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HIV EIA (3rd generation immunoassay)
UTA 5315 Advanced Pathophysiology Test 2
Questions and Answers Rated A+
✔✔can use urine, saliva, or serum (most accurate), need to wait until 12 weeks post exposure to see antibodies,
99% accurate 4th generation immunoassay- "gold standard" measures P24 antigen can test 10 days post exposure Mast cell ✔✔Cellular bags of granules located in loose connective tisssue close to blood vessels. Activation initiates inflammatory process. Histamine ✔✔Causes vasodilation, increases vascular permeability, increases blood flow to the site of injury- causes erythema and swelling. Cytokines ✔✔Soluble factors that contribute to the regulation of innate or adaptive resistance by affecting other neighboring cells. Can be pro- inflammatory or anti-inflammatory. Can react quickly or be more delayed. Leukotrines ✔✔Released when mast cells degranulate, prolong the inflammatory process. Cause vasodilation, attract neutrophils, monocytes, and eosinophils.target of inhibition for singular. Prostaglandins ✔✔Released when mast cells degranulate, are produced by the arachidonic pathway. Cause vasodilation, platelet aggregation at site of injury, pain, and fever. Chemotactic factors ✔✔Biochemical substance that attracts leukocyte to the site of inflammation Neutrophils ✔✔Predominant leukocyte at work during the early stages of acute inflammation
Monocytes ✔✔Become macrophages when entering the tissue, responsible for presenting antigens to the CD4 cell which triggers T-cell immunity and B-cell immunity. Releases additional cytokines IL1, IL6, TNF. Cytokine IL1 function ✔✔Causes fever, activates phagocytes & lymphocytes and also increases the release of IL6a Cytokine IL6 function ✔✔Stimulates production of acute phase reactants and promotes growth and stimulation of RBCs Cytokine TNF function ✔✔Causes fever, increases synthesis of proinflammatory proteins by liver, causes muscle wasting, induces thrombosis Cytokine growth factor function ✔✔Promotes production and maturation of neutrophils Complement ✔✔Functions include bacterial lysis, vasodilation and increased vascular permeability, triggers mast cell degranulation, chemotaxis, and opsonization. Kinin ✔✔Converted to bradykinin which is responsible for pain and chemotaxis, and it increases vascular permeability and vasodilation. Coagulation cascade ✔✔Factor XII activates kinin. Function is to form fibrin mesh to stop bleeding and trap micro organisms. COX1 ✔✔Prostaglandin of arachidonic pathway. Provides gastroprotection, platelet aggregation, fluid/electrolyte balance
Type 2 hypersensitivity ✔✔E. Antibodies directed against fixed antigens on the plasma membrane of cells C.M. Varies depending on alloimmune or autoimmune Alloimmunity and example of hypersensitivity ✔✔When an individuals immune system reacts against antigens on the tissues of other members of the same species Blood transfusions- causes clumping and lysis of RBC- fever, nausea, chills, low back pain, dark urine, hives, itching, SOB Rh incompatibility- hemolytic disease of newborn with jaundice, give Rhogam within 72 hours of birth (Rh- mother with Rh+ child) Autoimmunity and example of hypersensitivity ✔✔A breakdown of tolerance in which the bodies immune system begins to recognize self-antigens as foreign. Graves Disease- autoantibodies form against thyroid cells- bind to thyroid cells and mimic action of TSH, increases secretion of thyroxine Myasthenia Gravis- autoantibodies against acetylcholine bind to the post synaptic receptors and inhibit synaptic transmission of acetylcholine. Leads to muscle weakness and paralysis (mind to ground) Guillain-Barre' syndrome- antibodies bind with myelin sheath of the peripheral nervous system, triggering the immune response. Causes demyelination of the peripheral nerves and a rapidly progressive, ascending paralysis (ground to brain) Type III hypersensitivity ✔✔Widespread immune and inflammatory response not specified for any cell or tissue. SLE, RA Antibodies are formed against and bind to circulating antigens, antigen- antibody complex deposits in vessel walls or tissue. Causes cellular and tissue damage. IgG and IgM response, spread via circulation- not specific to a cell or tissue- widespread damage. Type IV hypersensitivity ✔✔T-cell lymphocyte mediated reaction that does not require antibody activation. Delayed response- 24-72 hours.
Contact dermatitis- poison ivy, topical drugs, chemicals such as nickel or formaldehyde. Antigens too small to cause a reaction bind to proteins, response includes rash, red bumps, itching, and blisters. Reactive tuberculin test- PPD cause and induration in 24-72 if person was previously exposed to tuberculin antigen Solid organ transplant rejection- 11-14 days after 1st exposure, 5-6 days after 2nd exposure, results in mononuclear infiltration, decreased circulation, and tissue necrosis. Systemic Lupus Erythematosus ✔✔E. Primarily women aged 20-40, Type III hypersensitivity. Antibodies are formed against DNA Genetic, leads to tissue damage. Exacerbated by infections, UV light, estrogen, meds, stress Diagnosed by serum ANA C.M. Butterfly rash (cheeks), photosensitivity, nonerosive arthritis of at least 2 peripheral inflammation joints, of serous sacs, proteinuria, seizures, anemia, leukopenia, thrombocytopenia Rheumatoid Arthritis ✔✔E. Primarily women 30-50, systemic autoimmune disease Progressive, irreversible leads to deformity and disability Tx includes PT, NSAIDS, corticosteroids C.M. Joint inflammation, pain, destruction of synovial membrane, widespread symmetrical joint swelling, erythema joints warm to touch, loss of function, morning stiffness- improves with movement, weight loss, weakness, anorexia -Osis or -philia ✔✔Elevated count of blood cells -penia ✔✔Low count of blood cells Leukocytosis ✔✔Increase in number of total WBC Leukopenia ✔✔Decrease in number of total WBC
What is the etiology, incubation, and mode of transmission for measles ✔✔Initial infection and From AIDS, chemotherapy, or steroid use Which antibodies and antigens do each blood type have ✔✔A has A antigen and B antibodies B has B antigen and A antibodies AB has AB antigens, and no antibodies O has no antigens, but A and B antibodies What is the etiology, incubation, and mode of transmission for influenza ✔✔Comes from one of three types- A, B, C Transmitted via aerosol Incubation is 1-4 days (usually 2) viral replication occur locally in tracheal and bronchial epithelial cells. After 2- 4 days, local lymphatic tissues are infected. Virus is disseminated to various organs, and rash appears. Transmitted by respiratory droplets, either airborne or on surfaces up to 2 hours Incubated 7-14 days (average 10-12 days) What is the etiology, incubation, and mode of transmission for HIV ✔✔Virus enters bloodstream and begins seeking out the CD4 (T-helper cells). The virus fuses to CD4 cells and integrates with host's DNA. More CD4 cells become infected, and eventually rupture. Overall CD4 count is reduced, leaving patient susceptible to opportunist infections. Transmitted via bodily fluids-blood borne. Incubates as long as 10 years in untreated individuals. Discuss some clinical implications of solid organ transplant rejection ✔✔rejection is an immune response, mostly T-cell mediated. Slow process, Type 4 hypersensitivity Patients are highly susceptible to infections r/t use of immunosuppressants
Describe the role of HLA in solid organ rejections ✔✔HLA is typed and matched on donor and recipient to decrease risk of rejection HLA is targeted response for rejection clinical manifestations of influenza ✔✔fever, sore throat, myalgias, headache, nasal discharge, weakness and severe fatigue, cough and other respiratory symptoms, tachycardia, red, watery eyes, pharyngitis clinical implications of influenza ✔✔prevention is key- vaccinate at 6+ months, annual diagnosed by rapid swab treat with antivirals- Tamiflu clinical manifestations of measles ✔✔fever >104, lasts 4-7 days, malaise, anorexia, 3c's- conjunctivitis, cough, coryza (inflammation of mucous membrane of nose), photophobia, periorbital edema, myalgias, Koplik spots (bluish-gray specks on red base, on buccal mucosa), rash- begins at hairline, spreads in 48 hours Clinical implications of measeles ✔✔One of most contagious infectious diseases, lasts 7-10 days Educate parents on importance of vaccination Immune globulin can be administered within 6 days of exposure Can be fatal for HIV patients Immunocompromised may have no rash Need serologic testing per CDC Tx is supportive- rehydration, Vit A Antiretroviral medications ✔✔Used to impede viral replication of HIV virus, come in 6 classes 1. Nucleoside reverse transcriptase inhibitors
- Non-nucleoside reverse transcriptase inhibitors 3. Protease inhibitors
PCP- pneumocystitis jiroveci pneumonia ✔✔fungus
butterfly infiltrates on CXR CM- worsening dyspnea, fatigue, night sweats, weight loss, poor appetite Tx- Bactrim MAC- mycobacterium avium complex ✔✔AFB- leads to systemic infection, grows slow- thick cell wall hard to penetrate CM- fever, night sweats, anorexia, weight loss, lymphadenopathy Tx- clarithromycin and ethambutol for 6-12 months CMV- cytomegalovirus ✔✔herpes virus greatest risk for CD4 < (ensure eye exams) CM- fever, myalgia, cervical lymphadenopathy, mild hepatitis, retinal detachment, vision loss, blindness Tx- resistant to medications, no prevention how is coagulation cascade altered by warfarin ✔✔blocks Proteins S and C blocks Vit K enzyme to prevent carboxylation, decreasing amount of functional K to be used in Vit K dependent coagulation factors how does low molecular weight heparin affect coagulation cascade ✔✔inhibits factor Xa and prevents formation of prothrombinase complex and consequently thrombin how do direct thrombin inhibitors alter coagulation cascade ✔✔prevent activation of fibrinogen and XIII give CM and an example of coagulopathy hemorrhage ✔✔CM- joint bleeding, tissue hematomas, large spontaneous central ecchymosis, delayed bleeding after surgery, trauma or injury DIC
in factor IX
normal platelets and PT, prolonged PTT, decreased factor IX CM: knee, elbow, and ankle bleeds, GI bleeds discuss DIC ✔✔activation of the coagulation system causes widespread intravascular fibrin deposition, fibrinolytic products attempt to break down fibrin- adhere to platelets to prevent adhesion. coagulation products are eventually consumed and bleeding occurs. may cause organ failure r/t micro- thrombi triggers: malignancy, sepsis, infection, ob complications, trauma, Sx, ARDS, rhabdo, venomous snake bites CM: oozing, bleeding from all puncture sites, bleeds from all body cavities, prolonged PT/PTT, elevated d-dimer, platelet count <100, discuss Vitamin K deficiency ✔✔CM: easy bruising, oozing from nose or gums, excessive wound bleeding, menorrhagia discuss liver disease ✔✔all factors of clotting can be affected Hageman deficiency ✔✔deficiency of factor XII- rare genetic disorder asymptomatic, causes prolonged clotting test with no clinical bleeding or risk present causes of thrombus ✔✔Triad of Virchow- injury to blood vessels, abnormality in blood flow, hypercoagulability some medications increase risks discuss macrocytic, microcytic, and normocytic anemias ✔✔classified by size of RBC macrolytic- MCV >100, includes pernicious and folic acid anemias, can be caused by ETOH microlytic- MCV <80, folic acid anemia normolytic- MCV 80-100 (normal range), sickle cell is an example
Risk factors and CM of anemia of chronic disease ✔✔AIDS, RA, CKD, chronic hepatitis, lupus 2nd most common, chronic disease leads to body's inability to use iron stores Risk factors and CM of sickle cell anemia ✔✔African descent, Mediterranean, middle eastern, or Indian descent, familial history Pain during crisis Pathophysiology and clinical implications of sickle cell anemia ✔✔Lack of O2 causes hgb S molecules to transform to sickle shape, treat with 0.45% NaCl to rehydrate cell and reverse shape change Autosomal recessive- can carry trait or active form. Define acute leukemia ✔✔Rapid onset- aggressive accumulation of immature cells, causes overproduction of leukocytes by the bone marrow, causes overcrowding, prevents formation of normal blood cells Chronic leukemia ✔✔Gradual onset, cells appear normal but do not function appropriately and accumulate Lymphocytic leukemia ✔✔Excessive production of lymphocytes Myelogenous leukemia ✔✔Excessive production of granulocytes Multiple myeloma pathophysiology and CM ✔✔Chromosomal abnormality that leads to production of malignant plasma cells, cells secrete antibodies which are deposited in organs (mostly bones) and grow malignant tumors, 3 yr life span Vertebrae, skull, ribs and pelvis most frequently affected CM: hypercalcemia, recurrent infections, renal failure
hepatomegaly, night sweats, weight loss, anemia, thrombocytopenia, petechiae, ecchymosis Risk factors for multiple myeloma ✔✔African descent Males more common Around 6th decade of life Etiology and pathophysiology of Hodgkin's Lymphoma ✔✔Malignant neoplasms of cells called CM of Hodgkin's Lymphoma ✔✔Large painless lump/mass- usually on neck, eosinophilia, fever, weight loss, night sweats, pruritus, adenopathy, thrombocytosis, leukocytosis, mediastinal or abdominal mass Epidemiology of Hodgkin's Lymphoma ✔✔Possibly Epstein Barr, unknown Etiology and Epidemiology of Non-Hodgkin's Lymphoma ✔✔Malignant transformation of lymphocytes, no Reed-Sternberg cells Caused by immunosuppression, AIDS, Hep C, EBV, post transplantation CM of Non-Hodgkin's Lymphoma ✔✔Generalized lymphadenopathy Late stages bring fever, night sweats, weight loss Acute Lymphocytic Leukemia (ALL) ✔✔Marked by >30% lymphoblasts in blood or marrow Most common in children Survival rate decreases with age CM: fever, pallor, bleeding, fatigue, lymphadenopathy, infection, joint pain, splenomegaly, Acute Myelogenous Leukemia (AML) ✔✔Marked by proliferation of immature myeloid cells, decreased apoptosis, and lack of cellular differentiation Most common in adults
