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COMPLETE Pathophysiology Notes - Part 2 (4.0ed the final exam!)

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Boston College
NURS 2080

Pathophysiology Exam 1 SG INFLAMMATION Inflammation = reaction of body to cell injury or death Minimizes effects of infection or injury Removes damaged tissue Generates new tissue – repair process Damaged tissue is removed and new tissue is generated “-itis” caused by: Inflammatory mediators Fluid movement & leukocytes migration to extravascular tissues “itis” = inflammation Cells of inflammation Endothelial cells Line blood vessels Have a function related to blood pressure Selective barrier to microbes & inflammatory stimuli Regulate leukocyte extravasation Help regulate & modulate immune responses Secrete colony-stimulating factors Stimulate production of neutrophils and macrophages when they are low Release WBCs into extravascular tissue Regulate immune cell proliferation Repair process Platelets Cells in blood that help with hemostasis Have granules that contain inflammatory mediators Leukocytes Granulocytes and agranulocytes Neutrophils (granulocyte) Phagocyte Engulf bacteria and debris First to appear during inflammatory response (within 90 minutes); first responders Most numerous WBC in blood Mobile - can fit in and out of tight spaces Short life span (24-48 hours) Eosinophils (granulocyte) Phagocyte Protects against parasites Seen in allergic reactions Longer life span; seen in chronic inflammation Show up 2-3 hours after neutrophils – part of acute inflammatory response Basophils (granulocyte) Most prominent in IgE allergic reactions Histamine release Seen in allergic reactions Mast cells (granulocyte) Develop from basophil when leaving circulation Seen in allergic reactions Often seen in tissue injuries; come into contact with allergens or microorganisms Monocytes/macrophages (agranulocytes) Phagocyte Longer ½ life than granulocytes Produce vasoactive mediators Prostaglandins Leukotrienes Platelet activating factors Inflammatory cytokines Growth factors Lymphocytes (also migrate to site) - agranulocytes B cells - produce antibodies T cells Th cells produce cytokines Tc cells kill infected cells Don’t have to memorize Cell mediators of inflammation Histamine Released from mast cells, basophils, and platelets Dilation of blood vessels and increased permeability Upon release, attaches to endothelial cells to activate them to contract Released in acute inflammatory response Serotonin Found primarily-platelets Released during platelet aggregation Dilation of blood vessels and increased permeability Upon release, attaches to endothelial cells to activate them to contract Released in acute inflammatory response Leukotrienes Activated mast cells synthesize this mediator Like histamine, but occurs later & much more potent Can stimulate neutrophil & eosinophil chemotaxis Prostaglandins Induces inflammation Increased capillary permeability/vasodilation Smooth muscle vasoconstriction (bronchoconstriction) Can also stimulate neutrophil chemotaxis Chemotaxis is like a perfume: can follow scent down a hallway Our immune response spreads perfume to attract cells to a certain injury In case of prostaglandins it attracts neutrophils to the area Platelet activating factor Activates platelets – enhances serotonin release Stimulates leukocytes, endothelial cells & vascular smooth muscle Stimulates inflammatory mediators (prostaglandins) Nitric oxide Relaxes vascular smooth muscle - vasodilation Affects platelets (prevents adhesion, aggregation & degranulation) Regulates leukocyte recruitment Oxygen free radicals Low levels Increase expression of cytokines and endothelial adhesion molecules amplifying the cascade that elicits inflammation High levels Can produce endothelial cell damage causing vascular permeability; RBC injury Cytokines Interleukins Produced by macrophages & lymphocytes IL-1 Tumor necrosis factor alpha Produced by macrophages and mast cells Chemokines Recruit and directs migration of inflammatory & immune cells to site of injury Induce leukocyte chemotaxis Like a perfume *Important slide – memorize These 2 cytokines are important because they can attract neutrophils & start acute-phase response G- bacteria have sugar coating (LPS) Macrophage realizes it’s something foreign – initiates inflammatory response That macrophage can release TNF-a and IL-1. Interferon gamma (IFNy) stimulates macrophage to release these cytokines. When these cytokines are released, they circulate body When they get to hypothalamus, it causes a fever (affects body’s thermostat) Fever is normal for acute inflammation Macrophages can tell neutrophils to come to area They also activate/stimulate endothelial cells to produce certain things – they can make endothelial cells sticky so leukocytes can stick to inner lining, and they can release other inflammatory mediators Once something is identified the body tries to control situation by attracting as many cells to the scene as possible Acute inflammation Triggered by tissue injury or infection Short duration (several minutes/days) Characterized by: Exudation of fluid & plasma proteins Lots of blood flow to scene Endothelial cells contract so leukocytes can get to scene Causes some leaking of plasma proteins Emigration of leukocytes Neutrophils are one of primary neutrophils coming to scene Hallmark signs of acute inflammation: fever, redness, loss of function, pain, swelling Heat and pain from leaking plasma, excess protein Fever occurs because hypothalamus adjusts thermostat Elderly have lower core thermostat Their baseline may be 97.6 Elderly sometimes do not mount fever; might get confused/disheveled May complain of W&F (could be sign of inflammatory response) Systemic Fever Leukocytosis (increased WBCs) What is not a sign of acute inflammation? Granuloma formation (occurs in chronic inflammation) 2 phases of acute inflammation: Vascular phase (1 phase) Vasodilation Warmth and redness Caused by histamine & nitric oxide Spasm occurs that can help heal certain area then vasodilation of arterioles, venules, and capillary bed Increased permeability Loss of fluid (exudate) Intravascular stagnation Endothelial cells in vessels normally tight but get gaps during acute inflammation Localizes spread of infectious organisms & dilutes it When fluid leaves scene, it dilutes infection in area and makes it less harmful Responsible for swelling, pain, and decreased movement/function Caundd by histamine, bradykinin, and leukotrienes Cellular phase (2 phase) – leukocyte migration Margination Stagnation slows down flow; allows neutrophils to attach to endothelial lining of vessel Makes it sticky (margination) Transmigration/diapedesis Neutrophils squeeze out of gap into extravascular space; helpful in containing injury Chemotaxis Phagocytosis PRR (pattern recognition receptors) or opsonization I.e. pattern of sugar (like LPS) that neutrophil can recognize Engulfment Fusion Destruction Once its engulfed, neutrophil lymph system helps drain debris Local manifestations of acute inflammation Range from severity Localized Abscess Deep infections within body Fistula Abnormal opening between two systems Ulceration (can affect epithelial lining) SIRS (if huge inflammatory response) Systemic inflammatory response syndrome Widespread systemic lining Rare but can happen with big infections ? Adjacent tissues injury Exudates Serous – yellowish color (lots of plasma proteins); watery Hemorrhagic – lots of blood Fibrinous – fibrous products Membranous Purulent – infections; pus; degraded WBCs Resolution Yes Complete-normal structure & function No Progression to Chronic Inflammation Chronic causes Scarring / Fibrosis Substantial tissue injury Inflammation occurs in tissue that do not regenerate Neurons of brain (cells can’t reproduce) Cells & nerves of spinal cord (cells can’t reproduce) Far advanced liver disease from ETOH Over time their liver is destroyed Rheumatoid arthritis caused by chronic inflammation Chronic inflammation Duration varies (days-weeks to years) Develops after acute inflammation Often gradual & asymptomatic Causes Low-grade persistent infection or irritant Infiltration of macrophages Macrophages and leukocytes are the WBCs seen in chronic inflammation Foreign bodies Sponge after surgery left in body Inhaled foreign bodies Viruses, some bacteria, fungi and larger parasites Autoimmune diseases Obesity Adipose tissue can cause mediators (possibly leading to type II diabetes) Dense infiltration of macrophages Epithelioid cells Giant cells Granuloma Giant and epithelioid cells Don’t need to know difference – they engulf bacteria and debris Granuloma = dense amount of macrophages surrounded by lymphocytes Granulomas can be encapsulated by fibrous collagen Cartilaginous Calcified Tuberculosis Airborne Produces delayed cell-mediated immune response Primary First exposure to mycobacterium tuberculosis Healthy people can combat it and don’t get the disease; wall off bacteria Some patients develop active disease upon first interaction Primarily HIV population Can never have PPD again Secondary Reinfection from inhaled germ or previously healed lesion (granuloma) can break down Usually happens with impaired body defenses; immune system problems Pathophysiology of TB Inflammation of lung (neutrophils and macrophages) Engulf bacteria (unable to kill) Cell-mediated immune response CD4+ (helper T lymphocytes) Macrophages and T cells (CD8+) Ghon focus (granuloma) Ghon complex (granuloma and lymph node) *If TB travels to a lymph node Healed lesion *Shrunken ghon complex – has calcification around it *Macrophages engulf bacteria  take it to T cells Symptoms of tuberculosis: Low-grade fever Night sweats Anorexia Have problems keeping food down; causes weight loss Weight loss Fatigue Cough Initially a hacking, dry cough  becomes productive and purulent cough Extra pulmonary disease (HIV) produces neurological deficits, meningitis, bone pain, urinary symptoms Can affect kidneys, brain, bone, other pulmonary diseases, etc. Diagnosis Positive tuberculin skin test Sputum culture (acid fast bacillus) Chest X-ray (nodules, calcifications, cavities, enlarged lymph nodes) Immunoassays Terminology Exudate Fluid rich in protein // any fluid released from the body with high concentration of protein, cells, or solid debris Serous Serum  yellow (from platelets), thin, watery fluid Sanguineous Bloody fluid Serosanguineous Consisting of both bloody (sanguineous) and serous (serum) fluid Purulent Pus, white in color from dead leukocytes Ecchymosis Superficial bleeding under the skin or a mucous membrane (a BRUISE) Edema Condition in which body tissues contain an excessive amount of fluid in the interstitial spaces  leads to swelling Erythema Reddening of the skin due to dilation of superficial blood vessels in the skin (sign of inflammation) IMMUNITY Neutrophils are granulocytes Agranulocytes Macrophages Scavengers; engulf bad cells; travel and take disease to other immune cells Dendritic cells Live under skin/epithelial tissue and found in most organs/tracts of our body Help capture microorganisms and present them to lymphocytes Both macrophages and dendritic cells can release cytokines B lymphocytes – mediate humoral immunity Produce antibodies (immunoglobulins) Antibodies job is to attack organisms/toxins going in circulation within body before they end up in body tissues T lymphocytes – cell mediated immunity Have antigen receptors – like a puzzle piece on outside of cell These receptors find infected cells then tag the cells to kill it (cell mediated – attacks infected cells) Natural killer cells Lymphocyte Contains granules Causes apoptosis by forming pores in cell membrane (puts granules into cell) Function as part of innate immune system – respond to infections but not antigens Attacks infected or stressed cells Viral infections Tumor cells or abnormal cells Intracellular pathogens Receptors Activating On a normal cell, we have both activating and inhibitory receptors Inhibitory NK cell sees abnormal cell without inhibitory receptor, fits in puzzle piece, and granules go into infected cell and kills it Terminology Antigens (immunogens) & haptens (smaller than antigen; too small to stimulate immune response unless they attach to another body protein) Substances that stimulate adaptive immune response Microorganisms Non-microbial agents (poison ivy, pollen, etc.) Poison ivy is a hapten: it attaches to a protein in some people, which is why some get it after exposure, and some don’t Epitopes Binding sites (this is how antibody knows to attack an antigen) Antigen presenting cells (APC) Dendritic cells & macrophages Engulf pathogen and bring it to lymph nodes to be processed Present processed antigens to lymphocytes Antibodies Made in response to antigen; they attack extracellular toxins and microbes (usually in circulation) Opsonins/Opsonization Tag microbe for ingestion Tissues of inflammation Central lymphoid tissues (provides environment for immune cell production and maturation) Bone marrow B and T cells born here; B cells mature and receive signaling proteins Thymus T cells migrate here to mature; become Tc or Th cells within 2-3 days Sent out into circulation, leave blood stream and enter lymph nodes Peripheral lymphoid tissues Lymph nodes Lymphocytes and macrophages circulating through lymph system APCs bring antigens to them Spleen Filters blood; has red pulp and white pulp B and T cells in white pulp; where they identify toxins in blood Secondary lymphoid tissues (MALT – mucosa associated lymph tissue) Found on respiratory tract, GI tract, etc. They process antigens brought by APCs Happens right outside organ where MALT cells are located – better to stop infection closer to where initially found Innate immunity functions Prevents the establishment of infection Prevents deeper tissue penetration of microorganisms Tries to prevent infection before it gets deeper in body Induces the inflammatory response Can initiate adaptive immunity by APC to lymphocytes Innate immunity (natural/native) Early & rapid response by body Recognizes self from non self Pattern recognition; innate immunity can recognize signs on microbes as something foreign First line defense Physical - Epithelial barriers – skin & mucosal membranes Cellular defense - Phagocytic leukocytes & NK cells Receptors on phagocytic leukocytes can recognize if that receptor will fit another microbe Chemical – Cytokines, opsonins, complement Molecular – Pathogen recognition Pattern recognition receptors Recognize microbes by its’ composed matrix (PAMPS) Many different types (toll like, scavenger, glucan, mannose) Innate immunity cells attach to microbes & initiate phagocytosis Cytokines (cont.) Produced by cells of innate & adaptive immune systems Regulatory proteins – functions Table 15-1 Interluekins, interferons & TNF- alpha, chemokines, colony stimulating factors Bind to specific receptors on target cell’s membrane surface Actions are brief – short half-life so they don’t over-stimulate More examples of cytokines Chemokines Direct leukocyte movement & migration Some attract leukocytes to sites of chronic inflammation Some attract neutrophils to site of acute inflammation Implicated in a number of acute & chronic diseases Colony Stimulating Factors Stimulates bone marrow or progenitor cells Results in increase production of what was stimulated Complement system Initial Activation Phase (phase 1) Attach to Complement C3 3 pathways (for recognition of microbes) Alternative Innate immunity Complement activated by microbial cell surface (recognition that microbe is foreign; complement cascade initiated) Classical Complement system activated by antibody bound to antigen Humoral immunity – B cells produce antibodies; these attach to microbes and initiate complement cascade Lectin Complement activated by plasma lectin to mannose on microbe Amplification of Inflammation (phase 2) There are different complement proteins circulating body in active form Once c3 is activated, we have cascade that goes down line to get rid of microbe C3 cleaves into c3a and c3b C3a induces inflammation – chemoattractant – brings more cells to scene of injury C3b – can tag microbes as foreign (opsonin) - opsonization occurs C3b attaches to c5; c5 breaks apart Induces more inflammation and can bring more cells to scene Vascular permeability and other inflammatory things then occur Membrane attack response (phase 3) In addition to tagging for opsonization, complement can also do direct killing Remaining complement ends up poking a hole in microbe and throws all its lysing enzymes in cell and that cell bursts apart **Complement can cause inflammation, introduction of more neutrophils to scene, opsonization, and direct killing** Adaptive immunity (specific or acquired) 2 line of defense Lymphocytes Antigen receptors Develop a specific immune response for each pathogen/antigen Ability to “remember” pathogens 2 types of adaptive responses: Humoral immunity – B cells  memory cells & plasma cell (plasma cell --> antibodies) Protects against extracellular pathogens Cell mediated immunity Defends against intracellular pathogens CD4 (t helper) master regulator Major histocompatibility complex Membrane bound proteins Peptide display molecule T lymphocytes MHC - I Found on all nucleated cells & platelets CD8+ cytotoxic T cells Become activated only when recognize antigen peptide associated with MHC I Attracted to INFECTED cells (endogenous antigens); especially virus infected cells Kills cell MHC – II Expressed on APC (dendritic cells & macrophages) & B lymphocytes CD4+ molecule of T helper cells recognize antigens on MHC II Become activated to secrete cytokines HIV: we lose these cells Helper T cell TH1 Help develop cellular immunity Cytotoxic T cell Memory cells Phagocyte mediated ingestion TH2 Help develop humoral immunity B Cell activation Antibody production Memory cells Macrophage release Other T cells Humoral immunity (B lymphocytes) Mature B cells migrate to lymphoid tissues & interact with specific antigens (develop Ig receptor) With assistance of Helper T cells, B cells differentiate into Antibody secreting plasma cells Memory B cells Can live throughout body in different tissues B cells have ability to initiate complement Antibodies IgG Most abundant Helps initiate complement IgA In mucosa (saliva, bronchioles, GI tract, genitals, tears, etc) IgM First one to show up, and first one made by a newborn Helps initiate complement IgE Hypersensitivity reactions Effector responses of humoral immunity Agglutination- antibodies disarm antigens by clumping them together Neutralization Antibodies combine with toxins released by bacteria & viruses neutralizing effects Phagocytes then engulf & remove from blood or tissue Precipitation – antibodies react with soluble antigens resulting in an insoluble complex, which then precipitates Lysis – adherence of antigen to immune cells, facilitating phagocytosis & complement activation Complement cascade (inflammatory response first, then tagging for opsonization) 2 responses of humoral immunity Primary Antigen first introduced in body Has latent period before noted in serum (processing of antigen) Activated CD4+ helper T cells B cells plasma cells antibody Fraction remain as memory B cells Secondary (memory) Occurs in repeat exposures Memory B cells Antibodies rise sooner (1-3 days rather than weeks) Reaches higher level Booster immunizations (every 7-10 years) Builds up level of
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