DUMDUMISMs CRACKING MS

Refers to excessive or inappropriate activation of the immune system Types

Type I immediate hypersensitivity disorders
Type II antibody-mediated disorders Type III- immune-complex mediated disorder

Type IV T cell mediated disorder

IgE mediated mast cell degranulation Examples are:

Hay fever, asthma, anaphylaxis

Formation of anti-bodies (IgG,IgM) against surface antigens. Complements usually involved Autoimmune hemolytic anemia, hemolytic disease of the newborn

IgG,IgM,IgA that interact with exogenous or endogenous antigens to form antigenantibody complexes that cause vessel or tissue injury Autoimmune diseases (SLE), rheumatoid arthritis, AGN

Synthesized T lymphocyte release cytokines that cause direct cell-mediated toxicity or delayed hypersensitivity disorders Tuberculosis, contact dermatitis, transplant rejection

Autoimmune disorders results from the breakdown in the integrity of immune tolerance such that a humoral or cellular immune response can be mounted against host tissue or antigens, leading to localized or systemic injury Immunologic tolerance is the ability of the immune system to differentiate self from nonself

Mixed connective tissue disease Polymyositis dermatomyositis Rheumatoid arthritis Scleroderma Sjogren syndrome Systemic Lupus erythematosus

Autoimmune hemolytic anemia Autoimmune neutropenia and lymphopenia Idiopathic Thrombocytopenic purpura

Acute idiopathic polyneuritis Atrophic gastritis and pernicious anemia Hashimoto thyroiditis IDDM MG Graves disease Ulcerative Colitis Primary biliary cirrhosis

Rheumatoid arthritis systemic inflammatory disease that attacks the joints by producing proliferative synovitis that leads to destruction of the articular cartilage and underlying bone.

Morning stiffness for at least 1 hour and present for at least 6 months Simultaneous swelling of three or more joints for at least 6 weeks Swelling of wrist, metacarpophalangeal or proximal interphalangeal joints for at least 6 wks Systemic joint swelling for 6 or more weeks

Rheumatoid nodules Serum rheumatoid factor Radiographic changes typical of rheumatoid arthritis on hand or wrist radiographs

Reduce pain, minimize stiffness and swelling, maintain mobility Rest (physical and emotional) Therapeutic exercise DMARD - methotrexate NSAIDS aspirn

Degenerative joint disease Pain worsens with activity and relieved by rest initially. In later stage, pain is experienced during rest. Arthritis of the weight bearing joints

No cure Physical rehabilitation Relieve pain NSAIDS

Chronic inflammatory disease that can affect virtually any organ system Dominant in females Common in african americans, latin americans, asians Idiopathic

Systemic lupus erythematosus (SLE) is an autoimmune disease. SLE is characterized by the production of unusual antibodies in the blood. SLE is eight times more common in women than men. The cause(s) of SLE is (are) unknown, however, heredity, viruses, ultraviolet light, and drugs all may play some role.

Up to 10% of people with lupus isolated to the skin will develop the systemic form of lupus (SLE). Eleven criteria help doctors to diagnose SLE. Treatment of SLE is directed toward decreasing inflammation and/or the level of autoimmune activity. People with SLE can prevent "flares" of disease by avoiding sun exposure and not abruptly discontinuing medications and monitoring their condition with their doctor.

fatigue, low-grade fever,loss of appetite, muscle aches, hair loss (alopecia), arthritis, ulcers of the mouth and nose, facial rash ("butterfly rash"), unusual sensitivity to sunlight (photosensitivity), inflammation of the lining that surrounds the lungs (pleuritis) and the heart (pericarditis), and poor circulation to the fingers and toes with cold exposure (Raynaud's phenomenon). Complications of organ involvement can lead to further symptoms that depend on the organ affected and severity of the disease.

Skin manifestations are frequent in lupus and can sometimes lead to scarring. In discoid lupus, only the skin is typically involved. The skin rash in discoid lupus often is found on the face and scalp. It usually is red and may have raised borders. Discoid lupus rashes are usually painless and do not itch, but scarring can cause permanent hair loss (alopecia). Over time, 5%-10% of those with discoid lupus may develop SLE.

Arthritis Thrombocytopenia Myositis Muscle pain and weakness Vasculitis Chest pain Carditis High blood pressure Renal failure psychosis

Malar (over the cheeks of the face) "butterfly" rash Discoid skin rash (patchy redness with hyperpigmentation and hypopigmentation that can cause scarring) Photosensitivity (skin rash in reaction to sunlight [ultraviolet light] exposure) Mucous membrane ulcers (spontaneous sores or ulcers of the lining of the mouth, nose, or throat)

Arthritis (two or more swollen, tender joints of the extremities) Pleuritis or pericarditis (inflammation of the lining tissue around the heart or lungs, usually associated with chest pain upon breathing or changes of body position)

Kidney abnormalities (abnormal amounts of urine protein or clumps of cellular elements called casts detectable with a urinalysis) Brain irritation (manifested by seizures [convulsions] and/or psychosis, referred to as "lupus cerebritis") Blood-count abnormalities: low white blood count (WBC) or red blood count (RBC), or platelet count on routine complete blood count testing)

Immunologic disorder (abnormal immune tests include anti-DNA or anti-Sm [Smith] antibodies, falsely positive blood test for syphilis, anticardiolipin antibodies, lupus anticoagulant, or positive LE prep test) Antinuclear antibody (positive ANA antibody testing [antinuclear antibodies in the blood])

Corticosteroids NSAIDS Hydroxychloroquine Immunosuppresants B cell suppresors (Rituximab)

Infection caused by HIV Characterized by profound immunosuppression with associated opportunistic infections, malignancies, wasting, and CNS degeneration AIDS is a secondary immunodeficiency disorder that results from HIV infection and is transmitted through blood, semen, or vaginal fluids

1 Attachment of HIV to CD4+ T cell receptors 2 Internalization and uncoating of the virus with viral RNA and reverse transcriptase 3 Reverse transcription 4 Integration of viral DNA to host DNA (integrase enzyme) 5 Transcription of the inserted viral DNA to produce viral mRNA

6 Translation of viral mRNA to create viral polyprotein 7 cleavage of viral polyprotein into individual viral proteins that make up the new virus 8 Assembly and release of the new virus from the host cell.

CD4+ cell count

Category 1 = >500cells/uL Category 2 = 200-499 cells/uL Category 3 = <200 cells/uL

Clinical category
Clinical Category A no symptoms or persistent

lymphadenopathy Clinical Category B symptoms of immunedeficiency not enough to be classified as AIDS Clinical Category C AIDS defining illness

8-12 years 3 phases

Primary infection phase (2-4 weeks)

Latency phase (8-10 years)

Overt or AIDS phase (2-3 years)

Fever Fatigue Rash Headache Lymphadenopathy Pharyngitis Arthralgia Myalgia Night sweats GI problems Aseptic meningitis Oral or genetic ulcers

PCP and PTB CMV and MAC Esphageal candidiasis Herpes simplex virus Kaposi Sarcoma Lymphoma Salmonella septicemia Cervical malignancies Histoplasmosis Etc.

ELISA Western Blot Assay Ora Quick Rapid HIV-1 Antibody test Polymerase chain reaction (PCR)

HAART
Highly active anti-retroviral therapy

 Entry inhibitors (or fusion inhibitors) interfere with

binding, fusion and entry of HIV-1 to the host cell by blocking one of several targets. Maraviroc and enfuvirtide are the two currently available agents in this class.

 CCR5 receptor antagonists are the first

antiretroviral drugs which do not target the virus directly. Instead, they bind to the CCR5 receptor on the surface of the T-Cell and block viral attachment to the cell. Most strains of HIV attach to T-Cells using the CCR5 receptor. If HIV cannot attach to the cell, it cannot gain entry to replicate.

 Nucleoside reverse transcriptase inhibitors (NRTI)

and nucleotide reverse transciptase inhibitors (NtRTI) are nucleoside and nucleotide analogues which inhibit reverse transcription by being incorporated into the newly synthesized viral DNA strand as faulty nucleotides; they both act as competitive substrate inhibitors.

 Non-Nucleoside reverse transcriptase inhibitors

(NNRTI) inhibit reverse transcriptase by binding to an allosteric site of the enzyme; NNRTIs act as non-competitive inhibitors of reverse transcriptase. Protease inhibitors (PIs) target viral assembly by inhibiting the activity of protease, an enzyme used by HIV to cleave nascent proteins for the final assembly of new virions.

 Integrase inhibitors inhibit the enzyme integrase,

which is responsible for integration of viral DNA into the DNA of the infected cell. There are several integrase inhibitors currently under clinical trial, and raltegravir became the first to receive FDA approval in October 2007.

 Maturation inhibitors inhibit the last step in gag

processing in which the viral capsid polyprotein is cleaved, thereby blocking the conversion of the polyprotein into the mature capsid protein Because these viral particles have a defective core, the virions released consist mainly of noninfectious particles. Alpha interferon is a currently available agent in this class. Two additional inhibitors under investigation are bevirimat and Vivecon.