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Pathophys 1st Exam
Dr. A's Pathophysiology Midterm 1
| Question | Answer |
|---|---|
| Define etiology | the cause of a disease |
| Define pathogenesis | the sequence in manifestation of an illness |
| What are morphologic changes? | size, shape and color, consistency changes |
| What are functional derangements and clinical manifestations? | signs and symptoms a patient presents with |
| What's the difference b/w focal and diffuse? | focal is well defined or a definitive space. diffuse is broad region, not well defined or spread out |
| What dictates the potential for a tissue or organ to adapt to an injury/stress? (6) | 1. The potential for regeneration 2. The severity of the injury 3. The duration of the injury 4. The condition of the cell 5. The location of the cell 6. The degree of cell specialization |
| What are labile cells? Example? | A continuously renewing cell population. epithelial cells |
| What are stabile cells? Example? | A (potentially) expanding cell population. hepatocyte, any -blast |
| What are permanent cells? Example? | A static (can't regrow) cell population. CNS cells and cardiac cells |
| What are the 5 cell adaptations? | 1. Atrophy 2. Hypertrophy 3. Hyperplasia 4. Metaplasia 5. Dysplasia |
| What is atrophy? | An adaptation to diminished need or resources for a cell's activities. |
| What occurs with atrophy? | Shrinkage of a cell or organ due to the loss of organelles. |
| What does atrophy involve? | Changes in both production and destruction of cellular constituents. A cell's reversible restructuring of its activities to help its survival and adapt to diminished use. |
| What causes pathological atrophy? Example? | Diminished blood supply, inadequate nutrition, loss of innervation, abnormal endocrine stim. loss, decreased workload. atherosclerosis, spinal lesion |
| What is hypertrophy? | An increase in cell size and functional capacity due to an increase in production and number of organelles |
| Where would you expect to find physiological hypertrophy? | muscles |
| Where could you find pathological hypertrophy? | heart: myocardial hypertrophy due to valve damage or MI |
| What is hyperplasia? | Increase in size of an organ or tissue due to an increase in the number of cells. Increased functional and/or metabolic demands on the cell or compensatory proliferation. |
| Where would you find physiological hyperplasia? | Lactating breast from hormonal stim. and increase in RBCs at high altitude. |
| When could you find pathological hyperplasia? | endometriosis, psoriasis, liver regeneration |
| What is metaplasia? | A change/substitution in which one terminally differentiated cell type is replaced by another terminally differentiated cell type. |
| Why would you find metaplasia? | Persistent injury/irritation (smoker) |
| What conditions could produce metaplasia? | Barret esophagus Myositis ossificans |
| What is dysplasia? | A disordered growth and maturation of the cellular components of a tissue. i.e. The morphologic expression of the disturbance in growth regulation. |
| What conditions may give rise to neoplasia? | hyperplasia, metaplasia, dysplasia |
| What are the 3 categories of cellular accumulations? | 1. Normal cellular constituent 2. An abnormal substance 3. A pigment |
| Why might substances accumulate in a cell/organ? | increased production, decreased metabolism, increased deposition, decreased transport |
| Give 6 examples of intracellular accumulations. | 1. Steatosis 2. Hydropic change 3. Pigments 4. Proteins 5. Glycogen 6. Cholesterol |
| What is steatosis and what is the most common organ involved? Caused from? | Steatosis is an accumulation of triglycerides w/in parenchymal cells. Commonly involved in the liver. Caused from protein malnutrition, toxins (alcohol #1), obesity, anoxia |
| What occurs in a cell with ischemia? | Low oxygen Low pH High lactate Low ATP |
| What is hydropic change/cellular swelling? | An increase in water accumulation within parenchymal cells. |
| What is the most common cause of cellular swelling? | Loss of ATP resulting in falure of the Na/K ATPase pump. |
| If you have hemosiderosis what has occurred? | Accumulation of iron w/in parenchymal cells and w/in interstitium; golden brown granules |
| What is focal hemosiderosis? | a common bruise (localized) |
| What is systemic hemosiderosis? | Body looks bruised, can be from blood transfusions, hemolytic anemias, hemochromatosis (increased absorption of iron) |
| What is lipofuscin? | An undigestable mixture of lipids and proteins thought to be result of oxidative stress. Wear and tear pigment (yellowish), increases with age |
| What diseases could lead to glycogen accumulation? | Enzyme deficiency diseases. |
| What are the 4 enzyme deficiency diseases and what enzymes are they associated with? | 1. Pompe: acid alpha glucosidase 2. McArdle: myophosphorylase 3. Cori: glycogen debranching enzyme 4. von Gierke: glucose-6-phosphatase |
| Where can cholesterol accumulate? | Macrophages and vascular smooth muscle cells w/in blood vessel walls |
| What is a disorder of cholesterol accumulation? | Xanthomas |
| Know the causes of cell injury and the biochemical processes that govern the manifestation | pg. 23 in notes |
| What are subcellular changes in reversibly injured cells? (2) | 1. cellular swelling 2. steatosis |
| What are structural cell changes in reversible injuries? (6) | 1. Plasma membrane bleb 2. Increased intracellular volume 3. Mitochondrial swelling and calcification 4. Disaggregated ribosomes 5. Dilated, vesicular ER 6. Aggregated cytoskeletal elements |
| What occurs in an irreversible injury of a cell? (3) | 1. Vacuolization of the mitochondria 2. Rupture of lysosomes 3. Nuclear changes |
| What are the 3 nuclear changes and how do they present? | 1. pyknosis: pinpoint nucleus (shrunken) 2. karryorrhexis: fragmented nucleus 3. karyolysis: nucleus no longer visible |
| Review free radicals and the reactions in the body. | pgs. 27 - 31 |
| What is dystrophic calcification? | Calcium deposition in dead (necrotic)/non-viable tissue |
| What is metastatic calcification? | Calcium deposition in normal tissues due to hypercalcemia. (over entire area) |
| What is necrosis? | A spectrum of morphologic changes that occur in cells following cell death in living tissue. |
| What are the 2 processes that give the sum of necrosis? | 1. denaturation of proteins 2. enzymatic digestion of organelles |
| What is coagulative necrosis? | Morphologic pattern of necrosis characterized by preservation of cellular outline, lacking nuclei |
| Where would coagulative necrosis occur? | heart, kidney tubular cells |
| What is liquefactive necrosis? | Morphologic pattern of necrosis characterized by destruction of the tissue, cellular debris, loss of architecture. |
| Where does liquefactive necrosis occur? | CNS |
| What is gangrenous necrosis? | Morphologic pattern of necrosis characterized by blue/black discoloration of the anatomy, visible with eyes. |
| When does gangrenous necrosis occur and what are the 2 types? | In limbs after disruption of blood supply. Dry = w/o bacterial infection and Wet = w/ bacterial infection |
| What is caseous necrosis? | Morphologic pattern of necrosis characterized by cheesy like consistency, necrotic debris resembles cheese. |
| Why would caseous necrosis occur? | TB |
| What is enzymatic fat necrosis? | Morphologic pattern of necrosis characterized by enzymatic degradation of fat/lipids |
| What is the word for turn to soap (fat react w/ minerals) giving a bubbly necrotic debris? | saponification |
| Where does enzymatic fat necrosis readily occur? | pancreas. pancreatitis gives severe, lancinating epigastric pain |
| review apoptosis | pg. 38 |
| What do HSP 60 and HSP 70 do? | Involved in protein folding and targeting to final destination. (chaperonins) |
| What does ubiquitin do? | Facilitates degradation of proteins. |
| Define inflammation. | A complex reaction to injurious agents such as microbes and damaged, usually necrotic cells that consists of vascular responses, migration and activation of WBCs and systemic reactions. |
| Give the 4 major players in the inflammatory process. | 1. WBCs 2. Blood vessels 3. CT cells 4. Extracellular Matrix |
| What are major causes of inflammation? | physical, chemical, microbiological, immune responses; anything that can damage a cell can cause inflammation |
| What is an acute inflammatory response both clinically and histologically? | Clinically: rapid onset, short-lived, symptomology Histologically: Neutrophils predominate, macrophages arrive later |
| What is a chronic inflammatory response both clinically and histologically? | Clinically: slow onset, long-lived, symptoms appear late, pronounced tissue damage Histologically: lymphocytes, macrophages, fibroblasts |
| What are the cardinal signs of inflammation? (both languages) | heat (calor), swelling (tumor), redness (rubor), pain (dolor), loss of function (functio laesa) |
| What is an edema? | Accumulation of fluid w/in the extravascular compartment and interstitial tissues |
| What is an exudate? | Edema fluid w/ a high protein [] which frequently contains inflammatory cells. Exudates are observed early in acute inflam. reactions and produced by mild injuries |
| What is an effusion? | Excess fluid in body cavities |
| What is a transudate? | Edema fluid w/ low protein [] |
| What is a serous exudate or effusion? | Absence of prominent cellular response with a yellow/straw-like color |
| What does serosanguinous mean? | A serous exudate, or effusion, that contains RBCs and has a red tinge. |
| What is a fibrinous exudate? | An exudate that contains large amounts of fibrin resulting from activiation of the coagulation system. Referred to as fibrinous pleuritis or fibrinous pericarditis when occurs on serosal surfaces |
| What is a purulent exudate and what conditions is it frequently associated with? | Contains prominent cellular components. Pus Pyogenic bacterial infections where PMNs predominate |
| What is supporative inflammation? | A condition in which a purulent exudate is accompanied by significant liquefactive necrosis. A pattern that is pus producing. |
| What is the sequence of events in inflammation? | 1. transient vasoconstriction 2. vasodilation 3. margination 4. adhesion/pavementation 5. emigration/migration via chemotaxis 6. aggregation 7. phagocytosis |
| Why does transient vasoconstriction occur? | To prevent bleeding out (hemorrhaging) |
| Vasodilation during inflammation does what? | Increases blood flow to the damaged tissue and slows blood flow so nutrients arrive but less blood is lost. Also increases vascular permeability. |
| What is an immediate-transient response? | Endothelial cell contraction (tight junctions open) |
| What is an immediate-sustained response? | Endothelial cell damage (large efflux) |
| What is delayed-prolonged leakage? | apoptosis? Cell exposed to damaging stim and then apoptoses b/c too damaged causing leakiness to begin. |
| What is stasis? | Decreased velocity of bloodflow |
| What does margination in inflammation mean? | Movement of WBCs toward vascular wall. |
| What do selectins do in the adhesion/pavementation stage of inflammation? | Rolls and sticks WBCs along the side of the vessel wall. |
| What do integrins do in the adhesion/pavementation stage of inflammation? | Sticks the WBCs firmly to the vessel wall. |
| What do immunoglobulins do in the adhesion/pavementation stage of inflammation? | Causes WBCs to squeeze b/w endothelial cells (transmigration). |
| What is not produced in the deficiencies LAD type 1 and 2? | 1. selectins 2. integrins characterized by recurrent bacterial infections |
| What is chemotaxis? | Movement along a chemical gradient. |
| What occurs with phagocytosis? | Recognition and binding of WBCs via opsonization (coat bacterium) Engulfment via endocytosis Killing via free radicals, lysosomal enzymes and production of AA metabolites |
| What are the opsonins? | C3b, IgG |
| What are the 3 systems associated with chemical mediators? | 1. Kinin system 2. Complement system 3. Clotting system |
| Kinin system cascade produces what? What are its effects and how is it activated? | Bradykinin Pain, vasodilation, increased vascular permeability. Activated by the coagulation system ->Hageman Factor |
| The complement system is a family of 20 proteins, what are the 4 most important and what do they do? | 1. C3a: VD and increased VP 2. C5a: VD and increased VP, chemotaxis; activates AA metabolism 3. C3b: opsonin (coats targets) 4. C5b-C9: membrane attack complex |
| What are other activators of the complement system and what do they do? (3) | 1. Classic pathway: antigen antibody complexes turn on C1 turns on complement system 2. Alternate pathway: Interaction with LPS turns on complement system 3. Mannose Binding pathway: Microbial surfaces can exhibit sugar to turn on system |
| Describe the Coagulation Cascade. | Prothrombin becomes thrombin. Thrombin + fibrinogen -> fibrin. Plasminogen + tPA -> plasmin. Fibrin + plasmin -> fibrin split products (review notes on pg. 56) |
| Name 2 vasoactive amines and what they do. | 1. Histamine: Major inflammatory chemical throughout body. Secreted by many cells and derived from basophils. Serotonin: Amine in GI tract and brain, augments blood flow (review notes on pg. 58) |
| What are the 2 Arachidonic Acid pathways? | 1. Lipoxygenase pathway (LOX) 2. Cyclooxygenase pathway (COX) |
| What type of products does the COX pathway produce? (3) | prostaglandins (PG) thromboxane (TX) Lipoxins (LX) |
| What type of products does the LOX pathway produce? (2) | Leukotrienes (LT) Lipoxins (LX) |
| What LOX product is the cell derived chemotactic agents for WBCs? | LTB4 |
| What protein of the complement system is a plasma derived chemotactic agent? | C5a |
| Which cytokine is a cell derived chemotactic agent for neutrophils only? | IL-8 |
| What condition do leukotrienes mimic and why? | asthma; increased vascular permeability and vasodilation, hypersensitivity to something inhaled, bronchus closes |
| PGE2 increases/is associated with? | pain |
| Prostacyclin inhibits what and which proastaglandin is a prostacyclin? | platelet aggregation; PGI2 |
| What does thromboxane do? | vasoconstricts and increases platelet aggregation |
| What is singulair's action on the arachidonic acid metabolites? | blocks leukotrienes by inhibiting LOX pathway |
| What are some examples of COX inhibitors? | Vioxx, Celebrex, NSAIDs |
| What do steroids inhibit? | Phospholipase, both LOX and COX |
| COX-1 is generally found in? COX-2 mainly produces? | GI tract Inflammation and pain |
| PGE2 and PDG2 cause what biologically? | induce vasodilation, bronchodilation; inhibits inflammatory cell function |
| PGI2 causes what biological activity? | Induces vasodilation, bronchodilation; Inhibits inflammatory cell function |
| PGF2a does what biologically? | Induces vasodilation, bronchoconstriction |
| TXA2 does what biologically? | Induces vasoconstriction, bronchoconstriction; Enhances inflammatory cell functions (especially platelets) |
| LTB4 causes what biological activity? | Chemotactic for phagocytic cells; stimulates phagocytic cell adherence; enhances microvascular permeability |
| LTC4, LTD4, LTE4 all cause what biologically? | Induce smooth muscle contraction; constrict pulmonary airways; increase microvascular permeability |
| What do fish oils do to arachidonic acid metabolism? | Inhibits AA present |
| Cytokines are categorized as and do what action? | Interleukins; tell cell's to do work |
| What are the roles of cytokines in inflammation? (5) | 1. Induce synthesis of endothelium adhesion molecules 2. Induce synthesis of NO 3. Induce aggregation of neutrophils 4. Induce systemic acute-phase reactions 5. Chemotactic for neutrophils (IL-8 mainly) |
| What stimulates cytokine secretion? | Endotoxins, immune complexes, physical injury and produced by lymphocytes and macrophages (released with indication of tissue damage) |
| What 2 interleukins are the dictators of inflammatory response/first 2 to cause release of inflammatory mediators? | Interleukin 1 (IL-1) and Tumor/Tissue Necrosis Factor (TNF) |
| IL-2 takes what actions while mediating inflammation? | Responsible for adaptive host response, activates WBCs, recruits to fight off infections/tumors |
| IL-6 does what when mediating inflammation? | Involved in systemic acute phase reaction (flu-like symptoms); induces fever, pain, loss of apetite, malaise |
| IL-8 takes what action while mediating inflammation? | Cell derived chemotactic agent; chemokine for neutrophils only |
| What does TNF do an inflammation mediator? | Causes cell death -> triggers apoptosis in surrounding area |
| IL-1 and TNF play a role in what condition? | arthritis |
| IL-6 is special in that it can do what? | Cross the BBB to reset temperature at the hypothalamus |
| NO is a _______-derived _________ factor. | endothelial; relaxing derived from arginine |
| NO is synthesized by what 2 cells? | endothlial cells and macrophages |
| In what 2 forms is NO found? | Constitutive and inducible (endothelial cells and macrophages can induce) |
| What 2 actions can NO have in mediating inflammation? | Vasodilator and cytotoxic as a free radical; it mediates vascular tone and degrades foreign material |
| Platelet activating factor is derived from and is what? | membrane phospholipids; very potent and versatile mediator |
| Platelet activating factor (PAF) is synthesized by? (3) | 1. all inflammatory cells 2. endothelial cells 3. injured tissue |
| Platelet activating factor has what functions? (5) | 1. increased permeability 2. vasodilation 3. platelet aggregation 4. increased AA metabolism 5. increased leukocyte adherence |
| Review cytokine production flow chart | pg. 63 |
| If a macrophage is autocrine, what happens? | self stimulating effect - macrophage has IL-2 receptor-activated when IL-2 released |
| If a macrophage is paracrine, what happens? | One cell secretes substance that has an immediate effect in neighboring cells |
| If a macrophage is endocrine, what happens? | Substance secreted and travels distance away and causes an effect |
| Review WBCs, their actions, what they release, etc. | pgs. 64-66 |
| What is natural immunity? (3) | 1. inflammatory response 2. Doesn't require prior exposure to offending agent (antigen) 3. Is non-specific and lacks memory |
| What is "acquired immunity"? (3) | 1. A specific response to a specific antigen 2. Requires a sensitizing exposure 3. Response is magnified by subsequent exposure |
| IgA antibodies are found where? | nose, breathing passages, digestive tract, ears, eyes and vagina |
| IgA protect what parts of the body? | Surfaces that are exposed to the outside from foreign organisms and substances |
| IgA is found where? | saliva and tears |
| IgG antibodies are found where? | All body fluids but mostly in the blood. |
| How is IgG different in its size and abundance? | smallest but most abundant in body |
| IgG antibodies known for fighting what? | Bacterial and viral infections |
| IgG is special in that it can do what? | Only antibody that can cross the placenta and confer immunity to the fetus. |
| IgM antibodies are special how and are found where? | largest type; blood and lymph fluid |
| IgM are produced when? | First antibody produced in response to an infection. |
| IgD are found where and in what amount? | Tissues that line the cavities inside the body; small amounts |
| IgD plays a role in what? | allergic reactions to some substances like milk, some medications and some poisons |
| IgE are found where? | lungs, skin, mucous membranes |
| IgE protect the body against what substances? | pollen, fungus, spores and animal dander |
| IgE antibody levels are high in what type of people? | Those with allergies |
| A type 1 hypersensitivity reaction is mediated by and is of what type? | IgE; immediate |
| What are some examples of a type 1 hypersensitivity reaction? | hay fever, seasonal allergies, B-cell reaction to foreign antigen, anaphylactic reaction |
| What happens to mast cells in a type 1 hypersensitivity reaction? | IgE antibodies bind mast cells, basophils, cross link IgE receptors causing degranulation |
| A type 1 hypersensitivity reaction leads to and releases? | vascular leakage, especailly venules; various mediators including histamine |
| What is the 3 step process that occurs in a type 1 hypersensitivity reaction? | 1. initial exposure to antigen = increased IgE production 2. IgE binds to mast cells 3. Subsequent exposure to antigen = binding to IgE and degranulation of mast cells -> histamine, leukotrienes, eosinophil chemotactic factor |
| A type 2 hypersensitivity reaction involves what antibodies binding to what? | IgG and IgM bind to fixed (not soluble) target antigens cytotoxic |
| What does an antibody do in a type 2 hypersensitivity reaction? | Antibody binds to fixed antigen, attracts complement and Ig-Fc receptor bearing cells. IgG or IgM bind to "self" antigens and trigger complement activation and tissue damage |
| What type of antibodies are found in a type 3 hypersensitivity reaction? | A type 3 is an immune complex mediated response and IgG and IgM bind to circulating antigens forming immune complexes |
| A type 4 hypersensitivity reaction is what type of reaction and what is not produced? | T-cell-mediated or delayed-type reaction; antibody not produced |
| What elicits a type 4 reaction? | the antigen itself |
| Type 4 is considered a delayed hypersensitivity why? | Foreign antigens elicit cytokine release (Il-1, 6, 12) by T helper cells and cytokines cause macrophage and lymphocyte activation |
| How long does a type 4 reaction take to occur? | 24-48 hours after exposure |
| What are the outcomes of acute inflammation? | Complete resolution Healing by fibrosis/organization Abscess formation Chronic inflammation |
| Define chronic inflammation | Inflammation of prolonged duration (weeks or months) in which active inflammation, tissue destruction and attempts at healing are all proceeding simultaneously |
| What could cause chronic inflammation to arise without a pre-existing acute inflammatory component? | Persistent microbial infection Prolonged exposure to exogenous or endogenous toxic agents Autoimmune diseases |
| How does a macrophage "adapt" to chronic inflammation? | Becomes flattened out -> epithelioid cell Many fuse to become a "multi-nucleated giant cell" |
| What is granulomatous inflammation and what occurs with it? | A distinctive pattern of chronic inflammation: the predominant cell is the activated macrophage which possesses a modified epithelial like appearance; multinucleated giant cells, lymphocytes, necrosis and fibroblasts |
| What is a granuloma? | A focal area of granulomatous inflammation consisting of a central zone of necrosis surrounded by microscopic aggregates of epithelioid cells, lymphocytes and fibroblasts. |
| What causes a granuloma? | General: immune reaction, chronic irritation, undigestable foreign material, unknown etiology. specific: TB, leprosy, syphillis, sarcoidosis, fungal infection, suture. |
| What type of reaction tends to be granulomatous? | 4 |
| What does the wound healing and repair process involve? | Total reconstruction (regeneration/resolution) Partial reconstruction Universal repair tissue = fibrous CT scar |
| What are the 4 components to wound healing and repair and what do they involve? | Angiogenesis: migration and proliferation of endothelial cells Migration and proliferation of fibroblasts Deposition of extracellular matrix Remodeling of CT |
| What is granulation tissue? | The hallmark tissue of early healing by fibrosis (scab) |
| What is granulation tissue made up of? | Proliferating small capillaries, proliferating fibroblasts/myofibroblasts, extracellular fluid, macrophages |
| What is the function of granulation tissue? | Fill in tissue gaps Remove dead cell debris Aid in wound contraction Form an early pre-scar |
| What are the 7 steps of healing by primary union/intention? | 1. blood clot fills incisional space 2. Neutrophil infiltration 3. Epithelial continuity restored 4. Macrophage infiltration 5. Granulation tissue fills space 6. Progressive collagenization 7. Remodeling |
| What are the 4 steps of healing by secondary union/intention? | 1.Large amounts of granulation tissue are required 2. Inflammatory reaction is more prolonged 3. More debris and inflammatory exudate 4. More pronounced scar formation -> More myofibroblasts |
| What local (4) and systemic (3) factors influence wound healing? | type, size and location, vascular supply, infection, movement; circulatory status, infection, malnutrition |
| What is proud flesh? | Excessive granulation tissue. i.e. tiny cut but huge scab |
| What is keloid formation? | Hypertrophic scar: excessive collagen deposition |
| What is wound dehiscence? | Mechanical stress/ mechanical failure of a wound |
| What is contracture? | Excessive wound contraction i.e. myofibroblasts do too good of a job and cause dimpling of the skin |
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