immunity? | It augments antibody response and enhances immunological memory |
| The complement system disposes of inflammatory wast and immune porducts how? (2) | 1. Clears immune compleses 2. Removes apoptotic cells |
| Complement is activated though 3 pathways to form the membrane attack complex (MAC) | 1. Classical pathway 2. Alternative pathwaw 3. Manose Binding Pathway |
| Activation of classical pathway is primarily triggered by what? | Antigen-antibody (Ag-Ab) complexes |
| 1. Specific immune activation 2. Innate immune activation (2) What pathways in complement system are associated with these? | 1. Classic pathway 2. Alternative pathway and Mannose-binding pathway |
| 1. The alternative pathway is initiated by products of ___. 2. give 4 examples | 1. Microorganisms 2. Endotoxins, Polysacharides, Cobra venom factor, Tumor cells |
| 1. The mannose-binding pathway has components common with the ___ pathway. 2. MBP recognizes what? | 1. Classic pathway 2. Carbohydrate patterns found on surfaces of microorganisms (bacteria, viruses, protazoa, fungi) |
| 1. Mannose-binding pathway uses protein similar to C1q of classical component. What is this protein? 2. This protein is part of the ___ family and is produced in the ____ | 1. MBL 2. Collectin familly and produced in the liver |
| The complement system is thightly regulated to generate ___ molecules. | 1. Pro-inflammator molecules |
| What is the endpoint of complement activation? | 1. Formation of MAC 2. Cell lysis1. |
| Proinflammator molecules that mediate smooth muscl contraction and increase vascular permeability 2. Give 3 examples | 1. Anaphylatoxins 2. C3a, C4a, C5a |
| Molecule binds to the surface of bacteria and a specialized receptor (Gl receptor or C3b receptor) recognizes it and binds with it...therefor increases phagocytosis | Opsonization |
| Chemotactic factors such as MAC and C5a activate ___ molecules such as what? | 1. Proinflammatory molecules 2. Leukocytes, Cytokines and Degranulation of mast cells and basophils |
| Cell lysis is done by what? | MAC (C9 polymerization is catalized to lyse the cell) |
| T or F: the complement system is regulates to act on the durface of microorganisms as well as normal cells and tissues | FALSE! it is a tightly regulated to act only on microorganisms... when this regulatory system is malfunctioning, normal tissues may be damaged |
| 1. Immune complexes activate what pathway? 2. What protein is invovled? | 1. Classic pathway 2. C1q |
| What happens to the complement system if immune complexes are formed continuously? | It results in its comsumption and therefor its net depletion |
| Cleavage fragments of C3 (2) normally bind to bacterial surfaces to promote ___ of it | 1. C3b and iC3b 2. Phagocytosis |
| Increased susceptibility to pyogenic infections such as haemophilus influenza and strep pneumonia is associated with defects in what? (3) | 1. Antibody production 2. Complement proteins 3. Phagocytic function |
| Ecosanoids are derived from 20 what? | Carbon essential fatty acids |
| Basically 2 types of ecosanoids | Prostaglandins and leukotrienes |
| Ecosanoids are derived from ___ and ___ fatty acids | Omega 3 and omega 6 |
| 1. Primary dietary omega 6 2. Primary dietary omega 3 | 1. Linoleic acid 2. Alpha-linolenic acid (ALA) |
| 2 active forms of ALA | EPA and DHA |
| Primary control enzyme for prostaglandins | Cycloxygenase |
| 1. Inflammatory FA 2. Less inflammatory FA | 1. Omega 6 2. Omega 3 |
| 3 things inflammation does | 1. Neutralizes injurious agents 2. Removes debris 3. Stimulates healing |
| What do prostaglandins do in general? | Liberates AA from cell membrane via phopholipase A2 |
| Function of PGI2 and TXA2 | 1. Vasodilation ; platelet inhibition 2. Vasoconstriction; platelet stimulation |
| 1. Prostacyclin is produced where? 2. Thromboxane A2? | 1. Endothelial cells 2. Platelets |
| 1. PGD2, PGE2 AND PGF2 alpha are found in ___ cells 2. 3 things these do | 1. Mast cells 2. Vasodilation, Smooth muscle contraction and Regulates mucus production |
| Inhibition of ___ by NSAIDS supress all ___ synthesis | 1. Cycloxygenase 2. Prostaglandins |
| What inhibits prostaglandins? | The inhibition of cycloocygenase |
| 1. The enzyme COX 1 is found where? 2. Steroids inhibit ___ | 1. Gastric mucosa 2. Phopholipase A2 |
| Prostaglandings and leukotrienes are derived from what? | Arachadonic acid |
| 1. Major control point enzymes for leukotrienes 2. Located where? | 1. 5-lipoxygenase 2. neutrophiles |
| 4 things leukotrienes promote? | 1. Chemotaxis (LTB4) 2. Vasoconstriction 3. Bronchospasms 4. Increases permiability |
| Enzyme in cell membrane that cleaves arachadonic acid | Phopholipase A2 |
| Primary control enzyme for protaglandins | Cyclooxygenase |
| Prostaglandins that makes mucous (3) | PGE2, PGD2, PGF2-ALPHA |
| COX 1 and COX 2: which is inducible? Which is always there? | 1. COX 2 2. COX 1 |
| 1. Has no selectivity and inhibits all ecosanoids 2. What can block this? (2) | 1. Phopholipase A2 2. Cortisol and prednsone |
| 1. Generic drug that inhibits COX enzyme 2. Primary example | 1. NSAIDS 2. Aspirin |
| What is unique about aspirin? | Noncompetitive, irreversible inhibitor of cycloygenase enzyme |
| 1. 2 important clotting factors produce by COX 1 2. Function of both | 1. Prostacyclin (PGI2) : inhibits platelets and vasodilator 2. Thromboxane A2 (TXA2) : increases platelets and vasoconstrictor |
| Aspirin, if taken every day will block what? | TXA2 and PGI2 |
| 1. PGI2 is produced where? 2. TXA2? | 1. Endothelium 2. Platelets |
| 1. What happens if aspirin is taken every other day? 2. How is this possible? | 1. Enhances PGI2 and block TXA2 2. Well...platelets don't devide so they only have "X" amount of COX 1 therefor can only make so much TXA2 (once it's blocked, it's blocked). Endothelial cells are contantly being reproduced as is COX 1 therefor PGI2, |
| (continuation) | after it's done being blocked, body produces more |
| 1. Druf that is not an NSAID and not an antiinflammatory and blocks COX 3 2. AKA? | 1. Acetaminophen 2. Tylenol |
| 1. Number one complication of antiinflammatory drugs (NSAIDS) 2. How does this happen? | 1. Gastric ulcers 2. Deteriorates mucous lining |
| NSAIDs block what? (in reguards to ulcers) | Mucous producing protaglandins (PGE2, PGD2, PGF2ALPHA) ... BAD!!! = ulcers |
| Why does increased stress create ulcers? | Because sympathetic drive contricts blood flow to GI tract which is essential for mucous formation! |
| 2 ways in which we can modify the affects of aspirin (or other NSAIDs) on gastric ulcers | Coating the aspirin and create a COX 2 inhibitor |
| What will coating the aspirin do? | Allow aspirin to enter GI tract before it dissolves in stomach to destroy the PGE2 (mucous production) |
| What do COX 2 inhibitors do? | Blocks COX 2 and leaves COX 1 alone... blocks inflammation without affecting mucous production! Happy day! |
| 1. Enzyme responsible for mucous production? 2. What else is it active in ? | 1. COX 1 2. Clotting: PGI2 and TXA2 (COX 1 produces these) |
| 2 examples of COX 2 inhibitors | 1. Viox 2. Celebrex |
| 1. Celebrex blocks ___ of COX 1 and ___ of COX 2. Celebrex was developed for what? | 1. 10% of COX 1 and 90% of COX 2 2. Treat chronic inflammation without causing gastric ulcers |
| Naproxen blocks both ___ and ___ | COX 1 and COX 2 |
| What does COX 2 do? | Controls inflammatory effects on cells (COX 2 inhibitors block this and leaves COX 1 alone) |
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LrB
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