Lymph nodes


Section
Question | Answer |
---|---|
Upper limb, lateral breast | Axillary |
Stomach | Celiac |
Duodenum jejunum | Superior mesenteric |
Sigmoid colon | Colic --> inferior mesenteric |
Rectum, anal canal above the pectinate line | Internal iliac |
Anal canal below the pectinate line | Superficial inguinal |
Testes | Superficial and deep plexuses --> para-aortic |
Scrotum | Superficial inguinal |
Thigh (superficial) | Superficial inguinal |
Lateral side of dorsum of the foot | Popliteal |
Right lymphatic duct | drains right arm and right half of the head |
Thoracic duct | drains everything else |
Question | Answer |
---|---|
Th1 | make INF-gamma and IL-2, inhibited by IL-10 (made by Th2 cells) |
Th2 | make IL-4, IL-5, IL-10, inhibited by INF-gamma (made by Th1 cells) |
What causes differentiation into the Th1 | IL-12 |
What causes differentiation into Th2 | IL-4 |
Th1 cells are humoral or cell-mediated | cell-mediated |
Th2 cells are humoral or cell-mediated | humoral |
What inhibits MHC II from binding antigen | lack of acidification in the lysosomes |
What does MHC I have that MHC II doesn't have | B2 microglobin |
Question | Answer |
---|---|
HLA-A3 | hemochromatosis |
HLA-B27 | Psoriasis, ankylosing spondilitis, inflammatory bowel disease, Reiter's syndrome |
HLA-B8 | Addisons disease, myasthenia gravis |
HLA-DR2 | Multiple sclerosis, hay fever, SLE, Goodpasture's |
HLA-DR3 | Diabetes mellitus type I |
HLA-DR4 | Rheumatoid arthritis, diabetes mellitus type I |
HLA-DR5 | Pernicious anemia --> B12 deficiency, Hashimoto's thyroiditis |
HLA-DR7 | Steroid-response nephrotic syndrome |
Question | Answer |
---|---|
NK cells mode of action | use perforin and granzymes to induce apoptosis in the infected cell |
How does endotoxin/lipopolysacchride cause it's response | Binds to endotoxin receptor CD14 on MACROPHAGES directly stimulating them |
What is the costimulatory signal | APC = B7 and Th cell = CD28 --> needed for the activation of T cell |
How are cytotoxic T cells activated | IL-2 from the Th cells |
What causes B cell switching | IL-4, IL-5, IL-6, CD40 ligand on Th cell |
How many antigens can one B cell make antibodies for | 1 |
Which portion of the antibody binds to the antigen | Fab |
Which portion of the antibody activates complement | Ch2 part of the heavy chain Fc (IgG and IgM only) |
Which part of the antibody detemines the isotype | Fc portion of the heavy chain |
Does the light chain contribute to the Fc portion | No, only the heavy chain does |
How does IgA exist when secreted | as a dimer |
Which antibody mediates the type I hypersensitivity reaction | IgE |
Ig idiotype | specific for a given antigen |
Ig isotype | Ig epitope common to single class of Ig |
Ig allotype | Ig epitope that differs among members of the same species |
What does an antigen need to be presented by MCH to T cells | peptide antigen (ie. polysaccharide capsule and LPS from gram - will not activate T cells) |
Question | Answer |
---|---|
IL-1 | Fever, osteoclast activating factor |
IL-2 | stimulates T cells |
IL-3 | stimulares Bone marrow |
IL-4 | stimulates IgE production |
IL-5 | stimulates IgA production, stimulates growth and development of eosinophils |
IL-8, LTB4, C5a | Neutrophil chemotactic |
What happens if a patient has a IL-12 deficiency | They can suffer from severe TB infections and you treat them with IFN-gamma |
How can you stain for monocyte, macrophages | CD14 - you will see them in PPD |
Since mature red blood cells are the only cells that do not express MHC class I what kills babesia and malaria | NK cells and they are stained with CD56 |
Which complement binds bacteria | C3b |
Which complement mediates anaphylaxis | C3a and C5a |
What happen if you are C1 esterase deficient | hereditary angioedema and you can't use ACE inhibitors in these patients |
Deficiency of C3 | increased susceptibility to type III hypersensitivity reactions and recurrent pyogenic sinus and respiratory tract infections |
Deficiency of C5-C8 | Neisseria bacteremia |
Deficiency of DAF | paroxysmal nocturnal hemoglobinuria |
What do inteferon-a and beta do | inhibit viral protein synthesis |
What does interferon-gamma do | increase MHC I and II expression and antigen presentation in all cells |
Stellate shaped granuloma | Cat-scratch fever (Bartonella henslae) |
What are patients with silicosis more at risk for | TB infections due to the inhibition of macrophages by the silica |
Question | Answer |
---|---|
Antihistone | Drug-induced lupus |
Anticentromere | Scleroderma (CREST) |
Anti-Scl-70 (anti-topoisomerase I) | Scleroderma (diffuse) |
Antimicrosomal | Hashimotos |
Antimitrocondrial | Primary biliary cirrhosis |
Anti-Jo-1 | Polymyositis, dermatomyositis |
Anti-Ro, Anti-La | Sjogren's syndrome |
Anti-U1 RNP | Mixed connective tissue disease |
Anti-smooth muscle | autoimmune hepatitis |
Question | Answer |
---|---|
Bruton's agammaglobulinemia | no germinal follicles (no maturation of B cells) - recurrent respiratory infections in a young boy (X-linked recessive) |
Hyper IgM-syndrom | No CD40 ligand on Helper T cells --> not able to switch Ig Class --> severe pyogenic infections |
Multiple Sclerosis | Type IV hypersensitivity ie. Th1 cells activate macrophages against self antigens --> demyelination |
Selective IgA deficiency | Most common immunodeficiency in the US --> increased susceptibility to Giardia Lamblia |
Wiskot-Aldrich | Thrombocytopenia, eczema, and increased IgE; X-linked disease; increased risk for non-hodgkin's lymphoma |
Syngeneic graft | between identical twins with the same HLAs |
Most important effector cells for MMR and other live viral vaccines | Cytotoxic T cells (CD8+ and CD3+) |
Question | Answer |
---|---|
Who causes damage to the lung during pneumonia | neutrophils - they come in and release cytokines that damage the area |
Digeorge syndrome | cardiac abnormalities, abnormal facies, thymic aplasia, cleft palate, hypocalcemia (tetany), and all from a problem on chromosome 22 (CATCH-22) |
Superantigens from S. aureus (TSST-1) and S. pyogenes | activate Th1 cells to produce a ton of IL-2 and INF-gamma; activate macrophages to produce a ton of TNF-a and IL-1 |
Question | Answer |
---|---|
Postvaccinal lymphadenitis characterized by multinucleated giant cells with eosinophilic inclusions | Measles |
What are the pathgnomonic Warthin-Finkeldey cells for and what are they made of | Measles, fused lymphocytes |
Pernicious anemia and Graves disease type of hypersensitivity | Type II noncytotoxic hypersensitivity |
What is the most important factor in getting rid of immune complexes | C3b |
Question | Answer |
---|---|
Vaccines to Pneumococcus and H. Influenza will only contain what if not paired with a peptide | IgM because the peptide is needed for the isotype switch |
What is the other name for DiGeorge syndrome | Velocardiofacial syndrome |
Patients with selective IgA deficiency have an increased risk for developing what | Atopy (they get higher IgE) |
People with severe AIDS will have which kinds of immunoglobins | IgM; they won't have the T cells needed for the switch |
What is the Arthus reaction | Swelling and inflammation following things such as a tetanus vaccine (Type III hypersensitivity - immune complex formation because you've seen it before) |
Reiter's syndrome | campylobacter, chlamydia, salmonella, shigella, yersinia infection |
Tertiary syphillus forms what type of reaction | granuloma mediated by Th1 and macrophages |
What orchestrates cell mediated immunity | Th1 cells |
It's TIME that I learned Wiskot-Aldrich syndrome | Thrombocytopenia, Infections, LOW IgM, and increased IgE (eczema) |
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