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| 5300637126 | Common INTRA-cellular accumulations | Fat Hyaline Ca++ Proteins Glycogen Pigments | 0 | |
| 5300651740 | Etiology | "Cause" | 1 | |
| 5300652160 | Pathogenesis | "Insidious development" Sequence of events from the initial stimulus to the ultimate expression of the disease | 2 | |
| 5300652161 | Morphology | "Abnormal Anatomy" | 3 | |
| 5300656003 | Apoptosis | Normal cell death | 4 | |
| 5300656004 | Necrosis | "premature" or "untimely" cell death due to causes | 5 | |
| 5300659886 | -plasia | Growth | 6 | |
| 5300659887 | METAplasia | normal cells, but they are in the wrong place! | 7 | |
| 5300661930 | DYSplasia | Cells which are growing abnormally, and frequently are referred to as pre-malignant/pre-invasive growth | 8 | |
| 5300663858 | -trophy | size of the cell | 9 | |
| 5300665245 | Atrophy | shrinkage of cell due to loss of CELL SUBSTANCE (not water) | 10 | |
| 5300666336 | What can cause atrophy | decreased workload denervation decreased blood flow decreased nutrition aging | 11 | |
| 5300668473 | Reversible cellular changes | - reduced oxidative phosphorylation - ATP depletion - Cellular "swelling" | 12 | |
| 5300670613 | Irreversible cell changes | !) If the mitochrondria die, the cell dies 2) if the membrane can't keep the sodium out, the cell dies 3) if the lysosomes start to auto digest the cell, the cell is dead | 13 | |
| 5300673099 | Three main causes of injurty | Physical - trauma/heat/cold Chemical Infectious - bacteria, viruses | 14 | |
| 5300674874 | What happens to nuclei when cells start to die | smaller, darker, fragmented, dissolved | 15 | |
| 5300676464 | Gangrenous necrosis | Just means dead, Might imply the loss of blood flow. Dry or wet | 16 | |
| 5300676909 | Fibrinosis necrosis | Means that the dead tissue will stain the same colour as fibrinous tissue. Often used to describe damage walls of blood vessels. | 17 | |
| 5300678140 | Caseous necrosis | A term used for tissues that can no longer hold their shape well. If you cut them, they will fall apart. "cheese" | 18 | |
| 5300680841 | Fibrinoid Necrosis |  | 19 | |
| 5300685197 | Gangrene |  | 20 | |
| 5300689334 | Shrinkage/Hyperchromasia | Shrinkage, increased nuclear staining, nuclear fragmentation. |  | 21 |
| 5300698993 | karyolysis | nuclear dissolution | 22 | |
| 5300698994 | Pyknosis | clumping of nucleus | 23 | |
| 5300699299 | Keryorrhesxis | Fragmentation of nucleus |  | 24 |
| 5300702872 | What is an obvious difference between apoptosis and necrosis? | apoptosis is neat and intentional necrosis is messy | 25 | |
| 5300722272 | Innate and Adaptive Immunity cells | | 26 | |
| 5300740285 | Toll Like Receptors are a type of | Pattern Recognition Receptors (PRRs) They are a part of the innate immune system | 27 | |
| 5300741992 | PRR's recognize | PAMPs Pathogen-associated molecular patterns | 28 | |
| 5300746138 | Principal cell of acute inflammation | Polymorphonuclear leukocyte (PMN) - Neutrophils | 29 | |
| 5300746891 | Principal cell of chronic inflammation | Mononuclear - leukocyte | 30 | |
| 5300748294 | Cells of the innate immune system | Neutrophils Monocytes (Mast Cells) Eosinophils Basophils *NK cells | 31 | |
| 5300750666 | Sequence of events in inflammation | 1) vasodilation 2) increased vascular permeability 3) leakage of exudate 4) Margination, rolling, adhesion 5) Diapedisis (transmigration) 6) Chemotaxis 7) PMN (neutrophils) activation 8) Phagocytosis | 32 | |
| 5300754159 | Possible outcomes of inflammation | resolution scar chronic inflammation | 33 | |
| 5300755120 | Mast Cells | Big bags of granules | 34 | |
| 5300755580 | Where are mast cells located | In the loose connective tissues in your skin. Anywhere someone can penetrate the skin. | 35 | |
| 5300756553 | When mast cells degranulate, like a squid squirting ink, what do they squirt out? | Histamine chemotactic factors | 36 | |
| 5300757858 | What does histamine do | boo i'm scared! -vasodilation -smooth muscle contraction Now that i'm empty of my granules, i'm gonna synthesis more stuff - leukotrienes -prostaglandins -Platelet-activating Factor | 37 | |
| 5300760712 | What do the chemotactic factors that the mast cells release do? | Attract other white blood cells ex. neutrophil chemotactic factor (Guess what cell this chemotactic factor attracts? :)) | 38 | |
| 5300763791 | sooo.. what do the mast cell granules do? | 1) stimulate inflammation (vasodilation and smooth muscle contraction) 2) release chemotactic factors to attract other white blood cells to the scene of crime | 39 | |
| 5300773425 | Leukotrienes | white blood cells talking to each other | 40 | |
| 5300774695 | prostaglandins | have a tendency to do things like sensitise the body to pain. They can also cause vasoactive effects. | 41 | |
| 5300779349 | Leukocytes |  | 42 | |
| 5300780576 | Which leukocytes are the first on the scene? | Neutrophiils | 43 | |
| 5300787575 | Neutrophils are especially eager to kill | bacteria and fungus (things that like to travel a lot) | 44 | |
| 5300788745 | Eosinophils are especially eager to kill | parasites they are also found when you have allergies | 45 | |
| 5300790192 | stages of white blood cells leaving the blood and entering the tissues | margination rolling adhesion transmigration (diapedesis) | 46 | |
| 5300790193 | heparin | anticoagulant | 47 | |
| 5300791156 | Monocyte | in blood (clark kent) | 48 | |
| 5300794326 | Macrophage | Monocyte once it is activated and enters the tissue (superman) "superMAcrophage" hehe | 49 | |
| 5300797475 | Macrophages are found all over the body, and they have different names depending on where they are in the body. What are they called when they are in the brain? | microglia | 50 | |
| 5300800580 | How do macrophages/monocytes contribute to inflammation? | They have specialised chemicals -interleukins IL-* (help communicate between white blood cells) -Tumor Necrosis Factor | 51 | |
| 5300804620 | Monocyte actions that affect inflammation |  | 52 | |
| 5300809196 | What cells use Nitric Oxide and Free Radicals to mess with (digest and kill) whatever they eat? | macrophages! Monocytes | 53 | |
| 5300812567 | Chemical messengers between white blood cells | Cytokines (this is an umbrella term for a number of different chemical messengers) | 54 | |
| 5300813786 | Main types of cytokines | Interleukins Tumor Necrosis Factor Interferon | 55 | |
| 5300814634 | Interleukins are released by? | Primarily macrophages and lymphocytes | 56 | |
| 5300815405 | Tumor necrosis factor is released by? | Macrophages | 57 | |
| 5300820502 | What role do interferons play in the immune system? | interrupt viral replication, are produced by virus-infected cells and help slow down viral infections | 58 | |
| 5300824748 | Why do macrophages or lymphocytes release interleukins? | They have detected a pathogen and they want to attract other white blood cells to the area, or they want to stimulate proliferation of other white blood cells (bone marrow?) | 59 | |
| 5300827004 | Tumor Necrosis Factor | It is also secreted by macrophages. It is released because of PAMPs. The PAMP stimulates a TLR to be fired and then "poof" TNF is released. | 60 | |
| 5300829912 | Interferons | Primarily released by virally infected cells. The cells release this to tell other cells to be careful and not get infected themselves. |  | 61 |
| 5300833582 | Tumor Necrosis Factor-alpha | Produced primarily by macrophage mediates acute inflammation directs WBC chemotaxis to tissue Stimulates liver enzyme release | 62 | |
| 5300836595 | Interleukin-1 | Promotes acute inflammatory response stimulates coagulation enhances WBC migration increase tissue temp stimulates liver enzyme release | 63 | |
| 5300839110 |  | 64 | ||
| 5300842873 | Acute vs Chronic Inflammation | Acute focuses on preventing spread and restorative healing chronic focuses on preventing spread and adaptive remodeling | 65 | |
| 5300863322 | What are the three protein cascade systems that mediate the inflammation response? | Complement System Coagulation System Kinin System | 66 | |
| 5300864885 | What does complement do? | It battles invaders! It either attacks it (punching holes in it's membrane), or it holds it down so that other parts of the immune system can get it. | 67 | |
| 5300868150 | Where do the protein cascade systems live? | They are always circulating in your blood waiting to be activated. as proenzymes "pro"= before activation | 68 | |
| 5300870617 | Types of complement cascade? | classical lectin alternative |  | 69 |
| 5300872428 | Which of the complement cascades is not part of the innate immunity (i.e. is part of the adaptive immunity)? | Classical! | 70 | |
| 5300873066 | What triggers the classical complement cascade? | It needs an antigen antibody complex to trigger it. | 71 | |
| 5300875154 | What triggers the alternative complement pathway? | It is spontaneously activated by pathogen surfaces. | 72 | |
| 5300876317 | Lectin complement pathway recognises? | mannose sugar on the pathogens | 73 | |
| 5300878267 | complement pathway can do..? | stimulates the inflammatory response - stimulates mast cells - attract white blood cells to the area will try to directly kill the bacteria or it will stick to it. | 74 | |
| 5300880953 | Where do all of the complement pathways converge? | C3 | 75 | |
| 5300882077 | What does C9 do? | Creates the membrane attack complex | 76 | |
| 5300884209 | What does complement do? | ALL PATHS activate membrane attack complex opsonization chemotaxis (attract other cells to the area) inflammatory response |  | 77 |
| 5300891267 | Compliment works with all other immune cells |  | 78 | |
| 5300896632 | Main component of the coagulation cascade? | Fibrin | 79 | |
| 5300923367 | Bradykinin | localised pain vasodilation smooth muscle constriction vascular leakage (oedema) | 80 | |
| 5300930404 | -When the liver is stimulated, it released proteins into the blood -granules -synthesised in blood |  | 81 | |
| 5300936523 | Adaptive Immune system |  | 82 | |
| 5300943055 | Active immunity | antibodies or t cells produced after either a natural exposure to an antigen or after immunization | 83 | |
| 5300943579 | passive immunity | preformed antibodies or T-lymphocytes are transferred from a donor to a recipient | 84 | |
| 5300959885 | What cells are antigen presenting cells? | Dendritic cells and macrophagesf | 85 | |
| 5300978328 | Two kinds of adaptive immunity responses | humoral and cell-mediated | 86 | |
| 5300986349 | players of cell-mediated immune response | antigen-presenting cells (macrophages, dendritic cells) Helper T cells Cytotoxic T cells infected cells T cell stuff! | 87 | |
| 5300996425 | CD8+ | Cytotoxic t cellz | 88 | |
| 5300996865 | CD4+ | Helper T cells (generals!) | 89 | |
| 5301004713 | Humoral Immune Response | When the helper t cells recognise an infected cell and then go and activate the B cells to create plasma (memory) cells and antibodies | 90 | |
| 5301006009 | Cell-Mediated Immune Response | When the Helper T cell is presented an antigen by an APC and stimulates more Helper T cell proliferation. Helper T cells bind with a B cell that has also coincidentally eaten the same antigen and is presenting it as well. This binding triggers the B-Cells to proliferate (plasma cells and antibodies). complement is also activated to poke holes in invader. | 91 | |
| 5301025201 | T Cells | They are there to kill virus infected cells and fungus cell. If you lose these cells, you get virus and fungus related problems | 92 | |
| 5301031143 | T Cell differentiation occurs in.... | Cell-mediated immunity | 93 | |
| 5301035524 | Humoral Immunity revolves around... | B lymphocytes. B cells throw antibodies out into the environment, these antibodies circulate through the blood and try to kill invaders/attract other WBC to help fight. | 94 | |
| 5301036203 | Humoral Immunity |  | 95 | |
| 5301037492 | B cells become | Plasma cells (pumps out antibodies) Memory cells (not there to fight, hides in the closet until next infection) | 96 | |
| 5301037939 | immunoglobulins are basically | antibodies | 97 | |
| 5301038447 | Which of the B cells crank out antibodies | plasma cells | 98 | |
| 5301040053 | Whats the difference between antibodies and immunoglobulins? | Antibodies - free floating in blood immunoglobulins - stuck to the surface of the cell | 99 | |
| 5301047504 | complement can be activated by | tons of stuff. antibodies, chemical messengers etc. just know that it happens | 100 | |
| 5301050348 | Classes of antibodies GAMED | IgG, IgA, IgM, IgE, IgE | 101 | |
| 5301050982 | most common antibody | IgG | 102 | |
| 5301051524 | Which antibody can cross the placenta? | IgG | 103 | |
| 5301052187 | Which antibody is in all of the secretions of the body? Blood, mucus, milk, tears, saliva. Basically lines the surface of the body and helps protect you from invaders. | IgA | 104 | |
| 5301056419 | primary antibody of the primary responce | IgM | 105 | |
| 5301057093 | Which antibody is associated with histamine and allergies. Makes mast cells and basophils more reactive. | IgE | 106 | |
| 5301059351 | IgE | for parasites and allergic reactions | 107 | |
| 5301059723 | Which granulocyte focuses on parasite attack | eosinophils | 108 | |
| 5301069205 | What glycoproteins identify the T cells | CD4 and CD8 | 109 | |
| 5301073055 | cytotoxic T cells secrete ____ to kill infected cells | perforin (they PERFORATE the cell) | 110 | |
| 5301075969 | Which T cells stop cytotoxic T cells from hurting self? | T regulatory Cells | 111 | |
| 5301076658 | CD4 Cells | The president of the immune system T Helper cells Tell the immune cells what to do | 112 | |
| 5301080750 | What triggers cell-mediated immunity | antigen presenting cells | 113 | |
| 5301081048 | cell-mediated immunity |  | 114 | |
| 5301082772 | cytotoxic t cells do... | either make cells commit apoptosis or secrete perforin to kill bad cells | 115 | |
| 5301084841 | T helper cells are gossips CD4 |  | 116 | |
| 5301097705 | T-Helper cells come in two flavours | Th1 and Th2 | 117 | |
| 5301098140 | Th1 cells | talk to T cells. They stimulate cell-mediated immunity. They talk to Cytotoxic T cells | 118 | |
| 5301099547 | Th2 cells | important for developing humeral immunity. They interact with the B cells and tell the B cells what to do. | 119 | |
| 5301101692 | Natural Killer cells | recognise self cells. | 120 | |
| 5301107607 | Types of adhesion molecules | secretins, integrins | 121 | |
| 5301108150 | secretins | the adhesion molecules on the surface of endothelial cells (lining the vessels) | 122 | |
| 5301110897 | integrins | the adhesion molecules on the white blood cells that are going to go through diapedesis | 123 | |
| 5301112368 | chemotaxis | the process by which the white blood cells travel to the site of injury. How do they know where to go? Through the use of chemicals. | 124 | |
| 5301115372 | When granulocytes arrive at the site of battle and are 'activated' they secrete three things | 1) they undergo degranulation 2) secrete cytokines 3) produce eicosanoids | 125 | |
| 5301116942 | eicosanoids | 20 chain fatty acids released by leukocytes (part of cell membranes) prostaglandins leukotrienes lipoxins | 126 | |
| 5301120479 | prostaglandins | think about what asprin does helps pain, fever, prevents clotting these eicosanoids: pain fever clotting | 127 | |
| 5301121771 | leukotrienes do the opposite of | lipoxins | 128 | |
| 5301122577 | leukotrienes are involved in | chemotaxis (bringing white blood cells where they need to be) vasoconstriction increased permeability | 129 | |
| 5301123012 | lipoxins | inhibit chemotaxis vasodilation decreased permeability | 130 | |
| 5301125322 | cytokines | proteins produced by many cells (primarily lymphocytes and macrophages) that have many roles in acute and chronic inflammation | 131 | |
| 5301126486 | cytokines of macrophages | TNF-a and iL-1 | 132 | |
| 5301127111 | Chemokines | small proteins which are attractants for PMNs | 133 | |
| 5301131697 | exudate types of acute inflammation | serous (watery) fibrinous (hemorrhagic, rich in fibrin) suppurative (pus) ulcerative | 134 | |
| 5301132369 | something to remember about fibrinous exudate | fibrin can be seen a lot, especially if there has been a lot of bleeding. Remember that fibrin is the end product of the coagulation cascade, so it's probably there to reduce further blood flow. | 135 | |
| 5301134775 | What is usually in purulent exudate | neutrophils | 136 | |
| 5301137660 | four components of granulomas | fibroblasts, lymphocytes, macrophages, giant cells | 137 | |
| 5301138088 | giant cells | macrophages that have fused and have multiple nuclei | 138 | |
| 5301143050 | What are the five pathological processes of disease | 1) immunology, inflammation and repair 2) cell injury, necrosis, 3) circulatory disturbances 4) disorders of growth 5) pigmentations and tissue deposits | 139 | |
| 5301148252 | inflammation ONLY occurs in | living tissue | 140 | |
| 5301150588 | Inflammation can be harmful. How? | -innate immunity has to potential to cause tissue damage -death of neutrophils releases free radicals -hypersensitivity of adaptive immunity | 141 | |
| 5301152680 | How do we classify an inflammatory response? | 1) What kind of exudate is present 2) Time course | 142 | |
| 5301153205 | Inflammatory time course | peracute acute subacute chronic | 143 | |
| 5301153314 | peracute | minutes to hours | 144 | |
| 5301153625 | acute | hours to days | 145 | |
| 5301153626 | subacute | several days to 1-2 weeks | 146 | |
| 5301153922 | chronic | many days, weeks, months, years | 147 | |
| 5301162723 | injury |  | 148 | |
| 5301164160 | cells of chronic inflammation | lymphocytes plasma cells macrophages | 149 | |
| 5301165805 | cells of acute inflammation | neutrophils, eosinophils, basophils | 150 | |
| 5301166807 | acute pneumonia |  | 151 | |
| 5301167447 | what is the difference between a leukocyte and an inflammatory cell? | They are all neutrophils, eosinophils, basophils and lymphocytes. When circulating they are called leukocytes, when in tissues, they are called inflammatory cells | 152 | |
| 5301170108 | to T or B cells dominate in circulation | B cells | 153 | |
| 5301171879 | Transudate is usually referred to as | oedema | 154 | |
| 5301171880 | transudate | ultrafiltrate of plasma, low specific gravity, lower protein concentration than that of plasma, low cellularity | 155 | |
| 5301173379 | exudate | lots of proteins, fibrinogen | 156 | |
| 5301174069 | what plasma protein is abundant in exudate? | fibrinogen! | 157 | |
| 5301175021 | what is the difference between inflammatory and non-inflammatory oedema? | exudate - inflammatory oedema transudate - oedema | 158 | |
| 5301185054 | features of acute inflammation | vasodilation increased fluid phase of exudate lots of neutrophils little repair haemorrhagic | 159 | |
| 5301185055 | features of chronic inflammation | lots of cells in the exudate mononuclear cells dominate repair (fibrosis) granulomas | 160 | |
| 5301190748 | morphological diagnosis of disease SEVERITY | minimal, milk, moderate, severe or marked | 161 | |
| 5301191552 | Morphological diagnosis of disease DURATION | peracute, acute, subacute, chronic, chronic-active | 162 | |
| 5301193853 | vascularity starts to decrease after | ACUTE INFLAMMATION | 163 | |
| 5301194436 | Morphological diagnosis DISTRIBUTION | focal multifocal locally extensive diffuse | 164 | |
| 5301198119 | When presenting a morphological diagnosis what is the order of your descriptors? | organ tissue specific site within tissue distribution pathological process severity duration | 165 | |
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| 5301206229 | 170 |
