Pathophysiology Exam 2 PDF

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Prof. Soontupe and Koplow...

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Chapter 15: Disorders of the Immune Response 1) Review of Physiology a) Normal immunity i) Protective functions ii)  proliferation of cancer cells iii) Healing process b) Immune alterations i) Hypersensitivities (inappropriate immunity) ii) Autoimmunity (misdirected immunity) (1) Lupis (2) Body determines that some tissues in the body it does like (goes and attacks it) ex: lupus, rheumatoid arthritis are all auto immune disorders iii) Immunodeficiency (inadequate immunity) (1) HIV/AIDS (2) Inadequate immunity, aids, HIV, exposed to antigen but body does not recognize it 2) Classification of Immunodeficiency State a) Primary (congenital or inherited) i) It is the exact cause ii) Exact cause! Genetic…couldn’t be avoided b) Secondary (acquired later in life)- something usually caused it. ex.: strep can lead to other things, must treat so it doesn’t evolve to something else… i) Malnutrition will cause a problem because you need proteins ii) Infection (e.g., acquired immunodeficiency syndrome [AIDS]) iii) Neoplastic disease (e.g., lymphoma) iv) Immunosuppressive therapy (e.g., corticosteroids or transplant rejection medications) (1) Steroids suppress to immune system (2) Steroids suppress immune system. No matter how close a transplant is, it does NOT have the same DNA. Body will recognize it does not belong..sometimes immune system activated=rejected…in transpalnt need immune suppressing drugs (3) When someone recieves organ transplant they need immunosuppressant drugs so they do not reject the new organ v) Compliment Complex Immunity (1) Ex. Strep 2) Hypersensitivity Disorders a) Definition i) Excessive or inappropriate activation of the immune system ii) Red eyes, runny nose, swelling, hives, etc. b) Types i) Type I, IgE-mediated disorders (1) Classic allergic response ii) Type II, antibody-mediated disorders (1) When your body comes in contact with something iii) Type III, complement-mediated immune disorders (1) Compliment complex systems (2) Rummathord Arthritis, when tissues in your body attack iv) Type IV, T-cell–mediated disorders (1) HIV 3) Types of IgE-Mediated Allergic Reaction a) Atopic Disorders i) Heredity predisposition and production of a local reaction to IgE antibodies produced in response to common environmental agents

(1) Urticaria (hives), allergic rhinitis (hay fever), atopic dermatitis, food allergies, some forms of asthma (2) Hives on the outside show that there is swelling on the inside which can be very dangerous b) Nonatopic Disorders i) Lack the genetic component and organ specificity of the atopic disorders 4) Phase of Type 1 Hypersensitivity Reactions a) Primary or Initial-phase Response i) Vasodilation ii) Vascular leakage- capillaries can not keep fluid in iii) Smooth muscle contraction b) Secondary or Late-phase Response i) More intense infiltration of tissues with eosinophils and other acute and chronic inflammatory cells (mass cells) (1) Release histamine which is vasodilation of blood cells ii) Tissue destruction in the form of epithelial cell damage 5) Type II (Cytotoxic) Hypersensitivity Reactions a) Action i) Mediated by IgG or IgM antibodies directed against target antigens on the surface of cells or other tissue components- Iga is in the mucus lining the GI, bladder, lungs and eyes (more likely to have asthma etc) ii) Endogenous antigens: present on the membranes of body cells iii) Exogenous antigens: absorbed on the membrane surface- absorbed into the membrane b) Examples i) Mismatched blood transfusion reactions- body can react ii) Hemolytic disease of the newborn when RBC’s starts destroying themselves iii) Certain drug reactions- Cytotoxic reactions may occur 6) Type III, Immune Complex Allergic Disorders a) Mediated by the formation of insoluble antigen–antibody complexes that activate the complement pathway i) Activation of the complement pathway by the immune complex generates chemotactic and vasoactive mediators that cause tissue damage by (1) Alterations in blood flow. (2) Increased vascular permeability (plasma seeps out into tissue spaces) (3) Destructive action of inflammatory cells. (4) Complex hide in tissues and destroy, complement come to eat them up (pac man) (5) Examples: (a) Strep and heart and kidney disease and R. arthirits b) Immune complexes formed in the circulation produce damage when in contact with the vessel lining or are deposited in tissues. i) They elicit an inflammatory response by activating the complement pathway. ii) Leading to chemotactic recruitment of neutrophils and other inflammatory cells c) Responsible for the vasculitis (inflammation of arteries) seen in certain autoimmune diseases- inflammations of the arteries d) Systemic immune complex disorders i) Serum sickness (1) 7-10 days after being exposed to the antigen without being treated with the steroid (2) Urinalysis will show protein in the urine (3) Can evolve into other immune automated disorders (4) Must treat allergies associated with bug bites or severe allergy reactions. If not treated joints will be sore and swollen, may have a fever, protein might be present in urine…can evolve into other immune automated disorders- kidney destruction e) Localized immune complex reactions i) Arthus reaction – joint reaction to something 7) Type IV hypersensitivity Reactions

a) Cell-Mediated Immune Response-microorganism enters body and cell responds to it! i) Cell itself can die based on the reaction ii) A microorganisms enter the body and the cell responds to it iii) The principal mechanism of response to a variety of microorganisms, including intracellular pathogens and extracellular agents iv) Can lead to cell death and tissue injury in response to chemical antigens or self-antigens b) Basic Types i) Direct cell-mediated cytoxicity (1) Hepatitis cells specific to the livers, the cells become inflamed depends on the virus that it is exposed to (a) Enters the body (b) Cell specific to the liver (c) Liver cells become inflamed depending on the type of hep virus ii) Delayed-type hypersensitivity (1) Allergic contact dermatitis- coming into contact with something on your skin 12-24 hours later something starts happening (a) Ex. mango skin (b) Come in contact with something (c) Than 24 hours later you start to see reactions (2) Hypersensitivity pneumonitis (a) Inflammation of inner lining of bronchi of the lung (b) Something you inhale 8) Autoimmune Diseases a) Systemic lupus erythematosus (SLE) b) Autoimmune hemolytic anemia (AIHA) c) Pemphigus vulgaris i) Strange rash ex. Poison ivy d) Hashimoto thyroiditis i) Inflamed thyroid 9) Mechanisms of Autoimmune Disease a) Heredity and gender- R. Arthritis and lupus are more common in females b) Failure of self-tolerance i) Disorders in MHC–antigen complex/receptor interactions ii) Molecular mimicry iii) Superantigens- devlope over time (1) Antigens that have been developed over time environmental exposure reaction 10) Criteria for Determine an Autoimmune Disorder a) Evidence of an autoimmune reaction i) 1. Must be reastion ii) 2. Look for a reaction (R. factor) b) Determination that the immunologic findings are not secondary to another condition c) The lack of other identified causes for the disorder 11) A systemic immune complex disorder hat is caused by insoluble antigen-antibody complexes being deposited in blood vessels joints, heart, or kidney is categorized by which type of hypersensitivity? a) Type III (this is lupus) 12) Characteristics of Systemic Lupus Erythematosus (SLE) a) Formation of autoantibodies and immune complexes b) B-cell hyperreactivity c) Increased production of antibodies against self (autoantibodies) and nonself antigens-happens in the joints the heart and kidneys d) Majority of people with lupus die of kidney failure (renal failure)

e) f) g) h) i) j) k)

Lupus-means wolf Systemic means throughout the body In whole body not just on the skin Joints, hearts, and kidneys Usually die from renal failure Complexes attack basement membrane of the kidneys The autoantibodies can directly damage tissues or combine with corresponding antigens to form tissuedamaging immune complexes. i) Autoantibodies (1) Antinuclear antibodies (2) Other antibodies (3) Platelets (4) Coagulation factors (5) Red blood cell surface antigens (6) Factors that are observed to see if someone has lupus l) Signs and Symtoms i) Remissions & exacerbations ii) Early (1) Arthralgia (swelling and aching) & arthritis (inflammatory response in joints) iii) Skin (1) Malar “butterfly” rash (2) Photosensitivity (3) Sun brings out rash iv) Renal (1) Interstitial nephritis- causes inflammation of the inner lining of the glomerulus (2) Renal failure often preceded by nephrotic syndrome

13)Categories of Clinical Manifestations of SLE a) Constitutional b) Musculoskeletal- joints c) Dermatologic d) Cardiovascular- endocarditis e) Pulmonary f) Renal g) Neuropsychiatric h) Test for lupus- antinuclear antibody test (A&A test)

Chapter 16: Acquired Immunodeficiency Syndrome 14) AIDS Epidemic and Transmission of HIV a) Caused by HIV b) Occurs worldwide c) There is no cure. d) Transmitted through blood, semen, vaginal fluids, and breast milk e) Not spread by casual contact or insects f) Is infectious, even if the person is asymptomatic 15)Cells Affected by the HIV a) A subset of lymphocytes called CD4+ T lymphocytes (also known as T-helper cells or CD4+ T cells) b) Macrophages c) Dendritic cells

16)Characteristics of AIDS a) Profound immunosuppression b) Associated opportunistic infections c) Malignancies d) Wasting e) Central nervous system degeneration- phago-go eat! Mono and macro are activated with certain virus 17) Functions of the CD4+ T Cells a) Necessary for normal immune function b) Recognizes foreign antigens c) Helps activate antibody-producing B lymphocytes d) Orchestrates cell-mediated immunity e) Influences the phagocytic function of monocytes and macrophages

18)Life Cycle of the HIV-1 a) Attachment of the HIV to CD4+ receptor b) Internalization and uncoating of the virus with viral RNA and reverse transcriptase

c) Reverse transcription, which produces a mirror image of the viral RNA and double-standard DNA moleculenew DNA that forms is not your DNA, wil have its own cellular reproduction. Your cells will not recognize this d) Integration of viral DNA into host DNA using the integrase enzyme e) Transcription of the inserted viral DNA to produce viral messenger RNA f) Translation of viral messenger RNA to create viral polyprotein g) Cleavage of viral polyprotein into individual viral proteins that make up the new virus h) Assembly and release of the new virus from the host cell 19)Three phases of HIV Infection a) Primary infection phase i) Inidividual is infected with the virus ii) Can still pass the virus to others b) Chronic asymptomatic or latency phase i) No symptoms but know they have been exposed c) Overt AIDS phase 20) CDC JIV/AIDS Classification System a) The clinical importance of the CD4+ cell count in the categorization of HIV-related clinical conditions i) Category 1: >500 cells/μL ii) Category 2: 200 to 499 cells/μL iii) Category 3: 1,000,000/L  i) Normal is 250,000 b) Etiology i) Splenectomy ii) Cancer iii) Chronic inflammatory conditions (RA, Crohn's disease) c) Pathophysiology i) Thrombus formation due to activation of the coagulation system (1) Genetic

(2) Secondary (acquired) disorder- cancer, secondary polysythemia (exposed to something else) d) ** Increases the risk of clot or thrombus formation in arterial/venous circulation 9) Increases Platelet Function a) Hypercoagulability due to increased platelet function results in platelet adhesion, formation of platelet clots, and disruption of blood flow. b) The causes of increased platelet function are disturbances in flow, endothelial damage, and increased sensitivity of platelets to factors that cause adhesiveness and aggregation 10) Causes of Bleeding a) Decrease in the number of circulating platelets i) Depletion of platelets must be relatively severe before hemorrhagic tendencies of spontaneous bleeding occur. b) Impaired platelet function i) Bleeding resulting from platelet deficiency commonly occurs in small vessels and is characterized by petechiae and purpura 11)Thrombocytopenia a) Definition i) Decrease in the number of circulating platelets ii) Platelet count...