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Immune System
Pathophysiology 3 - Disorders of the Immune System
| Question | Answer |
|---|---|
| define immunity | the bodies protection from (infectious) disease |
| define immune response | the coordination of cells that provide protection for the body |
| what happens when immune response is excessive | - unwanted effects - identifies self-tissue as foreign - causes problems |
| name the two types of immunity | innate and adaptive immunity |
| another name for innate immunity | natural immunity |
| (innate/adaptive) immunity is the first line of defense against pathogens, and can be activated immediately | INNATE immunity is the first line of defense against pathogens |
| what comprises the innate immunity system | - physical barriers (skin, epithelial c. lining GI and resp. tracts) - chemicals (keratin) - cellular response (WBCs) - molecular defenses |
| means of entry for pathogens | - skin - respiratory tract - GI tract - urogenital tract |
| the primary physical barrier is | the skin |
| what makes the skin the primary physical barrier | - closely packed cells in many layers - cells are continuously being shed and renewed - chemicals create an environment inhospitable for microorganisms - other antimicrobial protiens |
| what is the immune function of keratin in the skin | creates an environment that is too salty and acidic for microorganisms |
| what kind of microbial proteins does the skin contain that inhibit and destroy microorganisms | lysozymes |
| function of goblet (epithelial cells) in GI tract | trap pathogens and wash them away |
| function of cilia and mucous in respiratory tract | trap pathogens in mucus and move them up towards the throat where they can be expelled (via coughing or sneezing) |
| how does the immune system identify between self and non-self | most foreign microbes share a common structural characteristic (proteins, sugars and lipids) |
| (innate/adaptive) immunity produces a more generalized response. | INNATE immunity produces a more generalized response |
| list all the Cells in innate response | - neutrophils - eosinophils - basophils - monocytes - macrophages - dendritic cells (DC) - natural killer cells (NK) - Intraepithelial lymphocytes |
| where do all WBC's originat | hematopoietic stem cells in red bone marrow |
| name the two groups of leukocytes, and why are these groups named such | - granulocytes (presence of granules) - agranulocytes (absence of granules) |
| list the granulocytes | - neutrophils - eosinophils - basophils |
| list the agranulocytes | - monocytes - macrophages - lymphocytes |
| describe the neutrophils | - granulocyte - most abundant in body (55%) - early responder - use phagocytosis to kill |
| describe eosinophils | - 1-4% - parasite infections - allergic response |
| describe basophils | - <1% - release histamine and proteolytic enzymes - allergy response - parasitic infections - phaygocytose |
| describe monocytes | - largest in size - 3-7% - (released from bone marrow) mature to DC - inflammatory response - phagocytose (foreign substances and cellular debris) |
| describe macrophages | - longer life span - reside in tissue - 1st phagocyte responder - works with neutrophils |
| describe natural killer cells and intraepithelial cells | - NK spontaneously kill target (organism/some tumor cells/ infected cells) - NK does not need exposure to surface antigens - assist in development of adaptive immune response - produce cytokine. - help with viral infections |
| describe dendritic cells | - immature cells in lymphoid tiss. - capture foreign agents and transport to peripheral lymphoid organs - complex maturation process (during migration to lymph nodes) - key antigen-presenting cells (initiate adaptive immunity) |
| name the two antigen presenting cells | - macrophages - dendritic cells |
| what are antigen presenting cells | - process complex antigens into epitopes and present them on the cell surface - this activates lymphocytes (adaptive immune response) |
| name the two divisions of lymphocytes | - regulatory cells - effector cells |
| what is the function of regulatory cells (lymphocytes) | control immune response |
| what is the function of effector cells (lymphocytes) | work to eliminate the antigen |
| describe lymphocytes | - adaptive immunity - 36% wbc count - derived from lymphoid stem cells - differentiate in to B and T cells - distinguish between various pathogens |
| where do lymphocytes originate | lymphoid stem cells in red bone marrow |
| function of B lymphocytes | - produce antibodies (humoral immunity) |
| function of T lymphocytes | provide cell-mediated immunity |
| Define the term CD (i.e. CD4, CD8) | cluster of differentiation |
| why is CD important | the number specifies the surface proteins associated with a particular cell type/stage of cell differentiation and has a specific group of antibodies |
| about how many CD's are there in the human body | 371 |
| T lymphocytes mature in the | thymus gland |
| B lymphocytes mature in | bone marrow |
| (b/t) lymphocytes secrete antibodies | B lymphocytes |
| what other organs are involved in the lymph tissue | - lymph nodes - spleen - skin - mucosal tissue |
| what four properties are necessary for adaptive immune response | - specificity - diversity - memory - (self/non-self) recognition |
| what is specificity in adaptive immune response | (after first encounter) cells recognize and remember specific antigens ....targets a specific antigen |
| what is diversity in adaptive immune response | wide variety of lymphocytes able to respond to millions of antigens |
| what is memory in adaptive immune response | (after 1st encounter) the ability for T and B cells to remember the antigen and respond faster |
| what is recognition in adaptive immune response | the efficiency at recognizing and eliminating foreign antigens quickly |
| MHC | Major Histocompatibility Complex |
| describe MHC | - protein complex part of the Antigen Presenting Cells (APCs) - "hold and present" fragment of foreign antigen on cell surface - allows recognition and initiation of immune response |
| helper T cells | - recognize MHC - activates in presence of MHC - secretes cytokines (stimulating B cells to produce antibodies) |
| steps of adaptive immunity after antigen presents in body | - MHC activates T helper cells - t helper cells secretes cytokines - cytokines stimulate B cells - B cells produce antibodies - both T and B cells divide rapidly and differentiate into (effector or memory cells) |
| describe the differences of innate and adaptive immune response in regards to time of response | (Innate) immediate response - within minutes or hours of initial antigen presentation (Adaptive) time of response is dependent upon exposure - 1st exposure delayed response, 2(+) exposure is more immediate t/b cell response |
| describe the differences of innate and adaptive immune response in regards to diversity | (innate) limited to classes or groups of microbes (adaptive) very large - specific for each unique antigen |
| describe the differences of innate and adaptive immune response in regards to microbe recognition | (innate) general patterns on microbes - nonspecific (adaptive) specific to individual microbes and antigens |
| describe the differences of innate and adaptive immune response in regards to response to repeated infection | (innate) similar with each exposure (adaptive) immunologic memory - more rapid and efficient with exposure 2(+) |
| describe the differences of innate and adaptive immune response in regards to defense | (innate) epithelium, phagocytes, inflammation, fever (adaptive) cell killing - tagging of antigen by antibody for removal |
| describe the differences of innate and adaptive immune response in regards to cellular component | (innate) phagocytes (monocytes/macrophages, neutrophils), NK cells and DC (adaptive) B and T lymphocytes, macrophages, DC, NK cells |
| describe the differences of innate and adaptive immune response in regards to molecular components | (innate) cytokines, complement proteins, acute-phase proteins, soluble mediators (adaptive) antibodies, cytokines, compliment systems |
| define humoral immunity | antibody production (by B lymphocytes) |
| Antibody protiens are molecules that are more specifically referred to as _______________ | immunoglobulins (Ig) |
| name the five classes of Immunoglobulins | - IgM - IgA - IgD - IgG - IgE |
| describe the general structure of the immunoglobulins | four-polypeptide chains with at least two identical antigen binding sites. |
| another name for the IgG | gamma globulin |
| a majority of the circulating antibodies are _____________ what is the second most common antibodi | IgG; IgM |
| describe the IgG antibody | - 75% total circulating antibodies - antiviral -antibacterial -antitoxin - present in all body fluids - readily enters tissue and crosses placenta |
| describe the IgA antibody | - 15% all antibodies - secretory (saliva, tear, mucous, sputum) - *main function* local immunity on mucosal surfaces - prevents attachment of viruses and bacteria |
| describe the IgM antibody | - 10% of all antibodies - lysis of microorganisms - 1st antibody produced by fetus + immature B cells - 1st Ig produced in response to infection - high in labs = active infection |
| describe the IgD antibody | - low levels - relatively unknown functions |
| describe the IgE antibody | - least common antibody - responsible for inflammation, allergic response, parasitic infections |
| what is a primary immune response | when the human body first encounters a foreign antigen |
| antibodies are derived from | B cells that differentiate and mature into antibody-secreeting plasma cells |
| how does the adaptive immunity remember specific antigens | during the primary immune response, a portion of B cells form a population of memory B lymphatic cells |
| another term for secondary immune response | memory phase |
| what is the secondary immune response | a repeated exposure to an antigen |
| how does the adaptive immunity respond during the memory phase of an infection | there is a rise in antibody levels earlier and stronger |
| why are immunizations important. | the first vaccination causes a primary response, every subsequent vaccination allows for a memory phase |
| what is cellular immunity | this predominantly involve T lymphocytes, which activates an autoimmune processes, controls viral infections, activates delayed hypersensitivity reactions, and rejects foreign tissue. |
| the master regulators of the immune system are | CD4+ helper T cells |
| what happens with CD4+ helper T cells are activated | - cytokines are released (initiating an immune response) ---- activates WBC (macrophages, basophils, and neutrophils) ---- enzymatic and phagocytic functions - helper T cells differentiate into regulator and cytotoxic T cells |
| function of Regulatory T cells (Tr) | control immune system response |
| function of cytotoxic T cells (CD8+) | monitor the activity of all cells in the body and then eliminate any that compromise the integrity of the body |
| what two types of T lymphocytes are needed for the cell-mediated immune response | CD4+ and CD8+ |
| (humoral/cell-mediated) immunity plays a role in delayed hypersensitivity reactions (i.e. allergies or dermatitis) | CELL-MEDIATED immunity plays a role in delayed hypersensitivity reactions |
| purpose of the central and peripheral lymphoid organ | a network of organs/tissue that produce, mature, and store large numbers of immune system cells |
| the central (lymphoid) organs include | - red bone marrow - thymus |
| the peripheral lymphoid system includes | - lymph nodes - spleen - tonsils - appendix - Peyer's patches (intestine) - other mucosa-associated lymphoid tissue in respiratory, GI, and reproductive systems. |
| what is the function of the peripheral lymphoid system | - store immune cells - process antigens - support cellular processes |
| describe the thymus | - elongated - bi-lobed - in the mediastinum (above heart) |
| thymus function | production of mature, immunocompetent T lymphocytes |
| describe the lymph nodes | - small clusters of lymphoid tissues - located throughout the body - connected to each other by lymphatic vessels |
| function of lymphatic tissue | - transport lymph (clear/yellowish) along with cellular debris, and other organisms |
| two main functions of lymph nodes | - removal of foreign material from lymph - sites for proliferation and response of immune cells |
| what areas of the body are lymph nodes predominantly found | - axillae - groin - great vessels (neck, thorax, and abdomen) |
| function of the spleen | - filter antigen from blood - help with systemic infections |
| name the two systems of the spleen | - red pulp - white pulp |
| function of red pulp in spleen | - supplied by blood vessels (sinusoids) - function to eliminate old/injured RBC's |
| function of white pulp in spleen | - lymphoid tissue - location of B/T lymphocytes, macrophages, and dendritic cells |
| two types of adaptive immunity | - active - passive |
| how is active (adaptive) immunity aquired | an immune response where B/T lymphocytes are *activated* - vaccination - environmental exposure long-lasting but development may take days to weeks (after primary response) |
| how is passive (adaptive) immunity acquired | immunity is *transferred* from one source to another - mother to fetus via placenta (IgG's) - mother to baby via breast milk/colostrum short-term, lasting weeks to months |
| weakened immune system leads to | immunodeficiency |
| excessive immune response causes | - allergic reactions - autoimmune disorders |
| what are the causes of hypersensitivity immune disorderes | inappropriate immune responses |
| two types of hypersensitivity reactions | Type I hypersensitivity reaction Type II hypersensitivity reactions |
| what is type i hypersensitivity reactions | - IgE- mediated - develop quickly upon exposure - classic allergic response |
| what is an allergen | an antigen that causes a "classic allergic response" |
| list some type i hypersensitive reactions | - rhinitis - asthma - anaphylaxis - atropy |
| which WBC's play an important role in type i hypersensitivity reactions. Why | - mast cells - basophils - eosinophils - they contain histamine and heparin (chemical mediators) |
| what are the two distinct phases of a type i hypersensitivity reaction | 1) primary early response 2) secondary late response |
| after exposure to an allergen, how long does it take for the primary early response to occur | -5 to 30 minutes - subsides within 60 minutes |
| what happens in the primary early response | - mast cells are degranulated (histamine is released) |
| what is the function of histamine | - vasodilator - relaxes vascular smooth muscle - increases capillary permeability - causes bronchial constriction |
| which WBC releases histamine | Mast cells |
| how long does it take for the secondary late response take after exposure to an allergen | 2-8 hours after resolution of the primary early response and can last for several days |
| what happens in the secondary late response | - lipid mediators and cytokines released - (lipid med.) form arachidonic acid - (cytokines) promote migration of eosinophils (and other WBC's) to site of allergen |
| what is the function of arachidonic acid | - synthesis of leukotrienes and prostaglandins - symptoms similar to histamine (longer lasting) |
| what is anaphylaxis | - systemic life-threatening IgE-mediated hypersensitivity reaction |
| what causes anaphylaxis | - widespread release of histamine ------- causes vasodilation ------- hypotension ------- atrial hypoxia ------- airway edema |
| the severity of anaphylaxis is dependent on | the preexisting degree of sensitization |
| name the levels of clinical manifestations of anaphylaxis | - Grade I - Grade II - grade III - grade iv |
| describe grade i anaphylaxis | - cutaneous and mucosal tissue - erythema - urticaria - with or without angioedema |
| describe grade ii anaphylaxis | - multisystem involvement - hypotension - tachycardia - dyspnea - GI manifestations (n/v/d) - abdominal cramping (mucosal edema) |
| describe grade iii anaphylaxis | - life threatening - bronchospasm - cardiac dysrhythmia - cardiac collapse |
| describe grade iv anaphylaxis | - cardiac arrest - management is focused on resuscitation |
| management of anaphylaxis is focused on | - removal of offending agent - keeping airway open - obtaining intravenous access - volume resuscitation - administering epinephrine |
| what is atopy | local (atopic) immediate reaction that is confined to a particular area. |
| how do atopy type i hypersensitivity reactions present | - urticaria (hives) - allergic rhinitis, - atopic dermatitis, - bronchial asthma |
| an individual experiencing atopy will have high levels of which WBC/antibodies | - IgE - eosinophils - basophils - mast cells |
| symptoms of allergic rhinitis | - rhinorrhea (runny nose) - sneezing - nasal obstruction - watery eyes - allergic asthma - malaise - fatigue - headache (no fever) |
| how can a diagnosis of allergic rhinitis be confirmed | - presence of specific IgE antibodies - skin prick test - familial history of allergies |
| what are the mainstays of allergic rhinitis treatment | - antihistamines - nasal corticosteroids |
| name some antihistamines | - Benadryl - allegra - zyrtec - claritin |
| antihistamines work to | - reduce sneezing - reduce rhinorrhea - reduce nose/palate/eye itching - modest effect on nasal congestion |
| name some intranasal corticosteroids | - flonase - nasacort |
| function of intranasal corticosteroide | - improves all nasal symptoms - have delayed onset of action of about two weeks |
| function of mast cell stabilizers on allergies | - mast cell deregulation - release of intracellular mediators |
| if over the counter shots are not enough, what else can be done to prevent allergies | - allergy shots (desensitization via immunotherapy) |
| how is desensitization via immunotherapy accomplished | -patients given progressively higher doses of antigen, high levels of IgG, prevents activation of IgE |
| Most food reactions occur within ______________ of exposure, but some delayed reactions are possible | one hour |
| describe type ii (or cytotoxic) hypersensitivity reactions | - antibody-medicated reactions - IgG and IgM antibodies are directed against target antigens on specific cell surfaces or tissue - intrinsic or extrinsic |
| define intrinsic | naturally part of the host cell |
| define extrinsic | a foreign substance or infections agent becomes incorporated into the cell surface |
| what are tissue specific antigens | the antigens that are on the surface of cells and certain tissues |
| name the four ways type ii hypersensitivy reactions occur | - compliment-activated cell destruction - antibody-mediated cell cytotoxicity - compliment/antibody-mediated inflammation - antibody-mediated cellular dysfuction |
| what is complement-activated cell destruction | - two fold approach - results in cell lysis and activation of macrophages - macrophages destroys target cells via phagocytosis |
| give some examples of when complement-activated cell destruction is a mechanism for disease. | - mismatched blood transfusions - Rh incompatibility (negative women - positive fetus) |
| what is antibody-dependent cell cytotoxicity | components of both the innate and adaptive immune responses destroy target cells -- antibodies bind to the target cell surface -- release of chemotactic substances and destruction of target cell |
| name leukocytes involved in antibody-dependent cell cytotoxicity | - NK (primary response) - macrophages - eosinophils |
| antibody-dependent cell cytotoxicity is a common mechanism for which infections | this is common in ANTIVIRAL and the cause of some AUTOIMMUNE DISORDERS |
| describe compliment- and antibody-mediated inflammation | - antibodies are deposited in extracellular tissue components - activated leukocytes release injurious substances - causes inflammation and tissue damage |
| name a couple of ailments/diseases that the compliment- and antibody-mediated inflammation is responsible for | - some forms of glomerulonephritis - vascular rejection or organ grafts |
| what is antibody-mediated cellular dysfunction | - antibodies binding to receptors does not lead to cell death - leads to unwanted cellular function change |
| give some examples of antibody-mediated cellular dysfunction | - Graves Disease (antibodies directed against TSH receptors on thyroid) - myasthenia gravis (autoantibodies to Acetylcholine receptors either block or cause destruction of receptors...and decreased neuromuscular function) |
| what is an autoimmune disease | - when the body's immune system fails to differentiate self from non-self. - the body's immune system mounts an attack against the host cells |
| define self-tolerance | - the ability of the immune system to distinguish self from non-self |
| self-tolerance depends on what two processes | - central tolerance - peripheral tolerance |
| what is central tolerance | - elimination of autoreactive lymphocytes during maturation of the central lymphoid tissue |
| what is peripheral tolerance | the suppression of autoreactive lymphocytes in peripheral tissue that have escaped destruction in the thymus |
| define autoreactivity | an organism active against its own tissue |
| list some systemic autoimmune disorders (name 4) | - mixed connective tissue disease - polymyositis-dermatomyosis - rheumatoid arthritis - scleroderma -Sjogrens Syntrome - systemic lupus erythematosus |
| list some autoimmune blood disorders | - autoimmune hemolytic anemia - autoimmune neutropenia and lymphopenia - idiopathic thrombocytopenic purpura |
| list some autoimmune disorders that effect other organs (name at least 4) | - acute idiopathic poly neuritis - atrophic gastritis and pernicious anemia - autoimmune adrenalitis - goodpasture syndrome - hashimoto thyroiditis - DMI - premature gonadal (ovarian) syndrome - primary biliary cirrhosis - sympathetic ophthalmia |
| define anergy | when a lymphocyte fails to respond to an antigen, and thus fails to cause a cellular/humoral immunologic response ---- the state of immunologic tolerance to specific antigens |
| in many autoimmune disorders, the immune system loses its ability to recognize self and produces ___________________ , which act against host tissues | autoantibodies |
| describe how autoantibodies behave in Graves Disease | - autoantibody-induced hyperactivity of the TSH receptor - causes hyperthyroidism |
| how are T lymphocytes "trained" in the thymus during their maturation process | T cells are exposed to self-peptides bound to MHC molecules |
| what is positive selection | as maturing T lymphocytes are exposed to self-peptides bound to MHC molecules. T cells that display reactivity to the MHC. ---- these T cells are allowed to mature |
| what is negative selection | as maturing T lymphocytes are exposed to self-peptides bound to MHC molecules. T cells that have a high affinity for self-antigens that are sorted out and undergo apoptosis |
| study figure 3.8 in section 3.2 | see picture |
| even though the exact causes of autoimmune disorders are unknown. There are two main factors that play a large role in. what are these two main factors | - genetic - environmental - (lesser factor) biological sex (i.e. lupus more prevalent in women) |
| define susceptibility genes | genes that are often associated with disease development ---- the presence of these genes does not guarantee and autoimmune disorder. |
| define trigger event | - an event leading to the altered immune state - maybe a virus, microorganism, chemical substance, or self-antigen (previously hidden now present) |
| list some possible environmental factors that can lead to an autoimmune disorder | - viral infections - exposure to hazardous chemicals - maternal smoking - lack of exposure to maternal antibodies (breast feeding) |
| what is T cell anergy | when an immunocompetent, antigen-specific T cell is unable to respond to an appropriate stimulus |
| what is release of sequestered antigens | occurs when the body produces antibodies against self antigens |
| what is molecular mimicry | - a theory to describe mechanisms by which infections agents or other foreign substances trigger an immune response against autoantigens |
| what are superantigens | a family of related substances (like staph or strep exotoxins) that cause uncontrolled proliferation and activation of T cells, causing fever, shock, and death |
| what criteria needs to be met for the diagnosis of an autoimmune disorder | - evidence of an autoimmune reaction - immunologic findings not secondary to another condition - no other identifiable causes found |
| what are serologic assays used for | detection of antibodies against antigens of cellular components |
| name the three methods of serologic assays | - indirect fluorescent antibody assay (IFA) - enzyme -linked immunosorbent assay (ELISA) - particle agglutination of some kind |
| define positive titer | - used in serologic assas - serum is diluted until it is no longer produces a visible reaction |
| treatment of autoimmune disorders depends on | presenting symptoms and disease process |
| what are corticosteroids and immunosuppressive drugs used for in autoimmune disorders | - main therapies for autoimmune disorders - aimed to stop/revers cellular damage |
| use of plasmapheresis in autoimmune disorders | to remove auto reactive cells from circulation |
| describe Grave's Disease (cause, symptoms/signs, diagnosis) | - abnormal stimulation of thyroid gland by Thyriod stimulating antibodies - state of hyperthyroidism, goiter, ophthalopathy - between ages 20-40 |
| exophthalmos | - bulging of eyes anteriorly out of orbit - seen in Grave's disease |
| it is thought that Graves disease results from | accumulation of T lymphocytes sensitized to antigens along thyroid follicular cells and orbital fibroblasts that secrete cytokines |
| describe the effect of Grave's disease on the eyes | - cause of severe eye problems - exophthalmos - diopia - vision loss - corneal ulceration |
| main goal of treatment in Graves disease | - normalization of thyroid function -----antithyroid medication ----- ablation of thyroid tissue (radioactive iodine) ----- thyroid surgery ----- there is no safe/effective therapy able to correct the autoimmune process |
| describe Systemic Lupus Erythematosus (SLE) | - chronic inflammatory disease (the great imitator) - can affect almost any organs systems - mostly women in childbearing years - four types of lupus (SLE is most common) - causes is unknown |
| Systemic Lupus Erythematosus is characterized by | - presence of antinucclear antibodies (autoantibodies) and non-self-antigens - developed by a combination fo genetic environmental/hormonal/immunologic factors |
| possible environmental factors for SLE | - UV light - chemicals (drugs, hair dyes) - some foods - infectious disease agents |
| what are some clinical symptoms of SLE (list at least 5) | - arthalgias - arthritis - "butterfly" rash - renal disease - pleural effusions - pleuritis - pericarditis - hematologic problems |
| most common tests for SLE/Lupus | - ANA levels (nonspecific, results are elevated) - anti-DNA antibody test (more specific) |
| treatment for SLE (Lupus) | geared towards managing acute/chronic treatment, preventing organ damage and other long-term complications |
| NSAID use in Lupus treatment | - control fever - control arthritis pain |
| antimalarial use for Lupus treatment | - cutaneous and musculoskeletal manifestations |
| use of corticosteroids in lupus treatment | - more significant treatments (Renal and CNS disorders) |
| use of immunosuppressive drugs in lupus treatment | - more severs cases |
| what is inflammation | - response to cell/tissue injury - damaged tissue is removed - tissue is generated a new |
| inflammation is characterized by | - presence inflammatory mediators (neutrophils) - movement fluid - tumor necrosis factor alpha - vascular endothelial growth factor (VEGF) - serum amyloid |
| - itis | inflammatory condition of the organ - appendicitis - hepatitis - phlebitis |
| what are the 5 cardinal signs of inflammation | - rubor (redness) - tumor (swelling) - calor (heat) - dolor (pain) - functio laesa (loss of function) |
| in inflammation, what causes rubor (redness) | dilation of blood vessels |
| in inflammation, what causes tumor (swelling) | extravascular accumulation of fluid |
| in inflammation, what causes calor (heat) | increased blood flow |
| in inflammation, what causes dolor (pain) | increased pressure from accumulation of fluid and mediators |
| what is acute-phase response | - systemic manifestations that occur during acute inflammation ---- cardinal signs that appear at site of injury ---- fever ---- chemical mediators (cytokines) |
| acute inflammation | - immediate - last from several minutes to a few days - exudation of fluid/plasma components - migration of leukocytes (mainly neutrophils) to extracellular tissue |
| describe chronic inflammation | - lasts from days to years - associated with necrosis - proliferation of blood vessels - presence of lymphocytes and macrophages - fibrosis |
| compare acute and chronic inflammation | the processes between the two overlap |
| what are the two stages of acute inflammation | - vascular stage - cellular stage |
| describe the vascular phase of acute inflammation | - temporary vasoconstriction, followed by vasodilation - two cardinal signs appear (heat and redness) - increased vascular permeability - swelling - clotting |
| vasodilation in the vascular phase of acute inflammation occurs due to | the presence of histamine and nitric oxide |
| increased permeability in the vascular phase of acute inflammation leads to | protein-rich fluid (exudate) moves into the extravascular space, |
| what causes swelling in acute inflammation | increased fluid in the tissue spaces |
| the increased swelling in acute inflammation can also lead to | - pain - impaired function |
| what happens when fluid movement slows in the vascular phase of acute inflammation | - clotting occurs ---- d/t increased RBC's, leukocytes, platelets, and clotting factors - helps contain spread of infections mircoorganisms |
| describe the cellular phase | - leukocytes (neutrophils) arrive to the site of injury - adhesion and margination (accumulation) - transmigration (movement) - chemotaxes |
| describe adhesion and transmigration of leukocytes in the cellular phase of acute inflammation | - leukocytes move from vascular space to extravascular tissue - facilitated by complementary adhesion molecules on endothelial surfaces - migration occurs along with chemical gradient (chemotaxis) |
| describe chemotaxis in the cellular phase of acute inflammation | - directed cell migration that uses energy - at the site of injury, products are made |
| what are endothelial cells and their fuction | - cells that line the interior of blood vessels - help regulate blood flow |
| in inflammation situations, what are endothelial cells responsible for | - antiplatelet agents - antithrombic agents - produces growth factors that stimulate angiogenesis and extracellular matrix (ECM) - repair processes following inflammation |
| what are platelets (thrombocytes) and their functions | - cell fragments in blood - provides primary homeostasis |
| in inflammatory response, what do platelets do | - release inflammatory mediators to increase permeability - alters adhesive chemotactic and proteolytic properties of endothelial cells |
| what are neutrophils and their function | - primary phagocytes in inflammation - live only about 10 hours - constantly replaced |
| what is leukocytosis | - elevated white blood cell count - common with bacterial infections and tissue injury |
| the demand of neutrophils in an inflammatory response may be enough to produce an immature form of neutrophils called __________________ which may be elevated as well | bands |
| what are monocyte/macrophages and their regular function | - release potent vasoactive mediators ----- prostogandins ----- leukotrienes ----- cytokines ----- platelet-activating factors - promotes tissue regeneration |
| how do monocytes/macrophages function in CHRONIC inflammation | - surround and wall off foreign material that cannot be digested |
| how do monocytes/macrophages induce inflammation | - lipid mediators and cytokines produced by basophils, eosinophils, and mast cells |
| what are plasma mediators | - coagulation factors - complement proteins are synthesized in the liver - activated by a series of proteolytic processes |
| what are cell-derived mediators | - activated in response to microbes or damaged tissue |
| inflammatory mediators are classified by _____________ | function |
| name the four classifications of inflammatory mediators | - vasoactive/smooth muscle-constricting properties - plasma protease - chemotactic factors - reactive molecules |
| list some vasoactive inflammatory mediators that have smooth muscle-constricting proprties | - histamine - arachidonic acid metabolites ---- prostaglandins ---- leukotrienes - platelet-activating factor (PAF) |
| list some plasma protease that become active inflammatory mediators | - coagulation factors of the clotting cascade - vasoactive peptides of the kinin system |
| list some chemotactic factors that are inflammatory mediators | - complement fragments - chemokines |
| list some reactive molecules in the inflammatory mediators | - cytokines from leukocytes |
| acute inflammatory reactions can cause the formation of ________________ to ___________ or ________________. | exudates; abscesses; ulceration |
| what can be in the fluid of exudates | - plasma protein content - presence/absence of cells - serous fluid - RBC - fibrinogen - tissue debris - WBC breakdoewn |
| serous exudate | serous fluid in exudate |
| hemorrhagic exudate | RBC's in exudate |
| fibrinous exudate | fibrinogen in exudate |
| purulent exudate | tissue debris and wbc breakdown products |
| what is an abscess | - localized area of inflammation containing a purulent exudate - may be surrounded by a neutrophil layer |
| what is a good cure for an abscess and why | - a surgical incision and drainage of the abscess - antibiotics cannot penetrate the abscess wall |
| what is an ulceration | - epithelial surface that has become necrotic and eroded |
| peptic ulcers are caused by | traumatic injury to epithelium |
| diabetic foot ulcer is caused by | vascular compromise |
| three steps in formation of an abscess | - inflammation - suppuration - abscess formation |
| what is suppuration | - development of suppurative/purulent exudate containing degraded neutrophils and tissue depris |
| what is abscess formation | - walling off the area of purulent (pus) exudate |
| what can chronic inflammation result from | - progressive acute inflammatory processes - low-grade responses that fail to evoke an acute response |
| instead of neutrophils, which leukocytes are involved chronic inflammation instead | - macrophages - lymphocytes |
| what is a negative result of long term chronic inflammation | - scarring - deformities |
| list some causes of chronic inflammation | - foreign bodies (talc, silica, asbestos, surgical suture material) - pathogens (tubercle bacillus, syphilis) - injured tissue surrounding a healing fracture |
| what are the two patterns of chronic inflammation | - nonspecific chronic inflammation - granulomatous inflammation |
| what is nonspecific chronic inflammation | - accumulation of macrophages and lymphocytes at injury site - ongoing chemotaxis - fibroblast proliferation - scar formation |
| granulomatous lesion (granuloma) | - type of chronic inflammation - formation of granulomas (1-2 mm lesion) ----- focal collections of macrophages - granuloma is encompassed by lymphocytes - associated with foreign bodies (splinters, asbestos, sutures, and silica) - also seen with mic |
| normal WBC levels | 4000 to 10,000 cells/microLiter |
| when do WBC's increase in inflammation | acute-phase response |
| when can a decrease in WBC be caused | overwhelming infections due to an impaired ability to produce WBC |
| the body's response to foreign pathogens can vary depending on the source of infection (i.e. viral, parasitic, bacterial, allergens, and so one...give examples of each) | - bacterial infections = increase in neutrophils - parasitic infections/allergic response = increase in eosinophils - viral infections = decrease neutrophils, increase lymphocytes |
| ESR stands for | Erythrocyte Sedimentation Rate |
| CRP stands for | C-Reactive Protein |
| other than WBC count, what lab tests can signify an acute-phase response | - elevated esr (erythrocyte sedimentation rate) - elevated crp (c-reactive protien) |
| describe lymph nodes in response to an acute-phase response | - nodes are enlarged (due to drainage from the area) - painful and palpable |
| nonpainful yet palpable lymph nods are seen more with | neoplasms |
| define regeneration | - when damaged cells can be replaced with identical copies - as a result, there is no evidence of a previous injury |
| define repair/replacement | - alternative mechanisms are used to stabilize and maintain surrounding tissue - most often replacing the injured area with connective tissue - result is the formation of a scar |
| name the three categories of cells based on their ability to undergo regeneration | - labile - stable - permanent |
| define labile cells | - divide actively (throughout life) - capable of regeneration after injury |
| name some labile cells in the body (location, tissue types, etc.) | - epidermis - GI mucosa - genitourinary tract - hematopoietic cells (bone marrow) |
| define stable cells | - undergo few divisions but capable of division when activated - can be capable of regeneration after injury |
| name some stable cells in the body (location, tissue types, etc.) | - hepatocytes - renal tubular cells - numerous mesenchymal cells |
| define permanent cells | - incapable of division and regeneration - replaced by scar tissue after injury/cell loss |
| name some permanent cells in the body (location, tissue types, etc.) | - neurons - myocardial cells |
| define wound healing | the process by which the integrity of injured tissue is restored |
| name the three stages of wound healing | - inflammatory phase - proliferative phase - wound contraction and remodeling phase |
| each phase of wound healing is mediated by | - cytokines - growth factors |
| describe the inflammatory phase of wound healing | - begins at the time of the injury -blot clot forms - phagocytic WBC's migrate to area ----- neutrophils ingest bacteria and other debris ----- macrophages arrive after 24 hours, produce growth factors |
| what is the goal of the proliferative phase | - build new tissue to fill the wound space |
| what is the most important cell in the proliferative phase after wound healing | - fibroblast |
| what is a fibroblast | connective tissue cell that synthesizes and secretes the following substances: ---- collagen ---- proteoglycans ---- glycoproteins ---- growth factors |
| the function of growth factor released by fibroblasts | - angiogenesis - endothelial cell proliferation and migration |
| in which phase of wound healing does epithelialization occur | proliferative phase |
| what is epithelialization | - epithelial cells at the wound edges proliferate to form a new surface layer similar to the one that was injured |
| when does the wound contraction and remodeling phase of wound healing begin | - 3 weeks post injury - may continue for 6 month (or longer) - based on severity of the wound |
| describe the wound contraction and remodeling phase of wound healing | - decreased vascularity - remodeling of scar continues ------ collagen is simultaneously being synthesized and lysed by collagenase enzymes |
| why can scar sometimes increase in tensile strength then shrink to be less visible | in the wound contraction and remodeling phase of wound healing, collagen is simultaneously synthesized by fibroblasts AND undergoing lysis by collagenase enzymes |
| what cells/enzymes make collagen | fibroblasts |
| what cells/enzymes lyse collagen | collagenase enzymes |
| name the two types of wound closure healing | - primary intention - secondary intention |
| what is an example of a primary intention wound closure and healing | sutured surgical incision |
| what types of wounds would require secondary intention wound closure and healing | - larger wounds ----- burns ----- greater loss of tissue and contamination - results in larger amounts or scar tissue |
| describe secondary intention wound healing | - slower - greater loss of tissue - results in larger amounts of scar tissue |
| define a keloid | - abnormality in healing by scar tissue - tumor-like masses caused by excess production of scar tissue |
| list nine factors that negatively affect wound healing | - malnutrition - decreased blood flow - decreased oxygen delivery - impaired inflammatory response - impaired immune responses - infection - wound separation - foreign bodies - age |
| AIDS | Acquired Immunodeficiency Syndrome |
| what causes AIDS | the infection human immunodeficiency virus |
| HIV | human immunodeficiency virus |
| describe HIV | - extreme immunosuppression associated with opportunistic infections, malignancies, wasting, and CNS degeneration |
| name the two forms of HIV | - HIV type 1 (HIV-1) - HIV type (HIV-2) |
| describe HIV-1 | - responsible for most HIV infections |
| describe HIV-2 | - endemic (primarily in West Africa) - transmission is the same as HIV-1 - typically does not progress to AIDS |
| why have AIDS related deaths been on the decline since 1990's | - continual improvement of drug therapies and education |
| because of improved AIDS treatments and decrease in AIDS related deaths, AIDS is now considered | a chronic illness |
| what is the most frequent mode of HIV transmission | - Sexual contact (especially male-on-male) - use of needles/syringes/injection paraphernalia (anything with blood-to-blood contacts) |
| what is the mode of transmission for HIV | mucosal fluids ---- semen ---- vaginal mucus virus is transmitted into the mucous membranes or blood of another person |
| for children with HIV, what is the mode of transmission | - from mother to infant (most common) ----- during pregnancy ----- during birth ----- while breastfeeding |
| how is HIV NOT spread | - saliva or casual contact |
| how common is HIV infections in healthcare workers | - uncommon - 58 documented cases in 2013 due to accidental needle sticks |
| who is at risk for HIV infections | - healthcare workers (relatively uncommon) - those with preexisting STDS (syphilis, Herpes, gonorrhea, chlamydia, trichomoniasis) |
| for those with preexisting STD's, how will having HIV affect the treatment of these STDs | - recurrence of STD lesions - STD treatment failures - atypical STD presentations |
| can an HIV-infected person be infections even in the absence of symptoms | yes |
| define seroconversion | when an infected person's blood converts from being negative for HIV antibodies to being positive |
| what is the window period for HIV | can be between 1-3 months, but can take as long as 6 months |
| define window period | the time between initial infection and the seroconversion |
| HIV primarily targets which cells | CD4+ T Lymphocytes ---- also infects macrophages and dendritic cells |
| because HIV targets CD4+ T lymphocytes, what happens to people who are infected with HIV | - CD 4+ cells are responsible for coordinating the immune response to infection - those infected are significantly more susceptible to severe infections |
| because HIV carries genetic information in RNA, it is classified as a | retrovirus |
| before inserting its genetic information into the host's genome, a retrovirus (like HIV) must first | convert RNA to DNA |
| what has become a key step in to becoming a major target for antiviral theraputics | preventing viruses from converting RNA to DNA and inserting their DNA into the host's genome |
| what is located inside the viral caspid of an HIV microbe | - two copies of genomic RNA - essential viral enzymes ------ reverse transcriptase ------ protease ------ integrase |
| name the three enzymes encapsulated in the HIV microbe | - reverse transcriptase - protease - integrase |
| based on relative abundance receptor ______________ is most commonly the target for antibodies used in the screening | 924 |
| list the steps of the viral lifecycle of HIV | - attachement - internalization - DNA Synthesis - integration - transcription - polyprotein production - cleavage and assembly - release |
| in the search for a cure of HIV, which step of the viral lifecycle has become the focus of potential therapeutic interventions | all of the steps, could potentially prevent more viruses from ever being produced .... therefore each step has become the focus of potential therapeutic interventions |
| describe the attachment phase of an HIV lifecycle | - virus binds to CD 4+ T cells (and other surface molecules) ------ CXCR4 ------ CCR5 ------ chemokine co-receptors |
| describe the internalization phase of an HIV lifecycle | - viral envelope peptides fuse into CD 4+ membrane - virus is uncoated - contents of viral core enter host cell (RNA and enzymes) |
| describe the DNA Synthesis phase of an HIV lifecycle | - HIV reverse transcriptase converts HIV RNA to DNA - results in double stranded DNA - this can now be inserted into the host cell's DNA |
| what is the function of reverse transcriptase in HIV | - convert HIV RNA to DNA - DNA synthesis phase |
| describe the Integration phase of the HIV lifecycle | - newly synthesized HIV DNA enters the nucleus of the CD 4+ T cell - integrase enzyme assists HIV DNA insertion into host cell's DNA |
| what is the function of integrase enzyme in HIV | - fuse HIV DNA with host cell's DNA - in integration phase of HIV lifecycle |
| describe the transcription phase of the HIV lifecycle | - HIV phase that is newly fused to host cell genome - DNA transcription begins - proteins needed to build new viruses are produced |
| describe the polyprotein production phase of the HIV lifecycle | - during transcription - polyprotein chain of essential viral proteins and enzymes are created (by rRNA) |
| describe the cleavage and assembly phase of the HIV lifecycle | - protease enzyme cleaves the polyprotein chain into individual proteins/enzymes - the proteins and viral RNA are assembled into new HIV viruses |
| what is the function of protease enzymes in HIV virus | to cleave/cut the polyprotein chains into HIV viruses |
| describe the release phase of the HIV lifecycle | newly formed HIV are released from the cell and move on to infect other cells |
| name the two types of viral dissemination | - cell-cell fusion - budding |
| what are the three phases of HIV progression | 1) primary infection phase 2) chronic asymptomatic (or latency) phase 3) overt AIDS phase |
| the signs and symptoms primary infection phase of HIV infection (try to name at least 5) | - acute illness stage to acute mononucleosis ----- fever ----- lyphadenopathy (swollen lymphnodes) ----- sore throat ----- fatigue ----- myalgias ----- night sweats ----- maculopapular rash ----- headache ----- aseptic meningitis ----- ulcers |
| describe the primary infection phase of HIV | - acute illness to acute mononucleosis - pronounced decrease CD4+ T cells - signs and symptoms manifest 1 month after infection - beginning treatment during this phase |
| describe the latent phase of HIV | - few signs or symptoms of illness - median time is about 10 years - CD4+ T cell count slowly falls to 200(or less) cells/microL - swollen lymphnodes for 3 months in at least 2 locations (not including groin) ------ nodes can be sore or visible |
| describe the AIDS (last) phase of HIV | - when CD4+ cells fall to less than 200 cells/microL - when an individual exhibits an AIDS-defining illness - risk of infection and death is significantly increased - develops within 10-11 years in 60-70% of individuals |
| list the types of opportunistic viral infections that commonly infect those with HIV | - cytomegalovirus - Herpes Simplex Virus (HSV) - Human Papillomavirus (GPV) - Varicella Zoster Viruses (VZV) - JC virus (causes progressive multifocal leukoencephalopathy....PML) |
| list the types of opportunistic bacterial/mycobacterial infections that commonly infect those with HIV (name at least 3) | - bacterial pneumonia - salmonellosis - bartonellosis - mycobacterium tuberculosis (TB) - Mycobacterium avium-intracellular complex (MAC) |
| list the types of opportunistic fungal infections that commonly infect those with HIV | - candidiasis - coccidioidomycosis - cryptococcosis - histoplasmosis - penicilliosis - pneumocytosis |
| list the types of opportunistic protozoal infections that commonly infect those with HIV | - cryptosporidiosis - microsporidiosis - isosporiasis - toxoplasmosis |
| what are the two best diagnostic methods to detect HIV | - enzyme immunoassay (EIA) - Enzyme-linked immunosorbent assay (ELISA) |
| if the ELISA or EIA come back positive for HIV, what is the next step? | -Western blot test (confirmatory test) |
| what does the enzyme immunoassay (EIA) detect in HIV | - antibodies produced in response to HIV infection |
| negatives of the EIA test in HIV testing | - high false positive rate - this is why the Western blot test is a confirmation |
| what does the Western blot test, test for | - detects presence to specific viral antigens - high degree of specificity and sensitivity |
| what is a polymerase chain reaction (PCR) test in HIV | - amplifies and detects the presence of trace amounts of viral DNA in infected cells - helpful with diagnosing infants born to infected mothers - alternate strategy for detecting HIV presence |
| prevention of HIV | - abstinence - long-term mutual monogamy (two uninfected partners) - avoid recreational IV drugs - do not reuse syringes/needles - all people between 13-64 be screened - anyone engaging in high risk activities be tested annually |
| describe the function of HIV medications | - they decreased the amount of virus in the body - do NOT eradicate virus |
| general treatment of HIV involves | - HIV medications (highly active antiretroviral therapy (HAART)) - get a CD4+ count every 3-4 months - get viral load testing every 3-4 months - avoid, recognize and treat opportunistic infections early |
| HAART | highly active antiretroviral therapy |
| what is the current class of HIV medications | HAART (highly reactive antiretroviral therapy) |
| what are reverse transcriptase inhibitors | - HIV medication - inhibit HIV replication by acting on reverse transcriptase |
| list reverse transcriptase inhibitors | - nucleoside analog reverse transcriptase (NRTIs) - nucleotide analog reverse transcriptase (NRTIs) - non-nucleoside reverse transcriptase inhibitors (NNRTIs) |
| list the four types of HAART medications | - reverse transcriptase inhibitors - entry inhibitors - integrase inhibitors - protease inhibitors |
| what are entry inhibitors for HIV | - prevents HIV from entering/fusing with CD4+ cells - prevent virus from beginning its lifecycle within the cell |
| what are integrase inhibitors (INSTI) for HIV | - block the integration step of the viral cycle - prevents HIV genome from integrating into host's genome |
| what are protease inhibitors (PI) for HIV | - binds to protease enzyme - inhibits protease action - prevents cleavage of polyprotein chain |
| in most regions, what is the first line antiretroviral therapy regimen | - two NRTIs in combination with third agent (INSTI, NNRTI, or PI) |
| what is innate immunity | (aka, natural immunity) is the first line of defense. this typ or defense is in place before an infection takes place and can function immediately. it is comprised of physical, chemical, cellular, and molecular defenses. |
| what cells are involved in innate immunity | - neutrophils - macrophages - dendritic cells (DC) - natural killer cells (NK) - intraepithelial lymphocytes (IEL) |
| Describe adaptive immunity | (aka, acquired immunity) - 2nd line of defense - humoral and cellular mechanisms - responds to cell-specific antigens - acquired through previous exposure - destroys specific antigens - longer response time - extremely effective |
| what are antigens | are present on the surfaces of pathogens or other foreign substances that elicit the adaptive immune response |
| what are the primary cells of adaptive immunity | the primary cells of the adaptive immune system are the lyphocytes, APCs (antigen presenting cells), and effector cells |
| describe T lymphocytes and discuss their roll in immunity | provide *cell-mediated immunity*, recognize specific antigens presents on the surface of pathogens and to remember them in the future |
| describe b lymphocytes and discuss their role in immunity | produces antibodies ****humoral immunity****, recognize specific antigens presents on the surface of pathogens and to remember them in the future |
| study table 3.1 | to understand the difference between innate and adaptive immunity |
| what is the function of humoral immunity | b lymphocytes function in humoral immunity to produce antibodies |
| know the 5 classes of immunoglobins | see module |
| what is the function of cellular immunity | t lymphocytes make up the cellular immunity and the function to activate other B+T cells, control intracellular viral infections, reject foreign tissue grafts, activate autoimmune processes, and activate delayed hypersensitivity reactions |
| what is the master regulator of the immune system | CD4+ helper T cells |
| describe the differences between active and passive immunity (active immunity) | - acquired from an immune response either via vaccination or from environmental exposure - long lasting but takes days to weeks after the firth exposure to fully develop a response |
| descrbe the differences between active and passive immunity (passive immunity) | - immunity is transferred from another source. - the most common example is from mother to fetus, where the IgG antibodies are passed via placenta, breast milk, or colostrum. - short-term protection lasting only weeks to months |
| what are type i hypersensitivity reactions | IgE-mediated reactions that develop quickly upon exposure to an antigen |
| what cells are involved with type i reactions (know their role) | - mast cells - basophils - eosinophils - they play an important rol because they contain the chemical mediator histamine |
| know the different types of type i hypersensitivity reactions and their treatments | see module |
| what are type ii hypersensitivity reactions | (aka cytotoxic hypersensitivity reaction), - antibody-mediated reactions - mediated by IgG or IgM - directed against target antigens on specific host cell surfaces or tissue |
| what are autoimmune disorders | occur when the body's immune system fails to differentiate self antigens from nonself antigens and mounts an immunologic response against host tissues |
| what is self-tolerance | the ability to distinguish self from non-self |
| what is autoreactivity | the term that describes an organism acting against its own tissue |
| what is anergy | when the loss of lymphocytes response to an antigen occurs and causes a lack of cellular/humoral immunologic response, this is called anergy. Anergy is the state of immunologic tolerance to specific antigens |
| what are autoantibodies | in many autoimmune diseases, the immune system loses its ability recognize self and produces what is called autoantibodies |
| what are positive and negative selection (positive selection) | during the maturation in the thymus, T cells encounter self-peptides bound to MHC molecules. the T cells that display the host's MHC antigens and T-cell receptors for a nonself-antigen are allowed to mature, a process termed positive selection. |
| what are positive and negative selection (negative selection) | during maturation in the thymus, T cells encounter self-peptides bound to MHC molecules. The T cells that have a high affinity for host cells are sorted out and undergo apoptosis, called negative selection. |
| what are the 2 general causes for autoimmune diseases | - genetic factors - environmental factors |
| how do you diagnose an autoimmune disease | - history - physical - serological findings - following criteria must be met: evidence of an autoimmune reaction, immunologic findings (not secondary to another condition), no other identifiable causes found |
| what is Grave's disease | abnormal stimulation of the thyroid gland by thyroid stimulating antibodies (TSH receptor antibodies) that act through the normal TSH receptors. It is a state of hyperthyroidism, goiter, and ophthalmopathy |
| what is SLE | Systemic Lupus Erythematosus (SLE) is a chronic inflammatory disease termed "the great imitator" because it can affect almost any organ system. |
| what is HIV | - retrovirus - selectively attacks CD4+ T cells - the immune cells responsible for coordinating the immune response to infection - people with HIV infections are more susceptible to severe infections with ordinarily harmless organisms |
| how is HIV spread | - transmitted from one person to another through: --- sexual contact --- blood-to-blood contact --- mother to child (pregnancy/birth/breastfeeding -NOT spread via saliva or casual contact |
| what is seroconversion | when an infected person's blood converts from being negative for HIV antibodies to being positive |
| what is the window period | the time between infection and seroconversion is called the window period |
| know the S+S of the acute (primary phase) of HIV infection | see module |
| what is the latent and last phase of HIV infections | (latent phase) characterized by no signs or symptoms of illness. (last phase or AIDS) when CD4+ cell count falls to less than 200 cells/microLiter or the patient exhibits an AIDS-defining illness |
| what are opportunistic infections | infections that common organisms that do not produce infection without impaired immune function |
| what are the best diagnostic tests for HIV | HIV antibody tests - enzyme immunoassay (EIA) or enzyme-linked immunosorbant assay (ELISA) - Western blot assay as a confirmation test |
| in regards to HIV what does the EIA test detect | detects antibodies produced in response to HIV infection |
| the polymerase chain reaction (PCR) test detects (in regards to HIV) | - nucleic acid test - detects HIV DNA - detects for presence of the virus rather than antibody |
| describe the process of chronic inflammation and discuss how it develops | - results from recurrent of progressive acute inflammatory processes or low-grade responses that fail to evoke an acute response - involves collection of macrophages and lymphocytes (rather than neutrophils) - involves proliferation of fibroblasts |
| three stages of wound repair | - inflammatory phase - proliferative phase - wound contraction and remodeling phase |
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